Flock and Herd logo

ARCHIVE FILE


This article was published in 1960
See the original document

INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

Leptospirosis

L. A. W. MACTIER, B.V.Sc., Veterinary Inspector, Moree

In the last week in October, 1958, a pastoral company, whose property of 10,000 acres, and later referred to as property "A", is situated in the heart of what is known as the Watercourse country (located generally north-west of Moree), trucked a consignment of 117 steers and bullocks, aged from 18 months to five years old, from Moree to Flemington.

The stock train left Moree (409 miles from Flemington) at 10 a.m. and these cattle started going down in the trucks at Muswellbrook (235 miles from Moree) about 6 a.m. the next day. They continued to go down, and one bullock had to be taken out of the truck at Farley (292 miles from Moree). Another bullock was dead in the truck on arrival at Flemington and most of the other cattle were in a bad way. Many were passing blood-stained urine. Practically all the cattle were blood-stained and they sold at £6 to £7 per head less than other cattle in similar condition trucked from Moree on the same day.

The train drover who travelled with these cattle advised that even when the animals were being sold they were still passing bloodstained urine. He also stated that cattle from two other properties, adjoining "A", also got down in the trucks, but he had never noticed any from these other properties passing blood-stained urine.

Enquiries were made as to the calving percentages on the property "A" and it was ascertained that for the last ten years these would average only approximately 60 per cent. Also, quite a few calves died when they were about two weeks old.

As it was considered that Leptospirosis probably was occurring on this property, blood samples were collected from 20 cattle whose ages and breeding histories were known.

Submitted to the agglutination test for Brucellosis, one sample was positive (4/3/2) and two were doubtful (1/S/- and 1/1/S); whilst the remaining seventeen were negative.

Examination for Leptospirosis resulted in eleven samples being positive for Leptospira pomona (1 at a titre of 1/1000, 2 at 1/300, 5 at 1/100 and 3 at 1/30). Three of the positives for L. pomona were positive also for L. hyos (2 at 1/300 and 1 at 1/100).

As it was apparent that the cattle here were affected with Leptospirosis the advisability of vaccinating all animals had to be considered; particularly as the Watercourse country is periodically inundated with from a few inches to several feet of water, and the country is infested with thousands of wild pigs which probably are infected with Leptospirosis.

History of leptospirosis

Recourse to the literature revealed that Leptospirosis was first described in humans by Weil in 1886, but it was not until 1915 that Leptospires were first isolated from cases of Weil's disease in Japan; and independently in Germany in the same year. (Steele, Galton and Menges.)

Leptospirosis in cattle was reported in the U.S.S.R. by Michin and Azinov in 1935 and in Australia by Johnson in 1943. In 1944 Jungherr first described this disease in cattle in the U.S.A. In 1948 an outbreak occurred in a beef herd in Illinois (Bryan).

Prior to the actual isolation of bovine Leptospirosis in the U.S.A. in 1948, and its identification as L. Pomona in 1950, reports suggested the disease was prevalent and was probably the cause of unexplained cases of faulty lactation, abortion and deaths in cattle. By 1954, 34 leptospiral serotypes had been isolated; with at least 25 additional serotypes since then.

In Europe and Asia, Leptospirosis is primarily a disease of rodents and it is upon these hosts that the Leptospires depend for survival. Man and his domestic animals become infected quite by accident, although certain serotypes have become more or less well adapted to domestic animals (L. Pomona and L. canicola).

Leptospirosis in man is dependent upon his coming in contact with excreted leptospires in the course of his daily life.

In domestic livestock, Leptospirosis was causing a loss of over 100,000,000 dollars annually in the US.A. by 1954; or 25,000,000 dollars greater than losses from Brucellosis (Bryan).

Leptospirosis in dogs has been recognised in Europe and the U.S.A. for many years. Mather (1954) stated that 11 per cent. to 38 per cent. of dogs in parts of U.S.A. were temporary or permanent shedders of Leptospires and thus were of considerable importance to public health.

SYMPTOMS.

The disease in cattle varies in severity and mild cases may pass unnoticed. Eventually. Leptospire organisms localise in the kidney and are disseminated in the urine. This carrier state may last for up to three months in animals recovered from the disease.

Observations made by York indicated that in herds in which Leptospirosis has been diagnosed, 60-70 per cent. of the animals were serologically positive. Severe illness was shown by 10 per cent., mild illness characterised by fever and interrupted lactation by 40 per cent., whilst others showed no visible signs.

Usually 5 per cent. or less of infected animals died, although in some herds 25 per cent of the younger animals succumbed. The abortion rate reached 25 per cent. in some cases, but is usually 15-20 per cent. when the disease first strikes a herd.

