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Poisonous animals
 
Cnidarians (Jellyfish, Corals and Anemones)
 
Venomous fish
 
Scorpions
 
Spiders
 
Hymenopterans (Bees, Wasps and Ants)
 
Sea snakes
 
Terrestrial snakes
 
Miscellaneous animals
 
 
 
 
 
 
 
 

Clinic

 

Loxosceles spp.

Studies

USA
Rees et al. 1987: 17 L. reclusa bites. Identification: spiders brought in by the patients and conclusively identified.

Sams et al. 2001a: 19 L. reclusa bites. Identification: spiders brought in by the patients and conclusively identified and clinically characteristic lesion, and typical clinical course.

Chile

Schenone et al. 1989: 216 spider bites. Identification: spider brought in and identified as L. laeta (10%); 60% of patients saw a spider as a possible cause, 40% did not see the cause of the bite and the cause was inferred from the course of envenoming. Retrospective study.

Case reports

Brazil

Cardoso et al. 1990: 2 L. gaucho bites. Identification: detection of venom antigen (ELISA) from tissue fluid in the region of the bite.

 

Israel
Efrati 1969: 1 L. rufescens bite. Identification: the spider was brought in by the patient and conclusively identified.

South Africa
Newlands et al. 1982: spider bites. Loxosceles sp. a possible cause.

 

There have repeatedly been doubts expressed regarding the severe necrotising process that has been described in the literature and attributed to Loxosceles sp. bites, In a great number of cases it was not possible to identify the cause of the bite, and often the victim did not even see a spider, such as the 40% of 216 patients whose symptoms were attributed to L. laeta bites in the study of Schenone et al. (1989). The spider that caused the bite is rarely, and according to some toxicologists practically never, brought in for identification (Kunkel 1985). Careful analysis of the published case reports shows that in most cases a Loxosceles sp. bite is inferred to be the cause based on the presence of a skin lesion and the course of the illness (Kunkel 1985). Skin necroses may have many causes other than Loxosceles venom that should be considered in the differential diagnosis: e.g. infections, foreign bodies, focal vasculitis, self-administered injections, fat herniation with infarction, mechanical trauma, medications (heparin, coumarin), pyoderma gangrenosum (Wasserman and Anderson 1983–84). In none of the fatal cases of envenoming attributed to Loxosceles sp. was a Loxosceles sp. actually identified as the cause (Wang 1987, Wasserman and Anderson 1983–84).

There are no commercially available laboratory tests to identify the cause of a spider bite. The prerequisites for such a detection procedure were developed and published in 1973 (Berger et al. 1973). This is a lymphocyte transformation test to verify L. reclusa envenoming. However, the test only shows positive when the patient is already in the convalescent phase.

Signs & symptoms

Autopharmacological effects

Angio-oedema 4/17, urticaria 1/17 (Rees et al. 1987).

Local effects

A definite connection between skin necroses and L. laeta envenoming was established by Macchiavello (1947) in Chile and L. reclusa bites by Atkins et al. (1958) in the USA. Local necroses are explained as being caused by interaction between complement reactions, accumulation of polymorphonuclear leucocytes and local haemostatic defects (Futrell 1992).

Often no pain initially (thus bites often go unnoticed). If only a small amount of venom is injected, mild pain, erythema and oedema possible within 8 h; possibly development of insignificant necrosis (Berger 1973).

With severe envenoming strong local pain and local swelling within 2–8 h after the bite. Local cyanosis, within 12–24 h blisters, potentially haemorrhagic. Centre of the erythematous lesion becomes pale. Obvious necrosis within 24–48 h, often with irregular borders (Wasserman and Anderson 1983–84).

Local erythema 16/17, local cellulitis 7/17, local blistering 5/17, lymphangitis 1/17 (Rees et al. 1987).
Local pain, erythema, swelling, necrosis (Efrati 1969).

Local erythema 19/19, pain at the bite site 10/19, skin necrosis 11/19 (32% > 1cm2). Time to healing 5 to > 17 weeks (mean 5.6 weeks); for severity grad 1 (mild edema, punctum, no necosis) mean 8 days, severity grade 2 (erythema, mild edema, bulla, necrosis ≤ 1cm2) mean 22 days, severity grade 3 (extensive erythema, edema, bulla, ulcer / skin necrosis > 1cm2) mean 74 days (Sams et al. 2001a).

Haemolytic effects

Haemolysis (rare) appears to occur rapidly or with a long delay after the bite (24–72 h to 2–3 days) (Wasserman and Anderson 1983–84).

Haemolysis was observed in 4% of cases treated at the "Hospital Vital Brazil" (Lucas 1988).

