|Virus||Bovine Viral Diarrhea Virus||Virus||Hepatitis C Virus|
|Primary Host||Cattle||Primary Host||Humans|
|Disease(s) Caused||Bovine Viral Diarrhea||Disease(s) Caused||Hepatitis C|
|Symptoms||Fever, lethargy, loss of appetite, oral lesions, diarrhea, decreased milk production||Symptoms||Fatigue, nausea, muscle aches|
|Potential Complications||Secondary bacterial infections||Potential Complications||Liver cirrhosis, liver cancer|
|Transmission Mode||In utero, contact with secretions from persistently infected animals||Transmission Mode||Blood-borne|
|Sites of Community Outbreaks||Farms, ranches||Sites of Community Outbreaks||Healthcare settings, drug users|
Importance of Bovine Viral Diarrhea Virus
Bovine Viral Diarrhea Virus (BVDV) is an enveloped member of the Flaviviridae family. BVDV is a major pathogen for cattle and also serves as the U.S. EPA approved surrogate for Human Hepatitis C.
There are two types of BVDV, noncytopathic and cytopathic. The noncytopathic type is able to persist in the body by suppressing the immune response. This type is usually non-symptomatic in healthy adults, but can leave the animal more susceptible to other infections as a result of the immune suppression. The cytopathic type is responsible for mucosal disease, a fatal condition. Mucosal disease causes lesions on the intestinal walls, resulting in severe diarrhea and dehydration. Bacterial infection of the lesions contributes to mortality.
If a pregnant cow is infected with BVDV in the first trimester, the fetus’ developing immune system can ignore the virus, thus becoming persistently infected (PI). These animals, if they survive to birth, are the major source of transmission in a herd, shedding virus throughout their lifespan. Because the noncytopathic type suppresses the immune system, PI animals are more likely to become ill. Mucosal disease can arise in PI animals via either mutation of the persistent strain into the cytopathic type, or by secondary infection. This typically happens before the animal is 2 years old.
BVDV is accepted by the U.S EPA as a surrogate for disinfectant efficacy testing against Human Hepatitis C virus (HCV). A surrogate is necessary because HCV is difficult to propagate reproducibly in cell culture. BVDV works well as a surrogate due to a high degree of genomic similarity between the two viruses. Their genomes have been found to code for functionally identical proteins that can serve as targets for inactivation. Both viruses are of similar size and both are enveloped, indicating similar susceptibility to disinfection. In addition, both viruses establish persistent infections in their hosts at a similar frequency.
Importance of Hepatitis C
HCV is an enveloped member of the Flaviviridae family. HCV causes hepatitis C, a disease that affects the liver.
Infection with HCV can cause either an acute or chronic infection. About 15% of cases are acute, with the remainder being chronic. Acute cases typically cause mild symptoms such as fatigue, nausea, and muscle aches. The liver is not usually involved. Chronic infections can result in liver cirrhosis or cancer. Co-infections and excessive alcohol consumption greatly increases the chances of this happening.
HCV is blood-borne. Transmission can occur in several ways. Intravenous drug use is a major vector. Tattoos performed with a non sterile needle or contaminated dye is another way that HCV can be spread. Healthcare settings can also pose a risk when reusable equipment is improperly sterilized, or when accidental needle sticks occur.
Importance of Disinfection: Survival of Bovine Viral Diarrhea Virus and Hepatitis C on Surfaces and Potential for Transmission via Fomites
BVDV is spread primarily through direct contact with a PI animal. Transmission can also occur via surfaces contaminated with bodily fluids from a PI animal.
HCV has been shown to survive and remain infectious for up to 1 week. Infected surfaces, such as needles, can easily transmit HCV, as can contaminated suspensions.
Both BVDV and HCV are susceptible to a range of disinfectants, as with most enveloped viruses.
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- Ciesek, Sandra, et al. “How stable is the hepatitis C virus (HCV)? Environmental stability of HCV and its susceptibility to chemical biocides.”Journal of Infectious Diseases 201.12 (2010): 1859-1866.
- Doerrbecker, Juliane et al. “Inactivation and Survival of Hepatitis C Virus on Inanimate Surfaces.” The Journal of Infectious Diseases 204.12 (2011): 1830–1838. PMC. Web. 19 Jan. 2016.
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