This is an excellent med school parasite overview - very long, cut and paste into Word to read, or print out.

 

Introduction to Parasitology

               

                In any field of study, it is important that the learner is presented with the basic terminology used as well as application and limitation of the different terms used. This will enable the reader an easier way of understanding matters the concerns a particular subject matter.

                The following text aims to acquaint the reader of the various terms and basic information in the field of medical parasitology.

 

TERMINOLOGY

                Parasitology is a branch of biology that deals with the phenomenon of dependence of one living organism to another. Clinical (or Medical) Parasitology primarily deals with animal parasites of man and their medical significance and importance in human communities.

                Parasites are organisms that depend onto another living creature, referred to as the host, for survival. Obligate parasites are those that cannot survive without the assistance of the host. This means that the parasite is “totally” dependent and unable to multiply if it is not in the body of a host. Some parasites, however, are able to adapt to a free-living or parasitic existence depending upon the condition. These organisms are called facultative parasites or opportunists. In nature, there are some free-living organisms that are parasitic to other creatures but not to humans. Man may ingest these organisms and they pass through the alimentary canal, excreted in the feces, alive or dead, in the unchanged state. These organisms are referred to as spurious parasites.

                Parasites, like other living creatures, undergo different stages of development before reaching full maturity. Each set of metamorphosis results to a distinct stage of development. Some parasites may need a particular kind of host for a particular stage of development. The transformation and survival of a certain stage of development may not occur if the organism is in the body of a “non-appropriate host.” This phenomenon is called “host specificity.”

                There are some parasites that do not inhabit only a single host throughout their lifetime. Some organisms, while undergoing development, inhabit a host different from the one where the adult forms are found. An intermediate host is the one that harbors the immature or larval forms of the parasite. Some parasites undergo both asexual and sexua| reproduction. In these organisms, the asexual process takes place in the body of the intermediate host. On the other hand, the mature or adult forms of the parasites are found in the body f the definitive or final host. This is also the host where the sexua| cycle of some organisms takes place.

                Some animals, domestic or wild, may serve as respiratory host to a parasite. These are referred to as reservoir hosts. Man, in this case, is only “incidentally” involved but not a “natural host.” Reservoir hosts are of epidemiologic importance in the spread of some infection since they have served as the “ready and constant” source of the infectious organisms to the community.

                Some parasites require passage through an intermediate host before the infective stage (i.e. the specific developmental form capable of causing infection to man) is developed. The infective stage may not be transferred directly from an intermediate to the definitive host. Instead, it may be passed to a transport host, whereby no development or transformation of the parasite takes place but infectivity is preserved. Some animals serve as transport (or parathenic) host. They are not essential in the life cycle of the parasite but may serve as another source of infection to man aside from the natural intermediate host of the organism.

 

Interrelationship of Organisms

 

                Different organisms exhibit various kinds of association with one another throughout their entire life. Close association of two organisms, whereby a “give-and-take” relationship exists is called symbiosis. If the relationship is “beneficial” to both associates, it is referred to as mutualism. If the parasite derives benefits without reciprocating and/or without causing injury to the host, the relationship is called commensalism.

                Some big animals attack, kill, and use smaller ones for food. In this form of existence, the bigger animal is referred to as predator while the smaller is called prey. There are animals that derive their nourishment from already dead ones either by devouring those that died of natural causes or taking the leftovers of the predators. These kind of animals subsisting in such manner are called scavengers.

 

The Process of Infection

                Parasites that live on the surface of the host’s body are called ectoparasites and their condition is referred to as infestation. Those parasites found inside the body of their host are referred to as endoparasites in which the condition is called infection.

                Prior to the development of an infection, a person must be in a situation considered “at risk” of acquiring it. Such risk situation is called exposure, which simply means that the organism is given the chance to enter the body of the individual. The process of introducing the organism into the body of the host (e.g. man) is called inoculation.

                Parasites that successfully enter the body of a person may establish a colony through reproduction. These organisms, inside the person’s body, may be recovered in body fluids like blood, urine, CSF, or tissues at that times that the organisms are still unable to produce signs and/or symptoms of the infection. The period of time from the entry of the organism until they may be recovered in body fluids, tissues, or excreta, without any manifestation yet, is referred to as the biologic incubation period (also called pre-patent period). Disease producing organisms, as may be expected, will be able to produce signs and/or symptoms of the infection later after inoculation. The period of time from the entry of the organism into the body of the host until the earliest sign and/or symptom of the infection appear is referred to as the clinical incubation period.

                Disease-producing organism (also called pathogen or pathogenic organism), in certain conditions may not be able to cause damage to the host and therefore unable to produce signs and/or symptoms of the infection. This condition is referred to as inapparent infection, and the person who harbors such pathogenic organism but without manifestation of the infection (i.e. the person is asymptomatic) is called a carrier. Other susceptible individuals, who later manifest the infection, may acquire the infection from carriers.

                Parasites have “specific” developmental forms with the ability to enter the human body to initiate an infection process. The developmental form of the parasite capable to doing so is called infective stage. On the other hand, the pathogenic stage is the developmental form may or may not be able to cause pathologic damage but is the only stage that can enter the body of the host. There are some parasites whose infective form, as well as their mature stages, can cause pathologic damage or disease to man. In certain species, the infective stage may also be the pathogenic form and vice versa.

                Some animals serve to transfer the infective stage of an organism from one source to another. The transfer may be from one person to another, from an animal to a human being, or from inanimate objects into a person. Commonly, the animals that transfer the organism or parasite are various kinds of insects. These animals that transfer the infective form may be referred to as vectors (also called transmitters). Vectors, which are “essential” or needed in the life cycle of the parasite, are called biologic vectors. The life cycle of some parasite will not be completed without the participation or involvement of a particular biologic vector. On the other hand, some vectors are not necessarily needed in the life cycle and they merely act as mechanical transmitters of the organism – these are called phoretic or mechanical vectors.

                An organism coming from the body of a person and transferred to another individual is undergoing horizontal transmission. Man acquires many parasites, pathogenic and commensal ones, through horizontal transmission. An unborn baby may be infected with a parasite that came from the mother via placental transfer and this process may also be called vertical transmission. This process is responsible for congenital infection.

                Most parasites that cause infection to man originated from animals thus, commonly referred to as zoonotic infections. A person may excrete the infective form of an organism and this stage of development may re-enter the person’s body in the process of autoinfection. Autoinfection may occur via “retrograde” migration of the infective form (retroinfection) or through the outside part of the body (external autoinfection). This process may lead to a severe type of infection in an individual without necessarily acquiring infective forms from another person or other sources. Infective stages coming from another source of the same species, e.g. human-to-human, is called heterofection. An already infected individual and has been re-infected with the same species of the parasite is suffering from a condition called superinfection. On the other hand, a person may be harboring more than one species of organism at the same time and this condition is called mixed infection.

                There are some individuals who may think they are infected with some “bizarre” parasite but in reality, no such parasite exists in their bodies. Psychiatrists referred to this situation as delusional parasitosis.

 

Sources of Parasite Infections

                An individual may acquire parasite infection from a variety of sources. The infective cyst of some protozoa such as Entamoeba histolytica, Giardia lamblia, etc. may be present in unclean foods or water (or drinks) contaminated with fecal matter that came from an infected person. The infective egg of some worms like Ascaris lumbricoides, Trichuris trichiura, etc. may also be present in food and water, aside from being deposited in the soil around human habitation. People, who will be eating such food or drink such water contaminated by soil containing the infective eggs, may easily acquire the infection with these organisms. Some individuals may ingest contaminated soil, accidentally or intentionally (geophagia), which may contain the infective forms of organisms such as Ascaris lumbricoides. Trichuris trichiura, Toxocara sp., Strongyloides stercoralis, hookworms, etc.

                Various animals that serve as food to humans, if infected and eaten raw or inadequately cooked may also be the source of infections. Echinostoma ilocanum, a kind of fluke, is acquired from certain species of snails. Parasites such as Capillaria philippinensis, Diphylobothrium latum, and Opistrochis viverrini are know to come from certain species of fish that man eats. Individuals who are fond of eating raw beef or pork have higher chances of acquiring infections with Taenia saginata and Taenia solium, respectively.

                Mosquitoes of the genus Anopheles serve as vectors for malaria and some filarial worms such as Wuchereria bancrofti and Brugia malayi. Insects like fleas, which may be present on domestic pets, are known source of infections with Diplydium caninum and Hymenolepis diminuta. sexua| contact with an infected individual is a known source of infection with Trichomonas vaginalis.

 

Portals of Entry

                The specific site in the human body where the parasites enter is referred to as portal of entry. Some species of organisms may not be able to effectively cause infection if they enter the wrong portals thus in most instances each species has its own entry point in the host’s body.

                Internal parasites that inhabit the intestinal tract, expectedly, enter through the mouth. Examples of species that make use of the mouth as portal of entry include Ascaris lumbricoides, Trichuris trichiura, Taenia species, Enterobius vermicularis, Entamoeba histolytica, Giardia lamblia, Trichinella spiralis, Capillaria philippinensis, etc.

                Some parasites such as hookworms (Necator americanus, Ancylostoma duodenale) threadworm (Strongyloides stercoralis), and blood flukes (e.g. Schistosoma japonicum) gain access to the body via the skin.

                Parasites causing malaria, the filarial worms, leishmania, and the trypanosomes are introduced into the human body percutaneously by “blood-sucking” insects that serve as vectors or transmitters.

                The infective eggs of pinworm (Enterobius vermicularis), aside from using the mouth as portal of entry, may also enter through the nose through inhalation.

                The infective larvae of Strongyloides stercoralis and species of Ancylostoma may cause infection among babies of infected mothers through the milk (i.e. transmammary transfer) Trichomonas vaginalis enters the body of an individual through the genital organs during “unprotected” sexua| intercourse.

 

Pathogenesis of Parasitic Infections

                Each pathogenic parasite utilizes different mechanisms (pathogenesis) of causing disease among humans or other animals. These mechanisms maybe one or a combination of the following: 1] trauma or physical damage, 2] lytic (liquefaction) necrosis, 3] stimulation of host’s tissue reaction (cellular or immunologic), and 4] toxic and/or allergic response.

                Ectoparasites, such as Sarcoptes scabiei – causing scabies, produce intense pruritus (itchiness) due to local irritation of the person’s skin. The infective larvae of blood flukes, hookworms, and threadworm cause local damage as they enter the host’s skin. The adult worm of Ascaris lumbricoides may cause obstruction o the appendix, common bile duct, gall bladder, and the intestine. Entamoeba histolytica and Balantidium are examples of species that secrete proteolytic enzymes that can produce lysis (liquefaction) of the host’s tissues. The lytic process may occur in any organ that the parasite is able to invade such as the brain, lungs, liver and other organs. Obligate intracellular parasites, such as species causing malaria, can produce lysis of red blood cells that they infect.

                Eggs of schistosomes (i.e. Schistosoma japonicum), once in contact with the tissues of organs such as the liver, stimulate the tissues that eventually lead to production of fibrosis or scar tissue. Adults of filarial worms (e.g. Wuchereria bancrofti) cause stimulation and proliferation of the cells of the lymphatic channels reaching to the obstruction in the flow of lymph fluid and later on producing lymphedema that manifests with swelling of the affected part of the body such as the lower extremities.

                Leishmania donovani stimulates the bone marrow to produce plenty of phagocytes but reducing the ability to produce red cells at the same time. Thus, persons who suffer from leishmaniasis manifests with anemia with increase number of some of the white blood cells. Host tissue reaction to Entamoeba histolytica infection may result to granuloma (consists of fibrous tissues), which may stimulate a tumor that maybe mistaken for a cancer.

                Some species of parasites, while inhabiting the host’s body, excrete waste or toxic substances, which may be absorbed and later produce systemic toxic effects. Adult worms of the intestinal fluke, Fasciolopsis buski, that inhabit the duodenum can produce obstruction and also secrete metabolic wastes, which when absorbed may lead toxicity to the host. The larvae of Ascaris lumbricoides pass through the lungs sometime in its life cycle. This larvae can stimulate the immune system of the host and subsequent infections may lead to the development of allergic responses similar to bronchial asthma or urticaria. The cyst of a tapeworm, Echinococcus granulosus, aside from its ability to cause mechanical pressure on surrounding tissues where it is located, may spontaneously rupture resulting to the release of its fluid content. The fluid contained in this cyst is a very potent anaphylatoxin, which when systemically absorbed may end with shock.

 

Diagnosis of Parasitic Infections

                The medical technologist plays a very important role in the diagnosis of infections with parasites. Diagnosis of parasitic infection is, oftentimes, based on identification of organism in specimen submitted to the laboratory. The technologist, therefore, should be very accurate in the identification of the organisms.

                Different diagnostic tests in Parasitology may be classified as either “direct” or “indirect”. The direct approach is to demonstrate the organisms where they can be recovered. Patients who are infected with Ascaris lumbricoides, Trichuris trichiura, Capillaria philippinensis, Taenia saginata, Taenia solium, Schistosoma japonicum, and many other parasites are easily diagnosed by finding the eggs of the organism in the patient’s feces. Larval forms of threadworm and some species of hookworm may also be recovered in fecal specimen. Patients infected with Trichinella spiralis are diagnosed through recovery of the larval stage in biopsy material of muscle tissues. Malaria, filariasis, trypanosomiasis, and similar diseases are usually diagnosed by finding the causative parasites in blood films. Not infrequently, people who are infected with tapeworms may evacuate segments of the worms in their feces. The segments may be examined and identified with or without stain. Trichomonas vaginalis infection is easily diagnosed by finding the trophozoites of the parasite in the patient’s urine. Examination of CSF will also be of great help in the diagnosis of Naegleria fowleri and Acanthamoeba culbertsoni infections.

                In quite a number of instances, recovery of parasites in body fluids may not be that easy or impractical. Also, there are some conditions whereby the location of the organism is quite inaccessible or trying to get them, such as in biopsy, may entail more damages that benefits. In such situations, the indirect approach may be resorted to instead. These diagnostic procedures, however, are not readily available, more likely to be less accurate, and are of limited application.

                If the organism is able to stimulate the immune system of the host, antibodies may be detected in the blood such as in the case of schistosomiasis, where the patient’s blood will contain antibodies against the eggs of the parasite. This is the basis of the so-called Circumoval Precipitin Test (COPT), which may be used in the diagnosis of schistosomiasis. Serologic tests are also available, although expensive, for the diagnosis of human infections with Echinococcus granulosus, Trichinella spiralis, Leishmania donovani, etc.

                A certain laboratory technique called Xenodiagnosis may be used to diagnose infection with some parasites such as Trypanosoma cruzi. In this method, a laboratory-bred insect, the one that serves as vector to the organisms, is allowed to feed on the blood of individuals suspected to be infected with the parasite. The feces of the insect is then examined for the presence of the organism after sometime.

                Some parasites may also be grown in artificial culture media such as rice-starch agar for Entamoeba histolytica, as well as other protozoa parasites. Coproculture (i.e. stool or soil culture) will enable the recovery of the larval forms of hookworms and threadworms. Animals such as rabbits, hamsters, and monkeys may also be used to grow parasites in the laboratory to produce more parasites and therefore, make the diagnosis easier, more accurate, and to have high yield of positive result.

 

Treatment of Parasitic Infections

                Infections with parasites may be treated with chemotherapy (i.e. the use of commercially available drugs) or through surgical intervention or a combination of the both. Hydatid disease due to the larvae of Echinococcus granulosus is treated by surgical removal of the cyst. Cysticorcus larvae of Taenia solium located in the eye of a patient are also removed through surgical procedure.

                Infections with organisms such as Entamoeba histolytica, Ascaris lumbricoides, Trichuris trichiura, Giardia lamblia, Trichomonas vaginalis, etc. are effectively treated through the administration of specific drug for the particular organism.

                Vaccination against parasite infection is not yet perfect at the present time. Researches are still ongoing for the development of vaccine that may effectively protect humans from acquiring infection with some parasites. At the present time, vaccines are being developed and tested for organisms such as Plasmodium species (causing malaria), Schistosoma japonicum, Entamoeba histolytica, etc.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Protozoology

               

                Overview

               

                All living organisms may be classified according to either: a] Protozoa or b] Metazoa. Organisms that belong to Protozoa are oftentimes described as unicellular while Metazoa will include those that have numerous cells, tissues, and organs. Thus, Metazoa organisms have organ systems that perform the complex processes of life. Protozoa, although looking very simple, is capable of the various processes of life. Protozoa is a subkingdom of Animalia.

 

Stages of development of Parasites

                Parasites under Protozoa, generally, undergo different stages of development throughout their life. In most instances, these developmental forms will include a] trophozoite and b] cyst.

                The trophozoite (also called trophic form) is the vegetative or the motile stage of the organism. Among the pathogenic species, it is also the stage capable of producing pathology hence referred to as the pathogenic stage. Organelles of locomotion, generally, are present in the trophic forms. In general, different group of protozoa has their own type of locomotion organelles. The pseudopodia are found among members of Sarcodina, flagella in Mastigophora, and cilia in Ciliophora.

                Trophozoite forms are easily destroyed by adverse condition in the environment such as strong chemicals, urine, changes in temperature, presence of other organisms, and other physical, chemical, and biologic factors.

                The cyst on the other hand, is also considered the dormant or the non-motile form of the parasite. At times, the cyst may also be referred to as the “infective stage”. This is due to the fact that most cyst forms are, relatively, more resistant than the trophozoite forms. Cysts are likely to be found in formed stool samples, although, they may also be recovered in water fecal specimen. Being more resistant than the trophozoite, the cyst may easily be preserved using chemical agents such as 5 – 10% formalin solutions. The cyst may also be maintained, for a definite period of time, in the laboratory or longer in refrigerator temperature. In contrast, trophozoites are easily destroyed and quite fragile as compared to the cyst. Thus, stool samples suspected to contain trophozoites must be examined within 30 minutes after collection of such sample, lest the organism will disintegrate and making identification rather difficult if not impossible. If the examination of specimen suspected to contain trophozoites is to be delayed or cannot be done at once, preservatives may be used but the parasite becomes immotile. There are times that the motility of the organism in the living state is quite helpful in the identification of the parasite because there are parasites whose motility is quite characteristic. The most widely used preservative for trophozoites is polyvinyl alcohol (PVA). A long time ago, merthiolate-formaldehyde solution was being used to preserve trophozoite forms but because of the harmful effects of some of its ingredients its use was halted.

                Stoll sample preserved with PVA, whether it contains cyst or trophozoite, may be kept for quite a long time. The may also be smeared later and stained permanent stains and be kept as permanent record or for teaching purposes, or even in research. However, about 5 years or a little more, the quality if stain color tends to be lesser and lesser through passage of time.

 

Structures and Organelles (Protozoa)

1.       Nucleus – has the chromosomes, which is essential for life, reproduction, and the transmission of the composition of the organism. Inside the nucleus, an aggregate mass of granules is present and referred to as the karyosome (also called nucleolus or endosome). The nucleus may either be vesicular or compact. Vesicular nucleus has the karyosome suspended in a large amount of nucleoplasm while a compact nucleus has a very large granular chromatin filled karyosome and a very scanty nucleoplasm. Vesicular nucleus may be provided with chromatin particles arranged on an achromatic network or the chromatin granules may line the inner part of the nuclear membrane.

Compact type of nucleus does not have space anymore between the nuclear membrane and the karyosome. Organisms whereby vesicular nucleus is observed include Entamoeba histolytica, Entamoeba coli, Endolimax nana, etc. while compact type of nucleus is seen in Balantidium coli.

2.       Cytoplasm – is the interior of the cell where the different organelles are found. The cytoplasm has, more or less, two distinct portions, namely a] endoplasm – the dense granular part surrounding the nucleus and b] ectoplasm – the less granular and more homogenous part that envelopes the endoplasm. Stored food, mitochondria, Golgi apparatus, microsomes, and endoplasmic reticulum are located in the endoplasm. The ectoplasm may include functions such as a] locomotion, b] procurement of foods, c] respiration, d] excretion, and e] protection of the organism.

3.       Plasma membrane – is the semi-permeable, limiting boundary of the trophozoite stage. It controls the intake and output of nutrients, secretion and excretion, and maintains the normal concentration of the plasma substance.

4.       Cyst wall – is the relatively tough membrane, secreted by the ectoplasm, which envelopes and protects the cyst form.

5.       Contractile vacuoles – are pulsating vacuoles of various sizes seen in the endoplasm of some organisms like Balantidium coli. These vacuoles are presumed to act as “osmoregulators”.

6.       Food inclusion bodies – are structures present in the endoplasm of some protozoa, which serve as foods to the parasite. Synthesis of foods takes place in the endoplasm and may be stored in the form of a] chromatoidal bodies and/or b] glycogen mass. Chromatoidal bodies consist of proteins while glycogen masses are composed of carbohydrates. It is more likely that these inclusion bodies are observed in the cyst form of the parasite.

7.       Cytostome and cytopyge – some species of protozoa have a specialized “cell mouth” called cytostome and/or cell anus, which is referred to as “cytopyge”. Ciliates commonly have these structures and are mostly found in the trophozoite form.

8.       Locomotion organelles – in some species, like the amoeba, the plasma membrane has no constant shape. Its form changes by means of extension and retraction of temporary, finger-like structures called pseudopodia. The active protrusion and retraction of the pseudopodia enables the amoeba trophozoite to move from one place to another. Also, they may aid the organism to obtain particles of food from the environment. Member species of Zoomastigophora, mostly in the trophic forms, possess hair-like projections of the cytoplasm called flagella. The flagella arise from kinetoplast (consisting of parabasal bodies and blepharoplast) within the cytoplasm and constant whipping movement enables the parasite move. A small portion of the flagellum, within the cell wall, that is connected to the kinetoplast is called “axoneme”. In Ciliophora, there are numerous short, threadlike structures called cilia. The cilia arise from the so-called “basal granules” within the ectoplasm and are distributed throughout the entire body surface of the parasite.

 

Encystation and Excystation

                Protozoa parasites transform from trophozoite to cyst, and vice versa, during their existence. Encystation is the formation of cyst from trophozoite form. This process occurs when the organism is subjected to conditions, which are unsuitable for continued existence in the trophic forms. Conditions believed to favor encystations include:

                                1] deficiency or overabundance of foods in the environment,

                                2] accumulation of excessive waste products of metabolism produced by the parasite or other

    associated organisms such as bacteria around

3] significant changes in the pH of the surrounding medium,

4] loss of water or dessication of the medium,

5] diminished or too much supply of the oxygen, and

6] overpopulation.

                In most situations, encystations will involve two or more of these factors. In the process, the ectoplasm secretes a thick cyst wall, which will enable the organism to be more resistant to the adverse changes in the environment that the trophozoite may be unable to adapt to.

                There are two types of encystations, namely: a] protective, and b] reproductive. In the protective type, the parasite undergoes encystation without significant changes in the morphology. It is aimed to protect the organism. This type of encystations happens, for example, when the parasite is about to be excreted and transferred into a new host. Balantidium coli is an example of parasite that undergoes this type of encystations. On the other hand, reproductive type of encystations is characterized with multiplication of the nucleus in the cyst form thus resulting numerous daughter organisms when the parasite later transforms into the trophozoite form. Organisms that undergo the reproductive type of encystations include Entamoeba histolytica, Entamoeba coli, Giardia lamblia, etc.

                Cyst stage of parasite undergoes excystation to produce trophozoites. The process is, probably, favored by the following factors:

                                1] osmotic changes in the surrounding medium

                                2] enzymatic action of the enclosed organism on the inner surface of the cyst wall

                                3] favorable pH of the environment

                                4] enzymatic action of they tissue s to the parasite

                The last two items are affecting most of the protozoa, which are parasitic t man (e.g. the amoeba). It is noteworthy that the two processes do not necessarily happen outside of the outside of the body of the host that supports the existence of the parasite.

 

 

PARASITIC AMOEBA

                                Entamoeba histolytica                                                      Entamoeba coli

                                Entamoeba hartmanni                                                      Endolimax nana

                                Entamoeba gingivalis                                                       Iodamoeba buetschlii

 

General Characteristics

                Species of amoeba that commonly infect man are classified under Rhizopodea. Generally, trophozoite forms of amoeba parasites have pseudopodia as the organelle of locomotion. In the aforementioned list, only Entamoeba histolytica is pathogenic to man. It causes the disease “amoebiasis”. The others, in the above list, are “commensal parasites” of man. Entamoeba gingivalis exists in the trophozoite form only and inhabits the mouth while the others undergo cyst and trophozoite development and are inhabit the lumen of the large intestine, specifically the cecum. The presence of these commensals in a person’s stool serves as an index of fecal contamination of the food and/or drinks of that individual thus, the possibility for that person to acquire any “fecal-borne” infections.

 

Entamoeba histolytica

                This parasite has cosmopolitan distribution (worldwide) but prevalence is higher among countries with tropical and/or subtropical climate than the temperate regions. Incidence in cold countries, however, may also be high if the sanitary condition is poor. The parasite is a “lumen-dweller” (because it inhabits the cecum). The disease it causes is called “amoebasis”.

 

LIFE CYCLE

                Infection is acquired through ingestion of mature (quadrinucleated), viable cyst that contaminates foods and/or drinks. Ingested cyst passes through the stomach and later into the small intestine. The small intestine contains a very acidic medium. When the environment inside the intestine becomes neutral and alkaline, i.e. at the later part of the small intestine, excystation begins. The parasite becomes very active, goes out of the cyst, and multiplies. Each cyst produces 4 daughter organisms called “metacystic trophozoites,” which in turn multiply through binary fission continuously resulting to a colony. As the content of the colon of the colon moves towards the rectum, water is absorbed thus making fecal matter becomes more solid. The parasite, at this point, undergoes encystation that happens as the fecal matter passes through the length of the large intestine. As encystation takes place, the parasites store foods in their cytoplasm. A young cyst, one with a single nucleus, ripens by undergoing two successive mitotic divisions resulting to a cyst with 4 nuclei (mature). If the passage of fecal matter in the colon is fast, as in diarrhea, the organism does not have enough time to undergo encystations and thus trophozoites will be present in the feces. The trophozoites that go with watery feces during defecation eventually die and disintegrate since encystation does not occur outside of the body. On the other hand, the evacuated cyst now becomes the infective stage to next host for as long as it remains viable. Mature cysts can reach foods and/or drinks through fingers of food-handlers, kitchen utensils, fecal contamination of foods and or water, or use of night soils (human feces as fertilizers) in vegetable gardens. Insects such as flies and other animals like rats may serve as phoretic vectors by meant of transferring the cysts mechanically to foods or drinks.

 

Pathogenesis

                The biologic incubation period of amoebiasis may vary from 2-5 days (sometimes longer) and the clinical incubation period maybe as short as 4 days but maybe as long as 1 year. Some infected individuals may remain asymptomatic for many years, which are called “carriers”. Since the stool of amoeba carriers contains the infective cyst, they are also called “cyst passers”. In general, the expected incubation period is 1-4 months.

                Trophozoites do not colonize the small intestine. Oftentimes, the colony is located in the cecum. The slower or more turbulent flow of contents in the cecum as compared to other parts of the intestinal tract favors colonization.

