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Question

67. Infectious bursal disease (Gumboro-disease).

Answer 1

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.

Answer 2

􏰀 Influenza genus Alpha􏰁Influenza A virus (Ho, animals)!! 􏰀 Influenza genus Beta􏰁Influenza B virus 􏰀 Influenza genus Gamma􏰁Influenza C virus 􏰀 Isavirus genus 􏰁 infectious salmon anaemia 􏰀 Quaranjavirus genus 􏰁 Quaranfil virus, Johnstin Atoll virus 􏰃 human arbovirus 􏰀 Thogotovirus genus􏰁Thogoto 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!

Answer 3

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..

Answer 4

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!

Answer 5

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)

Answer 6

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

Answer 7

RVF: mosq, ru, hu NSD: tick, sheep RIFT VALLEY FEVER Bunya, phlebovirus Endemic in the tropical Africa after heavy rainfall 􏰁 Epizootics in 5-20 year cycles (outbreaks cycle) 􏰁 After abnormally heavy rainfalls 􏰁 Outbreak peaks in late summer 􏰁 Long intervals btwn outbreaks allows for development of a susceptible animal population that is consequently severely affected by the following outbreak Mosquito transmitted (vs nairobi tick) - biological! So rainfall - eggs!! - Mosq that can transmit present in europe! Africa. A matter of introduction. - but direct transmission and infected tissues aswell! Ru and hu are competent hosts. Otherwise most animals can be infected! (Severe disease and abortion in these) - Ca, fe: severe in young not adult - eq not severe disease - su/rabbit/birds resistant Bite/other -> viraemia -> endothelial cells, resp/gi mm/ liver -> haemorrh, bloody diarrhoea, icterus! - CNS (deadly form) - foetus (all foetal organs) Small ru: - Sudden very sharp high increase of abortion is the most prevalent sign!!! - Sudden death young, - Diarrhoea, icterus, muco-purulent nasal discharge. Cattle: similar Human: asympt or flu like, 1% mortality - heamorrhagic fever 50% mortality! bloody diarrhoea, icterus, haemorrhages, coma). - Retinopathy, encephaliltis (maybe together with the haemorrh fever) Pm Necrotic hepatitis; Enlarged, yellow, fragile liver + haemorrhages - GI! We only treat humans (supportive) Vax in endemic of ru; repeat, maternal! Arbo control Zoon - gloves! Prevent introduction quarantine, serological investigations, tourists! NAIROBI SHEEP DISEASE - Nairobi sheep disease orthonairovirus. - Not ND but OIE listed! (Almost same, should notify) - Africa prevent trasmission abroad is importance In africa, tick biological vector. Infection -> viraemia -> repl in all organs! Haemorrh gastroenteritis, haemorrhages in heart, enlarged PO, full GB, hyperemic genital organs --> SHOCK --> DEATH! (Up to 90%) Hu: mild/asympt (vs. Rift valley 50% mort!)

Answer 8

VS: euryxen vesicles saliva+arbo Eph: high yield dairy, mosq only! VESICULAR STOMATITIS Rhabdo, vesiculovirus, VSvirus - Found in americas - avoiding import!! - not uniform - several serotypes! But crossprotection sometimes, variable - euryxen: eq, ru, su, hu etc. wild = asympt! - IMPORTANCE ddx from fmd in su/ru! Primarily by biting flies and midges but also saliva - wounds!! INCREASED susceptibility with age!!!! Long immunity(1yr), high morbidity, low mortality Bite/saliva -> vesicles at entry -> generalization (gen signs) -> vesices oral (Salivation, anorexia), teats (decr milk prod), coronary bands(limping) -> healing after 2w Human: flu lilke, not really vesicles, fast recovery BENIGN EPHEMERAL FEVER Ephemeral = transient, lasting short time - rhabdo, ephemerogenus, Bo ephemeral fever virus - serologically uniform! Tropical, subtropical areas in high yielding dairy cows - Spread ONLY by mosquitoes = no anmial-animal spread! - Clinical signs only in cattle and buffalo - Seroconversion in other Ruminants - Seasonal differences(rainy!) - dont carry after recovery --> good immunity & antigenicity o High morbidity, low mortality (like vesicular) Bite -> endothel - gen signs and sharp mild prod drop! NO shedding!!! Vasculitis, polyserositis, pneumonia Will heal, sterile healing (no shedding remember!) problem is the economic loss of milk prod...

Answer 9

Lyssa, rabies virus Rabies free islands + countries due to vax (EU) - danger of spread in eu is from east Serotypes (each has own maintaining host): 15 but 7 most imp 1. : classical rabies virus is what we usually see 2. : Lagos-bat virus: Africa 3. : Mokola virus: Africa 4. : Duvenhage virus: S Africa 5. : European bat lyssavirus 1 (EBLV-1) 6. : European bat lyssavirus 2 (EBLV-2)) 7. : Australian bat lyssavirus (ABLV) Phylotypes depending on genetic relatedness, differences in protection. phylotype 1 includes the most imp spp in europe, and has decent level of cross protection! Good!! All animals susceptible, High: fox, cat, dog, Ov, Cap, Bo, Eq, Ho (less) Shedding in saliva (+milk, urine but not so imp) - bite. Car PO eating infected tissues. Herbivore dont bite - dead end, car spread! ``` Epi forms (differences in maintaining host) present in europe: (Urban: dog and cat) eradicated) Sylvatic: fox, racoon dog/magnut Bat: fruit bat (reservoir), aerogenic in bat cave urine!! ``` GENOTYPE 1: --> some differences in severity and signs may be seen in other genotypes Bite -> repl in wound -> periph nerve cell (2-5mm/h), slow!), retrograde axonal transport to SC, brain and salivary glands. From salivary gland spread FAST(centrifugal spread) to cornea, organs, fetus, brain, fat. --> shedding BEFORE signs!! ---> dose dependant (length of incubation period, severity of signs) --> in beginning hides in CNS, immunomodulation, = late IR, but good response! (What we take adv of in vax, good IR but EARLY! Incubation 2-8w (more or less...) Clinical forms - Furious rabies: introduction -> excitation/aggression -> paralysis - silent rabies: introduction -> paralysis More about the phases of the clinical forms^ - 1) Introductory phase - shyness, anorexia - 2) Excitation phase: aggressiveness, increased sex drive, abnormal appetite(eat stones), swallowing disorders, strabismus (first sign of paralysis!) - 3) Paralysis phase: jaw paralysis -> salivation, hoarse voice In dog we can see both forms, while in cat only furious. Ru: may only see tympany and stopped rumination, or more typical form(silent) Excited, breaks out, hoarse, painful swallow, increased libido, mooing, hides, dull su: mostly just furious rabies, exctiation, bite, paralysis Eq: furious form (excites, colic, itch entry site). In silent form we see only paralysis. Av: we see furious form, excited and aggressive (make themselves big with feathers, but can heal!) Wild - becomes brave and goes close to humans.. Bats: navigation issues, attacks, paralysis Pm - Dont see much, may see random things in alimentary tract due to weird eating habits. - HP! CNS: inflamation, lymphohistiocytic infiltr, degeneration, glia cell foci -> negri bodies (cytopl IB)

Answer 10

DIAGNOSIS EPI-HP, Pm-signsCNS --> lab!!!! - IF really sensitive, PCR - virus isolation + IF - ELISA for ab titre of vax (late immune response in dsease - useless...) PREVENTION, CONTROL - only way to stop infection is exterminate rabid/suspected rabid!! - herbivores exposed: revax asap and observe 45?d, or emergency slaughter within 24h (still at site of entry) after exposed and heat treated if for consumption) - car: if vaxed (proven) can observe 90d (very variable incubation) - or eg if car is suspected to be infected and has bitten hu - it is shedding before the signs has occured, so if bite before should see signs in some days. 14d observation and no signs - no rabies! Free countries: quarantine (long), regular vaccination (VN test for titre) Eradication of urban rabies - list of dogs + vaccination. + post exposition vax! - already done in europe (WW1) Sylvatic rabies more complicated.. - Kill foxes, PO vax (in food) Bat rabies - Avoid bat caves.. (urine aerogenic) Vaccines - domestic/pets: inactivated from cell culture (3m + every 6m/yearly cat) Post exposition 10doses in total! Slow spread to brain (sl. Gland!) so have time to incr titre and prepare for generalization!!! - fox: live attenuated vector vax Public health - bite, saliva, wound - surgery - transplant - urine aerogenic - bat cave! Signs: unwell -> aggressive -> spasm -> paralysis -> death Humans are less susceptible, but low survival still.. 70k deaths/year. Inactivated vax + post exposition Bat rabies 1 - common asympt, fruit eating bats in europe. Rare transmission to other species, human infection bite. Bat rabies in europe eg in same phylogroup, some crossprotection with the typical rabies vax!! Bat rabies 2 not in europe - bite infects hu, animals

Answer 11

Retro, deltaretrovirus, enzootic bo leukosis virus Only Bo susceptible Friesian more Worldwide, many countries has eradication program Forms: - Sporadic, non-infectious form of calf(unrelated to virus). - Enzootic, infectious form: Disease of cattle 6m-3y caused by enzootic leukosis virus. No onc gene - Rex, Tax responsible for tumor formation (--> SLOW SPREAD bc no own onc gene) - Malignant tumors (lymphosarcomas - lymphoreticular tissue tumor!) develop in 1-10% of cattle (adult animals), - Discharges (air, contact, po, ai, iatrogen, insects(blood) - Intrauterine (immunotolerant, shedding calves issue for eradication!) - Milk Infection after maternal - 6m - 3yrs, target is B cells 3 phases - 1) Incubation phase (1-4months): replication in lymphoid cells, seropositivity, asymptomatic – some stay in this phase for years 2) Pretumor phase (2-4 yr): persistent lymphocytosis, blood smear – still no CS 3) Tumor phase (4-5 yr): 1-10% develope tumor (lymphosarcoma), THIS IS WHEN WE START SEING SIGNS! Signs Generally bad condition. enlarged Ln compress esophagus/trachea -> 2dary complications), depression, fatigue, anorexia, weight loss, drop of milk production, infertility -> Death. Pm Tumors in GI lung heart bladder. Ln haemopoetic tissue. Lymphosarcomas. AGD/ELISA best!! - blood and milk - persistant seropos (slight decr during calving and vax) - maternal ab 6m --> we use PCR under 6m! (Immunotolerance) Ddx sporadic leukosis in calves - larger ln and in calf Lifelong infection -> remove infected, closed herd, iatrogenic, pasteurize milk/colostrum, AI from disease free bulls! Eradication like normal... Free state: 2x seroneg 3-6m apart

Answer 12

Retro, Lentivirus - EIA virus Worldwide, more frequent in wet areas (aka swamp fever), arbovirus. Lifelong. Eq is susceptible, horse mostly. Introduction with infected animals, then spread in area with blood sucking flies (not long distance so sick animal must be introduced). Mechanical. - painful bite - horse runs away and introduce elsewhere. Discharges has no epi role. Foetus can be infected (rare) -> abortion or infected foal. Bite -> lymphoid, bm damage - anemia: HA virus-->haemolysis, immune complexes, macroph phag. the damaged rbc - immunosuppression: decr lymphocytes - healing and carriage, but retro v mutogenic -> new variant and new wave!!! After 1-4m: - acute: general signs, weak, tired, abortion, mm haemorrhages, edema and death OR AFTER 3-5d ASYPTOMATIC CARRIER! - subacute: febrile WAVES for months (another disease too idont remember), weak, weight loss, decr performance, anemia, edema (No abortion, haemorrhages, death) - asympt Pm: - Acute: haemorrhages, oedema, spleen hyperaemia, liver dystrophy, flaccid heart(tired from anemia...), enlarged lymph nodes, white mm! (Ht 25%) - Subacute: spleen enlarged - purple-red, liver enlarged (nutmeg, due to HF, hemolysis), kidney glomerulonephritis (immunocomplexes). We diagnose with serology!! May be false neg in beginning - repeated. Agar Gel immunodiffusion (coggins test), ELISA aswell (more recent) to see if seropos. PCR may be pos for carrier cases v low ab... not used really No treatment OR vax! - cull to prevent spread. - serological testing, iatrog infeciton!!!

