Wesselsbron disease is an acute mosquito-borne viral infection that affects mainly sheep, cattle, and goats in sub-Saharan Africa and is associated with rainfall and flooding. Infection is common, but clinical signs are infrequent (though probably underreported). Newborn lambs and goat kids are most susceptible, and animals can die. Infection in adult sheep, cattle, and goats is usually subclinical; however, it can cause abortion, congenital CNS malformation, arthrogryposis, and polyhydramnios.
Wesselsbron disease is an acute viral infection of mainly sheep, cattle, and goats; clinical signs have also been reported in dromedary camels and in humans (1, 2). The infection is caused by a flavivirus, Wesselsbron virus (WSLV), transmitted primarily by mosquitoes of the genus Aedes. It is therefore associated with heavy rainfall and flooding, and cases can occur concurrently with and closely resemble Rift Valley fever.
Infection is common; however, clinical signs are infrequent (though likely underreported). Newborn lambs and goat kids are the most susceptible, and high mortality rates can occur. Infection in adult sheep, cattle, and goats is usually mild or subclinical; however, disease can be severe in pregnant ewes and in sheep with preexisting liver pathology. Abortion can occur in ewes, together with congenital malformation of the CNS with arthrogryposis of sheep and cow fetuses and polyhydramnios (excessive amniotic fluid) in ewes. Incidental spillover occurs to humans, causing a nonfatal, influenza-like disease.
Etiology and Epidemiology of Wesselsbron Disease
Wesselsbron disease is caused by a flavivirus, Orthoflavivirus wesselsbronense (order Amarillovirales, family Flaviviridae), an enveloped, positive-sense RNA virus in the yellow fever virus complex. The virus has been isolated from vertebrates and arthropods from many sub-Saharan African countries and Madagascar. Evidence of infection has been reported in cattle, sheep, goats, camels, pigs, donkeys, horses, dogs, rats, ostriches, lemurs, and wild ruminants and equids (3, 4, 5).
The main vectors of WSLV are floodwater-breeding mosquitoes of the genus Aedes, particularly the subgenera Neomelaniconion and Ochlerotatus; however, WSLV has also been isolated from other mosquito genera, including Culex, Anopheles, and Mansonia, and once from an ixodid tick.
Incidence of infection is likely greater than is generally realized, and clinical cases are likely overlooked because they tend to occur concurrently with cases of Rift Valley fever, a more severe disease sharing similar vectors and climatological risk factors.
The high prevalence of antibodies in warmer and moister coastal areas of southern and eastern Africa suggests that domestic herbivores play an important role in maintaining the virus, and activity appears to occur year-round. In drier areas, however, seroprevalence is generally lower, and irregular disease outbreaks occur, usually in conjunction with outbreaks of Rift Valley fever, when abnormally heavy rains lead to an abundance of floodwater-breeding Aedes mosquitoes.
Direct host-to-host transmission has not been reported; however, transmission from ewes to lambs via milk has been demonstrated experimentally (6). The wide range of potential mosquito vector species and wide vertebrate host range suggest a high potential for range expansion and emergence.
Humans can become infected with Wesselsbron disease via mosquitoes or by exposure to tissues or fluids from infected animals—for example, when performing necropsies or in the laboratory. Most infections in humans are subclinical and only detected serologically; however, infection can result in transient, nonfatal influenza-like symptoms.
Clinical Findings of Wesselsbron Disease
Wesselsbron disease has an incubation period of 1–3 days in newborn lambs and kids, after which nonspecific clinical signs of illness, including fever, anorexia, listlessness, weakness, and tachypnea, become evident. More severe clinical signs can include icterus, diarrhea, nasal discharge, and neurological signs. Death can occur within 72 hours. In calves and adult sheep, goats, and cattle, the incubation period is 2–5 days, and nonfatal febrile or inapparent infection occurs.
The virus is both hepato- and neurotropic, and efficiently crosses the placenta, resulting in abortion and polyhydramnios in ewes, as well as fetal arthrogryposis and congenital CNS malformations (see ).
Two sheep fetuses aborted in late gestation, showing arthrogryposis. Although a diagnosis was not made in this case, abortion and fetal arthrogryposis are typical outcomes of infection with Wesselsbron virus during early to middle gestation.
