Chapter 20 Management of pig health.
Profitable pork production in the commercial pig unit requires the development and maintenance of a herd health program based on the prevention and control of infectious and noninfectious swine diseases. Team effort is required between the producer and technical experts, including veterinarians, agricultural engineers, and swine husbandry specialists. The past emphasis on "putting out fires" has been replaced by the current emphasis on disease prevention. Veterinarians increasingly serve their clients primarily by working with them to develop herd health programs centered on sanitation, restricted human and animal traffic onto the farm premises, tailored vaccination and immunization programs, and routine monitoring of overall herd health and production. Early diagnosis, isolation, and treatment of sick animals is critical to the success of individualized herd health programs. The producer, therefore, is a major player in the management of pig health.
This chapter discusses the most common and important infectious diseases, noninfectious toxicants, and metabolic and nutritional disorders that affect swine. Some of the infectious diseases are of special significance because the pathogenic organisms can be spread to humans. Such diseases are termed zoonotic diseases or zoonoses. The chapter provides an introduction to the nature and clinical signs of swine diseases and disorders. No attempt is made to detail the etiology, diagnosis, or treatment of specific infectious diseases. For a more comprehensive discussion, see the benchmark text, Diseases of Swine (edited by Straw et al., 1999).
APPROACHES TO ENSURING PIG HEALTH
Pork producers on a given farm have unique health concerns. The pathogens present, and their virulence, are influenced by the microenvironment, the level of sanitation, the stockmanship, and the flow of people and animals through the facility. When farms are started and facilities are new, the only microorganisms on the farm that are pathogenic to the pigs are those that are brought in on the pigs themselves. After that, pathogenic organisms can be brought in by newly introduced pigs, people, equipment, feed, pets, and wildlife.
To keep pathogenic organisms under control, an effective program of biosecurity, sanitation, and vaccination should be in place (Biehl et al., 1997). The particular organisms that the farm vaccinates against will depend on the pathogens present. It is unwise to vaccinate against microorganisms not found on the farm, unless the farm's pigs are moved to a site that has those microorganisms.
To prevent introduction of new pathogens, an effective biosecurity program should be in place. Biosecurity refers to the barriers established to separate the pigs from the outside world. Some barriers are real and some are not. If two neighbors have pigs that are only 100 m (300 ft) apart, it is virtually impossible in the long run to keep pathogenic organisms from passing between the farms unless extensive and costly measures are in place.
The first rule of biosecurity is to put as much distance as possible between two groups of pigs. Authors argue about how much distance is enough to prevent spread of disease, but the greater the distance, the greater the barrier. Biosecurity protection is proportional to the square root of the distance to the nearest pig of a different origin.
The second rule of biosecurity is to isolate, test, and acclimate incoming pigs. Incoming pigs should be isolated at a great distance (1 mi or more would be better than shorter distances) from the resident pigs. While the new pigs are isolated, they should not have the same caretakers as the main herd to prevent early potential pathogen spread. Isolated pigs should be tested about 30 d (or 15 to 45 d) after arrival to ensure they do not have new pathogens. The exact testing to be conducted depends on what microorganisms the farm wishes to exclude, local regulatory requirements (e.g., testing for pseudorabies or brucellosis), and upon the advice of the attending veterinarian. It is a good idea to put a young pig from the resident herd in with the new animals to acclimate the new pigs to the microorganisms on the farm.
The third rule of biosecurity is to control traffic flow of people, feed, and equipment through the facility and near the pigs. People flow through the facility is often controlled by a shower-in practice that requires visitors and workers to remove their street clothes, shower, and wear clothes that are kept on the farm. This practice requires on-farm clothes-washing facilities. Facilities without walkthrough showers should at least require that visitors wear boots or footwear that remains on the farm. Visitors should avoid contact with pigs for a period of 48 hr or more before their visit. Supplies that enter the farm should be sanitized. Trucks that enter the farm should follow a route not used by the farm workers and, if possible, the wheels of the trucks should be sanitized.
SANITATION AND PIG FLOW
Pigs naturally shed microorganisms; some are pathogens and some are not. In some cases, animal stress leads to increased shedding of microorganisms and, thus, a normally healthy herd can begin to shed pathogenic microorganisms. To minimize the effective dose of bacteria, viruses, and parasites, an effective sanitation program should be in place.
Many newer farms use an all-in-all-out feature that helps to control pathogen spread. If a batch of pigs remains together in the same air space, and if the pigs are healthy to start with, they will probably remain healthy as long as the biosecurity program is not violated (there are rare exceptions). Typically, growing-finishing, nurseries, and farrowing barns are operated on an all-in-all-out basis. Sow breeding and gestation units are commonly in a mixed-batch, large air space. Thus, if the sows due to farrow next week are infected today by older sows, they will be sick and their new piglets may be in peril. Thus, all-in-all-out systems start at birth, often with mixing of the breeding herd. Because the breeding herd is often not managed as an all-in-all-out system, the breeding herd can incubate pathogens.
Effective sanitation (Becker et al., 1990) is performed between batches of pigs in an all-in-all-out system. Marginal sanitation controls can be used while the pigs are present, but clearly these measures will not be effective if the pigs are in the facility and able to re-infect the site immediately. Marginal, but necessary, sanitation measures include sweeping the aisle; timely removal of dead pigs and manure; cleaning; dusting cobwebs; and general housekeeping.
Effective sanitation begins with removal of all organic matter. This is best accomplished with a detergent, warm-water pressure sprayer. Pressure sprayers can be 200 to 1,000 psi, and while greater pressure removes organic matter more easily, it can chip paint and damage equipment. Steam-cleaning is even more effective than using just warm water. Sanitizing kills a large portion (99%) of the microorganisms. Sterilizing kills 100% of the organisms. Sterilization is difficult, but possible, if pressure washing and disinfecting are followed with a gas sterilizing agent. Sanitizing is performed by power washing, drying, disinfecting, and allowing the surfaces to dry.
Among outdoor units, the sun is a powerful sanitizing agent. Farrowing huts should be turned over between uses (flipped) to allow the sun to sanitize the inside of the hut. Pastures should be rotated to allow the sun to impact soil-borne microorganisms. The sun is not very effective against parasites that are in bedding or below the surface of the soil.
Sanitation with agents other than steam heat or sunlight can cause development of resistant microorganisms, which may reduce effectiveness of the agents and lead to food safety concerns. For these reasons, the sanitizing agents should be rotated periodically (at least every 6 m). Table 20-1 provides a list of sanitizing agents, adapted from the Pork Industry Handbook (Meyerholz and Gaskin, 1981). Consult vendors for up-to-date information--new agents are continually developed.
HERD HEALTH PROGRAM
THE OVERALL HERD HEALTH PROGRAM
Each commercial pork production unit should have an overall herd health program (Biehl et al., 1997). A herd health program is typically designed by an attending veterinarian with training and experience with pigs, who reviews the health status of the herd and recommends methods to treat current diseases and methods to prevent introduction of new diseases. The attending veterinarian may be in residence on large farms or may visit as infrequently as once/yr. Even if on-site visits by a veterinarian are infrequent, producers should conduct their disease surveillance efforts and biosecurity program in conjunction with their veterinarian. A valid and open producer-veterinarian relationship will benefit the pigs.
SLAUGHTER CHECKS AND OTHER MEANS OF DISEASE SURVEILLANCE
A method of disease surveillance should be in place (Smith et al., 1990). The veterinarian and the producer should discuss the particular diseases to be monitored. Overtesting is costly, but under-testing can be deadly. The common methods of disease surveillance include:
* Necropsy of ill (euthanized) or dead pigs on the farm and (or) at a diagnostic laboratory
* Blood collection for serology or organism isolation
* Fecal collection for internal parasite evaluation
* Urine collections for metabolic or infectious problems
* Skin scrapings for determination of external parasites
A common method of disease surveillance is to perform a routine slaughter check (Meyer et al., 1990). Some countries perform slaughter checks routinely. Pointon et al. (1999) recommend quarterly slaughter checks to account for seasonal effects. While "normal" pigs are being processed at a plant, the following features can be evaluated:
* Lung lesions, pneumonia, and pleurisy
* Liver lesions due to ascarids (roundworms)
* Snout turbinate damage (atrophic rhinitis)
* Mange or lice on the skin
* Kidney problems such as nephritis (perhaps leptospirosis)
The sample size needed to estimate the population of parasites depends on the incidence of the disease in the herd. If the disease incidence is low, more animals must be sampled. From 10% to 45% of the animals must be sampled at slaughter to get a representative sample. The person doing the sampling can use two scales: present or absent and degree of severity. For most conditions in a healthy herd, the owner simply wants to know if the problem is present or absent. Owners who are attempting to clean a herd of a problem should use a severity score, which better tracks how well the problem is being resolved. If the producer has little hope of resolving an endemic disease, a severity score is important so that control measures can be assessed. For these herds, the severity of disease problems at slaughter are more a reflection of management practices put in place to control the disease.
Euthanasia refers to humane methods of causing death (true or good death). Pigs that are severely ill or in significant or irresolvable pain should be euthanized. Timely euthanasia prevents the spread of disease because pigs that are ill from an infectious disease are likely to spread the disease organisms at a rapid pace.
