Board Review

1. Board Review

2. Gastrointestinal

3. Neonatal enteric disease: Colibacillosis Etiology: Usually haemolytic E. coli (eg. F4 [K88], F5 [K99]) can cause watery diarrhoea (any time), septicaemia (0-48 h), or enterotoxemia (eg. F18 post weaning). Pathogenesis: Attachment to receptors on enterocytes and elaboration of enterotoxin (attaching and effacing E. coli do occur but are uncommon). Toxin induces a secretory diarrhoea. Pathology: Dehydration, congestion of stomach and intestines, dilated, flaccid small intestine, mild or no villus atrophy. Diagnosis: Presumptive diagnosis based on absence of blood, no intestinal necrosis, isolation of profuse or pure culture of pathogenic serotypes.

4. Neonatal enteric disease: Colibacillosis Treatment and Control: Treat affected pigs symptomatically with antibiotics (e.g. gentomycin). Obtain a sensitivity screen and re-assess antibiotic selection. If not currently performed, institute a sow vaccination program. If vaccination is performed, determine the serotype involved and ensure that it is included in the vaccine. Assess the hygiene of the facility. Assess management for potential stressors (sow and litter). Dietary zinc (e.g. 3000 ppm zinc as ZnO in starter diets). – for 2 weeks after weaning, inorganic zinc

5. Post-weaning enteric disease: Edema disease Etiology: Verotoxin producing E. coli (eg. F18). Pathogenesis: As for colibacillosis except that the enterotoxin produced is edema disease principle. Absorbed toxin causes arterial degeneration and increased vascular permeability resulting in edema in various locations and focal malacia in the brain stem. Clinical signs: Sudden death (best pigs) and/or neurological signs usually within 10 days of weaning. Edema of eyelid, nose, or ears. Pathology: Dehydration, edema of greater curvature of stomach, congestion of stomach and intestines, dilated, flaccid small intestine, mild or no villus atrophy. Diagnosis: Presumptive diagnosis based on absence of blood, necropsy findings, isolation of profuse or pure culture of pathogenic serotype.

9. Neonatal enteric disease: Clostridial diarrhoea Etiology: Peracute/acute forms involving C. perfringens C affect pigs within hours after birth. Subacute/ chronic forms affect pigs 3-21 days. Pathogenesis: ?-toxin causes enterocyte damage then bacterial penetration and adherence to basement membrane. Pathology: Severe necrotizing-hemorrhagic enteritis, possibly gas bubbles in serosa (acute) or diffuse fibrinous necrosis of mucosa without haemorrhage (subacute/ chronic; note: latter lesion similar to coccidiosis). Diagnosis: Bloody diarrhoea with high morbidity and case mortality. Hemorrhagic enteritis observed on post mortem. Definitive diagnosis on demonstration of ?-toxin. May see hemorrhagic diarrhea, but may kill pig so fast that it is not seen clinically

12. Neonatal enteric disease: Clostridial diarrhoea Consider C. difficile when: Diarrhoea in piglets less than 1 to 7 days of age with high morbidity (10-90%) and mortality (up to 50%) and possible respiratory distress (ascites and fluid in peritoneum) Absence of “normal” pathogens such as E. coli, toxigenic Clostridium perfringens A or C, Rota virus, TGE Gross lesions of mesocolonic edema, occassional hydrothorax (causes resp. distress) and/or ascites Diagnosis confirmed by culture of organism

13. Neonatal enteric disease: Clostridial diarrhoea Consider C. perfringens type A when: Mild diarrhoea in piglets less than 3 days of age with high morbidity but low mortality Absence of “normal” pathogens such as E. coli, Clostridium perfringens type C, Rota virus, TGE Disease that is self-limiting and/or responds well to antimicrobials

14. Neonatal enteric disease: Clostridial diarrhoea Treatment and control: Treatment involves use of appropriate antibiotics. Control requires improved hygiene and sow vaccination. Clostridia can kill sows. If a sow is found dead and bloats extremely rapidly, suspect clostridia