Courtesy of Dr. Paul Reynolds.
Neurological signs secondary to Wesselsbron disease have been described in horses (7). Clinical signs described in an outbreak in dromedary camels include lethargy, shivering, lacrimation, dyspnea, tremors, recumbency, and death (1).
Wesselsbron disease and Rift Valley fever share many clinical and pathological features, and they can occur concurrently in the same area. However, Wesselsbron disease is usually milder, producing much lower mortality rates, fewer abortions, and less destructive liver lesions. The causative virus appears to be more neurotropic than the Rift Valley fever virus, and severe, teratogenic fetal CNS lesions occur after experimental infection (8, 9, 10). Use of the live attenuated virus vaccine in pregnant ewes can result in early embryonic death, teratogenic lesions of the CNS, arthrogryposis, polyhydramnios, abortion, or fetal mummification.
Infection in humans is usually subclinical but can produce transient mild to severe fever, headache, retrobulbar pain, myalgia, and arthralgia. No fatalities due to Wesselsbron disease in humans have been reported.
Lesions in Wesselsbron Disease
In newborn and young animals, moderate to severe icterus and hepatomegaly occur with Wesselsbron disease; the liver is yellowish to orange-brown, with small necrotic foci. Petechiae and ecchymoses are commonly found in the mucosa of the abomasum, the contents of which are chocolate-brown in color. Petechiae and ecchymoses can also be found on other serosal surfaces.
Histopathological examination reveals mild multifocal to extensive necrosis of the liver, with eosinophilic inclusion bodies in some necrotic hepatocytes (11). Lesions in adult animals are usually much milder.
Diagnosis of Wesselsbron Disease
Outbreaks of abortion and neonatal deaths associated with heavy rainfall and flooding
Virus isolation to distinguish it from Rift Valley fever
Outbreaks of abortion and neonatal deaths associated with heavy rainfall and flooding are an indication of Wesselsbron disease; however, the disease must be distinguished from Rift Valley fever via clinical findings or molecular detection.
The virus can be isolated or detected by PCR assay from almost all organs of lambs that have died during the clinical stage of the disease. Intracerebral inoculation of newborn mice is the best method of isolation.
In ewes and lambs, diagnosis can be confirmed histologically in the liver by immunohistochemical analysis (see ). In fetuses, however, liver sampling alone might be insufficient for diagnosis of Wesselsbron disease, especially in cases without obvious hepatic lesions. In ovine fetuses collected during the second trimester of gestation, the highest levels of viral antigen were detected in the placenta and fetal brain, while liver involvement was limited (10). Veterinarians investigating abortion, stillbirth, or congenital malformations should therefore routinely collect fetal brain and placental cotyledon samples, in addition to liver, to improve diagnostic sensitivity for WSLV infection.
Pearls & Pitfalls
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Immunohistochemical staining in a liver tissue sample from a young lamb. Note the Wesselsbron virus (WSLV) antigen staining red within the cytoplasm of necrotic hepatocytes adjacent to a portal canal. Original magnification 40X.
Courtesy of Dr. Lieza Odendaal.
Serological diagnosis has historically been based on hemagglutination inhibition, complement fixation, ELISA, and virus neutralization. However, a rising titer should be demonstrated to exclude preexisting seropositivity. Hemagglutination inhibition testing is limited by its cross-reactivity with other flaviviruses.
A variety of new single- and multiplex molecular assays have been developed to detect WSLV and other arthropod-borne viruses (arboviruses) in clinical samples and mosquito pools and may be available for research purposes (12, 13).
Treatment and Control of Wesselsbron Disease
Vaccination of nonpregnant animals
Housing animals indoors at night
No specific treatment exists for Wesselsbron disease. If necessary, standard supportive therapy to treat clinical signs and support liver function is recommended.
A live attenuated Wesselsbron virus vaccine is available, although not widely used. The vaccine may be administered to nonpregnant animals and likely confers lifelong immunity. Injudicious use of the vaccine in pregnant ewes can result in severe economic losses due to abortion and fetal malformations. Housing animals indoors at night and moving them away from low-lying wetland areas during high-risk periods might decrease exposure to vectors.
Attempts to control mosquito vectors are of little value as a preventive measure.