Answer 13

(Only bovine is zoonotic Deer and sheep are infectious btw animals) Diseases: o Scrapie: sheep, goat, moufflon 1732 o Mink transmissible encephalopathy: mink 1947 o Chronic wasting disease: elk, mule deer 1967 o Bovine spongiform encephalopathy (BSE): cattle 1985 o Feline spongiform encephalopathy: felidae 1990 Occurrence: worldwide (not all – but everywhere at least 1 present EXCEPT Australia/NZ) Etiology: Prion (proteinaceous infectious particles): - Normal prion: can find in healthy – cytoplasm membrane, many in neurons, unsure of function - Infective prion: resistance (proteases, heat, disinfectants), folding differences (normally dynamic synth and decomp of prions, but a difference in folding makes these prions unable to degenerate --> accumulation! o Origin: Mutated form, Infectious form (PO), Inheritable (Ho, familiar cumulative) o Atypical prion strains (eg. Atypical scrapie) Slow, no inflammation, degenerative processes o PO resistant infectious prions o The pathogenic prions trigger the misfolding of the physiological prion proteins in a chain reaction-like process o Chain reaction, trigger malformation of normal proteins -> beta sheet formation -> irreversible structural transformation that proteases cant degen! o PO -> int -> nerve endings of gut wall (vagus, splanchic) -> CNS -> chain reaction, accumulation -> normal structure of brain destroyed -> evident signs o Internal proteases unable to decomp -> accumulation -> amyloid plaque formation -> cell death -> pass through the peripheral nerves eyes, tongue and nasal mucosa No pm, HP: Vacuolisation of the nerve cells, amyloid plaques --> look like sponge Diagnosis --> signs and EPI give suspision... Difficulties 􏰁 No post mortem lesions 􏰁 Antibodies are not produced 􏰁 Methods detecting nucleic acids cannot be used (cannot use PCR) Detection of PrP threads (prion associated prion proteins) Fibril like. Scrapie associated fibrils. Prion detection - NO genome, no pcr!! - prions are non-immunogenic - BUT elisa, western blot can be used - proteinase K is v strong proteinase from fungi which can degr. The beta sheets --> the prp is exposed, and detected with eg. ELISA, western blot! - Hyperimmune sera can be made against the prp, and eg. Western blot: Ab in gel – ag will migrate according to molecular size with electric current • Pattern can be used to compair to typical pattern for diagnosis No treatment, no vax, killed!! Free countries, SRM, feed ban, no vax (CNS, skull, eye, gut) where it travels! SCRAPIE PrPSc (scrapie-associated prion protein) Everywhere except austr., NZ Sporadic due to breeding of resistant animals o 1.5-5 years of age o Long lasting presence in the flock o Carriage: tonsils (discharge), lymph nodes, gut (feces), nasal discharge - CAN BE SHED (unlike BSE) o Keeping different age groups together increases the risk o Genetic predisposition Infection PO (direct contact, discharges, environment) -> Gut, spleen, lymphoreticular tissues, lns, tonsils - Shed in discharges, foetal membranes, foetal fluids - Atypical scrapie: not present in lymphoreticular tissues, not shed o 1.5-5 years old sheep (incubation over 2yrs, rarely signs under 1.5yrs) o Altered behaviour: CNS signs (head tremor, nervous), ITCHING (--> NOT in the case of atypical strains), sticks out tongue, frequent drinking o Movement disorders: ataxia, hypermetria, weakness, staggering o Weight loss -> death eventually Pm like normal TSE Can detect prion (like before) but here also from nasal discharge!! Not only pm!!! breeding resistant lines - dominant inherited, stamp out, signs are seen over 18m, so we examinate sheep slaughtered above this age MINK - Only in mink farms. PO infected meat. - 6-9m incubation, so seen in over 1yr old - weird behaviour, squirrel tail. - movement disorders - Stamp out - feed!!!

Answer 14

History, 1986: dairy herd, wanted to incr milk prod – gave higher protien feed – BSE. Occurance improven with changes in protein processing - BOVINE, zoo ru, big cats, HUMANS - Swine and av are resistant to infection Europe is recognized as having a negligible/controlled BSE risk status (2017) o Only a few animals within a herd o No spreading from animal to animal, there is no transmission from cow to calf Po -> gut -> along nerves -> brain 3-5 year incubation!! Slow!! (Vs 2 scrapie) Mad cow disease - Change of behaviour: hypersensitivity, nervous, shy, head down, aggressive, resistance to milking - Movement disorders: weakness, ataxia, hypermetria, weight loss, drop of milk production, death HP like other, diagn like TSEs... only pm! o Notifiable disease o Feed ban on proteins of animals origin --> Except: milk, milk powder, colostrum, egg, fish powder (no shedding) o Meat powders from ruminants and carcasses cannot be used for nutrition o Import control o Examination of clinical cases (CNS) o Monitoring if: animals died in CNS signs, animals above 24 months (vs 18m scrapie) died, emergency slaughtered, animals above 30 (72) months of age (if 6 years negative -> prob negative!) o Specific Risk Material (SRM): CNS, gut, spleen, eye, brain spinal cord FELINE GB mainly, 2-5 y/o from infected food. Aggressive or shy, dilated pupil, movement disorder.

Answer 15

Bacillaceae fam, Bacillus genus, b. anthracis, - obligate pathogen - repl only in infected host - conditions of spore formation: oxygen (outside host!!), min 12C, water = open carcass is perfect! - Susceptibility: (Ov most) ruminants, horse, dog, cat, human (not as susceptible), swine, (birds quite resistant but can transmit) = Zoonosis Rel. Uniform, close A and B(mostly B) Due to the successful vax the disease is sporadic mostly. The diagnosis is easy. The problem is the spores, they live for decades and cannot rid of. The areas where these spores are present is hard to keep track of, and after eg a lifetime its easy to set up a new farm in a forgotten anthrax area. o Soil, pasture: soil disturbance (excavation, digging); environmental effects (drought, flooding); soil will be infected for a long time (people forget about the previous infection Water, Infected meat (Carnivorous animals, source of human infection) - eat! Role of scavengers (mammals, birds): oxygen exposure, transport skin Raptors can be quite resistant, but spores can be present in the gut & they can spread the disease over some distances! capsule - D-glutamic acid (L type in animals), so D gives protection as it survives in the body as it cant be decomposed. spore infection soil mostly PO – throat, intestines (local lesions, repl) – blood, septicemia (protected by capsule makes unlimited repl possible.. HUGE AMOUNT) – toxin production (edeam, lethal toxin) causing local lesions and blocking the resp center killing the animal - In human mostly also inhalation (work with skins) or wound infection also possible (possible but rare in animals too) Signs - 3-5d (12h) incubation period - Cattle – most susceptible – peracute or acute o You see them stop grazing and ruminating, fever, depression, ataxia, bleeding is seen (natural orifices) Horse – acute course o Horse is colicing, edema and fever are also seen Carnivore - acute o Enteral cases typical; haemorrhagic enteritis, vomitus, pharyngitis (voice change) and fever Swine – not so susceptible, local lesions (Throat, intestines) o Vomitus, diarrhoea Birds o Rarely see signs.. (fever, gen. Disease, haem. Diarrhoea) --> in all if untreated deadly! We typically find them dead with bleedings from orifices, foaming in oronasal area (gasping for air) – death by suffocation! PM Acute: o Most typical: no or late rigor mortis, incomplete clotting, black blood, huge spleen o Ln are large and haemorrhagic o Generally haemorrhages and edema typical o Haem enteritis, carbuncles intestinal (haem+edematic areas under mucosa – bump) o Kidney (?) - Local (su) o Inflammatory lesions in phanynx and tonsils (su typical, eg necrotic tonsillitis) o Gut, Ln (serous-haemorrhoagic lymphadenitis)

Answer 16

Diagnosis - Grazing animal, bleedings, pm lesions (blood-spleen-rigor mortis) - from this quite obvious.. - Lab o On suspicion we take blood smear (easy as blood doesnt clot..) and piece of cart from ear for PCR o Blood smear: meatchromatic stain of the capsule is typical, huge amount of bacteria - metachromatic staining (unique – toluidine blue: pink capsule, blue bacilli in blood due to the unlimited replication! Ddx all sudden death diseases.. - toxicosis, heat shock - ru: pasturellosis, gas gangrenous diseases - eq: pyosepticemia, EIA - swine: ASF, CSF, malignant edema - dog: lepto, ehrlichiosis, haemobartonellosis Treatment - Must treat asap – look for sign (FEVER) - We suppose the rest of the herd is infected aswell: source available for all.. - Penicillin is first choice (ttc, flouroquinolone) - Change possible souce!! Feed, pasture, water source.. Prevention, control - Movement restriction of area o Only vaxed animals can graze here - Isolation and treat animals with anthrax - Healthy animals should be observed for apperance of signs, and vaccinated - Dead anthrax cases o Dont open to avoid spore production (open first case to diagn, then no more dissection) o Proper disposal of the dead animals, bedding (burn), disinfection (super resistant spores, long exposure needed) - Vax has been successful for 100 years! o Live vax, sterne-strain (protects 1 season) o DONT combo hyperimmune sera and live vax as ab act against vax.. Public health importance - Humans are not so susceptible.. - The cutaneus form is the most typical o Infected IV needls, infected animal, meat processing, drugs (?) Haemorrhagic-edematous localized cutaneus lesion (round red spots) - Pulmonary anthrax o Inhalation, most severe form o Looks like flu so tricky to diagnose, pneumonia (invades everywhere in lung) - GI anthrax (gut and oropharynx) o Eat infected meat that hasnt been heat treated properly - Hard to diagnose, death with misdiagnosis.. - Sepsis - Ab as treatment like with animals - Cutan and lung form are typically occupational diseases, working with skins etc. - Prevention o During dissection wear gloves, avoid aerosolation in lab o War, terrorism.. o Vax of human tricky.. mainly soldiers in affected areas, several vax needed

