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This article was published in 1978
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Actinobacillus seminis Infection in Rams
J. Evers, B.V.Sc., Veterinary Inspector, Narrandera
This brief resume is intended to give some information on the epidemiological and clinical features of A seminis infection of rams as well as some idea of an approach to the problem as encountered in the field.
The disease itself is not yet well-characterised, although significant progress has been made over the past 10 years. There is certainly enough information available to allow its differentiation from other causes of Epididymitis in rams and probably assess its economic importance. Control or eradication of the disease is, however, not yet possible for a number of reasons, on which I will comment later.
1. THE ORGANISM
Historically, A. seminis has been under scrutiny for some 20 years as a cause of Epididymitis in rams. First reports described a Gram-negative pleomorph as a cause of suppurative epididymitis and being classified as Histophilus ovis. This early work was done in both N.Z. and Australia.
A little later the name Actinobacillus seminis starts cropping up in the work of several researchers - e.g. Baynes and Simmons in Queensland (1960).
More recently, van Tonder has attempted to clarify the issue by looking at the Actino epididymitis problem as being caused by a gram negative organism which may be any one of the following:
Actinobacillus seminis - 4 sub-types,
Histophilus ovis - 2 sub-types.
This may help to explain the variable clinical features seen by different workers. It should also be noted that Actino lignieresi has been reported as a cause of Ovine Epididymitis in N.S.W.
The main focus of research into the Actino seminis problem now appears to be South Africa, where van Tonder has done much to clarify epidemiological features.
2. EPIDEMIOLOGICAL FEATURES Infection with A. seminis has been described in many breeds of sheep, and occasionally in goats and bulls in South Africa. However, van Tonder sees it as a major problem in young stud Merino rams.
In Australia, scattered reports occur. Where problems have been encountered, it has usually been a Stud situation and most of these have involved Border Leicester rams. In commerical/flock rams, only odd clinical cases are seen in all breeds.
Van Tonder postulates that the disease exists sub-clinically in rams and under certain Stud management practices the clinical form becomes evident. The main predisposing factor appears to be a high plane of nutrition leading to rapid growth and early maturity. It is in hogget and 2-tooth rams that clinical outbreaks tend to occur.
Van Tonder further proposes two modes of transmission in a flock:—
a. Horizontal - by infected rams serving ewes. This leads to a vaginitis and cervicitis and possibly regional lymphadenitis.
b. Vertical - as a direct result of (a), foetuses can be shown to harbour the organism in kidneys, bladder, gonads and vagina by about 3 months gestation.
Some abortions and stillbirths do occur. Surviving ewe and ram lambs remain sub-clinically infected - ewe lambs for as long as 22 months, and ram lambs for perhaps a lesser period.
It is tempting to guess that this subclinical infection will terminate in rams in the absence of early maturation. Where the gonads do mature early, it readily persists and these rams remain as either latent or clinical carriers - probably for life.
Infected ewes continue to give birth to latent carriers of the disease.
It would appear that vertical transmission may be the important factor in maintaining infection in a flock. The horizontal spread from infected rams 'keeps the pot boiling', so to speak , but also facilitates the spread of infection to clean flocks.
3. CLINICAL FEATURES
In my experience, the epididymitis seen is indistinguishable from that caused by earlier cases of Brucella ovis. However, certain features may help to clarify the situation:
a. Sudden onset of epididymal lesions - van Tonder claims this can be literally seen 'overnight'.
b. Few cases appear to progress to the massive epididymal enlargement/testicular atrophy seen in advanced cases of Brucellosis.
c. Perhaps a higher frequency of involvement of the head of the epididymis than might be expected with B. ovis.
d. Increased incidence of soft, hypoplastic testes and fine adhesions between the tail of the epididymis and testes.
e. Rapid regression of clinical cases of epididymitis - this does not occur with B.ovis.
I would emphasise that these are my own field impressions.
4. DIAGNOSIS
Absolute confirmation of infection with A. seminis can be difficult. However, the elimination of Brucella ovis as a possible cause of clinical epididymitis is the first step.
If numbers of rams in the younger age group are affected, then clinical features can all but clinch the diagnosis - particularly, I feel, if the rams are run under Stud conditions. In Border Leicesters I have sometimes not even bothered with laboratory aids.
