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Feature Article

Human and animal bites: managing and preventing infection

STEPHEN MUHI, JUSTIN DENHOLM
OPEN ACCESS

Rodent bites

Rat bite fever (RBF) is caused by infection with either Streptobacillus moniliformis, a fastidious, slow-growing organism, or Spirillum minus, so-called due to the tightly coiled spiral shape of this unculturable Gram-negative organism.15 Although S. moniliformis occurs predominantly in North America, Australian cases have been reported.16 S. minus occurs predominantly in Asia, where the disease is known as ‘sodoku’ (Japanese: so, rat; doku, poison). Rats primarily transmit the disease, although other rodents such as mice, guinea pigs and ferrets are also associated with transmission.17 RBF occurs in about 10% of all rat bites, and those at risk include the homeless, children with pet rats, pet store workers and laboratory technicians.17

Symptoms of RBF usually present within one week of the bite and include fever, myalgia, sore throat, migratory arthralgia, headache and maculopapular rash.17 In S. moniliformis infection, the original wound and adenopathy have usually resolved before presentation, which may hamper the diagnosis.15 In contrast, S. minus has a longer incubation period of one to three weeks, and the indurated and painful wound often reappears or persists during systemic illness.17 Complications of infection may include meningitis, pneumonitis and endocarditis.18

Diagnosis requires a high index of ­suspicion, and S. moniliformis requires enriched media with prolonged incubation,17 thus the microbiologist must be informed if this diagnosis is being considered. The mortality rate of RBF is about 13% in untreated patients, and a lack of antibiotic therapy is associated with death.16 Although penicillin is the treatment of choice for S. moniliformis, it is also usually sensitive to cephalosporins and tetracyclines, but may demonstrate resistance to fluoroquinolones and trimethoprim-­sulfamethoxazole.17 Antibiotic susceptibility of S. minus is much less studied, given the difficulty in culturing the organism.15

A differential diagnosis which should be considered in unwell patients following rat exposure is leptospirosis, which is the most common zoonosis and distributed globally. It is classically transmitted following transcutaneous or mucous exposure to rat urine, although cases of transmission following rat bite have been reported.19-20 Doxycycline remains the drug of choice to treat leptospirosis.

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Monkey bites

Although monkey bites are uncommon, they do pose major health risks requiring prompt medical follow up. Theoretically, emerging infections resulting from ­monkey-to-human cross-species transmission could occur quite easily given the genetic similarity.53 Travellers, zoo workers and laboratory personnel are at risk of monkey bite, and travellers are at risk of the almost universally fatal rabies virus infection, which can be transmitted by monkeys. The increasing incidence of rabies in Indonesia, and in particular Bali,54 has ensured that Australian travellers remain at risk of exposure. Rabies post-­exposure prophylaxis must therefore be offered to all returned travellers from a rabies endemic area with a history of ­monkey bite.47

Simian herpes B virus is a herpes simplex virus-like infection of macaque ­monkeys. It is transmissible to humans and has caused cases of fatal encephalomyelitis.55 A few cases have occurred in laboratory personnel following macaque bites, scratches, needle-stick exposures and ­handling of infected bodily tissues. ­Travellers may be exposed to herpes B virus, with 81% of macaques in the Bali ‘monkey forest’ known to harbour the virus.56 Despite this frequent human–­monkey interaction, no infections have ever been reported from any of these ­destinations.57 Given the unknown risk and potentially fatal complications, patients bitten by ­monkeys should be referred to an infectious diseases physician for consideration of prophylaxis.32

Bat bites, rabies and Australian bat lyssavirus

Despite being free of rabies, Australian bats are enzootic for the closely-related Australian bat lyssavirus (ABLV), which carries a similarly high mortality rate. Three cases of fatal encephalitis due to ABLV have been reported, with the most recent case occurring in 2013, and a case in 2000 with a reported incubation period of two years.58 All people exposed to bats should, therefore, be assessed for post-­exposure prophy­laxis, regardless of the time elapsed since exposure. Recipients of bites from several other mammalian species, especially dogs, cats and monkeys, also require post-­exposure prophylaxis if they have returned from rabies-endemic areas.

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Rabies and ABLV exposures are categorised according to the WHO classification system (Box 1).47 People with category I exposures require no prophylaxis if the contact history is reliable.47 Immunocompetent patients with category II exposures require vaccination without human rabies immunoglobulin (HRIG).47 Post-exposure rabies vaccination in immunocompetent people is given in a four-dose schedule (on days 0, three, seven and 14). An additional dose is suggested on day 28 in the immunocompromised, although deviations of a few days are probably unimportant.47 The vaccine should be given in the deltoid muscle, as neutralising antibodies may be reduced if administered in other areas.5 Both immunocompetent and immunocompromised patients who have received a pre-exposure rabies vaccine course only require two further doses (on day 0 and three) in the event of an exposure.47

HRIG is recommended for non-­immune patients with category II exposures if:

  • they are immunocompromised and exposed to rabies, or 
  • the exposure is ABLV, regardless of their immunocompromised or immunocompetent status.47

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Dr Muhi is an Infectious Diseases Registrar at the Victorian Infectious Diseases Service, Royal Melbourne Hospital. Associate Professor Denholm is Medical Director of the Victorian Tuberculosis Program; Senior Staff Specialist at the Victorian Infectious Diseases Service, Royal Melbourne Hospital; and Principal Research Fellow in the Department of Microbiology and Immunology, University of Melbourne, Melbourne, Vic.