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Contact with a caterpillar of the genus Lonomia can result in a hemorrhagic syndrome. This was first described in 1967 by Arocha-Piñango in a case in Venezuela.1 In Brazil, the risk of Lonomia envenomation was considered low until 1989, when a high number of human cases were reported in southern Brazil. In 2004, 364 cases were reported in Brazil. The patients had a hemorrhagic syndrome after skin contact with Lonomia obliqua. Two species of the genus Lonomia are known to cause hemorrhagic syndrome: L. achelous, which is found in Venezuela and northern Brazil, and L. obliqua, which is found in southern Brazil. The symptoms of envenomation typically begin with a burning sensation at the point of contact, followed by erythema and edema. The skin around the site is warm to the touch. Headache, general discomfort, nausea, and vomiting may also occur. The hemorrhagic phenomena may appear as soon as 1 hour after contact or up to 12 hours later. Ecchymoses and hematomas are often seen and may be accompanied by bleeding from various sites. The bleeding is occasionally severe enough to be life threatening. Some patients with hemostatic disorders can develop acute renal failure (ARF).2–4 The L. obliqua venom activates both prothrombin and factor X and promotes fibrinogenolytic activity.5–7 Crude L. obliqua bristle extract has been shown to induce hemolytic activity in human and rat erythrocytes.8 However, there have been no reports of hemolysis in the cases of human contact. We report a confirmed human case of Lonomia venom-induced hemolysis.
A 64-year-old man accidentally came into contact with a caterpillar. Immediately after contact, he experienced burning pain, edema, and erythema at the site of contact (on his right hand). Subsequently, he began vomiting and developed a headache. Eight hours after the accident, he developed hematemesis, bleeding gums, and hematuria. Twenty-four hours after contact (day 1), he sought treatment and was admitted to a hospital where a saline infusion was administered. Laboratory testing showed a hemoglobin level = 11.9 g/dL, hematocrit = 36%, 17,800 leukocytes/mL, 57,000/platelets/mL, serum urea = 137 mg/dL, serum creatinine = 4.6 mg/dL, total bilirubin = 2.6 mg/dL, indirect bilirubin = 2.1 mg/dL, thrombin time = 22.8 seconds, international normalized ratio = 3.54; and activated partial thromboplastin time = 50 seconds. Based on these results, he was diagnosed with caterpillar contact-induced hemorrhagic syndrome accompanied by ARF.
On day 2, he was transferred to Emílio Ribas Institute of Infectology in Sao Paulo, Brazil. Upon admission, he showed dehydration and jaundice, and his blood pressure was 160/90 mmHg. There was mild edema and erythema in his right hand, without ecchymoses or other bleeding. Laboratory tests showed a hemoglobin level = 9.3 g/dL, hematocrit = 26.6%; urea = 197 mg/dL, serum creatinine = 6.4 mg/dL, fibrinogen = 0.06 g/L, fibrin degradation products = 640 µg/mL, D-dimer = 256 µg/mL, and lactate dehydrogenase = 5,028 mg/dL. He received a specific antivenom (antilonomic serum; Butantan Institute, Sao Paulo, Brazil) and renal replacement therapy was started. Twenty-four hours after receiving the antivenom, the patient showed a significant improvement in coagulation test results: fibrinogen increased to 1.41 g/L, fibrin degradation products decreased to 320 µg/mL, and D-dimer levels decreased to 16 µg/mL.
Despite the improvement in the coagulation test results and no further signs of hemorrhage, there was a significant decrease in hemoglobin levels (to 5.1 g/dL on the fourth post-incident day), and the patient showed lower platelet levels (18,000/mm3). We suspected hemolysis because the patient had higher serum levels of indirect bilirubin and lactate dehydrogenase (LDH) at admission. Hemolysis was confirmed by the observed levels of serum haptoglobin (10 mg/dL), and plasma free hemoglobin (1,220 mg/L) (Table 1
).
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The clinical course after Lonomia accident is probably related to the intensity of the contact, the particular larvae stage, and the type of immediate medical treatment provided.9,10 The bleeding syndrome may begin as soon as within a few hours or up to several days after the accident and can be severe enough to be life threatening.2 Early laboratory coagulation tests invariably showed prolonged prothrombin times, activated partial thromboplastin times and thrombin times, various degrees of hypofibrinogenemia, and typically normal or slightly decreased platelet counts.11 We report a proven case of hemolysis resulting from a Lonomia accident. The patient had intravascular hemolysis, as evidenced by low plasma levels of haptoglobin, high levels of free hemoglobin, and high serum levels of LDH. In addition, serum levels of unconjugated bilirubin were increased. In experimental studies performed in Wistar rats, it has been demonstrated that intravascular hemolysis and hemoglobinuria occur after exposure to Lonomia venom (Oliveira MRL and others, unpublished data). It has been shown that crude L. obliqua bristle extract has indirect and direct hemolytic effects on human and rat erythrocytes.8 In the same study it was shown that bristle extracts of L. obliqua caterpillars possess at least two components capable of lysing human and rat erythrocyte membranes in vitro. One has a phospholipase effect that lyses erythrocytes in the presence of lecithin. The other can destroy the erythrocyte membrane structure, possibly through a proteolytic effect.