Answer 17

FAST diseases, sudden death, endotoxemic!!! (No serology) INH: sheep, sometimes cattle (worldwide), maybe dyspnoea but death mostly, mostly liver pm. Alpha toxin BH: cattle, sometimes sheep (sometimes in europe). May be peracute see more signs! Red water disease, more pm seen. Beta toxin Infectious necrotic hepatitis (black disease), c. novyi B Occurance - Worldwide, But mostly places with high liver fluke occurance - Summer, early autumn (flukes during grazing period) Aetiology - C. Novyi B (Strict anaerobe!! Imp for pathogenesis) Epidemiology - sheep 1-4 years (rarely others, but sometimes cattle) - parasite infection (liver flukes) Pathogenesis - If abrasions GI, c novyi can enter circ in small amount - If fluke infection -> necrosis in liver -> the local necrosis in liver decr ox in tissues -> completely ox free environment, so novyi b can repl! - Toxic effect of the alpha toxin – haemorrhagic toxin absorbed into circ - hemolysis - causing the death of the sheep! Signs - FAST – hours - Depression, teeth grinding, laboured breath, tachycardia -> death Pm lesions - Typical! - Liver: necrosis, inflammation sorrunded by red ring (hemolysins are produced), liver flukes - Ascites and thoracic fluid accumulation - Blackish colour due to damaged circulation Diagnosis - Epi (season, fluke) – signs (sudden) – pm o Can diagnose based on this basically.. - Detect agent (fast course) o Micrpscoly o IF o Culture tricky bc anaerobe.. - Detect toxin - Ddx fascilosis alone.. (Inflammatory necrotic hepatitis should be seen aswell!) Prevention - Antiparasitic treatment - Combined vax with both the agent and its toxin (novyi) Bacillary haemoglobinuria (red water disease) Occurance - Australia and america frequent! (Europe) - Mainly in large beef cattle heards in americas (sometimes sheep) Aetiology - C. Haemolyticum (strict anaerobe) o BETA TOXIN – phospholipase C, lectinase (hemolysis, membrane damage) - Spore from soil (like normal) Pathogenesis - PO from soil -> Abrasion in gut -> circ -> liver - Liver damage needed to create anaerobe environment (eg fluke or other) - beta toxin -> IV hemolysis (anemia, haemoglobinuria = red water disease!) Signs - SUDDEN – sometimes no signs - Fever, depression - Hemoglobinuria, jaundice, anemia (tachypnoea) ``` Pm lesions - Anemic (thin blood) - Haemorrhages, edema - Liver necrosis - Bloody body fluids (abd, thor) - Red urine in bladder (In last we mostly see the liver signs) ``` ``` Diagnosis - Epi – signs – pm - Detect agent o Culture, IF - Detect toxin - Ddx: (sudden death) anthrax, anaplasmosis, leptospirosis, toxicosis ``` Treatment - Bc very fast often cant be treated. But herd, rest of hert prophylaxis!! If cases treat others - Penicillin, fluid, blood Prevention - Predisposing: liver fluke (antiparasitics) - Vax in endemic areas, 6month protection

Answer 18

- In tb free countries, wild ru, boar, badgers source! (Reservoir) M bovis and caprae (bovis mostly) - Obligate pathogen - shed in milk and discharges - carrier animals, wild animals introduce (hu) - cattle v susc, tiny amount needed for infection Since obl pathogen - dep on the balance of the bacteria (amount, virulence, spp), and the IR and resistance of host!! - Inhalation/PO (milk calf) (Rare intrauterine, veneral, per cutan, ascending teat) - Primary complex in resp: (phag by macroph, phagolysosome fusion inhibition, replication, macroph to Ln, lysis, cellular infilt (TNFa, gINF), tubercule formation (cellular infiltr forming layers around bact, plasma infiltr and caseous necr in center, granulation tissue capsule + fibrous capsule sorrunds it. May heal, inactive state, or move further to early gen - early gen: lymphogenous and haematogenous spread. Decent resistance of host, tubercule formation, miliary or larger, ln tubercules, death or inactive state - post primary: endogenous reinfection or from environment, ab present so cant enter blood - intracanalicular spread in eg lung, chronic organ tb: caseous necrosis, caverns, no ln lesions - exhaust phase/late generalization: exudative, caseus necrosis, plasma, ln lesions, death --> long, invisible spread, dont see signs until long time = monitoring vital!!! Signs - months to years incubation, then we see atypical signs... - primary focus: no sign - early gen: general signs, enlarged Ln, milk drop - postprimary: same but progressing - depending on which organ! Resp, diarrhoea, milk consistancy (udder tb), turbid urine, nodular testicles, vaginal discharge and infertility, movement disorder (CNS), movement disorder, deformation (bone, joint) Pm: TYPICAL! Imp! - rarely find primary complex.. imp is: Lungs o Tuberculosis nodosa – small tubercles, isolation, calcification, lesions in the lymph nodes Regional mediastinal o Chronic pstprimary tuberculosis – acinous, acino-nodosal pneum., caverns, no fresh lesions in lymph n. o Late generalization – fresh military tubercles, caverns, caseous lesions, fresh lesions in lymph nodes - Intestine – erosions, ulcers from lymphoid tissue - Liver, spleen and kidney – tubercles – caseous necrosis, calcification - Genitals – tubercles, - Udder – military, nodosus, indurations

Answer 19

Diagnosis of disease - Direct smear stained with ZN easiest: loads of ZN+ bacteria, HP is typical (tubercule morph), PCR, culture, spp identification by genome examination. Isolation • Second option, long incubation time. We do do it (determine of strain, ab resistancy etc) importance --> PCR is used with the isolate – examination of genome! (pcr replaced IF, IP) (!)Irregular shedding! Live animal, if negative result from eg tracheal discharge, may be false negative! Diagnosis of infection - we diagnose active infection, important in eradication! - cellular > humoral response importance as we deal with IC pathogen (only ab after the bacterium has generalized!) Cellular immune response: - gamma interferon test: Blood (lymphocytes) collected -> react with tuberculin -> if animal infected -> gamma interferon release! Avian and bovis tuberculin results in different gamma IF production. - (lymphocyte proliferation test, tricky) Humoral immune response: - ELISA, Not widely used, humural immunity not so strong. - But eg in wild living animals like badgers we use. But not used alone - complement method of others Tuberculin tests - allergic tests (cellular response) - these are the main!! - PPD (purified protein derivative) Antigen extract, used as immunodiagnostic tool, previously infected shows reaction! A) thermal test: rare. Used when the Clinical signs are tricky to interperet. The thermal test incr the signs, we measure the body temp 3x to make an average, then measure again after 6h, then every 2h until 22h. Positiv - 1.5°C increase, general (fever, depression) and organic (postprimary type of reaction...) reaction (stronger where lesions are located – pulmonary: coughing or dyspnea increased, enteral: diarrhea incr.) B) skin intradermal, - type 4 hypersensitivity/cell mediated. - v specific on genus (mycobacterium) level! Cant ddx species... (4mm thickness or signs = pos after 72h, under 2mm negative, btw inconclusive. ) IDT difficulties - false negative: preallergy, 1-3w PI too fresh infection to detect (cellular) immune reaction. Wont see in old isolated infection either. Anergy is in the exhaust phase where we have immunosuppression and false neg may occur - but signs should be v obvious... False positive: - (heteroallergy, antigenic rel to other bacteria, corynebact and actinomyces. Weaker reaction tho) - PARALLERGY: M. bovis is not present, but reaction is positive (other mycobacteria – m. Tuberc.C omplex = same reaction, other = weaker react.) Reacting animals in a herd without reaction history, if immediately large number of reactors appear, and if you repeat the test and different reactor animals appear. Need to find the source of the infection: Feed, water contaminated with soil, silage, pasture. (Saprophytic, facultative mycobacteria...) Also lab to ddx - parallergy or m. Bovis?; - EPI: new animals? Contact with wild? Is TB present in wild in area? A) compare tuberculin test (avian vs bo tuberculin), most widely used! - pos: fold is 4mm thicker than avian tuberculin or local reaction - inconcl: under 4mm thicker, no local reaction - neg: bovine reaction not positive, no local reaction, no difference from avian (avian and bovine ish same...) B) slaughterhouse, histo, stain, cultrue, PCR (time, money...) C) gamma interferon test (avian vs bovis tuberculin) RISK OF RE INFECTION: Positive reaction: close, isolate, stamp out all or repeated reactioning animals! Free herd: all animals above 6 weeks of age, twice 4-12 months apart, SID negative - Tuberculin test every year (every 3rd year), <1% positive, positive reactors are eliminated Treatment: not in farm animals, wont prevent coloniazation, and huge dose needed so ab resistancy!! Prevention: - general epi - we do not vax farm animals! - some places BCG strain PO in wild animals... Eradication, control - Principles – fetuses generally not infected, infected animals shed bacterium any time, tuberculin test is sensitive and specific, isolation of calves can prevent the infection - Methods: A) Selection using tuberculin test - small herds (false neg old animals) B) generation shift (calves) - tuberculin test at 6m C) herd replacement Tuberculosis free country at least for 6 years maximum 0.1% infection, individual identification of all animals o Regular and documented tuberculin tests, meat inspection of all slaughtered animals - maintaining: Tuberculin test above 6w of age (12m in case of long free state), every year (every 2nd or 3rd in long free state)

Answer 20

Bovis - obl, PO, head/neck, generalize, spread(human! Cull) Avium - fac, locus minores, mesenterial, predisposing, ddx importance Tuberculosis - obl, PO. Mesenterial, generalize, spread (human!) A) MYCOBACTERIUM BOVIS - PO infection - Can get infected by ingestion of dairy products, or by grazing on same pasture as cattle (pigs eat everything!) - Lymph nodes on head and neck are affected, can become generalized and reach liver, lungs and bones. (Like cattle!). Lymph nodes can become broken and become a fistula, and contents can be released. - M. Bovis and caprae - same pathogenesis as bovis. Clinical signs - Emaciation, fluctuating temperature, lethargy, lung/liver lesions, - TB involvement of joints is more common Intradermal skin test - Near the ear, reading after 36-48 hours (vs. 72) - Positive: erythema, edema, serum and necrosis (we look at the local reaction!!) Importance: can shead, spread and infect humans! Not so imp in maintaining. B) M. AVIUM & ATYPICAL MYCOBACTERIA - M. avium subsp. Avium - most resistant mycobacteria! (Facultative, but still v infectious among the opportunistic!) - other facultative pathogenic mycobacteria! - Infection via birds, environment -> per os (airborne, wound). - Lymphadenitis, local lesions mostly - avium can cause generalized, productive lesions - fac - need predisposing factors. PO -> Mestenterial Ln are affected (like cattle), but here some predisposing factors that may harm the gut mucosa, can lead to generalization of disease. - fac: is often subclinical, and seen at the slaughterhouse --> importance of slaughterhouse checks!!! - avium/fac parallergy - differentiation!! M. TUBERCULOSIS - Main agent of human tuberculosis, Pigs are susceptible, source of infection is usually via human contact - Pigs and dogs are capable of shedding M. tuberculosis (cattle NOT able to shed) - Infection via feeding swill (eg. From hospital...) without heat treatment - Primary complex in the gut & mesenterial lymph nodes, local lesions - generalization - Culling -> due to zoonosis (shead and spread like m. Bovis..)

Answer 21

M. Avium subsp. Paratuberculosis (MAP) Obl pathogen? V resistant, long incubation - differs from avium that it has even slower growth and infects mammals and not birds! But 99% same genome!) - Worldwide, large scale farms - Cattle mostly, other ru rarer signs. - FECAL and MILK shedding starts 3-5m PI, while incubation >9m! - we see signs if infected <6m, >6m asympt shedding --> signs at 2-5 years of age!! (= must be infected as calf, while only adults show signs.) - infection from feces, food or water. V resistant bacteria - 6-9m in environment!! - predisposing: immunosuppression! pregnancy, deficiency, BVD, parasite infection PO -> gut, macroph phagocyt, and repl start IC. Also in T-lymphocytes, in gut and mesent. Ln - 1st phase: tuberculoid phase (cell mediated), lysis of macroph, release bact and phagoc by other bact. Attracts cells - cytokine production (TNF and interferon gamma missing - So no tubercule form. Or necrosis, only productive infl with strong cellular inflamm in gut wall) --> atrophy of int follicles and decr absorption --> diarrhoea, weight loss, drop of milk prod 2nd phase - lepromatous: humoral response. Ab production. Signs >9m PI! - Weight loss, decreased milk yield, severe diarrhea (watery, smelly, squirt -> jet like - on wall not floor!), ventral edema - Sheep and goat have milder signs Pm - prox LI: thickening, gyri like transv folds cannot be smoothed away. - enlarged Ln - HP: epitheloid, giant cells DIAGNOSIS - Must consider which phase of the pathogenesis! (Long incubation, what phase) - detection of pathogen can only be done later in the pathogenesis, fac IC pathogen! (staining, IF, PCR, culture - Need iron tp material!) Immunodiagnostics (detection of infection) - tuberculoid phase: (interferon test, lymphocyte stimulation test(not really)) - lepromatous phase: serology! CFT, AGD, iIF, ELISA There is also an allergic test similar test to tuberculin test, paratuberculin (PPD), avian tuberculin No treatment - cull! (Long shed...) CONTROL, ERADICATION - In case of the disease = movement restriction -> infected animals should be transported only to slaughter - Disinfection, not using infected pastures for a year - Decreasing spread of the infection within the herd: Prevent infection of young calves, good hygiene (prevent fecal contamination), clean water, diseased animals culled. - Replacement animals from paratuberculosis-free herds - Vaccination (1st month 1x), attenuated and killed vaccines, tuberculin positivity: Not videly used but good protection. 1m protect Cant use tuberculin test tho? Eradication - test n slaughter tricky bc tricky diagnosis.. long incubation... - generation shift (milk shedding! Milk replacers) - herd replacement Zoon may be (chrons), not fully confirmed. Similar disease to cattle! Milk infectin - pasterization.