Symptoms are variable and may be acute or chronic. The outstanding indication is premature birth; both in cattle and swine.

Sudden reduction in milk flow in dairy cows may occur. Other symptoms include fever, anorexia haemoglobinuria, anaemia and icterus. Morbidity approaches 100 per cent. in a typical herd outbreak.

In swine up to 100 per cent of the pregnant sows may abort. This usually occurs two to four weeks before term; in cows at any stage of pregnancy but usually in the last trimester.

In cases of abortion in cattle, Brucellosis, Vibriosis and Trichomoniasis could be confused with Leptospirosis. In chronic cases one may have to rule out parasitism and malnutrition if there is general unthriftiness and poor weight gain.

In adult cattle, inapparent infections occur and symptoms range from slight malaise to a severe illness; with icterus and haemoglobinuria and a high death rate.

Between these two extremes is a common type in which the milk yield is reduced, is colostrum-like in appearance and may be blood-tinged. Affected animals may remain unthrifty for a considerable time and even on return to normal health. Full production is not regained. Abortions may occur in all forms of the disease. New Zealand workers reported an outbreak in which 28 per cent. of 88 milch cows produced dead full-time calves or aborted. The cows showed no symptoms and little or no loss of weight, appetite or milk production; although 75 per cent. had serum antibodies to L. pomona. In calves, symptoms vary but morbidity and mortality are often high in young animals, which may die quite suddenly after showing symptoms for only a few hours. Haemoglobinuria and icterus usually occur. Some calves may become carriers, although showing no symptoms (Te Punga and Bishop. 1953).

EPIDEMIOLOGY.

Leptospirosis frequently is introduced into a herd through an apparently healthy carrier. Urine from chronic carriers is the chief source of infection; which usually occurs through the mucous membrane of the eyes, nose, throat and vagina; though the organism can enter also through cuts and abrasions of the skin. Infection also may occur through contact with urine-contaminated bedding or organisms present in poorly drained pastures, pools and streams.

Semen of an infected sire may become contaminated from the urine in the urethra, and in fact many herd outbreaks have been traced to new additions of sires, especially boars.

Leptospires have been isolated from milk but they do not survive well in fresh raw milk. Pasteurised milk is safe, as leptospires are extremely sensitive to heat.

Rodents have been mentioned as infective carriers but it appears they do not play an important role in the transmission of L. pomona to cattle and swine.

Swine are the chief reservoir of infection.

Successful prevention of Leptospirosis depends upon avoiding the introduction of the disease to a healthy herd.

L. pomona has been recovered from streams and surface pools which had been contaminated with urine from recovered cattle. In one instance it was recovered from surface waters ten days after cattle had been removed from the area. In another case from a stream flowing at over 250,000 gallons per minute on the downstream side of the watering spot of infected yearling cattle (Stoenner, 1957).

Epizootics of Leptospirosis occurred in various environments, even in beef cattle grazing on large semi-arid areas, where ponds, potholes and slow-running streams used as sources of water provided the means of dissemination. During winter months the disease often spreads rapidly among cattle closely confined in muddy feed lots where contamination of food and water with infectious urine was precluded. Presumably the disease was spread by dermal contact with moist contaminated soil, since it spread slowly through a herd similarly fed and watered but confined in a dry, sandy, well-drained feed lot. Grazing on irrigated pastures and close confinement in muddy areas were associated frequently with rapidly spreading epizootics (Stoenner, Crews and Others, 1956).

Most outbreaks occurred in late autumn and winter when cattle were confined closely for supplementary feeding. At that time cows are in the last trimester of pregnancy, when abortions from this disease are more likely to occur. Unless heavy losses prevailed the disease easily could escape notice among non-pregnant cows widely scattered on summer grazing.

Calves aged three to ten weeks often are affected; with outbreaks generally confined to the wetter months of the year.

The incubation period is 4-10 days. Death may occur in 24 hours, but usually in 3-4 days. Mortality rate ranges from 5 to 80 per cent. Recovery without treatment is not uncommon, but may take up to six weeks.

In New Zealand the majority of fatal cases occur in the first few weeks of life.

Leptospires have been demonstrated in the kidney of an aborted foetal call and it is suggested that calves may be infected at birth. (Te Punga and Bishop.)

Urine of carriers is the source of infection. Cattle may shed the organisms for 3 months and pigs for periods up to one year.

Most domestic animals are susceptible to L. pomona but some are potentially more capable of disseminating the disease. Recovered pigs shed leptospires in their urine in greater numbers than do recovered cattle.

In areas where pigs and cattle are raised on the same premises, pigs play a more dominant role in the epizoology of the disease.

