Most Important Topics! Flashcards
9 - Derzsy’s disease of geese, parvoviral disease of ducks
Goose parvovirus, dependovirus genus.
(Dependo - need adeno/herpes to help replicate. But goose parvo v can use polym. Enz of dividing cells - dont need!)
Goose, moscovy ducs, Endemic in large farms, seen worldwide.
Important economical disease! Huge losses!
Fecal transmission horizontally, most imp transmission is vertical, (asympt) adult infect embryo - death or infected gosling infects other day old (most imp one)
Signs depend on age and pathogenicity (immunity)
very age dependent, under 10d up to 100% mortality - depending a lot on yolk immunity, after 5w losses are neglible due to progressive Resistance Development –> no signs!.
PERACUTE - HATCHING/DAY OLD INFECTION - after 1w incubation –> death 1-2d. (We se mortality up to 100%!) generalized signs, PD, flu-like, profuse white diarrhoea, fibrinous pseudomembranes tongue and oral cav, convulstions (liver damage), ascites with loads of fibrin - like a gel!
PARTIAL PROTECTED GOSLINGS - signs start end of 2nd week: growth retardation (dwarfism, curved legs, shorter beaks..), disturbed feather growth, ascites –> pengiuin posture
DAY 13-15: diarrhoea, excissosis main (heart, liver intact)
SURVIVE: (5-6w) development, growth stop - feather growing problems
Older duck no signs!
PM: ribrin rich ascites, ball shaped heart, tiger stripes, enteritis (swollen PO, petechiae)
No treatment just ab for secundary. Vax are obligatory, revax layers before end of season.
Duck: similar but only ducks, milder. Also dependo.
– Sign: lethargy, badfeather, diarrhea, weak legs(!), CNS. Chronic: growth stop, bad
feather. Mortality 30-60%
– Patho: acute: enlarged liver, chronic: kidney too. Muscles look cooked(!), ball heart, ascites. Inflammation with histiolymphocytes in liver, heart, muscles, brain, N.
ischiadicus
– Short beak and dwarfism syndrome (SBDS), 70s (huge loss)
18 - Infectious bovine rhinotracheitis (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions).
BHV 1, 5 - varicello
Virus has different tissue tropism, but mostly we see resp form. Genital and resp form does not occur at sime time. (If genital form we see mucosa degen, inflamm, nodules)
Introduction
- latency, semen (asympt bulls introduce)
- contact, airborne spread in herd.
- slow spread! (Good!)
- Feedlot cattle: resp! + predisposing –> secundary infections, may then become life threatning (no predisposing - recoved within 4-5d)
- resp form is usually associalted with conjunct, abortion(cow), encephalitis(calf, ascending from nose)!
- 1-6m calf - BRDC (younger if no colostrum)
- > 6m resp + red nose
- enceph under 5m, death within a week
- low mort alone, higher in brdc.
- abortion in heifers mostly (viraemic spread NOT genital form!)
Pm: upper resp inflamm, erosion, haemorrhages. Interst pneumonia (-> brdc, bronhcoalb pneum), abortin (liver, heart, skin necr foci), lymphocytic infiltr cns, intranucl ib
19 - Infectious bovine rhinotracheitis (diagnosis, prevention, control, eradication).
General prevention.
Specific protection: Short lasting (herpes) so repeat. Vax calf, cow before parturition(colostrum), and heifers at fertilization (most susc to abortion)
General eradication.
22 - Aujeszky’s disease (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions).
SHV-1 - varicello
- Pig natural host (general, abortion, resp, CNS), other mammals usually die from encephalitis! birds susc too
- NOT zoonotic.
- present in europe - wild boar! (Hunting dogs)
- Only pigs shed! Importance of waste - virus remain in resp tissue in slaughterhouse for 40d!
- spread some weeks during acute phase, then latency (reactivation)
- Introduction to pig herd: infected swine, fomites (things or rodents even)
- Within pig herd spread direct contact, water, mech vectors, semen, aerogenic, vertical
- Pig infect other spp: contact, liquid manure, contamination with pig by-product/eating it (esp resp).
- Wild boar may maintain it.
CNS primary repl after viraemia. Then lung and other PO.
Piglet: peracute or CNS -> death
Gilt: general, resp, mild cns like nose twitchy, wobbly movement.
Sow: abortion
Adult pigs: (resp, constip) often asympt –> slaughterhouse!!!
Other animals:
Ru: mad itch! Usually die 2d, gen signs
Eq: less susc, CNS
car; CNS, itching! (Rabies)
Pm: pneumonia, HP CNS!
piglet inflamed pharyngeal/tonsilla (primary repl), necrotic foci liver spleen.
23 - Aujeszky’s disease (diagnosis, prevention, control, eradication).
Separate age groups, other spp, proper disposal of by prod, manure, raw pork nem, hygiene (decr re-activation, virus load)
Vax never used in virus free country - only in eradication and decr signs!!
(Modified live vax usually - marker vax (gilts, sows, piget after maternal protection. Repeated - last some m only(herpes). Vax of infected pigs reduce shedding and incr survival. Vax other spp unreliable…), vertical, latency!
Eradication is obligatory!
Mostly we use selection with marker vax. Vax whole herd every 4m.
- vertical spread
24 - Diseases of horses caused by EHV-1 and EHV-4 viruses.
Varicello genus.
Resp and abortion disease of horses by infection of one or two agents (EHV-1,4). Most imp viral upper resp of horses under 2y, main cause of abortion. Found worldwide and is frequent. Only horses are affected.
These viruses are related and gives cross neutralization. Lifelong latency like all herpesv. (trigeminal ggl). Spread by direct contact, aerogenic and PO(snot!) Can cross placenta and infect foetus aswell.
Introduction: introduce studs, races - many horses) usually the carriers are source of infection of the young under 2.
- Foal of endemic studs: maternal protection –> 3-6m, the infection within 1st yr. No major symptoms, shedding during acute phase.(so mostly a spread importance!)
- ehv-4 mostly resp (but can cause abortion too rarely)
- ehv-1 resp, abortion(usually after resp), CNS but rare, (concurrent or after resp, mostly just cause spinal cord endothel damage - lumbosacral may heal, tetraplegia wont).
- resp signs we see mild upper resp and generalized.
- Breeding population –> usually starts with spread w/o signs from asympt carriers (stallion semen) –> dispersal in popultion -> we see SUDDEN abortion storms after 5m of pregnancy, 3w-3m PI! (30-40%). Repro heal after recovery.
- Before the abortion we see subclinical or resp infection. Subclinical infection may be detected with temp! Imp to check temp of mare everyday.
Pm: interstitial pneumonia in foal(uncomplicated), mare is healthy, foal (yellow edematic SC, liver, lung edema with necr foci, mucosal petechiae, CNS HP haemorrh and inflamm.
Diagnosis: store foetus at 4C, IF autolysis give false pos and cant see cells HP! Crossreactions, but since crossneutr dont really need to ddx the species!
Ddx influenza, equine arteritis (abortion), WNF (CNS)
Keep preggo alone or small groups - avoid travel…
Measure temp! It is hard to do anything once the abortion storm starts, but if diagnose early can influence (prevent further spread..)