Several methods of euthanasia are available, but the key result, regardless of the method, is a quick and painless 'death'. The American Veterinary Medical Association (AVMA) endorses a number of acceptable methods of euthanasia of pigs. Some methods that are acceptable to the AVMA are not practical on the farm (i.e., injection with lethal controlled drugs). For each method of euthanasia, the stockpeople should be trained until they reach an acceptable skill level. The acceptable and practical methods of euthanasia on the farm include:
* Any method of humane slaughter used at a processing plant; stunning, and exsanguination
* Penetrating captive bolt (while highly lethal, this method can cause personal injury)
* Lethal gunshot
* Blunt trauma (this method was allowed by the National Pork Board and the American Association of Swine Veterinarians in their recommended methods of euthanasia on the farm)
* C[O.sub.2] asphyxiation
Vaccinations, when available, should be used to control pathogenic microorganisms. Vaccinations can be given by injection (intramuscular [i.m.], subcutaneous [s.c.], or other means), orally, intranasally, or to the sow, which passes the antibodies to the piglets through the milk. Once the target disease is understood, the route of administration may be obvious. However, many vaccinations are given systemically for enteric diseases because the stomach and small intestine may lower the effectiveness of vaccines.
Some vaccinations are less effective than others. Vaccines can lose their effectiveness if stored or handled improperly. Producers should follow the guidelines on the product's label or seek advice from their veterinarian. In addition, the particular strain of microorganism on a given farm may be different enough from the vaccine strain to offer less-than-optimum protection. If pigs are stressed around the time of vaccination, they may be less able to build protective antibodies. If pigs are crowded in a non-sanitary pen and stressed, the microorganism challenge may overwhelm the pig's immune system.
Antimicrobial products are used in pigs to improve health and performance. The antimicrobials used most often are the antibiotics. Other antimicrobial agents include high levels of dietary copper or zinc and various "natural" immunomodulators including vitamins, some minerals, yeasts, bacterial cultures, and certain plant materials.
Antibiotics are given for two purposes. Subtherapeutic levels of antibiotics are often placed in the feed as a method of preventing disease and (or) stimulating pig productivity (weight gain and feed efficiency). Therapeutic levels of antibiotics are given to treat a particular disease. Regardless of the use of the antibiotic, withdrawal times must be followed. Each antibiotic has an FDA-approved number of days that the pigs must not be given the drug before slaughter (see Table 20-2). Some antibiotics have a zero-day withdrawal time, which means feeding may continue right up to slaughter.
Feeding antibiotics to pigs, particularly subtherapeutic antibiotics, is a source of controversy. The administration of antibiotics to animals and humans leads to an increase in the numbers of antibiotic-resistant strains of microorganisms. When resistant strains of a pathogen develop, antibiotics are not effective in treating human and animal diseases that formerly were treatable with a given antibiotic. Some scientists and physicians claim that the development of resistant strains of pathogens as a result of long-term feeding of antibiotics to animals creates a public health problem. The well-documented problem of resistant strains of pathogens in hospitals has led to a practice of frequently changing therapeutically administered antibiotics. It is still unclear whether the use of subtherapeutic levels of antibiotics in swine production contributes to the resistance problem in humans.
Clearly, the best option is to avoid the use of antimicrobials when the pig herd is extremely healthy. Healthy pigs do not need therapeutic antimicrobials. Subtherapeutic antibiotics are less effective at stimulating performance in very healthy pigs housed in a sanitary environment. If vaccines are available to control a particular disease, vaccination is the preferred method to prevent the disease. Still, in some cases, withholding antimicrobials is not in the best interest of sick pigs.
Handlers should perform needle injections carefully and only after receiving training. Table 20-3 shows needle sizes (length and gauge) commonly used for intramuscular and subcutaneous injections. Producers should select the smallest needle that can get the job done, read the instructions that come with the medications, and follow the recommended practices.
Injections should be administered (a) where the least discomfort will result, (b) in the neck or shoulder, but not in the ham, and (c) in the route recommended (under the skin, s.c., or in the muscle, i.m.) (see Figure 20-1).
[FIGURE 20-1 OMITTED]
INFECTIOUS AND NONINFECTIOUS DISEASES
Swine diseases can be classified in many ways, but for the purposes of this chapter, these diseases are grouped into three categories:
* Highly infectious diseases, not presently found in the United States, that would cause significant national and international concern if they were introduced; these diseases include African swine fever, hog cholera, and foot-and-mouth disease
* Highly infectious diseases under federal oversight with an eye toward eradication; these diseases include brucellosis and pseudorabies
* All other diseases found in the United States, including respiratory, enteric, reproductive, metabolic, and noninfectious diseases; these diseases are found on many farms and, in many cases, pork producers accept their presence and live with the conditions in their pigs
Infectious diseases can be classed according to the type of pathogenic agent (bacteria, virus, mycoplasm, and mycotic organisms). Table 20-4 lists the major infectious diseases of swine according to the three categories and the agents responsible for each. Table 20-5 lists other rare infectious diseases of pigs (not discussed here; detailed information on each is available in Straw et al., 1999). Some infectious diseases of swine are also zoonoses--diseases that can infect people as well as pigs. Because of the potential for zoonoses, workers should wash their hands regularly and practice other means of personal hygiene to minimize exposure to potential zoonotic agents.
HIGHLY INFECTIOUS DISEASES NOT FOUND IN THE UNITED STATES
African Swine Fever
African swine fever (ASF) is caused by a DNA virus that is the sole member of a separate viral family. ASF is not found in the United States, Europe, or Asia. ASF virus replicates primarily in the pig's macrophages (but also in other cell types in other organs and tissues). First described in 1921, ASF also infects other nondomestic pigs such as the warthog. Ticks are involved in spread of the virus.
ASF-infected pigs show clinical signs such as internal organ and skin hemorrhage, a very high fever, and loss of appetite. The condition can be confused with hog cholera or erysipelas.
Hog Cholera or Classical Swine Fever
Hog cholera, also called classical swine fever, was eradicated in the United States in 1976, following a 14-yr eradication program. Parts of Europe, most notably The Netherlands (1997), have had recent outbreaks of classical swine fever.
Classical swine fever is a highly contagious RNA virus, sharing the viral genus Pestivirus with bovine viral diarrhea. Symptoms include a very high fever of 41[degrees] to 42[degrees]C (106[degrees]F) and respiratory and enteric symptoms. The pig's eyes may be crusted shut.
Foot-and-mouth disease (FMD) is caused by an RNA virus. FMD was last reported in the United States in 1929. The same picornavirus that causes FMD in pigs also infects ruminants like cattle and buffalo. Pigs shed FMD virus at a greater rate than do cattle.
An outbreak of FMD in Taiwan in the late 1990s and in the United Kingdom and some countries in continental Europe in 2001 devastated the local pig industry and essentially halted pork exports. Hogs in parts of Asia remain infected.
FMD starts with vesicular lesions in the mouth and between the toes. A related, yet clearly different, disease is vesicular stomatitis (VS, one of several vesicular diseases). VS resembles FMD in the mouth lesions, but the morbidity and mortality do not occur in VS. Other symptoms of FMD include fever, chomping and salivation, and lesions of the feet, toes, and skin. Mortality in animals with FMD can be low (>5%) or higher (50% to 100%) depending on the strain of virus.
INFECTIOUS DISEASES THAT ARE BEING ERADICATED FROM THE UNITED STATES
Brucellosis is a bacterial disease of swine that also infects cattle, sheep, wildlife, and humans (Leman, 1979). The Brucella genus contains six species, one of which is Brucella suis. The species of Brucella that affects pigs is not thought to be infectious to people.
Most U.S. states have a low or zero incidence of Brucella infection. When a herd is discovered to have brucellosis, it is quarantined and an attempt is made to eradicate the disease from that herd. One major problem with eradication is that some wild or feral pigs in the southern United States are infected with Brucella. These reservoirs are difficult to eradicate. However, intense efforts at eradication of brucellosis from U.S. swine herds have been highly successful. Brucellosis-free status has been attained in many states and the prospects seem excellent for complete eradication of brucellosis in the entire U.S. swine population.
Symptoms of brucellosis in pigs include abortion, infertility, lameness, and variable signs of fever. Symptoms may not persist and death is not a major symptom. Bacterial shedding can be significant for 30 d but may persist for over 2 yr.
Pseudorabies, or Aujeszky's Disease
Pseudorabies (PRV) is caused by a DNA virus. Pigs are considered to be the natural host (Mare et al., 1991). PRV can infect cattle and other ruminants, causing a "mad itch." Pseudorabies has been present in the United States for nearly a century, but its importance was not fully appreciated until the 1980s. PRV is caused by a member of the herpes virus group and, unlike most herpes viruses whose host range is limited to a few species, PRV affects most mammals and many birds. Pigs are the major reservoir for PRV because most other animals, including cattle, sheep, dogs, cats, and mice, are killed by the infection. Mortality in swine infected with PRV is highest in baby pigs, but is usually nil in mature swine. The incubation period is about 30 hr. The first signs of the disease are sneezing, coughing, and a slight fever, followed by excessive salivation, muscle spasms, convulsions, and paddling, and finally death after 4 to 9 d. Pigs less severely affected may recover after a few days of fever. Pseudorabies virus crosses the placenta. If infection occurs prior to 30 d gestation, embryos are resorbed; infection after 30 d gestation may result in death of some or all fetuses or the birth of stillborn or weak-infected piglets. Many diagnostic procedures have been developed and vaccines are available.