                The trophozoites, which the aid of their pseudopodia, can move actively from one place to another. Trophozoites, aside from being very active, elaborate lytic enzymes that can lyze tissues (hence the name histolytica-lysis of cells). The trophozoites, with its lytic enzymes and activity of pseudopodia, cause lysis of the intestinal wall but the muscular layer is relatively resistant to such digestion resulting to sideward extension of intestinal ulcers created by the organisms. The typical lesion of amoebic ulcer in the GIT is described as “flask-shaped”, which has a narrow apex or entrance point and a wide base.

                Trophozoites also irritate the intestinal wall resulting to increase peristalsis and secretion of large amounts of mucus, which leads to production of “mucoid-watery” stools (also referred to as “mucoid-watery diarrhea”).

                Trophozoites, during the course of migration, may erode blood vessels resulting to the oozing of blood into  the feces thus amoebiasis may also manifest with “bloody-mucoid” stools. Therefore, the presence of blood into the feces of patients suffering from amoebiasis indicates that there is tissue invasion already.

                Occasionally, trophozoite forms in the intestinal tract may stimulate the growth of fibrous tissues resulting to formation of “granuloma”, which is referred to as “amoeboma”. This lesion may be mistaken for a tumor or malignant growth.

                In some instances, the trophozoites are overtly active and thus, they are able to pass through the walls of the intestinal tract allowing them to gain access to other organs resulting to the so-called “extra-intestinal amoebiasis”. From the cecum, the trphozoites can reach distant sites via lymphatics, blood vessels (hematogenous route), and through direct extension. The ability of the organisms to spread can lead to the development of amoebic lesion in the liver, brain, lungs, skin, and anywhere else in the body of the patient.

                The liver, among all other organs, is the most common site of extra-intestinal amoebiasis. The trophozoites, able to pass through the intestinal walls, enter the mesenteric vessels, are carried into the portal circulation, and lodged into the liver tissues resulting to an abscess, which is commonly described as having “anchovy-sauce like” appearance. The abscess material (exudates) contains trophozoites, pus cells, and digested liver cells. Encystation does not occur in the tissue and thus cysts are not expected to be present in the exudate.

                The abscess in the liver may create a sinus into the overlying skin of the abdomen, which may result to the formation of a skin lesion termed as “amoeba cutis”. This condition may also occur if the trophozoites from the recto-sigmoid colon reach the perianal skin. Amoeba cutis is characterized with edema, necrosis or gangrene of the skin, and may be transmitted sexually to result to a lesion in the penis in case of anal sex practices.

                The abscess in the liver may reach the lungs through direct extension via the diaphragm. Amoebic lung abscess produces the typical “liver-colored sputum”. The brain, although uncommon, may also be invaded by the trophozoites.

 

Clinical Manifestations

                In most cases, the onset of symptoms is gradual. There will be episodes of diarrhea, mucoid-watery with or without blood, and abdominal cramps. Changes in appetite or loss of weight may also occur. If there is already amoebic colitis, it may manifest with on and off diarrhea that may be mucoid with or without blood in character. The severity of signs and symptoms depends on the extent and magnitude of the lesion.

                Some individuals remain asymptomatic for a long time. Pain at the right lower quadrant of the abdomen may also be present, which may be mistaken as acute appendicitis.

                Patients suffering from amoebic lung abscess may manifest with fever, pain at the right lower quadrant of the abdomen, and leukocytosis. There may also be difficulty of breathing due to pressure exerted by the abscess in the liver to the diaphragm.

                Patients manifesting the infection in less than a month are labeled as “acute” while “chronic” cases will have on and off appearance of signs and symptoms for more than one month. Chronic cases may manifest with bouts of diarrhea alternating with constipation.

                The stools are, oftentimes, odorless and with very\(or none at all) pus cells. Red cells may be seen even in the absence of gross blood in the fecal sample. Usually, macrophages will be seen in watery stool samples with trophozoite forms.

 

Laboratory Diagnosis

                Diagnosis is made through demonstration of the organisms in stool smears. Direst fecal smear examination will allow recovery of cysts, trophozoites, pre-cysts, and/or metacystic trophozoites. In general practice, the cysts and trophozoites are the ones given importance in the identification of the organisms. It should be noted, however, that trophozoites predominate in watery or liquid stool samples. Cysts, on the other hand, are likely to be abundant in semi-formed or formed fecal samples. The portion of the feces with mucus and/or blood should be preferred in making the smear as it usually contains plenty of the organisms. If the stool sample is suspected to contain trophic forms, examination should not be delayed for more than 30 minutes from the time the evacuation since the trophic forms disintegrate easily making identification difficult if not impossible. However, the trophozoites may be preserved with the addition of PVA to the fecal sample but their motility is lost.

                Formed or semi-formed stools may contain very few numbers of cysts. Such specimen may be subjected to a concentration technique to produce high yield of positive results. Formalin-ether and Zinc sulfate methods are the commonly employed procedures for concentrating the cysts in the fecal sample.

                Before a negative result is reported, three fecal films made from samples taken from the different parts of the submitted specimen should be thoroughly examined.

                Stool specimens that are likely to contain cysts may be preserved with 5-10% formalin solution. PVA solution may be used to preserve cyst and trophozoite forms. Other preservative solutions that may be used to preserve both cyst and trophozoite stages include merthiolate-formaldehyde (MIF) and sodium acetic acid – formaldehyde reagents. One part of the stool is added to 4 parts of stool sample to ensure preservation. Preserved fecal specimens may also be stained later.

                Wet fecal smears that contain cysts may be added with dilute iodine solution (Lugol’s iodine) for better visualization but the examination should not be more than 20 minutes because the organisms become overstained thereafter. Permanent stains, such as Iron-hematoxylin, may also be used in specimen that contains cysts and/or trophozoites. Stained slides may be kept for a long period of time for future purposes.

 

Morphologic Characteristics

 

Trophozoite

 

1.       Measures 10 – 60 micrometers in diameter

2.       Shape is irregular due to its activity. Freshly evacuated specimens exhibit directional and progressive motility due to active and progressive protrusion of long and finger-like pseudopodia.

3.       Single, spherical, vesicular nucleus, which in permanent stained specimen will show the bull’s eye karyosome (diagnostic of the species) with fine and regularly distribute chromatin granules at the inner part of the thin nuclear membrane.

4.       Cytoplasm may have ingested red blood cells (diagnostic characteristic of this stage of development) and with food vacuoles.

 

Cyst

 

1.       Spherical or oval, 10 – 20 micrometers in diameter

2.       Refractile cell wall

3.       Nuclei, if unstained, are not discernible. Permanent-stained specimen will show 1 – 4 nuclei with bull’s eye karyosome and chromatin granules with the same appearance as that in the trophozoite.

4.       Cigar-shaped or with rounded ends chromatoidal bodies in the cytoplasm (diagnostic of this stage of development). Young cysts may also have mass of glycogen that is pinkish in color with Lugol’s iodine.

 

Culture

                Entamoeba histolytica, as well as other amoeba, may be grown in artificial culture media such as Diamond’s medium, Boeck and Drbohlav’s Locke Egg Serum (LES) and Triple N medium. However, culture methods are not routinely employed in the diagnosis because of unavailability, tedious process, and cost of reagents and materials. Culture methods are oftentimes of great value for research and teaching purposes.

 

Serologic Methods of Diagnosis

                Seroimmunologic tests, although very promising, are also not used in the diagnosis because of unavailability and costs of materials and reagents. However, some of the common tests include Gel Diffusion Precipitin test (GDP), Latex agglutination test (LA), indirect Hemagglutination test (IHA), countercurrent Immunoelectrophoresis, and Enzyme-Linked Immunosorbent Assay (ELISA).

 

Drug for Treatment – Metronidazole

 

Prevention and Control Of Amoebiasis

 

1.       Provision of adequate, clean, and safe drinking water.

2.       Proper disposal of human wastes with the use of sanitary toilets.

3.       Control of insects such as flies, conckroaches, etc., which may serve as phoretic vectors.

4.       Prevent and educate farmers and agriculturists in the use of human excreta as “nigh soils” in vegetable gardens and farms.

5.       Regular screening of food-handlers, as well as prompt and adequate treatment of infected individuals

6.       General public education.

 

Entamoeba coli

               

                Entamoeba coli is a commensal parasite that inhabits the cecum of man and it’s distributed worldwide. It is more prevalent in warm than old climates. Life history is similar to that of Entamoeba histolytica. Its presence in human feces indicates that there has been fecal contamination of his foods and/or drinks thus placing the individual into the risk of acquiring any illness that is “fecal-borne” in nature. Infection is acquired through ingestion of mature, viable cyst present in unclean food and/or drinks. Household insects and animals, like rodents and flies, may serve as mechanical vectors for this parasite, just like in other amoeba parasites.

 

 

 

 

 

 

Morphologic Features

               

Trophozoite

 

1.       15 – 50 micrometers in size with irregular shape due to activity of pseudopodia, which are short and blunt.

2.       Motility is described as sluggish and non-directional

3.       The single nucleus, when stained, has a relatively large karyosome and usually located near a portion of the nuclear membrane (eccentric location)

4.       Dirty appearance of the cytoplasm due to plenty of vacuoles that contain ingested food particles as well as bacteria.

 

Cyst

1.       Spherical and 10 – 31 micrometers in diameter.

2.       1 – 8 prominent nuclei even unstained. The nucleus, with stain, appears the same as that in the trophozoite.

3.       Young cyst may have glycogen mass that stains pink with Lugol’s solution. Chromatoidal bodies, if present, have splintered or jagged ends resulting to the so-called “whisk-broom chromatoidals”.

4.       Dirty-looking cytoplasm due to ingested bacteria.

5.       Cell wall is relatively thicker and less refractile than that of Entamoeba histolytica.

 

Laboratory Diagnosis

 

1.       Demonstration of cyst and/or trophozoite in fecal smears. DFS may be examined with or without stain.

2.       To increase yield of positive result, concentration techniques such as those employed in the diagnosis of E. histolytica may be used.

3.       Culture methods – similar in E. histolytica

 

Treatment

                No specific drug is needed to treat the infection (if t is a commensal). The infection is taken cared of if the individual will practice utmost care in the foods and drinks he eats as well as personal hygiene.

 

Prevention and Control

                Devising a program of control and prevention intended for E. histolytica infection will also eradicate the presence of E. coli as well as other fecal-borne organisms.

 

Entamoeba hartmanni

 

                Entamoeba hartmanni is a commensal of man that used to be thought of as capable of causing amoebiasis. During the old times, it was thought that E. histolytica cyst, which measures less than 10 micrometers are unable to cause disease while those that are greater than 10 micrometers are the ones capable of causing amoebiasis, hence the label “small race” and “large race” – E. histolytica. At present times, the so-called “large race” refers to Entamoeba histolytica and “small race” was given another name – Entamoeba hartmanni. This parasite is widely distributed but more cases are found in tropical and subtropical countries of the world.

                Incidence of infection is higher in communities with high incidence of Entamoeba coli infection. Humans acquire the infection through ingestion of foods and drinks that contain mature, viable cysts. The life cycle is the same with that of Entamoeba histolytica. Infection with E. hartmanni does not require use of specific drug for treatment since it is classified as a commensal. The clinical importance as well as prevention and control of infection are the same with that of Entamoeba coli.

 

Morphologic Features

 

Trophozoite

 

1.       Irregular shape, 4 – 12 micrometers in diameter

2.       Single vesicular nucleus with coarse chromatin granules lining the inner part of the membrane and a fairly large central karyosome in stained specimens.

3.       Cytoplasm does not contain ingested red cells but only vacuoles with food particles or bacteria.

4.       Motility in the living state is sluggish and slightly directional.

 

Cyst

 

1.       Spherical or oval in shape, 5 – 10 micrometers in diameter

2.       1 – 4 nuclei with features the same as those seen in trophozoite form

3.       The cytoplasm is coarse and may contain glycogen mass. Chromatoidal bodies, if present, are described as having “rice-grain” appearance (diagnostic).

 

Endolimax nana

 

                This parasite is a harmless commensal that inhabits the cecum of man. It has a cosmopolitan distribution but more prevalent in places or communities where Entamoeba coli is prevalent or present.

                Life cycle, clinical aspects, method of diagnosis, and prevention and control of infection with this parasite are the same as those in Entamoeba coli.

 

Morphologic Features

 

Trophozoite

 

1.       Uninucleated measuring 6 -15 micrometers with short and blunt pseudopodia

2.       Living specimens, in fresh-evacuated feces, show “slug-like” motility.

3.       Stained organisms will show clearly the nucleus with large, irregular and eccentric karyosome with a very thin nuclear membrane devoid of chromatin granules.

 

Cyst

 

1.       Spherical or oval, 5 – 10 micrometers in diameter

2.       1 – 4 nuclei, which are refractile due to large karyosome. In stained specimen, two nuclei maybe quite adjacent to one another and may give the so-called “cross-eye” appearance due o the positioning of the karyosome. At times, the karyosome may be detached and results to the so-called “punched-out nucleus”.

3.       Chromatoidal bodies, if present and stained, are described as “comma-shaped”

4.       Fresh-evacuated specimen, oftentimes, described with “ground-glass” cytoplasm because it is quite homogenous and smooth without noticeable inclusion bodies.

 

Iodamoeba buetschlii

 

                Iodamoeba buetschlii is also a harmless commensal inhabitant of the human cecum. This parasite is more prevalent in warm climates than cold countries. The infection is acquired through the oral route in similar ways as those of the earlier mentioned parasites. When present in the feces, it may be mistaken for other parasites able to cause disease among humans. It may be demonstrated in stained and/or unstained fecal specimens. Concentration methods may also be employed to increase the yield of positive result. Although it has a cosmopolitan distribution, it is much less common than E. coli and E. nana in occurrence.

 

Morphologic Features

 

Trophozoite

 

1.       Spherical or oval, but may also be irregular in shape and measures 6 – 15 micrometers in diameter

2.       The single nucleus in unstained and fresh specimen is not quite prominent. Stained nucleus will show a large and central karyosome with the chromatin granules surrounding it instead of being in the nuclear membrane hence the description “perikaryosomal” chromatin granules.

3.       Cytoplasm, oftentimes, has a large pinkish glycogen mass that is about ½ or 1/3 of the size of the organism, which when stained with Lugol’s iodine casts a “mahogany-brown” color.

 

Cyst

 

1.       Oftentimes with a single nucleus, characteristics of which is the same as that in the trophozoite form.

2.       6 – 15 micrometers in diameter, spherical or oval in shape.

3.       Cytoplasm has large, more than ½ or about 2/3^rd of the size of the organism, glycogen mass that stains deep mahogany brown with Lugol’s iodine (hence the name Iodamoeba). Due to its great affinity with iodine, it is also called “iodine cyst of Wenyoun”.

 

Entamoeba gingivalis

 

                Entamoeba gingivalis is a commensal that exists in the trophozoite form only. It inhabits the oral cavity of man and its presence is favored by poor oral hygiene. Morphologically, it is similar with the trophic forms of E. histolytica and E. coli. The incidence of infection in unhygienic mouths ranges from 71 – 96%. It is primarily recovered from pyorrhea pockets between the teeth and gums and also in the tonsilar crypts. Some observers reported that this organism is able to multiply in the bronchial mucus and may appear in the sputum. In case like this, the organism may be mistaken as Entamoeba histolytica from abscess in the lungs.

                It was believed that it is transmitted through “droplet spray” from the mouth of infected persons to another during close contact such as kissing or from use of drinking glasses or utensils contaminated with the saliva of infected individuals.

                The living trophozoite measures 5 – 15 micrometers with pseudopodia, which may be lobose or short and blunt. Red blood cells are very rarely seen in its cytoplasm. Most frequently, however, the organism ingests “fragments of leukocytes”. Nuclear fragments from white blood cells are usually demonstrated in the cytoplasm of stained specimens, which serves to facilitate identification of this parasite. Compared to other amoeba, it is only Entamoeba gingivalis that has the ability to ingest white blood cells and/or fragments of its nucleus.

                Although the organism is non-pathogenic, it is frequently recovered from the mouths of people suffering from pyorrhea alveolaris. Some researchers tried to find association between this organism and the development of oral disease but failed.

                In the past, amoeba-like organisms were found in cervical smears of women using contraceptive devices. They were identified as Entamoeba gingivalis. This amoeba in the mouth is usually found associated with a non-pathogenic flagellate, Trichomonas tenax, that inhabits the oral cavity, some oral fusiform bacteria, and oral moniliasis (caused by Candida albicans). In the female genital organs, E. gingivalis is oftentimes associated with Actinomyces infection.

                The organism multiplies through binary fission and can be grown in standard culture media used for growing other amoeba parasites.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

FREE-LIVING PATHOGENIC AMOEBA

                                Naegleria fowleri                                                Acanthamoeba castellani

                                Acanthamoeba culbertsoni                             Acanthamoeba astronyxis

                                Acanthamoeba polyphaga

 

                These species are classified as “free-living amoeba”, but there were instances that they caused disease among humans. Thus, it is more appropriate to refer to these species as “opportunists”. These parasites exist in the environment primarily in fresh, brackish and salt water, moist soil, and decaying plants. Species under the genus Naegleria are classified as “amoeboflagellates”. In their life cycle, the developmental forms consist of “flagellate” and “amoeboid” stages. The amoeboid form has no flagellum. Members of genus Acanthamoeba never produce flagellate form.

                Generally, disease caused by Naegleria is referred to as “primary amoebic meningoencephalitis (PAM)”. Species of Acanthamoeba (oftentimes A. culbertsoni) can also produce PAM but to a lesser extent than that of Naegleria. These parasites, generally, involve the brain but disease with these species is not limited to this organ only.

 

Naegleria fowleri

 

                Developmental forms of Naegleria fowleri include a] trophozoite – with amoeboid and flagellate forms, and b] cystic stage. The motile trophozoite colonizes water and moist soil. The resistant cyst is non-motile. Only the trophozoite form has been demonstrated in tissues of man.

Morphological Features

 

Trophozoite

 

                Amoeboid form – elongate anterior and distinctly tapered posterior end forming a single pseudopod at the

forward end and a knob-like process, called “uroid process”, at the posterior end. It measures 7 X 20 micrometers when active and 10 -5 micrometers in diameter when rounded. Each organism has a single nucleus with a large karyosome located at the anterior part of the endoplasm and the cytoplasm is filled with granules and vacuoles. The organism may have one or more contractile vacuoles.

                Flagellate form – pear-shaped with two flagella at the broader end. It may move forward rapidly or spin. It

does not divide but can easily shed-off its flagella to transform into the amoeboid form, at which time division occurs.

 

Cyst

 

                It is the stage that forms in agar culture media and also the one found in nature, spherical with a single nucleus, measuring 7 – 10 micrometers in diameter, with smooth, heavy and thick cyst wall. The single nucleus is not usually evident and the cyst looks empty. The nucleus, stained, has the same appearance as that in the trophozooite although smaller in size.

 

Medical Importance

 

                Man acquires N. fowleri through instillation of the trophozoite into the nose when the person swims in infected bodies of water. The trophozoite enters the brain via olfactory nerve epithelium. Some researchers consider that the flagellate form is the infective stage since it is aquatic in nature but others say it is the amoeboid stage that enters the nose.

                Cysts have not caused infection in experimental animals. In the brain, the parasite transforms from one stage of development to another as they multiply.

                Pathology is mostly limited in the brain tissues, which becomes soft and with hyperemia (blood congestion) of the meninges producing a moderate purulent appearance. The olfactory bulbs are congested or hemorrhagic and accompanied by necrosis.

                The infection is dramatic. A day or so of the prodromal symptoms of headache and fever is followed by rapid onset of nausea and vomiting with signs and symptoms of meningitis and involvement of the olfactory, frontal, temporal, and cerebellar areas. Meningeal irritation leads o stiff neck or generalized seizure or convulsion. Involvement of olfactory bulb results to disturbances in the sense of smell and/or taste. Patients, oftentimes, become irrational before going into coma. Death occurs early and the entire clinical course seldom exceeds 3 to 6 days.

 

Laboratory Diagnosis

 

                The organism may be recovered from the CSF obtained through lumbar puncture. A small amount of CSF diluted with distilled water and observe through hanging-drop preparation will show the organisms. Gram stain will not color the parasite. Iron-hematoxylin or Wright’s staining methods is preferred. Immunofluorescence and/or immunoperoxidase methods may also be used in the diagnosis.

 

Treatment

 

                No satisfactory drug, at present, can be used although Amphothericin B was tried but with considerable toxicity.

 

Prognosis

 

                Usually fatal but survival rate increases if the diagnosis is made at the earliest time

 

Prevention and Control

 

1.       Avoid contact with stagnant or thermal waters.

2.       Adequate chlorination of public water supplies, including swimming facilities.

3.       Salination of public water pools up to 0.7%

4.       Public education

 

Acanthamoeba species

 

                The disease produced by member species of genus Acanthamoeba is referred to as “granulomatous amoebic meningoencephalitis”. Unlike Naegleria, infection with Acanthamoeba is not associated with swimming. Brain involvement is secondary to an infection elsewhere in the body via the blood stream. The known portals of entry include ulcerated or broken skin, eyes, the lungs (possibly), and the genito-urinary tract.

                The onset of the disease is gradual with tendency to be chronic with a prolonged course and oftentimes occurring among debilitated or patients with immune deficiency. Corneal infection (keratitis), however, can occur among healthy individuals. A significant increase in Acanthamoeba infection occurred in different countries since 1985, which was linked to the use of contact lenses specially the soft ones.

                In reports, CNS infection only was associated to occur more with A. culbertsoni, A, polyphaga, and A. astronyxis while A. polyphaga and A. hatchet were found in cases of eye infection only. Most cases of GAE with eye infection were due to A. castellani.

                Mainly, Acanthamoeba infection produces granuloma in the brain. Alteration in mental status is a prominent feature of GAE. Headache, seizures, and neck-stiffness occur in about one half of the cases. Nausea and vomiting may also be present. Brain lesion with Naegleria infection tends to be diffuse but focal with Acanthamoeba. The organisms tend to be present in any of the infected tissues and around blood vessels.

                It was noted that Acanthamoeba infection occurs among animals such as beaver, cats, dogs, rabbits, turkeys, and water buffaloes.

 

Laboratory Diagnosis

 

                Laboratory diagnosis is through identification of trophozoites in CSF through hanging-drop preparation or recovery of trophozoites and cysts in brain tissues. Cyst of Naegleria species has never been found in any tissue. Culture, similar to one used in Naegleria, may also be done.

 

Morphological Features

               

                Stages of development include a] trophozoite form (active stage) and b] cyst (resistant form). There is no flagellate among species of Acanthamoeba. The trophozoite has irregular appearance due to spine-like pseudopodia and acanthopodia from the lobopodia.

 

Acanthamoeba culbertsoni

 

Trophozoite – 30 micrometers (average diameter) with prominent nucleus and a large nucleolus.

Cyst –­­­­­ spherical, with slight irregular outline, 20 micrometers or more double-walled, with polyhedral inner cyst wall (endocyst) and smooth or slightly wrinkled outer wall (ectocyst), centrally located nucleus with large, central karyosome.

 

Acanthamoeba polyphaga

 

Trophozoite – with broad, hyaline lobopodia with numerous delicate-looking acanthopodia, uroid process may be

prominent, the cytoplasm has a single and prominent contractile vacuole, 23 micrometers (average length) with vesicular nucleus and centrally located endosome

 

Cyst­ – double-walled with polyhedral or stellate endocyst and wrinkled ectocyst.

 

Acanthamoeba castellani

 

Trophozoite­ – elongate

 

Cyst­ – 16 micrometers average diameter, polyhedral endocyst and rippled or wrinkled ectocyst.

 

Acanthamoeba astronyxis

 

Trophozoite ­– 25 – 60 micrometers long, with conspicuous food vacuoles, endoplasm contains many small and yellowish refractile bodies.

 

Cyst ­– biconcave with folded ectocyst and stellate endocyst, 14 – 25 micrometers in diameter, with a single prominent nucleus.

N.B. Identification of the different species of Acanthamoeba is very difficult if based only on morphology. Differentiation is made easier with the use of immunoperoxidase and immunoflourescent staining methods.

 

Treatment

               

                No definite drug has shown significant effectiveness in treatment of GAE. Most early cases of acanthamoeba keratitis required corneal transplantation.

 

Prevention

               

                People wearing contact lenses should strictly follow the manufacturer’s instruction on the use, care, and disinfection of the lenses. Wounds in other parts of the body should be taken cared of properly since GAE is acquired through these wounds. Immune deficient individuals including patients with chronic diseases should be on the look out for being at high risk of infection with these parasites.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CLASS ZOOMASTIGOPHORA

ATRIAL FLAGELLATES

                                Giardia lamblia                                                    Trichomonas vaginalis

                                Chilomastix mesnili                                           Trichomonas hominis

                                Dientamoeba fragilis                                         Trichomonas tenax

 

                Member species of this group are characterized with one to several long, delicate, thread-like extensions of the cytoplasm called “flagella” in the trophozoite form, except Dientamoeba fragilis, which instead had pseudopodia. The neuromotor apparatus consists of blepharoplast (at times a parabasal body), which constitutes the kinetoplast (the energizing component), and an axoneme, with or without a free flagellum. The axial structure of the flagellum is a continuation of the axoneme, which consists of one or more fibrils. Some have rudimentary mouth called “cytostome”. Reproduction is through longitudinal binary fission whereby mitotic division of the nucleus and binary division of the kinetoplast precedes that of the cytoplasm.

                Both Giardia lamblia and Chilomastix mesnili have cyst and trophozoite forms in their life cycle, while others exist in the trophozoite stage only. The pathogenic ones include Giardia lamblia, Dientamoeba fragilis, and Trichomonas vaginalis. The others are commensal parasites of man.

 

Giardia lamblia

               

                It causes the disease called giardiasis or lambliasis. It also causes the so-called “traveler’s diarrhea”. The parasite has a worldwide distribution but more common in warm than cool climates. It is more prevalent among children than adult individuals and also the most commonly diagnosed flagellate infection of the human intestinal tract, especially in the west.

 

Morphological Feature

 

Trophozoite

 

                1. measures 9 – 21 X 5 – 15 X 2 – 4 micrometers

                2. bilaterally symmetrical and pear-shaped with rounded anterior, attenuated posterior, a convex dorsal side

                3. ventrally provided with a shallow and posteriorly notched concavity called “sucking disc”, which is for

attachment and enable the parasite to resist ordinary peristaltic activity of the intestine

                4. there are two spherical or oval nuclei with large, central karyosome that lie in the area of the sucking disc

at the anterior portion of the body thus giving the organism the appearance of “an old man with eyeglasses”

                5. there are four pairs of flagella

·          Lateral pair – crossed

·          Lateral pair – uncrossed

·          Central pair

·          Posterior pair

6. the parabasal bodies, usually two, are closely associated, slightly curved, sausage-shaped, and lie transversely or obliquely just posterior to the sucking disc.