TIME OF OUTBREAKS.

Leptospirosis has been considered to be a tropical disease because freezing temperatures were presumed to exert a deleterious effect on the organism. In contrast, most outbreaks observed in the State of Washington, U.S.A., occurred during mid-winter; indicating that the survival of the organism at freezing or near-freezing temperatures is adequate to perpetuate an epizootic (Stoenner. 1957).

CONTROL

Until March, 1954, repeated attempts were made to control Leptospirosis through serological testing and segregation, but in most herds the number of positive animals increased with each successive test.

TREATMENT

Streptomycin (5 mg. per lb. liveweight) given twice daily for three days has been reported as effective (Ringer and Others).

5 mg. of oxytetracycline (terramycin) daily for 5 days cleared 86 per cent of pigs from leptospiruria (Marshall). Terramycin fed at rate of 500-1000 gm. per ton of feed for 14 days eliminated the carrier state in 94 of 100 pigs (Baker and others). Aureomycin (200 mg. per pound of feed for 14 days) gave good results (Howorth).

IMMUNOLOGY.

Natural infection confers a long-lasting immunity in animals. Routine vaccination is recommended where the disease is endemic. When infection in the herd is extensive, antibiotic therapy is expensive, and it is then too late to vaccinate.

In New Zealand, most of the losses occur in calves aged three to six weeks, which is the time when seasonal demands on veterinary surgeons are at their highest and the personnel are not available for large-scale vaccination.

In experiments to test the possibility of preventing Leptospirosis in young calves by vaccinating their dams in late pregnancy, calves from cows vaccinated twice were challenged with 5 ml. of a 7-day culture of L. pomona (organisms per ml. in excess of 108) and 5 ml. of ground kidney tissue of an infected guinea pig, injected subcutaneously. Calves from unvaccinated cows in the same herd were challenged similarly as controls. The average age of calves in the first experiment was 10 days, and in the second 25 days (McDonald and Rudge, 1957).

In Experiment 1, nine out of 10 of the control calves were infected but none of the 10 calves from the vaccinated cows. In Experiment 2, all of the 10 control calves were infected and one out of 15 calves from vaccinated cows.

The criteria of infection were haemoglobinuria, leptospiruria, death with typical clinical signs, serological response and pathology or successful transmission to guinea pigs. It is apparent from these experiments that the vaccination of cows on two occasions in the last two months of pregnancy will protect calves from infection during their first month of life.

In a trial in the U.S.A. a single 5 ml, dose of vaccine produced a significant rise in the titre of 31 out of 32 young cattle within one week of vaccination. Five of these and five unvaccinated cattle were challenged 3 weeks later with live culture of L. pomona. Titres of vaccinated cattle did not rise significantly, but there was a sharp rise in the unvaccinated cattle. When 5 vaccinated cattle were challenged six months later, their blood titres remained low. In a similar experiment with young cattle, some were challenged 12 months and others 14 months after vaccination; when the treated cattle failed to show a significant rise in titre although vaccinated controls showed marked rise in titre and other signs of infection. This would indicate that a single dose of vaccine will protect for at least one year (Schiedy, 1957).

In another trial in U.S.A., 18 calves aged 1 to 2 months and 12 heifers aged 6 to 8 months were vaccinated with three different makes of vaccine which were all killed suspensions of L. pomona (Gillespie and Kenzy, 1958).

Vaccinated cattle were challenged with diluted urine from shedder cattle instilled into the eyes and nostrils. This was repeated daily four to six times. The drinking water provided in troughs also was contaminated by the addition of shedder urine each day for six to ten days.

The 17 very young calves aged 1 to 2 months when vaccinated (one died before challenge) were divided into two groups. One group was challenged at 6 months after vaccination; when 7 out of 9 became infected with Leptospirosis. The other group was challenged at 8 months, when 6 cut of 8 became infected.

All nine controls used became infected and one of these shed enormous numbers of Leptospires; estimated to exceed 100,000,000 per ml. of urine for up to eleven weeks after infection. The controls showed some evidence of being more severely affected than the vaccinated calves.

The heifers were challenged similarly: when only one of them became infected, in contrast to all 5 controls. Two of the controls shed for about three and five weeks respectively, when both excreted enormous numbers of Leptospires. One of these showed 24,500,000 and 25,000,000 per ml. on two successive days, and about ten days later was estimated to be shedding twice that number.

It is evident from the above trials that L. pomona vaccines induce in 6 to 8 months-old heifers a high level of immunity which persists for at least 7 to 8 months.

By contrast, calves vaccinated at one to two months acquire much less resistance and become infected when challenged six months after vaccination. Current studies by Gillespie and Kenzy (August. 1958) show that calves vaccinated at three to five months of age exhibit a high level of immunity when challenged 13 months after vaccination.

