while I realize this is the "alternative" parasites
forum, occasionally touching our feet in reality shouldnt cause much harm
read up folks and if you dont understand ... then read MORE
Take RESPONSIBILITY for YOUR health
the article that follows encompasses a VARIETY of flukes (not simply the all hallowed F. hepatica that seems to be so fixated on this site) There are hundreds if not THOUSANDS of different types of flukes, majority that inhabit the INTESTINES (not liver)that contiually appear to be over-looked on this forum and are much more dangerous than the average nematode. (nematodes produce one lava per ova, flukes produce over 100,000 larvae per ova ... that MIGHT be significant?)
this is LITEATURE ... not hocus pocus herbal new age stuff (no offense)
Question: what if I have a nematode infestation as well.
Answer: Albendazole combines with and compliments praz quite nicely, (as does levamasole)
Many of these may be testd for through SEROLOGY. Stool ova/ parasite
is dead end as many of us have determined. Serology testing exists for F. hepatica, paragonimus, strongyloides, schistosoma et al. This is definitive irrefutible results (its a GOOD THING)
ONE LAST NOTE:
much literature will have us to believe these parasites
dont replicate in the human body. This may be so in the normal scheme 0f things, but in the eventuality that you should happen to kill the unfortunate critters they will kick into survival mode and dessiminate the eggs which WILL hatch inside of you SANS snails. Literature dictates that eash bug lives up to 5 yrs but that infections may persist over 20 yrs.... come on folks .... this is BASIC math. DONT BELIEVE THE HYPE.
Helminthic Infections: Trematode Infections
From ACP Medicine Online
Wesley C. Van Voorhis, MD, PHD, FACP; Peter F. Weller, MD, FACP
Schistosomiasis, a chronic trematode (fluke) infection of humans, constitutes a major worldwide health problem: 200 million persons are infected, 120 million are symptomatic, and 10 million have severe disease.61 Three major species—Schistosoma mansoni, S. japonicum, and S. haematobium—infect humans. S. mansoni is found in Africa, the Arabian Peninsula, South America, and parts of the Caribbean; S. japonicum is found in Japan, China, and the Philippines; and S. haematobium is found in Africa and the Middle East. Two minor species, S. mekongi and S. intercalatum, are found in mainland Indochina and central West Africa, respectively. Transmission of schistosomiasis cannot occur in the United States because of the absence of the specific freshwater snail that is a requisite intermediary host [see Figure 11 -- omitted]. However, the disease may be encountered in immigrants or travelers from endemic areas.62,63
The diagnosis of schistosomiasis is suggested by a history of possible exposure, even exposure that occurred many years ago, along with compatible gastrointestinal or urinary tract symptoms, hepatosplenomegaly, eosinophilia, or a combination of these findings.
Clinical features. Three stages of disease may occur in schistosomiasis. The first stage, schistosomal dermatitis, may develop acutely within a day of cercarial penetration of the skin. Because this entity develops early after exposure, it usually will have subsided in patients before they are seen by physicians in the continental United States. Swimmer's itch, a similar reaction caused by exposure to animal schistosomes in freshwater and saltwater, is seen in the United States [see Figure 12 -- omitted].64 The schistosomes penetrate human skin and then die, causing no further infection.
The second stage of disease, acute schistosomiasis, or Katayama fever, develops 4 to 8 weeks after heavy (presumably, primary) infection. This stage is thought to be caused by a severe allergic response at the onset of egg-laying by the schistosomes. Patients have fever, cough (up to 10% also have pulmonary nodules), hepatosplenomegaly, malaise, myalgias, urticaria, and eosinophilia.65–67 Deaths have ensued. Katayama fever is more severe in infection with S. japonicum than with other species, because of the high quantities of eggs produced by S. japonicum.
