Viral Causes of Infertility and Abortion in Swine

CHAPTER 107 Viral 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 causes, such as nutrition, genetics, environment, management practices, and husbandry procedures. This chapter reviews infectious causes of reproductive failure attributable to viruses.


Several viruses have the potential to cause infertility and abortion of swine. The viruses described in this chapter are considered responsible for a majority of the infectious reproductive disorders seen in today’s high-technology swine industry. The viruses commonly associated with episodes of infertility and abortion in swine are porcine reproductive and respiratory syndrome virus (PRRSV), porcine parvovirus (PPV), pseudorabies virus (PRV) (the agent of Aujeszky’s disease), classical swine fever virus (CSFV) or hog cholera virus (HCV), porcine enterovirus (PEV), and encephalomyocarditis virus (EMC). Other viruses may be responsible for reproductive failure, but these pathogens are considered sporadic, with a more regional distribution. and typically causing isolated cases, such as porcine cytomegalovirus (PCMV) and blue eye disease virus (BEDV).


Viruses have the ability to cross the placenta and infect and kill the conceptus. Clinical signs will depend on the stage of gestation when the animals become infected, the pathogenetic mechanisms of infection for the virus, and the degree of virulence of the viral strains.


Gestation in pigs lasts about 114 days. 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 but is not completed until day 18 to 24 of gestation. Death of the conceptus before implantation 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 an irregular return to estrus after 24 to 28 days. Complete resorption of the embryos or an abortion may occur. Sows usually return to estrus between 2 and 10 days after loss of pregnancy.


Fetal death after day 35 typically is followed by mummification of the fetus, rather than by 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. If two or more fetuses survive, normal gestation and parturition can still take place.


At about day 70 of gestation, fetuses begin to develop immune competency. The epitheliomaternal placenta normally does not allow transfer of maternal antibodies to fetuses. Infection before 70 days by certain viruses may result in immunotolerance for the surviving fetuses. Immunotolerant-born piglets may be viremic at birth, and the virus is not recognized by the pig’s immune system.


Infection after 70 days of gestation may result in a successful immune response by the fetus, with the production of antibodies. Although a fetus may successfully produce antibodies, it may still succumb to the virus and be stillborn.


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. Abortions typically result from failure of some maternal system, rather than the effects of the viruses on the fetuses. These system failures and the resultant abortions usually are sequelae of systemic effects of viruses on the dam, such as high fever or viremia.


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). Certain viruses have tropism for fetuses at the end of the gestational stage. Stillbirths also may be caused by noninfectious agents or conditions and are known as intrapartum deaths.1


If less than the entire litter is infected transplacentally, the virus may spread within the uterus and infect littermates at different gestational ages, resulting in a variety of responses within the litter, including reduced litter size, mummification of fetuses, and stillbirths.


Viruses associated with reproductive failure also may cause increased neonatal mortality. 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, or weak piglets infected late in gestation may die soon after birth. In production records, neonatal death usually is captured within the preweaning mortality parameter.



PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS


Porcine reproductive and respiratory syndrome virus (PRRSV) is a fairly new virus first reported clinically in the late 1980s and isolated in Europe in 1991, and in the United States in 1992.2 PRRSV has become the most important virus affecting the swine industry, with estimated annual costs of U.S. $570 million in the United States alone.3



Epidemiology and Clinical Signs


PRRSV characteristically causes both reproductive and respiratory clinical signs.2 Reproductive clinical signs include late-term abortions, premature farrowings, weak-born piglets, and increased preweaning mortality rate. Respiratory clinical signs are due to the presence of interstitial pneumonia in nursery and finishing pigs, which can be complicated by secondary infections. Two main genotypes are recognized: European (or Lelystad virus) and North American. Within each genotype, significant strain variation exists. Differences in strain variation may influence virulence, pathogenesis, and clinical signs.