15. Neonatal enteric disease: Coccidiosis Etiology: Isospora suis, causing diarrhoea in suckling pigs, most commonly at 10-14-d Pathogenesis: Ingestion of infective sporulated I. suis oocysts from infected feces and contaminated pen fittings. Pathology: Gross lesions limited to jejunum and ileum which appear turgid, thickened with necrotic lining. Will see villus atrophy on histology (cf. chronic C. perfringens type C). Morbidity can be high but mortality likely <20%. Diagnosis: Clinical signs, age of pig, non-response to antimicrobials. Confirm by demonstration of organism on impression smears or histopathology.

17. Neonatal enteric disease: Rotavirus Etiology: Rotaviruses are ubiquitous and diverse group of enteric viruses which may cause diarrhoea from 3-d to 5-wks (mostly 10-21 d). Pathogenesis: Virus infects mature villus enterocytes causing swelling and shedding. Result is mild-moderate villus atrophy. Recovery may be complete within 7-d. Clinically significant diarrhoea is usually the result of bacterial superinfection of virus-damaged mucosa. Morbidity is about 100% but mortality usually <10%. Pathology: Flaccid, thin walled, fluid-filled small intestine and mild villus blunting. Diagnosis: Ubiquity of virus makes definitive diagnosis difficult. Clinical signs, pathology, EM of faeces and FAT can be employed.

18. Neonatal enteric disease: Rotavirus Treatment and control: Antibiotics will not be effective against the virus but will limit concurrent bacterial infection. Assess hygiene and attempt to improve immune status of sows pre-farrowing. Rotavirus vaccine efficacy is debatable.

19. Neonatal enteric disease: TGE Etiology: The corona, Transmissible GastroEnteritis virus Pathogenesis: Ingestion of infected droplets of fecal material. Main site of multiplication is mature enterocytes. Villus atrophy results in hypoglycemia and osmotic diarrhoea. Can get superinfection with E. coli and Clostridium Clinical signs: Epizootic characterised by vomiting in young pigs and the sows go off-feed for 2-3 days. Then explosive outbreak of diarrhoea in all ages of pigs. Mortality is 100% (0-7 d), 50% (8-14 d) and 25% (15-21 d). Mortality rare after this (older pigs faster at enteric repair). Pathology: Flaccid, thin walled, fluid-filled small intestine and villus atrophy. Diagnosis: Epizootiology and clinical signs confirmed by serology (x-reacts with PRCV – mutant TGE virus) or virus isolation. Main DDx is porcine epidemic diarrhoea (PED; another corona virus).

20. Neonatal enteric disease: TGE Treatment and control: There is no treatment. The management objective is to have all pigs infected by use of feedback and so become immune. Failure to achieve this objective may result in endemic TGE. Available vaccines are not efficacious.

21. Post-weaning enteric disease: Porcine Proliferative Enteropathy (PPE) Etiology: Obligate intracellular bacterium, Lawsonia intracellularis. Just below brush border of enterocytes Pathogenesis: Fecal-oral infection leads to invasion of intestinal crypt cells resulting in apoptosis and cellular hyperplasia and crypts filling with polymorphs (immature enterocytes) . Villus apical capillaries dilate and may rupture. These changes may regress, continue and result in benign adenomatosis or become necrotic. Usually seen in grow/finish. Pathology: Small intestine is thickened and reticulated (looks like brain). Lesions of PPE occur in ileum and proximal spiral colon. Can appear as adenomatosis (grow finish), regional ileitis, necrotic enteritis, proliferative hemorrhagic enteropathy (young adults) Diagnosis: Clinical signs, demonstration of organism on histology, PCR and serology.