Chronic schistosomiasis, the third stage, is caused by the heavy deposition of eggs in the intestine or bladder and in the liver. In S. haematobium infection, the principal symptoms are hematuria, dysuria, and frequent urination. Hydronephrosis and pyelonephritis may develop as a result of fibrosis and infection. In S. mansoni, S. mekongi, or S. japonicum infection, manifestations may include fever, malaise, abdominal pain, diarrhea, blood in stools, and hepatosplenomegaly. Presinusoidal hepatic trapping of S. mansoni, S. mekongi, or S. japonicum eggs and the consequent granulomatous reaction induce portal hypertension and collateral esophageal varices. Eggs may then be shunted from the liver to the lung, with the possible sequela of pulmonary hypertension. Death may occur as a result of variceal bleeding. Hepatic encephalopathy rarely develops because the hepatic parenchyma is spared. Coinfection with S. mansoni and hepatitis B or C virus is associated with accelerated clinical deterioration.61 Less common sequelae of chronic schistosomiasis include intestinal polyps, bladder carcinoma, and persistent Salmonella infections. An uncommon sequela of both acute and chronic schistosomiasis is focal neurologic dysfunction from aberrant localization of eggs in CNS tissue. Embolic deposition of S. japonicum eggs may produce cerebral granulomas, whereas S. haematobium and S. mansoni eggs may cause transverse myelitis involving the midthoracic or lumbar spinal cord.68,69
Laboratory findings and imaging studies. Computed tomography, magnetic resonance imaging, or ultrasonography may detect hepatic periportal fibrosis and calcification, colonic
wall calcifications, and changes in the bladder and ureter resulting from schistosomiasis. Serologic tests can help confirm the diagnosis; an indirect immunofluorescent test for gut-associated schistosome antigens is especially sensitive for the detection of acute schistosomiasis. Stool examination should include a search for eggs of all Schistosoma species [see Figures 13a -- omitted, 13b -- omitted, 13c -- omitted, and13d -- omitted]. Urine specimens for detection of S. haematobium should be obtained between 10 A.M. and 2 P.M. If stool and urine specimens are negative, microscopic examination of biopsy specimens of rectal or bladder mucosa may demonstrate eggs of all species. Detection of circulating antigens from adult worms and eggs are promising techniques that may supersede traditional egg demonstration.
Praziquantel is used to treat infection caused by any of the five Schistosoma species; it reliably cures 60% to 90% of infected persons and reduces egg burden substantially in most others. For S. haematobium and S. mansoni, two oral doses of 20 mg/kg are given in 1 day. For S. japonicum and S. mekongi, the dosage is 20 mg/kg given orally three times in 1 day. The efficacy, the paucity of side effects, and the convenience of single-day therapy make praziquantel the drug of choice for all forms of schistosomiasis.19 Resistance to praziquantel has been reported in S. hematobium and S. mansoni infections in Egypt and Kenya but has not yet become a widespread problem.61 In addition to praziquantel, corticosteroids are beneficial for patients with spinal cord schistosomiasis59 and acute schistosomiasis.
Humans acquire paragonimiasis after consumption of raw, salted, or wine-soaked crustacea (freshwater crabs or crayfish) infested with the metacercarial stage of lung flukes belonging to the genus Paragonimus (the life cycle of Paragonimus is illustrated in the CDC PHIL [
]; photograph 3415). It is estimated that 20 million people are infected with Paragonimus species.70P. westermani is endemic in parts of China, Korea, Japan, the Philippines, and Taiwan. Other Paragonimus species infect humans in western Africa and Central and South America. Although paragonimiasis is rare in the United States, it has developed in persons in Missouri from indigenous Paragonimus species.71
Ingested metacercariae undergo excystation in the duodenum and migrate through the wall of the gut into the peritoneal cavity. Most pass through the diaphragm and penetrate the parenchyma of the lung. Neutrophilic and eosinophilic reactions, followed by a mononuclear leukocytic inflammatory reaction, develop around the fluke. As the lung parenchyma necrotizes, a fibrous capsule begins to surround the fluke. By about 5 to 6 weeks after ingestion, the flukes have matured and start laying eggs, which causes the capsule to enlarge and rupture, often into a bronchiole. The most common presentation of paragonimiasis is the production of brown-tinged sputum or hemoptysis, which derives from the admixture of eggs, inflammatory cells, and blood in the sputum. Sputum is often gelatinous and purulent as well as bloody. Patients usually appear well but may have a chronic cough, pleuritic pain, or night sweats.
Young flukes may migrate to nonpulmonary sites. Localization in the CNS produces signs and symptoms from a cerebral or spinal inflammatory mass lesion, which may calcify.72 Less commonly, the parasites
lodge in cutaneous or peritoneal sites.
During the early stages of infection, when the larvae migrate, blood eosinophilia is prominent. The chest x-ray may show transient, often basilar, infiltrations, as in Löffler syndrome. Later in the course of the disease, blood eosinophilia commonly disappears, and the chest x-ray may show areas of cavitation; ill-defined, so-called cotton-wool and streaky densities; and bubblelike cavities.73 Pleural reaction, with or without pleural effusion or pneumothorax, can occur.