Most U.S. states have a low or zero incidence of PRV infection. When a herd is discovered to have PRV, it is quarantined and an attempt is made to eradicate the disease from that herd. Wild or feral pigs in the southern United States are infected with PRV. Effective vaccines are available for PRV, including a genetically modified virus whose inoculation can be separated from natural infection. A program of eradication of PRV in the United States is underway and, if successful (only 312 U.S. herds remained quarantined for PRV in November 1999), the effort will be a significant success story and will represent a major contribution to the future of commercial pork production.
Viral strains of PRV differ in symptoms. The most common symptoms include respiratory, enteric, and nervous system symptoms (especially ataxia) and reproductive problems (infertility, increased stillbirths).
INFECTIOUS DISEASES THAT SOME U.S.PORK PRODUCERS "LIVE WITH"
The primary mode of transmission of infectious respiratory diseases of swine is nose-to-nose contact. Pigs expose one another through social contact. In addition, aerosol transmission is possible for most respiratory pathogens. When respiratory pathogens are present, the air quality of the facility becomes especially important. Reducing dust and noxious gases can reduce respiratory symptoms.
Respiratory pathogens travel on particles of dust or water. The particles of smaller size, particularly those smaller than 10, 5, and 2.5 microns, will embed deep in the lung. Dust particles of greater than 10 microns are likely to be caught in the turbinates. Dust particles, with attached bacteria, that are less than 2.5 microns are considered a health risk. Lung alveoli are excellent culture media for bacteria. Every effort should be made to reduce respiratory pathogen concentrations and dust in the air to reduce respiratory symptoms.
Porcine respiratory and reproductive syndrome (PRRS) symptoms were first reported in the United States in 1987. The syndrome may have been present much earlier but was called other names. PRRS virus was isolated and reported in 1991 and, in that year, the name was agreed upon by the international community. PRRS is a troubling disease because it is now widespread in the United States and Europe, even though the virus has unique characteristics on each continent.
PRRS virus causes reproductive problems such as abortion and infertility. A lower farrowing rate and a slightly lower number of pigs born alive are the major symptoms in the sow herd. Among nursery and growing-finishing pigs, the major symptom is a respiratory syndrome. Increased morbidity and mortality associated with other respiratory pathogens will be observed if the PRRS virus is present.
Because the genetic variability of the PRRS virus is so great and because it is known to mutate rapidly, vaccines are less effective than for other pathogens. Also, because the PRRS virus infects the pig's macrophages, the virus is effective at lowering the pig's ability to mount an immune response.
PRRS can be controlled by strict biosecurity. To maintain a PRRS-negative herd, incoming animals should be held in isolation and tested before entry into the herd. No therapeutic agents are available. Modified live-virus and killed vaccines against PRRS are available and effective in controlling the respiratory, but not the reproductive, component of the disease. The effectiveness depends on the strain of PRRS virus involved. PRRS is widespread in the United States and interacts with Mycoplasma hyopneumoniae (discussed under Mycoplasmal Diseases) in affecting the clinical signs and lung lesions produced. Research at Iowa State University by Thacker et al. (cited by Carlton and Miller, 1999) showed that pigs inoculated with M. hyopneumoniae 21 d before PRRS virus inoculation had no observable Mycoplasma pneumonia, but did have PRRS-induced lung lesions that persisted for 4 wk after the PRRS virus inoculation. In contrast, PRRS-related lesions were resolved within 4 wk in pigs inoculated with only PRRS virus. This suggests that the chronic inflammatory response produced during the course of Mycoplasma pneumonia aggravated the adverse effect of PRRS virus on the lung lesions. Therefore, controlling M. hyopneumoniae infection may be critical in reducing the impact of PRRS-induced pneumonia. The respiratory syndrome, involved when PRRS virus and M. hyopneumoniae are present together, has resulted in the coining of the porcine respiratory disease complex (PRDC). Because vaccines against PRRS are less than totally effective, prevention of exposure is preferred. Cleaning up a herd without depopulation has been performed, but is very difficult.
Atrophic rhinitis (AR) is a disease of the snout of the pig with complications of pneumonia and other respiratory ailments. The bones of the snout contain four (two on each side of the nasal septum) spiral-shaped cartilages that serves to warm, humidify, and filter incoming air. In particular, respiratory pathogens are caught in the convoluted, moist turbinates and prevented from entering the lungs.
A pig with severe AR has a snout that is either twisted or snubbed. As the turbinates are damaged by bacteria, and the snout continues to grow, its growth will favor the less-affected side of the snout. If turbinate damage is very severe, both sides will be stunted resulting in a snubbed look.
AR is caused by more than one microorganism. Two leading candidates as the cause of AR are toxigenic Bordetella bronchiseptica and toxigenic Pasteurella multocida. Each organism alone causes variations in the AR syndrome, with both microorganisms, the full disease syndrome is present. When B. bronchiseptica infects the pig's nasal cavity, the organisms attach to the epithelial surface, proliferate, and destroy the cells in the region and diffuse into the nasal turbinates, which become distorted due to altered bone metabolism. The first clinical signs are sneezing, followed in about 3 wk by turbinate atrophy (see Figure 20-2) and nasal bleeding (turbinate atrophy is not detectable in the live animal until facial distortion begins weeks later). Positive diagnosis is made by post mortem examination of a cross section of the nasal cavity. There is no cure for the nasal turbinate destruction and facial distortion associated with severe AR. Noninfectious irritants, such as dilute acetic acid infused into the nasal cavity, can produce turbinate atrophy in young pigs free of B. bronchiseptica (Logomarsino et al., 1974). High levels of ammonia in poorly ventilated swine buildings may aggravate turbinate atrophy in B. bronchiseptica-infected pigs (Curtis, 1981). Cats, rodents, and other animals are carriers of B. bronchiseptica. Vaccination against B. bronchiseptica controls bordetellosis and AR in swine herds.
[FIGURE 20-2 OMITTED]
Because AR involves changes in bone metabolism, the possibility of a nutritional component in the syndrome has been examined. Distorted and abnormal turbinate bone and twisted snouts indicative of AR have been produced in growing pigs by dietary calcium levels below the requirement and phosphorus levels much higher than the requirement (Brown et al., 1966). Bone lesions are characterized by excessive bone resorption and replacement of bone tissue by fibrous tissue (fibrous osteodystrophy). Dietary calcium-phosphorus imbalance produces nutritional secondary hyperparathyroidism, resulting in excessive calcium removal from bone (Brown et al., 1966). When toxigenic Pasteurella multocida is present, the disease is considered progressive with significant morbidity and performance problems.
The primary symptoms of AR are respiratory tract problems, such as runny noses, sneezing, watery eyes, and bleeding nose and increased incidence of pneumonia. The primary diagnostic tool is the slaughter check, when the snouts are cut in cross section between the molars and the turbinates examined and scored for damage.
AR increases mortality somewhat due to respiratory tract infections, but more commonly, an entire herd has chronic respiratory morbidity. The loss due to reduced pig performance can be very costly.
Secondary respiratory diseases are common for pigs with AR. Mycoplasmal hyopneumonia is common among AR-affected pigs, but the two diseases can be found independent of each other.
Environmental problems in pig facilities exacerbate the symptoms and performance problems associated with AR. Management or facility practices that increase the severity of AR include a large number of pigs in a single air space, crowding, poor ventilation, high levels of dust and ammonia, continuous pig flow, poor sanitation, and indoor housing in general.
Vaccines are available to treat AR, but are considered only partially effective. Some antibiotics are effective, again in part. Even with the best medication a herd with AR will typically have measurable lung lesions and turbinate damage upon slaughter check.
Formerly known as enzootic pneumonia, mycoplasmal pneumonia is caused by Mycoplasma hyopneumonae (Hogg et al., 2001). Mycoplasmal bacteria do not have a cell wall, as do many other bacteria. Because many antibiotics inhibit bacterial growth by interference with growth of the bacterial cell wall, many antibiotics, particularly in the early years of therapy, were not effective in control of mycoplasmal pneumonia. Also, due to its unresponsiveness to antibiotics, the causative agent was thought earlier to be a virus; researchers now know the disease is caused by a Mycoplasma.
Mycoplasmal pneumonia is a chronic respiratory disease that shows high morbidity and relatively low mortality. The most common clinical sign is a nonproductive cough. Upon slaughter check or necropsy, characteristic lung lesions are observed. The typical lung lesions are at the tips of the lobes where small dust particles lodge and inoculate the lungs with the microorganism.
Some antibiotics are effective at reducing the symptoms. Vaccines are available. Complete control is not possible because herds that both vaccinate and use antibiotics still have morbidity. Medicated, very early weaning programs have been used to eliminate the causative microorganism in some herds.
The primary concern with mycoplasmal pneumonia is the performance set-back associated with chronic infection. In addition, when other respiratory pathogens are present, such as PRRS or AR, the herd has significant respiratory symptoms.