23. Post-weaning enteric disease: Swine dysentery Etiology: Brachyspira (Serpulina) hyodysenteriae. Pathogenesis: Oral infection leads to invasion of colonic crypts and then goblet and epithelial cells. The inflammatory response is associated with tissue loss, mast cell degranulation and failure to re-absorb Na and Cl causing a muco-hemorrhagic diarrhoea. Appetite may be normal. Pathology: Colon is flaccid, may be congested, and contents are brownish-red, fluid, foul smelling with varying proportions of mucus, and undigested food and necrotic material. Diagnosis: Clinical signs, pathology and confirmed by FAT or isolation/typing of B.hyodysenteriae. Ddx, trichuris suis (whip worm) No treatment – can only depopulate

25. Salmonella cholerasuis Swine specific / carriers triggered by stress, mixing Septicemia / pneumonia (interstitial) Sudden death, cyanosis Hepatomegaly, splenomegaly, hemorrhagic lymph nodes, hemorrhagic pneumonia Treat with antibiotics in feed, live vaccine

26. Salmonella typhimurium Ileum and colon inflamed and possibly ulcerated diarrhea in growing pigs culture from mesenteric lymph nodes (going systemic) salmonella normally in feces Contaminated feed Antibiotics Not swine adapted, won’t see pneumonia

27. Gastrointestinal Gastric ulceration pars esophaga keratinization - erosion – ulcer (can bleed out) causes: finely ground feed – acts like liquid splashing into esophagus empty stomach Gastrointestinal torsion irregular feeding, fighting Specific causes unknown

28. Rectal abnormalities Prolapse piling, zearalenone (estrogenic toxin), cough, diarrhea replace & purse-string, rectal ring, ampuate Stricture sequelae to salmonellosis or prolapse repair Atresia ani Congenital Fistulation possible in females – feces in vulva Will kill males

29. Other enteric diseases Cryptosporidia Spirochaetal colitis (Brachyspira pilosicoli) Nonhemorrhagic colitis in pigs Does not attach to colonic mucosa – stays in lumen Non-specific colitis

30. Respiratory Diseases

31. Mycoplasma (enzootic) pneumonia Etiology: M. hyopneumoniae Pathogenesis: Colonisation and destruction of mucociliary elevator. The compromised clearance activity results in pooling of infective material in the lung lobes. Clinical signs: Usually, pigs become infected >3 weeks of age resulting in a dry/barking cough spreading to most members of the group over 3-14 weeks (slow spread). A fever is unusual. Due to unequal infection, a gradual progressive variance in size develops. Secondary infections result in a more severe pneumonia (eg. M. hyorrhinis, P. multocida (capsule type A), H. parasuis – Not as serious without secondary infection P. multocida should not be in lung Pathology: Anterio/ventral plum-coloured lesions and areas of consolidation. – disease in airway, not alveoli Diagnosis: Clinical signs and distinctive lung lesions confirmed serology and by IFA,PCR or immunoperoxidase of lung section.

33. Control/eradication of enzootic pneumonia Treatment and control: Tiamulin injection (15 mg/kg) daily for 3 days (if severe). Continuous or pulse in-feed or in-water medication (eg. tetracyclines, tiamulin, valnemulin). Vaccinate at 3 & 5 wks (better than at 1 & 3 wks). Age segregated, All In-All Out pig flow (AI-AO). Eradication: Medicated early weaning at 5-10 days (not EU) Total depopulation (expensive) Partial depopulation; all animals except breeding stock which are then medicated for 2 weeks.

34. Other Mycoplasma sp. M. hyorrhinis: Infection is respiratory, often associated with lesions of enzootic pneumonia. Organism goes systemic and causes polyserositis. Affects pigs (usually) from 3 to 10 weeks of age. Distinguish from Strep suis and Haemophilus parasuis by absence of fever and low mortality. M. hyosynoviae: Infection is oronasal and the organism settles out in joints. Affects pigs >35 kg and is a cause of acute lameness in new breeding stock.

