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EPIDEMIOLOGICAL FEATURES AND CONTROL OF 
BOVINE TUBERCULOSIS
 V.N. Appaji Rao

Courtesy : Festschrift - Dr. S. Ramachandran

Mycobacterium bovis (M.bovis) is the specific cause of tuberculosis in cattle. However, M.tuberculosis and M.avium are also reported to affect cattle. Bovine tuberculosis is a disease characterised by the progressive development of granulomas or tubercles in the lungs, lymph nodes and/or other organs which affect the health of individual animal and has a detrimental effect on animal production and farm economy (1). Among infectious diseases, tuberculosis is still the leading cause of mortality in humans.

Tuberculosis caused by M.bovis is reported in almost every country of the world. The disease is recorded in 69 per cent of the countries in tropics and in 80 per cent of the countries in Africa (2). All species of cattle are affected although Bos indicus is reported to be more resistant than Bos taurus (3). In India the overall prevalence in buffalo was almost three times more than in cattle (4).

The primary mode of spread of bovine tuberculosis is by the introduction of infected animals into healthy herds. Most important factors determining the occurrence and spread of tuberculosis within a herd, are the number of infected animals, number of young stock exposed to these infected animals and the measures taken to prevent the spread. Managemental factors inclusive of zero grazing, constant housing in warm, humid and poorly ventilated premises, play important role in the spread of tuberculosis (5).

Infection is predominantly by respiratory route and in calves through ingestion of infected milk. After infection, a visible primary focus develops in 8 days and calcification commences 2 weeks later. Following infection, M.bovis is phagocytised by macrophages and is carried to lymph nodes, parenchyma of lungs and other sites. In macrophages the bacteria resist being killed by blocking maturation and fusion of phagosomal compartments (6) and natural resistance to the oxidative burst (7). Thus the bacilli are able to multiply, destroy the phagocytes and escape into intra-cellular space. This in turn stimulates accumulation of other phagocytes, creating the typical microscopic lesion-granuloma of tuberculosis. These granulomas continue to expand with new phagocytic cell infiltration, giant cell formation, fibrosis and the ultimate macroscopic lesion-tubercle (8). The clinical signs often become more pronounced after calving, expressed as progressive emaciation despite capricious appetite. 

M.bovis is a member of M.tuberculosis complex of mycobacteria which includes M.tuberculosis, M.bovis, M.africanum and M.microtia. Infection of humans with any of these organisms can result in tuberculosis, indistinguishable clinically, radiologically and pathologically (9). M.bovis does not establish itself in humans as readily as M.tuberculosis (10). More than 94 per cent of the world population live in countries in which control of M.tuberculosis in cattle and buffaloes is either limited or completely absent. The contribution of M.bovis to the prevalence of human tuberculosis is unknown in many of these countries, but the lack of control measures owing to financial constraints, lack of trained personnel and political will, mean that bovine tuberculosis will continue to persist as long as poverty and malnutrition exist. The control of bovine tuberculosis is rarely high on the political agenda of governments in developing nations worldwide. Approximately 40 percent of cases are expected to occur in South East Asia and 40 per cent in Sub Saharan Africa (11). In the United States of America the cost of bovine tuberculosis control has been estimated to be 300 million dollars (12). The current trend of increasing incidence of tuberculosis particularly in immuno-compromised humans prioritises the need for effective control of bovine tuberculosis (2).

The three principal reasons for the eradication of bovine tuberculosis are:

 a) the risk of infection to human population,
b) losses in productivity of infected animals and 
c) the risk of imposition of international trade restrictions. 

The control of bovine tuberculosis on a herd basis should consider the following aspects. 

  • Clean and well ventilated housing,

  • Appropriate stocking density,

  • Segregation of calf at birth and feeding with clean pasteurised milk,

  • Intra-dermal testing of all animals above the age of 3 months with PPD and segregation of reactor animals,

  • Periodic examination of all the animals and segregation of clinically suggestive cases,

  • A spectrum of sensitive and specific serological tests to confirm the disease in reactors, doubtful reactors and clinically suggestive cases and their removal from the herd,

  • Periodic intensive search by allergic tests, serological tests and clinical examination to identify fresh cases and their removal from the herd,

  • Routine periodic screening of farm workers for evidences of tuberculosis and exclude them from the farm premises, and

  • Intensive screening of all new animals before admission into the herd with allergic and serological tests.


BCG vaccination
Sufficient evidence is available to prove that calf-hood BCG vaccination and subsequent revaccinations have reasonably protected the calves reared in infected farms along with appropriate hygienic and managemental practices. BCG vaccination of calves (in a heavily infected farm) within 10 days after birth, again at 6 months of age and later once a year for 5 years provided significant protection (13,14). In another study, administration of 4 mg of dried BCG in two injections one month apart conferred considerable protection (13). Prior exposure to mycobacteria lowers the efficacy of BCG vaccine (15,16). Therefore, this type of exposure needs to be considered in the evaluation of cattle trials. In the future, DNA vaccines hold high promise (17).

In conclusion, the presence of bovine tuberculosis in any herd or region or country should be viewed with concern and should be controlled and eradicated by package of practices appropriate to the country.

References

  1. Dungworth, D.L. (1992). Respiratory system. In Pathology of domestic animals. Vol. 2, 4th Ed. p. 632. Eds. K.V.F. Jubb, P.G. Kennedy and N.C. Palmer. Academic Press Inc., San Diego.

  2. Moda, G. et al. (1996). Tubercle Lung dis., 77: 103.

  3. Office International des Epizooties (OIE) (2000). World Animal health in 1999, Part 2. p. 650. OIE, Paris.

  4. Lall, J. M. (1969). Vet. Bull., 39: 385.

  5. Neill, S. D. et al. (1988). Vet. Rec., 123: 340.

  6. Frehel, C. and Rastogi, N. (1987). Infection and Immunity, 55: 2916.

  7. McDonnough, K.A. et al. (1993). Infection and Immunity, 61: 2763.

  8. Neill, S.D. et al. (1994). Vet. Microbiol., 40: 41.

  9. Griffith, A.S. (1937). Tubercle, 18: 528.

  10. Francis, J. (1958). Tuberculosis in animals and man. p. 357. Cassel, London.

  11. Cosivi, O. et al. (1998). Emerg. infect. dis., 4: 27.

  12. Roberts, T. (1986). J. Food Protec., 49: 293.

  13. Govorov, A.M. (1955). Nauch, Trud. Ukrain Inst. Exp. Vet., 21: 82.

  14. Doyle, T.M. and Stuart, P. (1958). Br. vet. J., 114: 3.

  15. Berggren, S.A. (1977). Br. vet. J., 133: 490.

  16. Fine, P.E. and Vynnycky, E. (1998). Vaccine, 16: 1923.

  17. Huygen, K. (1998). Int. J. Lung Dis., 2: 971.

Authors Corresponding address: 

Dr. V.N. Appaji Rao
Associate Editor,
Indian Veterinary Journal, 11, Chamiers Road, Chennai - 600 035, India.

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