Swine Reproductive Diseases Notes 2024 PDF

Notes 12 – Reproductive Diseases Reproductive Diseases Overview of reproductive diseases Porcine parvovirus Leptospirosis Seasonal infertility Autumn abortion storm Vesicular diseases Systemic viral diseases Self-study – Reportable bacterial diseases...

Notes 12 – Reproductive Diseases Reproductive Diseases Overview of reproductive diseases Porcine parvovirus Leptospirosis Seasonal infertility Autumn abortion storm Vesicular diseases Systemic viral diseases Self-study – Reportable bacterial diseases 1 Reproductive Diseases Overview of Reproductive Diseases Reproductive failure in swine can either have an infectious or noninfectious etiology and can be present as reduced performance in only one reproductive parameter (such as farrowing rate), or as a syndrome of suboptimal performance in a number of reproductive measures. Reproductive failure is far more often a consequence of management mistakes and housing inadequacies than as a result of infectious disease. However, when infectious disease does strike a herd, the impact can have serious economic consequences, and for that reason, the following diseases should be considered as important. There are two types of infectious reproductive diseases in swine - systemic and urogenital. Both syndromes can occur as acute herd outbreaks or as chronic, endemic infections. Systemic reproductive diseases are most commonly diagnosed during acute outbreaks. Clinical signs tend to vary depending upon the time after mating that a sow is exposed. Exposure to a pathogen during the first 14 days post-service, followed by embryonic death and resorption, results in pregnancy termination and a regular return to estrus (18 - 24 days). Exposure after 14 days, but prior to the time of onset of fetal calcification at approximately 30 - 40 days post-service, results in complete resorption of fetuses and irregular return to estrus (> 24 days postmating). Fetal death after about day 35 results in incomplete resorption (mummified fetuses). Infections of the sow during the last few days of gestation results in fetuses dying during late gestation or in piglets born too weak to survive (stillbirths or increased preweaning mortality) and may cause prolonged gestation because there are not enough live fetuses to stimulate parturition. The duration of clinical disease in a herd, following infection with a systemic pathogen, is usually short: possibly affecting 2 - 3 months of farrowings. Only immunologically naive animals (incoming replacement gilts) remain susceptible in a chronically infected herd. Urogenital infections are most commonly the consequence of pathogens that ascend via the vagina and cervix. These pathogens infect the uterus, ascend through the urethra to the bladder, or ascend through the vagina and colonize the anterior vagina. Urogenital infections usually present as ongoing problems having persistent and somewhat insidious effects on performance. 2 Porcine Parvovirus (PPV) Incidence The virus is present in almost all herds worldwide. Herd outbreaks are rare because immunity is so widespread. Newly established herds are at greatest risk of being immunologically naive and susceptible to a major outbreak. In established herds, only the incoming replacement gilts are likely to be at risk of infection. Etiology PPV is a small, very stable DNA virus. It is unlikely that routine cleaning and disinfection of a pig barn would eliminate this organism. Pathogenesis Infection is via the oronasal route primarily, but venereal transmission is possible. The virus has been identified in semen. The virus will cross the placenta throughout the gestation period. Embryos and fetuses will die if infected before 67 days of gestation. The virus passes from infected to naive fetuses in the uterus. Fetuses at around 70 days can mount immunological resistance to the virus and survive. Sows shed virus for approximately 2 weeks after infection. Passive immunity is passed to piglets via colostrum and is protective for up to 4 - 6 months after birth. Clinical Signs Small litter size and mummified pigs. Sows do not go off feed or appear sick. Most producers don't realize they have a serious problem until litters of only 2 or 3 live pigs begin to occur. These litters will contain large numbers of mummified pigs. These mummified pigs may be differing sizes. Some sows that were thought to be pregnant will be found to be not-in-pig (NIP) at farrowing time. Sows may continue to be pregnant past their scheduled parturition date and finally farrow up to a week later. Usually these litters contain one or two large stillborn piglets and a number of mummified piglets. Abortion is not a usual feature of this disease syndrome. Epidemiology On rare occasions, the virus does disappear from a herd and these herds become susceptible to a major outbreak. Generally, this is only a problem with small, closed herds. Large herds may have periodic outbreaks amongst young sows. Serology has shown that about 1/4 of all gilts have negative antibody titres at the time of selection for breeding. Diagnosis 3 Fluorescent antibody testing of frozen lung smears from mummified piglets is the most definitive test. Serology demonstrates the presence of antibodies to parvovirus, and is of little value in diagnosing the cause of an outbreak. History and clinical signs are quite useful. Control Killed vaccines are commercially available. General recommendations are to vaccinate gilts one month and two weeks prior to breeding (this assumes gilts have been selected well in advance of breeding) and vaccinating sows when they wean their piglets (about every 6 months). On most farms, sow vaccination is probably unnecessary but this vaccine is almost always used in combination with other vaccines. It is easier to continue to vaccinate older sows than to create a more complicated vaccination program. Before commercial vaccines were available, producers were encouraged to grind up mummies