BROWN RECLUSE SPIDER BITES (Loxosceles reclusa)

TREATMENT INFORMATION FOR MEDICAL PROFESSIONALS

BROWN RECLUSE SPIDER BITES (Loxosceles reclusa)

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The recluse spiders, genus Loxosceles, belong to a unique family of arachnids known as the Sicariidae, or six-eyed spiders. The family consists not only of the recluse spiders, but also to the six-eyed crab spiders, genus Sicarius, of Central and South America, and South Africa. Recluse spiders were the first spider group to be recognized a causative agent of the disease state now known as necrotic arachnidism. When caused by a recluse spider is termed loxoscelism. This disease was first recognized by Chilean physician in 1872 when he linked a peculiar skin lesion known as the "gangrenous spot of Chile" to bites by the Chilean recluse spider, Loxosceles laeta. All recluse spiders as well as the six-eyed crab spiders, are now considered venomous to humans.

THE SPIDER

There are eleven indigenous species of recluse spider and two introduced from other countries. The most noted being the brown recluse spider, Loxosceles reclusa, which is found in the midwest and parts of the south: it ranges from southern Wisconsin east to Ohio, and south to northern Florida and central Texas. The adult brown recluses has a body length of 10 -12 mm. Frequently called the "violin" or "fiddleback" spider, due to the violin-like markings on the dorsal cephalothorax. NOTE: The apparent presence of a violin-like marking on the cephalothorax or elsewhere is not sufficient to identify a spider as belonging to the recluse group. Many other spiders have markings which somewhat resemble "violins".

This spider is not inherently aggressive but tends to bite only when trapped or crushed. The spider prefers warm dry locations. Their quest for warmth leads them into homes, firewood, boxes, and clothing. Because of the spider's nocturnal hunting habits, many bites occur while the victim is asleep, and thus go unnoticed.

VENOM

Recluse spider venom has the ability to cause major tissue necrosis. The primary dermonecrotic factor appears to be phospholipase sphingomyelinase D that acts by disrupting cell membranes. The patients' response to the foreign antigens in the venom may be responsible for the resultant tissue necrosis. The fact that reduced PMN leukocyte migration results in decreased necrosis support the role of immunity in the necrotic process. Altering the body's immune response to the spider's venom is the focus of many investigational treatment modalities.

CLINICAL PRESENTATION

Factors associated with the severity of any envenomation include: 1.) the amount of venom injected, 2.) host susceptibility, and 3.) the site where the envenomation occurred. The majority of bites probably go unnoticed or result in only a mild stinging sensation. A minority will however suffer more significant symptoms including: local pruritis, pain, swelling, induration, erythema, blister formation and even pustule formation. If none of the above occur within 48-96 hours significant envenomation and necrosis is unlikely.

Complications resulting from severe BR spider bite are related to the location of the bite. Areas of minimal subcutaneous fat appear to result in greater complication rates. The eyelids and extremities, specifically the dorsum of the hands and feet are at risk for complications. BR spider bites have been associated with deep venous thrombosis, pyoderma gangrenosum, and Pseudoepitheliomatous hyperplasia. Fever and malaise are the most common symptoms, but headache, anorexia, arthralgias, generalized maculopapular rash, nausea, vomiting, abdominal pain and chest pain may be systemic manifestations of BR spider bite. Other findings include: acute renal failure secondary to hemoglobinuria, leukocytosis, leukopenia, thrombocytopenia, disseminated intravascular coagulation, convulsions, and coma. Leukocytosis and an elevated ESR are the most common laboratory anomalies. The misdiagnosis of Lyme disease for BR spider bite has been reported.

TREATMENT

Early surgical excision of the BR spider wound is controversial. Several studies have associated increased wound breakdown and graft rejection with early surgical excision.

Dapsone treatment for BR spider bites has been found to alleviate the need for surgical intervention in some cases. Dapsone is an inhibitor of neutrophil function, a major mechanism of skin necroses brought on by envenomation. G6pd deficiency and methemoglobinuria are contraindications to Dapsone therapy due to potential massive hemolysis in individuals with these disorders.

High voltage, low amperage direct current shock has been used with great success in this and other types of envenomation. Treatment consists of using a modified stun gun that will produce 25 kilovolts at less than 350 milliamps. Because of the deep penetration of the venom of the BR spider it is necessary to shock "through the tissue" rather than surface shock only. This is accomplished by means of a jumper cable attached to one pole of the stun gun that will reach to the opposite side of the extremity. The central area as well as the surrounding area of erythema is shocked 6 to 8 times. This is like getting a shock from an electric fence and is tolerated quite well by most all patients. Patients should be observed for up to two hours since a sudden release of toxins and foreign proteins may result in some renal impairment. It is advisable to obtain a urinalysis several hours after treatment to check for hemoglobin and myoglobin. The mechanism of action is still debatable. Some feel that it inactivates the proteolytic enzymes and some feel that it gives the cell wall a higher energy state that inhibits the attack by the enzymes. It probably is a combination of the two.

Routine tetanus booster and antibiotic therapy is indicated. If Dapsone is used, 25 mg. two to four times a day seems to be an appropriate dose with minimal side effects.

© Stan Abrams, M.D. 1998

Published articles

• Ronald Guderian et all, High Voltage Shock Treatment For Snake Bite, THE LANCET, July 26, 1986, p 229.
• Krogel C. Meyer zum Buschenfelde K.H., Biological Basis For High-Voltage Shock Treatment For Snakebite, THE LANCET, December 6, 1986 p 1335.
• Mueller, L A Shocking Cure for Snakebite, Outdoor Life, June 1988, p.1: Outdoor Life, July 1988, p.2.
• Carl D. Osborn, M.D., Treatment of Venomous Bite by High Voltage Direct Current, THE JOURNAL of the Oklahoma State Medical Association, Volume 83, No. 1, January, 1990, pages 9-14.
• Carl D. Osborn, M.D., Treatment of Spider Bites by High Voltage Direct Current, THE JOURNAL of the Oklahoma State Medical Association, Volume 84, No. 5, June, 1991, pages 257-260.
• Carl D. Osborn, M.D., Multiple HVDC Shocks as First Aid or Therapy for Venomous Bites and Stings. THE JOURNAL of the Oklahoma State Medical Association, Volume 85, No. 7, July, 1992, pages 331-333.

There is a good possibility that for a small price, if you contact Erica Schwenneker who is the OSMA publications manager that she can get you copies of Dr. Osborn's articles that were published in the OSMA Journal. Her E-mail address is (For physicians only)

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