In small ruminants, C. pseudotuberculosis causes a disease called caseous lymphadenitis, which is characterized by pyogranulomatous abscess formation.

This bacterium uses the virulence factors phospholipase D and mycolic acid to damage eukaryotic cell walls and resist phagocytic lysosomal degradation, respectively.

[1] C. pseudotuberculosis also causes disease in horses, and it should be considered prevalent in areas where cases of "pigeon fever" and "ulcerative lymphadenitis" have been recorded.

It forms dry, pale yellow colonies measuring 1–2 mm in diameter after incubation on solid media for 48 hours.

[5] While strains of C. pseudotuberculosis are consistent in their morphology and growth on media, they show greater variation in biochemical properties such as fermenting ability.

[6] A multiplex polymerase chain reaction assay has been developed using a number of characteristic genes that can differentiate between the closely related species of corynebacteria – C. pseudotuberculosis, C. ulcerans, and C.

[8] C. pseudotuberculosis causes a disease known as caseous lymphadenitis that most commonly affects small ruminants, such as goats and sheep.

[11] Abscessation can occur in numerous areas, but it most commonly affects the cutaneous region and superficial lymph nodes.

[11] The internal manifestation of the disease is harder to recognize, as the clinical signs are not as obvious, but may include a reduction in reproductive ability and diminished body condition.

[13] C. pseudotuberculosis can also cause disease in horses, which also present with abscessation, but the lesions are most commonly seen on the underside of the abdomenal and pectoral regions.

[13] Diagnosis of C. pseudotuberculosis can be difficult due to vague clinical signs such as weight loss and general ill thrift.

[12][clarification needed] Confirming diagnosis in animals infected with the internal form of the disease is more difficult, but ultrasonography or radiography may be useful.

[15] Studies that examine the absence or mutation of the phospholipase D gene in C. pseudotuberculosis–infected mice have been shown to fail to develop chronic abscessation.

[20] The importance of this virulence factor has also been highlighted where mice that have been injected with mycolic acid were shown to produce a chronic abscessation that increased with higher doses.

[21] Superoxide dismutase is involved in evading the immune system by deactivating reactive chemicals secreted by the body that would otherwise kill the bacterial cell.

[15][23] Strains of C. pseudotuberculosis have shown to be susceptible to numerous antimicrobial therapies in vitro, including ampicillin, gentamicin, tetracycline, lincomycin, chloramphenicol, and others.

Treatment within live animals (in vivo) is thought to be limited due to the firm capsule and thick, caseous nature of the abscess lesions, which make them a difficult target for antimicrobial therapy.

[23] A vaccine using a recombinant form of the phospholipase D exotoxin is now in widespread use, and has been shown to decrease the occurrence of lung lesions and amount of tissue damage observed upon infection.

[17][neutrality is disputed] With antimicrobial therapy and vaccination protocols being somewhat limited, proper management practices are highly recommended for controlling caseous lymphadenitis.

[25] Good husbandry practices can decrease the occurrence and spread of caseous lymphadenitis among small ruminants, improving animal health and minimizing economic impacts on the producers.

C. pseudotuberculosis can persist on fomites such as straw bedding, hay, wood, and feces for weeks, and in the soil for up to eight months, making proper disinfection of facilities and pasture management essential to limit disease spread.