7. multiplication is through longitudinal binary fission

8. motility about the long axis producing the so-called “falling leaf” or “kite-like” motion

Cyst

 

                1. measures 8 – 12 X 7 – 10 micrometers

                2. usually ovoid in shape

                3. the finely granular cytoplasm is clearly separate from the cyst wall (i.e. referred to as “retracted

   cytoplasm”  – diagnostic)

4. recently formed cyst has 2 nuclei while mature ones have 4

5. the axonemes assume the appearance of four pairs of curved bristles (diagnostic)

 

LIFE CYCLE

 

                Man acquires the infection through the ingestion of mature and viable cyst contained in contaminated foods and drinks. The cyst passed unharmed through the gastric juices and undergoes excystation in the duodenum. Large number of the trophozoite attaches and inhabits the duodenum and the proximal jejunum. At times, the trophozoites can reach the bile ducts and the gall bladder. This, oftentimes, occurs if there is heavy infection. The trophozoites do not invade tissues and feed on mucus secretions. Encystation takes place in the intestine and the cysts are evacuated with the feces. The cysts may find their way to food and drinks through contaminated fingers, flies, and other insects, misconnection of drainage and water supply pipes, use of human excreta as vegetable fertilizer (night soil), or improper disposal of human waste.

                Promiscuous sexua| practices, particularly anal0oral contact, may favor transmission. This manner of transmission, probably, is associated with increasing prevalence of giardiasis among homosexual men.

 

Pathogenesis and Clinical Manifestations

 

                The pre-patent period varies from 2 – 3 weeks. In light infection, there may be no noticeable sign or symptom of the infection. Trophozoite forms, attached to the mucosal walls of the duodenum, cause shortening or blunting of the intestinal villi accompanied by foci of inflammation of the crypts and lamina propia of the intestine. Biopsy of the jejunum from patients suffering from giardiasis showed blunt or shortened villi, reduced height of the columnar epithelial cells of the mucosa and hypercellularity of the lamina propia.

                The trophozoites, attached on the mucosal wall, produce irritation with accompanying mucus secretion. Numerous trophozoites will “carpet the intestinal mucosa” preventing absorption of fats. The increase mucus secretion, irritation, and deranged fat absorption result to excretion of “fatty stools”. The condition is referred to as “steatorrhea” (i.e. plenty of fats in the soil). Thus, the patient suffering from giardiasis excretes “gruelly” or “steatorrheic” stool.

                There is also impaired absorption of carotene, folate, and vitamin B_12. Production of disaccharides and other mucosal enzymes can also be greatly reduced. Uptake of bile salts by the organisms may inhibit normal biologic activity of the pancreatic lipases. These abnormalities lead to “malabsorption syndrome”. Dehydration may also occur among patients with giardiasis and this is due to diarrhea.

                Patients with giardiasis may manifest with flatulence, abdominal distention, nausea, anorexia, and passage of foul-smelling and bulky stools. In chronic condition, it is likely to result to weight loss. Children are more frequently affected than adults, although all ages may exhibit symptoms ranging from mild diarrhea, flatulence, anorexia, abdominal pain and cramps, and epigastric tenderness.

                Among adults, giardiasis is seen as cause of the so-called “traveler’s diarrhea”. In the past, visitors to Soviet Union who became ill with giardiasis and experiencing severe diarrhea were labeled as having what they called “Leningrad’s curse”.

                Involvement of the gall bladder may produce gall bladder colic and jaundice due to obstruction of the bile passages or irritation and edema of the ampula of Vater.

 

Laboratory Diagnosis

 

                The diagnosis is based on finding the cyst and/or trophozoite in fecal smears. To increase the yield of positive results, concentration method such as the ones used for amoeba parasites, may also be employed. An old method of recovering the organism, especially the trophozoites, was the “string test”. The patient is asked to swallow a piece of string whereby a gelatin capsule is used as the weight. The string is then withdrawn later and the portion of the string with the bile stain is washed with saline solution and organisms are searched for under the microscope. This procedure may be done is duodenal aspiration is not possible. Duodenal aspirate, therefore, is the specimen of choice to recover the trophozoites.

                Immunologic tests that may be used for diagnosis, or research purposes, include ELISA, immunofluorescence, and counter immuno-electrophoresis.

 

Treatment – Quinacrine hydrochloride and metronidazole

 

Prevention and Control

 

                1. Drink only safe and clean water

                2. Prevent flies and other insects that may serve as phoretic vectors to come into contact with foods.

                3. Prevent people from using night soils as fertilizers in vegetable gardens plus thorough washing before

   eating.

4. Regular check of food handlers.

5. Prompt and adequate treatment of cases.

6. Public education

 

Chilomastix mesnili

 

                This is a commensal parasite that lives in the cecum of man. It has a cosmopolitan distribution but more prevalent in warm countries than places with cool climate.

Morphological Features

 

Trophozoite

 

                1. measures 6 – 20  3 – 10 micrometers

                2. asymmetric, pear-shaped due to the presence of the “spiral groove” at the tail end

                3. the nucleus is situated medially near the anterior end with a small and distinct karyosome

                4. the cytostome is well-defined located on one side of the nucleus with both ends rounded and constricted

    middle part hence described as “hour glass-shaped cytostome”

5. provided with three (2 short, 1 long) flagella and fourth one, which is delicate and lying in the cytostome

6. the cytoplasm is granular with numerous food vacuoles

7. multiplies by longitudinal binary fission

8. motility, in the living state, is described as “cork-screw” or with “boring motion” or it rotates along the

   longitudinal axis due to the spiral groove

 

Trichomonas tenax

 

                The organism primarily lives in the tartar around the teeth, cavities of carious teeth, in necrotic mucosal cells in the gingival margins of the gums, pyorrhetic pockets, and tonsilar crypts. It Is also associated with oral spirochete in Vincent’s angina and quite common among people with poor oral hygiene. T is quite resistant to changes in temperature and able to survive for several hours in drinking water.

 

Manner of Transmission

 

·          Droplet spray from the mouth of infected individual

·          Common use of contaminated dishes, eating utensils, and drinking glasses

 

Laboratory Diagnosis

 

                Identification of the trophozoite forms from tartar between the teeth, gingival margins of the gums, tonsilar crypts, or the mouth.

 

Preventive Measures – Proper and good oral hygiene

 

Trichomonas hominis

 

Characteristics

1. Maybe identified in diarrheic stools of infected individuals

2. Only the trophozoite form is identified and no cyst form has been found

3. More common in warm climate than cool climates

4. The usual habitat is the cecal region of the large intestine

5. It does not invade the intestinal mucosal cells.

6. The trophozoite form is considered the infective stage

7. It moves very rapidly with jerky, non-directional movement.

 

Pathogenesis

 

                It is non-pathogenic and considered as a commensal or “lumen-dweller”. Some workers believe, however, that it can produce diarrhea in very heavy infection.

 

Laboratory Diagnosis

 

1. Recovery of the trophozoite forms in the patient’s stool.

2. Diagnostic characteristics

·          Unstained trophozoite has successive wave-like movements of the undulating membrane, with spike-like posterior projection of the axostyle.

·          Stains trophozoite – with prominent costa and axostyle

 

Treatment – no specific drug for treatment is necessary

Preventive Measures – improvement of environment through proper sanitation and good personal hygiene

Trichomonas vaginalis

 

                Generally, infection with this parasite has been referred to as “pingpong infection”. However, other conditions maybe caused by this organism in specific areas such as in the vagina - producing trichomonal vaginitis, in the urethra – causing urethritis, in the prostate and adjacent structures – resulting to prostatovesiculitis, and in the cervix – causing cervicitis.

 

Characteristics

 

1. It is the most commonly acquired sexually transmitted infection

2. Only the trophozoite form is identified

3. The vaginal walls, cervix, urethra, prostate glands, and epididymis are the natural habitats.

4. The parasite prefers a medium or environment that is slightly alkaline or somewhat more acidic than that of the

     healthy vagina.

5. It can survive on wet sponges for several hours and in the urine for more than 24 hours.

6. The peak incidence of infection of “vaginal trichomoniasis” occurs between ages 16 to 35, at which time that sexual

   activity is at its greatest

7. The incidence tends to be higher among females with poor personal hygiene

 

Manner of Transmission

 

1. Transmitted in the trophozoite form through sexua| intercourse

2. Non-venereal (non-sexual) transfer is also possible such as:

·          Communal bathing or sharing of douche equipments or materials

·          Contaminated toilet seats or use of contaminated toilet articles

·          Direct contact wit infected females

·          From infected mother to female newborn

 

Pathogenesis

 

1. The incubation period ranges from 4 – 28 days

2. The trophozoites produce irritation and inflammation of the mucosal cells they are attached to

3. The proliferating colonies of the organisms cause degeneration and desquamation of the vaginal epithelium

    followed by white blood cell infiltration

4.The surface area is covered with a frothy, sero-purulent, creamy, yellowish discharge, frequently forming a pool in

    the posterior fornix of the vagina

5. Maybe associate with an increase incidence of endometritis (inflammation of the endometrium) after delivery and

   erosion of the cervix that may result to chronic cervicitis, which in turn pre-disposes the woman to the development

   of cervical malignancy

 

Clinical Manifestations

 

1. Female patients, oftentimes, complain of vaginal itching, chafing, and burning sensation accompanied by profuse

    irritating discharge (usually referred to as “leucorrhea” because the secretion contains plenty of white blood cells).

2. Large number of trophozoites and leukocytes are present in the vaginal secretion that is liquid, greenish or

    yellowish in color

3. There is vulvar and vaginal pruritus (itchiness), discharge, and difficulty of urination (dysuria).

4. In chronic infection, the secretion loses its purulent character due to decrease in the number of the organisms and

   leukocytes, increase in the number of desquamated epithelial cells, and the establishment of mixed bacteria flora.

5. Patients may also manifest with frequent urination and cystitis (inflammation of the urinary bladder).

6. Among male patients, the infection may be latent and essentially without signs or symptoms but the condition

   maybe responsible for persistent irritation of the urethra or recurrent urethritis

7. Male patients may also have dysuria or nocturia (increase urination at night), the prostate maybe enlarged and

    tender, and sometimes with associated epididymitis

 

Laboratory Diagnosis

1. The organisms are usually and ordinarily recovered in the urine (specimen of choice for diagnosis) of both male

     and female patients. The organisms, among female patients, may be recovered from vaginal secretions or

     scrapings, cervical swabs, and urine, while male patients maybe diagnosed using secretions from the prostate and

     in the urine.

2. N.B. – Proper collection of urine sample should be strictly observed to prevent fecal contamination since

   Trichomonas hominis, which maybe present in the patient’s stool, maybe mistaken for Trichomonas vaginalis.

3. The organisms, to increase the yield of positive result, maybe grown using the modified Diamond’s culture

    medium.

4. Serologic tests, such as indirect hemagglutination test (IHA) or gel diffusion test (GDT) may also be used for

   diagnostic or research purposes.

 

Treatment – Metronidazole is the drug of choice. To prevent re-infection, the sexua| partner should also be treated at the same time as the patient even though there is no sign or symptom of the infection. If only the patient is treated, there is great possibility for re-infection (hence the term pingpong).

 

Prevention and Control

 

1. Be morally upright. Practice safe sex and good personal hygiene. Monogamous sexua| practice.

2. Asymptomatic males must be diagnosed and treated promptly.

3. Public education

 

Dientamoeba fragilis

 

                This organism has a worldwide distribution. Only the trophozoite form has been demonstrated. The name “fragilis” is inappropriate because the organism, being in the trophozoite form, is not necessarily destroyed but can survive better than other trophic form of other parasite. This parasite used to be grouped under Rhizopoda. The organism is provided with pseudopodia and does not have any flagella. However, various protozoologist would prefer to classify it under “amoeboflagellates” instead because of its close affinity with other flagellates.

 

Morphological Features

 

Trophozoite

 

                1. 3 – 22 micrometers in diameter

                2. there is a distinction between the ectoplasm and endoplasm

                3. the hyaline pseudopodia maybe lobose or angular, broad, and leaf-like with characteristic serrate margin

                4. there may be 1 or 2 (rarely 3 or 4) nuclei, although most of the times the organism is bi-nucleated

                   (arrested telophase stage of nuclear division)

                5. The karyosome is beaded in appearance consisting of 4 – 8 beads or granules, which represent an

   incomplete binary fission. If there are four beads of the karyosome, it is described as “tetracoccic”. Others

   described the organism as having “fragmented karyosome”.

6. Living specimen in freshly evacuated stool assumes a form of movement described as “progressive”.

 

Manner of Transmission

 

                The exact manner of transmission is “unknown”. The trophozoite of Dientamoeba fragilis maybe carried inside the egg of some common nematode such as Enterobius vermicularis. Some workers claimed of having demonstrated structures similar to D. fragilis within the eggs of the mentioned nematode. The incidence of infection may support this claim. In Germany, both D. fragilis and E. vermicularis are highly prevalent parasites among pre-school children.

 

Pathogenesis

 

The organisms live in the mucosal crypts of the large intestine, particularly in the cecum. It does not invade tissues but causes irritation of the intestinal mucosa, which is followed by increase secretion of mucus together with hypermotility of the bowels resulting to the production of mucoid-watery stools.

 

 

Clinical Manifestations

1. Mucoid-watery diarrhea or stools has plenty of mucus.

2. Abdominal pain, tenderness, particularly at the right lower quadrant of the abdomen.

3. Flatulence, nausea, and vomiting.

4. Low-grade fever and fatigue.

5. Anal pruritus (itchiness) may also be present but not very common.

Diagnosis

 

                Identification of the organism in stool smears, which may be stained or unstained. Diagnostic points: Stained trophozoite, oftentimes, is bi-nucleated, whereby the nucleus has peripheral chromatin with 4 – 8 beads of karyosome. The cytoplasm may have some food vacuoles but without ingested red cells.

 

Treatment

 

1. Iodoquinol

2. Oxytetracycline or tetracycline

3. Paramomycin

4. Metronidazole

 

Prevention

 

                Since the exact manner of transmission is unknown, the incidence of infection may be lowered by good environmental sanitation, proper ways of waste disposal, good personal hygiene, and public education.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

BLOOD AND TISSUE FLAFELLATES

 

Leishmania donovani

 

Disease

 

·          Visceral leishmaniasis

·          Kala-azar

·          Death fever

·          Dum-Dum fever

 

Stages of Development

 

                Amastigote – inside (i.e. intracellular) different phagocytic cells of man

                Promastigotes – stages occurring in the body of the insect vector and in artificial culture media.

 

Habitat

 

·          Reticuloendothelial cells of visceral organs, especially in the spleen, liver, bone marrow, intestinal mucosa, and mesenteric lymph nodes

·          May also be present in the endothelial cells of the kidneys, suprarenal capsules, lungs, meninges, and CSF.

 

Life Cycle

 

                The amastigotes, within the intestine of sand fly after taking a blood meal, are transformed into promastigotes and multiply through longitudinal binary fission. The promastigotes migrate to the pharynx of the insect and are injected into the skin of man when the fly feeds on man’s blood.

                The promastigote are engulfed by reticuloendothelial cell, multiply as amastigotes through simple binary fission, until the host cell is filled –up with the amastigotes. The host cell is destroyed and the organisms are released. They are taken up by other phagocytes.

                The amastigote is the stage sucked by the insect when it feeds on the blood of an infected individual.

 

Pathogenesis

 

                The multiplying amastigotes inside phagocytes cause destruction of the host’s cells. Macrophages with amastigote forms in their cytoplasm are set free in the circulation, i.e. from the skin to the viscera.

                Amastigotes are released and are taken-up by the fixed macrophages in the spleen, liver, bone marrow, and the centers of reticuloendothelial activity. The host cellular defense is stimulated resulting to proliferation of macrophages in the bone marrow, which compromises the production of red cells and granulocytes. The end-effects are granulocytopenia and anemia.

                The spleen, liver, and lymph nodes are enlarged, whereby the spleen may end-up into hypersplenism (large and active spleen) that causes ore destruction of the red blood cells.

                The host humoral reaction is also stimulated resulting to increase production of globulin that may result to reversal of the albumin-globulin ratio.

                The infection, therefore, is a form of “reticuloendotheliosis”.

 

Clinical Manifestations

 

1.       Incubation period may be less than 10 days or more than one year.

2.       Early manifestations – headache, fever of irregular interval, and progressive enlargement of the spleen.

3.       Established infection – irregular undulant fever, which may have two peaks in a day, anemia with leucopenia (decrease white cells), edema of the skin and periosteum, emaciation (especially of the chest), diarrhea, and bleeding of the mucus membranes of the gums and nose. The degree of liver enlargement (hepatomegaly) is more than the enlargement of the spleen (splenomegaly).

4.       Death frequently occurs from complications such as hemorrhage, dysentery, toxemia, and overwhelming bacterial infections.

5.       Post kala-azar dermal leishmaniasis – due to incomplete treatment, whereby the organisms transform from viscerotropic (i.e. with affinity to invade visceral or internal organs) to dermatotropic (with greater affinity to infect phagocytes of the skin). Skin lesion consists of hypopigmented macules anywhere in the body but less likely in the face, hands, and feet. Later on, nodules on the face may be formed. The nose, chin, cheek, lips, forehead, and ears are the usual place for nodule formation and can mimic leprosy.

 

Diagnosis

 

1.       History of travel into endemic places

2.       Physical examination findings are not pathognomonic. Findings in the spleen, liver, and lymph nodes are not specific for leishmaniasis.

3.       Biopsy of tissues such as the spleen, liver and lymph nodes maybe used to demonstrate amastigote forms.

4.       Bone marrow aspiration to recover the amastigotes is preferred over biopsy because it is safer and les tedious.

5.       Biopsy or aspirate materials may be placed in artificial culture media to grow the organism.

6.       Serologic method, such as the Montenegro (leishmanin) test, maybe used to test for immunity.

 

Treatment

 

1.       Drug of choice – pentavalent antimony sodium gluconate

2.       Other drugs – pentamidine isethionate, amphotericin B

 

Trypanosoma gambiense

Trypanosoma rhodesiense

 

Disease

 

1.       T. gambiense – Gambian trypanosomiasis, Mid- and West-African sleeping sickness

2.       T. rhodesiense – Rhodesian trypanosomiasis, East African sleeping sickness

 

Habitat

 

                Blood, lymph nodes, cerebrospinal fluid, tissues of man, (and tissues of some animals that may serve as reservoir)

Vector

 

                Tsetse fly under genus Glossina (e.g. G. palpalis, G. morsitans)

 

Stages of Development

 

                Epimastigotes – in the salivary gland of the insect vector.

                Trypomastigotes (infective stage to man) in the proboscis of tsetse fly and in the body of man

 

LIFE CYCLE

 

                The trypomastigotes, n the salivary glands of the vector, are injected into the skin of an individual when the tsetse fly feeds on human blood, or other animal’s blood (anterior transmission –meaning coming directly from the salivary glands of the vector). The organisms enter the circulation and are able to enter the lymph nodes, spleen, and elsewhere in the body. The parasite transforms into epimastigote, reproduces through longitudinal binary fission, and later becomes trypomastigote. Multiplication goes on and on. The trypomastigotes circulate anywhere in the body of the person (or reservoir animals).

                The insect vector, on feeding on the host’s blood, sucks up the trypomastigote forms. In the vector’s body, the parasite becomes epimastigotes, multiplies, and transforms into metacyclic trypanosome that lodge in the fly’s salivary glands. The fly introduces the trypanosomes into the next victim in the saliva injected into the puncture wound during the act of feeding.

 

Pathogenesis, Pathology, and Manifestations

 

                The incubation period for Trypanosome gambiense, on the average, is 6 – 14 days. It is likely to be less for T. rhodesiense.

                The parasites lodged in the tissues at the site of injection, set up a local inflammatory reaction. The organism multiplies through longitudinal binary fission, which results to parasitemia. The organisms do not invade tissues but later circulate in the blood. There is no significant sign or symptom of the infection yet. This period is the patent, asymptomatic stage of the infection.

                The circulating organisms produce injurious effects on every tissue and organ of the body. In the lymph nodes, there is marked proliferation of endothelial cells lining the sinuses and leukocytic infiltration around blood vessels. Lymph node invasion leads to enlargement particularly in postcervical, submaxillary, inguinal, and femoral nodes. The spleen and liver may also enlarge and become congested. At this time, the patient has fever, which is irregular and usually occurring in the evening. Prominent signs include the so-called “Winterbottom’s sign” – i.e. enlarge nodes at the posterior neck triangle and “Kerandel sign” – delayed sensation to pain. During this febrile period, the trypomastigotes are released into the blood stream. The febrile attacks alternate with period no symptoms at all. The patient, at this stage of the infection, is still able to work.

                Later in the infection, the parasites invade the central nervous system, thus initiating the chronic or “sleeping sickness stage”. The patient develops severe headache, mental dullness, and apathy. At this stage of the infection, the patient loses interest to work. There will also be muscle spasms, trembling of hands and trunk, disturbed coordination, pain and stiffness of neck, and paralysis. These problems become progressive. Sleepiness sets in and the patient may not be awaken to eat or encounter accidents like fall or the patient may even sleep while walking. Death may be due to pneumonia, meningitis, dysentery, heart failure, or a severe fall.

                In T. rhodesiense infection, the CNS problems are usually lacking because of the rapidity of its course, which does not necessarily allow the condition to progress into the chronic stage of the infection.

 

Diagnosis

 

1.       History of travel or living in endemic places

2.       Physical examination findings (such as the Winterbottom’s sign and Kerandel sign).

3.       Demonstration of the parasites in the blood, which are quite numerous during the time of fever. The organisms may also be recovered from lymph node juice, bone marrow aspirate, and cerebrospinal fluid. Animal inoculation may also be done, especially if the mentioned specimens are negative for the organism.

 

Treatment

 

1.       Pentamidine isethionate

2.       Suramin sodium

3.       Melarsoprol

4.       Tryparsamide

 

Trypanosoma cruzi

 

Disease

 

1.       Chaga’s disease

2.       South American trypanosomiasis

 

Vectors

 

1.       Panstrongylus megistus

2.       Triatoma infestans

3.       Rhodnus prolixus

 

Habitat

 

                As trypomastigotes in the blood, as amastigotes in the reticuloendothelial cells and other tissues of man (and other mammals), an epimastigote and metacyclic trypomastigote in the intestine of the insect vector.

 

Stages of Development

1.       Occurring as amastigote, promastigote, epimastigote, and trypomastigote in man

2.       Existing as amstigote, epimastigote, and trypomastigote in the body of the vector

 

 

 

 

 

Manner of Transmission

 

                The vectors are referred to as “kissing bugs” since they prefer to bite on the mucus membranes of the lips and the eyes. They usually bite at night and it is painless. Children are more prone to be bitten by these bugs, whose feces contain the metacyclic trypanosome (infective stage).

                The bug, during its blood meal, defecates near the bite site. The feces, containing the infective stage, is deposited near the puncture site and rubbed into the wound allowing entry of the parasite. This method of transfer is called “posterior transmission”.

 

LIFE CYCLE

 

                The metacyclic trypanosome that enters the skin of man is engulfed by phagocytes and is deposited in the adipose cells of subcutaneous tissues. The organism becomes amastigote and reproduces by simple binary fission. The host cell ruptures releasing the amastigote. The area is infiltrate by polymorphonuclears, monocytes, lymphocytes, and later by histiocytes (major cells at the central area of inflammation). Fibrous encapsulation follows resulting to formation of “chagoma”, which causes blockade of lymph flow that produce edema of the affected area.

                Amastigotes invade the adjacent lymph nodes, multiply and develop continuously, later released into the blood as trypomastigotes, and then go anywhere in the body.

                The bugs during its blood meal takes up the trypomastigote stage that reproduces and transforms into metacyclic trypanosome. This stage of development is present in the gut of the bug, thus when it defecates, the infective form is released.

 

Pathogenesis, Pathology, and Manifestations

 

                The main pathology of Chaga’s disease is “destruction of the reticuloendothelial cells” due to the increasing number of amastigotes.

                The parasites prefer to invade cells of mesenchymal origin, especially adipose, myocardial, reticuloendothelial, and neuroglial cells.

                In acute Chaga’s disease, leukocytosis and lymphocytosis occur but later, the patient develops leucopenia. Anemia is also present. Fever may occur every now and then. During the febrile attacks, the blood has plenty of trypomastigote forms.

                Destruction of cells of various organs and blockage of the reticuloendothelial system lead to functional disability and may finally cause death.

                Neurotrophic strains specifically involves neuroglial cells. The parasite, in its amastigote form, destroys these cells causing death of the nerve cell. Depending on the principal location where this process occurs, encephalitis, encephalomyelitis, or meningoencephalitis may occur.

                The autonomic ganglia of hollow and viscous organs are destroyed. The segment of the organ that is above that which is denervated later becomes progressively dilated. This phenomenon commonly causes enlargement of the large intestine (megacolon), esophagus (megaesophagus), and ureters (megaureters).

                The heart is always involved in Chaga’s disease. Destruction of the heart muscles leads to acute myocarditis that is characterized with conduction defects, the typical one of which is right-bundle-branch-block.

                In chronic Chaga’s disease, there is cardiomegaly, here dilated and thickened ventricular muscle accompanied by thinning and fibrosis, oftentimes, at the apex. This may progress to ventricular aneurysm. One of the most important causes of death is rupture of the aneurysm.

 

Diagnosis

 

1.       History of residence or travel in an endemic place.

2.       P.E. findings, the most important of which is the so-called “Romañas sign” – swelling of the face with marked edema of the eyelids of one or both eyes.

3.       Demonstration of trypomastigotes in blood films or amastigotes in tissues.

4.       Serologic tests may also be used.

5.       Xenodiagnosis – a trypanosome-free, laboratory-bred triatomid bug is allowed to bite the individual suspected of having the infection. If the patient is infected, e bug’s fees will show the organism.

 

 

 

 

 

 

CILIATEA

 

Balantidium coli

 

                This parasite is considered the largest protozoa that can infect man. The parasite exists in the cyst and trophozoite forms. The trophozoite is provided with cilia and a cytostome. Cyst form is provided with a very thick cyst wall, which is hardly penetrated by stains. Cyst stage doesn’t have a cytostome. The parasite, either in cyst or trophozoite forms, is provided with a large, kidney-shaped macronucleus and a small spherical micronucleus, which is situated near the concavity of the macronucleus. Multiplication is through transverse binary fission.

 

Disease – Balantidiasis

 

Habitat – Cecal area of the large intestine

 

Manner of Transmission – ingestion of mature and viable cysts contained in contaminated food and drinks

 

Associate Animals – Monkeys and pigs

 

LIFE CYCLE

 

                The ingested cyst undergoes excystation in the intestine releasing the trophozoite form. There is no change in the number of nuclei (two: one micro- and one macronucleus) as the parasite transforms from cyst to trophozoite and vice versa. The trophozoite form in the cecum reproduces by transverse binary fission. Encystation occurs as the parasite is transported down the intestine and passed out with the feces in the cyst stage.

 

Pathogenesis and Pathology

 

                B. coli, once established in man, can invade tissues. The mechanical action of the cilia and, most probably, the secretion of lytic enzyme aid the organism in its entry into the mucosa of the intestine to produce a colony. The trophozoites produce a “flask-shaped ulcer” that is similar to the one produced by Entamoeba histolytica but with larger opening.