Key Points
In domestic ruminants, particularly sheep, abortions and neonatal deaths due to Wesselsbron disease are associated with heavy rainfall and flooding.
Wesselsbron disease is easily confused with, and can occur together with, Rift Valley fever.
Wesselsbron disease is a zoonotic infection, so care should be taken to prevent exposure to tissues and fluids from affected animals.
WSLV is considered to have a high potential for range expansion and emergence.
For More Information
Quan M, Coetzer JAW, Swanepoel R. Wesselsbron disease. Anipedia.
Smith DR. Waiting in the wings: the potential of mosquito transmitted flaviviruses to emerge. Crit Rev Microbiol. 2017;43(4):405-422.
Nelson AN, Ploss A. Emerging mosquito-borne flaviviruses. mBio. 2024;15(12):e02946-24.
References
Ishag H, Tigani El Tigani-Asil E, Zawde W, et al. Molecular detection of Wesselsbron virus in dromedary camels, Borana Zone, Ethiopia, 2024. Emerg Infect Dis. 2025;31(6):1263-1265. doi:10.3201/eid3106.250130.
Weyer J, Thomas J, Leman PA, Grobbelaar AA, Kemp A, Paweska JT. Human cases of Wesselsbron disease, South Africa 2010-2011. Vector Borne Zoonotic Dis. 2013;13(5):330-336. doi:10.1089/vbz.2012.1181
Swanepoel R, Coetzer JAW. Wesselsbron disease. In: Coetzer, JAW, Tustin, RC, eds. Infectious Diseases of Livestock. 2nd ed. Vol 2. Oxford University Press; 2004:987-994.
Diagne MM, Faye M, Faye O. et al. Emergence of Wesselsbron virus among black rat and humans in Eastern Senegal in 2013. One Health. 2017;3:23-28. doi:10.1016/j.onehlt.2017.02.001
Morvan J, Fontenille D, Digoutte JP, Coulanges P. The Wesselsbron virus, a new arbovirus for Madagascar. Article in French. Arch Inst Pasteur Madagascar. 1990;57(1):183-192. https://europepmc.org/article/med/1964039
Zimoch M, Grau-Roma L, Liniger M, et al. Mosquito-independent milk-associated transmission of zoonotic Wesselsbron virus in sheep. PLoS Pathog. 2024;20(12):e1012751. doi:10.1371/journal.ppat.1012751
Venter M, van Eden C, Wiliiams J, et al. Arboviruses associated with neurological disease in animals in South Africa and their zoonotic potential in humans. Int J Infect Dis. 2014;21(suppl 1):184. doi:10.1016/j.ijid.2014.03.804
Coetzer JAW, Barnard BJ. Hydrops amnii in sheep associated with hydranencephaly and arthrogryposis with Wesselsbron disease and Rift Valley fever viruses as aetiological agents. Onderstepoort J Vet Res. 1977;44(2):119-126. http://hdl.handle.net/2263/53772
Coetzer JAW, Theodoridis A, Herr S, Kritzinger L. Wesselsbron disease: a cause of congenital porencephaly and cerebellar hypoplasia in calves. Onderstepoort J Vet Res. 1979;46(3). http://hdl.handle.net/2263/53903
Oymans J, van Keulen L, Wichgers Schreur PJ, Kortekaas J. Early pathogenesis of Wesselsbron disease in pregnant ewes. Pathogens. 2020;9(5):373. doi:10.3390/pathogens9050373
Coetzer JAW, Theodoridis A, Van Heerden A. Wesselsbron disease: pathological, haematological and clinical studies in natural cases and experimentally infected new-born lambs. Onderstepoort J Vet Res. 1978;45(2):93-106. http://hdl.handle.net/2263/53987
Faye M, Seye T, Patel P, et al. Development of real-time molecular assays for the detection of Wesselsbron virus in Africa. Microorganisms. 2022;10(3):550. doi:10.3390/microorganisms10030550
Villinger J, Mbaya MK, Ouso D, Kipanga PN, Lutomiah J, Masiga DK. Arbovirus and insect-specific virus discovery in Kenya by novel six genera multiplex high-resolution melting analysis. Mol Ecol Resour. 2017;17(3):466-480. doi:10.1111/1755-0998.12584