- Uniform vax immunity among studs! Re-vax! Most imp as this is where the abortion storms starts. Vax against resp form, during abortion sheds in huge titre and break through vax so its not what we focus on!
- first fever -> sample collection -> vaccinate! Epi measures! Test ab levels, revax!
29 - Marek’s disease.
Galliherpesvirus 2, 3, mardiviru genus, alphaherpesvirinae but lymphotrophic aswell!
2 serotypes (with diff virulence strains:-))
- 1 causing mareks with 4 diff virulence strains
v virulent (tumors, break through vax),
virulent - tumours and transient paralysis,
lower virulence: neurological form,
avirulent: no sign.
- 2: another with non-pathogenic strains.
Worldwide, in all chicken farms basically.
V resistant - remains infective for a month, a year if in cell!
Vax are highly protective –> decr clinical apperance
–> not typical for herpes!
NOT germinative, but PO, aerogenic(dust)! !
Aerogenic –> resp –> macrophages (cell associated viremia)
- lymphoid tissue (thymus, bursa, spleen, cytolysis –> immunosuppression and compensating lymphoid prolif!, lymphoid tissue atrophy)
- feather follicles (skin leukosis, free virions)
- peripheral nerves (tumors, lymphocytic infiltr.)
- other organs (small focal tumors, cornea opacity, conjunctivitis, genitals, kidney, muscles)
- -> Virus spread: from cell to cell directly, no free virions, no VN effect of antibodies.
Visceral form endemic, neuriological form sporadic. Most susc 1-2w old, only signs usually if infected before 8w. FAST spread but chronic disease, no signs until 6(5)w!
- Classic neur form - CHRONIC!: (hen paralysis) low virulent strains (In layers or household birds because requires time to form, see in 6-12m old. Mostly in legs, last long - recover after 1year.
- Transient paralysis: moderate virulent strain in 6-7w non vaxed chicken, fast/sporadic/ quick recovery!
- In growers (after 7 weeks of age): skin tumours, nodules
- ACUTE tumor form (lymphoprolif): after 6w in non vaxed, vaxed in growers or beginning of laying, sporadic and long lasting!! (Cns signs may show)
- Peracute/anemia may be seen in 3-6w old
Free virions in epith cells of feather follicles only, other tissues its cell to cell transmission so ig cannot reach virus. Cellular immunity is central in protection!
Airborne -> resp mm -> macroph viraemia ->
- lymphoid tissues (immunosuppression, oncogenic transfer, atrophy = long lasting immunosuppr.)
- feather follicles - skin leukosis (maturation of virions - repl! In epith cells)
- lymphocyte infiltr in periperal nerves
- PO small tumors, corneal opacity
Acute: non typical signs, sign economic losses (weight, death)
After 7w old: mostly skin tumors and nodules seen
Chronic: 1-2%mortality, CNS.. wing paralysis, rare recovery
PM acute: High losses, bursa atrophy - loads of tumors in PO, enlarged organs, enlarged feather follicles
PM chronic: Less common, lasts longer, 1-2% sick! Macroscopically may not see anything, or periph nerves may be enlarged. (Plexus brach/isch) Muscle signs. Lymphomas may be. Ovary tumor. Gray eye in old.
Ddx
- avian leukosis! In avian leucosis we see signs after 4m (9w in J type can happen), and we see tumors in bm too here!min bone J type.), also marek - T lymphocytes, leukosis B lymphocytes!
- Newcastle(no onc)
MATSA (marek diss assoc tumor surf ag), but not imp anymore bc we use PCR!
The vax does not protect from infection, but from clinical apperance!.´chicken good, turkey weaker protection.
Alternate different vax in generations (chickens - layers)
Vax at day old or hatching (boosters doesnt help), there is also in ovo vax for 18d embryo. Vv strains can break trhough protection. New vax using fowl pox as vector marked or turkey
No treatment… since we assume present in all flocks, prevention is crucial. Vax, biosecurity, genetic resistance. (Collect eggs twice daily, disinfection to prevent early infection, staff separation,…) with acute marek we let the flock recover –> slaughter –> disinfect
- Bovine diseases caused by poxviruses.
Chordopoxvirinae - cow pox viruses:
- orthopox genus = real pox (cowpox, buffalo…
- parapox genus: irregular (bo popular stomatitis(saliva), pseudocowpox (zoon) –> benign infections!
- capripox genus: lumpy skin disease virus(ND!) - arbo!
- Most in ortho and parapox genuses are zoonotic!!!
- good antigens - lifelong = good vax! (exc parapox - months)
- genus cross protection
COWPOX
Orthopox, zoonotic, closely related to vaccinia, varola virus –> inspired first smallpox vax!
Euryxen!
- reservoir = rodents
- sporadic to cattle, not common anymore. (Used to be high morbidity and mortality)
- to hu from domestic cats
Contact infection. Cattle: mild, local: udder, mouth, genital (immuosuppr –> generalized possible)
–> takes a month to recover - long! Haemorrh, black crust. Gentle milking, disinfection, ab ointment (2.inf), hygiene. Very contagious, so if present all may be infected! Ddx herpesmammilitis
Prevent rodents!!
Cat, Rodent: local lesions around mouth
Human: localized lesions, immunosuppr –> generalized (cat mostly, milkers nodules)
PSEUDOCOWPOX
Worldwide, common, mild, self-limiting infection of udder, NO haemorrh, small vesicles, maybe marks after recovery (reddish marks with edge, horseshoe)
Introduction into a herd usually with infected animals - FAST dispersal
o INDIRECT transmission - milking (machines, milkers nodule)
Short term immunity -> re-infection!
zoon –> milkers nodules
BO PAPULAR STOMATITIS
- Parapox, like orf but in bo and milder. Direct or indifect contact with saliva (high titre!) licking…
- Sporadic, under 2yrs(!), spring and early summer!
- Poxlesions around nares, oral cavity (esoph forestomachs) –> may be tricky eating, salivation
- Reddened papule, necrotic center –> becomes depressed into skin. Extenstion of lesion peripherally with concentric rings of yellow (necrosis), gray (epith hyperpl) and red (eryth).
- Usually coinfection with BVDV (immunosupressive) - this is when we see the signs of the disease,
Spontanious healing after 3-4w! Typical!
No vax but not needed with this beningn self healing disease - BUT ddx FMD! (ND, must send to lab!)
Zoonotic, in human it looks like milkers nodules - we cannot ddx by signs in human
LSD (ND!)
Capripox - in cattle, ND
Fever, decr milk prod, enlarged Ln, moist/inflamed pocks in skin and mm(ent, resp), pockmarks after healing!, weight loss, sometimes abortion!
Buffalo, wild ru (reservoirs!) –> even with eradication will re-enter herd often…
Recent years cases are seen closer and closer to europe - ND! Might become endemic in europe… (orig. Africa)
Transmission by arthorpods! SEASONAL! Spread around easy, eg mosquitos fly (wind), also 50% of cases asympt –> carriers to new places…, tp from infected countries live cattle illegal…, iatrogenic
In body fluids too but direct contact not significant. AI transmission possible.