                The ulcers are round, ovoid, or irregular with undetermined edge, by which the ulcer floor is covered with pus and necrotic material. This lesion is commonly occurring in the cecum.

                The patient may manifest with diarrhea with or without blood. Right, lower quadrant, abdominal pain and tenderness may be present. Very rarely, the ulcer may perforate he walls of the intestine leading to peritonitis.

                Other signs and symptoms of balantidiasis include dysentery with abdominal colic, tenesmus, nausea, loss appetite, headache, insomnia, muscular weakness, and loss of weight.

 

Diagnosis

 

1.       Physical examination findings are not usually very suggestive or specific for balantidiasis.

2.       Demonstration of either or both trophozoite and cyst in fresh fecal smears. Watery stools are likely to show the trophozoite forms while it is usual to find the cysts in semi-formed or formed stools.

 

Treatment ­– Tetracycline is the drug of choice. Metronidazole may also be used to treat balantidiasis.

 

Prevention and Control

 

1.       Proper and sanitary disposal of human waste.

2.       Since monkeys and pigs maybe the source of infection, their feces should also be prevented from contaminating foods and drinking water.

3.       Early diagnosis and treatment of cases

4.       Public education

 

 

 

 

 

 

 

COCCIDIA

               

GENERAL CHARACTERISTICS

               

                Member species of Coccidia are classified under the class Sporozoa. They are intracellular parasites with no definite organelle of locomotion. Their movement, however, may be accomplished through body flexion, gliding or undulating of longitudinal ridges. The life history is characterized by alteration of generations that include a.) schizogony- asexual development that generally occurs in the body of the intermediate host, and b) sporogony- the sexua| cycle that occurs in the definitive or final host’s body. These two processes can occur in the same host such as Isospora belli where man is both intermediate and definitive host. In hemophilia, i.e. malaria, each process takes place in different hosts.

Schizogony involves multiplication of the organism through segmentation or division, whereby the nucleus divides followed by the division of cytoplasm resulting to organisms having their own nucleus (merozoites). Sporogony, on the other hand, involves union of sex cells and results to the formation of sporozoites.

                Isospora, Eimeria, and Cryptosporidium have only a single direct cycle of transmission whereby both asexual and sexua| stages of multiplication occur in a single host. In Sarcocystis and Toxoplasma, the sexua| stages are usually situated in the intestinal mucosa of a carnivorous host (the predator). This results in an oocyst or sporocyst that passes out in the feces to infect an intermediate host (the prey) where the asexual multiplication will occur.

               

Maturation Process and Stages of Development

               

                The smallest and earliest stage of coccidian inside a tissue cell is the trophozoite. The young trophozoite, inside a host cell, develops into a mature trophozoite, which undergoes schizogony resulting to production of the so called “segmenter” or schizont. The schizont grows and later causes rupture of the host cell releasing the merozoites, which invade other tissue cells and become young trophozoites again. Later, the trophozoite will become schizont that has merozoites. This process is repeated until some of the mature trophozoites differentiate into immature sex cells (male-microgametocyte, female-marcrogametocyte). The mature sex cells, called gametes, undergo union resulting to the formation of the zygote. The zygote secretes a cyst wall resulting to an oocyst, which has sporoblast inside. The sporoblast secretes a cyst wall resulting to the formation of the sporocyst that contains sporozoites. This is already the mature oocyst form. The sporozoites are released when the cyst wall ruptures. The liberated sporozoites invade other host cells and become young trophozoites.

 

Isospora belli – producing “human coccidiosis”

·          It has a worldwide distribution but rare.

·          Infection among humans is less common in temperate than tropical countries.

·          Both sexua| and asexual multiplication occurs in man.

·          They live in the distal duodenum and proximal ileum.

 

Life Cycle

 

Man acquires the infection through ingestion of the mature oocyst contained in contaminated food or drinks. Excystation in the small intestine results to the release of sporozoites. The sporozoites penetrate the epithelial cells and develop into trophozoites, which mature and undergo schizogony. Some trophozoites differentiate into gametocytes after a few processes of schizogony. The gametocytes mature into gametes and undergo union to form zygotes. A zygote will become an oocyst, which later matures and goes into the feces.

 

Pathogenesis

 

The infection is confined to the intestinal epithelial cells. The organisms cause destruction of the surface layer of the intestine. There is malabsorption, markedly abnormal intestinal mucosa with short villi, hypertrophied crypts, and infiltration of the lamina propia with eosinophils, neutrophils, and round cells.

 

Clinical Manifestations

 

·          The infection is oftentimes asymptomatic and self-limiting.

·          Some may manifest with mild gastrointestinal distress to severe dysentery producing pale yellow and foul-smelling stools that may suggests malabsorption process.

·          Chromic diarrhea may also happen and manifests with vague abdominal pain with cramps, weight loss, weakness, malaise and anorexia. Chronic diarrhea may be from several months to about 15 years.

Diagnosis

 

Diagnosis is through the demonstration of the oocyst stage in fecal smears. Concentration procedures, such as Zinc sulfate method, maybe employed to increase the yield of positive results.

 

Treatment

 

·          Rest and bland diet may be sufficient for mild or asymptomatic cases.

·          Drugs for treatment – co-trimoxazole, perimethamine and sulfadiazine.

 

 

Human Sarcocystis Infection

 

·          Sarcocystis hominis – producing “intestinal sarcocystis infection” produces oocyst, cattle and pig as intermediate hosts, and man as definitive host.

·          Sarcocystis lindemanni – producing “extra-intestinal sarcocystis infection,” produces sarcocyst, man serves as intermediate host, unknown definitive host (possibly carnivores).

 

Sarcocystis hominis

 

Morphology

               

·          Oocyst – almost identical with that of I. Belli, passed out in the feces fully developed (oocyst of I. Belli matures after evacuation in the stool).

·          Sarcocyst – in the skeletal muscle, containing numerous large round cells called “metrocytes” or “merozoites,” wall is covered with the closely set, thin villi giving the appearance of being striated.

 

Life Cycle

 

Man ingests the sarcocyst from improperly cooked beef or pork. The sarcocyst ruptures in the small intestine to release the merozoites, which invade the lamina propia of the intestinal mucosa and initiate the production of gametes. Sporogony occurs resulting to formation of oocyst that matures and later evacuated in the feces. Cattle or pig ingest the mature oocyst and schizogony takes place in the vascular endothelial cells. Sarcocysts develop in the skeletal and/or cardiac muscle fibers.

 

Pathogenesis

 

·          The organisms, while in the sporogony cycle, destroy the epithelial cells of the intestine.

 

              Clinical manifestation, method of diagnosis, and treatment are the same as in human coccidiosis.

 

Sarcocystis lindemanni

 

·          Producing sarcosporodiosis or extra-intestinal sarcocystis infection.

·          Sarcocysts are found in either skeletal or cardiac muscles, BUT NOT BOTH.

 

Morphology

 

·          Sarcocyst – several millimeters in length with tapered ends, diameters ranging from medium (100-200 micrometers) to large (over 200 micrometers), spindle-shaped or cylindrical in skeletal muscle, contains metrocytes that produce and maintain the cyst wall and generate fusiform merozoites (also called bradyzoites, cytozoites, or zoites) within the cyst.

 

Life Cycle

 

The infection is acquired through the ingestion of mature oocyst that came from the feces of the definitive host (presumed to be carnivores such as the dogs and cats). Excystation occurs in the intestine releasing the sporocyst, which excyst to release the sporozoites.

The sporozoites find their way to the vascular endothelium where they develop into schizonts and produce one or more generations of merozoites (called tachyzoites). The merozoites then invade the striated muscle cells and produce the sarcocyst.

 

Pathogenesis

 

·          Destruction of vascular endothelium

·          Inflammation of the involved muscle

·          Release of sacrcocystin from the sarcocyst may result to hyper-sensitivity reaction

 

 

Clinical Manifestations

 

·          Myositis may occur

·          Pain and tenderness of the involved muscle

·          Allergic manifestations

 

 

Diagnosis

 

·          Biopsy of the sarcocyst

·          Periodic Acid Shift (PAS) staining – areas of the cytoplasm will show PAS negative reaction.

 

 

Treatment – No specific treatment

 

Prevention of Infection

 

·          Protect uncooked foods from contamination with feces of flesh-eating animals.

 

Toxoplasma gondii – producing toxoplasmosis

 

                This organism has a cosmopolitan distribution and although infection is quite common, the disease is rare. Reproduction is through “endodyogeny” – whereby 2 daughter trophozoites are formed within the parent cell. The acute proliferative phase of the infection occurs in various tissues. The cyst is found in the muscle and other tissues, including the CNS, during the chronic phase of the infection. Domestic cats are likely to be the sources of the highly infective oocyst.

 

Morphology

               

       Trophozoite

·          4 – 8 X 2 – 3 micrometers, pyriform or crescent-shaped, one end is more round than the other with spherical to ovoid nucleus that is usually nearer the blunt end.

 

·          Tachyzoites are rapidly dividing trophozoites seen during the acute phase of the infection. Bradyzoites are the slow multi-plying forms within the cyst.

 

Diagnosis

·          History and physical examination

·          Demonstration of the organisms in biopsy material of the lymph node, bone marrow, spleen, brain and other tissues.

·          Serologic tests used that help in the diagnosis:

v       Complement Fixation Test.

v       Double Sandwich ELISA test.

v       Indirect Immunofluorescent antibody test.

v       Indirect Hermagglutination test.

v       Sabin-Feldman dye test.

v       Frenkel skin test, which is a type of delayed hypersensitivity reaction

·          Detection of the parasites’ DNA through Polymerase Chain Reaction (PCR)

Treatment

 

·          Pyrimethamine and sulfonamides

·          Spiramycin

 

Prevention

 

·          Proper and through cooking of meat

·          Environmental sanitation

·          Periodic examination of cat’s feces

·          Public education

 

Cryptosporidium parvum – producing cryptosporidiosis

               

                This parasite is distributed worldwide and maybe the common cause of diarrhea among travelers and patients of day-care centers. It can occur as a “water-borne” infection or “zoonotic” – i.e. from domestic animals. The infection is more common among children than adults.

 

Habitat

·          Brush border of the mucosal epithelium of the stomach or the intestine

·          May also inhabit the gall bladder and the pancreatic duct

 

Morphology

·          Trophozoite and schizont may measure 2 – 5 micrometers and are attached to the host cell membrane

·          Oocyst (4 – 5 micrometers) has 4 sporozoites but with NO sporocyst.

·          Schizont produces 8 falciform merozoites that are released to form new schizogonic cycle or initiate the sporogonic cycle by forming micro-and Fertilization occurs resulting to an oocyst that later becomes mature.

 

Life Cycle

 

Man acquires the infection through ingestion of the mature oocysts in contaminated foods and/or drinks. Excystation occurs in the upper gastrointestinal tract. Sporozoites escape from the oocyst and invade epithelial cells of the GIT. The organisms occupy the apex of enterocytes within the host cell membrane but NOT within the cell cytoplasm. Asexual multiplication (merogony) occurs to produce merozoite, which may invade other cells. Some of the merozoites undergo gametocytogenesis resulting to the production of micro- and macrogametocytes, which when fertilization of the macrogamete occurs will result to the development of an oocyst that contains 4 sporozoites capable of initiating a new infection.

 

Pathogenesis – Developing organisms destroy the host cells.

 

Clinical Manifestations

·          Self-limiting among persons with good immune functions

·          Nausea and vomiting, and abdominal cramps, weight loss, and fever among symptomatic individuals.

·          Diarrhea is a common presentation especially among children

·          Severe fluid loss due to diarrhea and vomiting may lead to fatal outcome among children

 

Diagnosis

·          History and physical examination findings

·          DFS of stool samples to identify the oocyst

·          Duodenal string test (Enterotest) to recover the oocyst

·          Modified acid-fast stain of stool samples will show red-stained oocyst. Yeast cells stain green.

·          Stool samples may be concentrated to increase the yield of positive results.

·          Serologic tests – ELISA and immunofluorescence

 

Drugs for Treatment

·          Spiramycin

·          Pyrimethamine and sulphadiazine

·          Somatostatin

 

Prevention

·          Proper personal hygiene

·          Proper disposal of human waste

·          Environmental sanitation

 

Pneumocystis carinii – producing interstitial plasma cell pneumonia or pneumocytosis

 

                This organism does not have yet a definition classification. The organisms are small with uncertain affinities to other organisms but more closely related to fungi. It lives in pulmonary alveoli. It assumed that it is an “airborne” infection. There had been reports, however, that transplacental transfer is possible.

 

Morphology

·          Trophozoite - measures 5 micrometers, amoeboid with a single nucleus and the cytoplasm has vacuoles, granules, and globules.

·          Cyst – measures 5 micrometers, with thick cyst wall, usually containing 8 trophozoites (referred to as intracystic bodies although some called sporozoites) each with a single nucleus.

 

Pathogenesis

·          It is NOT an intracellular organism NOR it invades the pulmonary epithelial cells of the interstitium. It adheres to the alveolar epithelium by means of its cell wall.

·          The presence and multiplication of the organisms in the lungs stimulate the exudation of serous fluid, histiocytes, lymphocytes, and plasma cells.

·          Interstitial tissues are thickened and are heavily infiltrated with mononuclear and plasma cells.

·          The lungs increase its weight and volume with thickening of the pleura with consolidation and prominence of interlobular septa.

·          There is immunosuppression or agammaglobulinemia.

·          Ventilation is impaired and death occurs due to respiratory failure.

 

Clinical Manifestations

·          Onset is insidious and with a gradual course.

·          Incubation period is about 1-2 months.

·          Illness begins with non-productive cough that gradually progresses to serious loss of ventilatory capacity, respiratory failure, and cyanosis.

·          The degree of respiratory distress far exceeds the degree of the abnormality in the clinical findings.

·          The physical signs in the chest, moderately deranged, with temperature that is normal or slightly elevated with normal or slightly increase white cell count.

 

Diagnosis

·           History and physical examination findings

·           Demonstration of the organisms in tissues or materials from the lungs like sputum, naso-tracheal washings, bronchial scrapings, biopsy, or materials obtained through percutaneous pulmonary needle aspiration.

·           Cysts are best demonstrated by Gomori’s methenamine silver staining of tissue sections or in smears. Giemsa or Papanicolau’s stains may also be used.

·           Chest X-ray will show symmetrical cloudiness with ground glass appearance that spread bilaterally from the bila. Alternating areas of lobular collapse and emphysema may produce a “honey-comb” effect.

·           Immunofluorescence may also be used for diagnosis

               

 

Drugs for Treatment

·          Trimetophrim – sulfamethoxazole

·          Pentamidine – compounds

·          Trimetrexate and Leucovorin

 

Prevention

·          Early diagnosis and prompt treatment of the patient

·          Build-up the resistance of the patient

·          Public Education

MALARIA

 

¥                    Malaria is from the word “mal” meaning bad and “aria” meaning air.

¥                    Malaria was also known as Paludism or Paludismo, from the word “palus” meaning miasma or mist.

¥                    The word Malaria and Paludism denote the early believed that the infection is acquired after being exposed to bad air.

¥                    It was learned later that the infection was due to small parasite carried by a female Anopheles mosquito.

¥                    The following produces malaria in man:

 

Plasmodium falciparum

 

- Producing malignant malaria, estivo-autumnal, falciparum malaria, subtertian malaria or pernicious malaria.

- It is most prevalent in the tropics and subtropics and “it still remains almost unchallenged as the greatest killer of the human race over most parts of Africa and elsewhere in the tropics”

- The most common Malaria in the Philippines.

 

Plasmodium vivax

 

- Producing vivax malaria or benign tertian malaria.

- It is more common in temperate than in tropical region.

- It is the second common Malaria in the Philippines.

 

Plasmodium malariae

 

- Producing malariae or quartan malaria

- Common in tropical Africa, Burma, Sri Lanka, India, Malaysia, and Indonesia.

- It is occasionally seen in the Philippines.

 

Plasmodium ovale

 

-Producing ovale malaria

- It is the least common Plasmodium infecting man.

- It occurs mostly in tropical Africa, principally on the West Coast and is endemic in Ethiopia.

 

¥        2 phases in the cycle of Malaria parasite:

1.       Extrinsic phase in the definitive host, the female Anopheles mosquito, in which sexua| reproduction occurs.

2.       Intrinsic phase in the intermediate host, Man, in which asexual reproduction occurs.

¥        Glucose 6-Phosphate Dehydrogenase Deficiency Trait

G6PD deficiency trait is believed to confer some protection against Plasmodium falciparum infection.

¥        Sickle Cell Anemia Trait

Responsible for some resistance to malaria

¥        P-aminobenzoic acid (PABA)

Deficiency of PABA has been noted to suppress the infection in vitro, in experimental animals and even in human populations.

¥        Duffy factor

It is thought to increase the individual’s susceptibility to malaria infection.

¥        Insect vector of malaria in the Philippines:

Anopheles flavirostris – rest out-of-door in day time, in seepages, springs, running streams, canals in either shade or sunshine

Anopheles minimus – the same as flavirostris

Anopheles balabacensis – rest either indoors or outdoors, in puddles, pools, ponds and in shades.

Anopheles lesteri – rest either indoors or outdoors, in pools, ponds lakes and in rice fields.

Anopheles philippinensis – rest either indoors or outdoors, in pools, ponds or lakes

Anopheles umbrosus – rest out-of-doors, inpools, ponds lakes, running streams and canals in shades

 

 

 

Manner of Transmission

 

1.       The infectious sporozoites from the salivary glands of an infected female Anopheles mosquito is injected during biting into the human bloodstream.

2.       Blood transfusion

3.       Contaminated syringes and needles

4.       Across the placenta

 

LIFE CYCE

 

1.       The female Anopheles mosquito introduces the sporozoites into the human blood stream. Within about 30 minutes, this slender motile stage of the parasite enter the liver parenchymal cell, initiating what is called pre-erythrocytic (PE) or primary exoerythrocytic (EE) stage of the parasite, because the red blood cells have not yet been invaded.

2.       Within the liver cell, the parasite begins an extensive multiplication called schizogony. The sporozoite developed into a trophozoite in which matures and multiply by segmentation.

3.       The schizont developed inside the liver cell.

4.       The schizont inside the liver cell develops and matures.

5.       The infected liver cell rupture, releasing the schizonts, now called merozoites.

In the case of Plasmodium vivax and Plasmodium ovale, the merozoites may enter another liver cells and this is called secondary exo-erythrocytic stage of the parasite. This secondary exo-erythrocytic stage of the parasite may be dormant and termed hypnozoite. Plasmodium falciparum and Plasmodium malariae does not have secondary exo-erythrocytic stage or phase.

6.       The merozoite enter the red blood cells and becomes the young trophozoite.

7.       Developed into growing trophozoite

8.       Mature trophozoite

9.       Young schizont

10.    Growing schizont

11.    Mature schizont

12.    The mature schizont rupture the infected red cell, release of merozoites and invade other red cells

13.    Young trophozoite

14.    Growing trophozoite

15.    Mature trophozoite

16.    Young schizont

17.    Growing schizont

18.    Mature schizont

19.    The infected red blood cells rupture releasing the merozoites.

20.    The merozoites invade other red cells may undergo schizogony or maybe differentiated into an immature sex cells.

21.    The immature sex cells are called gametocytes, the male is microgametocyte and the female is macrogametocyte. The female Anopheles takes a blood meal, ingesting the gametocytes.

22.    In the hemocoele of the female mosquito, the immature sex cells will develop into mature sex cells called gametes. The microgametocyte will mature by exflagellation wherein the nucleus divides and each division becomes the microgamete. The macrogametocyte will mature and develop to be ready for fertilization as macrogamete.

23.    The macrogamete is fertilized by the microgamete.

24.    The fertilized macrogamete is called zygote.

25.    The zygote developed into a motile, vernicule ookinete.

26.    The ookinete migrate outside the hemocoele.

27.    The ookinete attached itself outside the hemocoele and developed into an oocyst.

28.    Sporozoites develop inside the oocyst.

29.    The oocyst rupture.

30.    Releasing the sporozoites.

31.    About 20% of the sporozoites find their way into the salivary gland of the mosquito and when the mosquito takes a blood meal, she introduces the sporozoites to man.

 

 

 

 

 

Pathogenesis

 

¥        Relapses – the renewed parasitic and clinical activity

1. Recurrence or true relapses – the signs and symptoms are due to the parasite coming from the liver. (Plasmodium vivax and Plasmodium ovale).

2. Recrudescence – the signs and symptoms are due to surviving parasites from the red blood cells

    (Plasmodium falciparum and Plasmodium malariae).

Since EE schizogony appears to stem ONLY from sporozoites, there will be NO recurrences or “true relapses” in blood-induced malaria infection, in which NO sporozoites are involved.

 

Clinical Manifestations

 

¥        The infected individual begins to experience various general symptoms, such as headache, lassitude, vague pains in the bones and joints, chilly sensations and fever.

¥        Within a few more days, regular episodes of chills and fever become prominent but other systematic symptoms specially headache, muscle aches and pain persist.

¥        The malarial paroxysm occur at the end of the schizogony cycle, when the merozoites of the mature schizont together with their pigment and residual erythrocyte debris, erupt from the infected red blood cells and are released into circulation.

¥        Malarial or Febrile Paroxysm

1.       Cold Stage

- up to an hour

- with chilly sensations that processes to a teeth-chattering, frankly shaking chill

- peripheral blood vessels are constricted and the lips and nails are cyanotic

2. Hot stage

                        - lasts from 6 to 12 hours

                        - the body temperature begins to mount rapidly as the blood vessels dilate

                        - temperature peaks at 39 to 41°C, skin is hot and face flushed

                        - nausea, vomiting, headache, and a rapid pulse

                        - high fever may produce convulsion in children

3. Sweating stage

                        - may last for several hours

                        - the patient perspires profusely, temperature falls and headache disappears

                        - the patient is exhausted but symptomless

                        - the next day, the patient can feel quite well, before the next paroxysm occurs

Plasmodium falciparum produces pernicious malaria

Pernicious malaria

1.       Algid malaria – there is low blood pressure, the patient may be in shock and may lead to renal

    failure

2.       Hyperpyrexia – there is high temperature or high fever

3.       Gastro-intestinal type – there is diarrhea or dysentery

4.       Hemorrhagic type – there is hemorrhage in the skin and mucous membranes

5.       Blackwater fever – there is massive intravascular hemolysis and hemoglobinuria, it s believed

                                 to be due to erythrocytic auto-antibodies

6.       Cerebral malaria – there is involvement of the central nervous system

Warning signs for pernicious malaria:

1.       If 5% or more of the red blood cells are infected

2.       If 105 of the infected red blood cells have multiple infection

3.       If the intermediate stages of Plasmodium falciparum (growing trophozoites, mature trophozoites, young schizonts, growing schizonts, and mature schizonts) are demonstrated in the peripheral blood.

 

Diagnosis

 

¥        History

¥        Physical Examination

¥        Malaria smear

Thin smear - examined for at least 15 minutes

Thick smear – examined at least 5 minutes

 

An additional smear at intervals of several days is recommended if parasites are NOT found initially and Malaria is suspected in clinical ground.

               

·          Malaria smear should be reported in percentage

                                Thin smear – number of infected red blood cells divided by 1000 X 100

                                Thick smear – number of parasites per 100 white blood cells X 100

¥        Quantitative Buffy Coat (QBC Analysis)

- uses capillary tubes pre-coated with acridine orange dye

- under ultraviolet illumination, the dye will NOT stain the red blood cells will stain WBC, Platelets,

Plasmodia, Trypanosoma, and Microfilariae

- able to detect a very small number of Plasmodia which may not be detected in blood smear

- can NOT be used to identify the specific species of Plasmodia

- screening in mass blood donations

- available serologic tests can NOT differentiate current from past infections and therefore helpful only in

epidemiological studies

 

Drug Used

 

                Chloroquine                                                         Pyrimethamine-sulfadoxine

                Quinine                                                                  Pyrimethamine-sulfadoxine-mefloquine

                Amodiaquine                                                        Pyrimethamine-dapsone

                Pyrimethamine                                                    Primoquine

 

Preventive Measures

 

1.       Treatment of the patient

2.       Chemoprophylaxis

3.       Mosquito control

a.       Destruction of the mosquito

b.       Destruction of the breeding places

4.       Prevention of mosquito bites

a.       Mosquito repellent and nets, screen, wearing long-sleeved shirts and long trousers

5.       Development of Malaria vaccine

 

Genus Babesia

¥        Sporozoan parasites of red blood cells, transmitted by ticks

¥        Babesia bigemina was shown to be causing the so-called Texas cattle fever

¥        Babesia microti Is the most common species diagnosed in humans

o         Small rings within the red blood cells, very much like P. falciparum with a darkly staining nucleus and very little cytoplasm

o         Have no associate pigment in the red blood cells

o         Asexual multiplication by binary fission in the RBC with reproduction of merozoite that invade other RBC

o         When taken up by the ticks, there is complex cycle of multiplication that includes a sexua| stage, resulting ultimately in the presence of parasites in the salivary gland of the tick

o         Babesia is basically a hemolytic anemia, there is fever, weakness jaundice and hepatosplenomegaly

o         Diagnosis is by demonstration of the parasites from the RBC by stained smear and may be mistaken for Plasmodia

o         Combination of Quinine and Clindamycin have been very effective

 

 

 

 

 

 

 

 

 

 

HELMINTHOLOGY

 

Helminths

¥        Means worm

¥        Phyla

o         Annelida (segmented worms)

o         Nemathelminthes (Roundworms)

§          Nematoda

o         Platyhemlinthes (flatworms)

§          Trematoda (Flukes)

§          Cestoda (Tapeworms)

¥        Helminths belong to Metazoa.

¥        Integuments of parasitic Helminths

o         May be hardened, tough and elastic or relatively delicate

o         In most cases, resistant to digestion while alive

o         Frequently, it is provided with spines, hooks, cutting plates, stylets or other armature for attachment, penetration or abrasions of host’s tissues, particularly common in the region of the mouth.

¥        Sexes are separate in majority of roundworms

¥        Hermaphrodism is more in Trematodes and Cestodes.

¥        Many parasitic helminthes require one or more intermediate host.

¥        Among the unfavorable conditions that may be encountered by the egg or the hatched larvae:

o         Desiccation

o         Fermentation

o         Overgrowth by bacteria or fungi

¥        Unfavorable conditions that prevent embryonation or hatching or kill the larvae:

o         Inability to find or failure to e taken appropriate host

o         Death of intermediate host

o         Man-made barrier that kill parasite in the intermediate host or prevent it to arrive to the definitive host

¥        Malnutrition in helminthic infection:

o         Interferes with some types of antibody production

o         May decrease inflammatory reaction, lower resistance

o         Deficient diet with helminthiasis may cause:

§          Anorexia

§          Impaired liver function

§          Fever

§          Neutralization of digestive enzymes

§          Failure to absorb important vitamins

§          Aggravation of hemorrhages

 

NEMATODES

¥        Roundworms

¥        Include numerous free-living and parasitic species.

¥        Largest numbers of helminth of man belong to the roundworm.