Answer 22

R. Equi: Salmon pink, mucoid (capsule), non hemolytic colonies. Non-motile. Zoon from su Derm: 2-5 mm wrinkled yellow colonies, strong ß-hemolysis. Flagellated. Zoon! Both are slow RHODOCOCCUS EQUI - R. Equi in soil everywhere! - -> depending on area its endemic, sporadic or not present! - G+, branching filaments, fac IC EPI - R. equi is responsible for 10% foal mortality, 45% of pneumonia cases - morbidity rate: 5-17%, mortality: 80%! - foal 1-4m is infected, summer - windy, dry - dust inhalation - inhalation of dust infects - virulent strain accumulate in soil - high no. Of animals! Inhalatio, /PO, umbilical, intrauterine --> - In the lungs: Phagocytosed by alveolar macrophages -> inhibit phagosome-lysosome fusion -> propagation and cell lysis -> tissue destruction (similar to mycobacteria) - result: purulent bronchopneumonia - In the gut: replicates in the cells of peyers patches -> ulcers -> result: ulcerative enteritis, arthritis - The course of the disease takes longer than 3 weeks in half of the cases (long, also similar to mycob...) Signs: CHRONIC usually! - resp: General signs and resp signs. Loud moist rales on auscultation. - GI: 50% of pneumonia cases has, majority has no signs (diarrhoea, colic) - Aseptic polysynovitis, polyarthritis -> in 30% of pneumonia cases (Tibiotarsal and knee joint is affected -> lameness PM - purulent bronchopneumonia with abscess formation and purulent lymphadentitis (macroph brind r equi to Ln -> purulent inflammation) - Ulcerative enterocolitis, typhilitis(cecum inflamm), purulent lymphadenitis Diagnosis - usually common in area should indicate - lab, cytology, bacteriology, x-ray/US - culture! Treatment: - fac IC + abcesses --> rifampicin + macrolide for 4-10w!! - (Bacteriostatic, synergistic, concentrate in macrophages) Prevention - soil accumulation, dust formation - can measure temp for early diagnosis. - hyperimmune sera in endemic area age d7 and 30 - Human r equi comes from swine (not eq) 20% of swine carry this bact in submand Ln! Hu and su isolates same serotypes, plasmid and virulence types DERMATOPHILUS / EXUDATIVE DERMATITIS - D. Congolensis (only spp in genus) - G+ cocci forming filaments, flagellated - motile zoospores can survive in dry scabs up to 3yrs!!! - virulence fac: proteases, phospholipases, alkaline ceramidase - susceptible: ru and eq (hu!) Woldwide but likes warm weather. Regular introduction to europe. Introduction via symptom free infected animals, wool, skins, clippers and humans - Predisposing factors needed! Lesions to enter + activation of zoospores by persistent wetting (heavy prolonged rainfall), malnutrition, pregnancy, ectoparasites Wet, soggy, damaged skin -> 1m incubation --> exudative, pustular dermatitis (vesicles and scabs) (Only skin is affected!) - on dorsum (palpate papules through fur/wool) - Serous exudate cause matting of hair -> tufted appearance, irregular elevated crusty scabs - Tufts of hair can be readily plucked from lesions along with adherent scab material and underlying exudate - Lesions may resolve spontaneously within a few weeks - In severe infections extensive lesions, fever, anorexia and death (10-15%) in calves, lambs Dianosis: epi-signs! skin scraping! Smear, culture Treatment - dry! Clean! - im. (Parenteral) ab! Topical wont work (oxytetracycline) - isolation of herd Humans - wear gloves! Prevent wounds! Hand lesions some weeks...

Answer 23

OUTLINE: pathogenic characteristics of e coli + predisposing = tricky diagnosis AND treatment, PREVENTION! Enterobacteriaceae, echerichia genus, e. Coli spp - rod, capsule, flagella and fimbria - G- has thin cell wall, stain pink - most saprophytic e coli, but some facultative can cause even serious disease!! Antigens: - determining SEROTYPE O - cell wallO (LPS) K - Kapsule (PS - leat stabile or labile) F - fimbria (adhesion, all has F1 + diff types) H - flagellaH (60 types) Virulence factors - capsule: antiphagocytic - adhesin: adherance and colonization (fimbria attach) - endotoxin: LPS, at bacterial death we see endotoxic shock. Rapid death - Course of disease different, we see the signs of toxin effect, when the bacterial replication already occured - exotoxin: A) enterotoxin (heat stabile/labile, both incr secretion causing diarrhoes) B) verotoxin: vero or shigatoxin. Endothelial damage (eg. Eema disease) C) cytotoxic necrotic factor causing necrosis Some has invasive ability and can survive in blood! Extremely high genetic var. - chromosome + plasmids, these are shared btw e. Coli! Depending on which virulence fctors present we divide into STRAINS: Entero: -pathogenic(destroy villi), -toxogenic(intact villi), -invasive, -adhesive-aggregative, -haemorrhagic strains, verotoxigenic and necrotoxic strains.. Extra-enteric: septicemic, uropathogenic, avian pathogenic strains ``` - Toxogenic, vero in calves, car(ca, fe), su + pathogenic in car, cu - septicemia in calves, pigs, av - UTI in pigs - mastitis cows and pigs ``` Predisposing needed!! - Eg. Toxogenic (ETEC) strains use adhesins to attach, these are only present in calves for a week (neonatal diarrhoea), while piglets they stay till around weaning! (Neonatal + post-weaning diarrrhoea) DIAGNOSIS 1 - suspision (epi (age, spp!), signs, pm) 2 - isolation: culture! MacConkey is commonly used. Hemolysis in su, ca (we use blood agar) 3 - identify virulence factors, strain: PCR (exotoxins, adhesins(fimbria)) 4 - serotype determination (O K H F) - latex agglutination test Treatment - enteric: ab susceptibility, active in GI (colistin, enrofloxacin) - septicemia: generally too late (endotoxemia) - mastitis: milking out + metacam Vax of pregnant cow combo with rota to prevent newborn diarrhoea

Answer 24

A) FIRST WEEK - ACUTE IMPORTANCE OF COLOSTRUM AND HYGIENE!!! Coli septicemia - septicemic strain, survive in blood - no exotoxins! - sporadic, common - low colostrum/naval disinfection --> PO/naval infection -> pharynx lymphoid tissues or via gut -> blood -> septicemia, endotoxin effect - general + tachycardia, pneumonia, arthritis, meningitis, postsepticemic localization in the joints - acute, death within 2 days Pm: hemorrhages, enlarged lymph nodes, polyserositis (fibrinous) Isolation from blood, PO Generally too late for treatment Coli diarrhoea - enterotoxigenic - widespread, common - end of winter, large scale farms - Clinical signs: NO fever! anorexia, depression, diarrhea (yellow, stinking), dehydration, death within 1-3 days o In case of sufficient colostrum supply, the clinical signs are milder - Pathology: exsiccosis, liquid accumulation in the gut, stomach and gut are filled Colistin, enroflox, neomycin + re-hydrate Ddx rota Induvidual cages!! B) WEEK 2-8 - CHRONIC Calf dysentery: - verotoxigenic, damage endothel cause bleeding, edema - common asympt in older Destroy villus and produce verotoxins damageing endothel --> CHRONIC, haemorrhagic diarrhoea, spontanious recovery or death Bacteriostatic AB!! Kill releases more toxin... PUBLIC HEALTH IMPORTANCE! - (of calf dysentery) - Cattle is the most important source of this bacterial strain! 1-3% carry - PO, fecal contamination - Lethality 5-10% in children, 5-50% in elderly

Answer 25

< 10 DAYS Diarrhoea of newborn - worldwide, large scale farms, Enterotoxogenic strains - More frequent in litters of first farrowing sows (piglets of young sows) - colostrum! - pathogenesis, signs, pm like calf... - ddx: necrotic enteritis of suckling perfringens C), TGE, rota, coccidia - treat whole litter - mix 1st farrower and old sows before farrowing to boost colostral immunity - vax sows! Inactivated POST-WEANING (28D?) Coli diarrhoea of weaned piglets - Mostly enterotoxigenic strains! (Sometimes Verotoxin, cytotoxic necrotic factor producing) - fimbria stop binding after 10 of life, but after weaning a new fibria receptor is present - F18ac --> susceptibility is INCREASING with age!! - Pathogenesis like piglet/calf, BUT WEANING SPECIAL ... - changes in the gut flora - increased susceptibility to the F18 fimbria - -> causes shortening of the microvilli - overeating (high protein), insufficient production of enzymes(gut not ready), - slow peristaltic movement -> gastroenteritis Signs - seen 1-2w post weaning. - Diarrhea (watery, smelly with undigested protein), purplish discoloration of areas of the skin - VTEC, CNF producing strains – hemorrhagic feces - decr gain, uneven stock Pm gastritis and enteritis, enlargement of mesenterial lymph nodes (Filled GI, exciccosis in neonatal) Diagnosis - hemolytic E coli of F4 (both diseases), F18 (only weaner) -> blood agar!! Prevent overeating - gradual, fiber, ab, rehydration, stress Vax not really used... prev yes we use.