35. Pleuropneumonia Etiology: Actinobacillus pleuropneumoniae (12 serotypes) Pathogenesis: Via direct contact and aerosol, bacteria colonise the tonsils and enter the lung. Lesions, largely the result of toxin production (APX I and III), evident by 3 h in challenge model. (8-12 hours – dead pigs) Clinical signs: Acute disease in naïve pigs results in fever, dyspnea, possibly blood-stained froth at mouth in 15-30% of pigs and 30-50% case mortality within 36 h of onset of clinical signs. In sub-acute form, pigs are anorexic, show respiratory distress and coughing. Mortality is variable.

36. Pleuropneumonia Pathology: By12-24 h, fibrinous exudate on pleural surface over pneumonic areas. By 48 h, hemorrhagic/necrotic lesions observed especially in diaphragmatic lobe (does not have to be). Diagnosis: Acute, fatal respiratory disease with fibrous pleurisy and firm lung infarcts, confirmed by serology and culture of the organism. Main differential is A. suis (usually more diffuse as opposed to limited to diaphragmatic lobe)which is further differentiated on basis of toxin production (A. suis does not produce APX III or IV)

37. APP lungs

38. APP

40. Control/eradication of APP Treatment and control: Parenteral injection of clinical animals with an effective antimicrobial (eg. penicillin, tiamulin, oxytetracycline, ceftiofur [Exceed]) and in-feed or water for others (continuous or pulsed). All in-All out pig flow. Vaccination after about 8 wks (to avoid interference by maternal antibody); expensive. Medicated weaning at <21 days. Maternal antibody good for 21 days, then at risk (mother is source of infection) – not always effective Eradication: Total depopulation Could try a partial depopulation (eg. remove weaners-to-finishers) with vaccination/medication of sow herd and then weaning at <21 days.

41. Progressive atrophic rhinitis Etiology: Toxigenic Pasteurella multocida (usually capsule type D) facilitated by co-infection with B. bronchiseptica. Pathogenesis: Dermonecrotoxin produced by P. multocida causes demise of osteoblasts and enhances osteoclast activity resulting in turbinate atrophy, distortion of nasal septum and possibly shortening and twisting of upper jaw. Pigs predisposed to secondary infections due to absence of turbinates Clinical signs: Sneezing in pigs 1 to 8 weeks of age (may be paroxysmal with epistaxis), blockage of lachrymal ducts resulting in tear staining, mucopurulent nasal discharge progressing to shortening of upper jaw and corrugation of the skin of snout. Pathology: Rhinitis, turbinate atrophy and nasal distortion. Diagnosis: Clinical signs confirmed by culture of nasal swab for toxigenic P. multocida.

44. Control/eradication of atrophic rhinitis Control: For acute preweaning disease, parenteral or oral (TMP-sulpha – not in FA), ampicillin, tetracyclines, ceftofur. Prophylaxis by medication at 3, 10 and 21 days. Water/feed medication from weaning. Vaccination of sows (P. multocida toxoid and killed B. brochiseptica) to boost piglet passive immunity. Can vaccinate piglets at 7 and 21 days. All in-all out pig flow (with medication for improved efficacy). Eradication: Total depopulation If <20% of sows infected, testing/treatment of sows on entry to clean farrowing house and culling if infection not resolved.

45. Bordetellosis Etiology: B. bronchiseptica Pathogenesis: Colonisation and destruction of cilia in upper respiratory tract. May colonise lung causing broncho-pneumonia usually in the cranial and middle lobes (with Mycoplasma or P. multocida). Clinical signs: Sneezing in pigs >1 week of age (may be paroxysmal with epistaxis) and mucopurulent nasal discharge progressing to a cough when lung involved. May see mild (reversible) turbinate atrophy (regressive atrophic rhinitis). Pathology: Catarrhal rhinitis, conjunctivitis and possible bronchopneumonia (particularly cranial and middle lobes). Diagnosis: Clinical signs, confirmed by culture of nasal swab. Usually individual pig problem, not herd problem

46. Control of Bordetellosis Treatment and control: Severely affected pigs, use parenteral followed by oral administration of (TMP-sulpha), tetracyclines, For disease control, use in-feed medication of above or sulpha-tylosin mix (Tylasul, Elanco). Vaccinate sows prefarrowing and pigs at 7 and 28 days. Eradication: Requires medicated early weaning (<10 days), so not relevant in EU.