Other mycoplasmal microorganisms cause different problems. The second most reported mycoplasmal problem is associated with arthritis. The arthritis is responsive to antibiotics and cortisone. Infected pigs develop immunity to later infection.
Formerly known as Hemophilus pleuropneumonia, Actinobacillus pleuropneumonia is widespread and of particular concern in intensive pig units. The causative agent is the bacterium Actinobacillus pleuropneumoniae.
The onset of the disease is very rapid. Typically, certain pigs become ill very quickly, with a high fever and loss of appetite. There may be some diarrhea or vomiting. Pigs develop respiratory distress rapidly, with breathing through the mouth and may have a foamy, bloody discharge through the respiratory tract. The onset of the disease can be just hours after infection. Stressing the infected pigs will bring on a storm of morbidity and mortality. In the chronic form, there may be no fever and only an occasional death. The disease symptoms are much worse when other respiratory pathogens are present.
Upon necropsy, large areas of the lungs are affected, showing large, dark-red areas of damage and associated pleurisy.
Certain antibiotics are very effective; however, antibiotic-resistant strains have been reported. Vaccines are available. Most farmers prefer to keep the disease out by strict isolation of incoming animals.
Swine influenza (SI) is caused by a type-A influenza virus. The causative agent is an RNA virus in the Orthomyxoviridae family. The most prevalent strain of swine influenza in the United States is H1N1. A new strain, H3N2, previously found only in Europe, has recently been identified in the United States (Miller, 1999). There is evidence of cross transfer between pigs and people (as well as among other species).
SI has a rapid onset and a rapid recovery. Pigs will spike a fever and have respiratory symptoms. Pigs will have labored breathing and will not be willing to move. The mortality is usually low, but the morbidity can be 100% of the pigs in a given air space. Symptoms in an infected herd may be absent 7 d after its onset.
SI has no effective treatment. The symptoms can be treated by providing a warm, draft-free, low-dust environment. Vaccines are available. Affected pigs develop active immunity to subsequent exposure to a particular strain of the virus.
Pneumonic pasteurellosis is caused by Pasteurella multocida, a-gram negative bacterium widespread in the industry. Pasteurella is often associated with chronic respiratory disease in affected herds, especially in the porcine respiratory disease complex (PRDC).
A variety of antibiotics can be effective; however, many antibiotic-resistant strains are found. Antibiotic therapy is often reported to be ineffective at control of PRDC when Pasteurella is involved. Early weaning can control the disease. Some vaccines are available, with limited effectiveness.
The primary mode of transmission of infectious enteric diseases of swine is nose-to-nose and nose-to-feces contact. Pigs expose one another through social contacts as well. The primary symptom is diarrhea, which varies in color and consistency with the causative agent. Sanitation is especially important when enteric diseases are present. When enteric disease occurs, pigs become dehydrated, and dehydrated pigs are easily chilled. Replacement hydration and a warm environment are important.
Transmissible gastroenteritis (TGE) is a viral enteric disease of swine (Haelterman and Bohl, 1993). TGE virus is a coronavirus containing RNA. Surface antigens are similar on a related virus called porcine respiratory corona virus (PRCV) and laboratory assays may cross react.
When a herd is first infected, the onset of TGE often begins with vomiting, followed by severe diarrhea. A very high mortality (up to 100%) is observed among young pigs (nursing and recently weaned). If sows have protective antibodies in their milk, the symptoms will be worse among weaned pigs. While enteric symptoms are found among growing-finishing pigs, the mortality among older pigs is lower. After pigs are infected, surviving pigs have damaged villi in their small intestine and may have a severely reduced growth rate and feed efficiency. The incubation period is short (24 to 48 hr) and antibiotic treatment is ineffective, so the prevention of large losses due to an outbreak of TGE depends on diligent management and sanitation. The organism is carried mechanically on boots, and vehicle wheels contaminated with excreta from infected animals; strict isolation of infected from susceptible animals is essential. The economic impact of an infected herd is significant.
Survivors develop long-term immunity. Vaccination of the sow against TGE provides immunity of the newborn pig against the disease. In retrospect, it is of interest that perhaps one of the first oral vaccines of practical use in swine disease control was discovered empirically by pork producers who found that a degree of immunity against TGE in newborn pigs was attained by feeding the ground carcasses of pigs that died from TGE to pregnant sows.
Effective treatments for TGE are not available. The symptoms should be treated by attempting to keep the pigs warm, dry, and hydrated. Prevention of entry of the TGE virus is important. Vaccines are available. Some herds will re-feed dead or euthanized pigs to the sow herd to build immunity.
Escherichia coli is a natural inhabitant of the gastrointestinal tract. However, some strains of gram-negative E. coli are pathogenic. Other names for various forms of E. coli infections are collibacillosis (Kohler et al., 1994) and gut edema (Bergeland and Kurtz, 1992). Gut edema is believed to be a manifestation of an anaphylactoid response to the absorption of E. coli toxins absorbed from the intestinal tract. The syndrome often occurs following a sudden change in diet or management. Severely affected pigs may exhibit circulatory distress as indicated by dyspnea (labored breathing) and cyanosis (reddish patches on body surface and/or deep-red or bluish ears due to poor oxygen supply to tissues). E. coli infection can lead to a deadly septicemia. Other forms of E. coli cause mastitis or urinary tract infections.
E. coli most typically causes significant enteric problems for nursing piglets and weaned pigs. In weaned pigs, the condition is called milk scours or white scours. Morbidity is the primary economic concern, but short-term mortality can be observed. In gut edema, a severe edema is evident, including edematous eye lids. Post-weaning diarrhea is common when the maternal milk antibodies are no longer available to protect the gastrointestinal tract of pigs.
Antibiotics are effective in many cases. Vaccines are available. The environment contributes to the severity of the disease--a cool, drafty environment will cause greater problems for the affected pigs.
Swine dysentery, also known as bloody scours or vibrionic dysentery, is caused by the bacterium Serpulina hyodysenteriae (Harris et al., 1993). This gram negative bacterium causes a bloody diarrhea. Seven serotypes of the bacterium have been reported.
The incubation period (time from exposure to disease onset) is about 2 wk. Death losses may be 25% or 30% in growing pigs. Often, no fever is present in affected animals. The first indication of the presence of swine dysentery in a herd may be the sudden death of one or more animals with no previous symptoms. Infected animals that survive may be re-infected within a few weeks or months, suggesting that little or no immunity is acquired by infected animals. The primary symptom of bloody diarrhea is accompanied by signs of fever, loss of appetite, mucous discharge into the feces, arched back, and kicking indicative of gut pain.
Several antibiotics are available to treat the condition. Pigs are often treated through the water or the feed, but water medication is preferred. Sanitation and provision of a warm environment will prevent the disease from becoming severe after antibiotic therapy has started. Incoming animals should be free of this disease to maintain dysentery-free status of the herd.
Ileitis, or Proliferative Enteropathies
Ileitis is related to other conditions such as proliferative enteropathies, proliferative ileitis, and porcine intestinal adenomatosis (Lomax et al., 2001). The term proliferative enteropathies refers to the collection of diseases in this category--acute and chronic conditions with differing clinical signs and different causes. The primary microorganism is Lawsonia intracellularis, a bacterium that grows inside intestinal cells. Lesions found in ileitis include thickened mucosa in the distal small intestine and proximal large intestine.
The main symptom is loss of appetite and slowed growth with only occasional diarrhea in growing-finishing pigs. Some mortality may be observed, but the major problem is loss of performance due to loss of appetite and a wasting syndrome. Some antibiotics are reported recently to be effective against ileitis. Vaccines are not yet available.
Salmonellosis, known simply as Salmonella, is caused by one of several species of gram-negative bacteria, including Salmonella cholerasuis. Other species, including S. typhimurium, are zoonotic.
Salmonella is found most commonly in intensively kept, weaned pigs. In the form leading to septicemia, pigs develop a fever, loss of appetite, and some breathing difficulty. Stressful situations cause a rapid onset of the disease. In the enteric form, weaned pigs have a watery diarrhea that may later contain blood. Mortality is usually low, but morbidity is high.
While several antibiotics are effective, antibiotic-resistant strains are reported to be widespread. Sanitation and good management practices are important to control the disease. Most pigs are thought to be infected with one or more strains of Salmonella. Pathogenic Salmonella have been isolated from numerous species of birds and animals in addition to pigs and humans.
Coccidiosis and Toxoplasmosis
Coccidiosis is caused by the parasite Isospora suis and other parasitic species (Hall et al., 2001). Isospora must pass through the pig or other animals to complete its life cycle. The feces of infected pigs are contagious to other pigs.
Pigs with coccidiosis have a yellow-to-grayish diarrhea that turns very watery. Nursing and weaned pigs can be affected. Morbidity can be very high, but mortality is usually low.
Dehydration is the primary concern and supportive therapy should be provided. A warm, dry, clean environment is important. Some coccidiostats are available. Sanitation and prevention are important in the control of the condition.
Toxoplasmosis, a related parasitic disease, requires cats as an intermediate host. Toxo (as it is called) is caused by the protozoan Toxoplasma gondii. Most infections are subclinical. Toxo is a serious zoonotic disease. There is no reported effective treatment and vaccines are not available. Prevention of entry of the disease is important.
