Common Porcine Diseases

Common Porcine Diseases

Bacterial Diseases

Atrophic Rhinitis

Atrophic rhinitis is divided into two forms. The first form, regressive atrophic rhinitis, is caused by Bordetella bronchiseptica. It usually is mild and temporary, with little effect on performance (Fig. 25-1). The second form is progressive atrophic rhinitis, caused by toxigenic Pasturella multocida. Progressive atrophic rhinitis typically is severe and permanent, and it affects performance. Although each organism can cause nasal turbinate atrophy (Fig. 25-2) and nasal distortion independently, clinical signs tend to be more severe when combined. Although dogs, cats, and rodents can harbor B. bronchiseptica, their role in the spread of disease is unknown. Introduction of disease into a herd is usually through infected pigs. The disease can be intensified through overcrowding, mixing and moving of pigs, inadequate ventilation, and other concurrent diseases.

Clinical signs usually appear in animals between 3 and 8 weeks of age and include sneezing, coughing, tear staining at the medial canthus of the eye, blockage or inflammation of the lacrimal duct, epistaxis, decreased performance, and deformation of the upper jaw (Fig. 25-3).

A tentative diagnosis is typically made from the clinical signs and deformation and/or nasal turbinate atrophy upon necropsy. Nasal turbinate atrophy is best identified during necropsy by examining a transverse section of the snout at the second premolar. Remember, however, it is rare to find even healthy herds with no signs of atrophy. Culture growth of P. multocida is needed for a definitive diagnosis.

Treatment of atrophic rhinitis usually is attempted only when the disease rises to an unacceptable level within the herd. Some swine producers periodically measure the degree of turbinate atrophy and apply scores as a form of monitoring the disease. If treatment is indicated, antibiotics such as ceftiofur, sulfonamides, tylosin, and tetracyclines can be administered. Other treatments and preventive measures include vaccination, temporary closure of the herd to introduction of new pigs, better ventilation, increased hygiene practices, purchase of specific pathogen-free stock, segregated early weaning, and use of less dusty feed ingredients.

Atrophic rhinitis should not be confused with necrotic rhinitis (“bullnose”). Necrotic rhinitis results in abscesses on the snout as a result of unsanitary conditions.


Brucellosis in pigs is caused by the bacterium Brucella suis. The most commonly affected animals are breeding stock. Transmission of the disease is spread mainly by ingestion of infected tissues or wastes. Boars can also transmit the disease during service because the organism is found in semen. Suckling pigs can become infected from sows, although this is rare. Clinical signs include bacteremia that persists for 90 days, abortion, orchitis, lameness, spondylitis, paralysis, metritis, abscesses, and temporary or permanent sterility.

Diagnosis of brucellosis is often made when entire herds are tested using a brucellosis card test. Prevention should include purchase of stock from brucellosis-free herds and isolation for 3 months after purchase or return from fairs or shows. Control of the disease should include testing and slaughter of infected animals.

Clostridium Perfringens Type C Enteritis

Clostridium perfringens causes necrosis of all structural components of the villi. This necrosis causes blood loss into the intestinal wall and lumen (Fig. 25-4). These damaging effects cause necrohemorrhagic enteritis, which commonly causes hemorrhagic diarrhea (Fig. 25-5), followed by collapse and death in piglets younger than 1 to 3 days. When onset is less acute, brownish liquid feces develops between 3 to 5 days of age. Upon necropsy, the small intestine is often dark red and filled with hemorrhagic liquid. In piglets between 3 to 5 days of age, gas bubbles in the wall of the jejunum and necrosis of the mucosa within the jejunum and ileum can be seen.

Diagnosis is often made based upon necropsy findings. Treatment often is ineffective because the lesions are irreversible once diarrhea has become a clinical sign. Prevention of the disease should include vaccination.

Enteric Colibacillosis

Enteric colibacillosis is caused by Escherichia coli. The bacteria colonize in the small intestine of nursing and weanling pigs. Because certain strains of E. coli produce enterotoxins that cause fluid and electrolytes to be secreted into the intestinal lumen, diarrhea is a common clinical sign (Fig. 25-6). Other clinical signs include rapid dehydration, acidosis, and death.