In pigs, the chief sign of Leptospirosis is abortion. In one trial in which gilts were vaccinated prior to breeding and challenged with live cultures of L. pomona at mid-gestation, one group of 10 vaccinated gilts farrowed 89 pigs; of which 88 (98.9 per cent.) were healthy and viable. Another group of 10 vaccinated gilts farrowed 71 pigs; of which 68 (95.7 per cent.) were viable. A control group of 7 unvaccinated gilts farrowed 55 pigs, of which 27 (49.1 per cent.) were viable, 38.2 per cent. were dead and 12.7 per cent. were weak (Schiedy, 1957).

200 pigs had a titre of 1:1800 three weeks after vaccination, indicating that a higher titre can be obtained in pigs. There was a rapid decline in titre in the six months following vaccination. However, as the period when sows require immunity is during gestation it was of practical value (York, 1957).

In another trial with non-vaccinated gilts challenged in mid-gestation. 51 per cent. of the pigs farrowed were either dead or in a weakened condition. In contrast, vaccinated gilts produced only 5 per cent. dead or weak piglets; demonstrating the value of vaccination It is necessary to re-vaccinate sows before each breeding season (Bryan).

In cattle, re-vaccination is required after one year or 18 months.

During the 21 years prior to 25th April, 1957, 11 million cattle and pigs were vaccinated against L. pomona in U.S.A. (York).

It would be preferable to have a vaccine that produces a longer immunity, and that more rapidly, than the present killed vaccine. It may be possible to develop a modified or avirulent strain of Leptospires which could be incorporated into a vaccine; and might create a stronger and more rapid immunity.

The Manager of property "A" referred to in the opening paragraph of this article decided to vaccinate all the cattle on the holding, and has now vaccinated approximately 650 head. It is too early yet to assess the full results of this vaccination, but it was observed that prior to vaccination there were approximately 40 breeders out of 400 which should have had calves, but which obviously had lost them through abortion or early deaths.

Since vaccination, which was commenced in the middle of March, 1959, only one cow has been observed to have lost her calf and this occurred within a few days of vaccination; and before it could have taken effect.

Leptospirosis was suspected of occurring on another holding about 15 miles from property "A". Blood samples were collected from 10 cattle there. Results showed that one sample was positive for Brucellosis (4/4/4), while the remaining nine were negative. Examination for Leptospirosis showed that eight of the ten samples were positive for L. pomona; in two cases to the high titre of 1/3000, in one case to 1/1000. in two cases 1/300. one to 1/100 and two to 1/30. The other two samples were negative.

References.

  1. Baker and Others (1957) - See Mosier, Vet. Med., 52 : 11
  2. Bryan, H. S. (1957) - Vet. Med., 52 : 11
  3. Gillespie, R. W. H. and Kenzy, S. G. (1958) - Vet. Med., 53 : 8
  4. Howorth (1957) - See Mosier. Vet. Med., 52 : 11
  5. Johnson, D. W. (1950) - Med. J. Aust. fol. 724
  6. Johnson, D. W. (1943) - Aust. Med. J., fol. 659
  7. Jungherr, E. (1944) - J.A.V.M.A., 105 : 276
  8. Marshall (1957) - See Mosier, Vet. Med., 52 : 11
  9. Mather, G. W. (1954) - Vet. Med., 49 : 241
  10. McDonald. N. R. (1955-56) - Vet. Med. & Annots., 1 & 2 : 117
  11. McDonald, N. R., and Rudge, J. M. (1957) - New Zealand Veterinary Journal, 5 : 3
  12. Powers, Bohl and Ferguson (1956) - J.A.V.M.A., 129 : 568
  13. Ringen and Others (1957) - See Mosier. Vet. Med., 52 : 11
  14. Scheidy, S. F. (1957) - J.A.V.M.A., 131 : 8 : 366
  15. Steele, Galton and Menges (1957) - Vet. Med. 52 : 11
  16. Stoenner, Creks, Crouse, Taschna, Johnson and Wohleb (1956) - J.A.V.M.A., 129: 6
  17. Stoenner, H. G. (1957) - Vet. Med. 52 : 11
  18. Sutherland, A. K., and Simmons, G. C. (1949) - Aust. vet. J., 25 : 9
  19. Te Punga, W. A., and Bishop. W. H. (1953) - New Zealand Veterinary Journal, 1 : 143
  20. Toop, C. R. (1956) - J. Agr. West. Aust., 5 : 5
  21. York (1957) - Vet. Med. 52 : 11

Site contents Copyright 2006-2026©