JPC SYSTEMIC PATHOLOGY

RESPIRATORY SYSTEM

September 2026 P-B10

HISTOPATHOLOGIC DESCRIPTION:

Lung: Approximately 60% of the parenchyma is effaced and replaced by multifocal to coalescing poorly formed granulomas. Granulomas range up to 4mm in diameter and are composed of necrotic centers containing large numbers of viable and degenerate neutrophils and moderate numbers of macrophages mixed with eosinophilic cellular and karyorrhectic debris, basophilic mucin, and scattered mineralization. These areas of necrosis are surrounded by numerous epithelioid macrophages, few multinucleated giant cells (Langhans and foreign body type), and more peripherally by lymphocytes and plasma cells. Less mature granulomas lack a necrotic center. Some granulomas are circumscribed by a thin fibrous connective tissue capsule. Intervening alveolar lumina are filled by varying combinations and concentrations of edema fluid, small amounts of hemorrhage and fibrin, foamy alveolar macrophages, and neutrophils. Alveolar septa are occasionally lined by hyperplastic type II pneumocytes and expanded by congestion, hyperplastic interstitial and intravascular macrophages, and circulating neutrophils, and occasionally small amounts of collagen. Airways are filled and expanded by an exudate composed of abundant basophilic mucus and large numbers of viable and degenerate neutrophils and macrophages admixed with cellular debris. Multifocally, aggregates of lymphocytes and plasma cells surround blood vessels.

Spleen: There is diffuse severe follicular hyperplasia of the white pulp, and normal red pulp architecture is effaced by large numbers of macrophages filling sinusoids. At one edge is a cluster of granulomas similar to those previously described, but with abundant fragmented crystalline mineral within the necrotic center.

Liver: Essentially normal tissue.

SLIDE B: Acid-fast stain: There are rare, intrahistiocytic, 0.5x2µm, acid-fast bacilli.

HISTOPATHOLOGIC DESCRIPTION:

Lung: Affecting approximately 40% of this section, there are multifocal to coalescing granulomas that efface the pulmonary parenchyma, compress adjacent alveoli, and elevate the pleural surface. Granulomas are centered on large areas of lytic necrosis composed of abundant eosinophilic karyorrhectic and cellular debris with aggregates of mineral, surrounded by a layer of viable and degenerate neutrophils, surrounded by epithelioid macrophages with occasional multi-nucleated giant cells (Langhan’s and foreign-body type), further surrounded by lymphocytes and plasma cells with a rim of fibrous connective tissue. Adjacent alveolar septa are congested and thickened by macrophages, neutrophils, lymphocytes, and plasma cells. Alveoli occasionally contain pale eosinophilic fluid (edema) with increased numbers of alveolar macrophages. Blood vessels are occasionally surrounded by aggregates of lymphocytes and plasma cells. There is perivascular edema surrounding larger vessels. The pleural surface is moderately thickened by edema and increased fibrous connective tissue with scattered macrophages.

GENERAL DISCUSSION:

• Mycobacterium spp. are facultative intracellular, aerobic, gram positive (but poorly staining), non-motile, non-spore-forming bacilli
• Mycobacteria are acid-fast because of the mycolic acid and high lipid content layer of their cell walls; also very resistant to heat, pH changes and many disinfectants
• Mycobacteria are generally divided into three large groups
  • Tuberculosis group (referred to as M. tuberculosis complex or MTBC): M. tuberculosis, M. bovis, M. microti, M. mungi, M. caprae, and others
  • Leprosy group: M. lepraemurium, M. leprae, M. visibilis
  • Opportunistic “non-tuberculous” group:
    • Rapid-growing: e.g. M. fortuitum, M. chelonae, M. abscessus
    • Slow-growing: e.g. M. ulcerans, M. avium-intracellulare complex (MAIC) including M. avium spp. paratuberculosis
• Of the MTBC, M. tuberculosis and M. bovis are most common
  • “Tuberculosis” refers to disease caused by either M. tuberculosis or M. bovis, “mycobacteriosis” is used to refer to other nontuberculous mycobacteria
• Humans serve as reservoir for M. tuberculosis which most commonly infects non-human primates (and contact with humans is the primary route of exposure)

PATHOGENESIS:

• Bacteria are inhaled, then enter terminal bronchioles and alveolar spaces
• Cell wall glycolipids and waxes of bacteria help trigger initial macrophage response
• Bacteria are phagocytized by macrophages through interaction with pathogen pattern recognition receptors (PRRs) including complement receptors 1, 3, and 4, mannose, surfactant proteins, LAM, and CD14
• Bacteria are either killed or survive by inhibiting phagosome-lysosome fusion and antimicrobial mechanisms of macrophages
• Bacterial PAMPs activate macrophage PRRs -> more monocyte, macrophage, neutrophil recruitment -> more granulomatous inflammation
• γδ T-cells increased in early M. tuberculosis infection; may help bridge gap between innate and adaptive immune response
• Macrophages cause a delayed type IV hypersensitivity reaction by acting as antigen-presenting cells and secreting IL-12 which causes CD4+ TH1 lymphocytes to secrete IFN-gamma (which activates additional macrophages) and IL-2 (which induces proliferation and survival of T lymphocytes) leading to a cell-mediated immunity → tuberculoid granuloma
• Heavily infected macrophages die off forming the necrotic center
  • Combination of hypoxia and free radical-mediated injury
• Large numbers of organisms lead to extensive cell necrosis and tissue destruction; bacilli may become dormant within caseous center replicate extracellularly in the liquefied material
• In humans and non-human primates, infection can be maintained in a controlled state by the host immune system, spontaneously reactivate, or become reactivated if the host immune system is suppressed by another cause.
  • T-cell response critical for controlling disease
• Natural resistance-associated macrophage protein (Nramp 1 & 2) is a membrane protein involved in innate immunity to M. bovis (in humans and mice) that is primarily expressed in macrophages and tissues of the reticuloendothelial system
• Bacilli are released when tubercles rupture and enter the airways, spreading to other parts of the lung or may be coughed up and swallowed, entering the GI tract
  • Hematogenous spread can occur when a granuloma erodes a vessel wall
  • Leukocyte trafficking is another method of dissemination suggested in some host/species interactions

TYPICAL CLINICAL FINDINGS:

• Anorexia with listlessness, weakness, depression
• Reduced milk production
• Progressive emaciation
• Cutaneous abscesses and peripheral lymphadenopathy
• Hepatomegaly, splenomegaly
• Coughing, exercise intolerance, progressive dyspnea
• Blood smear – In rare systemic infections, bacilli may appear as clear rods within neutrophils or macrophages (do not stain with Wright stain)

TYPICAL GROSS FINDINGS:

• Classic gross lesion: Tubercles that are circumscribed, often encapsulated, tan to yellow foci of granulomatous inflammation with a central core of caseous necrosis and/or mineralization
  • Larger lesions may have a liquid or suppurative core
• Tubercle formation in the lungs is dependent on chronicity of infection—a recent study in NHPs only noted classic pulmonary granulomas within the chronic-active and latent reactivation stages, but not in early-activation or extrapulmonary stages (Pereira AHB, 2022)
• Other lesions depend on the Mycobacterial species, affected species and immune response, route of exposure, and stage of disease and include regional lymph nodes, spleen, liver, kidney, intestine, mesenteric lymph nodes, vertebra, spinal cord, eyes, bone, skin

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Tubercles are the classic lesion: Central core of necrosis with nuclear debris +/- mineral, surrounded by epithelioid macrophages and multi-nucleated giant Langhans cells (fused, activated macrophages), encapsulated by collagenous connective tissue with lymphocytes, plasma cells, +/- neutrophils; acid-fast bacilli variably seen within macrophages or extracellularly
• In elk and deer with M. bovis, suppurative inflammation may be prominent with less fibrosis and giant cells

ULTRASTRUCTURAL FINDINGS:

• Fibrillar, electron-opaque nuclear area
• Periphery is densely filled with ribosomes
• Capsule in close contact with cell wall

ADDITIONAL DIAGNOSTIC TESTS:

• Intradermal tuberculin skin test (eyelid or abdominal skin, I-M01)
• PCR, ELISA
• Special stains: Acid-fast (Fite-Faraco, Ziehl-Nielson) and more recently developed technique: Auramine O and Rhodamine B fluorescent stains
• Culture: Lowenstein-Jensen media, takes 4-8 weeks to culture
  • M. tuberculosis prefers glycerol and is niacin-positive; M. bovis is inhibited by glycerol and is niacin-negative
• TiKa – novel decontamination and culture technique to improve growth (Goosen W.J, J Vet Diagn Invest, 2022)
• Dry loop-mediated isothermal amplification (LAMP) assay: reduces need for cold chain storage, making use ideal for resource-limited diagnostic settings (Kapalamula TF J Vet Diagn Invest. 2023)

DIFFERENTIAL DIAGNOSIS:

• Foreign body granuloma or foreign body pneumonia (granulomatous pneumonia in pigs)
• Cestode cysts
• Pneumonyssus simicola (lung mite): Important differential in macaques
• Bacterial diseases: Nocardiosis, actinomycosis, actinobacillosis, Fusobacterium necrophorum, Mycoplasma bovis, Rhodococcus equi in horses
• Fungal diseases: Cryptococcosis, blastomycosis, aspergillosis, histoplasmosis, coccidiodomycosis

COMPARATIVE PATHOLOGY:

Mycobacterium spp. in other animals:

• MTBC affects old and new world primates
  • M. tuberculosis usually spread from humans; infection with M. bovis also possible
  • NW primates more resistant; may not always form pulmonary granulomas, especially in the early course of the disease
  • OW primates: disease spreads rapidly in captive populations, high morbidity and mortality
    • Cynomolgus monkeys may develop clinically silent disease
  • Non-human primates are also susceptible to M. avium-intracellulare complex (MAIC) and many atypical mycobacteria (M. marinum, M. kansasii, M. lepraemurium)
    • Atypical mycobacteria usually don’t cause clinical disease, but may cause positive intradermal TB tests
• Apes: All ape species susceptible to MTBC pathogens
  • Transmission usually from humans to apes; oral infection from unpasteurized milk fed to infant apes possible as well
  • Clinical course and lesions similar to OW primates
• Cattle: Respiratory and enteric syndromes
  • M. bovis - Pneumonia; extensive caseation and calcification of tubercles; May spread to pleura (hard, white nodules= “pearl disease”)
  • M. avium ss. paratuberculosis - Johne’s disease
• Horse: Usually enteric with lesions in retropharyngeal and mesenteric lymph nodes and intestine; most commonly MAIC, M. tuberculosis, or M. bovis
  • Hematogenous dissemination to lungs possible -> granulomas not caseous or calcified (often resemble sarcomatous nodules)
• Sheep and Goats: Usually respiratory syndrome (granulomatous pneumonia), similar to cattle; M. caprae is most common but M. bovis and MAIC also occur
• Swine: M. bovis, M. tuberculosis and MAIC
  • M. bovis, similar lesions as in cattle
    • Wild boar are considered spillover/dead-end host
      • Boar with higher Porcine circovirus 2 prevalence also have higher M. bovis prevalence and more severe disease
  • MAIC - usually enteric with lesions in retropharyngeal and mesenteric lymph nodes and spreads hematogenously to lungs
• Guinea pigs: Highly susceptible to M. tuberculosis and M. bovis but natural disease is rare
• Hamsters: Documented but rare infection with M. tuberculosis and M. chelonai
• Rabbits: Susceptible to M. bovis and M. tuberculosis but natural infection is rare
  • Prone to develop cavitary pulmonary lesions with dissemination to other organs -> valued as models for human tuberculosis
• Cat/dog: Uncommon; enteric disease in cats, respiratory disease in dogs
  • Cats: Usually M. bovis, M. microti also reported; M. tuberculosis infection is rare
    • Feline ocular mycobacteriosis reported species include M. bovis, M. microti, MTBC, MAIC
    • Feline leprosy – M. lepraemurium, and M. tuberculosis can both cause dermal lesions in cats
    • Recent study on ocular mycrobacterial lesions identified the choroid as the primary site of lesion development (Mitchell JL, Vet Pathol. 2022)
  • Dogs: More susceptible than cats; M. microti also reported
    • Tuberculosis in dogs and cats often appears as granulation tissue; discrete tubercles are uncommon
• Fish: M. marinum, M. fortuitum, M. chelonae, and others
  • Most common chronic disease of aquarium fish (also affects wild fish); infects kidney, spleen, other viscera, skin, bones; not specific to respiratory system (gills)
  • Mycobacterium persistent in biofilms in artificial aquatic systems
• Birds: Usually MAIC, rare reports of M. tuberculosis and other mycobacterial species; usually alimentary disease
• African clawed frogs: M. marinum; sarcoma-like inflammatory response
• Australian marsupials – Highly susceptible, MTBC and MAIC infections reported
  • Brushtail possums in New Zealand are M. bovis reservoir
  • Fibrous encapsulation not a prominent feature of granulomas in marsupials, may allow bacteria to be transmitted more easily
• Elephants: Most commonly M. tuberculosis with rare cases of M. bovis and other MTBC species
  • Both zoonotic and anthropozoonotic infections can occur
  • Infection most often result in pulmonary disease with spread to thoracic lymph nodes; typically chronic sub-clinical disease
• Free ranging rhinos: M. bovis and M. tuberculosis have been reported to cause granulomas in lungs and lymph nodes