Clostridium perfringens and Related Tetanus
Clostridium is a genus of gram-positive bacteria that includes Clostridium perfringens, C. tetani, C. botulinum, and others. The most common form is C. perfringens Type C.
C. perfringens can take several forms. The most common form causes a rapid death associated with an acute fever and hemorrhagic diarrhea. The body temperature may drop prior to death. In one form, piglets die within 3 d of life. Older pigs may have a nonhemorrhagic diarrhea with yellow-gray, mucous feces. While death is unlikely in older pigs, the performance setbacks can be significant. Once clinical signs are observed, the intestinal damage is already severe. One form of the disease infects the skin and can cause gangrenous lesions.
Some antibiotics are effective. Vaccines are available. Antibodies in the sow's milk are important and piglets should be vaccinated at 3 wk of age to minimize post-weaning effects.
Rotaviral diarrhea is caused by the RNA-containing rotavirus (Saif et al., 1987). There are many serotypes and the virus is widespread in nature.
Rotavirus causes significant diarrhea in young piglets, especially those less than 1 wk of age. The diarrhea is watery-yellow to white. Mortality can be very high, but morbidity is always high. The rotavirus causes lesions on the small intestine epithelium. Rotavirus diarrhea appears to be aggravated by the presence of E. coli and other pathogens, and following stressful changes in the environment (crowding, environmental temperature, change to solid feed).
There is no effective treatment for rotavirus infection. Antibiotics can be given for secondary bacterial infections. A warm environment is very important and fluid therapy is recommended. Most adult swine have serum antibodies against rotavirus and provide passive immunity to their offspring via colostrum. Management practices should be directed at sanitation, generating passive maternal immunity, and reducing the viral load, if possible. Vaccines are available.
Reproductive diseases of swine cause two main problems: (1) reduced farrowing rate and lower numbers of pigs born alive and (2) abortions and failure to cycle (Leman, 1979). Diseases that cause abortion may do so in an obvious manner wherein the aborted fetuses are observed, or in a less-obvious manner wherein the abortion is early enough in gestation that the aborted embryos or fetuses are reabsorbed. Diseases that increase the numbers of mummies (partially decomposed) or stillborn pigs are obvious to the animal caregiver. Seasonal variations in fertility should be considered when one attempts to understand variation in fertility.
Leptospirosis is caused by at least eight species of spirochete bacteria of the genus Leptospira. Leptospirosis (lepto) is widespread in the world, found in all the major pig-producing countries. Leptospirosis infects the urinary and reproductive tracts of pigs, causing both kidney and reproductive failures.
The majority of signs of lepto are subclinical. In its acute form, symptoms include septicemia, loss of appetite, and fever. The primary signs of chronic leptospirosis are infertility, late abortions, stillbirths, and unthrifty piglets. The reproductive failures can have significant economic cost. Lepto is a potential zoonotic agent.
The incidence of leptospirosis is high in deer and other wildlife as well as in farm animals. Transmission occurs by coitus, by the ingestion of contaminated feed and water, by eating infected rodents or their tissues, or by entrance of the organism through skin abrasions or conjunctiva. While antibiotics can be effective, most producers control lepto through vaccination.
Parvo virus (parvo) is a DNA-containing virus that can cause significant reproductive problems. Parvo is widespread in the United States and Europe. The virus can replicate in pigs of any age, but the main clinical sign is reproductive failure in pregnant sows.
The primary clinical sign of parvo is an increase in the number of mummified and stillborn piglets. Primary control is through vaccination. There are no effective treatments. Prevention of entry into the herd is critical.
EXTERNAL AND INTERNAL PARASITES
Many parasites affect swine, but most do not survive in humans.
Sarcoptic mange mite (agent: Sarcoptes scabiei). The sarcoptic mange mite burrows under the outer layers of the epidermis and causes irritation and thickening of the skin (McKean et al., 1999). (The subspecies of S. scrapiei that affects pigs apparently does not affect humans and vice versa.) In severe cases, the entire body surface is covered with thick, scurfy skin and alopecia is common. Appetite and weight gain may be reduced. Severe lesions resemble those of parakeratrosis, the zinc-deficiency disease of swine, but the microscopic examination of skin scrapings of affected pigs allows identification of the mange mite. The drug ivermectin, administered orally, parenterally, or topically, affords complete elimination of the mange mite, along with other external parasites and many internal parasites. Application of solutions of currently approved insecticides using liquid spray under pressure to penetrate the outer layers of epidermis is also somewhat effective in control of mange. Legal requirements for application and withdrawal before slaughter must be followed.
Demodectic mange mite (agent: Demodex hylliides or D. folliculorum). This mange mite is less common than S. scabiei, but occurs frequently in humans, dogs, sheep, and other mammals. It is easier to control because it does not penetrate the skin layers so deeply. Control is the same as for sarcoptic mange.
Louse. One species of lice, Haematopinus suis, occurs in pigs. Continual skin punctures made by the louse to suck blood result in irritation and in rubbing by the pig against any available object for relief. Control is by topical application of dry powder or spray containing any currently approved insecticide. Ivermectin is also effective in controlling lice. Legal requirements for application and withdrawal before slaughter must be followed.
Other External Parasites. Several other external parasites are pests of swine, including fleas, flies, and ticks. Their control is the same as that for lice.
Several internal parasites affect pigs (Biehl et al., 1993), but the most important economically are Ascaris suis and Trichinella spiralis. Other parasites include the whipworm (Trichuris suis), nodular worm (Strongulodes ransomi), lung worm (Metastrongylus species), liver fluke (Fasciloa hepatica), kidney worm (Stephanuses denatus), and Taenia solium, whose larvae invade the cardiac muscle, diaphragm, tongue, and other muscles. Currently approved oral medications are effective in controlling each of these parasites. Ivermectin, administered orally or parenterally, is effective against most.
Ascarids (agent: Ascaris suis or A. lumbricoides). The ascarid (Stephenson et al., 1980) is ubiquitous in swine populations and is economically important because of its negative effect on growth and feed utilization and tissue damage caused by its migration through the lungs and liver during the larval stage of its life cycle. The cycle is diagrammed in Figures 20-3a and 20-3b.
The adult lives in the small intestine where it mates. The fertilized eggs are excreted in the feces and go through a period of maturation on the ground; the duration of maturation depends on environmental temperature and humidity. The larvae, if ingested by a pig several weeks later, are swallowed. After dissolution of the protective covering by the digestive processes of the host, the larvae are absorbed into the blood from the intestinal tract. The developing larvae lodge in the liver where scar tissue is formed at the local site of intrusion. Heavy infestation results in severe liver damage seen at slaughter as white fibrous tissue scars on the surface of and within the liver. Severe scarring results in condemnation of the liver for human consumption. For comparison, note the smooth, dark surface of a normal liver shown in Figure 20-4.
The adverse effects of ascarid infestation are manifested both by competition between the adult ascarid and the host for nutrients and by the liver damage caused by the migration of the ascarid larvae. Small intestine weight is increased in direct proportion to the ascarid load. Nutritional research shows that the intestinal tract represents a disproportionate share of the energy requirement of the pig. Therefore, a heavy burden of ascarids undoubtedly decreases the efficiency of pig growth by increasing the energy required to maintain the hypertrophied small intestine. From the liver, migrating larvae are pumped by the heart to the lungs where they are expelled into the bronchioli and coughed up into the mouth. They are swallowed and enter the small intestine where they mature and repeat the cycle. The coughing associated with the migration through the lungs may be confused with signs of infectious respiratory disease. The migration and associated coughing usually persist only a few days. Ascarid larvae pass the placental barrier and infect the fetus in utero. Effective control of ascarids is accomplished by a choice of several treatments, including piperazine, and currently approved feed additives. Most of these antihelminhtics are effective against other internal parasites as well. Ivermectin administered parenterally or orally is also effective against ascarids and other internal parasites.
[FIGURE 20-3 OMITTED]
[FIGURE 20-4 OMITTED]
Trichinosis (agent: Trichinella spiralis). This parasite is highly infectious to humans and, for this reason, remains a detriment to pork consumption, even though the incidence of trichinosis in humans in the United States is nearly zero. However, the incidence worldwide remains significant (this issue is discussed in more detail in Chapters 3 and 9). The life cycle is diagrammed in Figure 20-5 and is described briefly here. Adults live and mate in the intestinal tract of the host (pigs, humans, rodents, and other animals) and fertilized ova are deposited in the intestinal mucosal lining. The larvae pass into the lymphatic system and blood and become encysted in the diaphragm and skeletal muscle of the host. The time required from original ingestion of infected meat to encysting of the larvae in skeletal muscle of the host is 1 to 4 wk. The encysted larvae can remain viable in the skeletal muscle of the host for several yr. The ingestion of infected pork by humans results in severe nausea, anorexia, and digestive upset followed by muscle pain as the larvae migrate to the skeletal muscle. Effective treatment is available.
Rapid laboratory testing allows detection of the presence of Trichinella in pork, so the source of infection often can be identified. Trichina organisms are destroyed by heat (77[degrees]C (170[degrees]F) for 30 min) or freezing (20 d at 5[degrees]F or -15[degrees]C). Irradiation of pork in U.S. slaughter plants has been approved recently. Irradiation destroys trichina and, therefore, represents yet another effective means of eliminating trichina from pork.
