Ovine rinderpest

Hyperacute cases are found dead without previous symptoms. They die with a serous, foamy, or haemorrhagic discharge coming out of the nose.

In acute cases, animals are recumbent, sometimes in self-auscultation position. Body temperature is high (40.5 to 41 °C) in the beginning of the onset in acute cases. The most typical signs are seen in the digestive tract. When entering an affected flock, one sees many animals with hind limbs stained by sticky faeces. Some sheep have an arched back and show pain when defecating. Tenesmus may be noticed when taking rectal temperature. Fluid faeces are olive green to brown. Examination of the mouth shows ulceration of the buccal mucosae, especially on the inner face of the lips, and neighboring gum. There can be periodontitis or serous nasal exudate and conjunctivitis.

Nasal discharge becomes mucopurulent and may obstruct the nose. A dry, fitful coughing develops. Death occurs from 5 to 10 days after the onset of the fever. Some animals may recover, but a dry, stertorous coughing often persists for some days.[10] Besides coughing, there is intensive labial dermatitis with scab formation, resembling orf.[11] Miscarriages may occur.[12]

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  Self-auscultation in an acute case
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  Hind legs stained with sticky diarrhoea
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  Arched back (painful defecation)
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  inflammation and erosion of the mouth
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  Periodontitis
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  Mucopurulent nasal exudate
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  Orf-like scabs on lips in a recovering case, Day 8

This virus appears to have evolved at the start of the 20th century in Nigeria.[14] The extant genotypes subsequently appeared in West Africa (lineages I and II), East Africa and Arabia (lineage III), and Pakistan–India (lineage IV).[8]

The first description of the disease was published in 1942 and relates to an outbreak in Côte d’Ivoire, West Africa, in goats and sheep in 1940.[15][8] It spread to East Africa and Arabia at the beginning of the 1980s and to Pakistan and India in the early 1990s (Calcutta goat markets) finally reaching Tibet in 2007.[8] The first description of this virus in India was in 1987.

The outbreak in Burkina Faso in 1999 was caused by the lineage I group. Genotype III has caused outbreaks in Ethiopia (1996) and also in Arabia, southern India, and Tamil Nadu (1992). This lineage was found in Yemen in 2001. Genotype IV has been isolated in Kuwait in 1999.

As of 2017, the disease is present in West Africa, part of Central Africa (Gabon, Central African Republic), East Africa (north of the Equator), the Middle East and the Indian subcontinent including Nepal and Myanmar. The disease is endemic in the Indian subcontinent and is a major threat to fast-growing goat husbandry in India, causing an annual loss of around 1800 million Indian rupees.

In North Africa, only Egypt was once hit, but since summer 2008, Morocco is suffering a generalized outbreak with 133 known cases in 129 provinces, mostly affecting sheep.[16] The outbreak has precipitated the vaccination of a large number of the 17 million sheep and five million goats in the country.[17]

The disease is transmitted by infected aerosols in situation of close contact of animals. The long-distance spread is by sick animals.[8] As the virus soon becomes inactive outside the body, indirect contamination is generally limited.

In an affected flock, even in pest-free regions, the disease does not progress very rapidly, in spite of the close contact between animals. New clinical cases may be observed daily for a 1-month period.[18]

Microscopic study of both natural and experimental cases revealed congestion and edema of the lungs, while in other cases it revealed a network of fibrin infiltrated with neutrophils, the formation of syncytia and gaint cells, and the presence of a pink-colored bacterial colony.  There was infiltration of neutrophils and mononuclear cells within the alveoli, bronchioles, alveolar wall, and interstitium of the lung.  Microscopic analysis also revealed that there was interstitial pneumonia followed by sloughing of the bronchial epithelium in the lungs and the prominence of type II pneumocytes. Numerous inflammatory cells were found in the submucosa and lamina propria of intestinal samples, and vacuolar degeneration and syncytial cells, which are microscopic features, were observed in hepatocytes of liver samples from goats. Periportal multifocal lymphocytic infiltrations were common in the liver parenchyma.

Leptomeningitis and nonsuppurative encephalitis were visible in brain sections under a microscope, and these conditions were characterized by vascular congestion, hemorrhages in the parenchyma, perivascular cuffing with mild to moderate mononuclear cells (mostly lymphocytes and few macrophages), focal to diffuse microgliosis, neuronal degeneration, satellitosis, and neuronophagia.[20]

In summary Epithelial cells, alveolar macrophages, lungs, and hepatocytes all showed histopathological alterations, primarily infiltrations of inflammatory cells, syncytia, and presence of intranuclear and/or intracytoplasmic eosinophillic inclusions.[21]