Mosre severe infection in peak lactation cows and younger animals..
local lesions, usually becomes generalized.
o Primary replication at the entry site (insect bite)
o Generalisation in some animals
Pock –> ulcer –> necrosis, contamination by flies –> scab falls off leaving plugs, holes, then recover.
Enter embryo –> embryonic death or newborn with signs! Maternal immunity. Virus in body fluids, dried hide (18d)
Pm
Lung: atelectasis, interlobular edema, tracheal mucosa lesions, organ lesions,
- Ddx: bo herpes mammilitis (AKA pseudo LSD), bo papular stomatitis, cowpox (not generalized)
- no marker vax is used, vaxed animals cannot be exported! We cant tell difference (elisa is not reliable here)
- Sheep and goat pox.
Similar to LSD, Skin lesion a bit different: pox: necrotic gray/black lesions –> star shaped scar
ND DISEASE!
Capripox: like LSD, similar features! Generalized disease! Only sheep, goat susceptible (some goatpox infect sheep and vice versa), local breeds less susc (=eu breeds more susceptible!)
serious, commonly fatal, skin eruptions. Sheep and goat pox are closely related viruses
Mainly africa, asia (EU, USA, australia free). Importance in inhib re-introduction from endemic countries!
Super resistant viruses; direct contact, airborne, fomites, biting arthopods (saliva, resp mucous, milk, scabs)
Primary replication resp epith –> viraemia –> 2dary repl in organs and tissues, skin pox nodules are seen. Aboriton.
Resp, GI: viral proliferation cause lymphoma like pocks, (ulcers)
Fever - flu like symptoms, peracute may occur (death)
Skin: pox: necrotic gray/black lesions –> star shaped scar
Crosses to foetus (abortion or signs in newborn), maternal immunity from healed ewes, does
More severe in sheep, wool covers skin lesions… (head, tail, genitals)
Decr milk prod.
High mortality! 70-80% lamb/kid, up to 10 in adult!
Weight loss, decr wool and milk prod.
Lifelong immunity!
Vax in endemic countries
Eu: maintain free staus (ø milk, raw meat import, live animals, on farm epi measures….)
36 - African swine fever.
dsDNA, enveloped.
Asfarviridae, ASF virus
Acute, contagious, haemorrhagic disease of swine and wild boar of all ages, wide range of signs and lesions which resemble CSF.
Arbovirus - biological vector. soft tick transmission: once tick infected, hard to rid of disease in that area! Endemic in sub saharan africa, there has been outbreaks in european part of russia and belarus which have spread to EU! Wild boar and export/import importance!!! (Sardinia endemic)
Mutations, many strains (but 1 serotype).
Very resistant, frozen for years, environment 200d, 15w in blood, 140d in salted, dry meats! (Even tho enveloped!!)
Sneaky virus! Has loads of proteins where many of these are not imp and used as bait to trick the immune system - ab prod but none of them neutr. Virus… –> exhaust immune system, long term viraemia, shedding, persiting infection. After a while the “right ab” is made (late phase neutr ab)
–> hides “real” ag like hand in pocked (surface structure) and only shows it before attachement, no time to neutr. Virus = NON-CONTROLLED VIRUS REPLICATION!
Spread from reservoir (wild boar) to domestic pig by soft tick, infected pig, fomites(farm-farm) or raw meat(international). Btw pigs oronasal, direct contact or ingestion of pig products (raw)
Tick to pig, pig further: Usually PO–> tonsil, Ln of head and neck –> blood –> generalized infection –> loads of viruses everywhere!!
Endothelium –> edema and haemorrhages!
Immunosuppression:
All wbc (take part of cell memb durin repl –> body rec as own
except lymphocytes, but love lymphoid tissue! (Spleen, bm, Ln)
CHRONIC: trick antigens -> All the useless immunocomplexes… –> occlusion (kidney –> death), SKIN!
1w icubation!
- Peracute/V virulent: suden death after 1w (virus everywhere) (90-100%mortality)
- Acute/Moderate: general signs –> death after 1-2w (leukocytopenia, thrombocytopenia, bloody stomach content, (poor blood flow -> ulceration) (<60% mort)
- Chronic/Mild: seroconversion, immune complexes: skin haemorrhages, necrosis, painless swelling of carpal/tarsal joint (<10% mort)
Acute: blood everywhere… black Ln, pneumonia, enlarged spleen
Chronic: lymphoid, splenic enlargement, fibrin rich fluid in cav and pericardium, pneumonia, skin haemorrhages
ND!
No treatment or vax available (vax soon probably)!
General epi measures (movement restr, protection and surveillance zones), tick control
Non-endemic coutnries: stamp out only way! Wild boar thinning! (Hunting, but run away if miss –> enter new areas…)
Desinfection, leave empty 1m before repopulation, movement restriction 1m after repop - serological control. Food waste. Regular surveillance!
37 - Teschovirus encephalomyelitis.
ND! Teschovirus genus(-virus 1, 2), 11 serotypes, 1 responsible for the disease, 2-11 are milder) Two types (not spp!) of the disease: more virulent teschen(czeck-poland border, first seen here) - central EU endemic!, and talfan which is basically everywhere and less virulent.
Only pigs susceptible. Teschen any age, talfan likes around weaning
Repl in gut - shed with feces - long, last for several weeks - resistant virus (3w environment) - contamination, indirect spread possible - dry form still infective…
CNS as source aswell. Swill feeding containing pig part/feces - good way for spread
3 phases of infection
Infection PO mostly (feces, pig organs) –> nose, olfact n. –> CNS
1 - enteral phase (repl, shedding (asympt), local immunity develops - very good, sometimes no more phases seen (stops virus)!)
2 - viraemic phase: fever (FIRST SIGN)
3 - neuronal phase: repl, encephalopmyelitis (signs)
General + CNS (localized adult - HL paralysis, general in piglet, grower), some recover (older ones)
Talfan: Basically same clinical signs (around weaning) But this paralysis can be transient - these animals can recover -> fewer losses!!
No path - HP needed, can only be seen in fresh samples - only disease where we must send live piglets as sample - after a few hours the HP signs cant be detected. Lymphocytic infiltr, necrosis(esp teschen) and degeneration is seen in gray matter brain stem, cerebellum and ventral horns of SC(HL signs!!!)
Not OIE listed anymore, but still ND in hungary
- no vax
- teschen: prevent introduction, if detect: movement restr and stamp out
Talfan: Losses not so high, we can wait a bit for seroconversion, own immunity fix, not too high losses
38 - Swine vesicular disease and vesicular exanthema of swine.
SWINE VESICULAR DISEASE
PICORNA
A) Zoonotic, europe is free (exc endemic in southern part of italy. One serotype, enterovirus, picorna. Resistant virus. Only pigs are susceptible.
Shed from ruptured vesicles, feces, raw pork, swill –> Gut replication (picorna!) -> viraemia (fever) -> epithelial cells oronasal, legs –> vesicles
- CNS, foetus rarely!
Fast recovery! No pm!
B) SVD can also be caused by another picorna virus (senecavirus A), we see vesicular signs in growers and fatteners on legs, while suckling general signs, salivation (oral inflamm, interst pneumonia), GI, CNS (encephalitis) no vesicles!
