JPC SYSTEMIC PATHOLOGY

RESPIRATORY SYSTEM

August 2023

P-B03

 

Signalment (JPC #2019267): 3‑month‑old Yorkshire pig

 

HISTORY: This pig went off feed, developed a hacking cough, and eventually died.

 

HISTOPATHOLOGIC DESCRIPTION: Lung: Multifocally, surrounding bronchi, bronchioles, and blood vessels, infiltrating adjacent alveoli, and expanding adjacent alveolar septa up to 5 times normal, are moderate numbers of lymphocytes, plasma cells, macrophages, and few eosinophils, admixed with fibrin. Bronchi and bronchioles are often either lined by attenuated, cuboidal epithelium devoid of cilia or the epithelium is lost; lumina often contain an exudate composed of amphophilic material (mucus) admixed with sloughed epithelial cells and degenerate inflammatory cells. Peribronchiolar and peribronchial lymphoid tissue (bronchial/bronchiolar-associated lymphoid tissue, BALT) is moderately hyperplastic. Interlobular septa are mildly expanded by increased clear space, pale eosinophilic fluid, mildly dilated lymphatics (edema) and low numbers of lymphocytes, plasma cells, and macrophages. Rarely, there are multinucleated giant cells within alveolar lumina.

 

MORPHOLOGIC DIAGNOSIS: Lung: Bronchointerstitial pneumonia, lymphohistiocytic, moderate, subacute, with bronchiolar-associated lymphoid hyperplasia, Yorkshire, porcine.  

 

ETIOLOGIC DIAGNOSIS: Pulmonary mycoplasmosis

 

CAUSE: Mycoplasma hyopneumoniae 

 

CONDITION: Porcine enzootic pneumonia (PEN)

 

CONDITION SYNONYM: Enzootic pneumonia

 

GENERAL DISCUSSION: 

• Cause of mycoplasmal pneumonia of swine, often known as enzootic pneumonia
• Although pigs as young as 5 weeks of age may develop disease, it is most important in grower-finisher pigs and may be a key component of fatal multifactorial pneumonia in 4- to 6-month-old hogs
• The cell membranes of many mycoplasmas, presumably including M. hyopneumoniae, contain superantigens that induce polyclonal proliferation of lymphocytes and result in the characteristic aggregates of lymphocytes around airways and blood vessels
• Many infections are subclinical, and carrier animals are important sources of infection of naive herds
• Primary M. hyopneumoniae infection is not expected to be fatal, but reduced mucociliary clearance and possibly impaired macrophage function may lead to fatal bacterial pneumonia caused by opportunistic pathogens such as Pasteurella multocida, Streptococcus suis, Bordetella bronchiseptica, or Haemophilus spp.
• Mycoplasmal infection exacerbates the severity and the duration of PRRS, although the effect of PRRSV infection on mycoplasmal pneumonia is apparently minor

 

PATHOGENESIS:

•  Predisposing risk factors increase likelihood of clinical disease (crowding, poor air quality, temperature or humidity changes, stress)
• A molecule called cilium adhesin expressed on the surface of the bacterium appears to be involved in the attachment and binding process, where it is thought to interact with glycosaminoglycan and heparin on cell membranes
• Superantigens that induce polyclonal proliferation of lymphocytes result in aggregates around airways and blood vessels 
• Bacterial inhalation → colonization of ciliated bronchi epithelium via outer-membrane proteins (97- & 145-kDa) → ciliostasis and lysis of ciliated epithelial cells  → neutrophil influx → loss of function (mucociliary apparatus) → cranioventral pneumonia 

 

TYPICAL CLINICAL FINDINGS: 

• High morbidity, low mortality; fatal cases often due to secondary bacterial infections
• Coughing; reduced feed conversion; poor weight gain

 

TYPICAL GROSS FINDINGS:

• Catarrhal to suppurative lobular bronchopneumonia

• Red-tan-gray discoloration, collapse, and rubbery firmness affecting cranioventral regions (“thymus-like”) of the lungs in a lobular pattern
• Pleural surfaces are usually not affected (unless secondary infection)

• Cranial to cranioventral lobes affected; dark red in early stages progressing to homogenous pale grey (“fish-flesh”) in more chronic disease
• Secondary infection by opportunistic bacteria, resulting in red, firm or hard, cranioventral consolidation that appears identical to the bacterial pneumonia that complicates PRRSV, PCV-2, or influenza

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Acute disease: Influx of macrophages and neutrophils into the bronchi, bronchioles and alveoli
• Subacute to chronic disease: Extensive BALT hyperplasia, increased numbers of alveolar macrophages, lymphocytes infiltrate the lamina propria of the airway mucosa, and alveolar edema
• Accumulation of exudate can occlude bronchioles with secondary atelectasis
• Goblet cells in the airway mucosa are increased in number, bronchial glands are hyperplastic 

 

ULTRASTRUCTURAL FINDINGS:

• Small, pleomorphic bacteria, lack cell walls, membrane-bound organelles, fimbria, and flagella
• Large numbers of mycoplasma attached to and damaging cilia

• Distorted, broken, and lost cilia with basal body degeneration
• Ballooning and blebbing of epithelial cell plasma membranes 

 

ADDITIONAL DIAGNOSTIC TESTS:

• Isolation and culture difficult due to fastidious growth requirements
• More sensitive by immunohistochemistry, or detection of M. hyopneumoniae DNA by PCR using lung tissue, nasal swabs, or transtracheal washes
• Detection of serum antibody by ELISA is a useful method of confirming prior exposure, or validating the M. hyopneumoniae–free status of minimal-disease herds

 

DIFFERENTIAL DIAGNOSIS:

Primary porcine pneumonias: 

• Mycoplasma hyopneumoniae 
• Porcine reproductive and respiratory syndrome virus (P-V25, genus Arterivirus): Causes interstitial pneumonitis in neonatal pigs, macrophage infiltrate in alveolar septa, and alveolar spaces filled with necrotic cells and proteinaceous exudates; little to no airway epithelial damage
• Swine influenza A virus (P-V18): Extensive necrotizing bronchiolitis and bronchitis, peribronchiolar mononuclear cuffs, migration of cells into airways, type II pneumocyte hyperplasia, and serofibrinous exudate in alveoli
• Postweaning Multisystemic Wasting Syndrome (Porcine circovirus 2, H-V11):   Granulomatous to lymphohistiocytic interstitial pneumonia with BALT depletion, with or without intracytoplasmic inclusion bodies and bronchiolar epithelial necrosis
• Actinobacillus pleuropneumoniae (P-B04): Fibrinonecrotic pleuropneumonia with caudal dorsal distribution
• Pasteurella multocida: Suppurative bronchopneumonia usually without pleuritis
• Salmonella choleraesuis: Pulmonary consolidation or fibrinonecrotic pneumonia with prominent extrathoracic lesions, especially necrotizing hepatitis, but also splenomegaly, lymphadenopathy, colitis, and cutaneous hyperemia
• Bordetella bronchiseptica (P-B09): Suppurative bronchitis with peribronchiolar fibrosis affecting suckling pigs
• Porcine respiratory coronavirus (PRCV): Necrotizing and proliferative bronchointerstitial pneumonia with squamous metaplasia, type II hyperplasia

 

COMPARATIVE PATHOLOGY:

Swine:

• M. hyorhinis: Fibrinous polyserositis and polyarthritis in weanling pigs
• M. hyosynoviae: Fibrinous polyarthritis in pigs >3 months old

Cattle:

• M. mycoides subsp. mycoides (small colony type) (P-B02): Contagious bovine pleuropneumonia
• M. bovis: Chronic pneumonia and polyarthritis in feedlot cattle; enzootic pneumonia of young dairy & veal calves; Mycoplasmal mastitis in cows
• M. bovigenitalium: Associated with bovine granular venereal disease
• Ureaplasma diversum: Reproductive failure in cattle (vulvitis, embryonic death, abortion, stillborn or weak calves)

Goats/Sheep:

• M. capricolum subsp. capripneumoniae: Contagious caprine pleuropneumonia
• M. mycoides subsp. capri: Mastitis; polyarthritis; pleuropneumonia

• M. mycoides subsp. mycoides (large colony type) nomenclature has been discarded and is now considered a serotype of M. mycoides subsp. Capri; pleuropneumonia, polyarthritis, and septicemia in kids, lambs; mastitis in does/ewes

Horses:

Rodents:

Dogs:

Avian:

• M. gallisepticum: Chronic respiratory disease in turkeys and chickens; sinusitis in turkeys; conjunctivitis in finches
• M. meleagridis: Air sacculitis, decreased egg hatchability
• M. synoviae: Infectious synovitis, sternal bursitis, air sacculitis; chickens, turkeys
• M. iowae: Reduced egg hatchability, late term embryo mortality in turkeys

Mycoplasmosis in Reptiles:

• Turtles/tortoises: Rhinitis with mucopurulent nasal discharge, conjunctivitis, and ocular discharge

• Alligators/crocodiles: Pneumonia and arthritis

 

REFERENCES:

1. Balestrin E, Wolf JM, Wolf LM, et. al. Molecular detection of respiratory coinfections in pig herds with enzootic pneumonia: a survey in Brazil. J Vet Diagn Invest. 2022;34(2):310-313.
2. Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents and Rabbits. Ames, IA: John Wiley & Sons, Inc.; 2016: 63-65,134-136.
3. Caswell JL, et al.  Respiratory system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 2. 6^th ed. St. Louis, MO: Elsevier; 2016: 534-535, 551, 563-564, 573, 579. 
4. Conley KJ, Shilton CM. Crocodilia. Terio KA et al., eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018: 861.
5. Fulton RM, et al. Bacterial Diseases. In: Boulianne M, et al, eds. Avian Disease Manual. 7th ed. Jacksonville, FL: American Association of Avian Pathologists; 2013: 203-221.
6. Jimenez Martinez MA et al. Suidae and Tayassuidae. Terio KA et al., eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018: 217-218.
7. Lopez A, et al. Respiratory System, Thoracic Cavities, Mediastinum, and Pleurae. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7^th ed. St. Louis, MO: Elsevier; 2022: 626-628.
8. Rodríguez CE, et al. Chelonia. In: Terio KA et al., eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018: 843.
9. Schlafer DH, Foster RA. Female Genital System. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier; 2016: 411.
10. Zachary JF. Mechanisms of microbial infections. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7^th ed. St. Louis, MO: Elsevier; 2022: 217-218.

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