Leptospirosis is a contagious disease of swine and many other animals (including humans) and is caused by infection with any one of a large group of Leptospira spp. serovars. Although the generalities of leptospirosis in swine are presented here, details of infection with different serovars may vary. Swine are susceptible to many different serovars.
Leptospirosis occurs in swine in all parts of the world where conditions are favorable for the survival of leptospires. The occurrence of any one serovar of Leptospira in an area depends on the presence of maintenance hosts in which the infection persists or the presence of incidental hosts. In both instances, leptospires can be effectively disseminated to swine. The disease occurs more frequently where the hosts are numerous or concentrated.
Early reports of “swine herder’s disease” in Europe described a disease among caretakers of swine that probably was leptospirosis. In the US, swine leptospirosis was recognized as an important disease of swine in the 1940s and 1950s. The disease continues to be endemic in areas where environmental conditions are favorable for leptospires. However, losses have been reduced by confinement, sanitation, management changes, vaccination, and the use of antibiotics. Leptospirosis is now relatively uncommon in modern swine production.
A new system of classification for Leptospira is based largely on DNA relatedness to known reference strains but universal agreement on taxonomy of the genus remains elusive. Under the most current classification, the family Leptospiraceae contains eight pathogenic species of which three are of most importance to swine: Leptospira interrogans (serovars pomona, icterohaemorrhagiae, canicola, and bratislava), Leptospira borgpetersenii (serovars sejroe and tarassovi) and Leptospira kirschneri (serovar grippotyphosa). Serovars pomona and bratislava are uniquely adapted to swine, others are maintained in other species but sometimes infect swine. Of additional note, serovar L. hardjo is the most important serovar of bovines and has been reported to infect pigs kept in close contact with cattle. Leptospira bratislava is reported to be the most common strain in swine, although the role of this serotype as a cause of disease is debated.
Leptospira are motile spirochetes, 6-12 microns long, and 0.1 micron in diameter. They usually are hooked on both ends and can be stained by Giemsa stain or, in tissue, by silver stains. In the laboratory they often are studied under darkfield microscopy. In laboratory media they are difficult to culture and grow very slowly (12-26 weeks). Many pathogenic strains can survive in the environment for long periods of time under moist conditions with a slightly alkaline pH. Most cannot withstand desiccation and are destroyed by common disinfectants.
Many of the pathogenic Leptospira serovars, including L. pomona, have a predilection for the kidneys and persist there. Both maintenance and incidental hosts pass large numbers of Leptospira in their urine, often lasting for weeks to months after clinical signs have concluded. Infection usually is introduced into a herd by infected, shedding swine (often replacement gilts or boars), by direct or indirect contact with incidental hosts (rats, mice, skunks, raccoons, foxes, opossums, etc.), or through Leptospira-contaminated water, soil, or effluent. Outbreaks have been reported in herds using untreated surface water for drinking.
Under ideal conditions, leptospires survive in water and damp soil. There they remain a persistent threat to a wide range of animals, including swine and man. Incidental hosts can be infected or merely act as passive transport hosts that carry leptospires to other premises. Carnivorous forms of wildlife may visit swine-raising facilities, feed on dead piglets and later visit other premises. They may be underestimated as transmitters of Leptospira.
Fetuses infected in utero may survive as infected piglets and, as adult carriers, transmit Leptospira to following generations. These inapparent carriers may be selected as replacement breeding stock or sold to other producers. When sold, they can introduce leptospirosis into recipient herds.
Some Leptospira serovars, especially L. bratislava, have a predilection for the genitalia of both male and female swine. The organisms can be transmitted from infected to negative animals during copulation. In addition, L. bratislava can be transmitted through urine.
Leptospira penetrate mucous membranes (eyes, mouth, nose, vagina), wounds, abrasions, and perhaps water-softened skin of the host. A leptospiremia then develops and organisms circulate throughout the body and probably affect many major organs. Many species localize in the kidney or in the uterus during the last half of gestation. Leptospira bratislava can localize in the oviduct and uterus of nonpregnant sows and in the genital tract of boars.