VESICULAR EXANTHEMA OF SWINE
Aka atypical FMD. Caliciviridae, vesivirus. Many serotypes.
Wide host range but not ru! Hu maybe. Transmitted to swine from natural host (seal) –> sea mammal/fish feed!
Swine: SALIVA! shedding spread in herd. Good resistance, but not as contagious as FMD!
General signs + vesicles oronasal, limb - lameness!
(Seal - skin lesions, abortion)
Stamp out!
Heat treat sea food given to pig!
- Foot and mouth disease (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions).
Bo (sheep, goat milder, swine shead high titre but only short time vs ru up to 3y!)
7 serotypes based on the neutr. Ab
O, A: worldwide (Oas, Allamand)
C: rare (Found 3 - ABC, but BC were OA! So only C is new. C may become exting´ct b so rare)
SouthAfricanTerritories 1,2,3: africa, arabia
Asia1: asia, middle east, turkey
Enviroment, animals, humans, (also meat, skin fur, milk…) –> PO/airborne –> primary replication in laryngeal, pharyngeal mucosa > viremia (9h) > spread
within the body > (3d) vesicles on mucosa (mouth, nose, tongue) and skin (teats, feet) - heal, but carry up to 3 YEARS! (Nd bc fast spread, fast shed bf signs, and long carry!)
Replicates fast (mRNA) - shedding 9h after infection no signs. = highly contagious and quick spread! No envelope - resistant (Wet cool dirty stalls weeks, manure up to 40d! Hygiene!!! Frozen meat, milk powder months!)
Signs are fever, decreased milk production, depression, high salivation (viscous, frothy), mouth vesicles w/tattered edge, red (bo, goat - severe, swine and sheep - mild)
base, bacterial superinfection!!, recovery after immune response
Feet: severe lameness (Bo, sheep), also loss of hoof - keratin layer - remove like a glove…(swine)
Myocarditis: young animals (bo, ov, sus), death
- Foot and mouth disease (diagnosis, differential diagnosis, prevention, control).
Sampling: 1 g of vesicular wall and fluid, orophar fluid, saliva (swab, probang) > buffered transport medium (pH 7.2-7.6) (!!!ph sensitive)> refrigerated or iced > submit ASAP!
EU we never use vax for eradication (still repl and shedding –> always stamp out), imp in diagnostics!
Ddx: pox, bvd mucosal disease, IBR red nose, bluetongue mouth/hoof erosions, malign cat fever pseudomemb (+SVD, VES in su!)
Treatment is prohibited - long shed!
Prevention is most imp! Practice how to react! Competition with time - have a plan. Everywhere in envronment - infective for long time!!
Once an outbreak occur the export of products + everything in contact is forbidden = basis of epi rules, 3km protection zone, 10pm surv zone.
UK 2001 - 6 million animals were killed…
(Hu moderatily susceptible, but benign disease.. not so important here)
- Rabbit haemorrhagic disease, European brown hare syndrome.
(Picorna order) Calici fam, lagovirus genus (both diseases!)
Cannot be cultured, good resistance (months in chilled, carcasses, fomites, insects), good antigens. Woldwide, present in europe. Austr biological weapon! These to are v similar disease, but not same host!!
(Strains? Serolgically different)
RHDV-1/1a mutant: rabbit 90% mortality OVER 2m
RHDV-2: rabbit and hare, younger susceptible too, longer incubation and a bit lower mortality (serol. Different from RHDV1 = no crossprotection)
European brown hare syndrome virus (EBHSV)
Host is the brown hare, also in eu, v similar to RHD
Same for both:
o PO, air-borne infections -> viremia, propagation in liver, vasculitis
o Liver dystrophy, thrombo-embolia in airways & visceral organs -> haemorrhages
o Mortality up to 100% due to liver damage, the hepatitis kills!
Basically you find dead rabbit with blood from oronasal region (dyspnoea, cns, die within 36h)
Haemorrh edema, necrosis in liver
Could be other septicemic disease, DIC, heat stress, posening… but since ND we send straight to lab!!!!
No treatment!
Sanitary prophylaxis: movement restrictions, humane slaughter & disposal of sick & in-contact animals, healthy animals in the same farm may be immunised-
Vax yearly!!
- Equine encephalomyelitis caused by togaviruses (Zoon.).
Notifiable, Zoonotic
Acute neurological disease of equine, only AMERICAs, transmit by mosquitoes, affects several species including Humans (birds maintain the virus)
Wild+domestic Bird: maintaining host. Migration of birds spread long distance.
Mosquito: transmit disease btw birds. Seasonal - seasonal epidemics: warm, rainy summers high enoug temp - the mosquitos must want to be active and repl, feed. Virus titre very high - easy transmission btw birds!
Horse, human - dead end host. In blood during viraemia the virus titre low - we see signs, but mosquito transmission the titre is too low.
3 SPECIES: (alphavirus genus of toga)
- Eastern equine encephalitis virus (M-B) (aka triple E :-))
(Bird - far, mosq - seasonal)
- Western equine encephalitis virus (R-M-B)
(Mosq prefer either bird or mammal!) - Venezuelan equine encephaltitis virus(R-M-H)
Enzootic - rodent maintain, less pathogenic. Epizootic - equine maintain, signs and death!!
Bite - ln - 1st viraemia - PO(repl) - 2nd viraemia
- if crosses BBB we see signs after 2nd! (5d)
Mortality (no. For eq mostly) - E up to 98%, W up to 50%, V up to 86% (virulence variants varies within spp, so depend more on this than the spp when its about mortality… )
Life long immunity, partial cross protection
Abortive infecitons: sometimes at first fever
Unapparant: Repl not successful in the body, low titre or due to immunity (prev infection, vax)
Signs: biphasic fever + (1st)Incr activity –> (2nd)apathy, icterus (colic, diarr Venezualian damage PO!) and CNS signs (movement(myelitis), convulsions(enceph)), after recovery permanent damage = should just euth. Them…
Zoonosis - see hu cases and horses simultaniously!!! (Pregnant - abort, children more sensitive…)
Vax in endemic coutries (trivalent for all spp:)) before mosquitoseason!
- Porcine reproductive and respiratory syndrome.
reproductive failure in adult females and deadly pneumonia in nursing pigs. Most imp disease in intensively raised pigs.
2 genotypes with their strains causing similar diseases; european and north american. 3 subtypes of the european genotype - Lelystad virus. Some strains are highly pathogenic.
Transmission from saliva and nasal discharge most imp (urine, feces, semen)
Inhal –> alv macroph (disrupt function, takes weeks to regenerate ((Blocks apopt in macroph until repl done, then Apoptosis after repl, no ag presentation (immunosuppressive virus))) -> viraemia 12h PI -> lymphoid organs, lungs, other tissues
- B cell activation, ab production but 99% not VN! -> interstitial pneumonia (B cells useless, no macr to clean up…) after 3w we see VN ab
- highest titre 14d PI, Virus can cross the placenta & replicates in the foetus from 14th day of foetal life
but is only efficient at crossing the placenta during the last trimester!
2 phases!
First phase lasting 2weeks we see resp in young, in sow we see abortion then return to oestrus.
