04/10/2022
Rift Valley fever is a peracute or acute mosquito-borne zoonotic disease of domestic and wild ruminants, largely confined to sub-Saharan Africa but with high potential for wider transmission. It is characterized by abortions and neonatal mortality in ruminant animals. Diagnosis depends on histopathological examination of samples of the liver and identification of the virus in tissues. Effective vaccines are available.
Rift Valley fever (RVF) is present in Africa, Madagascar, some Indian Ocean islands, and the Arabian Peninsula. The disease is due to infection with a Phlebovirus in the family Phenuiviridae. Sporadic, sometimes very large, outbreaks of disease in ruminants are usually associated with heavy rainfall and localized flooding. The virus is maintained between epidemics by silent circulation between mosquito vectors and susceptible domestic or wild ruminants and/or by vertical transmission by certain Aedes spp mosquitoes.
During epidemics, abortions in production animals and deaths among young animals, particularly lambs, together with an influenza-like disease in humans, are characteristic. However, infections in both animals and humans are frequently subclinical or mild. Diagnosis is based on identification of characteristic histopathological lesions in the liver and demonstration of the presence of the virus by immunohistochemical staining, PCR assay, and/or increasing antibody titer. Tissues and fluids from infected animals carry a high risk of infection for human handlers. Treatment is supportive, and effective prevention can be achieved by vaccination.
Etiology and Epidemiology of Rift Valley Fever in Animals
Rift Valley fever virus (RVFV) belongs to the order Bunyavirales, family Phenuiviridae, and genus Phlebovirus. An enveloped spherical particle of 80–100 nm in diameter, it has a three-segmented, single-stranded, negative-sense RNA genome with a total length of ~11.9 kilobases (kb). Each of the segments, L (large: 6.4 kb), M (medium: 3.9 kb), and S (small: 1.7 kb), is contained in a separate nucleocapsid within the virion. Remarkably little genetic diversity has been found among RVFV isolates from many countries, and no noteworthy antigenic differences have been demonstrated. However, some differences in pathogenicity occur.
The disease is endemic in many tropical and subtropical regions of sub-Saharan Africa, Madagascar, Comoros, Mayotte, and the Arabian Peninsula. Thought to have been originally confined to the Rift Valley region of eastern and southern Africa, since the 1970s the virus has spread, with major outbreaks having occurred in Egypt since 1977, West Africa since 1987, Madagascar since 1990, and the Arabian Peninsula in 2000. There has also been unconfirmed serologic evidence of RVFV infection in other parts of the Middle East. Particularly large epidemics including large numbers of human cases occurred in Egypt in 1977–1978 and in Kenya in 2006–2007. Between 2016 and 2018, 10 outbreaks of RVF occurred in Uganda, the first in almost 50 years. In 2020, two outbreaks were reported in Libya.
Sporadic large epidemics have occurred at 5–10 year intervals in drier areas of eastern Africa and less frequently in southern Africa. Outbreaks are usually associated with periods of abnormally heavy rainfall or, in some cases, with localized flooding due to dam building or flood irrigation. Smaller outbreaks are likely to occur more often and may frequently be overlooked due to suboptimal veterinary surveillance and confusion with other causes of abortion and neonatal mortality. RVF is considered a threat in other regions of the world, including Europe and North America, where competent mosquito vectors are present, and the potential exists for the virus to become endemic if introduced.
During interepidemic periods, the virus is thought to remain dormant in transovarially infected eggs of floodwater-breeding Aedes spp mosquitoes (subgenera Neomelaniconion and Aedimorphus) in the dry soil of small, ephemeral wetlands (dambos or pans). In some areas, this transovarial transmission is believed to be the most important interepidemic survival strategy of the virus; however, this has seldom been demonstrated, and it is unknown for how long RVFV can survive in this manner. Inapparent cycling of the virus between vectors and wild or domestic mammalian hosts has been reported to occur, and this may be the most important survival strategy for the virus in many areas. Serologic evidence of exposure to RVFV has been found in many wildlife species, either associated with outbreaks in animals or in the absence of reported outbreaks.
RVFV may also be transmitted and emerge or re-emerge by movement of viremic animals, (eg, via the production animal trade and possibly by wind-borne mosquitoes). When either the emergence of infected Aedes spp mosquitoes or the introduction of virus to an area coincides with abnormally wet conditions and the presence of a highly susceptible host population, a large epidemic may ensue. The virus is then amplified in ruminants and transmitted locally by many species of mosquitoes, particularly Culex spp, mechanically by other insects such as biting flies, or iatrogenically such as by reuse of needles between infected animals.
The incidence of RVF peaks during the late rainy season. In areas with cold winters, both the disease and vectors may disappear after the first frost. In warmer climates where insect vectors are present continuously, seasonality is less pronounced and outbreaks are likely to be smaller due to the maintenance of some level of herd immunity.
Humans are readily infected with RVFV via exposure to:
tissues or fluids from infected animals and aborted fetuses
aerosolized blood from infected animals during slaughter
mosquito bites (considered less likely)
Therefore, farmers, farm workers, slaughterhouse workers, and veterinarians are particularly at risk.
Clinical Findings of Rift Valley Fever in Animals
Clinical signs of Rift Valley fever tend to be nonspecific, rendering it difficult to recognize individual cases. The incubation period is 12–36 hours in lambs, and a biphasic fever of up to 108°F (42°C) may develop. Affected animals are listless and reluctant to move or eat and may also show signs of abdominal pain. Mortality in young lambs is high (90%–100%), and animals usually die within 2–3 days. Adult sheep are less susceptible, with 10%–30% mortality; the incubation period is 24–72 hours, and animals show a generalized febrile response, lethargy, hematemesis, hematochezia, and nasal discharge, although infection may also be inapparent.
Calves are less susceptible than lambs; however, mortality may still be as high as 70%. Clinical signs are similar to those in sheep, but icterus is more common. Disease in adult cattle is often inapparent; however, they may show anorexia, lacrimation, salivation, nasal discharge, dysgalactia, and bloody or fetid diarrhea, with a mortality of 5%–10%. Camelids, equids, pigs, dogs, and cats may be infected by RVFV but appear largely resistant to disease, whereas birds, reptiles, and amphibians appear to be refractory to infection.
Sometimes, abortion may be the only sign of infection; the aborted fetus is usually autolyzed. In pregnant ewes, abortion rates vary from 5% to almost 100% in different outbreaks and on different farms; abortion rates in cattle are usually 1 year and to confer colostral immunity to the offspring.
Zoonotic Risk of Rift Valley Fever in Animals
Because RVFV can cause severe and potentially fatal disease in humans, those involved in the food-producing animal industry should be made aware of the potential dangers of exposure to RVFV-infected animals and tissues. Appropriate protective measures should be taken when investigating cases of abortion, handling potentially infected animals, and collecting diagnostic samples.
