0332-B3
Dr. A. K. SINGH. 1
Tuberculosis in deer's caused by Mycobacterium bovis and rarely by Mycobacterium tuberculosis & Mycobacterium avium is undoubtedly the most important infectious disease affecting the deer family. The problem mainly lies in the control of infection reservoir existing in the wild animal population. The instinct of deer's to move in herds, contribute to the problem where infected and carrier animals within the herd add to the environmental contamination causing an easy spread of infection and disease. This report indicates the prevalence of tuberculosis in the wildlife of Satpura forests of Betul, in Madhya Pradesh, India. Two adult male spotted deer (Axis axis) died of tuberculosis within a fortnight's interval. Externally both showed similar degree of emaciation, cachexia, shrunken eyes and rough coat. On conducting postmortem, the gross pathological findings showed several pinheads to pea-sized yellowish-white nodules in both lungs filled with caseated pus. The mesenteric lymph nodes were also containing pus. Other organs especially spleen, liver, heart and kidneys appeared normal, however abomasum, small and large intestines were congested in both cases. Further examination of smears prepared from the lungs' nodular lesions revealed acid-fast bacilli of a more slender type distinguished as Mycobacterium species, and on culture they were typed as M. avium on the basis of standard biochemical tests. The mode of infection could possibly involve birds, which might have acted in transmission of the microbes from one location to other, and contaminating by their droppings.
Tuberculosis is caused by bacteria of the Mycobacterium family consisting of three specific strains Mycobacterium avium, affecting birds, Mycobacterium bovis, affecting cow, buffalo and sheep, deer, etc. and Mycobacterium tuberculosis, which affects humans. However, cross infection is very common, where any strain can affect any animal. Deer's are more vulnerable to tuberculosis, which spreads fast, mainly due to their herd behaviour (close proximity to each other). An infected animal may live 2 to 3 years before the disease becomes fatal, causing an increased risk of contamination of the environment and subsequent infection to other deer's of the same herd.
Two dead deer's at a gap of a fortnight were reported at the hospital for post-mortem, which was conducted by opening the body cavities & the visceral organs. Internal organs (specially lungs) were checked for any nodular lesions. Other organs like spleen, liver, heart and kidneys abomasum, small and large intestines, and lymph nodes were also examined for any lesions. Smears were prepared from the lungs' nodular lesions and stained with Zichl-Neelsen to find presence of tubercle bacilli. Also a culture of the lung tissue was subjected to standard biochemical tests to find out the type of Mycobacterium species.
The cause of death was tuberculosis, as proved by post-mortem findings and later proved by microbiological findings. The lungs' nodular lesions smear when stained with Zichl-Neelsen showed positive for a more slender type acid-fast bacilli, identified as Mycobacterium species in both cases. The culture of lung tissue revealed tuberculosis bacilli, which were typed as M. avium on the basis of standard biochemical tests. Both the deer's were affected by similar strain of tuberculosis.
Tuberculosis in deer is caused by Mycobacterium bovis and rarely by M. tuberculosis (Clifton-Hadley et al., 1991). There are very few reports on avian tuberculosis infection relating to M. avium, in deer in India, and is therefore considered less riskier than that of M. bovis and M. tuberculosis. However, this infection is not uncommon in deer in other countries (Griffith, 1928; Christiansen, 1931; Schmidt, 1938; Hopkinson and McDiarmid, 1964; McDiarmid, 1967; Hime et al., 1971; John, 1974; Kollias, 1978; Stacy, 1986).
The organism is relatively resistant and can survive in the environment for extended periods under the right conditions. Mycobacterium spp. can survive on pasture for up to 8 weeks protected in faeces, but is an obligate pathogen on entry into the host; thus ingestion of contaminated pasture or water, or inhalation of the organism as aerosols, will result in infection in a susceptible animal. It can gain entry via a number of routes including ingestion and inhalation. Inhalation is the principle mode of transmission however infection by ingestion is more likely on pasture where faeces or bird droppings contaminate drinking water. The source of infection could not be established, however, a possible hypothesis of the role of birds in the epidemiology of tuberculosis in deer can't be ruled out. Also, an infected deer sheds the organisms in the sputum, exhaled air, faeces, urine, milk, vaginal & uterine discharges, about 90 days post infection (Fenwick, S.1995).