One interesting feature of this case was the extremely low platelet count. In a study of coagulation and fibrinolytic factors in 105 patients who had accidental contact with L. obliqua caterpillars, Zannin and others observed significant thrombin production, intense consumption of fibrinogen, and high production of D-dimer, indicating a disseminated intravascular coagulation (DIC) process.11 Platelet counts were within normal ranges in most of the L. obliqua-envenomed patients studied. Only nine patients had (slight) reductions in their platelet counts.11 We believe that cases with significantly reduced levels of platelets are likely associated with hemolysis-induced DIC. A frank hemolytic transfusion reaction is unquestionably a triggering event for DIC. However, hemolysis of any etiology may trigger DIC. Lysed erythrocytes act as partial thromboplastin reagent in the intrinsic reactions, leading to generation of prothrombin activator (Factor Xa). They do so in an unusual way in that they can bypass the surface activation steps of the intrinsic mechanism.12 Cytokines may also play an important role in the development of DIC-related hemolysis.13
A remarkable feature in this case was the rapid development of severe anuric ARF after venom inoculation. Surprisingly, despite the fact that this patient was treated with hemodialysis for 24 days, he did not completely recover renal function until 1 month after the accident. We did not perform a renal biopsy on this patient. It is therefore likely that he had developed acute tubular necrosis. The etiology of ARF is multifactorial. Although this patient never developed hemodynamic instability, he did had severe hemorrhagic syndrome. Hemolysis is another leading cause of acute tubular necrosis.14 Hemolysis-related ARF is caused by hemoglobin, which is highly nephrotoxic, especially in volume-depleted patients. We cannot rule out a direct nephrotoxic effect of the venom. Another possible explanation for the ARF might be massive DIC-related deposition of microthrombi in glomeruli. However, although most of the patients in the study conducted by Zannin and others11 developed severe coagulopathy with pronounced fibrinogen reduction, none had renal failure. We can postulate that among the many possible causes of ARF, the etiology of the present case was hemolysis-related acute tubular necrosis or hemolysis-related DIC.
In conclusion, although Lonomia-induced hemolysis has previously been reported in an animal model, the case herein reported represents the first confirmed instance of such hemolysis in a human patient.
Received September 6, 2005. Accepted for publication December 15, 2005.
Acknowledgments: We thank the intensive care staff at Emílio Ribas Institute of Infectology for excellent assistance and patient care. We also thank Jefferson Davis Boyles for correcting the English and style of the manuscript.
* Address correspondence to Ceila M. S. Malaque, Instituro Butantan, Hospital Vital Brazil, Av. Vital Brazil 1500, Sao Paulo, SP, Brazil, 05503-900. E-mail: cmalaque{at}uol.com.br 
Author’s addresses: Ceila M. S. Malaque and Geraldine Madalosso, Instituto Butantan, Hospital Vital Brazil, Av. Vital Brazil 1500, Sao Paulo, SP, Brazil, 05503-900, Telephone: 55-11-3726-7962, E-mail: cmalaque{at}uol.com.br. Lúcia Andrade and Antonio C. Seguro, Disciplina de Nefrologia, Faculdade de Medicina da Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, Terceiro Andar, Sala 3310, Sao Paulo, Brazil, 01246-903, Telephone: 55-11-3066-7281, Fax: 55-11-3088-2267. Sandra Tomy and Flávio L. Tavares, Laboratório de Fisiopatologia, Instituto Butantan, Av. Vital Brazil 1500, Sao Paulo, SP, Brazil, 05503-900, Telephone: 55-11-3726-7222 extension 2163.
Reprint requests: Ceila M. S. Malaque, Instituto Butantan, Hospital Vital Brazil, Av. Vital Brazil 1500, Sao Paulo, SP, Brazil, 05503-900.
-fibrinogenase from Lonomia obliqua caterpillars. Thromb Res 113: 147–154.[Medline]This article has been cited by other articles:
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  K. Chan MD, A. Lee MD, R. Onell MD, W. Etches BM BCh, S. Nahirniak MD, S. M. Bagshaw MD MSc, and L. M. Larratt MD Caterpillar-induced bleeding syndrome in a returning traveller Can. Med. Assoc. J., July 15, 2008; 179(2): 158 - 161. [Full Text] [PDF]
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