Other signs & symptoms

Fine generalised macular rash 5/17 (Rees et al. 1987).
Fever (Wasserman and Anderson 1983–84).

Morbidity

If the wound is well cared for most Loxosceles bites heal by themselves. The black eschar falls off after 1–2 weeks. Complete healing of larger wounds after 6–8 weeks, at the longest 4 months (Wasserman and Anderson 1983–84). Anaemia. Renal insufficiency.

Case fatality rate

In none of the fatal cases of envenoming attributed to Loxosceles sp. was a Loxosceles sp. actually identified as the cause (Wang 1987, Wasserman and Anderson 1983–84).

Laboratory and physical investigations

Haemostatic defects/haemolysis

Rarely haemolysis, rarely thrombopaenia, very rarely disseminated intravascular coagulation (Futrell 1992).

Laboratory parameters should be assessed over a period of 3 days after the bite, as haemolysis in particular may develop after a long delay:

1. Haemoglobin, haematocrit,
2. LDH, haptoglobin,
3. clotting status, including platelets,
4. haemoglobinuria.

Treatment (symptomatic)

Very conflicting positions on treatment. There are no controlled clinical studies on the various recommended forms of treatment.

  1. Most Loxosceles bites heal by themselves with routine wound care (elevation of the affected extremity, local cooling to reduce local inflammatory reactions, dressing changes, antibiotic treatment if required) (King and Rees 1986, Futrell 1992).
  2. Early surgical excision creates more problems than it solves (King and Rees 1986; see below).
  3. The efficacy of corticosteroids has not been proven.
  4. Inhibition of segmented neutrophils: dapsone. Mechanism of action: delay of the migration of polymorphonuclear leucocytes into the area of the bite.
    Dosage: 50–100 mg, 12-hourly, for 2–3 weeks (Rees et al. 1985, 1987). 50 mg per day to be increased to 50 mg twice daily if G-6-PDH normal (Sams et al. 2001a,b)

However, severe adverse reactions to dapsone are possible, which in addition may be misdiagnosed as being systemic effects of the spider venom (vomiting, haemolysis) (Wille and Morrow 1988; Sams et a 2001a,b). Before administering dapsone it is necessary to rule out glucose-6-phosphate dehydrogenase deficiency and while taking the patient's history to find out if he/she has a sulfonamide allergy.

Studies

Rees et al. 1987: comparison of (1) dapsone 100 mg p.o., 12-hourly, (2) experimental L. reclusa antivenom, applied to the lesion, and (3) combination of (1) and (2). In addition, all patients received erythromycin and local cooling for relief of pain (further description of the study and clinical results, see above). Results: if the 2 patients who developed severe skin lesions are excluded from the 17 patients investigated, all wounds healed within 20 days regardless of the form of treatment. However, these patient numbers are too small to be able to make definite conclusions regarding treatment.

Rees et al. 1985: 31 spider bites. Identification: L. reclusa according to indirect criteria, such as patient history and clinical findings. Prospective study. Comparison of (1) early surgical excision (within 48 h) and (2) dapsone 100 mg daily for 14 days and subsequent surgical excision. Results: with dapsone pretreatment there was a statistically significant reduction in wound healing defects and the necessity for excision compared to primary, early surgical excision. There was no control group who were only treated conservatively.

Treatment (specific)

Antivenom
Loxosceles laeta antivenom is available in South America.

Assessment of the value of antivenom in the treatment of Loxosceles sp. envenoming

Antivenom treatment has little significance due to the purely practical reason that most patients do not consult a doctor until >24 hours after the bite. According to experimental investigations, antivenom no longer has an effect on the necrotising process at this point in time (Futrell 1992, Lucas 1988).

Treatment recommendations

The great majority of Loxosceles sp. bites heal well with good wound care and no further measures.

According to some authors in North America, local necroses due to Loxosceles sp. bites are best treated with analgesics and dapsone 25–100 mg, p.o., 12-hourly. Early surgical excision is avoided (Futrell 1992, King and Rees 1983, 1986, Rees et al. 1985). However, the indications for treatment with dapsone need to be considered carefully, as severe adverse reactions are possible (Wille and Morrow 1988, Kunkel 1988, Sams et al. 2001a,b). Note the contra-indications to dapsone. The evidence base for the use of dapsone is very weak.

Numerous differential diagnoses for skin necroses should be kept in mind, especially if no spider was seen and clearly identified to have caused the bite.

Severe systemic symptoms of envenoming, such as haemolysis, appear to be rare. However, they may occur with some delay (24–72 h to 2–3 days). It is therefore necessary to ensure that the patient is followed up for a corresponding period of time (Wasserman and Anderson 1983–84).