PRRSV is widely distributed throughout the world. Only few countries are considered free of the disease. Infected countries have widespread prevalence. PRRSV is readily transmitted by contact exposure of secretions of infected animals such as serum, saliva, milk, urine, and feces. PRRSV also is transmitted by semen, and this route of infection has gained greater importance since the increased use of artificial insemination and the establishment of central distribution boar studs. Infected animals can be viremic for prolonged periods of time. Duration of viremia will depend on the age of the animal, with longer periods of viremia in younger pigs than in older animals. After viremia has ceased, virus still persists in the tissues. Different studies show that such persistence may be detected in tissues for more than 100 days. Contact transmission has proved limited, however, in general lasting for up to 80 days after infection, although exceptions may exist.


PRRSV can be readily transmitted by contact with infected surfaces and through iatrogenic transmission by needles or materials that facilitate body fluid exchange.


Transport vehicles not properly cleaned and dried, contaminated fomites, exchange of material between infected and noninfected herds, and failure of farm personnel to follow biosecurity measures are considered important sources of infection between herds.46 Insects and aerosol transmission also have been described as possible sources of infection, but their relevance is still unclear or limited to very specific regions. PRRSV is an RNA enveloped virus that survives well in cold and wet environments, and its infectivity decreases as infected surfaces become dry.



Diagnosis


Late-term abortions, premature farrowings and significant increase in preweaning mortality rate are very suggestive of PRRSV infection.2 Acutely infected young piglets will be viremic for prolonged periods, up to 35 days. Blood samples and infected tissue specimens to detect presence of virus can be tested by virus isolation or polymerase chain reaction (PCR) assay. Several serologic tests that are based on enzyme-linked immunosorbent assay (ELISA) techniques are available commercially. Immunofluorescence assay (IFA) and IPMA tests also are available and are deemed more specific but less sensitive. Serologic tests measure exposure to the virus but not protection. When seronegative populations are monitored using these tests, serologic reactors may be found. In such instances, first performing a test with high sensitivity is recommended, followed by a more specific testing of the reacting samples. In the United States, the combination of ELISA followed by IFA has become the standard diagnostic laboratory procedure.


Infected piglets will be found to have microscopic lesions associated with PRRSV infection. In investigating a reproductive PRRSV infection, samples from weak-born piglets will constitute a good source of virus. Samples from mummified fetuses may yield false negative results because the virus may have become degraded.



Prevention, Control, and Eradication


Recent years have seen considerable advances in the area of prevention and control of PRRSV disease. Many new management techniques provide a means of control and even eradication of most PRRSV infections on swine farms. Control of PRRSV disease is directed at limiting damage from the viral infection; this strategy it is based on management of the replacement animals and prevention of reinfection by new viral strains.


A majority of new infections affecting commercial systems in the United States are considered to be a result of lateral transmission and not due to introduction of infected pigs or semen.6 Area spread from neighboring units, transport of pigs in PRRSV-infected equipment, lack of compliance with biosecurity protocols, and even potential introduction by means of insects58 are considered risks for PRRSV introduction into herds. Biosecurity protocols need to be properly thought out and implemented. Special effort should be made in selecting isolated areas for establishing new units and in reviewing all of the procedures that involve movement of farm inputs and outputs–—transport of pigs, supplies and materials, feed, water, and personnel; removal of manure; and reclaims. Because of the nature of the virus and its excellent survival in cold and wet conditions,4 procedures must ensure the cleaning and drying of all equipment and material used at the farm. In particular, all equipment used for transport of pigs should be properly cleaned and completely dry.5,9 All units also should have biosecurity measures in place to prevent infestation by pests such as rodents, insects, and birds.


Considerable advances in the control of PRRSV disease have been achieved during the last several years; however, control measures remain one of the most frustrating items for practitioners. The central component of PRRSV disease control is the reduction of the spread of the virus within the breeding herd, thereby preventing the infection of offspring before weaning.10 The perpetuation of infection in chronically infected herds may potentially be due to the presence of subpopulations of animals of differing immune status and virus activity.11 A step to prevent the development of such subpopulations has been the introduction of replacement animals that are previously exposed and immune to PRRSV infection before introduction in the PRRSV-positive herds.12 The consistent acclimatization of incoming breeding stock to PRRSV results in the stabilization of clinical signs of disease, the improvement of production parameters, and the production of PRRSV-negative piglets at weaning; therefore, gilt introduction remains the key to PRRSV control.13 Different methods for gilt acclimatization exist, and in general it is accepted that early exposure (at 2 to 4 months of age) will result in homologous protection of the exposed animals and introduction of the replacement animals at a time when shedding has stopped. A major challenge, however, remains the exposure method that will consistently induce PRRSV infection.


