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Swine Diseases

Chapter 25

Swine Diseases
LearningObjectives Describe and recognize clinical signs associated with specific diseases Describe the etiology of the diseases Describe common treatments of disease List the common and scientific names of parasites associated with this species List the common vaccinations and their schedules associated with this species

Atrophic Rhinitis
System: Respiratory Two Forms: Regressive atrophic rhinitis and progressive atrophic rhinitis Etiologic agent: Regressive atrophic rhinitis- Bordatella bronchiseptica; Progressive atrophic rhinitis- Pasturella multocida Signs: Sneezing, coughing , tear staining, epistaxis, deformation of upper jaw Diagnosis: Clinical signs and deformation Treatment: Antibiotics Control: Vaccination Zoonosis: No

Brucellosis
System: Reproductive Etiologic Agent: Brucella suis Signs: Clinical signs include bacteremia that persists for 90 days, abortion, orchitis, lameness, spondylitis, paralysis, metritis, abscesses, and temporary or permanent sterility Treatment: Slaughter Prevention: Control of the disease should include testing and slaughter of infected animals. Zoonotic: YES

Clostridium Perfringens Type C Enteritis


System: Intestinal Etiological Agent: Clostridium perfringens Signs: Necrohemorrhagic enteritis, which commonly causes hemorrhagic diarrhea (Fig. 25-5), followed by collapse and death in piglets younger than 1 to 3 days. 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: vaccination. Zoonosis: No

Enteric Colibacillosis
System: Intestinal Etiological Agent: Escherichia coli Signs: diarrhea is a common clinical sign Other clinical signs include rapid dehydration, acidosis, and death. Diagnosis: Culture 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
System: Circulatory Etiological agent: Eperythrozoon suis, a rickettsial organismspread by lice Signs: anemia, fever, pale mucous membranes, jaundice, emaciation, staggering or paralysis, weak neonates, unthrift appearances, and reproductive failure. Diagnosis: Giemsa-stained peripheral blood smears showing E. suis attached to the surface of red blood cells. Treatment: Tetracyclines Prevention should include use of disposable needles, sterilization of surgical equipment, and control of arthropod parasites.

Exudative Epidermitis
System: integumentary Etiological agent: Staphylococcus aureus Signs: reddening of the skin, erosions at the coronary band, depression, and anorexia during early stages of the disease and can progress to death Treatment: Treatment of the disease include administration of antibiotics. Amoxicillin, erythromycin, lincomycin, penicillin, tylosin, ampicillin, trimethoprimsulfonamide, aminoglycosides,and cephalosporins are effective Prevention: disinfection of the farrowing environment and of the sow, clipping of needle teeth in piglets, soft bedding, and efforts to prevent fighting. Zoonotic: No

Glasser Disease
System: Musculoskeletal Etiological agent: Haemophilus parasuis but possibly by Haemophilus parainfluenzae. Stress predisposes pigs to the disease. Mycoplasma hyorhinis may be the cause in younger pigs. Signs: fever of 104F to 107F, depression, difficult breathing, cough, and anorexia. Some pigs develop lameness associated with warm, tender, swollen joints Diagnosis: 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 Treatment: Antibiotics usually are effective treatments. Prevention: Reducing stress and possibly feeding medication in the food or water during times of high stress. Zoonotic: NO

Leptospirosis
System: Reproductive Etiological Agent: Leptospira pomona and L. bratislava Signs: Clinical signs include abortion 2 to 4 weeks before term, and SMEDI(stillbirth, mummification, embryonic death, and infertility) Treatment: Treatment and control of leptospirosis includes chlortetracycline and oxytetracycline if given early Prevention: annual vaccinations, confinement rearing, rodent control programs, fencing to prevent contact with contaminated water, and purchase of seronegative stock Zoonotic: YES

Mycoplasmal Pneumonia
System: Respiratory Etiological Agent: Mycoplasma hyopneumoniae. Signs: persistent dry cough, decreased growth rates, decreased feed efficiency, sporadic dyspnea, and a high incidence of lung lesions in slaughtered hogs and death Treatment: Treatment is limited Prevention: adequate ventilation, reduced crowding, all in/all out management, and vaccination. Zoonosis: No

