Swine diseases Ages of pigs are important Neonates

Swine diseases

Ages of pigs are important Neonates 0 -3 weeks Weanlings/nursery 3 -10 weeks Growers/finisher 10 -26 weeks Breeders/adults >6 -8 months <4 kg (8. 8 lbs) 4 -25 kg (8. 8 – 55 lbs) 25 -120 kg (55 – 264 lbs) >120 kg (> 264 lbs) (birth: 3 -4 lbs) (~ 25 lbs) (~ 50 lbs) (~ 220 - 240 lbs)

Orderly thinking. . . Multisystemic Diseases Respiratory Diseases Gastrointestinal Diseases Neurologic Diseases Musculoskeletal Diseases Reproductive Diseases Dermatology Miscellaneous

Multisystemic diseases Nutritional ◦ Vitamin E / selenium deficiency Infectious ◦ Erysipelas (Erysipelothrix rhusiopathiae): gram + rod ◦ Glasser’s disease (Haemophilus parasuis): gram coccobacillus ◦ Salmonella: gram negative ◦ PRRS (arterivirus) ◦ Pseudorabies virus (herpes virus)

Erysipelas Erysipelothrix rhusiopathiae Gram positive rod Environmental contaminant most herds have carriers Septicemia diamond skin, arthritis, endocarditis, necrosis

Erysipelas acute septicemia ◦ fever, prostration, anorexia, vomiting, reluctance to walk ◦ Hemorrhages may be present in multiple organs throughout the body. ◦ Mortality can be quite high. chronic forms of infection include endocarditis and arthritis

Diamond skin disease "Diamond skin disease" erythematous skin lesions • These may be the classic diamondshaped lesions or more diffuse edema and erythema. • The lesions are due to vasculitis and thromboembolism.

Valvular endocarditis

Erysipelas cont. . . Treatment Penicillin Tetracyclins Prevention and control Sanitation Vaccinate at weaning and then q 6 months Zoonotic: ‘erysipeloid’ occupational diseases for people such as veterinarians, abattoir workers and fisherman Direct contact

Treatment and prevention Penicillin – first choice people and animals cephalosporins and clindamycin -people. Caution and hygiene are important to prevent infection when working with potentially infected animals or in potentially contaminated environments

Glasser’s disease (polyserositis) Haemophilus parasuis small, pleomorphic, and fastidious, Gram-negative rod (coccobacillus) Endemic 3 wk – 3 month (have no active/passive immunity) initiated by stress ◦ weaning, changes in environment, commingling, or as coinfection with other disease agents Also associated with PRRS or swine influenza

Glassers - HX 1931 an organism, presumably the same one, was isolated from swine with influenza and named Haemophilus influenzae suis. 1943 it was clear that the organism was a pathogen in its own right, not necessarily associated with swine influenza, and the name was shortened to Haemophilus suis. 1976, definitive taxonomic studies resulted in the present name, Haemophilus parasuis

Glassers - CS Initially: fever, anorexia, depression Meningoencephalitis: ◦ tremors, incoordination, posterior paresis or lateral recumbency Polyserositis Polyarthritis Mortality at any age Less common clinical signs: ◦ rhinitis, dyspnea, reddening of the conjunctiva, cyanosis of the extremities and edema of the eyelids or ears

Glasser’s disease (polyserositis) Serosal surfaces: peritoneum, pleura, pericardium, joints, meninges Polyserositis (serous membrane inflammation with effusion, fibrinous), Pleuritis Pericarditis Peritonitis Pig with Glässer’s disease. Noticeable presence of fibrin in the peritoneal cavity (fibrinous peritonitis) and pericardiac cavity (fibrinous pericarditis

Glasser’s disease red, multifocal, disseminated and suggestive of septicemia and hematogenous spread

Glasser’s cont. . . Diagnosis Culture is difficult (but try it) Brain, visceral pleura and other serosal exudates are preferred culture sites Go with suspicion from gross lesions Molecular techniques for identifying H. parasuis (research) Treatment: Antibiotics and sulphonamides Penicillins Tetracyclins periodic evaluation of antibiograms is warranted. Mass: medicate, through the water (same age group)

