Chimpanzees and gorillas, when not inactive, engage primarily in short bursts of resistance physical activity (RPA), such as climbing and fighting, that creates pressure stress on the cardiovascular system. In contrast, to initially hunt and gather and later to farm, it is thought that preindustrial human survival was dependent on lifelong moderate-intensity endurance physical activity (EPA), which creates a cardiovascular volume stress. Although derived musculoskeletal and thermoregulatory adaptations for EPA in humans have been documented, it is unknown if selection acted similarly on the heart. To test this hypothesis, we compared left ventricular (LV) structure and function across semiwild sanctuary chimpanzees, gorillas, and a sample of humans exposed to markedly different physical activity patterns. We show the human LV possesses derived features that help augment cardiac output (CO) thereby enabling EPA. However, the human LV also demonstrates phenotypic plasticity and, hence, variability, across a wide range of habitual physical activity. We show that the human LV’s propensity to remodel differentially in response to chronic pressure or volume stimuli associated with intense RPA and EPA as well as physical inactivity represents an evolutionary trade-off with potential implications for contemporary cardiovascular health. Specifically, the human LV trades off pressure adaptations for volume capabilities and converges on a chimpanzee-like phenotype in response to physical inactivity or sustained pressure loading. Consequently, the derived LV and lifelong low blood pressure (BP) appear to be partly sustained by regular moderate-intensity EPA whose decline in postindustrial societies likely contributes to the modern epidemic of hypertensive heart disease.

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Four of 17 cirl buntings (Emberiza cirlus) involved in a trial translocation in 2004 for conservation purposes died and were examined postmortem. Two of the cirl buntings showed intestinal and hepatic lesions, including necrotising enteritis, consistent with isosporoid coccidiosis, and a third had an intestinal infestation of isosporoid coccidia. Sporulated oocysts from faecal samples from the birds were identified as Isospora normanlevinei, a parasite previously detected in cirl bunting populations in continental Europe. In a subsequent translocation of 75 cirl buntings from Devon to Cornwall in 2006, each brood of birds was placed in strict quarantine at low stocking density, with improved hygienic precautions and detailed health surveillance, and each bird was treated prophylactically with toltrazuril in an attempt to control the disease but not eliminate the I normanlevinei parasites. Seventy-two of the 75 birds were successfully reared and released, and there were no apparent clinical or pathological signs of isosporoid coccidiosis in any bird. I normanlevinei was detected in the released population, an indication that it had been successfully conserved.

Disease due to non-tuberculous mycobacteria (NTM) is common in fish. Current recommendations focus on outbreak management by depopulating entire fish stocks and disinfecting tanks. Treatment is not advocated. Treatment may be appropriate, however, where individual, valuable fish are concerned. ZSL London Zoo managed an outbreak of mycobacteriosis in a valuable group of imported F1 captive-bred Australian lungfish (Neoceratodus fosteri) by depopulation, isolation, extensive testing and daily oral antibiotic treatment. Four species of Mycobacterium (M. marinum, M. fortuitum, M. chelonae and M. peregrinum) were involved in this outbreak, each with unique antibiotic sensitivities. Triple therapy with rifampicin, doxycycline and enrofloxacin for 8 months was the most effective antibiotic combination, resulting in full disease resolution. No side effects were noted and, more than 18 months post-treatment, no recurrence had occurred. This is the first report of mycobacterial disease in lungfish and the first report of a polymycobacterial outbreak in fish involving these four species of Mycobacterium. This report demonstrates the value of extensive isolation and identification. Also, as therapies currently advised in standard texts did not reflect the antibiotic sensitivity of the NTM found in the fish reported here, we recommend that antibiotic treatment should always be based on sensitivity testing.

Cardiac disease has been implicated as a leading cause of death in captive great apes. Trans‐thoracic echocardiography provides clinically relevant information that may help differentiate between the myriad of different heart diseases and disorders, guide treatment and aid the management of great apes with underlying cardiac pathology. The purpose of this paper is to provide an outline of the procedures and methodologies required to conduct a thorough trans‐thoracic echocardiogram of great apes under general anaesthesia. Basic logistical considerations are discussed before a detailed description of the procedures required for the assessment of overall cardiac structure and function. Using a thorough systematic approach, it is our belief that veterinary professionals may be better able to diagnose, treat and manage captive great apes with, or at risk of developing heart disease.