Tuberculosis is a slowly spreading, chronic, granulomatous bacterial infection, characterized by gradual weight loss. All birds appear to be susceptible, although to variable degrees; pheasants seem to be highly susceptible, while the disease is uncommon in turkeys. Tuberculosis is more prevalent in captive than in wild birds. Tuberculosis is unlikely to occur in commercial poultry due to the short life span and husbandry practices used. (Also see Tuberculosis and other Mycobacterial Infections.)

Etiology and Epidemiology

Mycobacterium avium is the most common cause; although M genavense has been isolated. Serologic identification of isolates is essential to differentiate strains of M avium that cause disease in chickens and birds (serovars 1, 2, and 3) from other strains (serovars 4–6, 8–11, 21–28) that fail to produce disease in these species. M tuberculosis has infrequently been isolated from parrots and canaries. M avium is very resistant; it can survive in soil for up to 4 yr, in 3% hydrochloric acid for ≥2 hr, and in 4% sodium hydroxide for ≥30 min.

Tuberculosis is found worldwide, most commonly in small, barnyard flocks and in zoo aviaries; it is rarely found in young flocks. Wild birds, such as cranes, sparrows, starlings, and raptors, have been found to be infected. Tuberculosis has been found in emus and other ratites.

Infected birds with advanced lesions excrete the organism in their feces. Cadavers and offal may infect predators and cannibalistic flockmates. Rabbits, pigs, and mink are readily infected. Cattle exposed to contaminated feces may respond to M bovis purified protein derivative (PPD) tuberculin and to M avium paratuberculosis PPD tuberculin. M avium serovar 1, often isolated from tuberculous birds, has been isolated from people with acquired immunodeficiency syndrome.

Clinical Findings and Diagnosis

Signs usually do not develop until late in the infection when birds become thin and sluggish, and lameness may be seen. In chickens, granulomatous nodules of varying size are usually found in the liver, spleen, bone marrow, and intestine. Some exotic species may have lesions in the liver and spleen without intestinal involvement, but bone marrow and small mesenteric nodules may be found. Lesions are not calcified.

Live birds may be tested with avian tuberculins, although these are of little value in birds that do not have wattles. Large numbers of acid-fast bacteria in smears from lesions provide a tentative diagnosis. Mycobacteriologic examination is required to confirm a diagnosis. Isolates can be identified based on biochemical and seroagglutination tests and DNA analysis.

Control

Chemotherapy is ineffective. In commercial poultry flocks, relatively rapid turnover of populations, together with improved general sanitation, has largely eliminated this once common infection. Infected poultry should be destroyed, and housing facilities thoroughly cleaned and disinfected using cresylic (phenolic) compounds. Dirt-floored houses should have several inches of the floor removed and replaced with dirt from a place where poultry have not been maintained. All openings should be screened against wild birds.

Avian tuberculosis in zoos is difficult to eradicate. New additions to the aviary should be quarantined for 2–3 mo. The movement of ratites through sales and the long life of these animals have made tuberculosis a major concern for ratite producers. Isolation of ratites purchased at sales is essential to prevent the introduction of tuberculosis into established flocks.

Last full review/revision March 2012 by Charles O. Thoen, DVM, PhD