Glassers - Prevention and control Reduce stress Control of other diseases: PRRSV prophylactic antimicrobials Vaccine at weaning then again 3 -4 weeks later against one serovar of H. parasuis may not assure good protection against all serovars. (21 serovars)

Salmonella sp. 2000 serotypes: small, hardy, ubiquitous, Gram-negative bacilli ◦ Salmonella cholerasuis: mostly only in swine ◦ Salmonella typhimurium Zoonotic Contaminated pork products are not a primary source of food-borne salmonellosis outbreaks in people but efforts to reduce salmonellae in the pork food chain are a high priority for the swine industry disease in both people and swine include Salmonella serotypes typhimurium, enteritidis, agona and heidelberg

Salmonella Typhimurium “But S. Typhimurium’s success in swine isn’t just due to its increased motility when norepinephrine levels increase. It also has a mechanism for acquiring iron from its host to support its own growth and replication” 7/2009 Microbiologist Brad Bearson analyzes cultures for the presence of Salmonella enterica serovar Typhimurium in swine feces.

Salmonella - HX In 1886 the organism now known as Salmonella serotype choleraesuis was erroneously reported to cause hog cholera

Salmonella – Signalment, CS weaned or growing/finishing pigs Low-level endemnicity, carriers Septicemia pyrexia, anorexia purple discoloration of the ears (infarction) Small or large intestinal diarrhea (button ulcers) Pig, intestine. The intestinal lumen has Pneumonia reddened erosions and a fibrinonecrotic Rectal strictures exudate. Credit: Dr. B. Inskeep, AFIP

Salmonella

Salmonella cont. . . Diagnosis Aerobic culture Treatment Neomycin in the feed/water for whole group Naxcel (ceftiofur) for individual Prevention and control Sanitation: inactivated by chlorine, iodine and phenol-based disinfectants All in - all out operation Various vaccines (live avirulent) Pig, mesenteric lymph node. The mesenteric lymph node is enlarged and edematous. This lymph node is good for obtaining cultures. Credit: Dr. B. Inskeep, AFIP

PRRS Porcine reproduction (sows and gilts) and respiratory syndrome (young growing pigs but also occurs in naïve finishing pigs and breeding stock) Most important economic disease in USA (after eradication of classical swine fever) Arterivirus: SS enveloped RNA Virus (high mutation rates) persist in long-term carrier pigs (greater than 200 days) in reality stop shedding 60 days later

PRRS - HX 1987 -88 in North Carolina, Iowa and Minnesota 1989 – 90: Several outbreaks in Indiana were reported During the subsequent decade, PRRS spread rapidly, both in Europe and North America By the end of 1992 the disease was reported in Canada, Great Britain and several European countries. Two distinct strains of virus, one in Europe and one in the United States, were characterized as genetically different but are clinically similar in most respects. Both are now in the United States, along with a multitude of viral variants. Old name: swine infertility and respiratory syndrome (SIRS)

PRRS Transmission: direct contact (very infectious): It is present in nasal secretions, urine, semen, mammary secretions and feces. Clinical signs – neonates pulmonary intravascular macrophages (PIM) and pulmonary alveolar macrophages (PAM); anorexia, lethargy, fever cyanosis of the ears, respiratory distress secondary bacterial pneumonia delayed or abnormal estrus cycle with increased numbers of stillborns/mummies (3 rd trimester)

PRRS Abortions, mummies and weak pigs Lung affected with interstitial pneumonia of a pig with PMWS and co-infected with porcine reproductive and respiratory syndrome virus (PRRSV). This “infectious combination” is relatively frequent at field level; macroscopically it is not possible to distinguish between these two infections, so laboratory studies are required to confirm the etiologic diagnosis.

