There are five clinical forms of BVDV which makes it difficult for veterinarians to recognize the many clinical manifestations of this virus. To make matters more complex when na´ve pregnant cows are infected with the virus there is a risk of fetal exposure resulting in early embryonic death, abortion or congenital infection/defects. If pregnant animals are exposed between 90-120 days of gestation their calves can be born with immunological tolerance to BVDV which is known as persistently infected (PI). The PI calves although appearing clinically normal have prolonged (often lifelong) viremia and shed large quantities of the virus.
The five clinical forms of BVDV are: acute BVDV, Severe acute BVDV, Hemorrhagic BVDV, acute BVDV infection- bovine respiratory disease, and acute BVDV infection-immunosupression. The following tables summarize the subclinical and clinical manifestations of BVDV.
|Acute/asymptomatic||Mild fever , leucopenia, seroconversion to BVDV, short term viremia, short term shedding.|
|Acute/symptomatic||Fever, leucopenia, depression, anorexia ocular-nasal discharge, oral lesions, diarrhea, decreased milk production in lactating cattle, short term viremia (15d), short term shedding.|
|Severe Acute||Peracute course, fever, pneumonia, sudden death (10-15% mortality) Associated with BVDV type 2.|
|Hemorrhagic||Marked thrombocytopenia, bloody diarrhea, epistaxis, hyphema, bleeding from injection and branding sites, pyrexia, leucopenia, and death. Associated with BVDV type 2.|
|Acute/bovine respiratory distress||Fever, pneumonia, anorexia, prolonged treatment. Leading cause of death in feedlot cattle due to secondary infection with Pasteurella multocida, Mannheimia hemolytica and Mycoplasma bovis which complicate the pathogenesis.|
|Acute/Immunosuppressive||Leukoctye function diminished up to 25%, leucopenia, decreased CD+4 and CD+8 T lymphocytes, and decreased macrophage and neutrophil functions. Secondary or polymicrobial infections with bovine respiratory syncytial virus, popular stomatitis virus, malignant catarrhal fever virus have been reported.|
|Acute/ Chronic Disease Sequel to PI: Mucosal Disease|
|Mucosal Disease||Occurs in calves (6-18months) of age that are PI and are therefore immunotolerant to noncytopathic (ncp) BVDV. These calves may appear clinically normal, but upon superinfection with a homologous BVDV or mutation of the ncp to cytopathic (cp) variant or vaccination with MLV BVDV stain homologous to the ncp PI virus these calves can develop one of the two forms of mucosal disease described below|
|Acute MD||Acute mucosal disease is characterized by onset of clinical symptoms within 10-14 days postinfection. Symptoms include biphasic fever, anorexia, tachycardia, polypnea, decreased milk production, and watery diarrhea. Diarrhea is often characterized by the presence of mucosal shreds, fibrinous casts, blood and foul odor. Erosions and ulcers may be present on the tongue, palate, and gingival while epithelial erosions may be pronounced in the interdigital regions, coronary bands, teats, vulva, and prepuce. Other clinical signs may include nasal-ocular discharge, corneal opacity, hypersalivation, decreased rumination and bloat. Cattle with acute MD become progressively dehydrated and usually die within 3-10 days. Although mortality usually approaches 100%, a few animals may survive the acute MD but are prone to develop the chronic MD.|
|Chronic MD||Chronic MD is a sequel of acute MD. Affected cattle are “poor doers” and may have intermittent diarrhea, chronic bloat, decreased appetite, and weight loss. Nasal-ocular discharge is commonly seen. Cattle with chronic MD rarely survive past 18 months and are usually culled due to low performance or die of severe debilitation.|
Persistently Infected calf
Figure 1: Postmortem images of calf suffering from mucosal disease. Note the erosive lesions seen on the esophagus, gums, and abomasums these erosive lesions can typically be found all throughout the entire digestive tract in severe cases.
Bovine Viral Diarrhea Virus (BVDV) occurs in two biotypes: cytopathic (cpBVDV) which damages cells and noncytopathogenic (noncpBVDV) which does not damage cells. BVDV can infect a wide variety of cells and it is hypothesized that entry into the host cell is through receptor-mediated endocytosis. Replication of BVDV occurs within the cytoplasm of the host cell and viruses exit via exocytosis. The noncpBVDV replicates in leukocytes, lymphoid tissue, the proximal colon and the respiratory tract while cpBVDV was found to replicate in the gastrointestinal tract. In persistently infected males BVDV replicates within the seminal vesicles and the prostate gland. In acute BVDV, ncp BVDV is distributed widely throughout the host while cp BVDV is not as widely distributed. The ncp BVDV biotype induces humoral response whereas cp BVDV induces a cell mediated immune response. There are both low virulence and high virulence strains, in both strains the primary replication occurs in tonsils and the nasal mucosa with virus spreading to lymph nodes, spleen and thymus but in the high virulence strain there can also be spread to T cell dependent areas and to the bone marrow. The high virulent strain has faster and higher production of antigens and will eventually spread to all organs. There is persistent viremia with ncp-BVDV due to its ability to inhibit interferon 1 which decreases the cell’s ability to ward off infection. It is believed that the high levels of viremia facilitate transplacental and intrauterine infections. It has been shown that BVDV 2 strain has increased virulence and tissue distribution.
http://uwadmnweb.uwyo.edu/VetSci/Courses/PATB_4710/BVDV.ppt. BVD slide show
Bovine viral diarrhea virus: diagnosis, management, and control
By Sagar M. Goyal, Julia F. Ridpath
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