A definitive diagnosis can be made by culturing E. coli from the small intestine. Treatment typically consists of antibiotic therapy and correction of fluid and electrolyte imbalances. Prevention should include the use of slatted floors, prevention of chilling, and vaccination of gestating sows.


Eperythrozoonosis is caused by Eperythrozoon suis, a rickettsial organism that typically appears as a coccoid organism. The organism is transmitted most commonly by lice (Fig. 25-7). Other forms of transmission are contaminated needles and surgical instruments. Clinical signs commonly include anemia, fever, pale mucous membranes, jaundice, emaciation, staggering or paralysis, weak neonates, unthrift appearances, and reproductive failure.

Diagnosis is typically accomplished by Giemsa-stained peripheral blood smears showing E. suis attached to the surface of red blood cells. Treatment typically is accomplished with tetracyclines. Methods of prevention should include use of disposable needles, sterilization of surgical equipment, and control of arthropod parasites.

Exudative Epidermitis

Exudative epidermitis is also known as greasy pig disease. Infections are caused by Staphylococcus hyicus. The bacteria are unable to penetrate the skin and typically gain entry through lacerations on the legs and feet. Carriers tend to be the source of contamination in previously unaffected herds. Younger pigs tend to be more susceptible, but pigs gain immunity to the bacteria as they age. The main source of infection tends to be from sow to piglet during nursing. However, it can be spread through older more immune animals that carry the bacteria. Clinical signs include reddening of the skin, erosions at the coronary band, depression, and anorexia during early stages of the disease. As the disease progresses, the reddened areas of skin turn into brown spots, producing serum exudates that begin to cover the entire pig. As dirt builds up over the top of the sebum, it becomes black, giving a greasy appearance to the infected animal (Fig. 25-8). In the acute disease, death occurs within 3 to 5 days. Recovery from the disease tends to be time consuming, and decreased growth rates are common.

Treatment of the disease include administration of antibiotics. Amoxicillin, erythromycin, lincomycin, penicillin, tylosin, ampicillin, trimethoprim–sulfonamide, aminoglycosides, and cephalosporins are effective. High dosages and continued treatment for 7 to 10 days result in the greatest success. Antiseptics applied to the skin of the infected animal also can be beneficial. Efforts to prevent the disease should include disinfection of the farrowing environment and of the sow, clipping of needle teeth in piglets, soft bedding, and efforts to prevent fighting.

Glasser Disease

Glasser disease is also known as porcine polyserositis and infectious polyarthritis. The disease is thought to be caused by Haemophilus parasuis but possibly by Haemophilus parainfluenzae. Stress predisposes pigs to the disease. Mycoplasma hyorhinis may be the cause in younger pigs. The incubation period is 1 to 5 days.

Clinical signs of the disease include a fever of 104°F to 107°F, depression, difficult breathing, cough, and anorexia. Some pigs develop lameness associated with warm, tender, swollen joints. Pigs are capable of recovery, but chronic cases can lead to pericarditis and congestive heart failure (Fig. 25-9).

A presumptive diagnosis is made based on history and clinical signs. A definitive diagnosis requires culture of the organism from cerebrospinal fluid, cardiac blood, or joints. Antibiotics usually are effective treatments. Prevention should include reducing stress and possibly feeding medication in the food or water during times of high stress.


The two most common bacterial serovars found in swine are Leptospira pomona and L. bratislava. Other serovars that have been reported in swine include L. canicola, L. tarassovi, L. muenchen, L. icterohaemorrhagiae, and L. grippotyphosa. In swine, the bacteria are commonly transferred upon exposure to infected urine from wildlife or other swine. Clinical signs include abortion 2 to 4 weeks before term, and SMEDI (stillbirth, mummification, embryonic death, and infertility). For more information on leptospirosis, see Chapter 13. Treatment and control of leptospirosis includes chlortetracycline and oxytetracycline if given early. Prevention includes annual vaccinations, confinement rearing, rodent control programs, fencing to prevent contact with contaminated water, and purchase of seronegative stock (Fig. 25-10).