Pleuropneumonia
System: Respiratory Etiological Agent: Actinobacillus pleuropneumoniae, a gram-negative coccobacillus commonly referred to as APP. Signs: cyanotic extremities, thumps (abdominal breathing), open-mouth breathing with blood-stained frothy nasal and oral discharge, anorexia, reluctance to move, fever up to 107F, and acute death. Common clinical signs in adults include abortion and fatal infections. Diagnosis: 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. Treatment: The first treatment should be a systemic antibiotic because many animals with the disease do not want to eat or drink. Control: 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. Zoonotic: No

Streptococcal Infections
System: Multiple Etiological Agent: The first most prominent group is group D, followed by groups C, L, and E. Streptococcus suis. Signs: reddened patches of skin, enlarged lymph nodes, thickened joint capsules, congestion, edema, excess clear or cloudy cerebrospinal fluid, and bronchopneumonia Diagnosis: isolation and identification of the causative agent. Treatment: antibiotics in the feed and/or water, or systemic administration. Penicillins are effective but tend to inactivate in feed Prevention: reducing slurry gases, reducing overcrowding, and preventing introductions of carrier pigs.

Swine Dysentery
System: Gastrointestinal Etiological Agent: Serpulina hyodysenteriae, an anaerobic spirochete Signs: anorexia, passage of soft feces, dehydration, weakness, gaunt appearance, and possibly fever. The most common clinical sign is a mucoid diarrhea with flecks of blood and mucus that develops into a watery mucohemorrhagic diarrhea Diagnosis: A presumptive diagnosis is typically made from clinical signs and necropsy. Definitive diagnosis requires isolation of S. hyodysenteriae. Treatment: antibiotics in the water Control: facilities should try to improve sanitary conditions and eliminate rodent populations. Other forms of treatment/control include partial depopulation or a total depopulation. Prevention: purchase of specific pathogen-free stock or herds that have been free of dysentery for more than 2 years, and good husbandry practices.

Swine Erysipelas
System: Integumentary Etiological Agent: Erysipelothrix rhusiopathiae Signs: fever, lameness, lack of milk production in sows, abortion, skin discoloration leading to lesions, and death. Left untreated, the skin lesions become diamond shaped almost everywhere on the body Diagnosis: chronic and endocarditic forms of the disease is commonly made at necropsy. Acute forms of the disease are commonly diagnosed based upon the clinical signs Treatment: penicillin. Other effective antibiotics include ceftiofur and tetracycline. The acute form of the disease is often concurrently treated with antiserum. Zoonotic: NO

Hog Cholera-REPORTABLE DX
System: Reproductive Etiological Agent: virus of the pestivirus group of the family Flaviviridae Signs: poor reproductive performance and birth of piglets with neurologic disease. Clinical signs of the severe virulent strains include fever, decreased appetite, constipation, and depression Hog cholera has an incubation period of 2 to 6 days, with death occurring 10 to 20 days after infection. Diagnosis: virologic tests, antigen detection, virus isolation, nucleic acid detection, or serologic testing Prevention and Control: swift reporting of the virus to authorities and actions such as herd slaughter to prevent the spread of disease. Vaccinations for the disease are available.

Porcine Parvovirus
System: Reproductive Etiological Agent: Porcine parvovirus (PPV) Signs: Most asymptomatic but mummification of fetuses when sows are infected before 70 days of gestation. Abortions are rare because endometrial tissue is not affected. Most often the only indications that a herd is infected with PPV are increased mummification and stillbirth Diagnosis: Diagnosis is accomplished by fluorescent antibody testing of the mummies. Prevention: vaccination.

Porcine Reproductive and Respiratory Syndrome


System: Etiological Agent: PRRS virus is an enveloped virus that belongs to the Arteriviridae group of viruses Signs: increased preweaning mortalitythumps and show clinical signs of pneumonia upon necropsy. Initial outbreaks of the reproductive form of PPRS can last from 1 to 4 months. Reproductive PPRS loss is extremely high, sometimes as high as 70%. Porcine reproductive and respiratory syndrome can decrease average daily gains by 85% postweaning. Diagnosis: A presumptive diagnosis usually can be made from the clinical signs, but definitive diagnosis requires serologic tests and can be difficult. Treatment: None Prevention: purchase of PRRS-negative animals and vaccination.

Pseudorabies: A reportable disease


System:Respiratory Etiological Agent: Pseudorabies is caused by an enveloped deoxyribonucleic acid (DNA) herpesvirus. Transmission of the disease occurs from nose to nose, fecaloral route, and aerosolized virus. Signs: piglets infected at this age include tremors and paddling. Respiratory disease is the main clinical sign in weaned piglets and is often complicated by secondary bacterial infections. Clinical signs that can affect swine of any age include anorexia and fever Diagnosis: virus isolation, fluorescent antibody testing, and serologic testing Treatment: treatment of the clinical signs Control: vaccination, test and cull programs, and segregated weaning.