Answer 26

Avian pathogenic e coli strains (APEC) - invasive e. Coli strains, virulence variants! - predisposing like normal, infectious - mycoplasma! Infection: GENERALIZED - Embryonal infection (germinative, contaminated eggshell) – dead or weak chicken will be hatched - PO -> gut -> septicemia! LOCALIZED - Inhalation (hatchery) – replication in respiratory airways, local lesions (air sacculitis) - Percutaneous: cellulitis Replication in the gut -> septicemia -> endotoxin effect, parenchymal organs, endothelial cells, serous membranes inflammation, death Septicemia RESULT - Young -> endodoxin effect ->death - Grower, adult -> pericarditis, perihepatitis, airsacculitis, arthritis - Hen -> coli-granulomatosis -> liver&gut -> inflammatory granuloma around E.Coli - Death SIGNS: Day old - omphalitis, delayed absorption of the yolk sac, diarrhea, death --> enteritis, hemorrhages, fibrinous pericarditis Older - resp, general septicemia, arthritis, cellulitis --> fibr seroritis, granulomas skin/ovarium/gut, signs of septicemia (haemorrh, enlared PO) We isolate from BONE MARROW! Ddx newcastle, Infectious bronchitis Ab in drinking water; colistin Mycoplasma: tiamulin oxytetracillin

Answer 27

TYPHOID - typhisuis, chronic, growers-finishers, large int, stamp out PARATYPHOID - cholerasuis (murium, derby), acute/generalized, grower-finisher, small int, treatment! TYPHICOLITIS - typhimurium, acute I think, growers-finishers, treatment! Growers, finishers! A) SWINE TYPHOID - typhisuis, obl pathogen, only swine - rare due to eradication, chronic, growers/finisher - obl pathogen, but good management decr losses! Not present normally --> introduction needed (fecal contamination or animal) - long presence in the farm/herd -> slow spreading, chronic disease Oral infection, get into LARGE intestine -> replicate in lymphoid patches -> inflammation, necrosis of the mucous membrane and ulcers get into the gut wall and to the mesenterial lymph nodes -> blood stream - Parenchymal organs -> focal inflammation and necrosis = typhoma in lungs, spleen, liver, kidney etc. - Carriers and shedders for a long time, practically life long SIGNS - Chronic and slow, weight loss, anorexia, diarrhea (watery, yellow, stinking), abdominal pain, increasing cough(!), decr growth PM - Large intestine have enlarged lymphoid patches, ulcers (crater-like), fibrin between bowels, sometimes the bowels are attached to each other - Lungs have grey and congested areas, focal inflammation and necrosis on organs and tonsils DIAGNOSIS - Quite typical - diagnosis on spot! - aetiological - Antigenic structure is identical to S. cholerasuis, must do serotyping! (PCR) => also means we cant use serological tests... Treatment: ab Reduce signs but WONT TREAT!!! Not good to treat, stamping out better. May use to stop diarrhoea bf slaughter Stamp out - Obl pathogen - diagnosis of swine typhoid, closing herd asap! SWINE PARATYPHOID - cholerasuis (from swine), typhimurium, derby (from environment), fac pathogen - More common, acute-generalized, in grower-finisher No introduciton needed, but need predisposing for fac! Per os infection -> SMALL intestine, cause inflammation -> blood => septicemia -> parenchymal organs - Incubation period of 2-3 days SIGNS 42C fever, anorexia, depression, cyanosis, diarrhoea (yellow, creamy, watery) - if survive acute --> chronic phase: - pneumonia, cough, tenosynovitis (lame). (Typhi signs similar - both general, diarrhoea and resp! PM Acute - cyanosis, hemorrhages, hyperplastic spleen, enlarged lymph nodes, gastroenteritis (small Int.) - Liver - focal inflammation and necrosis (histology) Chronic (typhoid only chronic) - necrosis of mucous membranes of the gut (small int.), ulcer of lymphoid patches, sometimes ulcers in large intestine (typhoid - large intestines!) Should do aetiological - serology not widely used (crossreactions typhisuis) Here we can treat (this is general salmonella!) - (TTC) - herd, in water, well abs from gut!! - salmonella will still be carried after ab! Predisposing is imp! - vax imp - give protection from signs only! - eradication! Tricky but important TYPHICOLITIS OF SWINE - typhimurium (environment), - More common, acute disease(?) - growers, finishers, - 100% morbidity, 4-5% mortality - necrotizing enterocolitis, typhilitis --> yellow, watery, bloody diarrhoea! May be mucoid. (Here both SI and LI?) - Predisposing, rodents/bird. (Introducers) - no vax ASYMPTOMATIC CARRIAGE OF SALMONELLA BY SWINE - (typhimurium, derby) environmental - predisposing - human health impact, testing! Importance of keeping sero+ low! - rare signs, treatment wont stop shedding, predisposing!! ERADICATION - Aim: reducing infection below 1% and reach free state - Control of eradication - -> Bacteriological examination of ileocecal lymphoid tissue and slaughtered pigs, examination of antibodies in meat juice - Free: examination of the feces of EACH ANIMAL!, two bacteriological negative results with interval of 1 month (before slaughter) - Eradication, reduction in Denmark - -> Surveillance of blood, feces and meat juice, hygiene alone is not enough, nutrition (pellet, barley, dry/wet feed), introduction of animals only from negative herds, eradication can be reached with depopulation

Answer 28

Obl pathogen Pullorum: till 2-3w, Gallinarum: Grower/adult --> minor differences, main ags are identical! We talk about them as a collected disesase (some countries separates them) - used to be common (large farms), now sporadic (small farms) due to eradication (like swine typhoid) Most bird spp susceptible (chicken!!!) Infection: germinative, aerosol in hatchery, PO - feces, waste, dead eggs, fomites, RED MITES (blood sucking), infected animal, semen First vs second peak! Double mortality: vertical (death d 2-5), then horizontal (death 21-28d). Influenced by: first curve: grade of infection, second curve - management and treatment!! --> Massive or sporadic mortality - depending on circumstances... Young (I think) - PO infection -> gut -> blood -> Generalization - Germinative -> Embryonic infection -> death, weak chicken with omphalitis (will die in first days of life) Grower, adult (I think) - Oral or aerosol infection -> gut, septicemia, parenchymal organs (heart, ovary) -> focal inflammation, necrosis - -> All follicles always heavily affected in ovary - salmonella will always get to next generation... rooster infected too - and spread via mating - Long bacterium carriage! SIGNS Eggs - hatching % decrease, death increase Chicken - weak chicken, omphalitis, decr absorption of yolk. - "White diarrhoea" - febirle animals has incr production of uric acid -> white layer on feces! - Dyspnea, arthritis (leg, wing) Growers/adult - chronic arthritis and movement problems - atrophy and rupture of ovarian follicles -> peritonitis, diarrhea, - -> in egg prod., (weight loss, anemia => rare, but can happen in final phase) PM Chicken - Unabsorbed yolk, - focal inflammation & necrosis (typhi) in the heart muscle, lungs, liver and spleen, enteritis (hemorrhages, fibrin) Growers/adult - Focal inflammation and necrosis(typhi) in lungs, liver and spleen, - heart muscle necrosis, - enlarged lymphoid patches with ulcers, - atrophy of the ovaries Isolation from BONE MARROW! Plate aggl on farm if suspiscion (typical with the double peak, ab since born bc germinative!) ERADICATION - Eradication -> elimination of infected herds, disinfection of eggs, - selection (test & slaughter): cage birds, zoos - Isolated keeping of disease free stocks, only eggs from disease free flocks allowed to be hatched Maintaining free state: - in beginning of laying period, 2x plate agglutingation (full blood with stained antigen) - examine dead birds - bacteriology Europe is free from = no vax!

Answer 29

S. enteritidis, S. typhimurium, (S. infantis, S. hadar, S. Virchow) - -> non-host adapted! Human issue! - disease only in young, mostly these are carries, causing an issue for further spread to humans (AND other animals too) - worldwide, common, facultative - management influence shedding and spread! - UNDER 2w (4) --> disease of young!!! - Wild birds and rodents - Non infective: transport, management, stable, hygiene, mycotoxin - Infective: infectious bursitis, duck hepatitis, Derzsy-disease (complication), coccidiosis germinative, PO, aerosol (hatchery, feed) -> gut -> blood -> parenchymal organs, septicemia - Chronic (pigeon) -> wing arthritis in pigeons and cage birds (Typhoid: - Oral or aerosol infection -> gut, septicemia, parenchymal organs (heart, ovary) -> focal inflammation, necrosis) Signs: chicken like fowl typhoid, adult asympt, egg drop in prod! (Pigeon - diarrhoea, CNS, arthritis) Pm like fowl typhoid Diagnosis trickier, fowl typhoid easy to detect, while these we see in low amount from environment, and harder to culture. PCR is not good bc does NOT detect infection. Exclude convalescent herds from breeding, insect and rodent control, probiotics (restore bact. flora) - Vaccines -> S. enteritidis & S. Typhimurium, live and inactivated vaccines in breeders and layers!! - Eradication / reduction

Answer 30

Paratyphoid infections caused by non-host-adapted Salmonella are of public health significance because of contamination and mishandling of poultry products. S enterica Enteritidis, typhimurium is a major food safety concern in the egg-laying industry. Fecal contamination of the eggshell is the main mode of transmission from breeders to progeny, although S enterica Enteritidis is also transovarially transmitted. Meat contamination in slaughterhouse fecal. S. infantis (60%) strong ab resistance, long carriage, S. enteritidis (5%), S. typhimurium (3%) - these are imp! Low bc preventative measures! Paratyphoid v imp!!!) Aim of eradication/reducion: - S. enteritidis, S. typhimurium, (S. infantis, S. hadar, S. Virchow) - Breeding hens: all these 5 serovars <1% - Commercial laying hens: S. typhimurium, S. enteritidis <2% - Broiler: S. typhimurium, S. enteritidis: <1% - Turkey: <1% PREVENTION - Probiotics, vaccines, eradication/reduction CONTROL OF CARRIERS Breeding flock - check as much as possible!!! Germinative to layers and broilers, fecal contamination!! We want to test as much as possible. - farmer: first 5days do pm (10-60 birds), first 4w of laying we do boot samles and dust samples, every 2w of laying we test feces and dead eggs! - official: first 4 weeks of laying, middle of laying, last 8 weeks of laying (the important one...) Laying flock - egg to consumer! - farmer: first 5 days we do pm, 2 weeks before laying: feces (2 pairs of boot samples), every 15 weeks - Official: one flock/farm if farm size is >1000, 2 pair of boot samples + dust Broiler - slaughter machine isnt adapted to the different sized birds, guts can rupture and machine can spread bacteria to other birds. - Farmer – within 3 weeks before slaughter (only salmonella free birds can be slaughtered) PREREQUISITE(!!) (imp one) - Official – once 10% of farms/year if herd size is >5000, 2 pairs of boot samples PUBLIC HEALTH SIGNIFICANCE Usually we see salmonella gastroenterica - food poisening, carriage but no sign spread Rarely sepsis (cholerasuis, dublin, typhimurium) Rarely focal infection: colonization certain places eg Endocarditis, pericarditis, pneumonia, meningitis etc. Rarely enteric fever - similar to typhus! Give ab if septicemia, not needed in food poisening. Heat treat food!

Answer 31

Used to be common! Now due to good vax we rarely see signs.. but infection is present still! 2 pathogens must be present: - toxin producing B. Bronchiseptica: Dermonecrotoxin producing, widespread, found asympt often! - toxin producing p. Multocida D/A: Also dermonecrotoxin producing, but not so widespread, only found in infected herds, need to be imported by infected pig/other animal transport, mixing, quality of AIR in stable (humidity, NH3, dust, temp), overcrowding Clinical forms: - progressive (more severe clinical signs) - non-progressive form (milder) - Great economic impact, generally not lethal (gains, feed conversion rate...) eg. Shortening of maxilla, The teeth doesnt line up - chewing is abnormal - may explain poor feed conversion!! We ONLY se signs if infected as suckling piglet!! Otherwise carriers. 1. bronchiseptica - Mild damage of mucous membrane and turbinate bones by toxin. Recover. 2. mutocida D/A The prev. Mm damage is needed, the attachement of multocida isnt v good, need help! Then necrodermatotoxin prod prossible! Dermonecrotoxin inhib the osteoblasts, osteoclasts are still working, while osteoblasts not --> atrophy!! - inflammation of the mucous membranes of the nasal cavity, atrophy of turbinate bones, nasal septum, ethmoid bone, absorption of the turbinates -> deformation of the nose - Turbinate Filtration function important! Bacteria, fungi, spores...---> agents can now get directly to lungs, so pneumonia is common to find in AR aswell! SIGNS (takes time for signs to appear!!) - Piglets of 1-4 weeks -> rhinitis, nasal discharge, sneezing, blood present in the nares (stop here if no multocida) - Above 3 months of age -> block of lacrimal channel (as a result of distortion of the bones) and the skin around the eyes will be wet, deformation of the nose, wrinkles on the nose (if replication is happening on both sides of the nasal cavity) Pm - not deadly, but would see the lesions described. Diagnosis Typical pm but hard to spot - carcasses are halved in slaughterhouse! (Transverse to see...) - need to detect toxin with PCR to confirm! From nasal discharge. Treatment - only suckling with TTC.. but not really, damage already will be made if bacteria has replicated... Prevention! (Colostrum!! Suckling are infected!) - keep older sows in breeding for better colostrum! - shedding - dont breed infected animals! - toxoid vaccines! (Pregnant sow 2x in last month of pregnancy --> colostrum) (US they vax piglets but not so good, more animals must be vaxed, and young immune system...) ERADICATION - carrier animals must be eliminated! - SPF! (Specific pathogen free farms)

