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How to prevent and treat caprine viral arthritis and encephalitis

General News By Sophie Bennett 0 views
Caprine viral arthritis-encephalitis is a viral infectious disease. The clinical features are chronic polyarthritis in adult sheep, occasionally accompanied by interstitial pneumonia or interstitial mastitis; lambs often show symptoms of encephalomyelitis. This disease is distributed worldwide and in many

Caprine viral arthritis-encephalitis is a viral infectious disease. The clinical features are chronic polyarthritis in adult sheep, occasionally accompanied by interstitial pneumonia or interstitial mastitis; lambs often show symptoms of encephalomyelitis.

This disease is distributed worldwide and has a very high infection rate in many countries, with a long incubation period. Infected goats carry the virus for life, there is no specific treatment, and death is the eventual outcome, greatly affecting herd productivity and causing severe economic losses.

I. Pathogen. Caprine arthritis-encephalitis virus is a member of the family Retroviridae, genus Lentivirus. The virus's morphological structure and biological characteristics are similar to those of Maedi-Visna virus, with 20% genomic homology and serological cross-reactivity. It contains single-stranded RNA, the virus particle diameter is 80-100 nanometers, the buoyant density is 1.15 g/cm3, the molecular weight is 5.5×106, and it is composed of two fragments, 64S and 4S.

Chicken embryos, mice, guinea pigs, hamsters, rabbits and other laboratory animals do not develop the disease when infected. Aseptically collecting joint synovial tissue from diseased sheep to prepare single cells for in vitro culture, syncytia appear in the cells after 2-4 weeks. Goat fetal synovial cells are commonly used for virus isolation and identification. Inoculation materials include synovial fluid, milk and blood leukocytes, among which the virus isolation rate from the first two is the highest. Inoculating goat fetal synovial cells with attenuated virus, the virus begins to proliferate after 15-20 hours, peaks at 96 hours, cells begin to fuse at 24 hours after inoculation, and after 5-6 days the cell layer is covered with multinucleated giant cells of varying sizes. Experiments have shown that the formation of syncytia is a sign of virus replication. Therefore, it can be used for infectivity titration.

II. Epidemiological characteristics. Diseased goats and latently infected goats in the incubation period are the main sources of infection for this disease, and goats are the susceptible animals for this disease. The main mode of transmission of this disease is horizontal transmission, with intrauterine infection occurring occasionally. The main route of infection is the digestive tract. The virus infects lambs through milk, and contaminated forage, feed, drinking water, etc. can become transmission vehicles. Under natural conditions, it only spreads and causes disease among goats; sheep are not infected. There is no difference by age, sex or breed, but adult goats are mostly infected, with an infection rate of 15-81%. The incidence rate in the same year among lambs born to infected ewes is 16-19%, and the mortality rate is as high as 100%. Horizontal transmission requires cohabitation and grazing together for at least 12 months; contact between virus-carrying rams and healthy ewes for 1-5 days does not cause infection. The possibility of respiratory tract infection and transmission through medical instruments cannot be ruled out. Infected sheep often show no symptoms or inconspicuous symptoms under good feeding and management conditions. They can only be detected through serological testing. Once stress factors such as changes in feeding and management conditions, environment, or long-distance transport stimulate them, clinical symptoms appear.

III. Clinical symptoms. Based on clinical manifestations, it is divided into three types. Encephalomyelitis type, arthritis type and interstitial pneumonia type. They mostly occur independently, with a few overlapping. However, at necropsy, most cases have pathological changes of two or three of these types.

1. Encephalomyelitis type: incubation period 53-131 days. It mainly occurs in lambs aged 2-4 months, with obvious seasonality; more than 80% of cases occur between March and August, clearly related to late winter and spring lambs. At the beginning of the disease, affected sheep are depressed and lame, then develop rigidity of the limbs or ataxia. One or several limbs become paralyzed, the animal lies on its side unable to rise, with paddling of the limbs; some cases show nystagmus, fright, opisthotonus, head and neck deviation, or circling movements. Sometimes there is facial nerve paralysis, difficulty swallowing, or blindness in both eyes. The course of disease is from half a month to 1 year. A few surviving cases have sequelae. A small number of cases also have pneumonia or arthritis symptoms.