  • M. orygis reported in free-ranging Indian rhinoceros
• Hyrax: Specific variant of MTBC called “dassie bacillis” and M. microti-like bacteria reported in some cases
  • Weight loss, lameness, pneumonia, and reproductive failure have been associated with infections; granulomas are found in the lungs, liver, spleen, and kidney
• Mustelids: M. bovis and MAIC
  • Ferrets - Affects spleen, liver, intestines (hepatic lesions most common)
    • Feral ferrets in New Zealand are reservoir host; can amplify and transmit to cattle
  • Badgers – Pulmonary granulomas most common lesion
• Giraffes and non-domestic bovids: Sporadic infection with M. tuberbulosis reported; may be indistinguishable from M. bovis
• M. bovis reservoir hosts in wildlife species include African buffalo, lechwe (antelope), wood bison, white-tailed deer, waipiti, fallow deer, and red deer (cervids may be infected with M. caprae as well)
  • Kudu may act as maintenance host or spillover host
    • Kudu usually get swelling in parotid and submandibular areas with draining fistulae
  • Roe deer may be spillover host
  • Cervids may be infected for years without showing clinical sings, and shed bacteria during that time
    • Red deer identified as supershedders (susceptible and resistant breed lines)
  • Cervids: Tuberculous lesions in lungs, tonsils, several lymph nodes, ileocecal junction
• Camelids: Disease reported more frequently in Old World camelids New World camelids; M. tuberculosis, M. bovis, or other members of tuberculosis complex
  • Giant cells rarely seen in OW camelids but may be seen in M. microti infections in NW camelids
• Carnivores: Red foxes, gray foxes, wolves, coyotes, fennec foxes (captive), black bears, sloth bears (captive)
  • Infection with M. bovis – Transmission may occur by eating infected prey
  • Gross lesions often not seen (need histo or other testing)
  • Wild and captive felids mainly infected with M. bovis
    • Factors related to susceptibility to disease and recrudescence include inbreeding in lion populations and stress or concurrent disease
    • External lesions: Decubital ulcers, alopecia, corneal opacity, elbow and hock hygromas
      • In a recent study, 23% of 61 free-ranging leopards had no observed classic lung granulomas, but verified with histology and acid-fast stain to have mycobacterial pneumonia (Mitchell EP, J Comp Pathol. 2026)
    • Internal lesions: Systemic or granulomatous inflammation in the lung, lymph nodes, spleen, kidneys, adrenal glands, eye, arthritis, osteomyelitis (plus sequelae - pneumothorax, hydrothorax, pleural adhesions)
      • Typical granulomas are uncommon
• Meerkats - M. suricatta and M. microti
  • Spread by grooming (inhalation)
• Mongoose - Nasal lesions from M. mungi
  • Other lesions develop from hematogenous spread
    • Fibrosis is minimal, casesous necrosis in granulomas is variable in lung and lymph node lesions
  • M. bovis lesions in mongoose are typical granulomas
• Prosimians (ring-tailed, ruffed, black, and mongoose lemurs): M. tuberculosis
  • Sub-clinical or disease; clinical disease includes typical granulomatous inflammation or granulomas
  • M. xenopi described in a captive black and white-ruffed lemur with similar extra-pulmonary lesions
• Cetaceans: Diverse species of bacteria, large spectrum of lesions (atypical mycobacteriosis)
  • M. chelonae in a bottle-nosed dolphin
    • Panniculitis with blubber pyogranulomas, necrosuppurative pneumonia and lymphadenitis
  • M. abscessus in a bottle-nosed dolphin
    • Pyogranulomatous pneumonia
  • M. marinum in a beluga whale
    • Ulcerative dermatitis, panniculitis, and chronic proliferative pleuritis
  • Untyped mycobacterium in pygmy sperm whale
    • Pyogranulomatous lymphadenitis
• Pinnipeds - M. pinnepedii (member of MTBC)
  • Clinical disease - poor body condition, 2 main gross presentations:
    • 1 - Granulomatous to pyogranulomatous pleuropneumonia, thoracic lymphadenitis and mediastinitis with pronounced fibrinous or serosanguinous effusion
    • 2 - Multifocal caseating granulomas within the lungs and thoracic lymph nodes
• Captive Sirenia (manatees) - M. marinum, M. fortuitum, M. kansaii, and M. chelonei
  • Typical tuberculoid granulomas in lungs and lymph nodes
    • Lesions in pleura, testicles, skin also possible
• Reptiles and amphibians: Mostly non-tuberculous infections reported in captive reptiles and amphibians, less frequently in free-ranging animals
  • Pulmonary mycobacteriosis common in boids (typical reptilian granulomatous inflammation)

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