A chronic, rarely acute, contagious, granulomatous, debilitating disease of mammals characterized by the formation of tubercles in lungs and different organs
Mycobacterium species
More than 170 species, most of which are environmental organisms
All Mycobacterium types may produce infection in host species other than their own
Main recognized types of the Mycobacterium tuberculosis complex (mammalian tubercle bacilli)
M tuberculosis
M canettii
M bovis
M caprae
M pinnipedii
M microti
M mungi
M suricattae
M africanum
Dassie bacillus
Chimpanzee bacillus
Mycobacterium avium complex
M avium avium (avian tubercle bacilli)
M avium hominissuis (isolated from humans, swine, and other mammals)
M intracellulare
M tuberculosis
The most host-specific; it produces progressive disease only rarely in animals other than humans and nonhuman primates (mainly dogs, pigs, cattle, and elephants)
M bovis
Can cause progressive disease in many mammalian species, including humans
M caprae
An organism closely related to M bovis, has been isolated from humans, goats, cattle, and several wildlife species
M avium avium
The species of most importance in birds; however, it has a wide host range and is also pathogenic for pigs, cattle, sheep, deer, mink, dogs, cats, certain exotic hoofed animals, and some cold-blooded animals
M avium hominissuis
The cause of TB in immunocompromised humans, swine, and other animals
Pathogenesis Pathway
1. Infection through inhalation, ingestion, intrauterine and coital methods
2. Bacterium trapped in respiratory mucosa, phagocytosed by macrophages
3. If macrophages fail to destroy bacteria, they multiply and initiate infection
4. Bacteria spread aerogenously and via lymphatics
5. Primary (Ghon) complex forms
6. If not contained, bacteria disseminate via lymph and blood
7. Miliary tuberculosis can develop
8. Post-primary infection (secondary tuberculosis) can occur if immunity declines
Bovine tuberculosis pleurisy and peritonitis (pearl disease and grapes disease)
Bovine intestinal tuberculosis
Miliary tuberculosis
Multiple young tubercle nodules appear as small, grayish-white, firm, difficult-enucleated, millet-like tubercles
Granulomas consist of central aggregation of tuberculous bacilli or caseation surrounded by macrophages, epithelioid, and Langhan's giant cells besides lymphocytes surrounded by a thin rim of fibrous connective tissue at the periphery
Chronic nodular tuberculosis
Old tubercle nodules appear as grayish-white or yellow, hard, difficult enucleated pea or bean-like tubercles
Granulomas consist of central caseation and calcification surrounded by macrophages, epithelioid, and Langhan's giant cells besides lymphocytes encapsulated by fibrous connective tissue
Tuberculous bronchopneumonia
Nodules in the bronchi are either closed (bacilli remain in the tubercle) or opened (lesions reveal cavitations and bacilli come out)
Bovine tuberculosis pleurisy and peritonitis
Pearl disease: small rounded grayish elevated and velvety tubercles in the pleura or peritoneum
Grapes disease: clusters of white tubercles (grapes-like) in the pleura or peritoneum
Bovine intestinal tuberculosis
Begins as the pneumonic form and spreads to the intestine by coughing up and swallowing sputum, hematogenous or lymphatic spread, or less commonly ingestion
Associated with mucosal ulceration overlying Peyer's patches due to vasculitis, thrombosis, and ischemia
Clinical notes on TB in different species
Bovine: Calcification is typical, affects any organ
Sheep and goats: Lesions similar to cattle but calcification not common
Equine: Productive form with little connective tissue and softening of the center, rare calcification
Dogs: Exudative form similar to liquefactive necrosis
Birds: Extensive caseation without calcification, deficient cellular elements and connective tissue
Intradermal tuberculin test
The single most important diagnostic test for TB
Johne's disease (Paratuberculosis)
Chronic granulomatous enteritis of ruminants caused by Mycobacterium avium ssp. Paratuberculosis, characterized by persistent diarrhea, progressive weight loss, debilitation, hypoproteinemia, thickening and corrugation of the intestinal mucosa, and eventually death
Johne's disease pathogenesis
1. Ingestion
2. Intestine
3. M cells and enterocytes
4. Peyer's patches
5. Survival in macrophages/dendritic cells
6. Long delay (12 months or longer)
7. Granulomatous enteritis and mesenteric lymphadenitis
Johne's disease lesions in cattle
Chronic segmental diffuse (lepromatous) granulomatous enteritis with thickened intestinal wall, rough corrugated mucosa, and multiple ulcerations
Mesenteric granulomatous lymphadenitis, lymphangitis, and lymphangiectasia
Aortic and endocardial intimal mineralization
Johne's disease lesions in sheep, goats and deer
Nodular (tuberculoid) granulomas in the intestines, lymphatics, and lymph nodes, sometimes mineralized
Diarrhea doesnotoccur in sheep and goats (except pygmy goat develop explosive diarrhea and die unexpectedly)
Johne's disease is one of the most important diseases facing the dairy industry
Johne's disease progression
Infection acquired early in life, often soon after birth, but clinical signs rarely develop in cattle less than 2-year-old
Tissue specificity to ileocecal intestine related to greatest concentration and availability of iron in tissue macrophages
Bacteria disrupt phagosome-lysosome fusion and block degradative actions of lysosomes
Mechanisms of injury in Johne's disease
Death of cells of the monocyte-macrophage system and of all cell populations in the lamina propria of intestinal villi
Death of the epithelial cells of mucosa of the small intestine
Caseous lymphadenitis (Pseudotuberculosis)
Chronic suppurative lymphadenitis affecting sheep and goats (occasionally cattle, horses, and camels) caused by Corynebacterium pseudotuberculosis, characterized by enlargement and suppuration of one or more lymph nodes, and occasionally other organs
Caseous lymphadenitis pathogenesis
1. Infection by skin wounds, and less commonly across the mucous membranes via inhalation or ingestion
Enlarged and firm lymph nodes (mainly prescapular, prefemoral, mediastinal, bronchial, and supramammary)
Cut sections show onion-like lamination of fibrous connective tissue alternate with caseated friable mass
Whitish-yellow or greenish-yellow pus surrounded by connective tissue capsule
Microscopically, central caseous necrosis and calcification surrounded by macrophages, epithelioid cells, and lymphocytes encapsulated by fibrous tissue
Multiple abscesses in the internal organs may be present in caseous lymphadenitis
Chronic weight loss or emaciated carcasses present in severe cases of caseous lymphadenitis
The three types of inflammation are acute, chronic, and granulomatous.