2. Arthritis type: occurs in adult goats over 1 year of age, with a course of 1-3 years. The typical symptom is swelling of the carpal joint or lameness. The knee joint and hock joint may also be affected. The condition gradually worsens or occurs suddenly. Initially, the soft tissues around the joint are edematous, hot and damp, fluctuating, and painful, with lameness of varying severity, then the joint swells like a fist, movement is difficult, and kneeling on the front knees and moving on the knees are common. Sometimes the prescapular lymph nodes of affected sheep are enlarged. On fluoroscopic examination, mild cases show edema of the soft tissues around the joint; severe cases show tissue necrosis, fibrosis or calcification, and the joint fluid is yellow or pink.

3. Pneumonia type: relatively rare. There is no age restriction, the course of disease is 3-6 months, affected sheep progressively lose weight, cough, have difficulty breathing, dullness on chest percussion, and dull rales on auscultation. In addition to the above 3 disease types, lactating ewes sometimes develop interstitial mastitis.

IV. Pathological changes. The main lesions are seen in the central nervous system, limb joints and lungs, followed by the mammary gland.

1. Central nervous system: mainly occurs in the gray matter of the cerebellum and spinal cord. At the left vestibular nucleus site, when the cerebellum and medulla oblongata are transected, a brown area can be seen in the white matter on one side. Microscopic examination shows proliferation of lymphoid cells, monocytes and reticular fibers around blood vessels, forming cuffs, with proliferation of astrocytes and oligodendrocytes surrounding the cuffs, and varying degrees of demyelination of nerve fibers.

2. Lungs: mildly enlarged, firm in texture, gray, with scattered grayish-white small spots on the surface, and lobar or patchy consolidation areas on the cut surface. Bronchial lymph nodes and mediastinal lymph nodes are enlarged, bronchi are empty or filled with serous fluid and mucus. Microscopic examination shows infiltration of lymphocytes, monocytes or macrophages around bronchioles and blood vessels, even forming lymphoid nodules, alveolar epithelial hyperplasia, alveolar septal thickening, interlobular connective tissue hyperplasia, and atrophy or fibrosis of adjacent cells.

3. Joints: swelling and fluctuation of the soft tissues around the joint, with serous exudation under the skin. The joint capsule is thickened, and the synovium is often adhered to the articular cartilage. The joint cavity is dilated and filled with yellow-pink fluid, in which fibrin strands or blood clots are suspended. The synovial surface is smooth, or has nodular proliferations. Calcified plaques in the tissue can be seen through the synovium. Microscopic examination shows hyperplasia and folding of synovial villi, focal aggregation of lymphocytes, plasma cells and monocytes, and fibrinous necrosis in severe cases.

4. Mammary gland: in cases with mastitis, microscopic examination shows a large amount of lymphocyte, monocyte and giant cell exudation around blood vessels, milk ducts and between glandular lobules, followed by the appearance of large numbers of plasma cells, and focal necrosis often occurs in the interstitium.

5. Kidneys: in a few cases there are grayish-white small spots of 1-2 mm on the kidney surface. Microscopic examination shows widespread glomerulonephritis.

V. Diagnosis. On-site diagnosis can be made based on history, symptoms and pathological changes. For etiological diagnosis, the liver of diseased animals during the febrile period or near death, or of fresh carcasses, can be used to prepare a milk suspension for virus isolation tests, and mice or hamsters can also be selected for animal experiments. Serological diagnosis mainly uses agar gel diffusion tests or enzyme-linked immunosorbent assays to identify latently infected animals. Using immunofluorescence antibody technology to detect IgM antibodies in serum can serve as an indicator for judging new outbreaks.

VI. Prevention and control. There is still no effective treatment or vaccine. The main focus is on strengthening feeding management and epidemic prevention and sanitation work. Implement regular quarantine and promptly cull sheep that are serologically positive. Strict quarantine must be implemented for introduced sheep, especially when introducing foreign breeds; in addition to implementing a strict quarantine system, they must also be isolated and observed separately after entry, with regular re-examinations, and only after confirming health can they be transferred to normal feeding and breeding or put into use. In disease-free areas, self-breeding and self-raising should also be advocated, and strict prevention must be taken to prevent this disease from being brought in from other places.

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