In the second phase, lasting 1-4m(!), we see repro failure and high pre-weaning mortality!
o Boars: lack of libido, reduction in semen quality
o Suckling pigs: 2nd phase: high preweaning mortality (up to 60%)
B cells –> plasma cells (makes a bunch but not functioning..) - filling alv septa seen pm! Lymhoid depletion, periocular edema, edema of uterus! Pneumonia! Foetus (interst pneumonia, hydrothorax, ascites, edema in mesentery+perirenal aswell due to arteritis. (Arteriviridae;))
Eradication hard, virus variation, in larger farm. Need to know how virus acts in induviual farms, then we choose strategy of either eliminate (free from), or control, and live with PRRS. (Immunity in breeding stock to decr repro failure and transmission to piglets.)
There is limited crossprotection btw strains when using vax. Instead we should expose gilts and give time for seroconversion - testing.
Eradication rarely - closed herds only. (SPF)
- West Nile fever, disease caused by Usutu virus and other mosquito-borne flaviviral diseases.
!ND bc eq can die, high mortality in geese farms, zoonotic. In europe common sportadic cases in horses and humans.
Frequent in europe! 9 genetic lineages. Pathogenic are lin. 1 worldwide, and lin. 2 present in europe.
Mosq and bird (100d viraemia) cycle! Biological vector and migrating birds make it survive winter. Eq and hu (+more) are dead end hosts, too low titre. (Like eastern eq enceph)
Bite -> endothelial cells -> neuroinvasive (Inflamm of periph nerves, demyelinisation)
In most symptomatic ones we only see general signs
In under 1% CNS –> if see coma euth (will die)
Pm we see petechia on pericardium and serous fluid in epicardium. (Opposite??)
If suspect acute disease we do pcr and igm elisa to see if acute and notify!!! (IgG for serosurey, vax or not)
Prevent: mosq, vax horse and geese, indicator spp
There are other encephalitis viruses, cross reactions (japanese enceph serocomplex! Diagn value) eg usutu virus: enceph of wild birds, eg in central europe (HUN!), or japanese enceph, st. Louis enceph, murray-valley enceph, wesselbrondisease, turkey meningoenceph, …
Ddx. The crossreacting serocomplex, and togaviral enceph, rabies (most likely its WNF in europe!)
In europe inactivated vax are available. Before mosq season! Endemic areas hu should not donate blood.
Monitoring of birds and moquitos!
Other mosquito-borne Flavivirus – encephalitis mainly
1. Japanese encephalitis: human, horse, swine, mammals, birds
2. St. Louis encephalitis: horse human
3. Murray-valley encephalitis: children, wild bird reservoir, mammals
4. Wesselsbron disease: human, sheep, mammals. Fetus, abortion, hemorrhage, icterus, encep 5. Turkey meningoencephalitis: CNS, ataxia, enceph, mortality
6. Usutu virus: wild birds
7. Dengu virus: Dengue fever, human
8. Yellow fever: human, fever, hemorrhage, rash, liver dystrophy. VACCINE before travel
9. Zika virus: native in Africa, fever, rash, conjunctivitis, mosquitoes
Human: mosty asympt, flu like. Immunosuppressed, older: encephalitis… may recover or permanent encephalitis! No vax available for human!
53 - Bovine viral diarrhoea.
Flavi, pestivirus genus, BVD virus (not ND atm)
2 genotypes, BVDV1 is worldwide, BVDV2 is widespread too (from north america), in europe. Both has many subtypes, and each subtype has many strains… (only one serotype but NO crossreaction - imp for vax-..? Dont understand)
Problem is: when we see it its everywhere, immunosuppression = brdc etc incr disease, mucosal diease few but then high mortality, abortion. For others not lethal.
Suddenly huge problem and presence in herd.
- Basically lifelong shedding, fomites, feces survive weeks (nose-nose!!), semen, asymp animals.
- Spread invisibly in farm AND btw farm. And when we see it, we know we have a HUGE problem!
- We must ddx virulence variant!
- nCP more common, SPREAD INVISIBLE (no signs, cant be cultured)
- Cp strain: signs!
- Diff virus spp by subtypes, cp/ncp within spp, diff based on antigenitity: since so many different types, the ab specificity isnt necessarily good for cross protection even if closely related!
- (Gp53 is the neutralising antigen.)
All sort of transmission.. vertical, direct, veneral, indirect..
PO -> enteric mucosa, lymphatics -> viraemia (lymphocytes) -> P organs
–> endothelial damage = haemorrhages, mucosal damage = erosions, lymphatic tissue damage = immunosuppression (2dary; BRDC, other diseases (bo papular stomatitis)
NCp - no signs
Cp - the “normal” signs
- Calf: Fever, salivation, diarrhoea, respiratory disease, signs of co-infections (immunosuppression), central cataract
–> (ncp - maybe immunosuppr is seen, but asympt)
- Adult - asympt
Swine - see signs in foetus/piglet like ru!
Ncp + cp -> mucosal disease (or ncp mutation) –> High fever, haemorrhagic diarrhoea, Erosions on the mucosal surfaces: oral cavity, eyelids, hooves, legs, Weakness, exsiccosis, high mortality
Pregnant cow:
A) cp: enteric or resp in cow, and abortion… etc in foetus/embryo
B) ncp: asympt cow, embr death/infert, d40-120 IMMUNOTOLERANCE or seropos after immune system develops!
PM Mucosal disease
Sharp-edged, usually round/oval ulcers (FMD: red base, tattered edge)
Gums, palate, tongue, cheek, lips
Pharynx, oesophagus, rumen, reticulum
Inflamed enteric mucosa
Inflammation of the Peyer-patches, haemorrhagic ulceration
Croupous or diphteroid pseudomembranes
Haemorrhages under the serosal surfaces & on the kidney cortex
o Intrauterine infections - cerebellar hypoplasia, hydrocephalus, mictrophtalmia
o Histopath: degenerated villi, submucosal inflammatory cell infiltration
Diagnostic work is the key to fighting the infection!! Eradication - subclinical seropos, immunotolerant!
We treat symptomatically, and vax - live in outbreaks(not preggo, abort, also may induce mucosal disease), and inactivated repeatedly otherwise.
Eradication - smart, losses are huge… simultanious program of IBR is smart.
1. survey farm to see if present, serological high no of tests (coag. Blood sample, ab test at lab)
2. another sample 2-3w later (repeated)
3. cannot ddx tolerated and neg this way - vax - sample 2-3w later - tolerated still negative (no immune response), here we would sort out tolerated animals (-tive) + induce protection! Win-win
4. OR - direct virus detection aswell - ag or nucelic acid.
Always repeated sampling!!!
- Classical swine fever (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions).
(Like ASF (arbo/PO) but no arbo (direct, skin abrasions, vertical, veneral!)
ASF tricks the immune system with trick ag, while CSF repl in wbc hiding!
Both can cause viremia and shedding fast (A-2d, C-1d) - shedding in incubation period!!). ASF is dsDNA, CSF is RNA
Rel resistant for a enveloped flavi.
Serologically uniform, 3 genotypes. Wild and vaccine strains and other pestiviruses are ddx with monoclonal ab. Difference in virulence.
Transmission: (discharges) PO, air, conjunct, mating, trancut (iatrogenic, needles!), transplacental.
