CHAPTER 106 Bacterial, Rickettsial, Protozoal, and Fungal Causes of Infertility and Abortion in Swine

Losses due to reproductive failure are high in today’s swine industry. Many factors are involved in causing reproductive failure, including infectious agents, such as bacteria, viruses, protozoa, and fungi, and noninfectious factors, such as nutrition, genetics, environment, management practices, and husbandry procedures. This chapter reviews infectious causes of reproductive failure—primarily diseases caused by bacteria, protozoa, rickettsiae, and fungi. Such diseases have become less important in today’s high-technology swine industry with the improvement of the sanitation procedures and the widespread use of artificial insemination. Some of the diseases discussed in this chapter are still considered important at the individual animal level and in specific herds, but for the most part such diseases are considered sporadic in the U.S. swine industry.

Bacteremias, septicemias, toxemias, and viremias exert their effects directly when microorganisms invade the bloodstream and pose a threat to the life of the conceptus or the dam, or indirectly through mechanisms to induce fever. The degree to which these diseases influence the conceptus depends on the stage of pregnancy and the virulence of the organisms. In order to understand the clinical signs associated with reproductive failure in swine, it is important to review some of the terminology used and understand the stages of embryo and fetus development. Gestation, which is the period between conception and parturition, lasts about 114 days in swine. In the first 2 weeks of life, the conceptuses lie free in the uterine lumen. Damage to them during this stage is almost always fatal.¹ Implantation begins around day 12 of gestation; death of the conceptus before then will result in resorption of the conceptus, and the sow will undergo a regular return to estrus at approximately 21 days. Death of the embryo before calcification, between approximately 14 and 35 days of gestation, will result in abortion or complete resorption of the embryo. A delayed return to estrus may be observed after 24 to 28 days, resulting in an irregular return to estrus.

Fetal death after day 35 typically is followed by mummification of the fetus, rather than pregnancy termination, because the mineral content of the fetus prevents complete absorption. Mummified fetuses are characterized by discoloration and resorption of fluids and soft tissues.¹

Abortion refers to the delivery of an immature fetus, either live or dead, before the completion of the gestation period as a result of the failure of the mechanisms that control pregnancy. A stillbirth is a fetus that has matured fully in utero but is born dead. Stillborn piglets look normal, but their lungs do not float in water (respiration never occurred before death). Stillbirths may be caused by infectious agents; affected fetuses usually die before the end of gestation and around the prepartal period. Stillbirths also may be caused by noninfectious agents or conditions and are known as intrapartum deaths.¹ Most common noninfectious causes include hypoxia secondary to umbilical rupture or impairment of umbilical blood flow, high atmospheric carbon monoxide concentration, elevated temperatures (higher than 39° C) during farrowing, and prolonged parturition.¹ Neonatal death refers to that occurring primarily within the first 7 days of life. Death usually is due to events that take place during late gestation or shortly after parturition. In production records, neonatal death usually is captured within the preweaning mortality parameter.

Although a few bacteria such as Leptospira and Brucella are recognized to cause major reproductive economic losses, the reality is that in modern swine production systems these diseases are not significant, and they should be considered exceptional. On the other hand, sporadic losses due to infections caused by ubiquitous bacterial agents, often considered secondary to stresses and management practices, can result in significant economic losses because of the chronic nature and persistence of these diseases, which also typically are difficult to control and diagnose.

LEPTOSPIROSIS

Leptospirosis has been reported as a cause of reproductive loss in swine from all parts of the world.² Leptospirosis is caused by a variety of motile, aerobic spirochetes from the Leptospira genus. The leptospires that affect animal species (the parasitic strains) are grouped into about 23 serogroups containing approximately 212 serovars based on complicated agglutination reactions.² Reproductive signs in susceptible herds are characterized by abortion, birth of dead full-term piglets, weak-born piglets, and infertility.

Epidemiology and Clinical Signs

Leptospires persist in the kidneys and genital tracts of carrier swine. Shedding may occur intermittently for prolonged periods, for up to 2 years. Therefore, the primary mode of transmission of leptospirosis to pigs is through contact with voided urine from infected hosts. Contact of infected urine with the oral, nasal or ocular mucosa will result in a brief period of bacteremia of less than 10 days. During this time, bacteria can be isolated from most organs and fluids of the body, including the cerebrospinal fluid. Once the organism is cleared from the bloodstream, it will take up residence in the proximal tubules of the kidney.

Pigs act as maintenance hosts for serovars belonging to the pomona, australis, and tarassovi serogroups, whereas strains belonging to the canicola, icterohaemorrhagiae, and grippotyphosa serogroups are among the more commonly identified incidental infections in swine.²

Leptospira pomona has been the most common serotype isolated from pigs worldwide. Many strains of serovar pomona, especially those of type kennewicki, are adapted to pigs and have been found in the United States and Canada.³ L. pomona is reported to be endemic in North and South America, Australia, New Zealand, and parts of Asia and Eastern and Central Europe, but not Western Europe. Many strains within the pomona serovar have rodent hosts. Transplacental infection occurring during the short period of maternal leptospiremia in the second half of gestation may result in abortion. Chronic leptospirosis also will result in stillbirths and weak-born piglets, with a majority of the fetuses in the litter being affected. L. pomona does not appear to cause infertility.