 

Morphology

 

¥        Unsegmented, elongate-cylindroidal in shaped and tapered at both ends

¥        Bilaterally symmetrical but with secondary tri-radiate symmetry at the anterior end

¥        Body cavity is pseudocoele; t is not lined with mesothelium

¥        Parasitic Nematodes are generally light cream-white color, but the females of the smaller form may appear darker when filled with dark-colored eggs.

¥        Integument of Nematodes:

o         Cuticle – outer, hyaline and non-cellular

o         Hypodermis – subcuticular epithelium

o         Somatic muscle – layer of muscle cells

Nematodes do not have circulatory system.

Nematodes lack circular muscle.

Digestive System

 

¥        A simple tube extending from the mouth to the anus.

¥        The mouth is frequently provided with a capsular thickening.

¥        Oral, pharyngeal or buccal cavity may be tubular, funnel-shaped or long and capillary in type.

¥        Esophagus varies in shape, has striated muscular wall, a tri-radiate lumen, with associated esophageal glands, but at the distal end, it has usually an enlarged muscular bulb that is provided with strong valves, capable of closing the opening into the midgut or intestine.

¥        Intestine or midgut is a flattened tube with a wide lumen that follows a straight course from the esophagus to the rectum.

¥        Rectum is situated just behind the intestine and opens outward through the anus in female or in the male, through the cloaca, in male worm the spermatozoa is also discharged through the cloaca.

 

Excretory System

 

¥        It is consist of archetypical pair of lateral collecting tubules or canals may be asymmetrical and may be represented by a single lateral or median gland cell.

¥        Excretory pore opens midventrally in the cephalic and cervical region.

 

Nervous System

 

¥        Consist of a dorsal, a ventral and four lateral longitudinal trunks with transverse commissures.

¥        The most important commissure is the circumesophageal ring, which constitute a nerve center/

¥        Nerve endings terminate in all of the important organs and integuments, specially the sensory papillae.

¥        There is probably a pair of laterally placed minute receptor organs amphids or lateral organs in the cephalic or cervical region of all Nematodes.

¥        In species without caudal glands, there is a pair of minute lateral postanal phasmids or caudal chemoreceptor organs.

¥        Adult worms react to touch, heat, and cold and probably to chemical stimulus.

 

Reproductive System

 

Male

¥        All nematodes parasitic in man have separate sexes.

¥        Males are usually smaller than females, commonly have a curved posterior end and are commonly provided with special organ in the perianal or caudal region that facilitate copulation.

¥        Male reproductive organs are situated in the posterior third of the body as a single coiled or convoluted tube; the various parts of which are differentiated from its inner end and outwards into:

o         Testis

o         Vas deferens

o         Seminal vesicle

o         Ejaculatory duct

o         Cloaca

Male accessory copulatory apparatus include:

o         Telamon

o         Gubernaculum

o         Copulatory spicules

o         Copulatory bursae or Bursae copulatrix – the perianal and caudal cuticle is extended into an umbrella-like expanse that is reinforced by ribbed thickenings to serve as copulatory disk around the vulvar opening of the female worm.

¥        Spermatozoa are usually amoeboid rather than flagellate.

 

Female

¥        Female genital system may be single as in Adenophorea and double as in Secernentea.

¥        The genital system is also a delicate thread-like tubule that includes:

o         Ovary

o         Oviduct

o         Seminal receptacle

o         Uterus

o         Ovejector

o         Vagina

o         Vulva

¥        The ovum passes from the ovary into the oviduct where it is fertilized.

¥        The true shell, a secretory product of the egg begins to form immediately after sperm penetration, and the vitelline membrane separating from the inner layer of the shell.

 

Cycles of Development

 

¥        Developmental stages include:

o         Adult

o         Egg

o         First stage larva

o         Second stage larva

o         Third stage larva

o         Fourth stage larva

¥        The larva undergoes several molts.

¥        In most Secernentean Nematode parasite of man, the infective stage usually is the third stage larva.

 

Manner of Transmission

 

1.       Ingestion of the embryonated eggs (Ascaris lumbricoides)

2.       Ingestion of the larvae (Ancylostoma duodenale and Necator americanus)

3.       Ingestion of the encysted larvae (Trichinella spiralis)

4.       Skin penetration (Ancylostoma and Necator)

5.       Arthropod vector (Wuchereria and Brugia)\

 

Manner of Attachment

 

1.       Anchorage with their thin and attenuated anterior end. (Trichuris)

2.       Oral attachment to the mucosa (Ancylostoma and Necator)

3.       Penetration of the tissue or invasion of the intestinal mucosa (Strongyloides)

4.       Retention in the field of the mucosa and pressure against it (Ascaris)

 

Nourishment of the parasites

 

1.       Ingestion of lysed tissues and blood by embedded worms (Trichuris)

2.       Sucking and ingestion of blood (Ancylostoma and Necator)

3.       Ingestion of nourishment from the body fluids (Wuchereria and Brugia)

4.       Ingestion of intestinal contents (Ascaris)

 

Subclass

 

¥        Adenophorea – includes roundworm WITHOUT phasmids or caudal chemoreceptors

¥        Secernentea – includes roundworm WITH phasmids or caudal chemoreceptors

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ADENOPHOREA

Trichuris trichiura

 

Disease: Trichuriasis, Trichocephaliasis, Whipworm

Common Name: Whipworm

Geographical Distribution: Cosmopolitan in distribution, but is more common in moist region of the world. Prevalence rate may be as high as 80%.

Habitat: Wall of the cecum and less commonly the walls of the appendix, colon or most posterior level of the ileum

 

Morphology

Adult

¥        Trichuris – hair ail

¥        Flesh-colored worm

¥        Attenuated in the anterior three-fifths of the body and fleshy in the posterior portion.

¥        Esophagus is a delicate capillary tubule, resembling a string of beads, bit it has been shown to have anterior muscles with stylet.

¥        Life span may be from 4 – 8 years

Male

- 30 – 45 mm in length

- its caudal extremity coiled through 360 degrees or more

- genitalia consist of a long sacculate testis, vas deferens and ejaculatory tubule, which empty into the cloaca

-a single lanceolate spicule protrudes through a retractile (pineal) sheath that has bulbous termination, covered with many small, recurved spines

                Female

- 35 – 50 mm in length

- bluntly rounded at the posterior end

- genitalia consist of a single sacculate ovary, oviduct and uterus, which constricts as it joins the vagina, which in turn continues as serpentine tubule to the vulva, which lies ventrally at the anterior extremity of the fleshy portion of the worm

                Egg

- 50 – 54 um X 22 – 23 um

- barrel-shaped or lemon-shaped

- in addition to a vitelline membrane, have a triple shell, the outermost layer of which is brown

- have bipolar, unstained, intralaminar prominences that have the appearance of mucoid plugs

- described as Japanese lantern or like the ball of football (American football)

- discharged and evacuated with the feces in the unsegmented stage

- moisture is essential for the development of the egg

There is apparently no larval ecdysis with the egg shell

 

LIFE CYCLE

 

1.       Manner of transmission is by ingestion of the fully embryonated eggs through contaminated food and drink.

2.       The larvae hatch in the small intestine and enter the crypts of lower intestine and colon, eventually entering the epithelium of the cecum and the other parts of the large intestine.

3.       It grows into adult worm in about 3 months.

4.       The female is fertilized and lay eggs.

5.       The eggs are evacuated with the feces in the soil.

6.       The eggs become embryonated in about 3 weeks, after which an active first stage larva is coiled inside the shell.

 

Pathogenesis

 

1.       Mechanical and allergic processes may be involved.

2.       The anterior end of the worms, interlaced in the colonic mucosa, apparently produce little damage to the host unless present in large number.

 

 

 

 

Clinical Manifestations

 

1.       Light whipworm infections are usually asymptomatic.

2.       Depends on the intensity of infection (worm burden), the duration of infection and the age and nutrition of the host.

3.       In heavy infection in children (2 – 6 years of age), a diffuse colitis that causes chronic diarrhea typically occurs.

4.       In massive infection, worms attached to the mucosa of the rectum and chronic dysentery with abdominal cramps, and severe rectal tenesmus are produced.

5.       Anal sphincter tone is lost and rectum tends to prolapse

6.       Hypochromic anemia, which is seen in cases with prolonged massive infection, is due to the general malnutrition and blood loss from the friable colon and prolapsed rectum.

7.       There may be growth retardation and fingers may be clubbed.

8.       Clinical picture may be consisting of:

a.       Frequent, small, blood-streaked diarrheic stools

b.       Abdominal pain and tenderness

c.        Nausea and vomiting

d.       Anemia

e.       Weight loss

f.         Occasional rectal prolapse with worms embedded in the mucosa

 

Diagnosis

 

1.       Demonstration of the eggs in the patient’s feces by direst fecal smear

2.       Demonstration of the eggs from the feces by concentration technique like centrifugation flotation or sedimentation.

3.       Examination of the rectal mucosa by means of protoscopy or during prolapse.

 

Drug Used

 

1.       Mebendazole

2.       Oxantel/Pyrantel pamoate

 

Preventive Measures

 

1.       Treatment of infected individuals

2.       Sanitary disposal of human feces

3.       Washing of hands before and after meals

4.       Instructions of children about sanitation and proper hygiene

5.       Thorough washing and scalding of uncooked vegetables; especially important in countries using night soil for fertilized.

 

 

Capillaria philippinensis

 

Disease: Mystery disease, Pudok’s disease, Intestinal capillariasis

Geographical Distribution: Widely distributed in Northern Luzon, some parts of Mindanao, Thailand and isolated cases in Iran and Egypt

Habitat: Mucosa of the small intestine, predominantly the jejunum

 

Morphology

 

Adult

                Male

- 2 – 3.17 mm in length

- the anterior end has the esophagus

- there is ventrolateral caudal expansion

- the spicule starts at the posterior fourth of the parasite

- with an extraordinary long, smooth spicular sheath (overhanging sheath)

 

                Female

- 2.5 – 4.3 mm in length

- the body is divided into 2 almost equal parts:

¥        The anterior contains the esophagus and esophageal gland cells (schistosomes or stichocytes)

¥        The posterior contains the intestine and the reproductive system with slightly prominent vulva described as pouting.

 

Egg
- 20 – 40 um in size

- almost straight on the side

- the egg shell is coarsely pitted

- with flattened bipolar mucus plug

- require at least 10 – 14 days to be embryonated

- require at least 3 weeks to develop into the infective stage in fish

 

LIFE CYCLE

 

1.       The manner of transmission is by ingestion of the third stage larva from improperly cooked or raw fish.

2.       It goes into the stomach and small intestine, where they become adult male and female. These are the first generation adults.

3.       The first generation females are larviparous and lay larvae.

4.       The larvae develop into the second generation males and females.

5.       The second generation females are oviparous and lay eggs.

6.       The eggs are evacuated with the feces in a body of fresh or brackish water

7.       The eggs embryonate in the water and are ingested by fish.

8.       The eggs hatch in the intestine of the fish.

9.       Developed into the infective stage, third stage larva.

 

¥        Intermediate hosts are fish called Bagsit, Bagsang, and Birut.

¥        The finding of larval stages and of oviparous as well as larviparous females in the intestine, suggest that the parasite multiplies in the intestine and that overwhelming infections are the results of autoinfection.

¥        The adults, larvae, and eggs can be demonstrated in the feces.

 

Pathogenesis

 

¥        Most of the worms are seen between the mucosa and the basement membrane of the glands.

¥        There is derangement of intestinal function with malabsorption and loss of fluid, electrolytes and plasma protein into the intestinal tract.

¥        Hypoprotenemia, low blood calcium, potassium and cholesterol levels and other features of a protein-wasting enteropathy are encountered.

 

Clinical Manifestations

 

¥        There is intestinal malabsorption with symptoms of chronic diarrhea and borborygmus (gurgling stomach).

¥        There is abdominal pain with voluminous, sprue-like stools,

¥        There is protein losing enteropathy, the patient loses weight rapidly and becomes weak.

¥        The patient eventually appears emaciated, cachetic with generalized anasarca.

¥        Death may occur 2 weeks to 2 months after the onset of symptoms due o pneumonia, heart failure, hypokalemia or cerebral edema.

 

Diagnosis

 

                Demonstration of the eggs, larvae or adult worms from the feces.

 

Drug of Choice

 

1.       Mebenazole

2.       Alternating drug may be Albendazole

 

Preventive Measures

 

1.       Proper cooking of fish

2.       Proper disposal of human wastes

 

Trichinella spiralis

 

Disease: Trichinosis, Trichinelliasis, Trichiniasis

Geographical Distribution: Cosmopolitan in distribution but is much less important as an infection of man in the tropics and the Orient than it is in Europe and US.

Habitat: Duodenum and jejunum

 

Morphology

 

¥        Both female and male are minute and thread-like

¥        The anterior part of the body is largely filled with stichosomes, a compact cord of linearly arranged gland-like cells called stichocytes.

¥        Anterior to the stichosomes, the esophagus is muscular.

¥        The esophagus is extremely narrow.

 

Male

        - 1.2 mm in length by 60 um in maximum diameter

        - the slender anterior is relatively delicate with cephalic papillae

        - the posterior end bears a pair of conspicuous conical papillae, one on either side of the cloacal oroifice.

        - a single testis is situated a short distance from the posterior end of the body

Female

        - 2.2 mm in length, early 2 times s long as the male and one and a half times as broad.

        - a single ovary is in the extreme posterior part of the body, with the oviduct, seminal receptacle, uterus and

  vagina forming a nearly straight channel to the vulva

- the vulva is on the ventral side of the body about ¼ the body length from the anterior.

 

LIFE CYCLE

 

1.       The manner of transmission is by ingestion of the viable encysted larvae from improperly cooked or raw meat.

2.       The cysts are digested free from the meat in the stomach and the larvae excyst there or in the duodenum or jejunum.

3.       The larvae invade the mucosal epithelium and rapidly develop through 4 larval stages.

4.       They become mature worms early on the second day of infection.

5.       Mating may occur as early as 30 hours of infection and most of the females will be inseminated during the second day.

6.       Soon after insemination, the females began to produce eggs that develop into minute larvae in the uterus.

7.       By the sixth day of infection, they begin depositing motile larvae.

8.       larvae deposited by the worms in the intestine enter the lymphatic vessels and from there gain access to the general circulation and may become lodged in various locations, including the myocardium, brain, CSF and body cavities.

9.       The larvae later re-enter the blood stream and finally reach the striated muscles where they become encapsulate within the fiber.

10.    It becomes a dad-end cycle in man.

 

¥        Man usually acquires the infection from eating inadequately cooked or improperly processed infected lean pork.

¥        Country sausages and certain types of European style sausages prepared from a single heavily infective pig, provides the most common source of clinical trichinosis.

¥        Most heavily infected muscles are relatively poor in glycogen, those that are constantly active like, the diaphragm, muscles of the larynx, tongue, abdominal and intercostals muscles, biceps, psoas, pectoral muscles, gastrocnemius and deltoid muscles.

¥        The larvae are coiled in a spiral and gradually become surrounded by a sheath derived from the muscle fiber.

¥        The capsule is an adventitious, ellipsoidal sheath, resulting from round cells and eosinophilic infiltration around the tightly coiled larva and the long axis of the cyst, parallels that of the muscle fibers.

¥        The entire cyst wall results from host-tissue reaction and therefore is induced, rather than secreted by the larva.

¥        The encysted larvae may remain viable for many years, although calcification often occurs within 6 – 9 months.

¥        Two hosts are required to complete the cycle.

¥        Principal Maintenance Cycle:

1.       Pig to pig – in areas where the custom of feeding household garbage to pigs is widespread

2.       Rat – rat – in the presence or absence of appreciable infection in pigs

3.       Sylvatic – perpetuated by carnivorous or omnivorous wild hosts

 

Pathologic and Symptomatology

 

Intestinal Phase

·          Inflammation of the duodenal and jejunal mucosa caused by the penetration and development of the adult worm

·          May produce symptoms of malaise, nausea, vomiting, abdominal cramps and diarrhea.

Stage of Muscle Invasion

·          Typical findings are fever, facial edema, pain, swelling and weakness of the involved muscles.

·          Less common symptoms include headache, flushing of the face, conjunctivitis, pruritus, anorexia and thirst.

·          Lymph nodes are frequently become enlarged and tender.

·          Damage to muscles may cause difficulty in eye movement, breathing, chewing, swallowing and speech, or in the use of the extremities.

·          Eosinophilia reaches its peak in the third or fourth week.

·          Myocarditis is the most grave manifestation of Trichinosis and death from myocarditis usually occurs between the fourth and eight weeks of infection.

·          Encephalitis, meningitis and neurological disturbances also may occur in this stage.

Stage of Convalescence

·          Fever generally subsides and muscular symptoms begin to decrease.

·          If edema has been marked, diuresis may occur.

·          Appetite returns to normal and malaise subsides.

·          Myocarditis may still be present at this stage and physical exertion may precipitate congestive heart failure.

·          Bronchopneumonia, vascular thrombosis and encephalitis may also complicate convalescence.

·          Eventually, all symptoms subside and finally the larvae itself calcify.

·          The calcified cyst can be seen grossly in exposed muscle fibers.

 

Diagnosis

¥        History of having eaten raw or inadequately cooked or improperly processed meat, usually pork.

¥        Physical examination

¥        Laboratory examination

o         Demonstration of the free or encapsulated larvae in compressed small samples of the involved muscles obtained by biopsy.

§          Muscle strips obtained by biopsy and digested in artificial gastric juice for several hours at 37° C provided a concentrate that is more diagnostic

§          Xenodiagnosis – infected muscles are fed to uninfected albino mice, then killed a month later and demonstrate the encysted larvae.

o         Bachman intradermal test

o         Bentonite Flocculation test (BF)

o         Latex Agglutination Test

o         Complement Fixation Test

o         Indirect hemagglutination Test

 

Drug Used

 

1.       Mebendazole

2.       Albendazole

3.       ACTH or Adrenocorticosteriod drugs

 

Preventive Measures

 

1.       Proper cooking or deep freezing of all pork expected to be eaten by man.

2.       Avoid feed raw garbage to hogs.

3.       Exterminate rats around the farms.

SECERNENTEA

 

Ascaris lumbricoides

 

Common Name: Giant Intestinal roundworm, Large Intestinal roundworm

Disease: Intestinal ascariasis, Ascariasis, Ascariasis pneumonitis

Geographical Distribution: Observed and reported by many ancient people, the most cosmopolitan and most common of all human helminthes

 

Morphology

 

¥        The body is cylindrical, tapering gradually at the posterior end.

¥        A lateral line can be seen as a whitish streak along the entire length of the flesh-colored body.

¥        There are 3 lips, a broad median dorsal one and a pair of ventrolateral ones that are finely denticulated.

¥        The adult worm may live as long as 20 months but the usual life span is about 1 year.

Male

·          15 – 31 cm in length by 2 – 4 mm in diameter

·          The posterior end is curved ventrally.

·          Its genitalia consist of a long, single tubule made up of testis, vas deferens and ejaculatory duct, which is tortuously coiled in the posterior half of the worm and opens into the cloaca which is sub-terminal.

Female

·          20 – 35 cm, less common up to 49 cm in length by 3 -6 in diameter.

·          The vulva is situated midventrally near the junction of the anterior and middle thirds of the body.

·          Extending to the inside, there is vulva, a single vagina that branches to form the pair of genital tubules, each consisting of uterus, seminal receptacle, oviduct and ovary.

·          These tubules are coiled through the middle and posterior thirds of the body.

Egg

·          It is broadly ovoid with thick transparent shell consist of:

1.       Albuminoid layer – a coarsely mammilated layer, usually bile-stained, giving a yellowish brown color of the egg.

2.       Glycogen layer – a thick transparent middle layer.

3.       Vitelline layer – an innermost lipoidal vitelline membrane NOT found in unfertilized eggs, it is inert, being impermeable, it prevents toxic substances in the immediate environment from injuring embryo.

·          If the albuminoid layer of the egg was removed, it is called decorticated and the egg becomes colorless.

·          Daily egg-laying in light infection has been estimated to be 200,000 for each female.

Fertilized egg

        - 45 – 75 um by 35 – 50 um in lesser diameter, when spherical approximately 60 um in diameter.

        - the ovum is unsegmented and contains a mass of coarse lecithin granules.

        - this egg develops in the soil and becomes embyonated egg, which have a larva or embryo inside,

this is the infective stage.

Unfertilized egg

        - 88 – 94 um by 39 – 44 um

        - usually elongate with a relatively thin middle layer of the shell.

        - often with little or no outer mammilated layer.

        -contain disorganized refractile mass.

        - does NOT have a vitelline layer and does NOT develop into embryonated egg.

 

LIFE CYCLE

 

1.       The manner of transmission is by ingestion of the embryonated eggs from contaminated food and drink.

2.       The eggs hatch in the small intestine and the larvae escape from the eggshell.

3.       The larvae penetrate the intestinal wall until it comes in contact with the mesenteric venules and then goes into venous circulation. The larvae reach the liver, then to the right side of the heart, going to both lungs, into the pulmonary capillaries.

4.       The larvae break the pulmonary capillary, goes into the alveoli, into the bronchioles, bronchi, trachea, epiglottis, and then the larvae are swallowed.

5.       The larvae go to the stomach, then to the small intestine, where they become adult male and female. The adult worms mate and the female laid eggs. The eggs are evacuated with the stool in the soil. The eggs develop in the soil and become embryonated. The embryonated eggs contaminate the food and drink.

¥        There is blood-lung phase in the life cycle.

¥        The parasite has to pass the blood and lungs before becoming adult.

 

Pathology and Symptomatology

 

¥        Pathogenic Stage

1.       Migrating larvae

a.       Break the pulmonary capillaries – there will be pedicel hemorrhages in the air sac (alveolus), cellular infiltration and consolidation.

- There is Ascariasis pneumonia, where the patient has fever, cough, eosinophilia dyspnea, and rales.

- This is probably one of the causes of Loeffler’s syndrome.

                                b.     If the larvae fail to break the pulmonary capillaries, they are carried to the systemic circulation

     and may be brought to the different parts of the body. The larvae may reach the brain, eyes

     and spinal cord producing a more dramatic signs and symptoms.

2.       Adult worms

a.       Intestinal ascariasis tends to be tolerated unless the infection is heavy or the intake of nutrients by the host is inadequate.

b.       In children, there may be intermittent colicky cramps, loss of appetite, fretfulness and the abdomen may be protuberant.

c.        Allergic manifestations include asthma and urticaria.

d.       Significant nutritional impairment is more or less proportional to the worm burden, there may be protein-caloric malnutrition or impairment of growth.

e.       The worms may congregate in a closely packed mass (Bolus of Ascaris) and produce intestinal obstruction.

f.         May enter the appendix, biliary, or pancreatic duct resulting in obstructive appendicitis, acute biliary obstruction or acute pancreatitis.

g.       The worm may perforate the intestinal wall and penetrate the liver producing Ascaris Liver Abscess.

 

Diagnosis

 

1.       Ascaris pneumonitis (Loeffler’s syndrome)

a.       Demonstration of the larvae from the sputum or gastric washing.

2.       Intestinal Ascariasis

a.       Demonstration of the eggs from the stool.

b.       X-ray shadows may produce Tramway sign.

c.        In patient given Barium swallow, adult Ascaris also ingest barium, giving the String sign.

 

Drug Used

 

1.       Mebendazole

2.       Albendazole

3.       Piperazine citrate

 

Preventive Measures – same with Trichuris trichiura

 

 

 

 

 

 

 

 

 

 

 

ASCARIS OF CATS AND DOGS

 

                                                                                Toxocara canis                                                   Toxocara cati

                                                                                (Dog Ascarid)                                                       (Cat Ascarid)

Geographical distribution                                  Cosmopolitan                                                      Cosmopolitan

Disease produced                                              Toxocariasis or                                                    Toxocariasis or

                                                                                Visceral larva migrant                                         Visceral larva migrant

Mature male                                                         4-6 cm, up to 13 cm                                            4-6 cm

Mature female                                                      6-10 cm, up to 20 cm                                          6-12 cm

Cervical alae                                                        much longer than broad                                    broad, tapering anteriorly

Egg                                                                         subglobose, thick-shelled &                             subglobose, thin-shelled &

                                                                                Coarsely pitted eggshell                                    finely pitted eggshell

 

VISCERAL LARVA MIGRAN: (Toxocariasis)

¥        Most common cause is Toxocara canis

¥        Some cause by Toxocara cati

¥        Occasionally caused by Strongyloides, Hookworm, Gnathostoma, and Spirometra

 

HUMAN INFECTION:

1.       The manner of transmission is by ingestion of the embryonated egg from contaminated food and drink.

2.       The eggs hatch in the small intestine and the larvae escape from the eggshells.

3.       The larvae penetrate the intestinal wall until it come in contact with the mesenteric venules and then goes into venous circulation.

4.       Many of the larvae reach the liver and sometimes into the lungs: they remain in the liver and will NOT develop into the adult stage.

5.       After an undetermined period of migration, they become embedded in a matrix of epitheliod cells and encapsulated dense fibrous tissues.

 

Pathology

 

¥        Migration of the larvae causes eosinophilic inflammation followed by granuloma formation.

¥        The severity depends on the number of larvae, tissue invaded and the duration of infection.

¥        The most constant and striking feature is high, sustained eosinophilia.

¥        There is the triad of marked eosinophilia, hepatomegaly and hyperglobulinemia.

 

Diagnosis

 

1.       Microprecipitation test

2.       ELISA test

3.       Biopsy

 

Drug used

 

1.       Thiabendazole

2.       Corticosteroids

 

Preventive Measures

 

1.       Protect the children from contact with infected dogs and cats.

2.       Protect the children’s playground from the stool of dogs and cats.

 

 

 

 

 

 

 

 

 

 

 

ASCARIS OF SEA ANIMALS

Anisakis sp.

 

DISEASE PRODUCED:  Anisakiasis, Herring worm disease

 

HIMAN INFECTION:

 

Ø       Manner of transmission is by ingestion of the third stage larvae in the flesh of raw fish in Europe, the source is usually raw green herrin; in japan, the vehicle is likely sashimi

Ø       It may invade the stomach and the upper small intestine and produce an inflammatory response of varying severity.

Ø       Most commonly the stomach and the upper small intestine are involved, severe inflammatory reaction surrounds the larvae.

Ø       The local tissue response varies from a granulumatous, foreign body type reaction to massive eosinophilic infiltration with hemorrhages, fibrinus exudates and edema of intestinal wall that produces intestinal obstruction.

 

DIAGNOSIS:

 

v       Serodiagnostic test

v       Gastroscopy and surgery

 

TREATMENT:

 

v       Surgical Intervention

 

HOOKWORM

                                                                                      Necator                                                                 Ancyclostoma

Cephalic Curvature                                             Against the body                                                  Along the body

Vulvar Opening                                                    Anterior to the midpoint                                      Posterior to the midpoint

Buccal Capsule                                                   Semi-lunar cutting plate                                     With vental-teeth

Copulatory Bursae                                              Longer than broad                                              Broader than long                              

Copulatory Spicules                                           Long, fused at the tip (Barb)                              Separate and pointed

            Eggs are almost identical for Necator and Ancyclostoma

 

LIFE CYCLE:         

 

Ø       Just like Ascaris, there is “blood-lung phase” in the life cycle.