Su. Wild boars are the problem now - reservoir
Rarely seen in europe in domestic animals.
Survive in meat in fridge a month, freezer 6m!
Shedding in discarges. Carrier animals: adult, immunotolerant piglets.
–> Introduction with infected animal: large scale disease in the second week
–> Introduction with feed: large scale disease earlier (more animals affected)
(Discharges) Oronasal -> tonsils -> head/neck ln -> viraemia (till here same as ASF)
- lymphoid tissue -> immunosuppression
- BM damage -> thrombocytopenia, DIC
- endothelialdamage, bv dystrophy -> perivasc edema/circ issues!
- -> necrosis, heamorrhages!!!
(ASF all tissues, lymphoid, take memb of wbc, endoth damage, trick ag - immunocomplexes!)
Course dep on typical(classic/complicated bu secundary)/atypical, low virulence or vax strain.
Typical, Classic course:
- Peracute - death
- acute (Generalized, skin haemorrhages, CNS, eyes (diarrh bloody), up to 100% mortality),
- chronic (wasting, diarrhoea, crustae on skin(necrosis), (vs chronic CSF here we see skin haemorrh)
- Pregnant: abortion(weak)/immunotolerant/seropositive
- Weak strain/vax: subclinical
PM
- Peracute: sudden death, always check kidney first as its most sensitive (fine haemorrh at kidney cortex), some infiltr of brain (HP)
- acute: haemorrhages, erythema, edema EVERYWHERE, skin haemorrhages and necrosis (ear, leg), black ln, anemia, mild icterus (same asf but no skin haemorrh)
- Subacute: haemorrh or ichaemic infarcts at spleen edge!! (2dary infections - splenomegaly), GI (inflamm, buttons(lymphoid), pseudomemb, croupous pneumonia, necrotic tonsils (aujeszky!!), brain HP, atrophic thymus, eye signs.
Chronic: atypical, tricky! NO buttons, NO haemorrhages!!! LI thickened, necrotic and crustae. Lung is cropous-necrotic, post inflamm HP in brain.
- pregnant: edema, cerebellar hypopl. Anasarca
ASF:
1w icubation!
- Peracute/V virulent: suden death after 1w (virus everywhere) (90-100%mortality)
- Acute/Moderate: general signs –> death after 1-2w (leukocytopenia, thrombocytopenia, bloody stomach content, ulceration) (<60% mort)
- Chronic/Mild: seroconversion, immune complexes: skin haemorrhages, necrosis, painless swelling of carpal/tarsal joint (<10% mort)
Acute: blood everywhere… black Ln, pneumonia, enlarged spleen
Chronic: lymphoid, splenic hyperplasia, fibrin rich fluid in cav and pericardium, pneumonia, skin haemorrhages
Classical swine fever (diagnosis, differential diagnosis, prevention, control).
CSF is endemic in several EU countries in wild boar popultations (rare signs, experimental oral vax, like fox rabies in soil:))
- signs/pm suspision
- ND - must do lab
- lab
- elisa (antigen)
- RT-PCR (rev. Trancriptase, rna)
- virus isolation
- nucl sequencing
- IF of tissue sections
- serology (vaxed?) elisa, VN, CROSSREACTIONS BVD BD -> ddx with monoclonal ab!
Ddx
- fever, haemorrhages!
- ASF (lab), erysipelas(age, splenomegaly), skin assistere
o Salmonellosis – age, no skin haemorrhage, enlarged spleen
o A. pleuropneumoniae – high fever, dyspnoea, rapid death (no haemorrhages)
o Aujeszky’s disease – no skin haemorrhage, age
o Eperythrozoon suis – age, enlarged spleen, icterus
o Porcine circovirus 2 – age, course younger
o Poisoning – no fever, haematomas
(Same as ASF…)
Prevention: remember transmittion with fomites, humans, food, wild boar, wastes. Quick spread, fast shedding PI 24h.
- Avoid introduction! (Meat(catering), slaughter, import, home slaughter (hungary..))
- closed farm - wild boar!(maintain)
- Emergency vaccination in the restriction zone – with EU approval: marking,
quarantine, separate slaughtering, heat-treated pork, marketing restrictions
Eradication>vaccination!
Vax prohibited eu! (Vs ASF no vax available), serol monitoring tricky, vax sow infect foetus
Wild boar is main problem for introduction in eu as its endemic in many wild boars in diff eu countries. –> Hunting, “enzootic zones” in northern europe countries
- Transmissible gastroenteritis of swine.
Alphacoronavirus
Uniform serologically! (Crossprotection) PRCoV Spread in TGEs footprints
PRCoV TGE crossprotection. - outbreak rare nowadays! BUT if TGE present in farm ALONE = problem
(dog, fox, mouse can shed, but no disease)
- Seasonal epidemics! Nov-apr during farrowing. High mortality, rapid spread.
- Endemic farms: see in weaners! Mortality under 10%, slow spread.
Incubation 1-2d. oronasal route -> epithelial cells of lungs or intestines (jejunum) -> replication on top of the entire villi, villus atrophy, immature cells replace epithelium
o Decreased lactose digestion, increased osmotic pressure
o Na / K transport broken, electrolyte imbalance
o Viraemia (It can get into the milk, but not to the foetus) (too big). GI kills piglet.
Signs:
- Susceptible herd: FAST, vomiting, diarrhoea, suckling higher mortality,
2-3w mild. Adult - asympt/mild.
- Endemic herd: SLOW spread, signs in piglets of susceptible sows.
Nontypical pm. Dehydration, dilated int with undig. Milk, inflammation, villus atrophy.
Ddx e coli rota adeno PED..
Under 2w usually die.. after we should keep warm, treat dehydration, hygiene
Colostral immunity super important!! There are vax but not used in europe.
64 - bluetongue
Reo, orbivirus genus bluetongue virus (AHS, EE)
- Different serotypes - vax tricky. (Diff serot. in diff countries..) 29, mainly see serotype 1,2,4,9,16.
Endemic in europe! spreading further north! (Orig. Likes warmer..)
Mainly sheep, cattle less susceptible and can spread back to sheep, goats are not so susceptible. Spread with midges/gnats.
Seasonal depending on vector (and year), long distance spread with wind vector, tp of ru –> bigger restriction zones needed! (20, 100, 150km)
Sheep carry 2m, bo 1year!
Transplacental - immunotolerance if right time.
BITE -> primary multiplication in the lymphatic tissue -> viraemia in 5-11 days -> endothel damage ->
oedema, haemorrhages (due to destruction of membrane wall & increased permeability)
o MUCOSAL surface, SKIN, MUSCLE damages too
o Transplacental infection: abortion or developmental problems (hydrocephalus, cerebella
hypoplasia, jaw development disorder) - immunotolerance!
SHEEP: Can look like resp (gen+resp) but also: SC edema neck/head, swollen protruding cyanotic tongue (few), ulcers with necrosis (ox supply), hoof edema/laminitis/erosions, Muscle damage, lamb enteritis, Weight /wool loss
Abortion
CATTLE: subclinical, oronasal erosions, memb, ulcer. Congenital defects.