from parvo-infected litters and freeze this solution. When replacement gilts were introduced, they would be fed "ice cubes" of this parvo-infected material (live autogenous oral vaccine). This procedure worked, but one quickly ran out of vaccine and would need another outbreak before more material would become available. Leptospirosis Incidence Outbreaks of leptospirosis abortion are uncommon and unpredictable. Etiology L. pomona is the serotype most commonly associated with reproductive failure. More recently, L. bratislava has been shown to be present in a large number of herds and has on occasion caused a serious abortion problem and infertility due to fallopian tube infections. Leptospira spp. are sensitive to most soaps, disinfectants, and are rapidly destroyed by drying. They may persist for months in water. Open water sources that are exposed to wildlife can be reservoirs for Leptospira. Pathogenesis Infection is by ingestion, direct contact, and entry through abrasions, transplacental transmission, or by the venereal route. The organisms multiply to produce a septicemia, which may produce clinical signs. In L. pomona infections, organisms penetrate from the blood vessels through the interstitial tissue of the kidney to the basement membrane within 3 - 5 days of infection. Leptospira are shed in the urine from time-to-time for months after clinical recovery. Localization may occur in the pregnant uterus, cause fetal invasion, and abortion 10 days to 4 weeks after infection. 4 Clinical Signs Subclinical Infection: Most infected pigs do not show clinical illness. In finishing barns, leptospirosis has been diagnosed in certain instances because pigs at market show a high prevalence of white-spotted kidney lesions. Acute Infection: In rare circumstances, piglets can become infected and may show signs of dullness, anorexia, and diarrhea. As well, neurological signs may occur. Reproductive Disorders: Clinical signs include abortion, stillbirth, and neonatal mortality, sometimes accompanied by fever, and anorexia in the sow. Jaundice might occasionally be seen. Generally, abortion occurs late in gestation, often within one or two weeks of term. Mummified and macerated fetuses also occur commonly amongst litters of sows with leptospirosis. L. bratislava is believed to be responsible for cases of infertility characterized by repeat breeding. This organism localizes in the fallopian tubes and uterus. Epidemiology The disease is most commonly spread through the urine of carrier animals. Venereal transmission of L. bratislava is important. Spread from wild animals, particularly rodents, are important sources of infection as well. Leptospirosis has been associated with providing sows with water from a pond or other open water source. Human infection from infected pigs is a concern as it is a zoonotic disease. Diagnosis Clinical signs of late-stage abortion, birth of weak piglets, fever, and icterus in older piglets are characteristic of leptospirosis. Postmortem findings of kidney lesions may suggest leptospirosis. Diagnosis can be confirmed by demonstrating a rising titre of antibody to the appropriate strain. Treatment Abortions may be prevented and renal carriers eliminated by parenteral treatment with streptomycin (25 mg/kg) as a single injection. Feed medication with tetracyclines at a level of between 400 and 800 gm per tonne has been recommended as well. Control Killed bacterins containing 7 serotypes including L. pomona and L. bratislava are commercially available and used on almost all sows in Ontario twice before breeding gilts and at each weaning. These are usually combined with porcine parvovirus (PPV). Vaccination may not 5 prevent renal colonization and shedding of the organism during a herd outbreak, therefore herd medication is required. Eradication of the disease involves a thorough clean up of the environment, rodent elimination, and herd medication. This is typically done with injectable Streptomycin followed by in-feed Tetracycline. Leptospira can survive freezing. Feedback programs for parvovirus control could predispose to leptospiral infection. Reproductive Problems Seasonal Infertility Incidence There are herds, which experience lower reproductive performance in July, August, and September. This problem occurs on approximately 10% of farms, and its effects can vary from year to year. Where pigs are raised outdoors or in open-sided barns, the incidence tends to be much higher. Clinical Signs An increased number of sows returning to heat at irregular times (> 25 days) and/or an increase in not-in-pig (NIP) sows at farrowing are characteristic of this syndrome. A NIP sow is one which is found open in the farrowing crate. Regular 21 day returns are generally constant throughout the year. Delayed puberty often occurs along with the decreased farrowing rate. The weaning-to-breeding interval tends to be longer during the July-August-September period as well. Pathogenesis European wild boars are seasonal breeders. It is thought that there is still a tendency in domestic swine to prefer not to farrow at the beginning of winter. Therefore, weaned sows and gilts are less likely to begin to cycle in August. Likewise, sows, which have been bred are apt to lose their pregnancy more easily in the fall than at any other time of the year. Photoperiod is thought to be of importance in stimulating seasonal infertility to occur but the exact mechanism is unknown. Restricted feeding and heat stress appear to be factors. Melatonin is highest in sows in the late summer. Levels of progesterone in pregnant sows in autumn are lower than at other times. Treatment and Control The use of confinement housing, controlled photoperiod, and individual stalls tend to reduce the risk of seasonal infertility. If pens are used, sows should be housed according to parity to separate young parity sows from older parity sows. One theory suggests that increased sow feed intake for the first 3 weeks after breeding