Leptospira bratislava serotype has emerged as a major swine-maintained leptospiral infection in the last few years. Serologic data have indicated widespread infection in Europe, United States, Australia, Brazil, and South Africa. The epidemiology is poorly understood, because evidently many strains are maintained in pigs, dogs, horses, and hedgehogs and other wildlife. Although the renal carrier state does become established, urinary excretion is poor compared with pomona excretion. By contrast, venereal infection is thought to play an important role in the spread of the disease because the bacteria are known to persist in the upper genital tracts of boars and the oviduct and uterus of sows.² Abortion caused by L. bratislava infection is the result of presence of the leptospires the genital tract. L. bratislava has been recognized as a cause of infertility.

The serotype icterohaemorrhagiae is carried by the brown rat (Rattus norvegicus). Although serologic evidence of widespread infection has been reported in many countries, very few isolates are available from pigs.⁴ Field investigations suggest that infection between swine is inefficient.² The duration of urinary excretion is short (less than 35 days) in naturally infected pigs. In acute episodes of infection, L. icterohaemorrhagiae will cause jaundice and hemoglobinuria in young piglets younger than 3 months of age. In chronic episodes, weak-born litters have been reported as a feature of L. icterohaemorrhagiae infection.²

The serotype grippotyphosa is maintained in wildlife, and swine are considered only an alternate host. Infection in pigs is considered incidental. Some serologic evidence of its presence has been reported in Eastern and Central Europe and the United States, but in general, this serotype is not considered a significant pathogen of swine.² Of interest, L. grippotyphosa was one of the most common serotypes recovered in a study involving Iowa herds.³

The serotype canicola has been recovered from swine in several countries. Little is known of its epidemiology in pigs, however. The dog is the recognized maintenance host for this serovar. L. canicola is excreted in pig urine for at least 90 days and has the ability to survive in undiluted urine for at least 6 days, suggesting that between-pig transmission could be possible, although no studies are available in this subject. This serotype can cause abortions, stillbirths, and periods of infertility.²

Published information is limited regarding the tarassovi, hardjo, and sejroe serotypes. The pig is considered to be the maintenance host for some of the tarassovi strains found in Eastern Europe and Australia. In the United States, L. tarassovi has not been recovered from swine, but serologic evidence of infection has been described in pigs of the southeastern states, where it has been isolated from wildlife (raccoons, skunks, and opossums).² L. hardjo is maintained worldwide in cattle.² The organism has been isolated in pigs in the United Kingdom and the United States. Between-pig transmission is considered to be irrelevant because persistence in renal tissue is very limited. Serovar sejroe has been isolated from swine in Europe and is mostly maintained by small rodents.²

Diagnosis

Lesions associated with leptospirosis infection are not serotype specific and are not considered pathognomonic.² The primary lesion is damage to the membranes of the endothelial cells of small blood vessels. Lesions are very limited in acute leptospirosis. Petechial and ecchymotic hemorrhages can be seen in the lungs of some pigs. Minor lesions can be seen in the renal tubules. Focal liver necrosis, lymphocytic infiltration of the adrenal glands, and meningoencephalitis with perivascular lymphocytic infiltrations also have been described. In chronic leptospirosis, lesions are confined to the kidneys and consist of scattered small gray foci, often surrounded by a ring of hyperemia. These lesions are characterized by focal interstitial nephritis, manifested as interstitial leukocytic infiltrations by lymphocytes, macrophages, and plasma cells. Focal damage also may involve glomeruli and renal tubules. Bowman’s capsule may be thickened, containing eosinophilic granular material. Atrophy, hyperplasia, and presence of necrotic debris may be seen in the renal tubules. Chronic lesions may be noticeable as long as 14 months after infection. Leptospires can invade the pig’s mammary gland and produce a mild, focal nonsuppurative mastitis. Lesions in aborted fetuses are nonspecific and may include edema of various tissues, fluid in body cavities, petechial hemorrhages in the renal cortex, and small foci of interstitial nephritis. The liver may exhibit focal necrosis manifested as small grayish-white spots. Placentas from aborted fetuses are grossly normal.

Laboratory procedures most commonly used for the diagnosis of leptospirosis include serologic testing, culture, and immunofluorescence. Serologic testing is the most widely used method, and the microscopic agglutination test (MAT) is the standard serologic test. MAT is considered a herd test. Rising antibodies in acute and convalescent animals constitute a sign of recent infection. Titers of 1:1000 or greater are strongly indicative of recent infection. Chronically infected animals may have titers below the accepted minimum significant value of 1:100, for which this test has very low sensitivity. Presence of antibodies in fetal sera or thoracic fluid is diagnostic of leptospiral abortion. Culture of leptospires from affected tissues is the definitive diagnostic tool. The organism is fastidious, however, so culture is time-consuming, with special requirements, and is not performed on a routine basis. Immunofluorescence testing is the method of choice for diagnosis of fetal leptospirosis in fetal body fluids or kidney smears. Darkfield microscopy of fetal fluids or urine also has been used; however, precautions have to be taken so that the organisms are not confused with tissue artifacts.