Spirocercosis is a disease occurring predominantly in Canidae, caused by the nematode Spirocerca lupi. Typical clinical signs are regurgitation, vomiting and dyspnoea. The lifecycle involves an intermediate (coprophagous beetle) and a variety of paratenic hosts. Larvae follow a specific migratory route, penetrating the gastric mucosa of the host, migrating along arteries, maturing in the thoracic aorta before eventually moving to the caudal oesophagus. Here the worm lives in nodules and passes larvated eggs which can be detected using zinc sulphate faecal flotation. Histologically, the mature oesophageal nodule is composed mostly of actively dividing fibroblasts.Spirocerca lupi-associated oesophageal sarcomas may occur and damage to the aorta results in aneurysms. A pathognomonic lesion for spirocercosis is spondylitis of the thoracic vertebrae. Primary radiological lesions include an oesophageal mass, usually in the terminal oesophagus, spondylitis, and undulation of the aortic border. Contrast radiography and computed tomography are helpful additional emerging modalities. Oesophageal endoscopy has a greater diagnostic sensitivity than radiography. Endoscopic biopsies are not sensitive for detecting neoplastic transformation. Doramectin is the current drug of choice, effectively killing adult worms and decreasing egg shedding. Early diagnosis of infection is still a challenge and to date no ideal regimen for prophylaxis has been published.

The Egyptian fruit bat, Rousettus aegyptiacus, is currently regarded as a potential reservoir host for Marburg virus (MARV). However, the modes of transmission, the level of viral replication, tissue tropism and viral shedding pattern remains to be described. Captive-bred R. aegyptiacus, including adult males, females and pups were exposed to MARV by different inoculation routes. Blood, tissues, feces and urine from 9 bats inoculated by combination of nasal and oral routes were all negative for the virus and ELISA IgG antibody could not be demonstrated for up to 21 days post inoculation (p.i.). In 21 bats inoculated by a combination of intraperitoneal/subcutaneous route, viremia and the presence of MARV in different tissues was detected on days 2–9 p.i., and IgG antibody on days 9–21 p.i. In 3 bats inoculated subcutaneously, viremia was detected on days 5 and 8 (termination of experiment), with virus isolation from different organs. MARV could not be detected in urine, feces or oral swabs in any of the 3 experimental groups. However, it was detected in tissues which might contribute to horizontal or vertical transmission, e.g. lung, intestines, kidney, bladder, salivary glands, and female reproductive tract. Viremia lasting at least 5 days could also facilitate MARV mechanical transmission by blood sucking arthropods and infections of susceptible vertebrate hosts by direct contact with infected blood. All bats were clinically normal and no gross pathology was identified on post mortem examination. This work confirms the susceptibility of R. aegyptiacus to infection with MARV irrespective of sex and age and contributes to establishing a bat-filovirus experimental model. Further studies are required to uncover the mode of MARV transmission, and to investigate the putative role of R. aegyptiacus as a reservoir host.

Egyptian fruit bats (Rousettus aegyptiacus) were inoculated subcutaneously (n = 22) with Marburg virus (MARV). No deaths, overt signs of morbidity, or gross lesions was identified, but microscopic pathological changes were seen in the liver of infected bats. The virus was detected in 15 different tissues and plasma but only sporadically in mucosal swab samples, urine, and fecal samples. Neither seroconversion nor viremia could be demonstrated in any of the in-contact susceptible bats (n = 14) up to 42 days after exposure to infected bats. In bats rechallenged (n = 4) on day 48 after infection, there was no viremia, and the virus could not be isolated from any of the tissues tested. This study confirmed that infection profiles are consistent with MARV replication in a reservoir host but failed to demonstrate MARV transmission through direct physical contact or indirectly via air. Bats develop strong protective immunity after infection with MARV.

Rift Valley fever (RVF) is a mosquito-borne disease that affects both ruminants and humans, with epidemics occurring more frequently in recent years in Africa and the Middle East, probably as a result of climate change and intensified livestock trade. Sheep necropsied during the 2010 RVF outbreak in South Africa were examined by histopathology and immunohistochemistry (IHC). A total of 124 sheep were available for study, of which 99 cases were positive for RVF. Multifocal-random, necrotizing hepatitis was confirmed as the most distinctive lesion of RVF cases in adult sheep. Of cases where liver, spleen, and kidney tissues were available, 45 of 70 had foci of acute renal tubular epithelial injury in addition to necrosis in both the liver and spleen. In some cases, acute renal injury was the most significant RVF lesion. Immunolabeling for RVFV was most consistent and unequivocal in liver, followed by spleen, kidney, lung, and skin. RVFV antigen-positive cells included hepatocytes, adrenocortical epithelial cells, renal tubular epithelial cells, macrophages, neutrophils, epidermal keratinocytes, microvascular endothelial cells, and vascular smooth muscle. The minimum set of specimens to be submitted for histopathology and IHC to confirm or exclude a diagnosis of RVFV are liver, spleen, and kidney. Skin from areas with visible crusts and lung could be useful additional samples. In endemic areas, cases of acute renal tubular injury should be investigated further if other more common causes of renal lesions have already been excluded. RVFV can also cause an acute infection in the testis, which requires further investigation.