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VIRAL RESPIRATORY INFECTION IN CATTLE: Courtesy : Festschrift - Dr. S. Ramachandran |
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Introduction |
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Respiratory infection is an acute or sub acute inflammatory reaction within the nose, para nasal sinuses, larynx, trachea, bronchi and lungs. The causes may be one or more species of microbes including a battery of viruses. Factors such as stressful shipment, fatigue, inclement weather and management conditions may gravely alter the situation. Initially, workers associated with problem of pneumonia linked it with bacteria. Failure to reproduce pneumonia consistently with bacteria isolated from pneumonic lungs suggested the possibility of a viral involvement. Experimental reproduction of pneumonia in mice (1,2) and histopathological evidences (3) supported this hypothesis. The advent of tissue culture techniques, however, has facilitated recovery of a variety of viruses from cattle with respiratory diseases. The present consensus is that, viruses per se are responsible for devitalizing the epithelia of the respiratory passage destroying cilia in the bronchial tubes which otherwise keep the lower respiratory tract free of harmful pathogens. This event paves way for the invasion of ubiquitous bacteria resulting in clinical disease (4). It is common opinion that under intensive husbandry practices, physical stress reduces the natural resistance of the animal to infection. Potentially pathogenic viruses present in the environment of a cattle shed, without meaning any harm under normal situations, are then able to gain a foothold and initiate infection. The opportunity for rapid animal-to-animal passage presents itself when animals are kept huddled together so that, the virulence of the pathogen may get enhanced. Further, the short lifespan of animals yields a high rate of turnover of a population. This is further accelerated by slaughter and replacements providing a rapid supply of susceptible animals for the perpetuation of the transmission chain (5).
Local scenario Table 1 : Reported respiratory viruses of cattle
Operational strategy In the majority of cases, the severity of respiratory disease varies considerably from one outbreak to another and even from animal to animal within the same herd. There are situations in which only a few animals within a herd show gross signs of respiratory illness while the remaining animals do not show clinical disease. Therefore, in investigations into respiratory diseases, sampling should be resorted to on a herd basis from intensive units. This process of sampling should include clinical cases and the so-called ‘in-contact’ animals. In general, young animals between 2 and 6 months have been found to be active sufferers of many of the inapparent respiratory infections. It is therefore, necessary to focus our attention on the age of animals for sampling. The new-born calves under two months of age do not generally participate in the infection chain largely due to the influence of maternal antibodies they derive through colostrum and in the case of adults, resistance is due to relative indifference to viral agents (14) or due to an earlier experience with the infection.
The other factor, which may significantly influence the disease process is season. Fall and winter months greatly favour the distribution of respiratory infections. This is acceptable due to the fact that lowered ambient temperature and high humidity help otherwise vulnerable viruses to survive longer outside the host. Transmission of agents is further helped by animals coming closer and huddling together during such season (15). A successful virus isolation from an episode of respiratory illness, by itself, may not be adequate to incriminate the agent as the causal factor. In many situations, this process will have to be established by screening serum samples, preferably collected at acute phase and convalescent phase of the disease and demonstrating significant sero-conversions and/or by histopathology.
The broad picture that emerges out is that of a virus, widespread in animals, but existing normally at the minimal survival level only maintaining an equilibrium between the host and the pathogen. When this equilibrium is disturbed, the pathogen replicates unhindered exerting a variety of effects on the functions of the cell ranging all the way from a silent but prolonged process of cessation of macromolecular synthesis to rapid metabolic inhibition thereby halting cell activity and ultimately its death. Cumulative effects of these cellular changes become manifest in an injury to tissues and organs and are reflected in the characteristic disease in the host (5). Breaking the chain of events at an early stage by removing calf hood susceptibility to the initiators of infection - the viruses. Reduction of the environmental stress thereby lessening the severity of infection. From ‘virus’ angle, the use of vaccines can provide an effective prophylaxis. If a solution lies in vaccines, then they most surely be polyvalent, comprising as many of the more ubiquitous viruses as may occur commonly in an area.
The second element in respiratory disease control is reducing the ‘stressor’. Experience has shown that long distance travel, inadequate rest, food, water, exposure to cold and humid climate, dehorning, castration, branding, vaccination soon after long journeys critically reduce their resistance to disease. These are more severe in intensive units where animals are made to assemble from widely differing sources rendering them easy victims to a dense population of microbes especially viruses prevalent in a geographic site (4,5,19). |
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Authors Corresponding address: Dr. R. Raghavan |
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The views expressed in this article are of the author(s), and any clarifications can be obtained from the author(s). |
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