What Are Different Bites That Blister?

Vesicular stomatitis (VS) is also known as sore nose, sore mouth, pseudoaphthosis, "rotten tongue disease", "bovine and horse mouth ulcers" and so on. This disease is a viral disease in horses, cattle and pigs. It is characterized by blisters and erosions of the oral mucosa, nipple skin, and crown skin, but few deaths occur.

Vesicular stomatitis

Right!

Vesicular stomatitis (VS) is also known as sore nose, sore mouth, pseudoaphthosis, "rotten tongue disease", "bovine and horse mouth ulcers" and so on. This disease is a viral disease in horses, cattle and pigs. It is characterized by blisters and erosions of the oral mucosa, nipple skin, and crown skin, but few deaths occur.

Chinese name

Vesicular stomatitis

Foreign name

vesicular stomatitis

Alias

Nose

Features

Blisters and erosions on the skin of the hoof crown

The cause of vesicular stomatitis is vesicular stomatitis virus (VSV). It belongs to Rhabdoviridae and Vesicular virus. For the physico-chemical and biological characteristics of pathogens and the comparison with related viruses, see "Swine Vesicular Disease".

Vesicular stomatitis has two independent serotypes, the New Jersey type (NJ, first isolated and identified in 1926) and the Indiana type (IND, first isolated and identified in 1925). The latter has three subtypes, which are Indiana type I (IND-I, a typical strain), Indiana type II (IND-II, including Cocal and Argentina strains), and Indiana III Type (IND-III, Brazil strain). The latter two subtypes are less pathogenic to pigs, cattle, and horses than NJ and IND-. Although NJ and IND are independent in serology and immunology, they are indistinguishable in clinical symptoms. It is the virus glycoprotein that stimulates the body to produce specific humoral immunity, and the antigen with complementing activity is the nuclear protein of the virus.

Cultures of VSV-infected cells can produce hemagglutinin, which agglutinates goose erythrocytes at 0-4 ° C and pH 6.2, and the virus does not shed from the surface of erythrocytes. The suitable conditions for VSV to produce hemagglutinin in cell culture are similar to rabies virus, that is, the cell maintenance solution does not contain serum, but 0.4% bovine serum albumin is added.

Sequence analysis showed that the VSV genome is a single negative strand. In the process of the virus entering the susceptible cytoplasm, the genome is transcribed into mRNA by means of a polymerase that binds to the virion, and the mRNA can be translated into 5 proteins: the L protein (MW200000) and the NS core protein (MW25000) together constitute the viral polymerase G protein (MW57000) is a glycosylated membrane protein; M protein (MW26000) is an unglycosylated membrane protein; N protein (MW47000) is a nuclear protein. The virus replicates in the cytoplasm and matures through cell membrane buds. VSV replicates very high virus titers in cell culture and produces high interferon titers in the process. ^[1]

VS occurs mainly in the Western Hemisphere. NJ and IN-I endemic areas include the United States, Mexico, Panama, Venezuela, Colombia, Ecuador and Peru. Bolivia and Canada have only NJ models. It has also been reported in France and South Africa. Yichang and Zigui counties in Hubei Province, China had VS of pigs in the early 1990s, but they were not finalized. The disease mainly reduces the productivity of pigs and dairy cows and causes severe economic losses. ^[1]

Horses, cattle, and pigs are naturally infected in livestock, and serology has proven that wild animals (such as wild boars, raccoons, and deer) can be naturally infected. Anti-IND-I antibodies were found in the blood of arboreal and semi-arboreal animals in Panama. Anti-NJ antibodies have been found in the blood of bats, carnivores and some rodents. Human infections are mainly seen by laboratory workers and people in contact with livestock in endemic areas.

The ecological study of VSV is not clear. For example, where does the virus live in nature, how to save itself, how does it spread from one animal to another, and how does it spread to healthy herds. VSV-IND and VSV-NJ types may have different ecosystems. In endemic areas, IND-type infections often occur in wild arboreal or semi-arboreal animals, and pathogens have been isolated from Aedes albopictus and Culex. White pheasants can pass the virus to their offspring through the ovaries, and then pass on to susceptible animals through bites. In the VSV epidemic forest in Panama, monkeys also experienced varying degrees of serology. Another evidence is that VS often occurs during the vigorous period of arthropod growth. The above VSV-IND is circulating between wild animals and arthropods. However, there are several contradictory phenomena and views that the induced viremia is not sufficient to infect arthropods; sometimes neighboring farms are not affected during the outbreak, and the erratic distribution of the disease is difficult to understand; the epidemic During this period, the virus could not be isolated from arthropods; other speculations were: the virus exists in the soil or pasture, and the animal is infected through contact with the skin or oral mucosa; the host of the virus may be a plant or insect, vertebrate Only occasionally becomes the host. Whether the virus can replicate in arthropods after feeding them with natural host material has not been confirmed.

The disease generally occurs in the United States in May-October, increasing in the summer and disappearing after frost. But the epidemic of frost in the western United States in 1982 was still prevalent.

Humans can be infected through contact with sick animals, including nasopharynx, abraded skin, and inhalation routes. Possible direct sources of infection are saliva, vesicular exudates or epithelium, or infection by direct contact with the virus during laboratory operations. Humans have symptoms similar to colds after infection. Most people recover within a week and can produce neutralizing antibodies. ^[1]

The incubation period is 2-4 days. The International Animal Health Code stipulates a maximum incubation period of 21 days. The clinical symptoms of VS in pigs are similar to foot-and-mouth disease (FMD), swine vesicular disease (SVD), and vesicular rash (VE), and are not easily distinguishable. The clinical symptoms of bovine VS cannot be distinguished from FMD. VS is characterized by short-term fever, pimples and blisters on the oral mucosa, nipple epithelium, between toes, and crown of hoofs. The main lesions of horses are on the back of the tongue, and the disease characteristics of deer ^[1]

VSV is believed to penetrate the body through the epithelium and mucous membranes. Once the virus invades the epithelial layer, it will produce the primary lesion in the skin. At the same time, in the deeper skin, especially the spinal cell layer, the virus will be more active in replication. During the process from virus replication to causing cell lysis, exudates accumulate, and small blisters converge into large blisters. This phase usually occurs within 2-3 days of experimental infection. When the virus spreads throughout the germinal layer, it often seems to damage the columnar cell layer and the basement membrane, but it does not significantly damage the regeneration capacity of these cells. Although ^[2] blood, edema, and leukocyte infiltration occur in the dermis and subcutaneous tissue, the virus usually does not cause primary damage in these areas. If a secondary infection occurs, its damage may spread to deep tissues causing suppuration and necrosis. In the absence of complications, epithelial cells regenerate rapidly, usually recovering within 1-2 weeks without leaving scars. ^[1]