Control measures in the weaned pig population should be directed at minimizing the commingling of different pig sources at weaning, streamlining flows, strict implementation of all-in–all-out animal flow, implementation of nursery partial depopulations, and controlling other concurrent infections, mostly bacterial (e.g., Haemophilus parasuis, Streptococcus suis, Mycoplasma hyopneumoniae) and viral (i.e., swine influenza virus) aggravated by the PRRSV infection. Appropriate vaccination and medication protocols need to be determined for the individual infections. Finally, if the suckling piglet population is acutely infected, a series of management strategies directed at limiting the movement of piglets between litters in the initial 24 hours of life, humanely destroying chronically infected offspring before weaning, and maintaining strict all-in–all-out animal flow for the nursery should be helpful.14


Eradication of PRRSV is possible. Spontaneous elimination has been described in small-herd units.15 Consistent PRRSV eradication was not possible until recently, however.16,17 Total depopulation-repopulation, partial depopulation, segregated early weaning, testing and removal, and herd closure are among the most common strategies. The success of PRRSV elimination in the breeding herd resides in the introduction of seronegative nonexposed replacement animals into the breeding herd at a time when virus is no longer present.


Total herd depopulation-repopulation is a very successful technique, although it is costly and may be justifiable only if the elimination of other concurrent diseases is desired. Partial depopulation is indicated for the elimination of the virus from growing pigs when shedding from the breeding population has completely stopped. This technique alone has proved to be enough to eliminate the virus in small size farms.18 PRRSV elimination through the herd closure technique has gained considerable popularity in the United States.17 The principle of this technique is based in the fact that PRRSV infection tends to die out in an immune population over time. This strategy mimics the principles followed for eradication of transmissible gastroenteritis (TGE) in pigs, which ensure that all animals are exposed to the virus and that replacement animals that could perpetuate virus replication are not introduced during that time. In the case of PRRSV, longer periods of herd closure with no introduction of new replacement animals are required. Animals recovered from the infection will eliminate the virus from their tissues, although this will require prolonged periods (about 6 months). Introduction of seronegative replacement animals will be followed by attrition or scheduled culling of the previously infected animals. PRRSV elimination through the test and removal technique has also been used with successful results.16 Elimination of PRRSV by testing and removal consists of blood testing the entire breeding herd, identifying PRRSV-infected animals using tests for both antibody and virus, and removing seropositive animals from the farm.


Several studies have established that vaccination against PRRSV can result in protective immunity.3 Several commercial vaccine products are available today. Both attenuated and inactivated products are available on the various continents. In general, it is accepted that attenuated modified live virus vaccines induce a more efficacious immune response, although concerns regarding safety have been raised for some of the products. Inactivated vaccines also are available, but in general they are considered less efficacious when used in seronegative animals.


When used in the field, vaccines have met with various degrees of success in different countries. Differences may be due to differences in the commercial products available and how these products are utilized, and to differences related to presence of viral strains in different regions in which cross-protection is believed to be very limited. Also, induction of protective immunity among genetically different PRRSV strains, although it is possible, is very limited and difficult to assess. In addition, field reports that document the transmission of the vaccine virus and its reversion to the vaccine virus virulent form also can be found in the literature. Some vaccine virus strains may behave very similarly to field PRRSV strains in relation to persistence, transmission to virus-naive pigs, crossing of the placenta to cause congenital infection, shedding in semen, and length of time required to induce protective immunity. Therefore, issues regarding the safety and efficacy of the live virus vaccine products remain unresolved. Research to provide safer and more efficacious products is in progress.

Sep 3, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Viral Causes of Infertility and Abortion in Swine
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