[FIGURE 20-5 OMITTED]
JOINT AND ARTHRITIC CONDITIONS
The causative agent for erysipelas is the bacterium Erysipelothrix rhusiopathiae, a gram-positive bacillus that is widespread in the swine industry. Like brucellosis and leptospirosis, erysipelas is a zoonotic disease. In its acute form, the clinical signs include anorexia, apathy, and high fever that may persist for several days. The acute signs can be controlled by antibiotic treatment. The acute form may be followed by chronic erysipelas with inflammation, swelling, and stiffness of the joints. Occasionally, large, diamond-shaped red blotches may appear, accounting for the term "diamond skin disease." Chronic erysipelas can be treated and cured with antibiotics. Routine immunization against erysipelas is an effective control measure.
Other Joint Problems
Pigs can have swollen joints due to infection caused by a number of agents (Ross and Bailey, 1991) including streptococci, Mycoplasma hyosynoviae (Ross, 1981), or Actinobacillus suis as well as by physical injury or nutritional or genetic problems leading to osteochondrosis.
OTHER POTENTIAL PIG HEALTH PROBLEMS PSS/PSE
Porcine stress syndrome (PSS) is a condition in live pigs in which the pigs are highly susceptible to stress. The term malignant hyperthermia syndrome (MHS) has also been applied to PSS pigs, because of the elevated body temperature during stress. Affected pigs become red-skinned, have a spiraling hyperthermia (called malignant hyperthermia), and shake, lie down, and often die. If the PSS pig is stressed immediately before slaughter, even mildly, it will have light-colored (pale), soft and watery (exudative) meat (PSE) (see Chapter 9). Carrier pigs that have one copy of the mutated gene show some symptoms and pigs with two copies of the recessive gene have a high incidence of the condition (see Chapter 6). Selective breeding can easily eliminate the disease.
MMA or PPDS
When lactating sows either stop milking or significantly reduce milk production (Wagner et al., 1993), the cause may be what was formerly known as the syndrome mastitis-metritis-agalactia (MMA). MMA is known now as postpartum dysgalactia syndrome (PPDS). PPDS is known for a hypogalactia (low milk production) more often than complete cessation of milk production (agalactia).
PPDS is often, but not always, associated with metritis (inflammation of the uterus). Metritis is common particularly in sows that had a difficult or assisted farrowing. The fever and loss of appetite leads to constipation and a general malaise. The enclosure of sows in farrowing crates that restrict movement does little to help the constipation (exercise reduces the likelihood of constipation).
When sows get mastitis, their piglets may starve to death. The follow-up to PPDS is unthrifty piglets and difficulty in rebreeding sows. Piglets on PPDS sows can be saved by feeding them either supplemental feed while with the sow or by early weaning.
Swinepox (agent: swinepox virus and vaccinia virus)
Swinepox causes skin eruptions that persist over the entire body for 1 to 2 wk and then disappear. Swinepox virus and vaccinia virus are similar. Vaccinia virus is a laboratory strain that was used for immunization against smallpox in humans until the eradication of smallpox eliminated the demand for the vaccine. Pigs with swinepox reduce feed intake for a few days, then usually recover without complications. Death is rare. A high level of permanent immunity follows the disease.
Porcine Respiratory Disease Complex (PRDC) (agents: PRRS and Mycoplasma hyopneumoniae)
This common syndrome involves an interaction of PRRS virus and Mycoplasma pneumoniae to produce clinical signs distinct from those observed when either of these pathogens is present separately. The clinical signs of PRDC are therefore variable, depending on poorly understood relationships between PRRS and Mycoplasma hyopneumonia and their respective vaccines. The control of PRDC appears to depend on the selection of appropriate timing of vaccination against PRRS and Mycoplasma hyopneumonia, the strains of PRRS virus used in preparing the modified-live-virus vaccine, the level of maternal antibodies, the timing of sero-conversion to PRRS, and other unknown variables. The complex and poorly understood interactions between pathogens (in this case, viruses and mycoplasmas) in pig disease syndromes can be expected to receive continued attention in herd health management.
Mycotoxins in the Feed
Feedstuffs commonly fed to pigs can contain a number of natural plant contaminants (Carlson and Lloyd, 1981) or poisonous plants (Kingsbury, 1964). The most common are the mycotoxins and among those, aflatoxin is the most common mycotoxin (NRC, 1998). Certain regions of the world are contaminated with mycotoxins probably because of local weather conditions. Many of these molds and fungi have hormonal properties, especially estrogenic properties. Mold-infected feed should not be fed to breeding stock. Some low level of mold is tolerable in the diet of growing pigs. Feed intake can be negatively affected if the levels are too high.
Aspergillosis (agent: Aspergillus flavus)
This fungus is common in grain, peanuts, corn, and other crops harvested under wet conditions and stored at a high moisture content and may be present in fish meal if the moisture content is high (_18%). The toxicity of A. flavus is due to the absorption from the intestinal tract of mycotoxins (aflatoxins) produced by the fungus. Clinical signs of A. flavus toxicity are anorexia, diarrhea, poor growth, pulmonary distress, and death in severe toxicity. Aflatoxins have been associated with liver cancer in humans. Aspergillosis can be prevented by avoiding the use of feed contaminated with A. flavus.
Mold Toxicity (agents: Fusarium (Gibberella) roseum, Fusarium tricinctum, Gibberella zeae)
Harvesting and storage of corn and cereal grains at high moisture content (above 18%) is conducive to the growth of molds. Mold-contaminated corn and cereal grains may cause poor growth and reproductive failure and lead to major economic losses when fed to swine.
Ochratoxicosis (agents: Aspergillus ochraceas and Penicillium species)
Concentration of as little as 200 parts per billion (ppb) of ochratoxin A in swine feeds have been shown to produce kidney, liver, and muscle lesions. Other signs of ochratoxicosis due to contamination of pig feed with A. ochraceas or Penicillium species include diarrhea, dehydration, and liver necrosis. Reduced weight gain and feed utilization may not appear at 200 ppb ochratoxin contamination, but have been reported when the diet contains ochratoxin at levels above 1,400 ppb. Tests are available to measure the level of ochratoxins and aflatoxins in feedstuffs. The cost of obtaining this information on feedstuffs in questionable harvesting and storage conditions is usually a good investment.
Ergot (agent: Claviceps purpurea)
This fungus invades rye and other cereal grains and its toxic alkaloids cause reproductive failure in sows and gangrene of extremities (feet, ears, snout, tail). Withdrawal of ergot-infected grain from the diet reverses the adverse effects.
Prolapse, Ulcers, and Hernias
Pigs are susceptible to a variety of physical problems, including prolapse, ulcers, and hernias. These conditions can have a genetic component and, certainly, some environments make the conditions worse. Stockmanship is important in finding the conditions early and attempting to minimize the affected animals.
Pigs can have a prolapse (protruding) rectum or vagina. Among growing pigs and sows, the prolapsed rectum is a problem. Prolapse of the vagina can be observed especially after farrowing. The prolapse is a particular concern for pigs that are group-housed because pen mates will attack the prolapse, resulting in damage to the tissue and a potential for bleeding to death. Prolapses can be surgically repaired, but this practice is time-consuming and not always permanently effective. Prolapsed animals should be isolated until they are at least partially healed. Once prolapsed animals are repaired, they should be sent to market as long as drug withdrawal protocols have been followed.
Ulcers are common among some pigs. Pigs can develop a stomach ulcer very quickly (in a matter of minutes or hours). The ulcers can result in pigs bleeding to death in the acute form or becoming anemic if the condition is chronic. The incidence of gastric (stomach) ulcers in pigs remains relatively high despite its recognition as a health problem in pigs for several decades. The secretion of gastric juice with high acidity and high pepsin concentration increases the susceptibility to ulceration. The process of ulcer development can occur within minutes during a 2 to 3-d period of stress. Consumption of heated corn is associated with a higher incidence of ulcers than is consumption of unheated corn. Oats tend to protect the pig from developing stomach ulcers. An alcohol-soluble extract from oats has been shown to inhibit gastric acid secretion and to protect against ulcers in the growing pig. Stresses associated with marketing (fasting, long duration of shipment and crowding) increase the incidence. Finely ground feeds (particle size <750 microns) tend to improve growth rate and feed utilization, but are also associated with increased incidence of esophageal ulcers. Feeding a finely ground diet following a 24-hr fast may increase the severity of the lesions induced by the fast (Lawrence et al., 1998). Changing the particle size of the diet to >750 microns average diameter and feeding the diet for as little as 3 to 7 d has been shown to reduce ulcer severity in the esophageal region and to result in complete healing of the lesion within 2 to 4 wk (Lawrence et al., 1998). Transport of pigs for 4 hr results in a 40% to 50% reduction in feed intake over the ensuring 3 d (McGlone et al., 1993), indicating that even a relatively short duration of transport has the potential to precipitate ulcer formation. Lactating sows fed finely ground diets are also subject to pars esophageal ulcers. The physical restraint of the farrowing crate does not, by itself, appear to produce stomach ulcers as long as a high level of feed intake is maintained.
