Case report Clinical features of serum sickness after Australian snake antivenom Nicole M. Ryan a, * , Michael A. Downes b , Geoffrey K. Isbister a, b a Clinical Toxicology Research Group, The University of Newcastle, Newcastle, NSW, Australia b Department of Clinical Toxicology and Pharmacology, Calvary Mater Newcastle, Newcastle, NSW, Australia article info Article history: Received 10 August 2015 Received in revised form 17 October 2015 Accepted 20 October 2015 Available online 23 October 2015 Keywords: Serum sickness Snake envenomation Red-bellied black snake Tiger snake antivenom abstract Serum sickness is a delayed immune reaction in which the immune system responds to a protein in antiserum as a potentially harmful substance and mounts an IgG-mediated antibody response. A 32 year- old female patient had systemic envenoming following a bite by a red-bellied black snake (Pseudechis porphyriacus). She was treated with Tiger snake antivenom and recovered over 24 h and did not develop myotoxicity. She then presented with local pain, itching and swelling, which was partially treated with antihistamines. Eleven days after the bite she presented again with symptoms of worsening serum sickness including rash on the upper legs, joint and muscle pain in arms, ankles and knees, and nausea. The patient was prescribed five days of prednisone 50 mg/day, antihistamine 10 mg/day and analgesia 1000 mg/day and improved over 2 days. She had no further problems on follow up at 4 months. This case highlights that serum sickness can cause significant effects after the treatment of snake envenoming. It develops 5e14 days after antivenom administration and has characteristic clinical and laboratory fea- tures. Severe cases of serum sickness can result in morbidity but it appears to respond well to cortico- steroid treatment. © 2015 Elsevier Ltd. All rights reserved. 1. Introduction The significant morbidity and mortality associated with snake envenoming are well recognised. While antivenom is the main treatment for snake envenoming, adverse effects of antivenom can also be a significant issue. Acute reactions including severe anaphylaxis and pyrogenic reactions are major problems, particu- larly in countries where there is poor quality antivenoms (de Silva et al., 2011; Isbister et al., 2012). Although not life-threatening, the delayed antivenom reaction serum sickness can cause significant clinical effects, but is not always recognised nor treated in many patients. Serum sickness from snake antivenom has been reported to occur in 5%e56% of cases and can therefore have a higher inci- dence than acute reactions from snake antivenom. Serum sickness has an onset of about 5e14 days post- antivenom, and symptoms typically resolve within a few weeks although in some unusual cases the symptoms can persist for up to six weeks, (von Pirquet and Schick, 1905) and depressed comple- ment measurements of C3 and C4 have been detected up to 36 days after treatment (Nielsen et al., 1978). Clinically serum sickness manifests with rash, fever, arthralgia, myalgia, headache and gastrointestinal symptoms, but remains poorly defined with limited clinical descriptions. We present a case of serum sickness after Australian tiger snake antivenom which produced significant signs and symptoms. 2. Case presentation A 32 year-old female patient was bitten by a red-bellied black snake (Pseudechis porphyriacus) on the left index finger while gardening. She saw the snake which is relatively easy to identify. Visible fang marks were noted with bleeding and a pressure bandage with immobilisation was applied 5 min after the bite. The patient felt nauseated, vomited twice and had mild crampy abdominal pain en route to hospital. She presented to hospital 1 h post-bite. On examination there was mild local swelling but no evidence of systemic bleeding or altered neurology, (Fig. 1). Her initial laboratory tests were white cell count, 12.0 (RR: 4 e 11 Â 10 9 /L), neutrophils: 10.3 (RR: 1.7e8.8 Â 10 9 /L), creatine kinase [CK], 165 IU/L (RR: 1e300 U/L), activated partial thromboplastin time (aPTT), 26 s (RR: 25e37 s); international normalised ratio [INR],1.0; D-Dimer, 0.43 g/L (Upper Reference Limit: 0.5 g/L). Other laboratory tests were normal. She was initially treated with * Corresponding author. Clinical Toxicology Research Group, The University of Newcastle, Calvary Mater Newcastle, Edith St., Waratah, NSW, 2298, Australia. E-mail address: Nicole.Ryan@newcastle.edu.au (N.M. Ryan). Contents lists available at ScienceDirect Toxicon journal homepage: www.elsevier.com/locate/toxicon http://dx.doi.org/10.1016/j.toxicon.2015.10.012 0041-0101/© 2015 Elsevier Ltd. All rights reserved. Toxicon 108 (2015) 181e183