Mycoplasmal Pneumonia

Mycoplasmal pneumonia is also described as “enzootic pneumonia” and “viral pneumonia.” It is typically caused by Mycoplasma hyopneumoniae. Mycoplasmal pneumonia is chronic but clinically mild. Clinical signs commonly include persistent dry cough, decreased growth rates, decreased feed efficiency, sporadic dyspnea, and a high incidence of lung lesions in slaughtered hogs (Fig. 25-11). Concurrent infections of other mycoplasmas, bacteria, and viruses that can increase the severity of the disease are common. Mortality is high in endemic areas, but morbidity remains low. Pigs of all ages can be affected. Infection usually occurs in the first few weeks of life through contact with the sow or gilt. Young pigs 3 to 5 months old tend to show the highest incidence of lung lesions. As pigs age, regression and recovery from the disease are seen. A high percentage (probably 99%) of commercial swine herds in the United States are believed to be affected.

Diagnosis is commonly made upon slaughterhouse examination. Serologic tests can be used, but the results may be difficult to interpret. Treatment is limited. During an initial outbreak, antibiotics such as tylosin, lincomycin, timulin, or tetracyclines can be used to control the severity of clinical signs. Other practices that can limit the effects of the disease are adequate ventilation, reduced crowding, all in/all out management, and vaccination.


Pleuropneumonia is caused by Actinobacillus pleuropneumoniae, a gram-negative coccobacillus commonly referred to as APP. APP infection is a severe and contagious respiratory disease. The most severe effects are recognized in growing swine up to age 6 months. Onset is sudden, and the disease spreads rapidly in naïve herds. Clinical signs include cyanotic extremities, “thumps” (abdominal breathing), open-mouth breathing with blood-stained frothy nasal and oral discharge, anorexia, reluctance to move, fever up to 107°F, and acute death. Common clinical signs in adults include abortion and fatal infections.

Once established in a herd, chronic clinical signs include intermittent coughing and decreased growth rates, which make detection difficult. However, severe internal damage still can be present and exacerbated by transport, overcrowding, and temperature changes, resulting in death. Concurrent infections of Mycoplasma, Pasteurella, porcine reproductive and respiratory syndrome (PRRS), and swine influenza also are common. The pneumonia usually is bilateral, with pleurisy and pericarditis commonly seen (Fig. 25-12).

A tentative diagnosis of acute APP infection is made based on the rapid onset, clinical signs, and lesions found upon necropsy. A definitive diagnosis can be made by culture but may require growth with Staphylococcus aureus.

APP is most commonly spread through nose-to-nose contact. Pigs that have been infected with APP and have recovered often become carriers of the disease. Because of the acute nature of the disease in naïve herds and the significant lack of clinical signs in infected/carrier animals, treatment of the disease poses some difficulty. The first treatment should be a systemic antibiotic because many animals with the disease do not want to eat or drink. Some antibiotic choices are ceftiofur, tetracyclines, synthetic penicillins, tylosin, and sulfonamides. Once animals begin eating and drinking, treatments can be administered in the water or feed. Other suggestions for control include depopulation, early segregated weaning, all in/all out management, improved ventilation, and reduced stocking rates. If the herd is already APP free, new pigs should be purchased from other APP-free herds.

Streptococcal Infections

Streptococcal infections that commonly infect swine are broken into four groups. The first most prominent group is group D, followed by groups C, L, and E. Streptococcus suis, the bacteria belonging to group D, are gram-positive, facultative aerobes that are seen as oval diplococci or short chains. There are at least nine serotypes of Streptococcus suis. The two most common types present in the United States are type 1 and type 2. Type 7 also is commonly isolated from U.S. herds but is of little clinical significance.

Type 1 from group C randomly affects piglets up to 8 weeks of age (Fig. 25-13). Clinical signs in nursing piglets typically include polyarthritis and meningitis. Type 2 from group C tends to affect large, intensively managed herds, with transmission through carrier pigs or flies. Flies can travel 1 to 2 miles between farms and can carry the infection for up to 5 days. Type 2 commonly affects weaning pigs. Clinical signs of type 2 are fatal meningitis, abortion, depression, fever, tremors, incoordination, convulsions, bronchopneumonia, blindness, and deafness. Sudden death can occur from endocarditis or myocarditis.

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Aug 11, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Common Porcine Diseases

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