Answer 32

Acute(endotoxic effect) vs. Chronic, Temperature, water, exponential mortality, growers-adult OCCURRENCE, ETIOLOGY AND EPIDEMIOLOGY - Caused by P. multocida A (D, F) - capsule: polysaccharide, outermost layer -> hyaluronic acid capsule - Serotypes, different frequency, facultative pathogen - Virulence variants: High: acute fowl cholera; Low: mild, chronic or asymptomatic - Susceptibility INCREASE WITH AGE: turkey, duck, goose, hen (more resistant, high virulent strains must be), wild living birds, - Occurs in GROWERS and ADULTS - More common in warmer climate, summer or late autumn and in waterfowl, sporadic in moderate climate (better spread in warm) - typical epi curve: exponential ! D1 40 dead, 2nd 400, 3rd 4000, 4th all dead ... Differences depending on virulence A) Virulent strains -> cause ACUTE fowl cholera - introduction to the farm is necessary by convalescent - long shedding + predisposing = High morbidity and high mortality (if no treatment - exponential mortality) B) Less virulent strains -> CHRONIC forms, asymptomatic carriage (can be present in the farm normally) - Resistance is low in pasturella, but water transmission, short distances in excretes/feces can spread indirect! - Bacterium is present on mucous membrane of resp. tract or lymphoid tissues of the gut - Source of infection -> discharge from carrier animals, instruments, water (other hosts(mm), humans even!) - NO germinative infection! - Convalescent animals remain carriers - Predisposing factors (Primary pasteurellosis) - -> Stress, featherpecking, forcefeeding, transport, grouping, other stress, warm weather, temperature fluctuations PATHOGENESIS - Airborne or oral infection -> colonization of the upper respiratory epithelium - If predisposing effects -> see clinical signs Acute Septicemia: (virulent strain) o Endotoxin effect (from endotoxins released from the lysed bacteria): damage of blood vessels (increased permeability = hemorrhages) and will activate the coagulation cascade -> thrombocyte aggregation, release of procoagulants, formation of thrombi (focal necrosis - result of both bacterium & thrombi) o Elevation of corticosteroids, endotoxin shock (reason for death) Chronic (lower virulence) - arthritis, tendosynovitis, bursitis, inflammation of the upper respiratory tract and infl. of the comb and wattles - hide in the joint from abs CLINICAL SIGNS - Incubation period of 1-5 days (depend on predisposing Factors) - Peracute: dont see much other than death - Acute: Fever, anorexia, depression, diarrhea (sometimes with blood), nasal discharge, sneezing, drop of egg production, CONJUNCTIVITIS - Chronic - weight loss, LAMENESS, upper respiratory signs, diarrhea, fibrinous otitis media + bone (CNS signs - ataxia, stargazing), inflammation of the wattle (enlarged, warm and hyperemic) PATHOLOGY - Peracute maybe some haemorrhages - Acute Hemorrhages (serous membrane), hemorrhagic enteritis, fibrin in the gut, focal inflammation and necrosis in the liver (later also in other parenchymal organs), peritoneal fluid in the abdomen, fibrinous pneumonia, spleen is generally normal (sometimes enlarged) - Chronic o Focal inflammation and necrosis in the liver with fibrinous perihepatitis, salpingitis, fibrinous inflammation of the skull bones/otitis media (cranial pasteurellosis), arthritis, tenosynovitis and bursitis DIAGNOSIS - Due to exponential death curve - fast diagnosis is crucial! - Smear is fast: loads of G- bipolar bacteria, most used is isolation (takes a day) and then we can also check the ab sensitivity v imp!! Then treat ASAP! Ddx: Sudden death of loads - toxicosis!! Ddx other septicemic/Resp, main pm is the focal inflamm and necrotic lesions of liver - must ddx!! TREATMENT & PREVENTION - Immediate Antibiotic treatment -> Potentiated sulfonamides, Tetracyclines, Macrolides, Fluoroquinolones o Mainly per os (septicemic!, if parenteral treatment - can transmit infection with needle) o Elimination of the predisposing effects will increase efficacy of antibiotic treatment! - Prevention of introduction of a virulent strain - isolation, closed herd, rodent control, give tap water! - Movement restriction in the case of fowl cholera, risk of keeping convalescent animals - Prevention of predisposing effects - Vaccines o Inactivated vaccines (Europe only inactive) multivalent => contain most frequent serotypes present in an area, at 6-8w (grower - adult!)

Answer 33

Same family: Weeksellaceae A: ducklings >2m, no germ of importance, generalized, serous membrane, green feces OR: turkey, broiler growers, no germ, mainly localized resp, sinusitis, mucous Infectious serositis //rimiella anatipestifer - Large flocks, facultative - predisposing, - loads of serotypes, virulence var... - many birds susceptible but most severe in ducklings under 2m - LARGE SCALE DUCK FARMS. - like fowl cholera: Low resistance - mm and survive in water. Long shedding. Wild bird spread. - germ no importance here. (Vs. Cholera no germ) Infection airborne, P.O. or via wounds -> predisposing effects -> septicemia -> damage of the endothelium causing increased permeability, coagulopathy - Precipitation of fibrin, lesions in parenchymal organs, inflammation on serous membranes of the abdominal cavity and mucous membrane of resp. tract -> DEATH (but no exponential here..) CLINICAL SIGNS - Peracute - younger than 2 weeks, sudden death - Acute (v similar to fowl cholera) - anorexia, depression, diarrhea (watery, GREEN), sometimes with white uric acid crystals), nasal discharge, sneezing, conjunctivitis, CNS signs (ataxia, spasms) - Chronic - Stunting, the herd splits up, serous arthritis, fibrinous-purulent conjunctivitis, lacrimation, SINUSITIS (also similar to fowl cholera, but bursitis, wattle) PATHOLOGY (v similar fowl cholera!) - Hemorrhages, fibrinous serositis, perihepatitis (vs. Focal in fowl cholera), air sacculitis and meningitis - Fibrin in the abdominal cavity and in the pericardium - Sinusitis, fibrinous enteritis, arthritis Mostly acute disease no serology - isolation yes! Ddx: fowl cholera, duck hepatitis, duck plague, mycoplasmosis, ornithosis, borrelisosis, salmonellosis ORNITHOBACTERIUM RHINOTRACHEALE - Growers (no germ) - broiler, turkey - (farm mammals, wild birds) - facultative, many serotypes, - low resistance, need predisposing - Young - peracute, acute, older - asympt No predisposing, no disease.. o Non infectious: overcrowding, warm, accumulation of NH3, ventilation problems o Infectious: pneumovirus, lentogen NDV, infectious bronchitis(corona), mycoplasma, chlamydia Airborne infection, colonization of the upper airways -> predisposing factors -> Inflammation of the upper airways -> sinusitis, edema, tracheitis, air sacculitis, production of large amount of STICKING MUCOUS (will block sinuses and trachea -> cause of death = suffocation (similar to ILT, pseudomemb), sometimes pneumonia - Mainly limited to the airways, rarely cause septicemia -> brain and joints (then may look like anatipestifer and fowl cholera!) CLINICAL SIGNS - Peracute - depression, dyspnea, SUFFOCATION (due to mucous) - Acute - nasal discharge, lacrimation, respiratory signs, shortness of breath, swollen head, SINUSITIS, suffocation - Layers - respiratory signs, drop in egg production, thin and striated eggshell PATHOLOGY - Nasal cavity and trachea covered by thick mucous and fibrin, swollen mucous membrane with hemorrhages, pneumonia, fibrinous pleuritis, air sacculitis (serous, fibrinous) Typical, but must detect agent! Ddx: Infectious coryza, ILT (Infectious laryngotracheitis, herpes), TRT (Turkey rhinotracheitis, pneumovirus, paramyxo), mycoplasmosis, fowl cholera Predisposing factors!!

Answer 34

Franciella tularensis. (Franciella fam + genus) First seen in norway in 1653(lemmen fever) - G- cocci, resistant in environment, - Mainly in northern hemisphere!: o Subsp tularensis 􏰘 northAmerica, highly virulent o Subsp. HOLARCICTA 􏰘 NorthAmerica (beaver, muskrat), Eurasia (wild hare, small rodents) o Subsp. Mediasiatica 􏰘 middleasia o Subsp. Novicida 􏰘 North America, Australia - mainly rodent and wild hare (european brown hare) in europe (but super wide host range, bioterrorism) - zoonosis! Domestic rabbit not susceptible. - importance in spread to farm animals: Clinical signs appear in sheep, horse and piglet (ru(Not bo?) abortion, rodent and wild hare!) - Uniform, tricky to culture. (Francis blood agar) - Decent resistance; carcass, soil, water, tick (biological vector! Rest is mechanical). - Natural focal infections, size of the rodent population influence the number of human cases - Maintenance btw bloodsucking - wild rabbit and bird. (Vs tick, rodent, bird in q-fever) - Shed with URINE Either acute septicemic (tular-emia) of chronic disease (mostly in europe) - inflamm necrotic foci in parench (similar to primary pasturellosis!) organs. Can be lethal. Po/arbo/inhalation (urine) --> (fac ic) macroph --> ln --> septicemia --> POrgans Long immunity! CLINICAL SIGNS Ssp. Tularencis (acute disease - clinical signs) ssp. Holarctica (asympt. or mild chronic infection) - in europe! - In endemic areas, infection of farm animals are frequent, but clinical cases are rare - Clinical signs appear in sheep, horse and piglet; dog, cat, swine and cattle have seroconv. w/o clinical signs - Fever anorexia in sheep and rodents, rodents also get general symptoms with fever and death - Ruminants (not cattle?) will have abortions, and the European brown hare weight loss and weakness PATHOLOGY - Enlargement of spleen and lymph nodes, inflammatory and necrotic foci in parenchymal organs - European brown hare - macroscopic lesions in lung (80%), pericardium (28%), kidney (20%) Eg a lot of sheep affected, loads of ticks - think of this! Serology - many animals, tube agglutination test presumptive diagn --> can confirm serologically if paired. Isolation of agent - tricky culture, fastidious --> special media. Can aslo use pcr Subspecies detection by serology, 16s rna gene (PCR??) Ddx: Rodentiosis, Brucellosis Ab if early - streptomycin, TTC - Serological examination of European brown hare before export, killing of seropositive hares, hunting of European brown hares - Protection from ectoparasites (removal of ticks) - Prevention of hunting of dogs and cats in endemic area - No vaccine is available for animals Hu: infection from ticks, rodets, or european brown hare - ulcerogaldular, oculoglandular, oroglandular or septic/pulmonary form. (Skin, conjunct, vomit/diarr, pneumia) - there is vax for human!