The exact way in which Leptospira produce their pathogenic effect is not known but capillary damage is a major feature. Localization in the kidney, first in the interstitium and later in the tubules, results in vascular damage and at least temporary damage to tubules. Interstitial nephritis, if extensive, can lead to kidney failure and uremia. The liver may also be affected. In addition, Leptospira produce hemolysins which result in the hemolysis of erythrocytes and causes hemoglobinuria and hemolytic anemia. The severe effects of hemolytic anemia occur mostly in very young piglets. Toxic materials from autolyzing dead fetuses impair the health of the dams and may trigger abortions.
The acute phase of leptospirosis largely coincides with an initial stage of leptospiremia as well as virulence of the particular serovar involved. Signs often go unnoticed in mature, nonpregnant swine or in growing pigs. A careful observer might notice mild fever and inappetence for a few days. In very young piglets, however, there may be fever, anorexia, hemolytic anemia, hemoglobinuria, icterus, convulsions in occasional pigs and a failure to grow and gain weight.
Chronic infection in dams usually is apparent only as various forms of reproductive failure, including poor conception rates. Pregnant, infected animals often abort in late gestation. In many cases, fetuses are carried almost full term but may be mummified, dead, or weak at birth. Although many infected neonatal pigs die within a few days, some often survive. The dams usually recover promptly. They often conceive again and carry their litters to term.
Lesions seldom have been described in sows since most infected adults recover. Grow/finish swine may have scattered foci of interstitial nephritis or generalized kidney scarring which may only be noticed at slaughter as “white-spotted kidneys.” Lesions in small piglets include patchy areas of hepatic necrosis, excessive fluid and fibrin in the peritoneal cavity and evidence of inflammation in multiple organs. Microscopically, there is a marked focal, disseminated, interstitial nephritis; tubules and glomeruli often have degeneration and inflammation. Occasionally, a nonsuppurative meningitis can be observed. Placental lesions seldom are marked or significant but may include edema and scattered hemorrhages.
A history of abortions in late gestation, along with lesions in neonates, may suggest leptospirosis but mere observation is inadequate for accurate diagnosis. Diagnosis of outbreaks is usually based on serologic herd testing. The microscopic agglutination test (MAT), one of several tests available, often is used. Sera from a minimum of 10 animals, including both affected and unaffected animals, should be tested. High antibody titers are usually present at the time of abortion or farrowing but paired samples may be required. Microscopic agglutination testing is serovar specific so the use of multiple assays may be required to arrive at a diagnosis. Breeding animals are commonly vaccinated against multiple Leptospira serovars so interpretation of serologic results must also consider vaccination history of the animal. Titers from infection are much higher than those induced by vaccination.
Several other methods of diagnosis sometimes are used but have limitations. These include isolation and identification of leptospires (tedious, laborious), phase contrast identification of leptospires in urine (expensive equipment, not specific), and identification of leptospires in kidney sections with silver stains (lacking sensitivity and specificity). Two rapid and useful techniques, where available, are immunofluorescent microscopy on a homogenate of tissues (kidney, liver, lung, placenta) and immunohistochemistry (IHC). Some laboratories have polymerase chain reaction (PCR) tests that are sensitive but generally not serovar specific.
Control usually is attempted by prevention of exposure, immunization through vaccination, and/or the use of antibiotics. Prevention of exposure is difficult to achieve because so many species can act as carriers of leptospires. These include infected swine, rodents (especially mice and rats) and many kinds of wildlife. Once leptospires are introduced into a favorable wet environment, they often persist there as a source of infection. Nonetheless, leptospirosis can be effectively controlled (perhaps even eradicated) from swine populations raised under confinement conditions using a combination of medication, vaccination, vector control, and providing a treated or non-contaminated drinking water source. Immunization through use of bacterins, widely practiced in breeding herds, usually will reduce the prevalence of infection and abortions. The bacterin must be appropriate for the serovar of Leptospira causing the disease. Many bacterins are multivalent. The level of immunity obtained and its duration may not always be satisfactory. Also, bacterins usually will not eliminate infection in carriers. Antibiotics used judiciously may reduce the impact of leptospirosis. It is doubtful that all carriers can be eliminated by the use of permitted antibiotics. Research suggests that oxytetracycline, tylosin, and erythromycin are among the most effective agents.