Leptospira spp are spirochaetes, which infect a wide range of hosts. There are quite a few species and serovars and each serovar tends to have a restricted host range.
Nomenclature of leptospires is a typical example of out-of-control taxonomists so I will refer to L pomona and L hardjo as if that were the names of the particular serovars.
Leptospirosis became a serious disease of cattle during the early 1970's, at which time it was also a significant zoonotic infection. After several years, leptospirosis became a less significant disease of cattle to the point of being a very rare diagnosis although it has remained a sporadic human infection.
Seddon (1953) reported that leptospirosis, particularly L pomona was a cause of icterohaemoglobinuria in calves and that it occurred in all mainland states.
Hoare and Claxton (1972) reported that L hardjo had been identified as a cause of a novel syndrome in dairy cattle in the Illawarra, Moss Vale and Camden districts during late 1969. The syndrome comprised of fever, inappetance and reluctance to move with a marked (50-90%) drop in milk production. The udders of affected animals had no sign of swelling or inflammation but the milk sometimes contained yellow slimy clots.
Subsequent to these incidents, some 5-10% of affected cows aborted. The authors reported that this syndrome seemed to appear suddenly over a wide area.
During 1972 whilst I was at the Rural Veterinary Centre at Camden there were quite a few cases of "milk drop syndrome" associated with L hardjo.
Prior to 1973, there were few reports of leptospirosis in the Riverina. The years 1973 to 1975 were extremely wet years in the Riverina. Since the spirochaetes survive better in stagnant water this created an ideal environment for the spread of leptospirosis at the same time that a new serovar had entered a na ive population. For several years, leptospirosis was a significant disease in the Riverina producing a range of syndromes.
"Milk drop syndrome" was probably the most common condition with a significant percentage of dairy herds having a large number of cows affected. The syndrome was as described by Hoare and Claxton (ibid).
There were numerous cases of icterohaemoglobinuria, "redwater" in calves and even a few cases in adult cows and sheep. In affected calf herds, morbidity often reached 25% and case mortality in the absence of treatment was around 90%. Affected animals were lethargic with severe jaundice and haemoglobinuria and unless treated died within a day or so. Early treatment with antibiotics (penicillin/streptomycin in those days) produced cure rates over 75%.
Abortions were not of the same intensity as brucellosis but 10% of a herd aborting was not uncommon.
Which serovar was causing which syndrome was somewhat confused. We did not isolate any organisms and seroconversion was variable. The only consistent association was that herds with milk drop syndrome converted to hardjo whereas herds with abortions or redwater could convert to either pomona or hardjo or both.
One feature of the infection in those days was the level of seroconversion. Serum agglutination titres over 10,000 were not uncommon with an occasional titre of 60,000. Seroconversion was mostly to hardjo although there was evidence of quite a bit of pomona as well.
Leptospirosis was a relatively common human infection at that time, particularly in dairy farmers and veterinarians. The syndrome was usually described as "flu like" which is usually code that the clinician neglected to record the clinical examination.
Those who were affected described their condition as being febrile and lethargic with headaches and generalized joint and muscle pain.
A series of droughts coincided with the release of a bivalent vaccine and probably a level of adaptation in the hosts and organisms and leptospirosis essentially disappeared as a disease of livestock by the end of the 1970's. We saw occasional abortions but nothing of the scale seen earlier.
The level of seroconversion during those few incidents has also dropped. A titre of 900 is considered to be a strong reaction these days.
The microscopic agglutination test used today does not correlate directly with the serum agglutination test but the differences are still dramatic.
Over the past thirty years or so the main impact of leptospirosis has been as a zoonosis. Anecdotes abound of high levels of leptospirosis in dairy farmers although not much comes to light from the sort of literature review of which I am capable.
I am aware of a few cases in dairy farmers and, interestingly, one case in a mechanic who had been working on a header, presumably from contact with infection from rodents.
We have long suspected, possibly for no good reason, an association between leptospirosis and mice and during the mouse plague of 2010-11 we alerted the local cattle producers of the likelihood of leptospirosis infection and recommended vaccination. As it eventuated, the only leptospirosis diagnosed in the Riverina through the period was in humans. Several farmers were diagnosed with leptospirosis over that summer (McPherson pers comm.).
Reported clinical findings were headache, fever, general aches and elevated liver enzymes. It was interesting to note that the serovar which was diagnosed as the cause of this syndrome was Leptospira borgpetersonii sv arborea. This is a serovar which is reported as having emerged in Australia over the past decade (Slack, 2010).
The working hypothesis is that these infections were derived from mice.
Leptospirosis, in particular disease caused by L hardjo, is an example of coadaptation between a pathogen and its primary host. When it was first identified in Australia it caused widespread and serious disease but is now an insignificant disease in cattle and the main cause for concern is its role as a zoonotic infection.