It is perhaps the odd clinical case which poses the big problem. Two methods may allow confirmation:
a. Semen smears and culture - observation of organisms and typing on culture is the best method of confirmation. For subclinical cases it is the only reliable method. However, culture techniques are in need of further refinement at most diagnostic institutions, and the organism is inherently difficult to work with. An added complication is the blockage of the epididymis in advanced clinical cases, in which seminal excretion does not occur.
b. Serology - a Complement Fixation Test is available, but its accuracy leaves much to be desired. The presence of multiple antigenic strains in the field is probably responsible to some degree for this situation.
A titre of 20 may be regarded as indicative of infection in the presence of lesions. In subclinical rams, a titre of 10 should be looked for. In ewes serology is totally unreliable.
As an example, van Tonder lists results for a group of 31 sale rams from an infected stud:
No. Clinical cases - 3.
No. A. seminis isolated -22
No. C.F.T. >20 - 9.
The important point to remember is that identification of the flock problem is your objective; not the identification of individual infected rams. This is where most seem to get into trouble with serological interpretations.
5. ECONOMIC IMPORTANCE
There is no doubt that B. ovis is the major infectious cause of epididymitis in local rams. At present, A. seminis epididymitis appears to be a scattered problem which occasionally assumes economic importance as a cause of ram wastage in some Stud flocks.
Is it an emerging problem? Currently, increased interest in the problem may give an impression of a growing prevalence, on the other hand it may have been with us all along.
Comments of several Regional Diagnostic Centres are as follows:—
a. Armidale - A. seminis and B. ovis constitute sporadic problems of no economic significance. Only one outbreak was seen, this being in Border Leicester yearling rams.
b. Wagga - A. seminis constitutes a minor cause of epididymitis. Serologically, only 2.2% of 4,200 sera tested gave titres >20.
Unlike the South African situation, it does not appear to be a significant problem in our Merino studs. In British breeds, the following outbreaks were recorded in my area over the past two years:
PROPERTY 1.
Border Leicester Stud - 16 yearling rams culled by management for palpable lesions; all B. ovis negative; A. seminis C.F.T's 5 x 40, 4 x 20, 1 x 10, 6 negative.
The genitalia were taken from 4 of the 5 positives 6 weeks later, at which time palpable lesions had almost completely regressed in 1 ram.
The titre from the ram showing regression of lesions was then found negative, but a light growth of A. seminis recovered from the tail of the epididymis. The other 3 rams gave positive cultures from seminal vesicles and epididymii.
PROPERTY 2.
Poll Dorset Stud. A. seminis titres from 10 to 40; Brucellosis negative; hypoplasia of testicles.
Six rams with titres were semen sampled - 2 yielded B. ovis on culture.
PROPERTY 3.
Border Leicester Stud - tested regularly and Brucellosis negative; 3 positive (40) and 3 doubtful (10) in absence of lesions to Brucella C.F.T.; 7 weeks later 4 of these 6 rams were positive on palpation and negative on serology; a further 8 weeks later all were negative on serology and only 1 had lesions - it was then culled. No A. seminis serology was performed.
Other odd cases have been recorded in the area, and one Corriedale Stud does claim to cull 1 - 2% rams per year on A. seminis lesions. The organism has been recovered from some of these cases, including 1 ram which had undergone extensive treatment with broad spectrum antibiotics.
6. CONTROL MEASURES.
In the absence of B. ovis titres, palpation and culling of clinical cases is the only measure available. Reliance on serology is likely to cause a shambles and decimate a Stud flock. Culture from large numbers of semen samples doesn't impress as a practical approach in most situations. For confirmation of A. seminis infection in the first instance, I prefer submission of genitalia to semen samples when an owner is willing to make the sacrifice.
Premature culling of rams with lesions may be a serious cause of economic loss - I now prefer to segregate such clinicals and only cull after a re-examination 3 months later. In other words, cull on breeding soundness not A. seminis infection - there's little point in the latter course when you appreciate the extent of flock infection.
Modification of management procedures may be a method of reducing further incidence of clinical cases in some flocks. It is unlikely to appeal to owners, though, when 'good, big stretch rams' are fetching premium prices.
Attempts at identifying and culling 'carrier' ewes are definitely contra-indicated at present.
7. CONCLUSION
There is not a lot we can do for studs afflicted with A. seminis infection at present. We can identify the problem and give some idea of predisposing factors. More importantly, we can advise on a rational approach to the culling of rams with Epididymitis and avoid unnecessary wastage of sound animals.