PRRS cont. . . Diagnosis virus isolation (VI), detection of PRRS antigen by fluorescent antibody tests (FAT) or immunohistochemistry (IHC), or detection of PRRS virus genome by polymerase chain reaction (PCR) and be coupled with presence of typical lesions. serology provides indirect evidence of infection but does not determine if there is actual disease caused by PRRS virus. Supportive care, treat secondary bacteria moderately resistant to environmental degradation, the virus is easily inactivated by phenol, formaldehyde, and most common disinfectants

PRRS CONTROL closed herds: ◦ replacements do not enter male or female replacements from PRRSv positive herds outside the pyramid ◦ Enter only PRRSv free replacement seedstock into a production pyramid. semen: ◦ Do not use PRRSv positive semen from a stud outside the pyramid. ◦ Assure any outside semen is from a stud that is confirmed PRRSv free before entering it into a production pyramid. commercial modified live vaccines ◦ Live vaccines pose a dilemma as vaccine virus may act as a foreign introduction Change feed with mycotoxins

Pseudorabies Aujesky’s disease Type 1 Herpes virus: alphavirus The disease was eradicated from the US commercial pig industry in 2004 but remains in some localized feral swine populations Species: cattle, sheep, dogs, cats, and goats but not horses AND rats, mice, raccoons, opossums, rabbits, and several fur-bearing mammals ◦ Close contact with infected swine central nervous system (CNS), respiratory system or reproductive system Not humans!

Pseudorabies The disease is named after the Hungarian veterinarian Dr. Aladár Aujeszky who linked the disease in cattle, dogs, and cats in 1902. Pseudorabies was not identified as a viral disease in swine until 1909 Prior to 1960, the disease in swine was important in Eastern Europe but major outbreaks did not occur in the US until the mid-1970 s In 1989, the US embarked on a 5 -stage Federal/State/Industry program for eradication of PRV in swine; eradication of PRV from the commercial industry was achieved in 2004

Pseudorabies cont. . . Baby piglets up to 100% mortality high fever, depression, anorexia, tremors, incoordination, dog-sitting position, vomiting, foaming at the mouth, blindness, paddling, coma and convulsions Weanling/growers up to 60% mortality in weanlings, 0 -15% in finishers pneumonia impt, neurologic dz, vomiting, extreme pyrexia Adults - often inapparent can cause stillbirth/abortion

Pseudorabies Dead pigs (and a cat), a result of Pseudorabies Mummified pigs, a symptom of Pseudorabies

Pseudorabies Lesions on postmortemed lung Lesions on nose of piglet

Pseudorabies cont. . . Reportable disease! Diagnosis Necropsy histologic lesions in brain, ulcers in gi tract Serum neutralization is standard test ELISA can be used as a screening test Treatment - none Prevention closed herd! quarantine! restrict wildlife The virus can be destroyed by many disinfectants, including orthophenylphenol, quarternary ammonium or iodine compounds, and 5% sodium hydroxide vaccination

Pseudorabies

Pseudorabies Regulation ◦ use of vaccine regulated by states ◦ federal regulations for monitoring all animals over 6 mo old must be tested 25% of herd tested q 3 months or. . . 10% of herd tested q 1 month

White muscle disease / Mulberry disease heart Nursery or grower pigs (few weeks – 4 months) Vitamin E / Selenium deficiency Feeds high in the concentration of polyunsaturated fatty acids, copper, vitamin A or mycotoxins can either destroy vitamin E or make it less bioavailable Grains from soils deficient (midwest) in selenium, or selenium antagonists in mixed feeds, can result in feeds low in selenium. Both vitamin E and selenium work as antioxidants.

Vit E / Selenium cont. . . Clinical signs acute death (mulberry heart disease) muscle weakness (white muscle disease) more common in lambs, calves and chickens rather than swine Diagnosis Necropsy - hydropericardium, fibrinous epicarditis, myocardial hemorrhage Diffuse hepatic necrosis - hepatosis dietetica Liver selenium < 0. 5 ug/g

Mulberry heart disease The condition was named after the mottled appearance of the heart muscle in affected pigs. Typically, there alternating areas of necrosis and hemorrhage throughout the myocardium.

Hepatosis dietetica consists in a degenerative lesion caused by vitamin E and selenium insufficiency.

Vit E/ Selenium prevention or treatment of a deficiency, pigs can be injected with vitamin E and/or selenium and tissue levels will be increased rapidly. supplementation of feed or drinking water Sows injected in late gestation give birth to pigs with increased levels of both compounds. MHD is more responsive to vitamin E; HD more so to selenium

Respiratory diseases Atrophic rhinitis: Bordetella bronchiseptica and Pasteurella multocida (primarily type D) Swine influenza: influenza virus Mycoplasma pneumoniae: “enzootic pneumonia, ” Actinobacillus pleuropneumoniae: Gramnegative Pasteurella: Gram negative Verminous pneumonia

Atrophic rhinitis Bordatella bronchiseptica ◦ aerobic, Gram-negative rod Pasteurella multocida ◦ Gram negative coccobacillus High ammonia Restricted to swine (described in dog and goat) In the United States, AR is becoming a rare disease as ◦ early weaning, age segregation and/or vaccination.