The diagnosis of paragonimiasis should be considered for patients from endemic areas with compatible clinical presentations.74 Examination of the sputum for ova may confirm the diagnosis by revealing the operculated eggs of Paragonimus. Swallowed eggs appear in the stool; therefore, examining the stool for eggs may be helpful, especially in children. Fine-needle aspiration of pulmonary lesions also yields diagnostic eggs.75 Paragon imiasis may resemble pulmonary tuberculosis both clinically and radiographically, yet Paragonimus eggs are usually not seen in acid-fast stains. Serologic tests are available.70
Praziquantel is an effective treatment of paragonimiasis, although its use remains investigational. The dosage is 25 mg/kg orally three times a day for 2 days.19 Bithionol is somewhat effective, but its use is limited because of side effects such as diarrhea. Triclabendazole has been used and has been reported to cure cases in which praziquantel and bithionol had failed.70
Clonorchis sinensis, the Chinese liver fluke, infects approximately seven million persons in the Far East, including South China, Hong Kong, Taiwan, Japan, Korea, and Vietnam.76 Humans become infected with C. sinensis, a parasite
of freshwater fish, by eating raw or undercooked fish containing encysted metacercariae (the life cycle of C. sinensis is illustrated in the CDC PHIL [
]; photograph 3385). Larvae, liberated by trypsin in the duodenum, migrate to the common bile duct and then to the distal biliary tree. There they mature into adult worms, which may persist for more than 20 years. Less commonly, adult worms are found in the gallbladder and pancreatic ducts.
In the acute phase of the infection, the epithelium of the biliary tree undergoes early desquamation, which is followed by hyperplasia and increased mucin production by the epithelial cells. The hyperplasia may progress to adenomatous changes. With chronic infection, fibrosis develops around dilated bile ducts. Clinically, the syndrome of acute clonorchiasis, manifested by fever, chills, and tender hepatomegaly, may develop 1 week after ingestion of infected fish. Later in the course of the infection, however, most patients with light infection and many with heavy infection are asymptomatic.77 Occasionally, adult worms block pancreatic ducts, causing pancreatitis. By occluding the biliary tract, worms may contribute to acute suppurative Cholangitis
. Clonorchiasis predisposes to intrahepatic bile duct stone formation and to recurrent pyogenic Cholangitis
; infection with C. sinensis has been associated with cholangiocarcinoma.78
Leukocytosis, prominent eosinophilia, and elevation of alkaline phosphatase levels occur in symptomatic acute clonorchiasis. Sonography often detects diffuse dilatation of small intrahepatic bile ducts without dilatation of large intrahepatic or extrahepatic ducts. Adult flukes may be visualized in the gall bladder by ultrasonography and in the bile ducts by cholangiography.79 In asymptomatic chronic clonorchiasis, eosinophilia is not present, and liver function tests and liver scans are normal. Egg laying begins within 2 to 3 weeks after infection; eggs may be found either in the stool or in duodenal aspirate. Diagnostic serologic tests are neither sensitive nor specific. The diagnosis should be considered in patients who have a history of travel or residence in the Far East, have eaten undercooked fish, and have a compatible clinical syndrome.
Praziquantel, which is considered investigational for clonorchiasis, constitutes effective and well-tolerated therapy for this disease. Praziquantel is administered at a dosage of 25 mg/kg orally three times a day for 1 day.19 An alternative investigative therapy is albendazole, 10 mg/kg/day for 7 days.19 Initially, complications of C. sinensis infection, including calculi, Cholangitis
, and pancreatitis, are managed medically, although surgical drainage may be required.
Opisthorchiasis represents infection by either Opisthorchis felineus or O. viverrini. O. felineus infects 1.5 million persons in Kazakhstan, the Ukraine, central Europe, western Siberia, and parts of Asia; O. viverrini infects nine million persons in Thailand, Laos, and Cambodia.
Cats and wild carnivores are the definitive hosts of these species. Humans acquire infection by eating raw or undercooked fish that contains metacercariae of the parasite. Metacercariae undergo excystation in the duodenum and migrate into the bile ducts, where they mature.
Clinical features of opisthorchiasis are similar to those of clonorchiasis; complications include the development of cholangiocarcinomas.77,78,80 The diagnosis is made by finding eggs in feces or in duodenal aspirate.
Therapy, which is considered investigational by the FDA, consists of praziquantel (25 mg/kg orally three times in 1 day).19 Complications involving biliary tract sepsis require the administration of antibacterial agents.
Fasciola hepatica, the liver fluke of sheep and cattle, is a major veterinary problem and can give rise to human fascioliasis.78,81,82 Human infection with F. hepatica shows a wide geographic distribution that includes Europe, China, Africa, and Latin America; the disease is considered a public health problem in the Andean countries of South America, Iran, and western Europe.82 Despite the prevalence of the parasite
in sheep and cattle of the southern and western United States, autochthonous human cases are rare. Humans generally become infected by ingesting parasitic cysts attached to aquatic plants, most notably wild watercress.
