SalivaSaliva : The patient was admitted to a Pietermaritzburg, KwaZulu Natal hospital on the 2nd May 2012 with migratory pain in his arm and shoulder, unilateral ptosis, fever, confusion, and progressively hypersalivation and hydrophobia. The patient was already unwell on the 29th April 2012. Rabies was considered as a differential diagnosis when the patient reported contact with a stray dog that died and with which he had contact two months prior to his illness. The patient provided shelter for the animal which was initially well, but reportedly developed signs and symptoms consistent with rabies within a couple of days. The animal was buried on the farm. The patient did not report any bites or serious injuries from the animal and therefore did not receive any rabies post exposure prophylaxis at the time. It is however likely that the patient was in contact with the saliva of the dog (which may be a source of infection on broken skin or mucous membranes). Once rabies was suspected in the human patient, the dog was exhumed and tested positive for rabies. On admission the patient received rabies immunoglobulin (human origin at 20IU/kg) and rabies vaccination in the Emergency Department. Once the diagnosis of rabies was likely, the patient was managed according to a modification of the Milwaukee protocol . Pending laboratory confirmation of rabies he was treated empirically with acyclovir for possible herpes infection and quinolones for rickettsial disease. Laboratory tests for rabies were carried out at the Centre for Emerging and Zoonotic Diseases, National Institute for Communicable Diseases of the National Health Laboratory Service (NICD/NHLS) in Johannesburg. Ante- mortem tests using PCR on multiple samples of saliva, skin and cerebrospinal fluid over the course of his illness were consistently negative. Rabies specific IgG was positive in serum likely reflecting the recent passive and active immunization of the patient. Initial serological tests on cerebrospinal fluid were negative, but rabies specific IgG was detected at low titers on repeat samples, without an increase in titre over 4 weeks. Extensive testing for other infectious causes of encephalitis yielded negative results (including testing for West Nile fever, Rift Valley fever, herpes, malaria, enteroviruses).