Tuberculosis in deer may take either a subacute form where animals are severely affected within six months of infection or a chronic form without obvious signs for several years. Clinical signs are unpredictable owing to the variable distribution of the lesions but usually there is progressive emaciation, lymph node enlargement. Animals, which are chronically infected without overt clinical signs, serve as carriers and can harbour significant numbers of bacilli, which are disseminated through the environment (Buchan and Griffin,1990).
Deer's pathological condition to become an asymptomatic carrier or to develop clinical disease depends upon the amount of mycobacterium taken aboard, and the resistance of the host animal. An animal is most at risk immediately following infection, which is determined by factors exogenous to the host such as the presence of agent in the environment and the dose received. This is influenced by coughing frequency of infected animals, confinement, stocking density and the length of time of exposure. The risk of progression to active infection is dependent on endogenous factors, which may involve the presence of concurrent disease, immunosuppression, and stress.
Tuberculosis in deer is a major issue due to the inability to control the infection reservoir, which exists in the wild animal population. Infected and carrier animals within the herd contribute to environmental contamination and spread of infection and disease. Tuberculosis can affect any age of animal and the organism can gain entry via a number of routes including ingestion and inhalation. Two deer were tested positive for tuberculosis in their post-mortem examinations. The tissue changes pertinent to tuberculosis were seen in the lungs, and bacteriological culture of swabs of the lungs' nodular lesions yielded M. avian from both deer. The source of infection could not be established, however, a possible hypothesis of the role of birds in the epidemiology of tuberculosis in deer was concluded. This information is important to wildlife and forest officials, in order to initiate appropriate measures to protect an indiscriminate spread of tuberculosis.
*Buchan, G.S.; Griffin, J.F.T.(1990): Tuberculosis in Domesticated Deer (Cervus elaphus): A Large Animal Model for Human Tuberculosis. J. Comp. Path. 107:11-22.
*Christiansen, M. 1931. Intensive tuberculosis in deer caused by avian tuberculosis. Zeitschr. Infekt. Hyg. Han., 40: 165171. Reprinted in Vet. Bull., 2: 316.
*Clifton-Hadley, R.S.; Wilesmith, J.W.; (1991): Tuberculosis in deer: a review: The Veterinary Record, July 6 1991.
*Fenwick, S.(1995): Notes for Veterinary Microbiology 16.301. Massey University, N.Z. p14.1-14.19.
*Griffith, A.S.1928. Cited by Hamerton, A.E. 1935. Distribution and comparative morbid anatomy of tuberculosis in captive animals. Br. J. Tuber., 29: 145-151.
*Hime, J.M., Keymer, I.F., Boughton, E. & Birn, K.J. 1971. Tuberculosis in a red deer (Cervus elaphus) due to an atypical mycobacterium. Vet. Rec., 88(23): 616-617.
*Hopkinson, F. & McDiarmid, A. 1964. Tuberculosis in a free living red deer (Cervus elaphus) in Scotland. Vet. Rec., 76: 1521-:1522.
*John, H. 1979. Tuberculosis in deer. New Z. Vet. J., 27(8): 151.
*Kollias, G.V.1978. Immuno-pathologic studies of mycobacterial infections in captive cervids. In F.J. Montali & G. Migani, eds. 1980. Comparative pathology of zoo animals, p. 295-303. Washington, DC, Smithsonian Institute Press.
*McDiarmid, A. 1967. A list of bovine tuberculosis in fallow deer. J. Brit. Soc., I: 78. Cited by Wilson & Harrington (1976) in Vet. Rec., 98: 74.
*Schmidt, H.W. 1938. Tuberculosis in the Roe deer. Deutsch. Tierärztl. Wschr., 46: 482-485. Reprinted in Vet. Bull., 9:752.
*Stacy, V.T. 1986. The existing and potential importance of brucellosis and tuberculosis in Canadian wildlife: a review. Can. Vet. J., 27: 119- 124.
1 Veterinarian
Government Veterinary Hospital, Khedi, Betul, M.P. India
Tel: 91-07141-231907
E-mail: [email protected]