Hernias can be of two forms: umbilical or scrotal. Some genetic lines may be predisposed to develop hernias. Hernias form when a sphincter weakens, loosens, and allows the intestines to fall through. The hernia grows when the influx of intestinal mass exceeds the outflow. Some hernias can be so large that they drag on the ground, posing a risk of being punctured. Hernias can be repaired surgically, but this is time-consuming and not totally effective. Affected pigs may need to be euthanized.
Pigs can experience a number of behavioral problems, but the most common problem--tail biting--is resolved by docking the tail. The last two-thirds of the tail is removed near birth to prevent tail biting. If the tails are left on, and pigs are housed indoors on slats, the incidence of tail biting can be very high. Ear chewing is a related anomaly (see the discussion on behavioral problems in Chapter 18).
Early weaned pigs show some behavioral problems, including ear, navel, and prepuce suckling. The urine-drinking piglet--probably with a strong drive to suckle--can consume large quantities of urine, which is unhealthy.
When sows are hungry and particularly when they are waiting in line to eat, vulva biting can develop. The vulva is a blood-rich organ. If it is punctured, sows can lose a large amount of blood and experience discomfort.
Sows housed individually in indoor units show two distinct behaviors: (1) During gestation, limit-fed sows lick, chew, and bite the bars or other pen materials. It is not known why sows do this behavior, but some scientists have speculated that this is a sign of stress. Such claims have led to the banning of the crate for gestating sows. (2) Sows show nest-building behaviors in pens or paddocks if they have nesting materials. Interestingly, even if they do not have nesting materials, they still show nest-building behaviors. Pre-farrowing sows show what is called phantom nest-building behaviors. It is not known if this phantom behavior is a sign of a stressful situation for the sow.
Pigs that are penned in one environment for a long period (usually months) have a difficult time moving through novel environments. Thus, when some pigs are moved through chutes and onto and off of trucks, there is variation in the ease with which pigs are handled. Suggestions were made that some of the more lean, heavily muscled pigs are more difficult to handle due to inadvertent genetic selection for behaviors that make handling pigs difficult. Regardless of the origin of this behavior, difficult handling of pigs is a serious behavioral problem for the producer and the processor.
Each behavioral problem is a function of both genetics and environment. The selection program and the specific features of the environment (including stockmanship) should be examined closely when behavioral problems arise.
This chapter provided an overview of pig health for use by nonveterinarians involved in pork production. Standard approaches to ensuring pig health in commercial pork production units include biosecurity, sanitation, control of pig flow, and overall planned herd health programs in collaboration with a herd veterinarian. Infectious disease-control programs include vaccination, subtherapeutic and therapeutic antimicrobeal administration, and biosecurity measures. Major infectious viral, bacterial, mycoplasmal, and fungal diseases and internal and external parasites were described, as well as their causative agents, signs of infection, and control. Pigs can experience noninfective physiological diseases such as stomach ulcers and behavioral problems.
QUESTIONS AND ACTIVITIES
1. Create a table of common enteric diseases of swine with the name of the disease in the left column. In the other columns, list the causative microbe and the major and distinguishing symptoms and the treatment or prevention tools available.
2. Create a table of common respiratory diseases of swine with the name of the disease in the left column. In the other columns, list the causative microbe and the major and distinguishing symptoms and the treatment or prevention tools available.
3. Select one disease and provide an in-depth review of the causative microbe, the clinical signs, treatment, and prevention.
4. Describe what might be the cause when the following symptoms are present (there is more than one answer to some symptoms):
a. Bloody feces
b. Vomiting among sows
c. A transient respiratory problem
d. Abortion early in pregnancy
e. Increased numbers of mummified piglets
f. Swollen joints
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McGlone, J. J., J. L. Salak, E. A. Lumkin, R. I. Nicholson, M. Gibson, and R. L. Norman. 1993. Shipping stress and social status effects on pig performance, plasma cortisol, natural killer cell activity, and leukocyte numbers. J. Anim Sci. 71:888-896.
McKean, J., D. Holscher and S. Quisenberry. 1992. External Parasite Control on Swine. Pork Industry Handbook No. PIH-40. North Carolina Agricultural Extension Service, North Carolina State University, Raleigh.
Meyer, K., L. Biehl, and D. Reeves. 1990. Slaughter Checks-An Aid to Better Herd Health. Pork Industry Handbook No. PIH-93. North Carolina Agricultural Extension Service, North Carolina State University, Raleigh.
Meyerholz, G. W. and J. M. Gaskin. (1981a). Environmental Sanitation and Management in Disease Prevention. Pork Industry Handbook No. PIH-79. North Carolina Agricultural Extension Service, North Carolina State University, Raleigh.
Miller, M. 1999, December. A new flu virus uncovered. Pork'99: 46.
National Pork Board. 2002. Swine Care Handbook. NPB, Des Moines, Iowa.
NRC. 1998. Nutrient Requirements of Swine. 10th ed. National Academy Press, Washington, D.C.
Pointon, A. M., P. R. Davies, and P. B. Bahson. 1999. Disease surveillance at slaughter. In: B. Straw et al. (eds.) Diseases of Swine. Pp. 1111-1132. Iowa State Univ. Press, Ames, IA.
Pond, W. G. and J. H. Maner. 1984. Swine Production and Nutrition. AVI Publishing Co., Westport, CT.
Ross, R. F. 1981. Mycoplasmal diseases. In: A. D. Leman et al. (eds.) Diseases of Swine. 5th ed. pp. 535-549. Iowa State University Press, Ames.
Ross, R. and J. Bailey. 1991. Swine Arthritis. Pork Industry Handbook No. PIH-36. North Carolina Agricultural Extension Service, North Carolina State University, Raleigh.
Saif, L. J., O. A. R. D. C. Wooster, J. G. Lecce, and A. Torres. 1987. Rotaviral Diarrhea in Pigs. Pork Industry Handbook No. PIH-61. North Carolina Agricultural Extension Service, North Carolina State University, Raleigh.
Smith, W. J., D. J. Taylor, and R. H. C. Penny. 1990. Color Atlas of Diseases and Disorders of the Pig. Iowa State University Press, Ames.
Stephenson. L. S., W. G. Pond, M. C. Nesheim, L. Krook, and D. W. T. Compton. 1980. Ascaris suis: Nutrient absorption, growth and intestinal pathology in young pigs experimentally infested with 15-day old larvae. Exp. Parasitol. 49:15-25.
Straw, B. E., S. D'Allaire, W. L. Mengeling, and D. J. Taylor. 1999. Diseases of Swine. 8th ed. Iowa State University Press, Ames.
