Rift Valley hemorrhagic fever.

Rift Valley hemorrhagic fever is a zoonosis and is primarily seen in various animals, but much less commonly causes severe disease in humans with high mortality.

Livestock fatalities (epizootics) from fever cause serious economic problems. During the last major outbreak of Rift Valley haemorrhagic fever in Saudi Arabia and Yemen in 2000, the fatality rate was over 14%.

The virus was first isolated and identified from sick sheep in Kenya (the Rift Valley) in 1930, and later in parts of sub-Saharan North Africa. In September 2000, the first case of Rift Valley hemorrhagic fever outside Africa (Saudi Arabia and Yemen) was reported.

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Epidemiology of Rift Valley Hemorrhagic Fever

At least 30 mosquito species belonging to five genera are possible carriers of the infection. The diversity of carriers is of particular concern in terms of the spread of the disease among animals and humans. In a certain endemic area, a specific carrier may predominate (in the Arabian Peninsula, this is mainly Aedes (Aedimorphus) vexans). Mosquitoes of the genus Aedes can transmit the infection transovarially. In this way, the offspring of mosquitoes already infected and capable of transmitting the infection to animals and humans are born. It is important that infected mosquito eggs can survive for a long time (months, years) in dry conditions. The intensity of transmission increases during the rainy periods of the year.

Many species of wild and domestic animals can be affected by the virus, including cattle, sheep, camels, goats (sheep are more susceptible than other animals). In case of epizootics among sheep, the mortality rate among lambs reaches 90%, among ewes - 10%. An important signal of the beginning of an epidemic among animals is 100% abortions in sheep.

Transmission of infection to people is possible:

• by transmission (through mosquito bites);
• through contact with the blood (other fluids, organs) of an infected animal, through consumption of milk from sick animals;
• inhalation route of infection (a case of laboratory infection has been described).

Pathogenesis has been studied mainly in experimental animals (lambs, rats), and in humans it has been little studied. High hepatotropism of the virus has been established; massive necrosis of hepatocytes and eosinophilic infiltration have been detected in newborn lambs. Liver and CNS lesions (encephalitis) develop in experimental rodents.

Marked changes in the lymph nodes were noted, accompanied by necrotic changes with serous or hemorrhagic exudate. Lesions of the glomerular and tubular parts of the kidneys were established. In humans, liver damage, degenerative processes in the myocardium, and interstitial pneumonia were established (in isolated studies).

The reduced functional state of the MFS and the high level of proinflammatory cytokines (especially when the vascular endothelium is damaged) are of great importance in the pathogenesis of the disease.

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Symptoms of Rift Valley Hemorrhagic Fever

The incubation period is from 2 to 6 days. Rift Valley hemorrhagic fever begins acutely. There are pronounced symptoms of Rift Valley hemorrhagic fever: intoxication, moderate fever; patients are often bothered by weakness, myalgia, back pain, headache, vomiting, abdominal pain. Uncomplicated course of Rift Valley hemorrhagic fever is observed in 98% of all cases, the duration of the disease is from 4 to 7 days, while the titers of specific antibodies increase, viremia is not observed. In severe cases, symptoms of liver damage with the development of jaundice, renal failure, hemorrhagic syndrome prevail.

Currently, 3 types of complicated course of Rift Valley hemorrhagic fever are considered:

• development of retinitis (more often in the central parts of the retina) in 0.5-2% of cases (1-3 weeks after the onset of the disease) - the prognosis is usually favorable; based on the characteristic changes in the retina, it is possible to judge in retrospect the possible presence of a history of Rift Valley hemorrhagic fever;
• development of meningoencephalitis in 1% of cases, the prognosis is unfavorable;
• development of hemorrhagic syndrome (bleeding, hemorrhagic rash, etc.), DIC syndrome; characterized by prolonged viremia of up to 10 days or more; mortality can reach 50%.

Diagnosis of Rift Valley Hemorrhagic Fever

Microbiological diagnostics of Rift Valley hemorrhagic fever is performed in the first 2-3 days of the disease, the virus is isolated from blood, feces and pharyngeal washes by infecting newborn white mice and cell cultures. Serological diagnostics of Rift Valley hemorrhagic fever is based on the determination of specific antibodies in ELISA (IgM). RIF is used to detect virus antigens. In vivo detection of virus markers is performed in the blood, and posthumously - from tissues using PCR.

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Treatment of Rift Valley Hemorrhagic Fever

Specific antiviral treatment for Rift Valley hemorrhagic fever has not been developed. Ribavirin has been shown to be effective in experimental settings, but its clinical effectiveness in humans has not been proven. Pathogenetic treatment for Rift Valley hemorrhagic fever is mainly aimed at detoxification and relief of hemorrhagic syndrome. Currently, in hospital settings, with adequate pathogenetic therapy, mortality may not exceed 1%.

How is Rift Valley Hemorrhagic Fever prevented?

Prevention of Rift Valley hemorrhagic fever is aimed at:

• vaccination of animals with two types of vaccines - live attenuated and killed; after vaccination with the attenuated vaccine, immunity lasts for life;
• prevention of the disease in humans using a formalin-killed vaccine; the method is currently at the clinical trial stage;
• containment of mosquito populations, as well as individual prevention of mosquito bites.