Atrophic rhinitis – clinical signs Hx: Described in 1830 and in US in 1944 Clinical signs: 1 wk weaning early stages: snuffling, sneezing, snorting, ◦ Epiphora, +/- epistaxis which may progress: atrophy and distortion of the turbinates, nasal and facial bones of some affected pigs twisted snouts

Atrophic rhinitis cont. . . Dff: rhinitis: porcine reproductive and respiratory syndrome virus (PRRS), pseudorabies virus (PRV), inclusion body rhinitis (cytomegalovirus), or excessive dust or ammonia Diagnosis Necropsy - 2 nd premolar or 1 st cheek tooth in pigs less than 6 months of age Nasal culture for either organism

Atrophic rhinitis Toxigenic P. multocida produce a potent toxin that causes a rhinitis with progressive osteopathy of facial and turbinate bones

Atrophic rhinitis Treatment tetracyclines in the feed: farrowing/weaning LA 200 (oxytetracycline) to neonates Control or eradicate ◦ improvement of husbandry: management and housing, including ventilation, all in all out, reduce stress ◦ vaccination program for the breeding stock, pigs, or both.

Swine influenza Influenza virus: type A influenza viruses (family Orthomyxoviridae). Zoonotic Serologic surveys show that nearly all of the herds in the Midwest have antibodies to SIV Outbreaks associated with movement or extreme weather changes up to 100% morbidity low mortality unless secondary bacterial infection complicates things

Swine influenza - Hx Swine influenza subtype H 1 N 1: ◦ 1 st appeared in western Illinois in 1918 ◦ influenza pandemic that killed an estimated 20 million people worldwide interspecies transmission: among swine, chickens, ducks, turkeys, many wild birds and people 2 or more strains of virus: potential for reassortment (genetic “shift”). H 3 N 2 and H 1 N 2 emerged during the 1990 s: triple reassortment” variants that are comprised of swine, human, and avian viral genes

Swine influenza - CS inflammation with widespread degeneration and necrosis of cells lining bronchi and bronchioles Sudden: sudden onset of fever, occulonasal discharge, prostration and weakness Progression: paroxysmal coughing over a relatively short course of 5 -7 days low mortality Both lungs are non-collapsed. There is diffuse tan consolidation of cranial lobes, and multifocal lobular consolidation of the caudal lobes, consistent with bronchointerstitial pneumonia Credit: Dr. B. Janke, Iowa State University, College of Veterinary Medicine, Veterinary Diagnostic Laboratory

Swine influenza cont. . . Diagnosis Necropsy - cranioventral pneumonia: fluorescent antibody technique on fresh lung sections immunohistochemistry techniques on formalin-fixed lung sections Treatment - supportive Prevention closed herd control secondary infections keep away from humans (no shows!) inactivated by many disinfectants (2 wks environment)

Mycoplasma hyopneumoniae Enzootic pneumonia: acute and severe disease, PRDC (porcine resp dz complex) Weaned – grower/finisher increases the severity of several other infections: (PRRS) and influenza Carrier swine very costly, widespread disease of swine, largely because of its negative effects on growth rate and feed efficiency

Mycoplasma hyopneumoniae Transmission: direct, aerosal, transplacental Most common cause of chronic pneumonia ◦ Chronic, non-productive cough Low mortality Secondary bacterial complication Dff

Mycoplasma cont. . . Diagnosis Necropsy - “plum colored”or pale cranio-ventral pneumonia Culture to rule out secondary bacteria fluorescent antibody, immunohistochemical, or polymerase chain reaction (PCR) techniques

Mycoplasma cont. . . Treatment - Lincomycin in feed Prevention - improve management

Actinobacillus pleuropneumonia (APP) Gram-negative, capsulated, coccobacillary rod Host specific Intensive swine operations Inapparent carriers Release toxins

