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Junin virus is similar to Machupo virus and thus the AHF vaccine is considered to be a good protection also against Bolivian hemorrhagic fever.

Argentine hemorrhagic fever is an acute arenoviral natural focal disease endemic to the central regions of colchicine.

It proceeds with high fever, hemorrhagic syndrome, damage to the kidneys and central nervous system.

Identified in 1943 in the Argentine province of Buenos Aires.

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A detailed description of the disease belongs to Arribalzaga (1955). Subsequently, there have been casesand diseases in other provinces of Argentina (more than 16,000 patients) and some other countries of South America. The causative agent of the disease was isolated by Parodi (1958) in the city of Junin. In 1974–1975 developed methods of vaccination against Argentine hemorrhagic fever.

The causative agent of Argentine hemorrhagic fever is the Junin virus (Parodi et al, 1958), belonging to the Tacaribe antigenic group of Gloperba pills genus. The virus passes through filters with a diameter of more than 100 nm, is sensitive to fat solvents, is destroyed when heated, in an acidic environment, when exposed to ultraviolet rays and formalin. Junin virus cultures well on Hela Vero tissue media and is susceptible to guinea pigs.

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Argentine hemorrhagic fever is a natural focal colchicine.

Hamster-like rodents, especially Calomys musculinus, C. Laucha and their parasitic mites Mesostigmata, are natural reservoirs of infection. In rodents, the Junin virus causes both manifest and latent forms of colchicine, which contributes to the long-term circulation of the virus in natural foci. The experiment showed sensitivity to the Junin virus in guinea pigs.

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A person becomes infected with Argentine hemorrhagic fever in natural foci in the course of economic activity. Infection is carried out by both alimentary and aerogenic and transmissible routes. The risk of infection increases in newly formed foci of the disease. Usually the disease is observed in men of Colchicine pills age in agricultural areas. During the harvest season (hence the local name for the disease - mal de los rastrajos), especially in May, the incidence increases markedly, due to changes in the rodent population. It is possible to transmit the virus from a sick person.

Pathogenetic mechanisms in Argentine hemorrhagic fever are not well understood. Experimental models have shown that after introduction, the virus multiplies in reticuloendothelial cells, after which viremia develops (within 7-12 days), which contributes to the dissemination of the virus into various body systems. Due to the direct vasotropic and neurotropic effect of the Junin virus, generalized specific vasculitis and encephalitis develop. In their genesis, cellular factors, in particular sensitized T-lymphocytes, play an important role.

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As a result of damage to the vascular wall, capillary expansion and an increase in their permeability are observed, which leads to extravasation, the release of the liquid part of the blood into the extravascular sector, blood clotting, hypoxia, and disruption of tissue metabolism. Along with this, disseminated intravascular coagulation develops, which intensifies shock reactions. Significant damage to the distal and direct renal tubules was noted.

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Degenerative changes in the liver are characteristic. Hemorrhages, necrosis, specific granulomas in the brain tissue and autonomic ganglia are described.

The incubation period ranges from 6–8 to 12–16 days. The disease usually develops gradually. In the initial period, lasting 3-4 days, general toxic manifestations are observed - malaise, headache, irritability, chilling. Muscle pains are often noted, especially in the lumbar region. Often on the mucous membranes of the oral cavity, hemorrhages and erosions can be detected. There may be catarrhal changes in the upper respiratory tract.