will reduce 6 the problem of seasonal infertility. Anticipate from previous experience and breed more gilts. Autumn Abortion Syndrome In cold climates, there is a higher incidence of abortion in October and November than at other times of the year. This occurs with stalled sows in barns where the barn temperature drops substantially from day to night. Autumn abortion can be minimized by increasing feed intake and/or increasing ambient temperatures in gestation barns. Swine Vesicular Diseases Swine Vesicular Disease (Picornaviridae) Affects primarily swine, but humans have occasionally been infected. It is very difficult to eradicate from the environment. First diagnosed in Italy, later other European countries but has not occurred in North America. Vesicular Stomatitis (Rhabdoviridae) Seldom causes disease in pigs, more commonly a cattle problem. Vesicular stomatitis can affect horses, wildlife, and humans. It is endemic in certain areas of southeast USA, but not in Canada. Vesicular Exanthema or San Miguel Sea Lion Disease (Caliciviridae) This disease still exists in marine life along the California coast, but has not been diagnosed in pigs since 1956. A widespread epidemic occurred in the USA from feeding uncooked fish waste to pigs. Systemic Viral Diseases (FAD) (***important) In general, these diseases are characterized by high fever (> 41°C), anorexia, and lethargy. Usually systemic diseases are associated with one predominant sign (central nervous system {CNS} signs, lameness, etc.). However, there are a few systemic diseases that affect a wide variety of body systems and do not present a clear-cut predominant sign. These latter diseases tend to be severe and include diseases such as hog cholera (HC), African swine fever (ASF), and salmonellosis. Clinical presentation of these three diseases can be similar and differential diagnosis may be difficult. These diseases cause vasculitis, resulting in hemorrhage and edema. Postmortem lesions include petechiae and ecchymosis on skin, kidney, and lymph nodes. There may be splenomegaly and infarction. Hemorrhage may occur in the brain and CNS signs might be observed. ASF or HC are reportable diseases in Canada and the United States and federal veterinarians must be notified immediately. 7 ***Hog Cholera or Swine Fever (Pestivirus, Togaviridae) Canada and the United States are free of this important pathogen. The clinical signs include depression with drooping head, fever (> 41°C), huddling, diarrhea or constipation, and nervous signs. Mortality can be very high. Gross lesions include petechial hemorrhages throughout the body including kidney (turkey-egg kidney) and often, splenic infarcts. (Clinical signs similar to Salmonella cholerasuis). ***African Swine Fever (Iridoviridae) This disease is difficult to distinguish from Hog Cholera based on clinical signs and gross lesions. Originally, mortality generally was higher than for HC, approaching 100% but milder forms have evolved. African Swine Fever has spread via food wastes, from ships and air travel to the Caribbean, Brazil, and Europe. (Clinical symptoms similar to Salmonella cholerasuis) Japanese B. Encephalitis (Flavivirus) This disease is spread by mosquitoes, can cause disease in other domestic animals as well as some birds, reptiles, and humans. Pigs are a reservoir for the disease. Geographically, the disease is restricted to eastern Asia including Japan, Korea, India, and Nepal. In swine, the clinical signs are restricted to the fetus and occasionally suckling pigs. Stillbirths, weak newborns, and CNS disease of piglets is typical. Blue Eye Disease (Paramyxovirus) This disease has only been diagnosed in swine and has only been observed in Mexico. Clinical signs include encephalomyelitis in young and growing pigs (ataxia, muscle tremors, paddling, blindness). Corneal opacity occurs in 1 - 10% of piglets. Teschen and Talfan Disease (Enteroviruses) Teschen is a severe disease causing high mortality occurring in Central Europe and parts of Africa. Clinical signs are due to a polioencephaloymelitis. Talfan is a milder disease that has occurred infrequently in North America. Enteroviruses are widespread, but generally not associated with disease problems in Canada At one time stillbirth, mummification, embryonic death & infertility (SMEDI) syndrome was attributed to these viruses. In an outbreak of mummies and infertility that is not caused by parvovirus, one should consider enteroviruses as a possible cause when investigating. 8 Self-study Reportable Bacterial Diseases Anthrax (Bacillus anthracis) Anthrax occurs when grazing animals ingest spores from contaminated pastures, but more likely in swine, infection results from ingestion of contaminated feed containing animal components such as bone meal. Clinical signs may be absent - sudden death (systemic anthrax). Swine with pharyngeal anthrax, the most common form show marked cervical swelling and marked dyspnea leading to suffocation. Intestinal form of anthrax causes bloody feces. Brucellosis (Brucella suis) Canada is free of B. suis and the incidence in the USA is quite low. B. suis can infect humans and cattle. It can be transmitted via semen, but more commonly from ingestion of infected fetuses. The organisms survive in the environment if sanitation is poor. Abortions can occur at any time during gestation. Tuberculosis (Mycobacteria avium, M. bovis, M. tuberculosis) Most tuberculosis (TB) lesions observed in market pigs in abattoirs are due to M. avian. It spreads to swine by birds, especially poultry. A less common but an important source of mycobacterium is sawdust bedding. Herds with outbreaks are encouraged to bird- proof the barn and feed area. Intradermal tuberculin test is seldom used in swine and may fail to identify infected animals. Localized TB infections seldom produce signs of disease. Lesions are generally detected at slaughter as enlarged lymph nodes. These pigs are condemned and the producer is not compensated. 9