Actinobacillus pleuropneumonia Peracute, and chronic forms Clinical signs severe respiratory distress death marked dyspnea with mouth breathing +/- bloody discharge from the mouth and nose

Actinobacillus cont. . . Risk factors: ◦ Overstocking, inadequate ventilation, coinfection with other respiratory pathogen, stress Diagnosis necropsy - fibrinous pleuropneumonia often diaphragmatic lobes most severe culture is difficult complement fixation serology Treatment ceftiofur (Naxcel) and procaine penicillin Control vaccination of young pigs

Actinobacillus • Classic lung lesions caused by Actinobacillus pleuropneumoniae. • Focal areas of necrotizing pneumonia isolated in the dorsal and caudal portions of the lungs is a diagnostic feature. • the entire lung lobe can also be involved. • fibrinous pleuritis is common

Pasteurella multocida Gram negative coccobacillus Most common bacterial isolate from pig lungs opportunistic pathogen mycoplasma, influenza, actinobacillus, stress clinical signs moist productive cough dyspnea some die

Pasteurella cont. . . Diagnosis necropsy - suppurative cranio-ventral bronchopneumonia may be pleuritis similar to actinobacillus culture Treatment - penicillin, tetracyclines Control look for underlying disease medicate feed and water (tetracyclines)

Pasteurella pneumonia

Verminous pneumonia Ascaris suum - direct life cycle ◦ pneumonia, hepatitis, and ill thrift Metastrongylus elongatus - earthworm intermediate Problem with pasture pigs Clinical signs poor doer respiratory distress Secondary bacterial infection “Milk spots” liver, worms in the GI Levamisole, ivermectin

Verminous pneumonia • 15 -40 cm long, thick bodied, round worms • Eggs persist in environment 15 yrs

Gastrointestinal diseases Stomach Ulcers Small intestine E. coli (piglets): Gram-negative, flagellated bacilli TGE (piglets): coronavirus Clostridium (piglets): large, anaerobic, Gram positive bacillus Coccidiosis (>7 days): protozoa Rota virus (post weaning) Salmonella (any): Gram-negative bacilli

Gastrointestinal disease cont. . . Large intestine Swine dysentery (grower/finishers): Gram-negative, anaerobic Proliferative enteropathy (grower/finishers) Hemorrhagic bowel syndrome Proliferative illeitis Whipworms (growers) Salmonella (any): Gram-negative bacilli

Infection with and/or agent Unweaned piglets Nursery pigs Grow/finish pigs Enterotoxigenic E. coli ++++ + (early grower) Rotaviral infection ++++ + (early grower) Transmissible gastroenteritis virus ++++ (TGE) +++ Adults +++ Clostridium difficile ++++ Clostridium perfringens Type A ++++ Clostridium perfringens Type C ++++ + (rare) ++++ ++ ++++ +++ ++++ ++ +++ Coccidiosis Isospora suis Salmonellosis Swine dysentery Brachyspira hyodysenteriae Proliferative enteropathies Lawsonia intracellularis Porcine epidemic diarrhea virus (exotic) Whipworm infection Trichuris suis +++

Gastric ulcer disease Almost always the pars esophagea (nonglandular stomach) Non-specific lesions Can lead to “bleed-out” Predisposing factors. . . Finely ground feed Stress Vit E/Selenium def Weaning onwards

“Bleed out” Melena, ulceration of squamous portion of stomach, anorexia

Colibacillosis E. coli: Gram-negative, flagellated bacilli Most impt cause of diarrhea in piglets <5 days old!!! O 157: H 7, does not appear to cause disease in swine Toxins Clinical signs clear watery to pasty brown feces dehydration and depression death losses higher in younger pigs

Colibacillosis cont. . . Diagnosis ph of feces (>8) culture of organism (large number) necropsy - dilated gas filled small intestine Treatment Ampicillin, tetracyclin, gentamicin, fluids Control sanitation, vaccination of sow

Colibacillosis

TGE - transmissible gastroenteritis Coronavirus (similar to FIP) Epidemic form (all ages) Endemic form (1 -8 weeks old) WINTER disease Clinical signs Neonates (1 -8 days)– watery diarrhea with undigested milk, vomiting and high mortality rates in piglets Growers, finishers - diarrhea recovers <7 days Morbidity and mortality high in pigs <2 weeks old

