EPI MT 2 DECK 3 Flashcards
Classical Swine Fever Cause?
- An acute, contagious disease of swine, characterised by general, febrile signs, haemorrhages, CNS disorders.
• Classical swine fever virus (Flaviviridae).
• Stenoxen: domesticated swine + wild boar.
• Relatively resistant (enveloped virus) –>pH 3, 60oC – 30’; 80oC – 5’ sensitive to high. PH–>Use alkylytic Detergent.
-In meat, blood: 4oC – 1 month, frozen ½ year survival. Invisceral organs longer survival. Survives in marinade, smoked meat (1/2 year).
• Faeces, urine: 7 days, cadaver 1-2 days.
• Differences in virulence: low virulence strains – subclinical, foetopathogen.
Classical Swine Fever Pathogenesis?
• Infection: PO, airborne, conjunctival, mating, transcutaneous (iatrogenic! – fomites,
boots, gloves, needles, syringes), transplacental.
• Oronasal → tonsils → head, neck LNs → viraemia (from the 16-24th hour) quick post
infection! Clincal signs come much later, animals can shed the virus without clinical
signs.
• Lymphatic tissue (LNs, spleen, lymphoreticular cells) → damage of the immune system
(immunosuppression) → secondary bacterial complications.
• Damage of the BM stem cells → thrombocytopenia, DIC → haemorrhages.
• Endothelial damage, hyaline dystrophy of the BVs → perivascular oedema →
circulation problems → necrosis, haemorrhages (day 3-4).
• Generalised infection (day 5-6).
• Direct damage: lymphocytes, megacaryocytes.
• Indirect damage: endothel damage, immunocomplexes.
CSF Acute, Subacute Clinical Signs?
- Permanent fever (40.5-40oC), depression,Suffusion, haemorrhages in the skin, oedema.
- Weakness of the hindlegs, ataxia, swaying, nystagmus.
- Conjunctivitis, blindness.
- In the beginning obstipation, later bloody diarrhoea.
- Haematuria, bloody nasal discharge (rarely seen these days).
- High morbidity (90-100%). Death after 1-2 weeks illness. 10-30% mortality.
- Red dots on the skin similar to circoviridae & ASF (can’t differentiate!).
CSF Chronic Clinical Signs?
- Retarded growth, BW loss, Diarrhoea, crustae on the skin.
• Pregnant sow – transplacental infection. First half of the pregnancy: abortion, premature birth, weak, trembling piglets, splayleg, immunotolerant piglets!
• Third part of the first trimester–>when the BM, spleen & LNs are formed in the foetus so immunotolerance occurs always at this time.
• Second half of pregnancy: less damaged, immunocompetent piglets
• Weak virulence strains/vaccine strains ▪ Subclinical infection, serological response.
CSF Peracute Pathology?
▪ Brain lymphocytic infiltration !
Leukoencephalitis (perivascular cuffing) ▪ +/- fine haemorrhage in the kidney cortex.
CSF Acute Pathology?
- Praesetais, stasis, haemorrhage, oedemas. Skin haemorrhage, necrosion (ears, legs)
Haemorrhages (also feature of ASF). - On the mesenterium, on the serosal surfaces .
- On the light kidneys, in the renal pelvis, on the mucosa of the urinary bladder.
- In the gastric mucosa, in the regional LNs
- In the small & large intestine, colon, haemorrhagic enteritis
- In the larynx, lung, bones, muscles (by electric immobilisation too!).
- Rarely in the liver, gall bladder, retina, conjunctiva ▪ RBC infiltration of the LNs ! ▪
Post-haemorrhagic anaemia, mild icterus .
CSF Subacute Pathology?
- Spleen: Haemorrhagic or ischaemic infarcts at the edges . In uncomplicated cases
normal size spleen (if bacterial complications then there is splenomegaly!) - Stomach: gastritis, croupous pseudomembranes, buttons (in ~4% of the cases) .
- LI: buttons (also in chronic form) – origin of button = lymphoid follicle in MM wall
- Lung: Lobular (lobar) haemorrhage, croupous pneumonia o (normally viruses cause
interstitial pneumonia. Enlarged interstitial tissue, oedematisation. Pleural LNs are
infiltrated with RBCs. - Tonsils: necrosis – characteristic (DD = Aujeszky’s disease).
- Brain: meninx, brain, spinal cord; 2-3 layer lymphoid cell cuffing, meningitis; poly- &
leukoencephalitis - Thymus: atrophy, lymphocyte numeric atrophy - immunosuppression.
