Chromobacterium violaceum is a facultative anaerobic, gram-negative rodshaped bacteria normally found in soil and stagnant water of tropical and subtropical countries. Infections of Chromobacterium violaceum are rare among mammals, but the first human infection were reported in Malaysia in 1927. This clinical case reports two separate cases of Chromobacterium violaceum infection in two sub-adult male Black-handed Gibbon (Hylobates agilis). Both animals were presented with the history of diarrhea, pyrexia and inappetance. From the physical examination, the findings were high body temperature, dull, inactive, soft fecal stained at the rectum and small open wound at lower limb of one of the case. The treatment given was antipyretic and multivitamin. Unfortunately, due to poor prognosis both patients died within 48 hours after presentation and treatment. Autopsy examinations wereperformed to find out the cause of death. Post mortem examination findings revealed hepatomegaly with multiple size whitish-yellow spots on the liver surface, congestion and enlargement of spleen and lymph node, congestion of lung and loss of demarcation between renal cortex and medulla of the kidney. The cellular changes via histopathological findings of kidney, spleen, lung and liver were suggestive of septicaemia. The gross and histopathologicalfindings were supported by the isolation of Chromobacterium violaceum via bacterial isolation and identification from lung, liver, spleen and kidney. Thus, the cause of death of the two sub-adult male Black-handed gibbon in this case are due to septicaemiadue to Chromobacterium violaceum infection.

Thoroughbred foal body temperature data were collected from shortly after birth until shortly after weaning during the 2007/2008 season on a stud farm in the Western Cape Province of South Africa. Equine encephalosis (EE) caused by EE virus (EEV) serotype 4 (EEV-4) occurred in the foal group during the first autumn after their birth (March and April 2008). A descriptive study was undertaken to provide data on the EEV maternal antibody status, the association between pyrexia and EEV infection, and the incidence of infection amongst the foals prior to and during the episode. This included the frequent capturing of foal body temperature data and regular collection of serum and whole blood during pyretic episodes. Infection by EEV was determined using both virological and serological methods. A high EE incidence of at least 94% occurred amongst the foal cohort, despite the fact that 37% of foals had previously shown maternal antibody to EEV-4. Pyrexia in foals was not directly associated with EE infection and 41% of infected foals showed no detectable pyretic episode. Information obtained from this EE episode showed the high incidence of EEV infection in foals during the first autumn after their birth. Monitoring foal body temperature can alert farmers to outbreaks of infectious disease, such as EE. These results are relevant to the epidemiology of EE and facilitate greater understanding of it as a differential diagnosis of African horse sickness (AHS), given that EE and AHS have similar epidemiologic profiles.