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VIRAL RESPIRATORY INFECTION IN CATTLE: 
PROFILE AND PERSPECTIVES
R. Raghavan

Courtesy : Festschrift - Dr. S. Ramachandran


Introduction 
The lungs are highly complex organs designed to effect the exchange of gases between inspired air and blood. The structural pattern of the lung is basically the same in all mammals with species variation in relative size and lobe distribution. Consideration of the vital role of the lungs and their position of relative exposure to infectious agents sheds light on the significance of pulmonary involvement in the functional economy of the body. A pulmonary disease of any kind may decrease or interrupt the free and adequate supply of air to the alveoli, exchange of oxygen to carbon dioxide, or adequate supply of blood to and from the lungs. 

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 
Animal husbandry programmes in India involving intensive rearing of dairy animals, importation of exotic breeds, replacement of pastoral style of farming by stall feeding have immensely altered the profile of respiratory infections in course of time. Outbreaks of respiratory infection, either by themselves, or as a complex of pneumoenteritis have assumed serious proportions and represent, with the spectrum of nutritional deficiencies, the bulk of illness. 

Causative agents 
Advanced virological techniques have helped in the identification of the causative agents and their association with specific respiratory ailments in cattle (Table-1). Some of these viral agents although widespread within the cattle population have a questionable role in the disease; yet, under conditions of physiological insults can take on a pathogenic role.

Table 1 : Reported respiratory viruses of cattle

Agent

Type

Group

Ref. 

BHV 

Herpes 

6

Parainfluenza 

Paramyxo 

7

Respiratory Syncytial virus 

Bovine 

Paramyxo 

8

BVD 

Flavi 

9

Reovirus 

1,2,3 

Reo 

10

Rhinovirus 

Bovine 

Picorna 

11

Adenovirus 

1,2,3 

Adeno 

12

Influenza 

Myxo 

13 

Operational strategy 
Viruses are obligate parasites displaying a high degree of host and cell selectivity. An operation involving virus research especially isolation should comprise appropriate in vitro models. 

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. 

Interpretation 
Despite the general similarity in the clinical picture, it should be in the back of mind of all investigators that in majority of the viral respiratory infections unique and pathognomonic clinical picture is seen in early stages of the disease but seldom recognized unless sought after. Evidence is also accumulating leading to speculation that a severe clinical syndrome met with under field conditions results from the interaction of two or more agents acting in concert.

Cause and effect 
Most of the respiratory involvements in cattle are caused by a large segment of viruses, which are treated as ‘latent’ or ‘inapparent’. In such instances or in some cases of ‘carrier’ state, altered host factors such as physical stress often tilt the relationship from one of commensalism to parasitic (16). Physical stress appears to exert its most important effect on epithelial surfaces, specially of the respiratory tract (17). Rapid changes in humidity and temperature in the environment could adversely depress the metabolism inside the epithelial cells and their associated immunologically competent tissues to such an extent that production of surface acting antibodies would be inadequate to cope with the infective challenge (18). There is a growing awareness that in respiratory ailments greater losses are inflicted by viruses producing insidious infections than by those responsible for diseases of a highly dramatic and spectacular nature.

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). 

Containment 
In a situation such as this, the problem of pneumonia has two aspects which require addressing. 

  1. Breaking the chain of events at an early stage by removing calf hood susceptibility to the initiators of infection - the viruses.

  2. 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). 
In conclusion, it is logical that a proper appraisal of the etiological factors - microbial and ecological, and their relationship at different levels in the causation of respiratory ailments needs to be made to devise ways and means for their control.

References

  1. Baker, (1943). J. Exp. Med., 78: 435.
  2. Watt, J.A.A. (1952). J. comp. Path., 62: 102.
  3. Jarrett, W.F.H. (1956). Br. vet. J., 112: 431.
  4. Thomas, H.S. (1998). The Angus J., 19: 28.
  5. Raghavan, R. (1971). Studies on isolation and biological characterisation of viral agents harbouring the respiratory tract of cattle, sheep and goats. Ph.D., Thesis. Agra Univ.
  6. Madin, S.H. et al. (1956). Science, 124: 721.
  7. Reisinger, (1959). J. Am. vet. med. Ass., 135: 147.
  8. Paccaud, M.F. and Jacquier, C.L. (1970). Arch. ges. virusforsch. 30: 327.
  9. Olafson, P. et al. (1946). Cornell Vet., 36: 205.
  10. Rosen, L. et al. (1963). Am. J. Hyg., 77: 38.
  11. Bogel. (1962). Zentbl. Bakt., 187: 2.
  12. Darbyshire, J.H. et al. (1965). Nature, (London). 208: 307.
  13. Romvary, J. et al. (1962). Nature, (London). 193: 907.
  14. Wenner, H.A. (1962). Ann. N.Y. Acad. Sci., 101: 398.
  15. Rosen, L. (1962). Ann. N.Y. Acad. Sci., 101: 61.
  16. Schwabe, C.W. (1969). Veterinary Medicine and Human Health. 2nd Edn. p.160. The Williams and Wilkins Co. Baltimore.
  17. Lidwell, O.M. et al. (1965). J. Hyg., 63: 427.
  18. Phillips, J.L.H. (1970). Vet. Rec., 86: 280.
  19. Stoltenow, C. and Lardy, G. (1999). Preconditioning Programs. North Dakota State Univ. http.www.ext.nodak.edu/as 1160W.htm.

Authors Corresponding address: 

Dr. R. Raghavan
Former Professor and Head,
Veterinary Microbiology, U.A.S., 56, 2nd Main, Ganganagar Layout, Bangalore - 560 032, India


The views expressed in this article are of the author(s), and any clarifications can be obtained from the author(s).