To the Editor:
Centipede bites usually cause benign local reactions. Systemic complications are rare, but rhabdomyolysis, proteinuria, and acute myocardial infarction have been described.Citation1 Until now, only one fatal case of a seven-year-old girl bitten by a centipede in her head was reported.Citation2 However, to our knowledge, there are no reports of neurological disorders. Here, we report a case of acute disseminated encephalomyelitis (ADEM) following biting by a scolopendra subspinipes mutilans.
A 54-year-old man, previously with excellent health and no history of any infection or vaccination, was admitted to our hospital with a 20-day history of headache, fever, and urinary retention. Three days before onset, he was bitten by a centipede on the right foot and the bite caused immediate local swelling, pain, and redness. The patient was able by description and pictures to identify the centipede as a scolopendra subspinipes mutilans, a common species in mid-east of China.
Neurological examination on admission found stiff neck and bilateral Kernig sign. Routine blood test revealed mildly increased leucocyte counts (11310/ml). Renal and liver function tests, electrolytes, blood glucose, erythrocyte sedimentation rate, serum antinuclear antibody, anti-DNA, rheumatoid factor, anti-neutrophil cytoplasmic antibody, angiotensin-converting enzyme level, and tumor biomarkers were within normal ranges. The cerebrospinal fluid (CSF) was clear, with an elevated opening pressure of 380 mmH2O, 6 white blood cells/ml, 1175 mg/l protein, and normal glucose level. Oligoclonal bands were not detected. CSF cultures were sterile. Polymerase chain reaction (PCR) analysis for HSV 1 and 2, and EBV was negative. Serological studies for HIV, Treponema pallidum, hepatitis viruses, cytomegalovirus, toxoplasma, HSV, rubella, measles, and EBV were unremarkable. Serum NMO-IgG antibody was negative. The results of visual evoked potential, brainstem evoked potential, and electromyographic studies were normal. Contrast-enhanced cranial magnetic resonance (MR), MR angiography, and MR venography were unremarkable. Enhanced spinal MRI scanning disclosed the enhancement of spinal meninges. Dexamethasone of 10 mg was administered for 10 days and tapered by prednisone. After the treatment, the patient was gradually free from headache and fever, and finally discharged with a urethral catheter.
Just after discharge, he felt numbness on both feet which gradually spread upward to xiphoid level as well as walking difficulty. The patient was readmitted on the 12th week after the centipede bite. Neurological examination disclosed reduced pinprick sensation below T6 level and symmetric upper motor neuron paralysis and deep sensation defect at both lower limbs. A second lumber puncture revealed a normal opening pressure, 8 white blood cells/ml, 836 mg/l protein, and normal glucose level. MRI-enhanced scanning of cervical and thoracic spine showed multiple partially enhanced lesions in the spinal cord.
The symptoms, neurologic findings, and MRI features were compatible with those of ADEM. The patient was given intravenously 500 mg methylprednisolone for 7 days and tapered slowly by prednisone. His neurological deficits gradually improved and disappeared after 4 weeks of treatment. One-year follow-up showed no recurrence.
ADEM often occurs after vaccination or systemic viral infection.Citation3 The disease has also been reported after the use of some drugs or being exposed to some kinds of biotoxins (such as snake venoms or bee stings),Citation4,Citation5 but never been reported after centipede bite.
The pathogenesis of ADEM is unclear, but an allergic or autoimmune reaction is believed to be most likely.Citation3 The patient in the present case had not been exposed to centipede venom before; therefore, allergic reaction was unlikely. Venoms of the scolopendra subspinipes mutilans are mainly composed of proteins. We deduce that some peptides in the venom may share structural similarities with important proteins of myelin and subsequent generation of pathogenetic auto-antibodies causes myelin damage. The above auto-immunological mechanism has been proved by Jean Neil and her colleagues.Citation6 They found a specific cross-reaction between GM2 ganglioside and glycosidic epitopes of venom proteins in a patient suffering from Guillain–Barre syndrome after a snake bite.
In the conclusion, ADEM may be added to the list of systematic complications after biting by a scolopendra subspinipes mutilans and a high-dose methylprednisolone therapy may be effective.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
- Fung HT, Lam SK, Wong OF. Centipede bite victims: a review of patients presenting to two emergency departments in Hong Kong. Hong Kong Med J 2011; 17:381–385.
- Pineda EV. A fatal case of centipede bite. J Med Assoc 1923; 3:59–61.
- Lublin FD, Miller AE. Multiple sclerosis and other inflammatory demyelinating diseases of the central nervous system. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J, eds. Neurology in Clinical Practice. Philadelphia: Butterworth-Heinemann; 2008:1609–1612.
- Malhotra P, Sharma N, Awasthi A, Vasishta RK. Fatal acute disseminated encephalomyelitis following treated snake bite in India. Emerg Med J 2005; 22:308–309.
- Boz C, Velioglu S, Ozmenoglu M. Acute disseminated encephalomyelitis after bee sting. Neurol Sci. 2003; 23:313–315.
- Neil J, Choumet V, Le Coupanec A, d’Alayer J, Demeret S, Musset L. Guillain-barre syndrome: First description of a snake envenomation aetiology. J Neuroimmunol. 2012; 242:72–77.