Ingested metacercariae burrow through the intestinal wall into the peritoneal cavity and then penetrate the hepatic capsule and parenchyma; they then enter the bile ducts, where they mature into adults after 3 to 4 months. Acute fascioliasis runs its course during the months of penetration and maturation. Symptoms may be minimal or include fever, upper abdominal pain, hepatomegaly, and malaise. Pruritus, urticaria, jaundice, nonproductive coughing, and anemia occur less often.78,83
After the flukes mature in the biliary passages, hyperplasia and dilatation of the biliary ducts, as well as periductal fibrosis, develop. Clinical manifestations in the chronic stage of infection are variable and may include the same signs and symptoms experienced in the acute phase. Obstruction of the biliary tract, cholecystitis, and biliary cirrhosis are uncommon. In rare instances, flukes migrate to other tissues, including the lungs, muscles, and CNS.
Ingestion of raw sheep or goat liver containing young flukes produces halzoun, a disease recognized in the Near East. Lodging of the flukes in the pharynx produces a pharyngeal inflammatory mass lesion with attendant dysphagia and dyspnea.
Acute fascioliasis usually produces leukocytosis, marked eosinophilia, and cholestatic-type abnormalities on liver function testing. Eggs are not found until approximately 3 months after infection, when they may be detected in the stool or, with a higher yield, in biliary or duodenal fluid samples. Thus, the triad of fever, marked eosinophilia, and hepatomegaly suggests acute fascioliasis. A history of ingestion of potentially infected watercress supports the diagnosis. Serologic tests are available but may reflect cross-reactions with other helminthic parasites. Nodular hepatic lesions with diminished density may be visualized by CT or MRI.84,85 In chronic fascioliasis, the extent of the abnormalities in liver function tests and cholangiograms correlates with the magnitude of biliary tract obstruction and hepatocellular damage.
Triclabendazole, given in a single oral dose of 10 mg/kg, is the drug of choice for fascioliasis, but in the United States it is available only from the manufacturer (Novartis). Bithionol (30 to 50 mg/kg on alternate days for 10 to 15 doses) and nitazoxamide (500 mg p.o., b.i.d. for 3 days) are alternatives.19 Praziquantel is not effective for fascioliasis.
Fasciolopsiasis results from infection with the intestinal fluke Fasciolopsis buski, which is found in many parts of Asia.86 This fluke principally parasitizes the intestine of the pig. Human infection is acquired by ingestion of water plants such as water chestnuts, which bear metacercariae of the parasite. The larvae undergo excystation in the duodenum and develop into large adult flukes, up to 7 cm
long, that attach to the mucosa of the proximal small intestine. Inflammation and ulceration may occur at these intestinal sites. Light infection is asymptomatic; heavy infection is associated with abdominal pain, ulceration, hemorrhage, intestinal obstruction, malabsorption, and facial and generalized edema.87 Blood eosinophilia is common. Diagnosis is made by finding adult flukes or, more commonly, by finding in feces the eggs of F. buski, which are difficult to distinguish from the eggs of Fasciola hepatica. Fasciolopsiasis is treated, on an investigational basis, with praziquantel, 25 mg/kg orally three times in 1 day,10 although some sources advise that a single 15 mg/kg dose is effective.86
Other Intestinal Flukes
Infection with two small intestinal flukes, Metagonimus yokogawai (found in the Far East and Indonesia) and Heterophyes heterophyes (found in Tunisia, Egypt, and the Far East), occurs when humans ingest raw or undercooked fish that contains metacercariae of the parasites. The adult flukes are 2 to 3 cm
long and attach to the mucosa of the small intestine. Heavy infection may cause abdominal pain and diarrhea.88 Diagnosis is made by finding eggs, which resemble the eggs of Clonorchis species, in feces. Therapy consists of the investigational drug praziquantel (25 mg/kg orally three times in 1 day).19
Human infection with the intestinal fluke Metorchis conjunctus, acquired near Montreal, Canada, by consumption of the white sucker fish, has been described. Illness consisted of upper abdominal pain, low-grade fever, eosinophilia, and elevated liver enzyme levels. Diagnosis was made by finding eggs in the stool and by serology. Praziquantel (25 mg/kg three times in 1 day) is beneficial.19,89
The intestinal fluke Nanophyetus salmonicola has been recognized in humans who ate raw or kippered salmon. In most patients, symptoms and infection resolved without therapy, although treatment can be provided with praziquantel (20 mg/kg given three times in 1 day).19,90
Click here to subscribe or purchase the full chapter. Van Voorhis, Wesley C; Weller, Peter F, 7 Infectious Disease, XXXV Helminthic Infections, ACP Medicine Online, Dale DC; Federman DD, Eds. WebMD Inc., New York, 2000.
Figures, tables, references and sidebars are available in the subscription edition of ACP Medicine .
Wesley C. Van Voorhis, MD, PHD, FACP, Professor of Medicine and Adjunct Professor of Pathobiology, University of Washington School of Medicine
Peter F. Weller, MD, FACP, Professor of Medicine, Harvard Medical School, Co-Chief, Infectious Diseases Division, and Chief, Allergy and Inflammation Division, Beth Israel Deaconess Medical Center
to YOUR health ,