47. Inclusion body rhinitis Etiology: Porcine cytomegalovirus Clinical signs: Sneezing in pigs <3 weeks of age, nasal discharge and epiphora. If chronic, may lead to otitis media. Pathology: Rhinitis and conjunctivitis. Diagnosis: Turbinates plugged with mucus/debris (problems suckling if cannot breathe through nose). Basophilic intranuclear inclusion bodies in nasal mucosa. If herd is naïve, (eg. a new herd) any age can be affected and 25% mortality in affected litters may be seen.

48. Swine influenza (SIV) Etiology: Swine influenza virus. Pathogenesis: Virus replicates in bronchial epithelium within 2 h and, by 24 h, most cells are infected as are alveolar septae and ducts. Small bronchi become blocked by neutrophil-rich exudate, and alveolar necrosis/bronchial epithelial hyperplasia cause the clinical signs. Clinical signs: Rapid involvement of almost 100% of animals which become apathetic, prostrate, erythema of skin, anorexia and fever. Severe cough, sneezing, dyspnoea, reddened eyes and conjuntival discharge. Recovery is rapid at 5-7 days. May see abortions. – any disease that makes sow sufficiently ill can cause abortion, does not have to be reproductive disease Pathology: Sharply demarcated patchy lesions mostly in apical and cardiac lobes, interstitial pneumonia. Diagnosis: Clinical signs, paired serology and virus isolation from nasal or tonsilar swabs or lung.

49. Lung - SIV

50. Treatment and control of SIV Treatment: Antimicrobial treatment for secondary infections. Control: If disease is prevalent in the vicinity, pigs can be vaccinated Multivalent available Eradication: If the herd becomes enzootically infected, will require total depopulation

51. Porcine reproductive & respiratory syndrome (PRRS) Etiology: PRRS virus Pathogenesis: Virus replicates in, and destroys, alveolar macrophages and endothelial cells causing vasculitis. Clinical signs: Usually in weaned pigs, will observe tachypnea and a “thumping” respiration. May also see eyelid edema and conjunctivitis. Pathology: Moderate to severe interstitial pneumonia. Diagnosis: Clinical signs and gross pathology confirmed by serology and virus isolation from lung, tonsils.

52. PRRS-lung

53. Porcine circovirus:Postweaning Multisystemic Wasting Syndrome Etiology: Porcine circovirus (PCV) 2 Pathogenesis: Largely unknown Clinical signs: Usually in weaned pigs (5-6 weeks of age), may observe icterus or dyspnea; will observe wasting. Increased mummies. Pathology: Moderate to severe interstitial pneumonia, enlarged lymph nodes. Many other “suggestive” lesions. Fetal myocarditis. Diagnosis: Clinical signs, confirmed by serology and demonstration of cytoplasmic inclusion bodies in ileal lumphoid tissue (Peyers patches) – pathogneumonic *.

54. Porcine circovirus:Postweaning Multisystemic Wasting Syndrome Treatment/Control: Ensure all piglets receive colostrum. Dose manually with 10 mL any pig <1 kg or born >2.5 h after start of farrowing (colostrum quality may be declining).