TGE cont. . . Diagnosis ELISA, immunoflourescence of gut contents Necropsy undigested milk in small intestine thin walled, transparent small intestine Treatment - supportive Control isolate new additions for 2 weeks, keep dogs and bird away (carriers) Immunization of sows or piglets Grind up piglet guts and feed to pregnant sows

TGE

tge Distended intestine with fluid ingesta thin translucent intestinal wall

TGE

Clostridial enteritis Clostridium perfringens type C: gram + sudden death in 1 -2 day old piglets Clinical signs BLOODY DIARRHEA Diagnosis Necropsy - blood in jejunum with flecks of mucosa, necrosis of small intestine Clinical signs Histopathology - large gram positive rods

Clostridial enteritis

Clostridial enteritis cont. . Treatment usually die too quickly type C antitoxin Control Sanitation Type C antitoxin within minutes of birth Vaccination of sow Prophylactic bacitracin or penicillin to piglets

Coccidiosis Isospora suis piglets 5 days old to weaning Clinical signs diarrhea (7 -10 days of age) no blood acidic feces (in contrast to E. coli) Dehydration

Coccidiosis cont. . . Diagnosis Diarrheas in pigs <7 days old are not Isospora! Necropsy - fibrinonecrotic enteritis Histopathology - oocysts, merozoites Fecal flotation can be falsely negative Treatment Adding coccidiostats to feed is ILLEGAL amprolium to piglets Control - disinfection of farrowing area

Coccidiosis

Rota virus Reovirus Almost all pigs are infected Diarrhea in post-weaned pigs Diagnosis - difficult Necropsy-thin walled small intestine Histopathology Flourescent antibody test Electron microscopy

Rota virus cont. . . Treatment Glucose and fluids Antimicrobials for concurrent infections E. coli Isospora Control Wean pigs on good nutritional diet MLV vaccine at 7 and 21 days (in water)

Dont forget Salmonella typhimurium Salmonella cholerasuis Fibrinonecrotic enteritis or colitis at necropsy Rectal strictures Culture of organism

Swine dysentery Serpulina hyodysenteriae: anaerobe spirochete Grower / finishers Mortality can be up to 30% Clinical signs diarrhea sometimes with blood eventually watery, bloody, mucoid most recover in 2 weeks but 30% may die

Swine dysentery cont. . . Diagnosis Necropsy - mucohemorrhagic colitis histopathology Spiral shaped organism on dark field microscopy Culture is definitive Treatment Lincomycin in water Control medicated water, depopulation, close herd vaccine only reduces clinical signs

Swine dysentery

Swine dysentery

Proliferative enteropathy Lawsonia intracellulare proliferative illeitis, hemorrhagic bowel syndrome Large intestine Weanlings and older Clinical signs intermittant diarrhea can be hemorrhagic diarrhea anemia (think gastric ulcer first)

Proliferative enteropathy cont. . . Diagnosis Necropsy - “garden hose” ilium and colon can be hemorrhagic or fibrinonecrotic Histopathology - intracellular, silver positive DNA probes Treatment and control No specific treatment Reduce stress Medicate feed - tetracyclines, carbadox

Proliferative illeitis

Whipworms Trichuris suis 2 -6 months of age Large intestine Clinical signs diarrhea with mucus and blood anemia (2 DDX? ) Diagnosis - fecal float, fibrinnecrotic colitis Control - dichlorvos and fenbendazole

Whipworms

Don’t forget Salmonella! Salmonella typhimurium Salmonella cholersuis associated with rectal strictures? Can be large intestine Fibrinonecrotic colitis Rectal strictures Culture

Parasites of pigs Trichuris suis - colon Ascaris suum - small intestine, milk spots Stephanurus edentatus - kidney Macrocanthorynchus hirudinaceous -small intestine

Neurological diseases Hypoglycemia Streptococcus suis Salt poisoning Edema disease

Hypoglycemia Newborn piglets Blood glucose <50 may develop signs Clinical signs convulsions shivering hypothermia gait abnormalities