Answer 35

Post weaning, after maternal, lung (marble) cytotoxin; alv macr for repl, endothel - thrombus - necrosis. Resp, cyanosis, bloody/foamy nasal discharge. Chronic - decr gainz A. Pleuropnumonieae - Common, high economic impact! - 2 biotypes: 1 NAD is needed, 2 doesnt need. - virulence factors: 4 cytotoxins: adhesins, capsule, outer membrane proteins, LPS! - -> virulence var depend on combo of these! - 19 serotypes! 16 detected by hungarian - on mm, low resistance, G- - only pig susceptible - must be introduced with carrier pig - after 6-8w due to maternal ab Predisposing factors o Quality of air, nutrition, overcrowding, mixing, ventilation, mycotoxins o Infective agents circovirus, PRRS, mycoplasma, Pasteurella - Difference between biotypes o 1 - high virulence - high morbidity and high mortality o 2 - low virulence - low morbidity and low mortality Aerosol infection by inhalation -> colonization of the respiratory tract - Predisposing factors -> replication in the lungs o Cytotoxins damage the alveolar macrophages causing release of cytokines, which will help the replication of the bacterium --> pleuropneumonia! - Also damage endothelial cells, result in microthrombi -> block blood vessels -> necrosis - Sometimes (rare) hematogenic spreading to kidney, brain, joints (cause local clinical signs) - Remain carriers after recovery CLINICAL SIGNS & PATHOLOGY - Peracute - fever, depression, cyanosis, respiratory signs - death - Acute - fever, cyanosis, labored breath, dyspnea, nasal discharge (blood, foam (due to incr. breathing rate) - Chronic - respiratory signs (mild), decreased production (weight gain), sometimes returning cough Pathology - both biotypes cause same lesions PM, so cannot differentiate! o HAEMORRHAGIC-NECROTIC pneumonia, foci, most typically in the diaphragmatic lobe! - Have a mottled, marble-like appearance due to the different lobes are in different phases of the disease o FIBRINOUS PLEURITIS on surface of the lungs o Chronic - demarcation of lesions o Histopathology - strong cellular infiltration, elongated nuclei in alveoli (due to cytotoxic effect) Dont need aetiological - typical!! Detection of antibodies against APxIV - 4th cytotoxin (only produced by A. pleuropneumoniae), Specific, good for screening to be sure its actinobac pleuropn Macrolides concentrate in the lung!! But remain carriers after treatment... - Prevent introduction, prevent predisposing factors - Vaccine 􏰘 inactivated bacteria (type specific protection), TOXOID (inactivated cytotoxins and surface proteins = wider protection), recombinant vaccines - Eradication (with ab, not allowed anymore?) 􏰘 selection + antibiotic treatment, generation shift + antibiotic treatment, herd replacement

Answer 36

Hemophilus, G-, mm, poor resistance - 11 serotypes - Found on mm (resp bo, genital sheep), poor resistance, close contact needed for infection, invades with predisp factors - management! BRDC predisposing! o Non infectious: shipping, cold, overcrowding, nutrition, quality of air o Infectious: adenovirus, IBR, PI-3, BRSV, mycoplasma Aerogenic/PO -> repl in resp tract (BRDC) and enter blood, where it can cause necrosis, vasculitis, inflmamation, and thrombi in CNS, JOINTS, LUNG and FOETUS. In sheep mostly infected SEMEN can colonize mm and cause ascending infection (orchitis, epididimytis CLINICAL SIGNS Cattle o Respiratory signs: fever, nasaldischarge, laboredbreathing o Arthritis o TEME: thromboembolic meningoencephalitis -> SOMNOLENCE (h somni), spasms, ataxia, forced movements o Abortion, endometritis, infertility, mastitis Sheep - young rams: orchitis and TREepididymitis, rarely generalized signs (Young full of energy,jump eachother, spread!) PATHOLOGY - Cattle o Pneumonia - sero-fibrinous inflammation in anterior lobes, pleuritis o TEME: hemorrhages, hemorrhagic-necrotic foci in the brain o Blood vessels: thrombosis Sheep: epididymitis and orchitis (Huge testicles!!!) - Give ab for pneumic form (macrolides?) - vax pregnant cow and calves 2x each. Inactivated.

Answer 37

BORDETELLA FAM - upper resp of birds and mammals - short G- rods - survive in environment some weeks - antigens: flagella, capsule, fibria - virulence factors: capsule, fimbria, HA, exotoxins: 1. Adenylate cyclase -> responsible for clinical signs 2. Tracheal toxin: inhibits ciliary action, kills ciliated cells 3. Dermonecrotoxin: induces skin necrosis, impairs osteogenesis 4. Osteotoxin: toxic for osteoblasts (only osteoclast action... atrophy) ``` B. bronchiseptica: o Pig: swine atrophic rhinitis o Dogs: part of kennel cough o Kittens: pneumonia o Horses: resp. infections o Rabbits: upper resp. infections, pneumonia o Lab rodents: bronchopneumonia ``` B. avium: turkey coryza BORDETELLA BRONCHISEPTICA - Primary (part of normal flora of upper resp tract) - Secondary (virus, bacterium - mixed infections) EPI - carrier animals maintain in nasal mm! - predisposing! - resistance: survive in environment, water (if prevent dehydration) few weeks & discharge - mammals are susceptible! PATHOGENESIS airborne (PO) and Predisposing factors (only clinical signs if these present!) --> Upper airway (adhesin attaches) -> Toxins -> rhinitis, bronchitis, bronchopneumonia, conjunctivitis, LONG carry SIGNS Swine: toxin producing strains, see in young piglet until 8 weeks old 1. Atrophic rhinitis (REVERSIBLE until multocida...), bloody, nasal discharge 2. Bronchopneumonia: day old piglets - nasal discharge, cough, dyspnoe 3. Secondary infections: Mycoplasma hyopneumonia, Pasteurella, Actinobacillus Dog: 1. Young: kennel cough (canine infectious tracheobronchitis) - canine adenovirus 1-2, C. parainfluenza-2, C. distempervirus, C. herpesvirus-1 2. Adult: Secondary to distemper --> bronchopneumonia Cat: sneezing disease - Secondary infection (calici virus, infectious rhinotracheitis, chlamydia, mycoplasma) - 2-10 weeks, alone: nasal discharge, sneeze, cough, conjunctivitis Rodents: - Overcrowd, young: conjunctivitis, pneumonia (with pasteurella multocida) DIAGNOSIS - must diagnose the predisposing infectious... many - TTC - vax: inactivated/live avaliable! AVIAN BORDETELLOSIS Turkey coryza - B. Avium. (Rhinotracheitis) - On mm of turkey and other Av.. - Widespread in major turkey producing regions (USA, Canada, Oz, Germany, GB, France, Israel, S. Africa) o Good resistance, facultative pathogen (like before) - same virulence factors as mammals! - mostly 2-6w turkey (but older too...) - super contagious! Infection is spread through direct contact with infected poults (or litter, drinking water) - High morbidity, LOW MORTALITY - predisposing! Noninfectious/infectious! PATHOGENESIS PO (drinking water), by inhalation, colonise & replicate in airways (resp epithelium) o Cytotoxins: Damage of the epithelium, inhibition of cilia, damage of the tracheal cartilage - Generally limited to the respiratory tract (septicaemia rare) - Sometimes generalisation in turkey: dermonecrotoxin SIGNS - general signs, stunting, sneezing, CONJUNCTIVITIS, eye/nasal discharge, beak breathing, altered vocalization - Mucous accumulated in the nares with swelling in the submaxillary sinuses, SINUSITIS, PERIORBITAL EDEMA - Older turkeys: dry cough - Signs begin to subside after a course of 2-4 weeks PM - mucous in the upper airways, TRACHEITIS (flattening, COLLAPSE), pneumonia, complications - Nasal and tracheal exsudates (initially serous, then tenacious and mucoid), tracheal lesions (softening and distortion of the cartilaginous rings, dorsal-ventral compression and fibrinomucoid luminal exsudate) - Cilia associated bacterial colonies DIAGNOSIS - Isolation and identification of B. avium from tracheal mucosa: swab sample, MacConkey agar, early course of infection, pure culture can be obtained from trachea - Virulent strains can haemagglutinate guinea pig RBC (can use to check virulence of strains isolated) Can try TTC early, but most cases wont help much (toxin prod), and remain carriers too... We give modified LIVE vax for mucosal protection at 3w of age. Inactivated to breeder hens BARTONELLOSIS ``` 1 - B henselae: cat, Ho: bacteria live in blood of cats -> Cat scratch disease --> Bacteria alive in flea faeces 2 - B Quintana: (cat, dog) Ho 3 - B bovis: Bo 4 - B vinsonii sbsp berckhoffi: Ho, Dog ``` - prev regarded as rickettsia! - Repl in RBC - Spread by ARBO mechanically, self limiting, mild or asympt. Arthropod bite -> replicate in endothelial cells􏰀bacteremia replicate in RBC􏰀generalised infection􏰀Persistant infection (frequently asymptomatic) B bovis: Cattle: asymptomatic, endocarditis B vinsonii sbsp berkhoffi Dog: lymphoadenitis, sometimes endocarditis in human B henslae: - Cat: asymptomatic, sometime endocarditis (persists!) - Human: cat scratch disease, vesicles -> papules -> pustule -> lns -> conjunctivitis, parotitis, muscle aching, CNS Blood smear! Isolation tricky Doxycycline, still carry... Incecticide, disinfect wound!

Answer 38

GENERAL - CHRONIC - female - abortion in the last trimester (ND! Zoon.!) - Male - epididymitis and orchitis - Zoonosis and notifiable disease! (Except.: B. ovis!) - Brucellosis has significant economic impact, mortality isnt significant (exc abortion obviously) - Brucella spp tend to infect specific animal species. However, most Brucella species can infect other animal species as well. - Brucellosis in cattle (B. abortus) in sheep and goats (B. melitensis) and in swine (B. suis) are diseases listed in the OIE. - koster stain: modified ZN brucella (abortus, melitensis, suis) red, other blue! (Ovis, canis + other) - fastidious culture: blood agar (+yeast and Bvit. B!) - fac IC - antigenic structure, in cell wall we have A and M polysaccharide, different predomination! Mel - A, abort - M, suis - both - crossreactions: Melit-abort-suis + ovis-canis + crossreactions with yersinia enterocolitica! Average resistance - in tissues, protected! But cannot tolerate disinfection! - Brucellosis is a highly infectious zoonosis for humans. The spread to humans most often occurs by drinking raw milk from infected animals = Human brucellosis is best prevented by controlling the infection in animals! - Pasteurisation of milk from infected animals is an important way to reduce infection in humans. Brucella is shed in milk, foetus, genital tract discharges! B. SUIS - Eradicated in europe, persists in wild swine (PROBLEM) - biotype 1, 2, 3 cause disease, - 2 in wild boar and hares in europe(!), (4 arctic in north america and russia, 5 in russia.) - wild boar/dogs, fomites, mating --> PO or veneral infection. --> genital tract, vertebral abcess - sow - abortion, disch, temporary infertility - boar - excrete in semen -> orchitis, sterility, Lameness, incoordination, posterior paralysis (vertebral abscess, fractures) PATHOLOGY - Fetus - edema of fetus and fetal membranes, small hemorrhages, maceration, mumification - Sows - necrotic foci in the uterine wall, - Boars - enlarged testicle, inflammatory necrotic foci - Lesions in bones and joints - vertebral body deformities Isolation, herd serology (slide agglutination) - no treatment!! - herd replacement as eradication!! - Control of import of susceptible animals, examination of abortion cases, serological survey of breeding boars in each 6 months, serological examination of sows in each year - Keeping wild boars away from swine herds!

