Rift Valley haemorrhagic fever

Hemorrhagic fever in the Rift Valley is a zoonotic disease and, first of all, is observed in various animals, it is much less likely to cause severe illness in people with high mortality.

Mortality of livestock (epizootic) from fever leads to serious economic problems. During the last large outbreak of Haemorrhagic fever in the Rift Valley in Saudi Arabia and Yemen in 2000, the mortality rate was more than 14%.

The virus was first isolated and identified from sick sheep in Kenya (the name of the area is the Rift Valley) in 1930, later in some parts of North Africa below the Sahara. In September 2000, the first reported cases of hemorrhagic fever in the Rift Valley outside Africa (Saudi Arabia and Yemen).

[1], [2], [3], [4],

Epidemiology of hemorrhagic fever in the Rift Valley

Possible vectors of infection are at least 30 species of mosquitoes belonging to five genera. The variety of vectors causes some concern in terms of the spread of the disease among animals and humans. In a particular endemic area, a specific vector can prevail (on the Arabian Peninsula, it is basically Aedes (Aedimorphus) vexans). Mosquitoes of the genus Aedes can transmit the infection transovarially. Thus, there is a progeny of mosquitoes, already infected and capable of transmitting infection to animals and humans. It is important that infected mosquito eggs can persist (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 to other animals). In epizootics among sheep, lethality in lambs reaches 90%, in sheep - 10%. An important signal of the beginning of the epidemic among animals is 100% of abortions in sheep.

Transmission of infection to people is possible:

• by the transmission route (through mosquito bites);
• when exposed to blood (other fluids, organs) of the infected animal, when milk is used from sick animals;
• Inhalation route of infection (described in the case of laboratory infection).

Pathogenesis was mainly studied in experimental animals (lambs, rats), but in humans it has been little studied. High hepatotropicity of the virus was established, neonatal lambs showed massive necrosis of hepatocytes, eosinophilic infiltration. Experimental rodents develop liver and CNS (encephalitis) lesions.

Significant changes in the lymph nodes were noted, accompanied by necrotic changes with serous or hemorrhagic exudates. Defects of the glomerular and tubular parts of the kidneys have been established. In humans, liver damage, degenerative processes in the myocardium, interstitial pneumonia have been established (in single studies).

Of great importance in the pathogenesis of the disease are the reduced functional state of MPS, a high level of pro-inflammatory cytokines (especially with damage to the vascular endothelium).

[5], [6], [7], [8], [9]

Symptoms of hemorrhagic fever in the Rift Valley

The incubation period is from 2 to 6 days. Hemorrhagic fever in the Rift Valley begins acutely, marked symptoms of hemorrhagic fever in the Rift Valley: intoxication, mild fever; patients often are troubled by weakness, myalgia, back pain, headache, vomiting, abdominal pain. The uncomplicated course of hemorrhagic fever in the Rift Valley 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, no viralemia is noted. In severe course, the symptoms of liver damage prevail with the development of jaundice, the phenomena of renal insufficiency, hemorrhagic syndrome.

Currently, there are 3 types of complicated course of hemorrhagic fever in the Rift Valley:

• the 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 forecast is usually favorable; by the characteristic changes in the retina in retrospect, it is possible to judge the possible presence in the anamnesis of the transferred haemorrhagic fever of the Rift Valley;
• 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 up to 10 days or more; lethality can reach 50%.

Diagnosis of hemorrhagic fever in the Rift Valley

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

[10], [11], [12],

Treatment of haemorrhagic fever in the Rift Valley

Specific antiviral treatment of hemorrhagic fever in the Rift Valley has not been developed. In experimental conditions, the effectiveness of ribavirin has been established, its clinical effectiveness in humans has not been proven. In general, the pathogenetic treatment of hemorrhagic fever in the Rift Valley is aimed at detoxification, relief of hemorrhagic syndrome. Currently, under steady-state conditions with adequate pathogenetic therapy, lethality may not exceed 1%.

How is hemorrhagic fever in the Rift Valley prevented?

Prevention of haemorrhagic fever in the Rift Valley is aimed at:

• vaccination of animals with two types of vaccines - live attenuated and killed; After vaccination with an attenuated vaccine, immunity persists for life;
• prevention of the disease in humans with the help of formalin-killed vaccine; currently the technique is at the stage of clinical approbation;
• containment of the mosquito population, as well as individual prevention of their bites.