55. Jaundice - PCV

56. Lymph node - PCV

57. Nephritis - PCV

58. Neurological

59. Strep suis (type II zoonotic) Lancefield group D septicemia, meningitis, arthritis Sudden death – large killer in nursery usually young pigs Penicillin/ceftiofur vaccine somewhat effective Autogenous vaccines available Zoonotic – can cause meningitis in humans

60. Haemophilus parasuis Glasser’s disease polyarthritis, polyserositis, meningitis young pigs – on sow/in nursery Can kill older pigs as well vaccination / penicillin Similar conditions M. hyorhinis (3-10 wks (off sow), no fever, low mortality) M. hyosynoviae (>10 wks, no fever, only arthritis)

61. Salt Poisoning Water deprivation (> 2 d) eosinophilic meningoencephalitis Sodium crosses BBB, give water after deprived, Na causes huge water intake, fluid drawn into brain, dead pigs Introduce water back slowly

62. Skin

63. Erysipelas soil borne neuraminidase arthritis, (vegetative valvular) endocarditis, skin lesions diamond skin disease penicillin – vaccination (3 & 6 wks) Lesions gone after first injection – isolate affected pigs

64. Erysipelas

65. Greasy Pig Disease Staph hyicus culture from subcutis abrasions / mites – needs to get into skin to cause disease 1-5 wks of age (on sow or in nursery) penicillin and topicals Cut needle teeth (1/2 down teeth to remove tips) If done at gums, can crack tooth or lead to osteomyelitis

67. Ringworm Agents Microsporum nanum Trichophyton mentagrophytes sows treatment with topical enilconazole, copper salts possible zoonosis

68. Ringworm

69. Swine pox typical pox lesions growing pigs associated with biting insects lice slaughter concern carcass blemish / mistaken for erysipelas self limiting

70. Swine pox

72. Reproduction

73. Porcine Parvovirus 90% of farms infected timing of infection determines if clinical diseases occurs – only a problem is if infection occurs in naïve, pregnant population Mummies of various size / small litters Goes into uterus and kills a few pigs of different stages Gilts affected Serology of little value in individual Virus is almost ubiquitous Vaccine

74. Porcine Reproductive and respiratory Syndrome virus Increased returns Abortion at any stage of gestation Premature farrowing (108-110 days of gestation) Increased loss of neonates Normal – 112-118 days Increased stillbirths and neonatal deaths All roughly the same size mummies

75. Abortion - PRRS

76. Leptospirosis Major serotypes Pomona; bratislava(swine specific, minimal antibody response, difficult to diagnose) canicola, icterohemorrhagica, hardjo, grippo Increased returns to estrus (possible vulvar discharge) Regular (before 10 days) or irregular returns (after 21-24 days) Can be in ovarian duct or uterus late term abortion – esp. pomona acute and convalescent serology uremia at slaughter

77. Pseudorabies (Aujeszky’s Disease) Herpes virus - latency in ganglia Neurological signs and pneumonia (young pigs) Abortion and increased mummies (adults) Focal necrosis in liver Reportable disease Gene deleted vaccines - G1 Can differentiate vaccine and disease titer “mad itch” in other animals

78. Cystitis / Pyelonephritis Actinobaculum (Eubacterium) suis found in prepuce of boars Sexual transmission? hunched back - kidney pain Individual pigs, not herd problem treatment ineffective water accessibility Decreased water, decreased urination, increased risk of ascending infection

79. Eperythrozoonosis (“epe”) red cell organism Rarely clinical – problematic if it is Spread by fomites, iatrogenic via syringe anemia and jaundice in piglets Giemsa stain of blood tetracycline

82. Nutritional Iron Piglets require supplemental iron as low in milk 100-200 mg Selenium/vitamin E Free radical damage, mulberry heart disease Hemorrhagic streaks in myocardium

83. Porcine Stress Syndrome Halothane gene (napole gene - Hampshire) DNA test Single (?) recessive gene Calcium transport deficit Malignant hyperthermia, acidosis rapid post-mortem autolysis associated with extreme muscling

84. TuberculosisM. avium (M. tuberculosis, M. bovis, M. intracellulare) sawdust / birds / peat moss not a public health hazard

85. Zearalenone Fusarium Estrogenic effect Affects implantation - return to heat occasional weak litters swollen vulva and rectum

86. Vesicular diseases Swine vesicular disease and foot and mouth disease are clinically indistinguishable. Do Not Miss Them!