Hypoglycemia cont. . . Diagnosis Blood glucose Empty stomach Treatment 20 ml/kg 5% glucosa, warm em up Control make sure the milk is flowing

Salt poisoning Usually due to water deprivation rather than too much Na Causes hyperosmalarity of CNS resulting in swelling and edema Clinical signs thirst, constipation depression, blindness, convulsions

Salt poisoning cont. . . Diagnosis History Clinical pathology-eosinopenia, hypernatremia Histopathology - eosinophilic meningitis Treatment None Control provide free access to water reduce salt in diet

Musculoskeletal diseases Arthritis S. suis, Erysipelothrix, A. pyogenes Mycoplasma hyosynoviae Myodegenerative disease Malignant hyperthermia (PSE) White muscle disease

Suppurative arthritis Streptococcus suis Erysipelothrix rhusiopathiae Actinomyces pyogenes May see loss of cartilage Due to fighting, surgical contamination Distended joints, abscesses Penicillin - treatment often no good

Suppurative arthritis

Mycoplasmal arthritis Mycoplasma hyosynoviae 4 -12 weeks of age acute or chronic lameness non-suppurative arthritis/synovitis edema of synovial tissue Lincomysin to treat

Mycoplasmal arthritis

Reproductive disease Parvovirus Leptospirosis PRRS Brucellosis

Porcine parvovirus 100% prevalence Signs depend on time of infection <30 days - embryo resorbed 30 -70 days - mummy >70 days - dead or weak, survive normally no other signs of illness SMEDI - stillbirth, mummy, embryonic death, infertility Diagnosis - detection of virus in mummy by immunofluorescence or by rising titer Poor conception rates, reabsorbed litters, mummies and small litters

Parvo - SMEDI

Porcine parvovirus cont. . . Control ◦ ◦ Natural infection of gilts before breeding Commingle gilts with sows Grind up mummies and feed to gilts Vaccination! may still get some losses

Leptospirosis Leptospira interrogans serovar pomona - most common serovar bratislava Clinical signs Pyrexia, last trimester abortion, stillbirths, weak litters, sudden mortality in piglets Diagnosis Culture difficult Dark field microscopy of fetal fluids, urine Serology (<1: 800)

Leptospirosis cont. . . Treatment Chlortetracycline in feed Control Vaccination Gilts twice before first breeding Sows before every breeding

PRRS Porcine reproductive/respiratory syndrome Premature farrowing Small weak piglets or stillborns increased numbers of mummies Delayed or abnormal estrus Serology to diagnose Vaccination for prevention Abortions, mummies and weak pigs

Brucellosis Brucella suis Clinical signs abortion at any time in gestation infertility - many sows coming back into heat abortions in first trimester) infected sows recover and deliver normally Lesions mild endometritis arthritis orchitis

Brucellosis

Swine diseases

Dermatologic diseases Mange: Sarcoptes scabei var suis Greasy pig disease: Staphylococcus hyicus: Gram-positive coccus Swine pox: Swine pox virus Erysipelas: Erysipelothrix rhusiopathiae: Gram -positive, aerobic, slightly bent, thin bacillus

Mange Sarcoptes scabei var suis (not zoonotic) represents the most important ectoparasitic disease of swine nursery or grower pigs

Mangy piglet Clinical signs intense pruritus, lichenification, papules, crusts poor production susceptible to other diseases

Mangy piglet

Sarcoptes scabei Diagnosis - clinical signs, skin scrape Treatment and control, acaricide (amitraz) topically, ivermectin injection ova, larvae, nymphs, adults develop in the epidermis 0. 5 mm in length, gray to white, and just visible to the naked eye when on a black background Place the scraping on a piece of black paper for a few minutes. Then carefully blow off the superficial debris and examine the site on the paper for the small, light colored mites.

