Vet Column 11-30-09
Fort Collins, Colo.
IBR, which stands for infectious bovine rhinotracheitis, is a viral disease primarily of cattle that can affect the respiratory, reproductive, ophthalmic and other body systems. IBR is a herpes virus, more specifically now known as BHV-1 (bovine herpes virus, class 1). When involved with the respiratory system, this viral pathogen is part of the bovine shipping fever complex, targeting the upper respiratory system.
So what is the upper respiratory tract? This generally refers to the nasal cavity, sinuses, oropharynx (back of the throat area), tonsils, and the trachea (windpipe). In the nasal area, the convolutions of the anatomy creates turbulence and enhances the trapping of particulates, including viruses and bacteria. The irritation results in mucous production and facilitates subsequent swallowing of the trapped particulates, removing them from the respiratory area. The fine hair like structure on the surface of the cells that line the trachea, called cilia, also aid in moving mucous up out of the trachea. This mucociliary escalator from the trachea also aids in preventing contamination of the lungs. Importantly, the mucous also contains substances such as interferon and immunoglobulin that can aid in combating viruses and bacteria, both directly and indirectly. The problem comes when the number of viruses and bacteria contaminating this area overwhelms the animal’s ability to remove them from the upper respiratory tract.
Most of the pathogens (harmful agents or germs, such as bacteria and viruses) affecting the bovine respiratory system have envelopes or capsules that make them susceptible to desiccation and ultraviolet light. They can survive, however, for undetermined periods of time in moist conditions with favorable temperatures and out of sunlight. Inhalation is thought to be the most common form of transmission, but one cannot ignore the potential of oral contamination with the viruses and bacteria potentially affecting the bovine respiratory system. Nose to nose contact, coughing and sneezing associated with short distance aerosol, and contamination of instruments, equipment, and hands of people treating or handling cattle can all be potential disease transmission events.
Cold, wind, dust and other environmental conditions can contribute to mechanical degradation of the upper airways, and when combined with increased numbers of bacteria and viruses, can also circumvent its immune defenses. High ammonia levels can also compromise the non-specific micro-anatomical and physiological defense mechanisms. Nutrition can also play a role, including micronutrients necessary for immune function and dietary changes that can results in a relative acidosis or other physiological imbalances resulting in a negative impact on non-specific defenses.
BHV-1 enters the surface cells (and eventually nerves) in the upper airways. Erosions and ulcers in the upper respiratory tract, notably the trachea, are the pathological hallmark of BHV-1 infections. These lesions occur from the destruction of infected cells resulting in cell death. Widespread destruction of ciliated epithelium in the trachea by the BHV-1 virus disrupts the housekeeping functions of the mucociliary escalator, and results in a failure to clear bacteria from the upper airways. This contamination by the bacteria of the lungs due to the viral predisposition often results in the classical clinical signs associated with shipping fever.
Once a calf is infected, the virus can be shed for eight to 10 days, with a peak occurring around four days after infection. What’s important is to remember that BHV-1 virus is a herpes virus and can be stored in the trigeminal and sciatic nerves following infection. When cattle are stressed, the virus can then be released and cause clinical disease. This is called recrudescence of BHV-1.
BHV-1 vaccines, when properly used according to label directions, are excellent vaccines. Since the preponderance of cattle populations are exposed to BHV-1 sometime in their lifetime, it is useful to immunize calves at about three to four months-of-age. This is when the antibody against BHV-1 from the colostrum has waned and the calves have generally not yet been excessively exposed to BHV-1.
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