Bites and Stings Recurrent necrotising arachnidism
MJA 1998; 169: 642-643
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To the Editor:
A 35-year-old male carpenter presented with an area of
increasing central blackness of the grafted sites of his right lower
leg.
Twelve months previously he had had a small ulcer which progressed to necrosis of the skin over the distal third of the right leg and dorsum of the right foot following a spider bite, and required partial thickness skin graft. The spider was not caught, but the patient confirmed its identity when he visually identified another white-tailed spider. At this second presentation, about 49 weeks after complete graft healing, he described a small area of blackness at the original bite site, increasing in size over two days, associated with general pallor of the larger graft site. On examination, there was blackening, well demarcated to the graft sites only, and surrounding areas of erythema and swelling. He had no lymphadenopathy or constitutional symptoms and denied any recent trauma or bite. His white cell count, differential count, erythrocyte sedimentation rate and C-reactive protein level were all within normal ranges. Cultures of the necrotic graft showed no pus cells or organisms. A junctional punch biopsy showed necrotic tissue with acute inflammatory cell infiltrate around many small vessels, but no features suggesting vasculitis. Unfortunately, there are no laboratory tools available to test for venom or antivenom antibodies in the involved tissue. With the help of a psychiatrist, the patient was questioned about any possible self-inflicted act, which he denied. He was treated with intravenous flucloxacillin and penicillin, followed by debridement and regrafting.
Three weeks later, he presented again with lower leg pain and blackness of the new graft with surrounding erythema, increasing over 6-12 hours. The graft had almost completely healed prior to this. However, in this presentation, there was involvement of new areas medially. Again, markers of inflammation were normal, and new biopsies and cultures were negative. The wounds were extensively debrided and regrafted. To date (six weeks after regrafting), there has been no complication with this current graft. I believe the patient had recurrent necrotising arachnidism, although a literature review of all MEDLINE journals to date (search terms necrotising arachnidism, spider bites and necrosis) revealed no reports of recurrent necrotising arachnidism. Similarly, another search (search terms human, skin graft rejection/failure and necrosis delayed/late) showed no reports of delayed skin graft failure. Necrotising arachnidism describes a rare complication of spider bite, which is characterised by progressive necrosis and inflammation of the bite site, occasionally requiring extensive debridement and skin grafting. The white-tailed spider (Lampona cylindrata) has been implicated in this condition,1,2 but there is currently little evidence to confirm this, and considerable difference of opinion among experts.3 The disease has some similarity with loxoscelism, a syndrome of tissue necrosis associated with the bite of the brown recluse spider (Loxosceles reclusa) in the United States. Mycoplasma ulcerans infection may be involved with this condition, but this is rare.1
Sor Way Chan Acknowledgements: Dr Ken Winkel, Deputy Director, Australian Venom Research Unit, The University of Melbourne, for providing relevant information and expert advice.
Comment: Chan's letter documents another case of significant local tissue injury where a spider bite may have been causal. The bite is ascribed to the white-tailed spider (Lampona cylindrata), although the spider was clearly not formally identified. The apparently successful healing of the skin graft was fortunate, as some cases of "necrotic arachnidism" prove rather resistant to successful grafting. However, once grafted, lesions affected by "necrotic arachnidism" tend to recur early, not 12 months later. It is most unlikely that venom would remain active but quiescent over such a period, and so the cause for the subsequent graft failure is unclear. An immune mechanism might be invoked, and infection is also worth considering, even in the absence of positive cultures. I have seen a number of cases of suspected necrotic arachnidism over the last 20 years in which local relapse has occurred after a prolonged period of apparent healing. The cause for such relapses has never been clearly documented. "Necrotic arachnidism" encompasses bites from any spider where tissue injury occurs, from any mechanism, including direct venom effects, as in loxoscelism, or indirectly, through infection, vasculitis and immune reactions. The best-described and best-researched cause of "necrotic arachnidism" is loxoscelism,1 caused by the bite of recluse spiders, genus Loxosceles, which causes distinct and sometimes severe local tissue injury. Experience in treating these bites in North America has shown that early debridement may extend the area of damage and that grafting is often unsuccessful, especially if undertaken in the first five weeks.1 Optimal treatment is still debated, with hyperbaric oxygen therapy currently enjoying some support.1,2 In Australia, the white-tailed spider is often mentioned in association with "necrotic arachnidism", but confirmatory reports are rare.2 Most reported bites by this spider cause no significant tissue injury,3 and research on the spider's venom has failed to show necrotising ability.4 Until there is a clear body of evidence to incriminate the white-tailed spider, it is inappropriate to suggest this spider is the likely cause of "necrotic arachnidism" in Australia, especially as Loxosceles is now found here and has caused confirmed cases of necrosis.5 It is more likely that a number of spider species occasionally cause necrosis and that the necrosis has different causes, including direct venom effect, infection introduced at the time of the bite and immune reactions mounted by the patient.
Julian White
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