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What is PPR (Peste des petits ruminants)? Used for sheep detection.

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What is PPR (Peste des petits ruminants)? Used for sheep detection.

Update Time:2023/3/8
What is PPR (Peste des petits ruminants)? Used for sheep detection.

Detection and prevention of animal epidemics.
Infection with peste des petits ruminants virus, peste des petits ruminants (PPR), commonly known as sheep plague, also known as pseudorinderpest, pneumonoenteritis, stomatitis pneumonoenteritis complex, is a kind of infectious disease and parasitic disease, which is an acute viral infectious disease caused by small ruminant disease virus, It mainly infects small ruminants and is characterized by fever, stomatitis, diarrhea and pneumonia.
Small ruminant epidemic virus belongs to the family Paramyxoviridae and measles virus. It has similar physicochemical and immunological characteristics with rinderpest virus. The virus is polymorphic, usually rough and spherical. The viral particle is larger than the rinderpest virus, and the nucleocapsid is a spiral hollow rod-shaped and characteristic subunit with a capsule. The virus can proliferate on testicular cells and Vero cells of fetal sheep kidney, fetal sheep and newborn sheep, and produce cytopathic effect (CPE) to form syncytium.

Epidemiology

The disease mainly infects small ruminants such as goats, sheep and American white-tailed deer, and is prevalent in western and central Africa and parts of Asia. In the epidemic area, the disease occurs sporadically. When the number of susceptible animals increases, the epidemic can occur. The disease is mainly transmitted through direct contact. The secretion and excreta of infected animals are the source of infection. The sheep in the sub-clinical type are particularly dangerous. Artificial infection of pigs does not cause clinical symptoms and disease transmission, so pigs have no significance in the epidemiology of this disease.


Virus

PPRV belongs to the measles virus genus of Paramyxoviridae, and there are also dolphin measles virus, canine distemper virus, mouse seal measles virus, rinderpest virus and measles virus in the same genus. PPRV has only one serotype. The PPRV genome is a single-stranded negative-stranded RNA with a size of 15948nt. The 3 'end of the genome is the genome promoter region, and the 5' end is the reverse genome promoter region. The six genes are arranged in the order of 3 '- N-P-M-F-HL-5'. The six structural proteins encoded in turn are nucleocapsid protein (N), phosphoprotein (P), matrix protein (M), fusion protein (F), hemagglutinin (H) and large protein (L). The P gene also encodes two non-structural proteins C and V.
N protein forms nucleocapsid particles through self-assembly, and cooperates with P protein and L protein to regulate viral RNA transcription and replication. N protein is also a highly conserved immunogenic protein, which can cause a strong antibody reaction when infected by virus. In addition, N protein contains T cell epitopes, which play an important role in cellular immunity.
According to the nucleotide sequence of N or F gene fragments, phylogenetic analysis can be carried out. The results show that PPRV is divided into four gene lines. The first and second lines are distributed in West Africa, the third line virus is prevalent in East Africa, Arabia (Oman and Yemen) and southern India, and the fourth line virus is only found in the Middle East, Alab and the Indian subcontinent. Comparing two phylogenetic analysis methods based on partial sequences of N and F genes, N gene phylogenetic analysis can more effectively cluster virus strains according to geographical sources, and the analysis results reflect the global spread of small ruminant disease virus from west to east (from West Africa to Asia), and carry out independent evolution in four regions. The F gene phylogenetic analysis more reflects the evolution process of the virus along the time axis, thus providing clues for the transmission route of the virus between different geographical regions. More specific results depend on more reports of the full sequence of N or F genes.


Disease symptoms

The incubation period of small ruminant disease is 4-5 days, with a maximum of 21 days. Natural disease is only found in goats and sheep. Goats are seriously ill, and sheep occasionally have serious cases. The lip of some rehabilitated goats formed aphthous-like lesions. The clinical symptoms of infected animals are similar to those of cattle with rinderpest. The temperature of acute type can rise to 41 ℃ and last for 3-5 days. The infected animals are restless, with dull back hair, dry mouth and nose, and loss of appetite. Mucous purulent rhinorrhea, exhaling foul gas. In the first 4 days of fever, the oral mucosa was congested, the buccal mucosa was extensively damaged, resulting in salivation, and then necrotic lesions appeared. At first, the oral mucosa appeared small rough red superficial necrotic lesions, and later turned pink. The infected sites included the lower lip, lower gingiva, and so on. In severe cases, necrotic lesions can be seen in the tooth pad, palate, cheek, nipple and tongue. In the later stage, bloody watery diarrhea, severe dehydration, emaciation, and subsequent temperature drop occurred. Cough and dyspnea occur. The incidence rate rate is as high as 100%. In severe outbreaks, the mortality rate is 100%. In mild outbreaks, the mortality rate does not exceed 50%. The incidence of serious disease and death of young animals are very high,


Pathological mechanism

The pathological changes of autopsy were similar to those of cattle with rinderpest. The lesions range from the mouth to the tumor-reticulum appetite. Conjunctivitis, necrotizing stomatitis and other gross lesions can be seen in infected animals, and severe cases can spread to the hard palate and throat. The abomasum often has lesions, while the rumen, reticulum and omasum rarely have lesions. The lesion often has regular and contoured erosion, and the wound is red and bleeding. Erosion or bleeding can be seen in the intestine. Characteristic bleeding or zebra stripes are common in the large intestine, especially at the junction of the colon and rectum. The lymph nodes are enlarged and the spleen has necrotic lesions. There are bleeding spots on the turbinate, throat and trachea. Typical lesions of bronchopneumonia can also be seen.
Because the virus has special affinity for gastrointestinal lymphocytes and epithelial cells, it can cause characteristic lesions. Generally, eosinophilic cytoplasmic inclusion bodies and multinucleated giant cells appear in infected cells. In lymphoid tissue, small ruminant epidemic virus can cause lymphocyte necrosis. Spleen, tonsil and lymph node cells were damaged. The multinucleated giant cells containing eosinophilic cytoplasmic inclusion bodies appeared, and there were few intranuclear inclusion bodies. In the digestive system, the virus causes the necrosis of the epithelial cells in the deep part of the Marki's layer, the infected cells produce nuclear pyknosis and nuclear rupture, and the formation of multinucleated giant cells containing eosinophilic cytoplasmic inclusion bodies in the epidermal germinal layer
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