Rhodococcus equi infection in Angora goats
By Dr Mackie Hobson BSc(Agric),BVSc

1. Diseases

Rhodococcus (previously Corynebacterium) equi infection is associated with horses. Very rarely it is associated with other species like goats, cattle, sheep and pigs. Cases in horses in the Karoo (Colesberg) have been detected since 1957. Rhodococcus equi was diagnosed in Angora goats through culture liver lesions by Dr Louw in Feb 23. The infection may be more common than we think as the lesion’s appearance very similar to Corynebacterium pseudotuberculosis (previously ovis) abscesses.

Hepatic necrobacillosis occurs most commonly following naval infection in kids or as a complication of rumenitis in adult goats, where bacteria invade the bloodstream at the primary site of infection (umbilicus/rumen) becoming bacteremic with bacterial septicemia and seeding of the liver.
Fusobacterium necrophorum involve various bacterial toxins leading to the prominent abscess-inducing capabilities. Mixed infections with other bacteria are frequent, and synergism between F. necrophorum and other pathogens, such as Truperella pyogenes, may also contribute to the pathogenesis of liver necrosis and abscess formation.

Where does Rhodococcus equi occur?

It can be isolated from faeces and soil previously contaminated by faeces. It can survive for over a year in soil exposed to sunlight. It can also survive without multiplication in transit through intestines of non-susceptible animals. Manure and dust build up contamination over years and so the infection becomes endemic on some farms. It is usually oral transmitted but can occur by inhaling contaminated dust. It has a predilection for lungs and lymphoid tissue (especially large intestine)

How does the bacterial infection develop?

Rhodococcus equi enters intestinal mucosa. Lung lesions may develop through inhalation or from secondary lesions when organisms are disseminated via intestinal lymph nodes and thoracic ducts. The immune response and immunity determines the outcome of the infection (age, stress, concurrent infections, and extent of exposure).

Clinical signs

The incubation period is unknown but may be in region of weeks before signs appear. In foals the lungs are most commonly affected followed by the intestine (caecum, colon) and regional lymph nodes. More widespread involvement of organs and tissues may occur. The mortality rate is high.

Clinical signs are not always shown but possibly:

• Listless
• Lung tissue- respiratory sounds
• Fever
• If the liver is badly effected ataxia and depression due to hepatic encephalopathy may occur
• Endocarditis
• Lameness- suppurative arthritis
• Regional lymphadenitis
• Weight loss
• Diarrhoea

Post Mortem

• Often lung lesions
• Caseous foci resembling abscess (a few mm diam to 100mm in chronic cases) of organs, liver.

Liver lesions

• Content of lesions may be fluid, slimy or inspissated with a colour from whitish-yellow to grey-yellow, green.
• Intestinal lesions may be ulcerative in caecum and colon.
• Pyogranulomatous lesions of mesenteric lymph nodes.

Rhodococcus lesion- ribs

Diagnosis

Culture (aerobic, anaerobic) and ID from lesion

Control

Colostrum intake, immunity (nutrition, stress factors) Hygienic environment Prolonged use of antibiotic (4-9 weeks) in valuable animals post culture (examples in previous culture sensitive to Chloramphenicol, Sulphamethoxazole/ Trimethoprim but resistant to the penicillins)

REFERENCES
Infectious Diseases of Livestock J. Coetzer,G. Thomson, R. Tustin
Dr R. Last -Vetdiagnostix
Dr Juan Louw (Bosberg Vets)