Swine Influenza
System: Respiratory Etiological Agent: orthomyxovirus of the influenza A group. In North America, outbreaks are commonly seen in the fall or winter. Signs: fever up to 108F, depression, difficult breathing, anorexia, and mucous discharge from the eyes and nose Diagnosis: acute nature of the disease and clinical signs. A definitive diagnosis requires virus isolation or demonstration of virus- specific antibodies. Treatment: no effective treatment of swine influenza Prevention/control: reducing stress levels, especially due to overcrowding, reducing dust, vaccination, use of all in/all out management, and strict import regulations

Transmissible Gastroenteritis
System: Gastrointestinal, reproductive Etiological Agent: coronavirus. Transmissible gastroenteritis is spread via aerosol and pig-to-pig contact Signs: vomiting, osmotic diarrhea, and dehydration, death up to 100% and abortions Diagnosis: clinical signs. Treatment: nonspecific Prevention: vaccination, increasing farrowing room temperatures, all in/all out management, and good sanitation

Swine Vaccination Protocols


TABLE 25-1 Swine Vaccinations

Non Infectious Diseases


Anemia is a regularly diagnosed problem in baby piglets. Clinical signs often present between 1 and 2 weeks of age. The signs include difficulty breathing, roughened hair coat, and poor growth. The lack of iron can be corrected by administration of iron intramuscularly or orally. Piglets must be supplemented with iron because of the lack of iron in sows milk.

Malignant Hyperthermia-Porcine stress syndrome (PSS)


Pale soft exudative pork (PSE): Animals with the Hal gene produce inferior quality meat that is pale (grayish), soft, and watery, which devalue the carcass. These changes occur after death of the animal, due to an abnormally rapid fall in pH in the muscle cells that damages the cell membrane and allows water to leak freely out of the cells. PSE affects a large percentage of animals that are homozygous for the Hal gene as well as many animals that carry the gene as heterozygotes. 2. Malignant hyperthermia: This is a drug-induced phenomenon characterized by muscle rigidity; tachycardia; tachypnea; metabolic acidosis; and a rapid, extreme, progressive rise in body temperature. Cardiovascular collapse and death usually occur. The condition may be triggered by halothane gas or by some of the neuromuscular blocking agents. 3. PSS: This is an acute manifestation that requires a stressful trigger to initiate clinical signs. Physical stressors such as restraint, exertion, fighting, breeding, parturition, veterinary procedures, fighting, transportation, overcrowding, and high environmental temperatures may initiate a sudden attack of dyspnea and open-mouth breathing,

PSS
Treatment: Treatment of malignant hyperthermia and PSS consists of intravenous dantrolene, a muscle relaxant specific for skeletal muscle Prevention: judicious planned breeding and culling, the incidence of the condition is decreasing and theoretically could be eliminated.

Parakeratosis
Parakeratosis is a metabolic condition due to a deficiency of zinc. The condition is more severe when calcium levels are high in the diet. The main clinical sign associated with parakeratosis is rough, scaly skin. Parakeratosis is prevented and treated by balancing zinc and calcium levels in the diet.

Prolapse
Occurs during parturition Treatment involves sedation or anesthesia of the sow, cleansing the prolapsed tissues, and repositioning the organ. A Buhner retention suture can be used to prevent reoccurrence. The sow must be closely watched so that the suture can be removed at the onset of labor.

Rickets
Rickets is caused by a lack of calcium, phosphorus, or vitamin D in the diet. To prevent rickets, it is extremely important that the swines diet provide the correct ratio of calcium to phosphorus. Clinical signs of rickets include slower than normal growth rates and crocked legs. Prevention and treatment of the disease include proper balances of nutrients in the diet.

Swine Parasites
Table 25-2 list the major swine parasites. YOU ARE REPSONSIBLE FOR THEM

Case Study
Mrs. Kay owns about 300 head of sows in her farrow-tofinish operation. Increased stillbirths are occurring in her farrowing house. When the piglets become growers, she is seeing increases in respiratory disease and death. A veterinarian diagnoses the herd with porcine reproductive and respiratory syndrome (PRRS). Is there a treatment of this disease? What can Mrs. Kay do to prevent this disease?

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