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General pig health sites:
Major Pig Pharmaceutical sites:
TABLE 20-1 Selected, Common Disinfectants and Their Use in Commercial Swine Operations. FORMALDEHYDE AND OTHER CHLORTEXIDINE ALDEHYDES Spectrum of Activity Gram + bacteria S.A. not Yes pyogenic cocci Gram - bacteria S.A. not Yes pseudomonads Tuberculosis bacill S.A. Yes Bacterial spores S.A.at 1% Yes concentration Fungi S.A. Yes Viruses S.A. not Yes parvovirus Special Properties Resistance to organic debris Good Good Effect of hard water None None Detrimental effect of heat No (4) Residual activity Yes (6) Most effective pH range Alkaline Not affected by pH Compatibility with anionic Yes Yes surfactants (soaps) Compatibility with nonionic Yes Yes surfactants Disadvantages Reduced Irritating activity fumes (8) against certain organisms Commonly Used Concentrations Disinfecting solution 1% 2-8% Sanitizing solutions 0.5% 1-2% Appropriate Uses E--Equipment CE--Clean Equipment E,P,F E,P,F P--Premises F--Foot baths Common Brands and Names (12) Nolvasan (3) Cidex[R] DC & R[R] Formaldegen[R] Formatin CHLORINE HYPOCHLORITES CHLORAMINES IODOPHORS Spectrum of Activity Gram + bacteria Yes Yes Gram - bacteria Yes Yes Tuberculosis bacill S.A. S.A. Bacterial spores S.A. S.A. Fungi Yes Yes Viruses S.A. S.A. Special Properties Resistance to organic debris Very poor Poor to fair Effect of hard water None (2) None (2) Detrimental effect of heat (5) (5) Residual activity (7) Yes Most effective pH range Acid Acid Compatibility with anionic Yes Yes surfactants (soaps) Compatibility with nonionic Yes Yes surfactants Disadvantages Inactivation Inactivation by organic by organic debris debris Commonly Used Concentrations Disinfecting solution Hypochlorites 50-75 ppm 3-5% (10,11) Sanitizing solutions Hypochlorites 12-25 ppm 2-3% (11) Appropriate Uses E--Equipment CE--Clean Equipment CE CE P--Premises F--Foot baths Common Brands and Names (12) Chloramine-T[R] Betadine[R] Chlorox[R] Iofec[R] Halazone[R] Isodyne[R] Losan[R] Tamed Iodine[R] Weladol[R] QUATERNARY SODIUM AMMONIUM HYDROXIDE COMPOUNDS Spectrum of Activity Gram + bacteria Yes Yes Gram - bacteria Yes S.A. Tuberculosis bacill S.A. No Bacterial spores Yes No (5-10% solution) Fungi Yes S.A. Viruses Yes S.A. Special Properties Resistance to organic debris Good Fair Effect of hard water None (3) Detrimental effect of heat No No Residual activity Yes No Most effective pH range Alkaline Alkaline Compatibility with anionic Yes No surfactants (soaps) Compatibility with nonionic Yes Yes surfactants Disadvantages Caustic Incompatible w/soaps-- limited spectrum Commonly Used Concentrations Disinfecting solution 2-10% 400-800 ppm Sanitizing solutions 200 ppm Appropriate Uses E--Equipment CE--Clean Equipment P CE P--Premises F--Foot baths Common Brands and Names (12) Lye Germex[R] Hi-Lethol[R] San-O-Fec[R] Warden[R] Zephiran[R] CRESOLS PHENOLS Spectrum of Activity Gram + bacteria Yes Gram - bacteria Yes Tuberculosis bacill S.A. Bacterial spores No Fungi S.A. Viruses S.A. Special Properties Resistance to organic debris Excellent Effect of hard water None Detrimental effect of heat No Residual activity Yes Most effective pH range Acid Compatibility with anionic Yes surfactants (soaps) Compatibility with nonionic No surfactants Disadvantages (9) Commonly Used Concentrations Disinfecting solution Variable Sanitizing solutions Appropriate Uses E--Equipment CE--Clean Equipment E,P,F P--Premises F--Foot baths Common Brands and Names (12) Cresl-400[R] Environ[R] Laro[R] Lysol[R] Orthophen- ylphenol Sodium or- thophenyl- phenate (1) S.A.--Some Activity. (2) Unless hard water is alkaline. (3) Reduces speed of kill. (4) Formaldehyde gas works best at 80-140[degrees]F. (5) Use at less than 110[degrees]F, active principal driven off by heat. (6) No, except slow-release formulas. (7) Hypochlorites: No, chloramines: Yes. (8) Glutaraldehyde is less irritating and is superior to formaldehyde as a germicide. (9) Strong odor with coal and wood tar distillates. (10) 3.3% Chlorox inactivates parvovirus on clean surfaces. (11) Chloramines variable. (12) Products listed are intended as examples, not endorsement; many suitable products are not listed. Source: Adapted from Meyerholz and Gaskin (1981). TABLE 20-2 Withdrawal Periods for Antibiotics Used in Commercial Pork Production in the United States. Consult the FDA for Updates to This Information. DRUGS FOR LABELED USE DAYS Parenteral unit dosage form drugs Ceftiofur 0 Erythromycin 2 Gentamicin (neonatal pigs) 40 Lincomycin 2 Oxytetracycline (varies by label) 18-26 Procaine penicillin G 7 Tylosin 14 Oral unit dosage form drugs, water soluble Ampicillin trihydrate 1 Bacitracin methylene disalicylate 0 Chlortetracycline 5 Chlortetracycline and sulfamethazine 15 Levamisole 3 Lincomycin 6 Neomycin 20 Spectinomycin, oral pump suspension 21 Spectinomycin, water soluble 5 Sulfachlorpyridazine 4 Tetracycline hydrochloride 4 Thiabendazole 20 Tiamulin (see labeling) 3-7 Tylosin 2 In-feed dosage forms (maximum, as times may vary with dose) Apramycin 28 Carbadox 70 Chlortetracycline 0 Chlortetracycline, procaine penicillin, and sulfamethazine 15 Chlortetracycline, procaine penicillin, and sulfathiazole 7 Hygromycin B 15 Levamisole 3 Lincomycin 0-6 Neomycin and oxytetracycline 10 Penicillin and streptomycin 0 Tetracycline 5 Tiamulin 0-2 Tilmicosin 7 Tylosin 0 Tylosin and sulfamethazine 15 Virginiamycin 0 Source: Adapted from Henry and Apley (1999). TABLE 20-3 Needle Sizes for Intramuscular and Subcutaneous Injections. Intramuscular Injection Gauge Length Baby pigs 18 or 20 1/2 in. or 5/8 in. Nursery 16 or 18 5/8 in. or 3/4 in. Finisher 16 1 in. Breeding stock 14 or 16 1 in. or 1 1/2 in. Subcutaneous Injection Gauge Length Nursery pigs 16 or 18 1/2 in. Finisher 16 3/4 in. Breeding stock 14 or 16 1 in. [ILLUSTRATION OMITTED] Source: Adapted from NPPC. TABLE 20-4 Major Infectious Diseases of Swine. DISEASE AGENT Bacterial Brucellosis Brucella suis, B. abortus, B. melitensis Bordetellosis (Atrophic rhinitis) Bordetella bronchiseptica Colibacillosis Escherichia coli Edema disease (ED) (a form of Escherichia coli (hemolytic) enterotoxemic colibacillosis) Erysipelas Haemophilus infections Erysipelothrix rhusiopathiae Polyserositis and arthritis (Glasser's disease) Pleuropneumonia Haemophilus parasuis Leptospirosis Haemophilus pleuropneumonia, H. parahaemalyticus Pasteurellosis (hemorrhagic Leptospira pomona (and other septicemia) serovars in some countries) Salmonellosis Pasteurella multocida Streptococcal Salmonella choleraesuis and S.ryphimurium Cervical lymphadenitis (jowl abscess) Septicemia, arthritis Streptococcus beta hemolytic (Group E.Streptococcus) Arthritis, septicemia, Group C (S.equisimilis) and meningitis Group L (Streptococcus) Swine dysentery Streptococcus suis (Group D) Treponema hyodysenteriae Viral African swine fever Pestes africana suum Congenital tremors Infectious congenital tremors virus Foot and mouth disease Foot and mouth disease virus Hog cholera (swine fever) Togaviridae Pestivirus suis or hog cholera virus Porcine parvovirus infection Parvovirus species Porcine rotavirus infection Rotavirus species Pseudorabies (Aujeszky's disease) Pseudorabies virus,a herpes virus Swine influenza Type A influenza suis Swinepox Swinepox virus Transmissible gastroenteritis TGE virus (TGE) Mycoplasmal Arthritis Mycoplasma hyosynoviae Polyserositis and arthritis Mycoplasma hyorhinis (see also Haemophilus parasuis) Mycoplasma pneumonia Mycoplasma hyopneumoniae Mycotic Aspergillosis Aspergillus flavus Moniliasis Candida albicans, Oidium albicans,Monilia albicans Ergot Claviceps purpurea Mold toxicity Fusarium (Gibberella) roseum, F.tricinctum, Gibberella zeae Ochratoxicosis Aspergillus ochraceas and Penicillium species Miscellaneous Atrophic rhinitis Bordetella bronchiseptica, Mycoplasma hyorhinis, noninfectious irritants, nutritional factors Enterotoxemia (edema disease, Toxin from E.coli gut edema, intestinal edema, gastric edema) MMA-complex (metritis, Streptococcus species, mastitis, agalactia) Staphylococcus species, Actinomyces bovis, Actinobacillus lignieresi, Corynebacterium pyogenes, Mycobacterium tuberculosis, Spherophorus necrophorus, possible endocrine factors RESIDENCE INTERNAL PARASITES PARASITE OF ADULT Ascariasis Ascaris suum Small intestine (ascarid) Trichinosis Trichinella Small intestine spiralis Whipworm infection Trichuris suis Cecum and large intestine Nodular worm infection Oesophagostomum Cecum and species large (Strongylid intestine nematodes) EXTERNAL PARASITES Sarcoptic mange Sarcoptes scabiei var. suis Lice Haematopinus suis TABLE 20-5 Other Infectious Diseases of Swine. DISEASE AGENT TYPE Anthrax Bacillus anthracis Bacterial Botulism Clostridium botulinum Bacterial (Bacillus botulinus) Corynebacterial infections Corynebacterium species Bacterial Listerosis Listeria monocytogenes Bacterial Malignant edema Clostridium septicum Bacterial Necrotic rhinitis Spherophorus necrophorus Bacterial Tetanus Clostridium tetani Bacterial Tuberculosis Mycobacterium Bacterial tuberculosis avium, bovis, hominus Actinomycosis Actinomyces bovis Mycotic Encephalomyocarditis Cardiovirus species Viral Eperythrozoonosis Eperythrozoon suis Rickettsial Hemagglutinating Hemagglutinating Viral encephalomyelitis encephalomyelitis virus Porcine adenoviruses Adenovirus species Viral Porcine enteroviruses Teschen virus, Virus Viral T80, Virus F7, Virus Californianos Porcine cytomegalovirus Cytomegalovirus species Viral infection (inclusion body rhinitis) Rabies Rhabovirus species Viral Reovirus infection Reovirus Viral Vesicular exanthema Vesicular exanthema Viral virus Vesicular stomatitis Vesicular stomatitis Viral virus Coccidiosis Eimeria and Isopora Protozoan species Toxoplasmosis Toxoplasma gondii Protozoan
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|Title Annotation:||SECTION V Pig Production Applications That Make Business Sense|
|Publication:||Pig Production, Biological Principles and Applications|
|Date:||Jan 1, 2003|
|Previous Article:||Chapter 19 Management of growing pigs.|
|Next Article:||A Human resources.|