Ø       The infective stage Hookworm to man is the filariform larva.

Ø     The manner of transmission for Necator americanus is more of skin penetration of the filariform larva than ingestion of the filariform larva.

Ø       The manner of transmission for Ancyclostoma duodenale is more of ingestion of the filariform larva rather than skin penetration

¥        Skin Penetration of Filariform Larva

1. Skin penetration of filariform larva

2.  The larvae find their way into the venules, then goes to the venous circulation.

3. The larvae reach the liver, then goes to the right side of the heart, going to both lungs, through the pulmonary capillaries.

4. The larvae break the pulmonary capillaries, goes into the alveolus (air sac), into the bronchioles, bronchi, trachea, and epiglottis and then the larvae are swallowed.

5. The larvae go to the stomach, then to the small intestine, where they become adult male and female.

6. The adult worms mate and the female laid eggs.

7. The eggs are evacuated with the stool in the soil.

8. The eggs develop in the soil and become embryonated.

9. The eggs hatch, the embryo or larva escape from the eggshell.

10.    The larva develops into rhabditiform larva (feeding stage) then develops to filariform larva (parasitic stage) which is the infective stage.

 

 

¥        Ingestion of the Filariform Larva

1.       The filariform larvae are ingested.

2.       The larve go to the stomach, then to the small intestine, where they become adult male and female.

3.       The adult worms mate and the female laid eggs.

4.       The eggs are evacuated with the stool in the soil.

5.       The eggs develop in the soil and become embryonated.

6.       The eggs hatch, the embryo or larvae escape from the eggshell.

7.       The larvae develop into the rhabditiform larvae, and then develop into filariform larvae which are the infective stage.

Ø       There is NO blood – lung phase if the filariform larvae are ingested.

 

Necator americanus

Common Name: American hookworm, American murderer

Disease produced: Necatoriasis, Uncinariasis

Geographical distribution: Predominant hookworm of Central and South Africa, South Asia, Northern, Central and South America

 

Morphology

 

Ø       They are attenuated at the anterior end with buccal capsule.

Ø       Provided with a ventral and a dorsal pair of semi-lunar cutting plates.

Ø       The living worms are grayish yellow, at times with reddish undertones.

Male

¥   7 – 9 mm in length X 0.3 mm in greatest diameter.

¥   Copulatory bursa is longer than broad.

¥   Copulatory spicules are long and slender, fused at the tip, forming a delicate barb tip.

Female

¥  Vulva is anterior to the midpoint.

Egg

¥   Resemble those of Ancylostoma duodenale but tend to be longer and somewhat more elongated

¥   64 – 76 um X 36 – 40 um

¥   The eggshell is relatively thin, clear and transparent with two to eight cell stages inside.

Larva

¥  Rhabditiform larva of Necator americanus and Ancylostoma duodenale

o         Stouter, larger, more attenuated posteriorly

o         Have a longer buccal capsule or cavity (open mouth), with rhabditiform type of esophagus

o         Small genital primordium

¥   Filariform larva of Necator americanus and Ancylostoma duodenale

o          close mouth, with slender, filariform type of esophagus

o         have short esophagus, about 20% of the body

o         the posterior end is pointed

o         with tightly fitting sheath and for Necator, the sheath is pitted

 

Pathology

 

Ø       When the larvae penetrate the skin, they produce maculo-papules, localized erythema and itchiness

Ø       In the lungs, they break the pulmonary capillaries (Loeffler’s syndrome), just like in Ascaris, there is blood-lung phase in the life cycle, producing the same signs and symptoms.

Ø       The adult worm suck and ingest blood.

o         Necator americanus consumed as much as 0.03 ml/worm/day

o         Ancylostoma duodenale consumed about 0.15 to 0.26 ml/worm/day

Ø       There is ontinuous blood loss and depletion of the iron reserve.

o         There is Hookworm anemia.

o         There is iron deficiency anemia.

o         There are microcytic hypochromic red blood cells

 

 

 

 

 

Ø       Hookworm anemia

o         The presence of hookworm eggs in the stool of an anemic patient may be incidental or casual.

o         There are some factors to be considered like:

§          Species of hookworm

§          Worm burden (Number of worms)

§          Duration of infection

Ø       The appetite may be poor or enormous and associated with pica or geophagia

 

Diagnosis

 

Ø       Demonstration of the eggs from the stool.

o         Direct Fecal Smear

o         Kato – Katz Method

o         Zinc Sulfate Centrifugal Flotation test

o         Formalin – Ether Concentration

Ø       Harada Mori Method – for the demonstration of the larvae.

 

Drug Used

 

Ø       Just like in Ascaris plus iron preparation for anemia.

 

Ancylostoma duodenale

 

Common Name: Old world Hookworm

Disease Produced: Ancylostomiasis

Geographical Distribution: Southern Europe, China and Japan but less common than Necator

 

Morphology

Ø       They are relatively stout, cylindroid, slightly constricted anteriorly

Ø       Have two pairs of ventral teeth and a pair of inconspicuous teeth

Ø       Has a cervical curvature, so that the anterior end is directed dorsoanteriorly

Ø       The living worm is pinkish or creamy gray in color

 

Male

§          8 – 11 mm in length X 0.4 – 0.5 mm in greatest diameter

§          Copulatory bursa is broader than longer

§          Copulatory spicules are separated and pointed

 

Female

§          Vulva is posterior to the midpoint

 

Egg

§          Almost identical with the egg of Necator americanus

 

Pathology and Symptomatology

Ø       They are the same with Necator.

Ø       The signs and symptoms observed following ingestion of Ancylostoma duodenale larvae suggest that not only do larvae pass directly to the small intestine where they develop, but others penetrate the mucous membrane of the mouth and pharynx carrying out a lung migration.

Ø       The syndrome caused by these migrating larvae has been called Wakana disease in Japan.

 

Diagnosis:

Ø       The same as in Necator.

 

Drug Used:

Ø       The same as in Necator.

 

Preventive Measures: (Hookworm infection (Necator and Ancylostoma)

1.       Sanitary disposal of fecal waste.

2.       Protection of susceptible individual.

3.       Treatment of infected individual

4.       Prevent skin from the filariform larvae.

 

Cutaneous Larva Migrans (Creeping Eruption)

Ø       A dermatitis characterized by serpiginous, intra-cutaneous lesions caused by migration of Nematode larvae that normally do not infect the human host.

Ø       The most common cause is Ancylostoma braziliense.

¨        With a pair of large ventral teeth and a pair of small, inconspicuous teeth

Ø       Also by Ancylostoma caninum

¨        With three pairs of large ventral teeth

Ø       Prevalent in the tropical and subtropical countries of the world.

Ø       Larvae of Hookworm of lower animals can not pass through the skin of humans

Ø       At the point of larvae invasion, indurated reddish, itchy papules developed.

Ø       In 2 or 3 days, narrow, linear, slightly elevated, erythematous, serpiginous, intracutaneous tunnels are produced by the migrating larvae.

Ø       The itching is intense especially at night and scratching may lead to secondary infection.

Ø       The feet, legs, and hands are most commonly involved.

Ø       Systemic treatment with Thiabendazole and locally by spraying the larvae with Ethyl chloride

Ø       Avoid skin contact with contaminated soil.

 

Strongyloides stercoralis

Common Name: Threadworm

Disease Produced: Strongyloidiasis, Strongyloidosis, Cochin-China diarrhea

Geographical Distribution: Primarily adapted in warm climates, but it has been reported, sporadically in temperate and cold regions

Morphology

                Free Living Generation (Rhabditoid)

                                Male

                                                - 0.7 – 1.0 mm in length  40 – 50 um in diameter

                                                - broadly fusiform

                                                - with 2 spicules and gubernaculum

                                                - the tail portion is pointed and curved ventrally

                                Female

                                                - 1.0 – 1.7 mm  X 50 – 75 um

                                                - stout and had two-horned uterus

                                                - short vulva opens near the middle of the ventral side

                Parasitic Generation (Filariform)

                Male

                                - the same as in free-living male

                Female

                                - delicate and filariform

                                - 2.7 mm in length X 30 – 40 um in width

                                - cylindrical esophagus extend through the anterior third or two-fifths of the body

                                - with paired uteri and short vulva

 

                                                                Hookworm                                                           Strongyloides stercoralis

Rhabditiform larva               Longer buccal cavity                                                           Shorter buccal cavity

                                                Small genital primordium                                                  Conspicuous genital primordium

 

Filariform larva                     Short esophagus, 20%                                                      Longer, 40% of the body

                                                Pointed posterior end                                                         Bifid or notched posterior end

                                                With tightly fitting sheath                                                    NO sheath

 

Life Cycle

Free Living generation (Indirect Development)

1.       The rhabditiform larvae are in the soil on the feeding stage.

2.       Under favorable condition in the soil, the rhabditiform larvae will develop into adult male and females.

3.       The females will be fertilized.

4.       The females lay eggs, hatch and rhabditiform larvae escape from the eggshell.

5.       The rhabditiform larvae are in the soil.

Parasitic Generation (Direct Development)

1.       Under unfavorable condition in the soil, the rhabditoform larvae in the soil develop into filariform larvae.

2.       The filariform larvae penetrate the skin of man

3.       Come in contact with the venules and then goes into venous circulation.

4.       The larvae reach the liver, then go to the right side of the heart, going to both lungs, into the pulmonary capillaries.

5.       The larvae breaks the pulmonary capillaries, goes into the alveolus (air sac), into the bronchioles, bronchi, trachea, epiglottis and then the larvae are swallowed.

6.       The larvae go to the stomach, then to the small intestine, where they become adult males and females.

7.       The adult worms mate and the females lay eggs.

8.       The eggs hatch and the rhabditiform larvae are evacuated with the stool in the soil.

Autoinfection (Internal Autoinfection)

1.       The rhabditiform larvae in the large intestine develop into dwarf filariform larvae.

2.       The dwarf filariform larvae penetrate the intestinal wall, until they come in contact with the venules, then go to venous circulation, the continue the cycle.

Autoinfection (External Autoinfection)

1.       The rhabditiform larvae in the large intestine develop into dwarf filariform larvae.

2.       The dwarf filariform larvae crawl of the anus.

3.       The dwarf filariform larvae penetrate the skin at the perianal region.

4.       Until it come in contact with the venules, goes into venous circulation and continue the cycle.

 

Pathology and Symptomatology

Ø       Strongyloides infection are light and go unnoticed by the human host, as they produce no significant symptoms.

Ø       There is blood-lung phase in the life cycle, that it is another cause of Loeffler’s syndrome.

Ø       Moderate infection with the parasitic females embedded primarily in the duodenal region, may cause a burning, dull or sharp, non-radiating, mid-epigastric pain.

Ø       Nausea and vomiting may be present, diarrhea and constipation alternate.

Ø       Long-standing and heavy infections result in weight loss and chronic dysentery accompanied by malabsorption and steatorrhea.

 

Diagnosis:

                Demonstration of the motile rhabditiform larvae

                                - from the stool

                                - from the duodenal fluid

                                - from String test

                                - use of Baermann technique

 

Drug Used:

                Mebendazole

                Albendazole

                Thiabendazole

 

Preventive Measures:

                Like in Hookworm infection

 

Enterobius vermicularis

 

Common Name: Pinworm, Seat worm, Society worm

Disease Produced: Enterobiasis, Oxyuriasis

Geographical Distribution: Cosmopolitan in distribution, more common in temperate and in cold regions

 

Morphology

                They are characterized by having cephalic alae.

                With prominent bulbous esophagus.

               

Male

                                - 2 – 5 mm in length X 0.1 – 0.2 mm in diameter

                                - Posterior end strongly curved ventrally

               

Female

                                - 8 – 13 mm in length X 0.3 – 0.5 mm in diameter

                                - Tail portion is sharply pointed

                                - The vulva opens mid-ventrally, just in front of the middle third of the body

                                - In gravid females, the uteri are tremendously distended, so that the entire body is packed with

   eggs.

                Eggs

                                - 50 – 60 um X 20 – 30 um

                                - elongate-ovoidal, distinctly compressed laterally, flattened on one side

                                - no intermediate host is required for development

                                - infective within few hours after they are deposited

 

Life Cycle

1.       Manner of transmission is by:

- direct anus to mouth by finger contamination

- anus to mouth by soiled night clothes

- sleeping in the same bed or bedroom with carriers

- airborne eggs that are dislodged from bed linens and clothes

- autoinfection

                2. The eggs reach the small intestine.

                3. The eggs hatch and the larvae escape from the eggshell.

                4. On reaching the cecal region, the larvae develop into adult males and females.

                5. The females are fertilized and become gravid.

                6. The gravid females migrate down to the colon and out to the anus to crawl on the perianal and perineal

    skin.

                7. The females lay their eggs on the perianal and perineal skin.

                8. The eggs become infective.

 

Pathology and Symptomatology

                - More common in children then adult

                - Oviposition at the perianal and perineal skin produces pruritus, this condition results in scratching the

   area, and at times causing scarcification.

- Oviposition usually takes place between 10 pm to 2 am.

- This is Nocturnal Pruritus Ani

- In female patient, the female worm may enter the vagina, producing vaginitis.

- The adult worm may also go to the appendix, producing appendicitis.

- In children, nervousness. Insomnia, nightmares, and even convulsions have been attributed to

   Enterobiasis.

 

Diagnosis

1.       Recovery of the eggs from the stool (less than 5%) perianal scrapings or swabs, or from under the

fingernails.

2.       Using NIH swabs or Graham Scotch Tape technique, usually in the morning before bathing.

3.       Capture of the adult worm, following enemas, or when females migrate from the anus.

 

Drug Used and Preventive Measures:

                Same as in Ascaris

 

Gnathostoma spinigerum

Disease Produced: Gnathostomiasis

Geographical Distribution: Found in many countries of the Orient, but the most important foci for human infection are Japan and Thailand

 

Morphology:

¥        They are stout, reddish and slightly transparent.

¥        With a subglobose cephalic swelling separated from the remainder of the worm by a cervical constriction.

¥        They are usually curved ventrally at both ends.

¥        The anterior half of the worm is covered with leaf-like spines.

¥        The cephalic swelling is covered with 4 – 8 transverse rows of sharp recurved hooks.

Male

                - 11 – 25 mm in length

                - has pseudo-bursa, with 4 pairs of perianal nipple-shaped papillae

                - the copulatory spicules are chitinoid rods.

Female

                - 25 – 54 mm in length

                - the vulva is slightly postequatorial in position

                - vagina is long and is anteriorly directed

Egg

                - 65 – 70 um X 38 – 40 um

                - ovoid, transparent and superficially pitted

                - with a mucoid plug at one end

                - unembryonated when laid

 

Life Cycle:

1.       The adult male and female worms inhabit the tumor which they produced in the wall of the stomach of cats, their wild relatives and dogs.

2.       The eggs are extruded from the lesions and are evacuated with the feces into a body of water, where they embryonate and hatch.

3.       The larvae are ingested by species of Cyclops (Copepods) in which they transform into the second-stage larvae (L₂)

4.       When the infected Cyclops (Copepods) are eaten by fishes, frogs, or snakes, the larvae develop into the third-stage larvae (L₃) in the flesh of these animals. This is called “primary infection”.

5.       Then the cats, their wild relatives and dogs ingest the third-stage larvae (L₃) from fishes, frogs or snakes, the larvae will become adult male and female in the stomach wall.

¥        Man is an accidental host and the larvae do not mature in man, but migrate throughout the body.

¥        Man becomes infected after ingestion of the third-stage larvae from improperly cooked or raw fishes, frogs or snakes.

¥        In Thailand, domestic duck and chicken probably constitute the more important sources of infection in man.

¥        Infection occasionally may be acquired directly from copepods swallowed in drinking water taken from ponds or streams.

 

Pathology and Symptomatology

                Gnathostomiasis Interna

                                - The adult worms are coiled inside the tumors of the digestive tract of the definitive hosts.

                                - This condition has never been described in man.

                Gnathostomiasis Externa

1.       Development of abscess pockets or indurated nodules with abscessed centers.

2.        Formation of deep cutaneous or subcutaneous tunnels in which the worm migrate, causing Cutaneous Larva Migrans or Creeping Eruption.

§          The lesions are deeper compare to those produce by Hookworms.

§          Subcutaneous or even frequently in the muscle.

§          They appear as intermittent migratory swellings that are circumscribed.

§          If the swelling is subcutaneous, there are usually signs of inflammation, redness and pain.

§          The swelling appears most frequently on the upper extremity, shoulder, neck, thorax, face, scalp, abdominal wall, thigh and dorsum of the foot.

§          The swelling is believed to be due to allergic reaction to the worm and its products, and to involve a little mechanical damage.

§          Any parts of the body may be invaded such as the mucous membrane of the mouth, pharynx, intestine, anus and cervix producing Visceral Larva Migrans.

§          May enter the central nervous system migrating along a peripheral nerve, into the spinal cord, to the brain

·    Pain, paralysis, seizures or coma may be produced

·    Eosinophilic meningitis is more severe, than Angiostrongylus cantonensis., frequently fatal course with paralysis or coma and with bloody or xanthochromic cerebrospinal fluid.

·    There are nerve root pain, paralysis of the extremities of sudden change in sensations

 

Diagnosis:

1.       Demonstration and identification of the worm from the lesion.

2.       Intradermal Test

3.       Precipitin Test

4.       ELISA Test

 

Treatment:

1.       Surgical removal

2.       Mebendazole

 

Preventive Measures:

1.       Proper cooking of fishes, chicken, ducks, and frogs

2.       Drinking clean water.

 

Angiostrongylus cantonensis

 

Common Name: Rodent Lungworm

Geographical Distribution: Has been found in China, Tahiti, Hawaii, Philippines, Sumatra, Cuba and India

 

Morphology:

§          The worm is delicate filiform, almost imperceptibly narrowed at both extremities.

§          In the living state, it has pallied hu.

§          The cuticula is smooth and is slightly thickened at the two extremities.

§          Lacking a buccal capsule, the mouth opens directly into a muscular esophagus.

 

Male

        - 16 – 19 mm in length X 0.26 mm in diameter

        - the small bursae copulatrix at the posterior extremity in directed ventrally

 

Female

        - 21 – 25 mm in length X 0.30 – 0.36 mm in diameter

        - the posterior end is shaped somewhat bluntly

        - with subterminal anal pore on the ventral aspect

 

Egg

        - 46 – 48 X 68 – 74 um

        - elongate ovoid with a delicate hyaline shell

        - unembryonated at the time of oviposition

 

Life Cycle

1.       The adult male and female in the pulmonary arteries of rodents (Ratus norvegicus and Ratus ratus).

2.       The female lay eggs and the eggs hatch in the lungs of the rodent hosts.

3.       The larvae migrate up to the trachea, epiglottis, and then swallowed.

4.       The first stage larvae are expelled with the feces in the soil.

5.       The first stage larvae are ingested by molluscan intermediate host (Achatina fulica, the Giant Africa snail or Giant Japanese snail and Pila luzonica or Pila conica) in which the larvae develop into the second stage larva, then the third stage larva, the infective stage.

6.       The third stage larvae are ingested by rats, migrate to the brain.

7.       After the final molt, the young adults migrate to the pulmonary arteries, here the female lay eggs.

 

Ø       Man is an accidental host.

Ø       Man becomes infected after ingestion of the third stage larva from improperly cooked snails (Achatina fulica or Pila luzonica).

 

Pathology and Symptomatology

Ø       The third stage larva are ingested by man, they penetrate into the blood vessels in the intestinal tract and are carried in the meninges, but are unable to migrate to the lungs, as they do in rats.

Ø       Rarely, worms develop to the young adults’ stage in the meninges, but they soon die and it is the death of the larvae or young adults and the inflammatory reaction provoked by the dead worms that causes the characteristic signs and symptoms of the human infection.

Ø       It is the most important cause of Eosinophilic meningitis in man, in Asia; although the disease is self-limiting and most of the cases are mild.

Ø       The chief complaint was severe headache, in others it was convulsions, weakness of the arms and legs, paresthesia, vomiting, facial paralysis, stiffness of the neck and fever.

 

Diagnosis:

1.       Demonstration and identification of the larvae and the young adult from the CSF.

2.       Eosinophilia in CSF

3.       ELISA

4.       Computerized Tomography (CT)

 

Treatment:

1.       For severe headache, in Eosinophilia meningitis, spinal puncture to remove about 10 ml of CSF.

2.       Being usually self-limiting, anthelminthic drug is not necessary.

3.       Surgical removal of the parasite is required when it is found in the anterior or vitreous chamber of the eye.

 

Preventive Measures:

1.       Properly cooked snails.

2.       Eradication and control of rodents.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

THE FILARIAE

v       The filariae live in the tissues or body cavities of a vertebrate host.

v       The females produce microfilariae that are highly motile, thread-like prelarva, that in some species retains the egg membrane as a sheath (it becomes “sheathed” form), whereas in others, the microfilariae ruptures the egg membrane and becomes naked or “unsheathed” form.

v       On being extruded by the female in their habitat, the microfilariae enter the blood or lymphatic vessels and they are ingested by blood-sucking arthropods.

v       In the appropriate arthropod vector, the microfilariae migrate through the wall of the digestive tract into the hemocoele, through the thoracic muscles, malphigian tubules or fat bodies.

v       There is development of two distinct larval stages (first- and second-stage larvae) L1 and L2 before reaching the infective stage, which is the third-stage larvae (L3) or filiform larva.

v       The infective stage (L3) migrates to mouth parts and escapes into or unto the vertebrate host’s skin when an arthropod host takes blood meal.

v       There is Periodicity which is biologic adaptation of the parasite to the time of maximum biting activity of the parasite vector.

v       There are new insights that link immune response to the clinical outcome of the infection.

v       Filariae that are relatively common as parasites of man:

1.       Wuchereria bancrofti – “sheathed” microfilariae in the lymphatics with nocturnal periodicity

2.       Brugia malayi – “sheathed” microfilariae, in the lymphatics with nocturnal periodicity

3.       Loa loa ­– “sheathes” microfilariae in the cutaneous or subcutaneous tissues with diurnal periodicity.

4.       Onchocerca volvulus – “unsheathed” microfilariae in the subcutaneous nodules, rarely found in the blood.

5.       Mansonella ozzardi – “unsheathed” microfilariae, in the subcutaneous tissues and possibly the body cavities

6.       Mansonella (syn. Dipetalomena) perstans – “unsheathed” microfilariae in the body cavities and non-periodic

7.       Mansonella (syn. Dipetalomena) streptocerca – “unsheathed” microfliariae in the skin and subcutaneous tissues, non-periodic

 

Wuchereria bancrofti

Common Name: Bancroft’s filarial worm

Disease produced: Bancroft’s filariasis, Fialriasis bancrofti, Wuchereriasis, Elephantiasis

Geographical distribution: Throughout the tropics and subtropics including the Philippines

Morphology:

v       The adult worms are minute and thread-like in form with a smooth cuticula.

v       Tapering towards both ends, their terminations are bluntly rounded.

v       The head is slightly swollen and is surrounded by two rings of small sessile papillae.

v       The mouth is unarmed, a buccal vestibule is lacking.

 

Male

§          40 mm in length by 0.1 mm in diameter

§          caudal extremity is curved sharply ventrally

§          up to 12 pairs of perianal pedunculated papillae (8 preanal and 4 postanal) supporting narrow inconspicuous alae

§          copulatory spicules are distinctly unequal and dissimilar, the gubernaculums is crescent-shaped

Female

§          80 – 100 mm by 0.24 – 0.30 mm

§          vulva is cervical in position

§          from the short vagina, the outer segment of the uterus is single

Microfilariae

§          244 – 296 um in length by 7.5 – 10 um in diameter

§          sheathed with graceful, sweeping curve

§          body nuclei are equidistant with each other

§          the tail is tapering to delicate point, no terminal nuclei

 

Miocrofilarial Periodicity

v       The numbers are high during a 4-hour period at midnight and scanty or absent during daylight hours

v       This type of circulation fluctuation is referred to as nocturnal periodicity.

v       In some parts of the Pacific region, microfilarial fluctuation is relatively slight, with an increase in numbers during the afternoon and evening but with microfilarial present in the blood continuously throughout the day and night and this is referred to as diurnal subperiodic.

v       The term subperiodic when applied to Wuchereria bancrofti is understood to be diurnal.

v       In the Philippines, there is modified periodicity, the number during the day is just being about one third during the night.

v       When absent from the peripheral circulation, the microfilariae are found primarily in the capillaries and small vessels of the lungs.

 

Intermediate Hosts (Vectors)

v       Culex quinquefasciatus (syn. C. fatigans) others include Anopheles spp., Aedes spp., and Mansonia spp.

 

Life Cycle

1.       The infective stage is the filiform larvae (third-stage larvae) (L₃) which escape from the mosquito, most frequently during flexure of the proboscis at the time of the blood meal is being drawn up and the (L₃) or  filiform larvae enter the skin by active migration through the puncture wound.

2.       After entering the skin, pass through peripheral lymphatics, in which they migrate, and then settly down in certain lymphatic vessels retrograde to lymph nodes.

3.       The worms in infected individuals are coiled up in nodular dilatations of the lymphatic vessels, most frequently, in the cortex of lymph nodes and the testicular tissues.

4.       The worms grow to maturity and mate.

5.       This process is followed by production of microfilariae by the gravid females.

6.       The microfilariae discharged by mature female worms may be expected to appear in the peripheral blood in 8 to 12 months. Filariasis without microfilaremia is not uncommon.

7.       The mosquito vector takes a blood meal and the microfilariae go to the stomach.

8.       In the course of 4 to 17 hours reached the thoracic muscles.

9.       The filiform larvae (third-stage larvae) (L₃) developed and migrate through the hemocoele within the labium down to the labella of the mosquito.

v       Man is the only known definitive host of Wuchereria bancrofti

 

Pathogenesis:

v       Filarial symptoms are caused mainly by adult worms, living as well as dead and degenerating.

v       The inflammatory filarial infection is an immunologic phenomenon caused by the sensitization to the products of the living and dead adult worms.

v       The presence of the worms, their molting fluid and other products and their cast-off sheaths provokes a reaction within the lymphatic vessels.

v       The effect on the host is dilatation and slowing of the lymph fluid in vessels occupied by the worms.

v       The worms become larger and immunological reactions definitely occur.

v       Infiltrations of plasma cells, eosinophils, and macrophages in and around the affected vessels becomes evident.

v       There is lymphangitiswith swelling, redness and pain. On chronic inflammation, the lymph valves proximal to the worms become damaged and incompetent. This damage contributes to the hydrostatic pressure already increased by the dilatation and consequent slowing of the lymph flow.

v       There is leakage of fluid with high concentration of protein into the surrounding tissues because of the permeability of the vessel walls.

v       This results in the characteristic hard or brawny edema of filarial elephantiasis.

v       Regional lymph nodes proximal to the worms become initially enlarged, and then shrink as fibrosis takes place.

v       Proximal lymphatic vessels become stenotic and obstructed.

v       Finally, there are dilated, tortuous lymphatic channels, proximally obstructed, fibrosed lymph nodes with obliterated lymph spaces and lymphedema with high protein content.

v       This is the classic picture of filarial elephantiasis.

