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This article was published in 1967
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Brucella ovis Infection
K. L. HUGHES, M.V.Sc., Department of Veterinary Medicine, University of Sydney, Camden, New South Wales
The earliest report of infection with the organism now known as Brucella ovis stems from New Zealand, although in this initial description the disease condition was first mistaken for one caused by a psittacosis lymphogranuloma agent, similar to that which had been implicated as the causal factor of enzootic abortion of ewes in Scotland. However, in follow-up investigations a bacterium was later isolated from ram genitalia, and which, when inoculated into pregnant ewes, produced in foetal membranes pathological changes indistinguishable from abnormal placentae recovered from ewes lambing in the field. Later, both Australian (Simmons and Hall, 1953) and New Zealand (Buddle and Boyes, 1953) workers described the detailed bacteriology of the causal agent.
While there is still some argument as to its taxonomic validity, since its original isolation Br. ovis has been incriminated as a specific cause of epididymitis in rams, placentitis in ewes and neonatal death of infected lambs.
Infections in Rams
Following infection with Br. ovis a mild inflammatory response occurs around bacteria localised in the tail of the epididymis.
Macroscopic lesions caused directly by the organism are rarely evident, but the end result of infection is often the formation of spermatic granulomata in one or both epididymides. These may resemble abscess formation and if extravasated sperm enter the cavity lined by tunica vaginalis a severe inflammatory response with resultant adhesions may be produced. Extensive fibrosis may be produced also in the tail of the epididymis. Other features such as testicular degeneration, calcification and hypertrophy of the epididymis proximal to the primary lesion are common sequelae.
Passive venereal transmission during mating and passive infection during the act of sodomy are believed to be the two main methods of spread from ram to ram. Artificial infection has been produced by administration of the virulent Br. ovis by the intravenous, intra-testicular, intra-epididymal, intra-preputial, supra-conjunctival, subcutaneous and oral routes, although infection by either of the last two routes has often been difficult to demonstrate.
About 10-14 days after intravenous infection with virulent organisms antibody to Br. ovis may be detected by a CF test conducted on serum of the rams. Those rams which become infected may first excrete the organism some 3-8 weeks after experimental inoculation. Palpable lesions usually develop within 5-17 weeks following natural infection or artificial infection by intravenous or intra-preputial inoculation of virulent organisms. Some rams may excrete Br. ovis in the semen for months or years without developing detectable palpable lesions in the external genitalia. Whether these rams ultimately develop lesions or whether they remain silent excreters indefinitely is problematical. Some workers consider the latter to be a distinct possibility.
Br. ovis is of relatively low virulence and usually produces a chronic reaction. However, an acute form has been seen in experimentally infected rams and more rarely in natural infection.
Testing for serum CF antibodies to Br. ovis, culture of ram semen, microscopic examination of MZN stained semen smears, and palpation of the external genitalia have all been used as methods to detect infection with Br. ovis. The CF test is highly reliable and it has been employed extensively to eradicate Br. ovis infection from King and Flinders islands. In eradication programmes it is preferable to commence the culling of rams reacting to the CF test at the conclusion of mating. False positive and false negative reactions are relatively uncommon. Vaccination against Br. ovis infection is permissible in some states and not in others. Where vaccination has been practised, vaccination titres may persist for some time and confusion may arise when vaccinated rams are transported to a state where vaccination is not permitted. Initially, a killed Br. ovis saline-in-oil adjuvant vaccine, given at different sites simultaneously with strain 19. was used but it is now accepted that two treatments of the saline-in-oil vaccine given eight weeks apart will provide comparable protection (Buddle, 1962).
Examination of semen by culture and smear methods alone will often fail to detect rams with a positive CF titre. This is particularly the case in rams very early in infection and in rams with old lesions. In the latter culture of seminal vesicles may sometimes be rewarding. Intermittent excretion of Br. ovis may further limit the value of smear and cultural methods. Smear methods alone would appear to be slightly inferior to culture.
In a recent first examination of 123 flock rams with recognised Br. ovis infection (Hughes and Claxton, 1967) the following results were obtained:
| CF Test | Culture | Smear | Palpation | |
|---|---|---|---|---|
| Recognised | 98.4% (121) | 66.7% (82) | 60.2% (74) | 40.7% (50) |
| Not Recognised | 1.6% (2) | 33.3% (41) | 39.8% (49) | 59.3% (73) |
| Total 123 | ||||
Although palpation methods should be regarded as non-specific, the number of rams with clinical lesions has been shown for comparison.
Gunn et al. (1942) drew attention to the prevalence of occurrence of "epididymitis with spermatocele" in a large sample of rams examined in N.S.W. and Queensland, and noted that degenerative changes were evident in the semen of many of the rams with lesions. Subsequently, the practice of examining the external genitalia of rams was adopted by veterinarians as a technique for the detection of infertile rams. Most of the available evidence indicates that in general rams with Br. ovis infection have lowered fertility but some individual rams may be quite fertile. Effects due to lowered fertility of infected flock rams are probably disguised by over-mating.
