Nocardiosis occurs in several animal species and is an acute, subacute or chronic disease characterized by focal or disseminated, suppurative or granulomatous lesions caused by infection with Nocardia asteroides or, less commonly, Nocardia otitidiscaviarum or Nocardia brasiliensis. Mastitis (cattle and goats), abortion (cattle, pigs, sheep and horses), corneal ulceration and chronic dermatitis (cattle), and often fatal, disseminated, granulomatous disease or granulomatous pneumonia (cattle and horses), have been recorded. Disease caused by Nocardia spp. has been reported from various countries in the world, but is sporadic and, except when associated with rare outbreaks, of little economic importance.

The first recorded cases of nocardiosis were reported from cattle with farcy on the island of Guadeloupe in the French West Indies, by Nocard in 1888.29 Bovine farcy characterized by a pyogranulomatous lymphangitis and lymphadenitis of the lower limbs was common in France at the end of the nineteenth century, but has since disappeared. Nocardia farcinica, the original isolate from bovine farcy, is now known to be represented by two strains—one indistinguishable from Nocardia asteroides, and the other a Mycobacterium- like strain.15

In South Africa nocardial infections are mainly seen in dogs (most frequently in the form of a pyogranulomatous pleuritis) and rarely as a cause of mastitis and abortion in cattle.16

Aetiology and epidemiology

The informal term, nocardioform, signifies Actinomycetes that form a Gram-positive fugaceous mycelium and reproduce by breaking up into rod-shaped or coccal elements. Both the pathogenic nocardioform Actinomycetes (Nocardia and Rhodococcus) and the non-pathogenic Actinomycetes (such as Oerskovia, Nocardioides, and Promicromonospora) are soil inhabitants. Members of the genus Nocardia are aerobic, catalase-positive, and their cell wall (type IV) contains large amounts of meso-diaminopimelic acid (meso-DAP), arabinose, and galactose.15 Mycobacterium, Rhodococcus, and Corynebacterium also have a type IV cell wall, but these genera are distinguished from Nocardia by differences in their respective mycolic acids, ribotyping or PCR-restriction enzyme pattern analysis.24, 48 Nocardia spp. grow best on blood agar, Loewenstein-Jensen or brain-heart infusion agar. Chloramphenicol should not be added to the medium. The colonies are orange, glabrous, heaped and folded, or may be white or pink with aerial hyphae. The colonies are dry and crumbly and are adherent.20

Nocardia spp. occur widely in soil.32 Nocardia asteroides grows over a wide temperature range and is resistant to 50 °C for several hours, but all Nocardia spp. are inactivated by pasteurization. Various serotypes (I to IV) of N. asteroides, differentiated by immunoprecipitation, have been recorded.38

African cattle breeds appear to be fairly resistant to skin infections. When they do occur these infections may be spread by Amblyomma variegatum ticks.31 Transstadial transmission by ticks has been demonstrated experimentally.3

Localized, subcutaneous infections also develop after injury to the skin, and pulmonary infections result from inhalation of the organism. Systemic nocardiosis results from a primary focus, usually the lungs. External contamination of the vulva with soil may cause a localized infection of the uterus, and abortion.12

Nocardial mastitis, which may occur as sporadic individual cases or as isolated outbreaks in cattle, usually results from infection via the teat canal by contaminated intramammary infusions used for mastitis therapy17, 25, 45 or from the environment, if heavily infected.13, 14 Concomitant infections with other pathogens such as Staphylococcus aureus, Trueperella (Corynebacterium) pyogenes and Pseudomonas aeruginosa may be present.16


Scant data exist on the pathogenesis of nocardiosis. Delayed hypersensitivity reactions may be associated with the development of the lesions. In experimental infections, a delayed hypersensitivity reaction and the inhibition of migration of those inflammatory cells present in the peritoneal exudate have been demonstrated33, 34 as soon as one week after the initial infection. These responses coincide with the appearance of the initial lesion, which is an abscess. The response reaches its maximum after two weeks, when the central suppurative reaction becomes surrounded by epithelioid and giant cells.18

Clinical signs


Acute, chronic or subclinical mastitis has been reported.45 At the onset of the mastitis, one or all the quarters are swollen and the milk may be pinkish.>1 This is eventually followed by induration of the udder.44 Blackish spots, crusts and nodules, which may rupture and exude a thick pus, are present on the affected parts of the udder.2

The milk yield of affected animals is severely reduced. In chronic cases, the granulomatous lesions may cause obstruction of the lactiferous ducts, and extensive fibrosis and draining sinuses may develop.5, 22 Acutely affected animals may die or have to be culled. Severe cases may succumb within 12 hours of the clinical signs first being noticed,17 and the mortality rate may be as high as 10 per cent.45

Abortions may occur at six to eight months of gestation16, 27, 49 in clinically healthy cows.49

A number of rare syndromes include a severe, progressive dermatitis in...

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