- Eyes: conjunctivitis, uveitis, retinitis, papillitis, neuritis
CSF Chronic Pathology?
- Non-typical lesions, complicated diagnosis. Buttons are erased, no haemorrhages.
- Thickened wall of the LI, necrotic mucosal surface, crustae.
- Lung croupous-necrotic pneumonia, sequestra, adhesions, subacute-chronic pleuritic.
- Post-inflammatory reparative processes in the brain.
- 6-8 costal bone-cartilage developmental problems.
CSF Epidemiology?
- Transmission ▪ Live, infected swine → transportation, trade.
• Raw pork meat, raw pork products (also frozen) → slaughter house, home. slaughtering, trade, tourism.
• Raw pork wastages → slaughterhouse, home-slaughtering, restaurants, tourism.
• Fomites → transportation, trade, tourism.
• Humans → technician, vet, butcher, salesman .
• Wild boar! – no domestic pig cases in the last 5 years
• Very contagious: Quick spread in the herd, Virus shedding in the discharges w/in 24h
after infection. Introduction with infected animal: large scale disease in the second
week. Introduction with feed: large scale disease earlier.
• Low virulence & vaccine strains: Subclinical circulation in adult swine or mild clinical
signs. Foetal damages. Immunotolerant piglets. Long-term carrier & shedder animals.
Seropositive animals in the population (even if no clinical symptoms).
Reoviral Disease Poultry Epidemiology?
Susceptibility: mainly chicken, but turkey, goose, guinea fowl, Muscovy duck, quail
pigeon, parrot & many other bird sp too.
• Age-dependent resistance: over 10 weeks of age only infection but no signs.
DANGEROUS NO CLINICAL SIGNS. Only clinical signs in young animals.
• Shedding with faeces & discharges. Litter, fomites play a role in the transmission.
• Extremely Resistant in the environment (20oC – 1 year, 4oC – 3 years!)
• PO, airborne, transcutaneous infections (injuries).
• Germinative infections!
Reoviral Disease Poultry Pathogenesis?
- Trypsin resistant strains – mainly PO infections, diarrhea (frequent).
• Trypsin sensitive strains: airborne or transcutaneous infections (severe). Trypsin can inactivate this orthoreovirus.
• Multiplication in the enterocytes & in the bursa fabricii.
• Epithelial damage, viraemia → inflammation of the tendon sheaths & joints, necrotic
& inflammatory foci in the visceral organs.
• Several strains can be isolated from clinically healthy birds too (orphan).
RDP Tenosynovitis- Arthritis?
- CLINCAL SIGNS: Mainly seen in 4-8 week old broiler chickens, Lameness, swollen
knee, Arthritis, haemorrhages under the skin. - In roosters we can see the rupture of the gastrocnemius tendon. Swollen thoracic
bursa. - PATHOLOGY: Arthritis in joints, deformed toes, haemorrhages in the synovial
membranes, erosions of synovial cartilage, accumulation of fibrinous exudate
RDP Generalized form?
- Necrosis, inflammation & degenerative processed in the visceral organs.
- Focal necrosis in the liver, liver dystrophy.
- Pancreas-atrophy, pancreatitis ▪ Nephrosis.
- Haemorrhages, perivasculitis in the brain stem .
- Thymus-atrophy, lesions in the bursa of Fabricus & in the BM – immunosuppression
- Myocarditis, ascites (in goslings)
- Hydropericardium – in chicken, together with adenovirus.
STUNTING DISEASE, POULTRY ENTERITIS & MORTALITY SYNDROME (PEMS) ?
Runting Stunting Syndrome
Together with parvo-, adeno-, astro-, hepe-, cornoa-, enteroviruses
Enteritis, diarrhoea, retarded development.
Feather, bone developmental problems, cartilage necrosis
Enlarged intestines, watery content
Blue tongue Cause?Properties?
• Sedoreovirinae–>smooth surface, no spikes.
• Orbivurses: Equine Horse sickness, Equine encephalitis.
• Rotaviruses.
• DsRNA, linear, segemented, double layer capsid, non enveloped.
• Reassort segments = High variability
• RESISTANCE:
- Orbiviruses: PH 5, sensitive in environment
- Orthoreoviruses: PH3, resistant in the environment
- Rotaviruses: PH 3-11. Resistant in the environment