The following may also be incriminated as a cause of palpable lesions in ram external genitalia:
Actinobacillus seminis
Pasteurella pseudotuberculosis
Corynebacterium ovis
Corynebacterium pyogenes
An unclassified gram negative pleomorphic bacillus (Dodd and Hartley, 1955; Claxton and Everett, 1966.)
Cysticercus tenuicollis
Sertoli cell neoplasia, cystic condition of the epididymis, trauma and vasectomy.
Infection in Ewes
Contrary to popular belief abortion "storms" due to Br. ovis infection are not a common finding and abortions due to this bacterium are usually of a sporadic nature in individual ewes. However, absence of even sporadic abortions should not be taken as an indication of the absence of Br. ovis infection.
Both natural and experimental infection of ewes may result in a placentitis of variable severity. The foetal membranes appear thickened with gross gelatinous oedema of the chorioallantois; yellow-white necrotic cotyledons may be present and in the area between the cotyledons similarly coloured plaques often may be found. Br. ovis may be seen in MZN stained cotyledon smears and the organism can be cultured directly from abnormal cotyledons and occasionally from foetal membranes which appear macroscopically normal. Br. ovis also may be recovered from the vaginal discharge and milk of aborting ewes. Abortions have been recorded from the fortieth day of gestation to term.
Natural infection has been demonstrated following mating of clean ewes with infected rams, but only two of 25 ewes gave birth to dead lambs and infected membranes (Buddle, 1955). Both ewes also developed serum agglutinin titres after infection. Carry-over of infection from one season to another has been recorded but this appears to be rare. Natural transmission from ewe to ewe in the absence of rams has been demonstrated and oral infection from contaminated pasture would appear to be of little importance. CF titres may develop in ewes after mating with infected rams and these usually vanish completely after parturition. However, titres may persist for three years or more in some cases. There is only fragmentary evidence that fertility of ewes may be impaired following infection.
In one field experiment conducted in U.S.A. (McGowan and Shultz, 1956) two similar ewe flocks were mated to two groups of rams, with and without palpable epididymal lesions. The overall reproductive efficiency was similar in two groups but ewes mated to affected rams lambed over a longer period, suggesting that in this group there was a higher return to service rate during mating. Lowered fertility of the affected rams was probably an important factor.
Neonatal Mortality of Lambs
Naturally or experimentally infected ewes may give birth to dead lambs associated with grossly diseased placentae. Infected lambs are often small and light for gestational age and immature lambs may be born completely enclosed in their foetal membranes. Br. ovis may be recovered from the stomach contents, lungs and other organs of affected lambs. Post-mortem features are not remarkable. Foot plaques or hyperkeratosis of the ventral aspects of the hooves are often seen in lambs from which Br. ovis can be isolated.
There are about five reports of congenital Br. ovis infection in lambs in Australia, mostly at a low incidence and associated with abortion and premature birth. Rickard-Bell (1963) reported that on one N.S.W. property 2 per cent of lambs born to 1000 ewes were associated with placentitis and Br. ovis-like organisms were demonstrated in smears of cotyledons and abomasal contents. He also recognised similar organisms in smears made from material taken from an unspecified number of postpartum deaths. This is not a common finding, although CF antibodies may be detected in lambs born of infected ewes. Foetal antibody has also been demonstrated in some cases.
In 1963 congenital Br. ovis infection was demonstrated in laboratory specimens taken from 11 lamb carcases collected from 15 flocks in the Oberon-Orange area (Hughes et al. 1964). Infected lambs came from five flocks. Premating examination in 1964 of the rams of all 15 flocks indicated that seven ram flocks were clean and eight infected. In only four of these eight infected flocks was congenital infection demonstrated in the previous year. One infected carcase originated from a flock which had no demonstrably infected rams at the pre-mating examination in 1964.
The number of lamb carcasses per flock examined in the laboratory is a critical factor in determining flock status in relation to congenital infection. The evidence suggests that although congenital Br. ovis infection may be widespread at a low level of incidence it is not of major economic importance as a cause of perinatal lamb mortality. Within individual flocks Br. ovis infection may contribute significantly to perinatal lamb mortality and it should also be remembered that Br. ovis is only one of the pathogens which may be recovered from dead lambs and their associated foetal membranes.
REFERENCES
Buddle, M. B. (1955) — N.Z. vert. J. 3:10
Buddle, M. B. (1962) — NZ. vet. J. 10:111
Buddle, M. B. and Boyes, Betty W. (1953) — Aust. vet. J. 29:145
Claxton, P.D. and Everett, R. E. (1966) — Aust. vet. J. 42:457
Dodd, D. C. and Hartley, W. J. (1955) — NZ vet. J. 3:105
Gunn, R. M. C., Sanders, R. N. and Granger, W. (1942) — Bull. Counc. sci. industr. Res. Aust No. 148
Hughes, K. L. and Claxton, P. D. (1967) — Aust. vet. J. In press
Hughes, K. L. Hartley, W. J. Haughey, K. G. and McFarlane, D. (1964) — Proceedings of the Australian Society of Animal Production 5:92
McGowan, B. and Schultz, G. (1956) — Cornell Vet. 46:277
Rickard Bell, L. (1963) — Aust. vet. J. 39:409
Simmons, G. C. and Hall, W. T. K. (1953) — Aust. vet. J. 29:33