GOAT: subclinical usually
Pm: haemorrhages in resp, gi, cyanosis/edema/erosions on mm. –> myocardial and mm dystrophy,
ND - must diagnose serotype! (Pcr)
Serology/vax before transport(attenuated!) live only as emergency vax during outbreak to blow fire out.
Zones, slaughter, vector, isolate pos/immunotolerant, vax to blow fire out. (Attenuated) (kinda like bvd)
66 - African horse sickness, equine encephalosis.
Orbivirus genus (bluetongue), AHS virus
Vector transmitted disease of equids with acute, febrile, endothelia damages, oedema, haemorrhages,
pulmonary & cardiac disorders -> circulatory problems of the lungs -> HIGH MORTALITY in horse
(Other eq less susc)
Africa, introduction to europe! Midges and gnats are biological vectors, mosq are mech.
Pathogenesis Difference: virus in lungs aswell!! Fluid accumulation in body cavities - lung edema.
Signs:
- pulmonary form (foamy nasal discharge) with sudden death in 24h
- acute resp form, death within 1w
- subacute cardiac, edematic form, most frequent. Hippo head. Dies or not within a week.
- mixed resp and cardiac.
- chronic febrile form. Recurrent fever in evening
(Bluetongue: resp, cyanotic tongue, head edema, laminitis-hoof edema, wool loss.)
Pm:
Edema, haemorrhages, pulm edema, hydrothorax, epi and endocardial haemorrhages + on serosal surfaces.
Ddx: Equine infectius anemia, equine viral arteritis
Dogs are potential carriers (eat infected tissue)
Prevent
- introduction, insecticides, slaughter, restrict, vax in safety zone.
Equine encephalosis is imp bc similar but milder! Abortion too!
(Eq and elephant)
- Infectious bursal disease (Gumboro-disease).
Birna, avibirnagenus, IBDV, non-enveloped.
2 serotypes, only 1 is pathogenic. Virulence variants; classic virulent, v virulent and attenuated vax strains (different strains based on level of attenuation)
highly contagious disease of young chickens characterised by immunosuppression & mortality generally at 3-6 weeks of age. Present in basically all chicken farms!
Super contagious and resistant, shedding 1d PI. HYGIENE, contaminated environment is main source. Easy spread btw farms. Contaminated egg shell infect hatchlings.
Highest level of b fabricius is btw 2-8w, so until 2w the mortality is low, but imunosuppression is permanent. In the 2-8w timeframe there is immunocompetance, but up to 100% mortality! Over 8w asympt shedding.
(Weakens the b cell response, eg vax will be ineffective if under 2w)
Signs are seen due to immunocomplex formation and necrotizing formation.
3-6w, general, diarrhoea, anemia(pale comb - cyanosis), retarded growth, more susc to other diseases..
General signs, 2-8w chicken -> check bursa!! (Edema, inflamm, haemorrh, caseous exsudate)
–> ND!!
Hygiene!! Disinfect egg shells!!!
Flock samples - is there ab present - how much, against which strain is there protection? From this we choose vax:
Lab important! Ab levels, which strains.
Immunocomplex vax is good - mix btw live and hyperimmune sera. Full protection many strains, blocks replication and shedding and thus mutations too!
Inact vax for Parent generation for good yolk immunity –> knowing what type of vax for offspring starts with uniform immunity of parents.
68. Characteristics of influenza viruses, epidemiology of influenza (Zoon.).
Influenza genus AlphaInfluenza A virus (Ho, animals)!!
Influenza genus BetaInfluenza B virus
Influenza genus GammaInfluenza C virus
Isavirus genus infectious salmon anaemia
Quaranjavirus genus Quaranfil virus, Johnstin Atoll virus human arbovirus
Thogotovirus genusThogoto virus, Dhori virus human, arbovirus
INFLUENZA A VURUSES:
Enveloped, rel resistant if humid/disch.
Seasonal outbreaks
o Direct, airborne infection
o 1-3 days incubation, fever, loss of appetite, depression, headache, muscle ache, nasal discharge,
sneezing, coughing, sometimes pneumonia
o Avian virus can infect humans directly if bad hygiene
o If many occur together, genetic re-assortment may occur
Influenza viruses are unstable, variable & mutations often occur
Proteins!!
- PA, PB1, PB2: replication
- NP: nucleoprotein and M1: matrix protein: used for detection of GENUS!
- M2 matrix: ion channel for decaps
- HA: haemagglutinin, surf protein - for the neutr abs! (Ddx of STRAINS! And HOST SPECTRUM) Depending on SA receptor for host cell attachement, birds have 3-galactose while mammals 6-galactose. SWINE has both. Sporadic rare spread from bird to human. Swine can be infected by both, and can cause mutations so bird receptor can be adapted to human, so hu-hu infection possible!!
Resp and enteric mm (bird), resp in mammals.
High virulence strains bc More proteases can cleave so virus can enter cells all over body/tissue
-NA - neruaminidase, release from SA receptor and SPREAD!!
HA + NA = SEROTYPE (H1N1 eg)
(HA 18 serotypes and NA 11 serotypes, these combine making different serotypes. Total variance = 18x11 = 196 difference variants can occur!! change vaccine regularly)
Accidental hosts with high dose from bird. Serious signs, no transmission!
HA & NA together determines serotype (H1N1)
–> Hypervariable - serials of point mutations causing antigenic drift (slow change): seasonal influenzas
–> 18 x 11 = 1-200 combos possible! o Segmented genome
If simultaneous infections: segment reassortment (Eg many birds together)
–> H1N1 + H2N2 Combo (H1N1, H2N2, H1N2, H2N1)
–> Vaccine and infusion less effective!!
–> aka Antigenic shift = pandemic!
Host adaptation! Some strains are highly adapted to a species, eg. In swine, eq, hu (basis for epidemics!) –> see ind. Topics!
- Avian influenza
In waterfowl all serotypes are present.
In poultry we see mostly HA H1-H5
NA N1-9
Forms: Apathogenic avian influenza (AAI) Low pathogenic (LPAI) Middle pathogenic (MPAI) Highly pathogenic (HPAI) - notifiable - STAMP OUT
We talk about high and low pathogenic strains.
Zoonotic, wild birds maintain (asympt, spread direct, feces, natural waters, discharges! Long distance spread!)
–> persist in water long time so waterfowl often affected, they are less susceptible and we rarey see signs in waterfowl (duck, goose…)
o Oronasal infection -> respiratory & enteric epithelia
o Shedding with excretes, faeces; sometimes long-term carry
o LPAIV strains: immunosuppression, enteric & resp signs
o HPAIV strains: blood vessel damages, generalised infections
LPAI
- signs 1-2w PI: mild resp and enteric signs. Immunosuppression is seen so 2dary infections! (Mycopl, chlam)
- pm mild inflamm lesions
HPAI
- signs 1-3d PI, mass mortality, edema, skin hemorrhages, respiratory signs, cyanosis Bloody diarrhoea, catarrhal
CNS: Convulsions, torticollis, paralysis
- pm: haemorrh everywhere, resp - enteric tract inflamm and haemorrh, Necrotic pancreatitis (goose, H5N1)
Serous, lympho-histiocytic encephalomyelitis
Diagnosis: feces, swabs dead birds, rt-pcr, virus isolation and confirm isolate with HA + molecular methods eg neutr it with antiserum.