 

Symptomatology:

Biological Incubation or Prepatent Period (From the entry of the third-stage infective larvae into the skin until microfilariae first appear in the peripheral blood)

·          Approximately 6 months after infection to about one year or more.

 

 

 

Acute Stage

·          The worms settle down and develop into adults, the parturient females and microfilariae produce tissue reactions.

·          Reactions to the worms consist of an accumulation of different cells in the lumen of the vessels around the worm. There is hyperplasia of the endothelium and perilymphatic cellular infiltrations occur.

·          Acut inflammatory reaction takes place, there is reddened, swollen, raised lymph tract immediately around and extending distally from the site of blockage.

·          It is tender painful and usually associated with fever.

·          Not uncommonly, an attack id preceded by a prodrome of malaise or urticaria.

·          Gradually, attacks become less severe and involved lymph channels less painful; this is referred to as “acute allergic filarial lymphangitis”.

·          The cardinal manifestations are lymphangitis, usually with associated lymphadenitis, mild fever of short duration.

·          Febrile attack is sometimes called “filarial” or “elephantoid” fever.

·          The lymphangitis may originate in an upper extremity, mostly epitrochlear, but eventually there is a concentration of lesions in the scrotum consisting of inflammation of the spermatic cord, epididymis and testes.

 

Chronic Stage

·          Acute inflammation subsides and fibrosis advances.

·          The worms die and are absorbed or become calcified.

·          The sites involved are the groin, with the development of nodular inguinal gland varicosities; the lower extremities, one or both of which become elephantoid and also the external genitalia, male or female.

·          There could be abscess formation of inguinal nodes.

·          Microfilaremia is not likely to be present.

·          The elephantoid mass consists of fat in a matrix of fibrous tissue containing distended lymph spaces.

·          It is possible that secondary streptococcal or other bacterial infection or some host factor is responsible for its appearance.

·          Elephantiasis, the enlargement of one or more limbs, the scrotum, breast, vulva with dermal hypertrophy and verrucous changes, is a relatively uncommon and late complication of filariasis.

·          The two most serious sequelae of filarial infection, elephantiasis and hydrocele, affect only a portion of the people who have been exposed to repeated infections over a period of years.

 

Organs and Tissues Involved in Lymphangitis, Adenitis, and Elephantiasis

·          Lymphangitis of the scrotum, penis or prepuce in the male and of the external genitalia of the female will result with blockage and inflammation in the thoracic duct or median abdominal lymph vessels.

·          If the groin is involved,  “varicose groin glands” develop.

·          Involvement and hypertension of lymphatics of the bladder of the kidney may result in the rupture of the lymph vessels concerned with consequent lymphuria, more frequently chyluria.

·          With similar tension of tunica  vaginalis, lymphocoele, or chylocoele may develop.

·          In the case of peritoneum, lymphous or chylous ascites may result.

 

Tropical Eosinophilia

·          There are chronic pulmonary infiltrations, hypereosinophilia of the peripheral blood, chest pain, cough, and asthmatic attacks especially at night.

·          A distinctive feature of the syndrome is the prompt relief of symptoms afforded by treatment with Arsenical drugs or Diethylcarbamazine.

·          The syndrome has also been referred to as Weingarten syndrome, Eosinophilic lung and Tropical pulmonary eosinophilia.

·          Wuchereria bancrofti and Brugia malayi are probably the etiologic agents in most cases of Tropical Eosinophilia.

·          Presumably, the syndrome is due to a failure of suppression of host-immune mechanisms against the microfilariae.

·          Meyer’s and Kouwenaar’s syndrome (lymphadenopathy and splenomegaly, transient pulmonary infiltrates and hypereosinophilia).

 

 

 

 

Pathogenesis and Clinical Course of Human Filariasis

1.       Filariasis with microfilaremia

·          Relatively asymptomatic infection with marked and prolonged microfilaremia.

·          Recurrent lymphangitis and eventual chronic manifestations of lymph stasis.

2.       Filariasis without microfilaremia

·          Early lymphangitis and lymphadenitis in persons moving from an area without filariasis to an endemic area.

·          Tropical Pulmonary Eosinophilia

·          Extreme filarial elephantiasis following a chronic course of recurrent lymphangitis, often complicate by cellulites due to streptococcal or other bacterial infection.

 

Laboratory Diagnosis

1.       Demonstration of the microfilariae from the blood, lymph, or chylous urine (Microfilariae may not be found in the blood during the early months of clinical inflammatory filariasis and late in the disease when elephantiasis has developed).

·          Thick or Thin smear

·          Nuclepore Filtration Technique

·          Knott Concentration Method

2.       Immunodiagnostic Methods

3.       Lymphangiography

 

Treatment

1.       Drugs → Diethylcarbamazine (DEC, Hetrazan) and Ivermectin (Mectizan), Antihistamines and corticosteroids

2.       Pressure bandaging

3.       Surgical removal of elephantoid tissue by a modified Kondoleon operation.

 

Prognosis

                Depends primarily with:

1.       number of immature or mature worms that gained entrance to the patient’s body;

2.       their potentialities for mating

3.       opportunities for re-exposure and therefore superinfection

4.       activity of the reticuloendothelial system and degree of sensitization of the patient

5.       number of times acute cellular reaction occurs at the same anatomical location

 

Prevention

1.       Use of insect repellent

2.       Vector or mosquito control

3.       Mass treatment of the patients.

 

 

Brugia malayi

 

Common Name: Malayan Filarial Worm

Disease produced: Malayan Filariasis

Geographical Distribution: Eastern Asia, Southwestern Pacific Islands, India, Philippines

Morphology:

v       The adult worms are silicate, whitish, thread-like that live in dilated lymphatics.

v       The tapering anterior end is provided with a nonlabiate mouth surrounded by two rows of minute papillae.

               

                Male

·          13-23 mm by 70-80 um

·          Caudal extremity is curved

·          With  long left spicules and shorter right spicules

·          The gobernaculum is more or less crescentric like that of Wuchereria bancrofti

 

Female

·          43-55 mm by 130-170 um

·          The vulva consists of a transverse slit

Microfilariae

·          Sheathed, stiff, with secondary kinks

·          Body nuclei are large and with irregular distribution

·          The tail is often constricted between 2 terminal nuclei

 

Microfilarial periodicity

v       In peripheral blood of patients, this embryo exhibits nocturnal periodicity.

 

Intermediate Hosts (vectors):

v       Mansonia species, Aedes togoi, and Anopheles mosquito

 

Life Cycle:

v       The life cycle of Brugia malayi is similar to that of Wuchereria bancrofti, except that in most areas, the principal mosquito vectors belong to the genus Mansonia.

 

Pathology:

v       The pathogenic mechanisms of human filariasis due to Brugia malayi are essentially the same as those of Wuchereria bancrofti.

v       The syndrome discovered from patients was allergic in nature.

 

Symptomatology:

v       There are symptoms of high eosinophilia, bronchial asthma and adenopathy

v       Patients with more advanced Malayan filariasis may be asymptomatic with microfilariae in the peripheral blood at night, or they may have elephantoid enlargement of one or more limbs, occasionally the groin, rarely the scrotum.

v       The presence of elephantiasis is predominantly seen in an extremity.

v       The prominent features are primarily affecting the lower limbs.

 

Laboratory Diagnosis:

v       Same as in Filariasis bancrofti

 

Treatment:

v       Same as in Filariasis bancrofti

 

Preventive Measures:

v       Same as in Filariasis bancrofti

 

 

Loa loa

 

Common Name: Loa Worm, Eye Worm

Disease Produced: Loaisis, Calabar swelling, Fugitive swelling

Geographical Distribution: Tropical Africa

Morphology:

v       The body is whitish and tapers somewhat toward the cephalic end

v       The cuticula is ornamented with small bosses.

 

Male

·          30 – 34 mm in length by 0.34 – 0.43 mm

·          Caudal ends curve ventrally and with narrow allae

·          Copulatury spicules are unequal in length and dissimilar in shape

 

Female

·          40 – 70 mm in length by 0.5 mm

·          Vulva opens in the cervical region

 

Microfilariae

·          250 – 300 um long and 6 – 8 um wide

·          Sheathed, tapering gradually, stiff, with secondary kinks

·          Body nuclei are large, non-equidistant and caudal nuclei continuous with those of the trunks

Microfilarial Periodicity

v       Exhibits diurnal periodicity, they appear in peripheral blood only during the day.

 

Intermediate Hosts (Vectors)

v       Chrysops diminuta and Chrysops silacea, (mango fly) day-biting flies

 

Life Cycle:

1.       A person, when bitten by the fly, is infected by the escape of the third-stage larvae from the membranous labium to the skin near the bite wound.

2.       Within an hour the larvae penetrate the subcutaneous and muscular tissues, where they become adult worms.

3.       The adult, thread-like, cylindrical worms inhabit the subcutaneous tissues.

4.       The life span of the worm in human has been variously reported as 4 to 17 years.

5.       The sheathed microfilariae usually have a diurnal periodicity in the blood.

6.       The principal intermediate insect hosts are Chrysops dimidia and Chrysops silacea.

7.       These flies take a blood meal and ingest the microfilariae.

8.       The ingested microfilariae pass through a cyclic development in these flies until they become the third-stage larvae.

 

Pathology and Symptomatology

v       The adult worms migrate back and forth in the subcutaneous tissues, provoking a temporary inflammation (“fugitive swelling” or “Calabar swelling”) in the course of their wandering.

v       They may migrate through all the viscera of the body.

v       Swellings develop rapidly, may reach the size of a hen’s egg, are at times painful and last for 2 – 3 days.

v       They are regarded as local reactions to sudden liberation of the worm’s metabolites.

v       Adults are particularly troublesome, although not necessarily painful, when passing in front of the eyeball or across the bridge of the nose.

v       Produces remarkable periods of allergic reaction.

v       Edema of orbital cellular tissues causes proptosis, called “bug-eye” or “bulge-eye”.

v       There is a high grade eosinophilia.

 

Laboratory Diagnosis

1.       Demonstration of the microfilariae in the peripheral blood during the day.

2.       Removal of the worms from the skin, subcutaneous tissues or conjunctiva.

 

Treatment:

1.       Surgical removal of the worms.

2.       The same as in filariasis bancrofti.

 

Preventive Measures:

v       Same as in Filariasis bancrofti

 

Onchocerca volvulus

 

Common Name: Convuluted Filaria

Disease Produced: Onchocerciasis, “River Blindness”

Geographical Distribution: Tropical Africa, North Yemen, Guatemala, Venezuela, Brazil, Columbia and Ecuador

Habitat:

v       Adult worms are commonly located in skin and nodules in subcutaneous connective tissues.

v       Nodules may appear on any part of the body but most common in the region of the pelvic arc, at the junction of the long bones, and the temporal of occipital region of the scalp.

v       Nodules containing up to 20 females and 13 males have been observed.

 

Morphology:

v       The worms are filiform and blunt at both ends.

v       The living worms are white, opalescent and transparent.

v       There is a distinct transverse striation of the cuticula.

 

 

 

                    Male

·          19 – 24 mm in length by 130 – 210 um

·          With tightly recurved ventrally at the posterior end

·          Has several perianal and caudal papillae

 

                    Female

·          33.5 – 50 cm by 270 – 400 um

·          Vulva opens slightly behind the posterior extremity of the esophagus

 

                    Microfilariae

·          Unsheathed, mostly in the cutaneous lymphatics (skin) occasionally in peripheral blood, urine and sputum

·          Anterior and posterior ends of the microfilariae are nuclei-free

 

Intermediate Hosts (Vectors):

v       Simulium species (Black Fly or Buffalo gnat) ingest blood and tissue fluid

 

Life Cycle:

1. The filiform or third-stage larvae (L₃) enter man when the Simulium fly takes a blood meal.

2. The developing worms wander through the subcutaneous but settle down, usually in groups and become encapsulated.

3. Nodules are produced by encapsulated of the adult worms in a fibrous tissue tumor-like mass.

4. The nodules are most frequently subcutaneous but may occur in connective tissues deeper in the body.

5. The adult worms mate and females produce microfilariae.

6. Microfilariae make their way out of the nodules and migrate actively through the dermis and in the connective tissues.

7. Simulium fly takes a blood meal and ingest microfilariae.

8. The microfilariae undergo developmental cycle transforming into the filiform or third-stage larvae (L₃).

 

Pathology:

v       The basic mechanism of the disease is the provocation of the host’s allergic reaction to the adult worms and to the microfilariae.

v       Fibroblastic reaction in the host which causes the worms to become enveloped in a fibrous scar forming the onchocercal nodule or onchocercoma.

v       These nodules tend to occur over anatomic sites where the bone is superficial, such as scalp, scapula, ribs, elbows, trochanters, iliac crests, sacrum, and knees.

v       Typical onchocercoma is firm, round or ovoid, non-tender, fully movable, well-circumscribed subcutaneous tumors.

 

Onchocercal Dermatitis

·          Sowda – from Arabic word “aswad” meaning black, it is localized Onchocerciasis, common in young adult males in Yemen

·          Leopard skin – tends to be generalized, in older males, in long standing Onchocerciasis, with spotty depigmentation.

·          Peau d’ orange – diffuse, poorly pitting swelling of lymphedema.

·          Lichenoid change – consist of dryness and scaling in a pattern that has been called “lizard skin”.

·          Atrophy – the skin is glossy and thin appearing, dry and unevenly pigmented.

·          Hanging groin – a sac of tissue forms in the inguinal region.

Ocular manifestations

·          Punctate keratitis – whitish ocular opacity, relatively symptomless, disappears without residue.

·          Sclerosing keratitis – corneal haziness, may be with anterior uveitis and calcification of the cornea may occur.

·          Iridocyclitis – may have mild uveitis, precipitates corneal epithelium of lens capsule, fibrosis retracts the iris, causing distortion of the pupil.

 

Laboratory Diagnosis

1.       Demonstration of microfilariae in skin snips or in the eye by ophthalmic examination with a slit lamp.

2.       ELISA

3.       Mazzotti test using DEC

Treatment

1.       Nodulectomy – surgical removal of palpable nodules

2.       Drugs – Ivermectin (mectizan), Diethylcarbamazine (DEC, Hetrazan), and Suramin

 

Preventive Measures

                The same as in filariasis bancrofti

 

Mansonella ozzardi

 

Common name: Ozzard’s filarial

Disease produced: Mansonelliasis ozzardi

Geographical Distribution: Tropical America

Habitat: Subcutaneous tissue mesenteries, visceral fat and possible the body cavities

Morphology:

                Male

·          24 – 28 mm in length by 70 – 80 um in diameter

·          The tail is tapered to a rounded tip and flattened dorsoventrally

 

Female

·          65 – 81 mm in length by 0.21 – 0.25 mm in diameter

·          Vulva anterior to the base of the esophagus

 

Microfilariae

·          Non-periodic, unsheathed microfilariae found in the blood

·          Tail tapered, contains a column of 4 to 6 ovoid bar-like nuclei, don’t extend to the tip

 

Intermediate Hosts (Vectors)

v       Culicoides species (midges) and Simulium species.

 

Life Cycle

v       Basically the same as in Wuchereria bancrofti

 

Pathology and Symptomology:

v       Generally an asymptomatic infection

v       Inguinal adenopathy had been reported

v       May have pruritic and maculopapular skin lesions, arthritis, fever and marked eosinophilia.

 

Laboratory Diagnosis

v       Demonstration of the unsheathed microfilariae from the peripheral blood and biopsy specimen of skin.

 

Treatment:

v       Ivermectin (Mectizan)

 

Preventive Measures:

v       The same as in filariasis bancrofti

 

Mansonella perstans

Former Name: Dipetalomena perstans

Disease produced: Perstans filariasis

Geographical Distribution: Tropical Africa and Tropical America

Habitat: Body cavities, most commonly in the peritoneal cavity, next the pleural cavity

Morphology:

v       The adult worms are delicate filariae with smooth cuticula

v       Bluntly rounded anterior end and caudal extremity curved ventral in both sexes

 

Male

·          45 mm in length by 60 um diameter

·          Posterior end have 4 preanal pairs of papillae and 1 postanal pair

 

 

Female

·          70 – 80 mm in length by 120 um in diameter

·          Vulva lies in the cervical region

 

Microfilariae

·          200 by 4.5 um in diameter

·          Unsheathed, non-periodic found in the peripheral blood

·          Nuclei extended to the tip of the tail

 

Intermediate Hosts (Vectors)

v       Culicoides species (Midges)

 

Life Cycle

v       Basically the same as in Wuchereria bancrofti

 

Pathology and Symptomatology

v       Infections are often asymptomatic

v       May cause transient abdominal pain, subcutaneous swelling, rashes, pain in the limbs and fatigue

v       Eosinophilia is common

 

Laboratory Diagnosis

1.       Demonstration of the unsheathed microfilariae from the peripheral blood day or night.

 

Treatment:

1.       Ivermectin (Mectizan)

 

Preventive Measures:

                    The same as in filariasis bancrofti

 

Mansonella streptocerca

Former Name: Dipetalomena streptocerca

Geographical Distribution: Tropical Africa

Habitat: Skin and subcutaneous tissues

v       Microfilariae are found primarily in the skin and also in the blood.

v       Nuclei in the microfilariae extend up to the tip of the tail

v       The intermediate insect host is Culicoides species (Midges)

v       The worm is usually nonpathogenic, but it may cause cutaneous edema and elephantiasis

v       Most of infected persons are symptomless

v       The patient may have pruritic dermatitis, with hypopigmented macules and inguinal adenopathy.

v       May be treated by Diethylcarbamazine (DEC, Hetrazan)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

THE TREMATODES

(Class Trematoda)

 

                    The trematodes or flukes are classified under phylum Platyhelminthes. Most member species are hermaphrodites and many are capable of self-fertilization. All species have complex life cycles, requiring one or more intermediate hosts.

 

                    Trematodes are subdivided into:

 

A.       Monoecious trematodes are characterized with flattened or leaf-shaped bodies, hermaphroditic, needing two intermediate hosts (whereby the first is almost always a certain species of snail), and are producing egg with operculum.

 

B.       Diecious flukes are, on the other hand, described with cylindrical bodies, sexes are separate, requiring only one intermediate host, and are producing non-operculate egg with an embryo (miracidium inside).

 

                    The most characteristic feature of flukes is the presence of “acetabula” (suckers), hence the name Trematoda (meaning – body with holes).

                    This group of helminthes may also be classified based on the habitat of the adult worms. Flukes, whose adults are inhabiting the intestinal canal are called “intestinal trematodes”, those that inhabit the lungs are called “lung flukes”, species inhabiting the biliary tree are referred to as “liver flukes”, and those that live in the blood vessels (commonly the mesenteric vessels) are the “blood flukes”. Diecious trematodes include the blood flukes while the monoecious include the intestinal, lung, and liver flukes.

                    The following is the list of organisms that will be given emphasis in this text.

 

                    Blood Fluke                                      Schistosoma japonicum

                                                                                Schistosoma mansoni

                                                                                Schistosoma haematobium

                   

                    Intestinal Fluke                                                Fasciolopsis buski

                                                                                Echinostoma ilocanum

                                                                                Heterophyes heterophyes

                                                                                Haplorchis yokogawai

                                                                                Metagonimus yokogawai

 

                    Lung Fluke                                        Paragonimus westermani

 

                    Liver Fluke                                        Fasciola hepatica

                                                                                Clonorchis sinensis

                                                                                Opistorchis felineu

                                                                                Opistorchis Viverrini

 

Organ Systems of Flukes

 

                    Generally, the flukes are provided with organ systems such as 1) Nervous, 2) Excretory, 3) Digestive, and 4) Reproductive Systems.

                   

                    The nervous system consists of paired ganglion cells situated at the anterior part, at the back of the esophagus or pharynx, and nerve trunks that send fibers to the back, lateral and ventral sides.

                   

                    The excretory system of flukes is bilaterally symmetrical, which opens at the dorsal and posterior portion of the worm. The flame cell (also known as “solenocytes”) is the basic unit of the excretory apparatus. The flame cells joined to form the capillaries, which in turn are united forming the excretory tubules.

 

                    The digestive tract, in most species, consists of an oral cavity (surrounded by the oral suc***), followed by the prepharyngeal tube, a muscular pharynx, esophagus, and two intestinal ceca with “blind” ends.  The digestive tract is, oftentimes, described as having an inverted Y figure. There is no opening that serves as the anus and wastes inside the ceca are excreted through regurgitation through the oral cavity. Some species have straight ceca while others have branched intestinal ceca. Foods of trematodes consist of liquid and semi-liquid nutrients, which the worm gets from the environment. Unused foods, as well as wastes, are regurgitated or vomited out through the oral cavity.

 

                    Flukes are not provided with special structures that will serve as respiratory and/or circulatory system. If the worm needs oxygen, it is taken in through the skin.

 

                    A monoecious fluke, being hermaphroditic, has one ovary, oviduct, ootype, multiple vitelline gland that produce the ground substance for the eggshell, seminal receptacle, Mehli’s glands, uterus, and genital pore. In a monoecious trematode, the genital pore serves as the “common opening” for male and female reproductive organs. Thus, it is referred to as the “common genital pore”.

 

                    The male reproductive organs include the testes, which is oftentimes paired but multiple among blood flukes, vas deferens, vas efferens, seminal vesicle, ejaculatory duct, prostate glands, genital atrium, and genital pore.

 

Stages of Development

 

                    The pattern of development among flukes is egg, larva, and adult. Generally, monoecious flukes produce operculate eggs, while the diecious trematodes are producing non-operculate eggs. The egg of diecious flukes already contains an embryo (miracidium) when laid.  Monoecious flukes, on the other hand, may either lay embryonated or immature eggs. However, the embryo that is formed in either case will still be a miracidium.

 

                    The miracidium is a free swimming, non-feeding, ciliated embryo. It is provided with penetration glands that secrete lytic enzymes, which help in the entry of the parasite into the body of the intermediate host. It has primitive organelles, which are still non-functional. It assumes a very brief free-living existence in water. It however, should be taken-up by the intermediate host in less than 24 hours, otherwise, it dies. It exhibits “phototaxis” (i.e. attraction to light), hence, it is more likely to swim on or near the surface of water. This characteristic favors the miracidium in invading the body of the intermediate host, since the snail host is more likely to liver the water surface. The miracidium is also attracted to the mucus secreted by the snail host, thus, making it easier for the parasite to the appropriate intermediate host.

 

                    There are species of monoecious flukes whereby it is the miracidium that enters the body of the snail host, while in others it is the embryonated egg that serves as the infective stage to the molluscan (snail) host. The miracidium, once inside the body of the intermediate host, develops into sporocyst stage. Generally, the sporocyst is an elongated sac-like structure without a mouth but always provided with a small opening at the anterior part that serves as the birth pore. Inside sporocyst are proliferating germ cells, which may become the next stage of development, the redia, or a second-generation sporocyst depending upon the species of the worm.

 

                    The redia has mouth, a muscular pharynx, a blind and a non-forked cecum, a birth pore, and locomotor organelles (in some species only). The rediae are release through the birth pore of the sporocyst and transform to the next stage of development called cercaria. The cercaria is the end-stage of development in the snail host.

 

                    The cercaria is free-swimming, non-feeding, larval stage, provided with penetration glands, exhibits phototaxis, and has a short life span. It is, therefore, important for the cercaria to find and be taken up by the next appropriate host, otherwise, it dies. Cercariae are of different types, namely 1] simple-tail lophocercus, 2] keel-tailed lophocercus, 3] microcercus, and 4] fork-tailed. The cercaria can develop from redia, or in some species having no redia stage, from the second generation sporocyst. The keel-tailed lophocercus differs from the simple-tailed by the presence of a “flute” or a “rudder” on its tain hence the term “keel-tailed”. The microcercus cercaria does not have a tail but there is a small spherical appendage at the posterior portion. The fork-tailed cercaria has a bifurcated tail assuming the appearance of a fork with two prongs.

 

                    The cercaria of monoecious flukes leaves the snail host, which can be due to the death of the snail or due to overpopulation of the cercaria. It swims in the water and finds the second intermediate host where it becomes encysted due to a fibrous capsule secreted by the intermediate host. The tail of the cercaria is cast off when it enters the body of the intermediate host. The encysted form, present among monoecious flukes, is called metacercaria.

 

                    Diecious flukes do not need a second intermediate host thus the cercaria is the infective stage to the definitive host. Among monoecious trematodes, the metacercaria serves as the infective form to the definitive host. Infection with monoecious flukes is acquired by man through ingestion of the metacercaria contained in the flesh of the second intermediate host. Ingested metacercaria undergoes excystation in the upper level of the small intestine and the released organism migrates to tissues or organs where is going to mature. The cercaria of diecious trematodes (blood flukes) enters the body of the final host (man or other animals) via skin penetration. The cercaria may also be taken-in orally through drinking water that is contaminated with the organism. However, the cercaria will still enter the surface area of the oral cavity to enter the circulation, or lymphatics to reach their predilection site for the maturity.

 

The BLOOD FLUKES (Schistosomes)

                    The blood flukes are cylindrical worms with separate male and female that lives in the blood vessels. They need only a single intermediate host in their life cycle. Blood flukes causing disease to man include 1] Schistosoma japonicum, 2] Schistosoma mansoni, and 3] Schistosoma haematobium.

 

Geographical Distribution

Schistosoma japonicum, also known as the “oriental blood fluke” causing schistosomiasis japonica is confined to some areas in the Far East including Japan, China, the Philippines (Leyte, Samar, Mindanao, Mindoro, and Sorsogon), and Thailand.

 

Schistosoma mansoni, also known as “Manson’s blood fluke” and causing schistosomiasis mansoni or Manson’s intestinal schistosomiasis or bilharziasis, is found in some specific areas of Africa, South America, islands at the Carribean Sea, Congo Basin, Northeastern Brazil, Guinea island, Kenya, Malawi, some parts of Venezuela, West Indies, and Puerto Rico.

 

Schistosoma haematobium, also called “vesical blood fluke”, and causing vesical schistosomiasis or urinary bilharziasis or schistisimal hematuria is present in Africa.

 

Habitat

                    The adults of schistosomes, oftentimes in copula, are located inside particular blood vessels. Schistosoma japonicum inhabits the superior mesenteric vessels (the vessels that drain the small intestine and first part of the large intestine). Schistosoma mansoni lives inside the inferior mesenteric vessels, which drain the greater part of the large intestine and the rectum. There are cases, however, that S. mansoni, is found inside blood vessels that drain the urinary bladder. Schistosoma haematobium inhabits the vesical plexus that drain the urinary bladder and the rectum. But this parasite may also inhabit the inferior mesenteries.

 

Morphology

                    Adult schistosomes have cylindrical bodies, male is more stout and shorter than the female, and provided with two suc***s (oral and ventral suc***s) located at the anterior end. The male blood fluke is provided with “gynecophoral canal,” holds the posterior part of the female during copulation. The intestinal ceca bifurcate somewhere at the level of the ventral suc*** and re-unite later somewhere at the posterior part. The level where the intestinal ceca re-unite is one of the bases for identifying the adult male. The female adult, oftentimes and for practical purposes, is identified based on where the ovary is situated.