Greasy pig disease Exudative dermatitis Staphylococcus hyicus: Gram-positive coccus Affects late preweaning pigs: few days to about eight weeks of age

Greasy pigs Sebaceous glands secrete excessively and there is accumulation of greasy exudate over lesions Clinical signs exfoliation of skin, excess sebaceous secretion pruritis not a feature unless complicated my mange Diagnosis - clinical signs and culture or histopathology

Greasy pig disease cont. . . Treatment: frustrating Injectible penicllin, oxytetracyline Tetracyclines in feed Topicals: 10% bleach, chlorhexidine, Virkon® (Durvet) or dilute tamed iodine Control Sanitation: sanitation for pregnant sows, especially in housing, and washing of sows may be of value Control external parasites Good nutrition

Swine pox virus ◦ Poxviridae family Only pigs less than 4 months old

Swine pox “round to oval cutaneous lesions that heal in three to four weeks” Clinical signs papules 1 -6 mm in diameter pustules, crusts clear spontaenously Diagnosis - clinical signs, biopsy intracytoplasmic inclusion bodies Treatment - not necessary: herd immunity

Erysipelas Erysipelothrix rhusiopathiae ◦ Gram-positive, aerobic, slightly bent, thin bacillus Diamond skin disease: zoonotic pigs 3 months - 3 years old

Diamond skin disease Clinical signs widespread ecchymotic hemorrhages due to microthrombi arthritis, endocarditis

Erysipelas cont. . . Diagnosis Diamond skin lesions pathognomonic Culture of blood, joints, lung, liver Treatment Penicillin is the drug of choice Control General sanitation Bacterins or attenuated live vaccines

Miscellaneous diseases Swine lice: louse, Pediculosis Baby piglet anemia

Swine lice Haematopinus suis: zoonotic, 6 mm long (largest louse) Lifecycle ◦ sucking louse (anemia) ◦ entire LC on host Indicator of poor management

Swine lice Clinical signs pruritis (mild), anemia, poor growing Diagnosis visible to naked eye Treatment - same as for mange

Baby pig anemia Iron deficiency Piglets iron demand is greater than the sows milk (15 -50%) Pigs raised in the outdoors may not need iron Vit E/ selenium deficiency : Fe toxicity !!

Baby pig anemia Clinical signs anemia within 2 -3 days of birth dyspnea, edema, pale skin, lethargy Diagnosis - clinical signs, CBC Treatment - 200 mg iron dextran at 1 -3 days of age

Foreign diseases Africa Swine Fever Foot and mouth disease Hog cholera / classical swine fever Swine vesicular disease Malignant catarrhal fever

Hog Cholera / classical swine fever Virus family Flaviviridae, genus Pestivirus Highly contagious viral dz 1978: ‘hog free’ Swine and boars Direct/ uncooked meat CS: High Fever: 106 -108 o. F (>41 o. C) Depression Conjunctivitis Constipation, then Diarrhea Skin hemorrhages/Cyanosis Stillbirths, deformities, mummies neurologic Renal petechiation

African Swine Virus African swine fever genus asfivirus in the family Asfarviridae Only DNA virus ~ arbovirus hemorrhage in multiple areas: hot sick red pigs is a tick-borne (ornithodorus), contagious, febrile, systemic viral disease of swine 100% mortality No vaccine

ASF 1. Greatly enlarged dark red to black friable spleen 2. Enlarged hemorrhagic gastrohepatic lymph nodes 3. Enlarged hemorrhagic renal lymph nodes

Hog cholera vs. ASF ◦ African Swine Fever pigs do not develop conjunctivitis or encephalitis ◦ Despite high fever, ASF infected pigs stay in good condition, whereas hog cholera infected pigs drastically lose weight

Vesicular diseases of swine Foot and mouth disease - apthavirus* Swine vesicular disease - enterovirus Vesicular exanthema - calicivirus Vesicular stomatitis - rhabdovirus

THE END!!!

References http: //www. aphis. usda. gov/animal_health/an imal_dis_spec/swine/ http: //www. ncsu. edu/project/swine_extensio n/ncporkconf/2002/roberts. htm http: //www. vetmed. wisc. edu/pbs/zoonoses/ Erysipelas/erysipelasindex. html http: //vetmed. iastate. edu/vdpam/newvdpam-employees/food-supply-veterinarymedicine/swine-diseases/haemophilus -parasuishttp: //vetpath. wordpress. com/category/necr opsy-cases/

References http: //www. fmv. utl. pt/atlas/figado/pages_us /figad 015_ing. htm http: //www. cfsph. iastate. edu/Disease. Info/dis ease. php? name=influenza&lang=en http: //microgen. ouhsc. edu/a_pleuro/a_pleur o_home. htm