Ddx Newcastle!! IBD (no CNS)
Low path avain infl - we can let live till end of prod term then slaughter. Kill to avoid more mutations aswell.
Highly path present kill immediately - avoid spread.
Vax is prohibited - human danger! Hides presence we dont see signs –> mutations, zoonotic!!! Dangerous new pandemic strain may occur..
72 - Rinderpest, peste des petits ruminants.
Emerged in egypt first 3000bc!! 1/10 plagues described in bible! First disease ever to be eradicated! 2011 annouunced free from globally.
Belgium outbread after WW1 - found out these disease must be faught in cooperation internationally - OIE was founded in 1924
Morbillivirus, natural host are clovenhooved animals, mainly cattle are maintaining spp - so eradication of cattle rinderpest most imp
May be passed to other ru, pigs.
(Rinderpest is prob origin of PPR and distemper.. measles in hu after adaptation to new host!)
Close contact needed, market!!! Low resistance
- only PO direct! (aerosol not sign!) (frozen meat)
Morbidity is 100%, while mortality dep a lot on breed, eg african breeds less susc. Can be up to 90%!
PO infection -> replicate in throat LNs -> Viremia -> spleen, lns, bone marrow, mucous membrane ->
leukopenia, inflammation of mucous membranes -> lifelong immunity! (good antigen, sterile healing due to good IR!)
Peracute
- young and newborns.. die after 3d due to high (42C) fever)
Acute - classic form
- most common, incubation 3-9d
- shedding 2d before pyrexia
- febrile phase + mm congestion –> erosiva phase of oronasal, pain salivation –> diarrhoetic phase, watery then mucous, blood, epithelia tissue debris –> death d8-12
Mild subacture/endemic
- one or more of the classic form phases! Usually no diarrhoea, fever not so high or long lasting. Mortality not really.
- may turn chronic - mild signs
Atypical: irregular pyrexia and maybe mild diarrhoea. Gradual recovery
Sheep and goat milder, no mm lesions! Variable signs
Pig mainly in asia. Pyrexia, erosions, diarrhoea, milder maybe death.
Pm:
- mucosal lesions in upper resp and gut - linear blackening of LI = zebra stripes
- white necrotic foci in peyers patches; lymphoid necrosis and sloughing leaves the supporting
architecture engorged or blackened!
- enlarged and edematic Ln
Samples: blood, ocular & nasal secretions, spleen, prescapular or mesenteric LNs, tongue,
retropharyngeal LN, 3rd eyelid
Ddx mucosal disease, malign cat… etcetc FMD list!
- ND to make sure doest come back
- No long carrying in cattle, low resistance of virus made eradication possible
- vax - good protection. Live vax life long protection (having storage in case outbreak)
- serological survallence - checking for presence of disease, sentinels
Close herd, stamp out if outbreak.
PESTE DES PETITES RUMINANTES (PPR) ND!
Sheep, goat (indian buffalo, gazelle) - NOT cattle/su!!!
A virus closely related to rinderpest, mostly infecting small ru. Esp goat - breed predisposition.
“More infectious” than rinderpest as it also commonly infects by aerosol!
No carry!
Morbidity and mortility up to 100% in susceptible herd!! Lower in endemic, and adult animals
Pathogenesis is similar to rinderpest, no repl in spleen, bm.
Peracute
Acute;
Also fever, erosions, diarrhoea, but more typical is Profuse catarrhal exudate which crusts over & occludes the nostrils, resp distress! Erosions etc too. Like rinderpest we see diarrhoea a bit later also similar. Death 5-10d later!
Subacute
- typically in areas with local breed susceptibility, less susceptible! Inconsistent signs, after a week; fever and SEROUS nasal discharge, then diarrhoea.
Pm
Lesions v similar in cattle affected with rinderpest, except prominent crusty scabs along the outer lips & severe interstitial pneumonia
- free: close and stamp out. Strategic ring vax to prevent further spread.
- Endemic: live attenuated vax - life long immunity, of convalescent too!
- Newcastle disease (aetiology, epidemiology, pathogenesis, clinical signs).
Paramyxo, avula genus, NDV aka avian paramyxovirus 1
- several genotypes, variants..
V similar to AI, was first differentiated from eachother in 1927!
Only birds susceptible! But euryxen bc many spp!
Velogenic, mesogenic, lentogenic and apathogenic strains of the virus (highest virulence is velogenic)
o Mesogenic, lentogenic & apathogenic strains used as vaccines (isolate the virus to make vaccine) presence of these viruses is NOT notifiable!
- velogenic strains are not present in eu (import!!)
- in eu lentogenic strains are endemic.
Velogenic
- viscerotropic strains - high mortality and haemorrh (100% mortality!)
- neurotrop, pneumotropic strains (neural and resp sympt stonger - 50-60% mortality.
Meso; less virulent, used in vax (not europe), maybe resp cns in young
Lento: less virulent, immunosupressive, endemic europe
Apathogenic: good for vax, apathogenic and asympt, can use in day old chicks!
Long survival in faeces, excretes, secrets, raw meat, soiled egg shell may infect embryo!!
Virus is shed during the incubation period, during clinical stages & for a limited period during
convalescence.
Wild birds - reservoir lentogenic strains (mutations after establish in domestic -> virulent! Closed flock)
BUT long distance spread is due to human actions like illegal import of exotic birds - not migratory birds!!
Inhalation (PO) -> resp -> viraemia -> lung, int, CNS -> endothel damage, Immunosuppression,
CNS: neuron death, inflammation, oedema
Oviduct damage -> egg production problems, lethal for embryo (so NOT due tp germ infection!!)
Lento: mild resp disease
Meso: acute resp, CNS, under 10% mort
Velo: sudden death, severe resp and CNS, up to 100% mortality (general, edema –> green/white diarrhoea –> inflamed/cyanotic head/neck, dysponoea –> CNS, drop in egg prod
(Vaxed - asympt, sporadic cases)
- Newcastle disease (post mortem lesions, diagnosis, prevention, control).
Tentative diagn –> lab definitive!
Only velogenic strains sign pm:
Swollen periorbital or even whole head, edema sorrunding resp tract esp around thor inlet. Resp tract congestion or even haemorrhages and diphteric membranes.
Petechiea proventriculus forming circle typical.
Lymphoid tissue of resp/gi: edema, haemorrh, necrosis, ulceration! (payer patches=suggestive! )
Edema, degen of ovaries
Younger esp may bsee haemorrh of thymus and bursa.
Samples should be collected from recently dead birds or moribund birds that have been killed humanely (dead: swabs from PO, live: swabs) keep on ice!
For detection of agent we can isolate virus in embr egg and confirm with HA and molecular methods (ab). BUT PCR is most widely used…
Serology just to ddx vaxed
Ddx fowl cholera (no cns), HPAI,
We dont treat - stamp out!
Prevent: wild birds, human import, carcass disposal, pests, general epi measures
Many vax types but eg
Day old: apathogenic strain - homogenization of immunity
Spray/drinking water booster vax lentogenic strain (immunosuppr)
- layer several times
- growers