                    The eggs of schistosomes are already embryonated (i.e. with miracidium) when laid by the female worm. The characteristic feature, other than the presence of the embryo, is the appearance and location of the “spine.” Schistosoma mansoni has a prominent lateral spine (but actually positioned at the infero-lateral side), Schistosoma haematobium has prominent terminal spine, and Schistosoma japonicum has an abbreviated lateral spine or a rudimentary knob on one side. The eggs of Schistosoma japonicum and Schistosoma mansoni are recovered in the feces, while for Schistosoma haematobium, they are recovered in the urine. However, eggs of Schistosoma mansoni may also be seen in urine and that of Schistosoma haematobium may also be found in stools, but to a lesser extent.

Basic Differences of Human Schistosomes

	Schistosoma japonicum	Schistosoma mansoni	Schistosoma haematobium
Integument	Smooth cuticle	Coarse trabeculations	Fine trabeculations
Male: Testes Intestinal ceca	12 – 20 mm X 0.5 - 0.55 mm	6.4 – 12 mm long	10 – 15 mm X 0.6 – 1 mm
	7 in a row	6 – 9 in a row	4 – 5 in clusters
	Very late union	Early union	Late union
Female: Position of Ovary	26 mm X 0.3 mm long	7.2 – 17 mm long	20 X 0.25 mm
	A bit behind the midplane	Anterior to the midplane	Posterior to the midplane
Egg:	70-100 X 56-65microns	114-175microns diameter	112-170 X 40-70microns
Recovered	Feces	Mainly in stool, less in urine	Mainly in urine, less in stool
Intermediate Hosts	Oncomelania species O. quadrasii	Biomphalaria sp. B. glabrata	Bulinus sp. B. truncates

Life Cycle

 

                    The adults, in their natural habitat, copulate and the female produces eggs. The already embryonated eggs accumulate inside the blood vessels. The mucus that comes with the eggs as they are laid causes irritation of the wall of the intestine or the urinary bladder, which results to hyperperistalsis. The eggs are then able to pass through the walls of the intestine (or the bladder) and are discharge with the feces (or urine). On defecation (or urination), the embryonated eggs are deposited in water where hatching takes place. The released embryo (miracidium) swims freely and attaches to the mucus trail left by the snail host. The miracidium enters the body of the snail host and developed into sporocyst, which in the mother sporocyst (S₁) that produces the daughter sporocyst (S₂). The daughter sporocyst develops into the “fork-tail cercaria,” which will be released from the snail host. The cercaria is a non-feeding, free-swimming, short-lived organism. It also exhibits phototaxis.

 

                    The fork-tail cercaria, the infective stage to man, comes into contact with skin of the definitive host. It actively penetrates the skin and enters the capillaries. It passes through the inferior vena cava, to the right side of the heart, and later into the lungs. At this point, the organism is already on the schistosomula stage. It breaks into the veins of the lungs and goes against the flow of blood until it reaches its habitat (i.e. depending on the species). It matures and copulates. The female produces eggs, which are already embryonated.

 

Pathogenesis, Pathology, and Clinical Manifestations

 

                    The pathology in schistosomiasis is practically similar for the three species. The liver and the intestinal tract are the organs most severely affected. The severity of the infection is mainly dependent on the number of worms present. At times, cases of light infection may also show severe manifestations. The eggs and cercaria are antigenic to man. Thus, the immune system of the host may be stimulated to produce antibodies against the eggs and/or cercaria.

                    Schistosomiasis may also be subdivided into four stages for easy understanding of events taking place in the disease.

 

                    Stage I – Stage of Invasion

                   

                    The fork-tailed cercaria, the infective stage to man, produce a form of dermatitis as it enters the skin in man. The skin lesion may be referred to as “schistosomal dermatitis” (also called clam diggers or swimmer’s itch). Urticarial rashes, edema of the subcutaneous tissues, fever, and pruritus may develop at this stageof the infection. These lesions are commonly observed at the lower extremities (i.e. the part of the body in contact with the water the cercariae are likely to be located).

                    The host’s immune system may be stimulated at this stage of the infection. Antibodies against the cercaria are produced. This is the basis for the development of the serologic test called “Cercaris Huellen Reaction” (CHR), which may give a positive result at this stage of schistosomiasis.

 

                    Stage II – Stage of Migration and Maturation

 

                    The parasite, its schistosomula stage, migrating to the right side of the heart, through the lungs, and back to the venous circulation is not producing significant effects to the host. At the end of this stage, the females may already be producing some eggs. The parasites are already at the final site for habitation.

 

                    Stage III – Stage of Established Infection

 

                    Sexually mature worms copulate and the female lays eggs. The eggs are discharged in the blood vessels where the adults live. The maturing larvae (miracidia) inside the eggs secrete mucus that causes irritation of the intestines. This results to the escape of eggs from the vessels into the perivascular tissues or into the lumen of the intestines. The eggs in the tissues are sequestered by eosinophils. The eggs maybe carried to different sites by the circulation. The liver, however, is the predominant site for the accumulation of the eggs. Granuloma formation occurs at the site where the eggs are. The granuloma is referred to as “pseudo-tubercle.” The liver, due to scattered granuloma around the eggs, enlarges resulting to acute hepatitis (peristaltic hepatitis). Organs where the eggs may also accumulate and produce pathologic damages include the spleen, brain, lungs, and intestines. It is also possible that eggs may also go to other sites. Pseudo-tubercles also develop in the walls of the intestines.

                   

                    Eggs in the tissues also stimulate the immune system to produce antibodies. This leads to the development of a serologic test called “Circumoval Precipitin Test” (COPT).

 

                    This stage of infection is also marked with plenty of eggs being extruded in the feces (or urine depending upon the species of the worm.

 

                    Stage IV – Stage of Chronic Infection and Complications

                   

                    This stage of schistosomiasis is characterized with massive scar tissue formation (granuloma) in organs where the eggs are deposited. Since eggs accumulate in the liver more than the other organs, this organ bears the greater burden. Significant parts of the liver parenchyma are replaced by granulomas. This condition can lead to the development of “liver cirrhosis” (i.e. shrunken liver due to fibrosis caused by the eggs).

 

                    The liver condition can cause obstructive pressure on blood vessels passing through the liver, such as the portal veins. The blood flow is impeded resulting to dilatation of the smaller branches of the vessels. Thus, there will be enlargement and engorgement of the superficial vessels of the abdomen and development of esophageal varices. They may rupture and the patient may vomit blood. The dilated superficial vessels on the abdomen may be seen as “spider nevi” or the so-called “caput medusa” (dilated vessels at the navel). Some patients may develop hemorrhoids.

                   

                    The cirrhotic liver is also not producing enough amounts of proteins because the parenchyma is replaced by scar tissues. The condition leads to accumulation of fluid in the abdomen (ascites).

 

                    During this late stage of schistosomiasis, the females are producing lesser number of eggs (or had stopped laying eggs already), therefore, lesser chance of finding the eggs in stool (or urine). The antibodies against the cercariae and the eggs are likely to persist for a long time. The walls of the intestines and rectum will show the eggs trapped in granuloma.

 

STAGES OF SCHISTOSOMIASIS

Stage of Infection	Parasitologic Events	Clinical Events	Pathologic Events
Stage I – Invasion	Fork-tail cercaria penetrates the skin   Migration of the cercariae later becoming schistosomulae	Skin reaction to the cercaria   Fever and cough may be present	Papular dermatitis     Inflammatory reactions in the lungs and liver
Stage II – Maturation	Maturation completed early egg production and migration to the final habitation sites	Acute febrile response may not be present always	Local or generalized allergic reactions to the products of egg
Stage III – Established Infection	Massive egg-laying or peak of egg production and extrustion in feces	Early part of chronic infection, may have diarrhea or other digestive manifestations	Local inflammatory reaction to the eggs, formation of granuloma but fibrosis is not the predominant feature
Stage IV – Late infection and Complications	Prolonged infection, markedly reduced egg production and extrusion or no egg production at all	Possible development of sequelae such as cor pulmonale, obstructive uropathy, formation of varices	Progressive fibrosis of varying intensity relative to degree of infection involving the liver, intestines, kidneys, urinary bladder, lungs, and other organs

 

Laboratory Diagnosis of Schistosomiasis

 

·    Eggs of Schistosoma japonicum and Schistosoma mansoni maybe recovered in the feces. Urine sample is used to demonstrate the eggs of Schistosomia haematobium. However, eggs of Schistosoma mansoni may also, to a lesser extent, be recovered in the urine, while the eggs of Schistosoma haematobium may be seen in the feces.Specimens (urine or feces) should not be mixed with plain water as such may cause hatching of the eggs resulting to the release of the miracidium. It is harder to identify miracidium that to identify the eggs.

 

·    CHR maybe done during the early stage of schistosomiasis. This test may also show positive result at the later stage(s) of the infection.

 

·    COPT is likely to show positive result during stages III and IV of schistosomiasis. This tests for the antibodies against the eggs of the particular species of blood fluke. Lyophilized eggs are prepared from mice previously and artificially infected in the laboratory. The serum of the patient is incubated with the eggs. Positive result is seen as “bleb formation” around the eggs. This is due to precipitation reaction of the antigen and antibody.

 

·    Ultrasonography of the liver may also helo in the diagnosis, but this may not be very specific.

 

·    Biopsy of the rectal mucosa may also be done to demonstrate the eggs in the tissues. Liver biopsy may also be considered but rather a dangerous procedure.

 

Prevention and Control

 

1.       Strict implementation of proper and sanitary disposal of human waste.

2.       Control of snails. The intermediate hosts of schistosoms are operculate snails, which enable them to survive in dry areas for a long time. Snail may be filled with use of molluscicides such as pentachlorophenate.

3.       Control of rats. It was also noted that rats play an important rle in the maintenance of schistosomiasis in the Philippines and Japan.

4.       Provision of source of clean, safe, and potable drinking water.

5.       Early diagnosis and treatment of cases.

6.       Public education.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

MONOECIOUS FLUKES

 

General Features

·          Bodies are dorso-ventrally flattened

·          Require two intermediate hosts to complete the life cycle, the first of which is a certain species of snails.

·          Adult worms are hermaphrodite (a single worm has both male and female reproductive organs)

·          The second intermediate host forms the metacercaria, which is the infective stage to the definitive host

·          Eggs they produce may either be mature (i.e. with miracidium) or immature but they are operculated

·          Based on the habitat of the adults, each species may be classified as follows:

 

ü        Liver Flukes – are those whose adults live in the biliary tree

ü        Intestinal Flukes – the adults live mostly in the duodenum and/or jejunum

ü        Lung Flukes – adult worms inhabit the lung parenchyma

 

 

Liver Fluke

 

Fasciola hepatica

 

v       Also known as the “sheep liver fluke”

v       Disease may be referred to as “sheep liver rot” or “fascioliasis hepatica”

v       It has cosmopolitan distribution but most prevalent among sheep-raising countries

v       Adult worms inhabit the proximal biliary tracts rolled like a mat

 

Intermediate Hosts:

                1^st intermediate host – Lymnea philippinensis

                2^nd intermediate host – Nasturtium officinale (watercress)

 

Morphology

·          Moderately fleshy may be up to 30 mm in length by 13 mm in breadth

·          Flat, leaf-like with spine on the skins

·          With a prominent “cephalic cone” – diagnostic – at the anterior end

·          Ventral suc*** (1.6 mm diameter) slightly bigger than the oral suc*** (1mm diameter)

·          Highly branched intestinal ceca extended to the posterior end, two highly dendritic (branched) testes – one behind the other – positioned at the posterior 3^rd and 4^th of the body, branched vitellaria distributed throughout  the entire lateral side, and a dendritic ovary situated at the right side of the anterior testis.

·          Egg, measuring 130 – 150 X 63 – 90 micrometers, is large, ovoid with broad operculum, light yellowish brown in color – oftentimes describe as “hen’s egg shaped ovum,” and immature when laid.

 

Pathogenesis and Pathology

·          Metacercaria passing through the intestinal wall does not produce any significant pathologic damage

·          The parasite traversing the liver parenchyma produces linear necrotic lesion accompanied by infiltrates of eosinophils with hyperplasia (increase number of cells) of the bile ducts begins

·          Adult worms in the bile ducts cause inflammation, adenomatous hyperplasia (increase of glandular cells), and fibrosis (scarring) of ducts. Numerous worms may cause pressure atrophy (shrinkage) of the liver with extensive fibrosis around the ducts. Similar changes occur in the gall bladder.

·          Heavy worm burden may result to formation of abscess pockets due to wandering worms that lay eggs. The adult worms feed on liver cells and they may also ingest red blood cells although such is not needed in their biologic activities.

·          The larvae that pass through the intestinal walls and later into the peritoneal cavity on their way to the liver may be “trapped” in different sites. Ectopic locations may result to abscess formation and fibrosis in the blood vessels, lungs, subcutaneous tissues, ventricles of the brain, or in the eyes.

 

Clinical Manifestations

·          Physical signs and symptoms include colic, obstructive type of jaundice, cough, vomiting and possibly generalized abdominal rigidity.

·          Urticaria may be present, leukocytosis may reach up to 60%

·          Irregular fever and/or diarrhea may be present

·          Gall stone (cholelithiasis) is developed – eggs serving as nidus

·          “Halzoun” – pharyngeal fascioliasis – is due to temporary lodgement of adult worms in the pharynx. It may happen when an individual eats liver of infected animals (e.g. sheep, goats, etc.). The adult worms contained in the liver that come into contact with different tissues result to edema of the soft palate, pharynx, larynx, nasal fossai, and Eustachian tubes. Halzoun manifests with dyspnea, deafness, dysphagia, or asphyxia.

 

Laboratory Diagnosis

·          Demonstration of eggs in feces or fluid from duodenal aspiration and/or biliary drainage

·          False fascioliasis – the patient in this condition does not really have adult worm in the liver but the person has just ingested infected animal liver. Remedy – tell patient to undergo a “liver-free” diet for 3 days or more. If the stool examination showed no eggs, then it may be false fascioliasis. Diagnosis of “true fascioliasis” is made based on the positive stool examination even after a period of liver-free diet.

 

Prevention and Control

·          Proper and sanitary way human waste disposal. However, this measure will not totally eliminate the parasite due to presence of reservoir hosts such as goats, sheep, and cows.

·          Sanitary protection of watercress beds against the infection

 

Opistorchis felineus

·          Also known as “Cat liver fluke”

·          Disease – opistorchiasis or cat liver fluke infection

 

Intermediate Hosts:

                1^st intermediate host – Bithynia leachi

                2^nd intermediate host – fresh water or cyprinoid fishes such as Idus melanotus and Tinca tinca

 

Morphology

·          Adult worm is lancet shaped with smooth cuticle, attenuated anterior and rounded posterior, thin and transparent, measures 7 – 12  X 2 – 3 mm, and live worms in the bile tract are reddish – bile in color

·          Oral- and ventral suc***s are nearly equal in size. Oral suc*** is subterminal in location, simple intestinal ceca, two lobed testes in oblique arrangement placed at the posterior part of the worm, small, slightly lobed ovary at the median and midway of the body, “transversely compressed” vitellaria distributed at the middle 3^rd, lateral part of the body

·          Egg is elongate – ovoid with a prominent operculum resting on a thickened or prominent rim, appears like that of an “old fashioned electric bulb,” with a miracidium inside, light yellowish – brown, and with a minute thickening at the posterior part of the shell.

 

Pathogenesis, Pathology and Manifestations

·          Maturing parasite in the distal bile ducts (habitat) cause inflammation and proliferative changes in the biliary epithelium leading to fibrosis. Degree and severity of pathologic changes dependent on the number of worms present. Heavy infection affects the proximal biliary tracts as well as the gall bladder ending up with massive periportal fibrosis.

·          Liver may enlarge and later leads to passive congestion of the spleen.

·          Bile stones may form around nest of eggs and may lead to cholecystitis (inflammation of gall bladder) – manifesting with obstructive type of jaundice.

·          Edema and formation of collateral circulation causing engorgement of superficial veins of the abdomen and esophageal varices may develop.

·          Uninhabited bile ducts also undergo hyperplastic changes.

 

Laboratory Diagnosis

·          Demonstration of the eggs in DFS or duodenal aspirates

 

Prevention and Control

·          Abstain from eating raw or inadequately cooked fishes

·          Parasite is hard to eradicate due to presence of reservoir hosts such as dogs, cats, foxes, swine, rat, beaver, rabbit, seal, and lion. These animals including man pollute water with fecal matter that contains the eggs.

·          Proper and sanitary disposal of human waste

·          Public education

Clonorchis sinensis

·          Also known as “Chinese liver fluke”

·          Disease – chlonorchiasis or Chinese liver fluke infection

 

Intermediate Hosts:

                1^st intermediate host – snails under genus Parafossarulus, Bulimus, Semisulcospira, Alocinma, and

also Melanoides tubeculatus

                2^nd intermediate host – fresh water fishes of family Cyprinidae such as the ide (Ctenopharyngodon

idellus – most common source of infection)

 

Morphology

·          Adult worm – flat, transparent, spatulate with attenuated anterior and slightly rounded posterior part, measures 10 – 25 X 3 -5 mm, inhabiting the “distal biliary tract,” integument has no spines, oral- is slightly bigger than ventral suc***, two deeply lobed or branched testes (characteristic), one behind the other, situated at the posterior 3^rd of the body, vitellaria consist of small granules distributed at the middle 3^rd at the lateral field of the body

·          Egg has the same appearance woth that of Opistorchis felineus

 

Pathology, Pathogenesis, and Manifestations

·          The same as that of Opistorchis felineus

·          Clonorchis sinensis as well as other related species – Opistorchis sp. were associate with the development of malignancy of the bile ducts due to marked and significant hyperplasia that occur.

 

Intestinal Flukes

 

Fasciolopsis buski

 

v       Also referred to as “Giant Intestinal Fluke”

v       Disease – fasciolopsiasis

v       A common parasite of man and pigs in central and south China, Taiwan, Vietnam, Thailand, Borneo, Sumatra, Bengal, and other countries of the Orient. Some dogs in China were found to be infected.

 

Intermediate Hosts:

                1^st intermediate host – Segmentina hemisphaerula, Hippeutis cantori

                2^nd intermediate host – water caltrop (Trapa natans or Trapa bicornis), water chestnut (Eliocaris

tuberosa – apulid), lotus, water bamboo, and other vegetations

 

Morphology

·          Adult worm – large and fleshy, often elongate ovoid, and measuring 20 – 75 mm long, 8 – 20 mm wide, and 0.5 – 3 mm thick, integument has spines, and without cephalic cone, oral- is about 4 – 6 times smaller than the ventral suc***, simple intestinal ceca with indentations (diagnostic), two highly branched testes one behind the other occupying the posterior half of the body, with finely granular vitelline follicles throughout the lateral part

·          Egg – indistinguishable with that of Fasciola hepatica

 

Pathogenesis, Pathology, and Manifestations

·          The adult worms attached mainly at the duodeno-jejunal area of the intestine may produce traumatic, obstructive, and/or toxic effects. At the attachment site they produce inflammation and ulceration of the mucosa, which may lead to hemorrhage. The worms can cause increase mucus secretions, which lead to intestinal obstruction. The worms’ waste products may be absorbed and lead to intoxication or sensitization.

·          Abscess may develop at the attachment site. Heavy infection may lead to acute ileus (paralysis of intestinal tract – absence of peristalsis).

·          Infection may manifest with toxic diarrhea, hunger pains, generalized toxic and allergic symptoms such as facial edema, abdominal wall, and of lower extremities.

·          Ascites (fluid in the abdomen) with abdominal pain is quite common. Death may occur due to severe intoxication.

 

 

 

Laboratory Diagnosis

·          Recovery of eggs in fecal smears. Possibility of echinostomiasis and/or fascioliasis should be excluded, especially in endemic areas.

 

Prevention and Control

·          Vegetables may be immersed in boiling water for few minutes of their skin peeled off followed by thorough washing although not very satisfactory.

·          Prohibit use of night soils (human excreta) in vegetable gardens

·          Use of molluscicides to kill snail hosts

·          Public education

 

Echinostoma ilocanum

 

v       Also known as “Garrison’s Fluke”

v       Disease – echinostomiasis

 

Intermediate Hosts

        1^st intermediate host – planorbid snails such as Gyraulus convexiusculus and Hippeutis umbilicalis

        2^nd intermediate host – large snails such as Pila conica, Pila luzonica (kuhol), and Viviparus javanicus

 

Morphology

·          Adult – reddish gray when alive, with plaque-like scales of its cuticle, measures 2.5 – 6.5 mm long and 1 – 1.35 wide, attenuated posterior, anterior and has a prominent “circumoral disk” (surrounding the oral suc***) provided with a “collarette of spines” (this is diagnostic of genus Echinostoma).

·          Ventral- is about 4 times bigger than oral suc***, two deeply lobed testes arranged one behind the other situated at the 3^rd fourth of the body, ovary is just in front of the anterior testis, vitellaria consist of medium sized follicles distributed at the lateral field at the posterior 3/4^th of the body

·          Egg – straw colored, immature, and measures 83 – 116 X 58 – 69 micrometers, with a small operculum, and oftentimes with a “prominent germ ball”

 

Pathology, Pathogenesis, and Manifestations

·          Adult worms cause inflammation at the attachment sites.

·          Waste products of the worm, when absorbed in the intestine, can cause generalized toxic process

·          Infection may manifest with intestinal colic and/or diarrhea – due to inflammation caused by the worms

 

Laboratory Diagnosis

·          Diret Fecal Smear (DFS) for the eggs, which should be differentiated carefully from the eggs of Fasciola hepatica and Fasciolopsis buski.

 

Prevention and Control

·          Refrain from eating raw or inadequately cooked snails

·          Molluscicides to kill snail hosts.

·          Proper and sanitary procedures of human waste disposal

·          Public education

 

THE HETEROPHYDS (also under intestinal flukes)

                Member species are small or tiny species of flukes of birds and mammals. Oftentimes, the worms are less than 1 mm long, pyriform or ovoid in shape with the skin covered with spines. Quite a number of specimens will show a “genital pore” (often loosely called as genital suc***) that is closely associated with the ventral suc***. Generally, member species are with simple intestinal ceca, coiled uterus, and 6 – 8 polygonal vitelline follicles on each of the lateral sides. For practicality of identification, it is the number and appearance of the testes that is used. Important species of heterophyds include Heterophyes heterophyes (two ovoid testes of equal size), and Metagonimus yokogawai (two, ovoid testes of unequal size). Other species that were reported to cause infection to man include Haplorchis yokogawai (single, large ovoid testis) and other species that were considered insignificant already because of rarity.

 

 

 

 

Heterophyes heterophyes

 

v       Adults are attached deep into the walls of the intestine. Egg measures 28 – 30 X 5 – 17 micrometers, ovoid, operculate, with a miracidium inside and vary hard to differentiate from the egg of Clonorchis sinensis

 

Intermediate Hosts

                1^st intermediate host – freshwater snails (Pironella conica, Cerithidea cingulata)

                2^nd intermediate host – freshwater fishes – Mugil cephalus (mullet), Tilapia nilotica, and Aphanius

fasciatus

 

Pathogenesis, Pathology, and Manifestations

·          Adult worms produce mild inflammation at the attachment site. They may burrow into the intestinal mucosa to produce further irritation, which may lead to superficial necrosis.

·          Eggs may be filtered into the mesenteric lymphatics, cardiac valves, myocardium, or even the brain. In the heart, eggs can cause myocarditis, which may develop into heart failure and thus, death.

·          Diarrhea is common among infected individuals.

 

Laboratory Diagnosis

·          Identification of the eggs in Direct Fecal Smear.

 

Prevention and Control

·          Most important is to refrain from eating raw freshwater fishes that serve as the source of the metacercaria.

·          Other measures applicable to other flukes are also of great help in reducing, if not eliminating, the infection in a community.

 

Metagonimus yokogawai

 

v       Also known as “Yokogawai’s fluke”

v       Disease – metagonomiasis

v       Pathogenesis, pathology, manifestations, diagnosis, prevention and control, and other aspects of infection are similar with Heterophyes heterophyes

 

Intermediate Hosts

                1^st intermediate host – Semisulcospira libertine

                2^nd intermediate host – freshwater fishes – Plectoglossus altivelis, Odontobutis obscurus, Salmo

perryi, Tribolodon hakonensis

 

Lung Fluke

 

Paragonimus westermani

 

v       Also known as the “Oriental lung fluke”

v       Disease – Oriental distomiasis or paragonomiasis

v       Places once heavily infected include Far East, which include Japan and Korea. Some isolated areas exist in China, Taiwan, the Philippines, Thailand, Malaysia, and Bengal. It was reported to be endemic in New Guinea, Solomon islands, Java, Sumatra, Zaire, Nigeria, Peru, Ecuador, Columbia, Costa Rica, Mexico, and Venezuela.

 

Morphology

·          Adult – plump, ovoid, with rounded anterior and tapered posterior (assuming the shape of “coffee bean”), measures 7.5 – 12 mm long, 4 – 6 mm wide, and 3.5 – 5 mm thick, with reddish-brown hue when alive, and provided with scale-like spines on its skin

·          Oral- and ventral suc***s are sub-equal, with two irregular, deeply lobed testes situated side by side at the posterior side of the body, with large and lobular ovary, vitellaria consist of branching follicles, and with “zigzag intestinal ceca” (diagnostic)

·          Egg – ovoid with “flattened operculum”, 80 – 118 X 48 – 60 micrometers, posterior part of shell is thick (thickened aboperculum)

 

Intermediate Hosts

        1^st intermediate host – snails like Semisulcospira libertina, Brotia asperata, and Brotia costula episcopalism

        2^nd intermediate host – freshwater crabs under the genera Parathelpusa (such as Parathelpusa mistio),

Potamon, and Siamthelpusa

-          crayfishes under the genera Cambaroides, Procamburus, and Palaemon.

 

Pathogenesis, Pathology, and Manifestations

·          Metacercaria that passes through the intestinal walls do not produce significant lesion.

·          Maturing parasite in the lungs induce leukocytic infiltration followed with production of a broad layer of fibrous tissues resulting to the formation of a thick cystic capsule – called pulmonary pocket – that enclose the organisms.

·          Small blood vssels form around pulmonary pockets and there is production of blood-tinged, thick, purulent fluid with flecks of rust material that contains cluster of eggs. Sputum – rusty color with blood. Patients manifest with hemoptysis, chest pain, fever, and cough.

·          Sites other than the lungs may also be infected due to entrapment of the migrating worm as it finds its way to the lungs. Ectopic sites of infection may occur in the liver, mesenteric lymph nodes, muscles, testes, brain, peritoneum, or pleura.

 

Laboratory Diagnosis

·          Demonstration of eggs in sputum (may also be recovered in patients’ stools). The “rusty colored” portion of the specimen is likely to contain plenty of eggs.

·          Serologic test – intra-dermal test (uses specific antigen), which shows persistent positive result

-          complement fixation test – gives positive result only when the worms are still alive

 

Prevention and Control

·          Refrain from eating raw or inadequately cooked freshwater crabs or crayfishes

·          Proper and sanitary disposal of human waste

·          Eradication of the snails (e.g. use of molluscicides)

·          Public education