Cache Valley virus – an outbreak of congenital malformations in Ontario lambs

Maria Spinato, Margaret Stalker, Josepha DeLay, Jan Shapiro, Jim Fairles, Paula Menzies, Jocelyn Jansen

During the last week of December 2015 and the first 2 weeks of January 2016, the AHL received several submissions of deformed stillborn and aborted ovine fetuses for postmortem examination. Similar cases were also reported to OVC and OMAFRA small ruminant veterinarians, and included flocks located in eastern, central, and southwestern Ontario. Gross examination of these fetuses revealed flexural limb deformities, kyphoscoliosis, torticollis, and hypoplastic musculature (Fig. 1). Most lambs had various degrees of brain malformation ranging from cerebellar hypoplasia (Fig. 2) to hydranencephaly (Fig. 3). In some affected flocks, normal lambs were reportedly born co-twin to deformed littermates.

Histologic lesions included skeletal myofibrillar hypoplasia, disorganized cerebral and cerebellar development with porencephaly. A few cases had mild placentitis typified by occasional small necrotic foci within cotyledonary villi, and rare stromal mineralization or neutrophilic infiltrates. Since similar outbreaks of deformed ovine fetuses caused by Cache Valley virus (CVV) were previously diagnosed in Ontario flocks in 2011-2013, this orthobunyavirus infection was the most likely culprit.

Fetal thoracic cavity fluid and serum samples from affected ewes were forwarded to the Texas Veterinary Medical Diagnostic Laboratory for CVV virus neutralization. As maternal antibody does not cross the ruminant placenta, fetal antibody is considered to be diagnostic for in utero infection. Positive fetal and maternal antibody titers for CVV ranged from 1:64 to 1:512, confirming CVV as the cause of fetal abnormalities in this outbreak. Fetal tissues and placenta were also submitted for CVV RT-PCR testing; results for this test were negative. This is not unexpected, as malformations are caused by viral infection at 28-48 days of gestation, and the virus is usually cleared when abortions or stillbirths (full term in sheep is 150 days) occur.

CVV is a mosquito-borne virus. It is transmitted to sheep by infected mosquitos that previously fed on infected white-tail deer, or that are offspring of infected mosquitos.  Late summer and early autumn are the months when the highest amount of virus is present in the mosquito population. CVV is considered endemic in most parts of the United States, Mexico, and Canada, and infects a wide range of domestic and wild animals, as well as humans. Since 2010, a new strain of CVV originating in Mexico has emerged and is now the dominant lineage in the Northeastern US. Whether this new variant is responsible for the recent Ontario outbreak, or the unusually warm autumn of 2015 facilitated a protracted period of mosquito transmission, is unknown. Attempts at virus isolation are in progress, but may be unrewarding at this stage.

Similar to Schmallenberg virus in Europe, a related orthobunyavirus that causes lesions identical to CVV, periodic outbreaks of deformed lambs at 3-5 year intervals may just be related to the immune status of the ewe population, which is eventually replaced by naive animals. Infected animals develop life-long immunity. There are no vaccines or treatments available to protect livestock against CVV. Shifting the time of breeding or keeping sheep away from cedar bushes and from wet areas during the breeding season may help to reduce exposure to infected mosquitos.   


Lamb born with arthrogryposis, kypho-scoliosis and poorly developed musculature.

Cerebellar hypoplasia.




Figure 1: Lamb born with arthrogryposis, kypho-scoliosis and poorly developed musculature.

Figure 2: Cerebellar hypoplasia.


Figure 3: Hydranencephaly.