Answer 39

B. Abortus, melitensis, suis. - Well controlled in eu, eradicated most eu countries. - Asymptomatic animals (horse, dog, cat) introduce or milk, fomites. - Btw animals it spreads from placenta, foetus/fluid, vaginal discharges. - Acute abortion outbreaks occur mainly after 5m of pregnancy - several newly infected cows - abortion storm! New animals - new abortion storms.. - Shed lifelong. Infection P.O. (ingestion), or through broken skin/mucous membranes of genital organs (venereal contact) - Settle down in the regional lymph nodes 􏰀 carried in macrophages to blood stream 􏰀 septicemia within 2-3 weeks 􏰀 settle down in predilection organs (pregnant uterus, placenta, udder) 􏰘 necrosis in chorionic villi, abortion, fetal membrane retention Shedding: - Uterine discharges after abortion: 2-4w - Brucella eliminated from the uterus after about 3 weeks, but they survive in the UDDER, lymph nodes, joints, tendon sheaths and bursae -> subsequent pregnancy -> shed at parturition!! - rare repeat abortion, need heavy re-infection - Males: settle down in epididymis, testicles, accessory genital glands -> shed in the semen SIGNS - incubation varies from 2w-3m bc Abortion happens around 6-8 month of gestation! - 1-2 days before the abortion: vulvovaginitis and greyish-white or reddish vaginal discharge - Fetal membrane retention -> brown, turbid, smelly uterine discharge - Udder: no signs, only shedding, hu risk - Bulls: mucosa of penis and preputium is flushed, enlarged and painful testicles - Arthritis, tenosynovitis and bursitis => In affected herds: decr fertility and milk production, testicular degen. Of bulls, abortions in susc. repl. animals! PATHOLOGY - Fetal membrane: Placentitis, hyperemia, edema, yellowish paste form a coating material, necrotic lesions, edema of umbilical cord - Fetus: edema, small hemorrhages, small necrotic foci in the liver - Testicles, epididymis: purulent, necrotic foci DIAGNOSIS - abortions in first-calf heifers & repl. animals - Fetus, fetal memb + blood of cow to lab! - smear - MZN+ coccobacilli! - PCR - serology: slide aggl./rose bengal test is a great screening test in RU! (Hu) NO TREATMENT! WE WANT FREE HERDS! Quarantine min 1m, or till after neg test after calving if pregnant. - Examination of abortion cases in diagnostic institute, regular serological survey of livestock - Freshly calved livestock: ELISA from milk - National eradication schemes - detection and slaughter of inf. cattle. Detection with serological methods ERADICATION - selection rarely successful - generation change: Separate seropos - let grow and slaughter. Keep seroneg away - herd replacement: Best method: safest, fastest, but mostexpensive - eradication in wild animals nearly impossible... VACCINATION - Aim - reduction of losses in infected livestock, young heifers - strategic measure during early years of eradication schemes! - NEVER in free countries! - live attenuated of 2-4m female calves - protection 3 gestations! Will be sero- at 18m (male would remain +) - inactivated in other, 2x + yearly booster

Answer 40

B. Ovis. - NOT eradicated in europe! Common - The RAMS introduce (asympt) - Ewe get free from after infection while ram shed for life!! - shedding in URINE and SEMEN - No septicemia. Colonize in urogenital mucous membranes - ascending infection. - epididymis, testicles and accessory glands -> resulting in inflammation, necrosis, edema, fibrosis and spermatocele Incubation period of 5-9 weeks! - Skin of scrotum is flushed; painful and enlarged epididymis and testicles, abnormal gait - Unilateral or bilateral testicular atrophy with swelling and hardening of the epididymis - Decreased quality of semen and sexual activity, reduced fertility in rams - Chronic lesions: abscesses and necrotic foci in the testicles, uneven surface and calcification - In ewes sporadic abortion, but it is rare, increased perinatal mortality Diagnosis Normal things... + microscopy and cultrue from semen (need CO2), NGs in sperm seen Ddx. B. Melitensis, H. Somni, actinobacillus Seminis No treatment - castration / slaughter. Eradication like before, separate rearing of young rams, remove seropos!

Answer 41

Less signs, shorter shedding/may heal! Melitensis: OIE listed! - Newly infected cause abortion storms. - Mideterranian countries, rest are free in europe. - 3 biotypes! - main host is sheep and goat - PO from milk or sexually transmitted (semen, vaginal disch) - Pathogenesis like in cattle, but spontanious regeneration is common!(?) - Infection of a kid - till reach the age of reproduction, can heal! - No clinical signs, abortion (sporadic), palpable inflammatory nodules in the udder (not in bo!) - SOMETIMES orchitis and epididiymitis - Chronic infection - reproduction characteristics decrease with 30-40% - Epidemiological data and clinical signs - Isolation of the causative agent from fetus, fetal membranes and milk - Serology 􏰘 Slide agglutination (Rose-Bengal test), CFT, ELISA, o Intradermal brucellin test 􏰘 0.1 ml, lower eyelid, 48h, 2mm 􏰘 used for surveillance of unvaccinated flocks and herds TREATMENT, PREVENTION AIM IS FREE! A different approach than in bo: Support the self-limiting nature of the disease - closed flock or herd - mod live vax under 6m, protect years! (never pregnant, will abort) (Generation shift): Separation and rearing of weaned kids or lambs of animals which were vaccinated for years - a brucellosis free flock can be established! CANINE: - Sporadic in europe. - B. Canis, but dog can also colonize and shed melitensis abortus and suis! - narrow range, Infects Canidae and HUMAN! - Infection PO, mm (conjunct! Need lower infective dose, oral cav, mating!). Shedding (not milk?). - bitch: vaginal discharge from estrus and mating, fetus, 6w AFTER ABORTION - male: prostate and epididymis, SEMEN AND URINE 2 YEARS SIGNS - No characteristic clinical signs, frequently asymptomatic, enlargement of lymph nodes - Pregnant bitches: o Abortion (btw. 45-60 days(90d pregn)), reproduction failures (decreased Fertility), reduced litter size, increased neonatal mortality o Most that have aborted have subsequent normal gestations! Males: - infertility, epididymitis, orchitis, prostatitis, scrotal dermatitis (licking) - Chronic infection - aspermic, rare - discus spondylitis (lameness, paresis, paralysis), uveitis DIAGNOSIS - semen: microscopy 5w PI, inflammatory cells and abnormal sperm - isolation of B. Canis: from female disch, foetus, blood PI 2-4w - serology after 3-12w Castration and treat with ab - inform owner zoon. Risk! - Combination of tetracyclines (minocycline) and aminoglycoside (streptomycin) for at least 4 weeks - Serological examination o In breeding dogs every 6 months and 3-4 weeks before mating o When a new dog is introduced into a kennel 􏰘 two times in 1 month interval o If a dog leaves the kennel + before readmission - Do not get dogs from a kennel where reproductive problems occur! - No vaccine is available = aim is seronegativity!

Answer 42

Malleus: from animal, always chronic in horse (others can be more acute) Pseudomalleus: from soil, acute or chronic in horse too BURKHOLDERIA MALLEI Glanders - Eq, Fe, Ca... human! - by itself poor resistance - but the contain lots of water: prevents dehydration of the bacterium - survive in environment for long time! Thick cell wall - thick lipopolysaccharide(LPS) layer prevent from drying out! --> also makes it hard to treat... Epidemiology - INTRODUCTION by carrier animals - Infection: discharge (nasal, ruptured nodules), feed, water, contact, shared trough, utensils, poor hygiene - -> Discharge drops into the water - consumed by other animals - High animal density helps spreading Mainly PO (aerogenic) -> colonize and replicate in the pharynx -> lymph vessels -> LNs -> blood - -> Spread to organs: lung, nose, skin lymphatic vessels, LNs - Granulomas: necrosis, suppuration, demarcation with CT (purulent granulomas), ulceration, star-shaped cicatrices (CT fibres contracted - scar) - Remain carriers SIGNS Horse - (least susceptible species) - Chronic disease (can be asymptomatic), incubation at least 2 weeks- several months! CHRONIC - Sometimes general CS: Anorexia, fever, weakness - Nose: Serous, sticky mucous-purulent DISCHARGE, blood Nodules, ULCERS (like crater), star-shaped cicatrices - Lung: cough, nasal discharge - Skin: ULCERATING NODULES ALONG THE SUBCUT. LYMPHATICS. Enlarged lymph nodes (CANT BE MOVED - due to prolif of CT (ddx strangles!) Donkey, mule - (more susceptible): acute disease; septicemia -> pneumonia -> death Camel: mucous nasal discharge, ulcer (not as fast as donkey/mule, faster than horse) Cats: Infected when eat MEAT of horses that died of glanders: o ACUTE septicaemia o Pneumonia, enteritis, conjunctivitis o Purulent-haemorrhagic nasal discharge o Nose: granulomas, ulcers (Additional here is the enteritis, conjunctivitis, and lacking skin lesions) PM - Nose: granuloma, ulcer, cicatrices - Pneumonia: - -> Proliferative: granulomas isolated by CT surrounding (less susceptible animals e.g. horse, cat) - -> Exsudative: necrosis, cavern (more aggressive - more susceptible sp. e.g. donkey) - Generalised malleus: Parenchymal organs, LNs - focal inflammation, necrosis, purulent granulomas DIAGNOSIS Disease: - confirm diagnosis using 2 methods e.g. isolation + PCR Infection: - mallein test (allergic test) A) Eye: 0.2 ml drop on conjunctiva of 1 eye (compare with other), 8-12h, 16-24h (repeating!) +ve case = purulent conjunctivitis (B) Skin (intradermal): 0.1 ml: neck/lower eyelid, 24-48h, >5mm incr in thickness) - (Horse is chronic - can detect ab too) ELISA, immunoblot - serological crossreactionw with pseudomalleus TREATMENT - free: stamp out - endemic: long high dose wide spectrum eg. Doxycycline. Remain carriers! Zoon.: Humans are moderately susceptible - Occupational disease: veterinarian, farmer, slaughter house worker - local or generalized - doxycylinde if early - biological weapon! Use mask MELIODIOSIS - B. Pseudomallei: Zoonotic, malleus derived from pseudomalleus! - wam areas! sporadic import to europe, - su, bo, cap, eq, camel - pigs carry often! (Import of sick animal, bc wont spread further..? - wet soil, mud, water - more resistant! - Warm, rainy and stress may cause infection - NO SPREAD BTW ANIMALS - SOIL BACTERIA! So rain, warm... predisp. - msdvet said host-host transmission isnt ruled out... soil -> aerogenic, PO, skin -> Septicaemia -> Abscesses: parenchymal organs, brain Clinical signs: (facultative.. can have short or long incubation depending on circumstance...) 􏱌 Acute: variable, fever, depression, purulent nasal discharge, cough, dyspnoea (Ddx. Glanders, no ulcer nose/skin!) 􏱌 Chronic: variable, respiratory signs, dyspnoea, diarrhoea, CNS: ataxia, circling Pathology: abscesses (lung, spleen, liver, kidney, brain, nose), purulent inflammation Remember: Detection of antibodies: CFT, ELISA -> cross with B. mallei Ab - wide spectrum (thick cell wall of bacteria), large doses, long lasting treatment (need time for the AB to diffuse into the lesions) Zoon.: diagnosed during vietnam war! We dont know the trigger for the disease... • Acute septicaemia: fever, depression, anorexia • Different clinical signs: fever, pneumonia, dyspnoea, diarrhoea • Antibiotic treatment: large doses, long treatment

Answer 43

Campylobacter: G-, on mm of birds and mammals - poor resistance, dont like dry! But poor hygiene, moist, survive some days! Jejuni, lari: - thermophilic (42C), gut -> feces - virulence variants, great variety!! - -> surface proteins (bind epith), LPS(cell damage), (CDT) cytolethal distending toxin - cell damage BIRD: C. Lari, jejuni - widespread asymptomatic carriers o Infection: (fecal contamination): environment, litter, faeces, feed, water, rodents, NO germinative infection, fast spreading w/in flock! o Pathogenesis: colonise gut (cecum, colon) -> change flora -> asymptomatic carry o Sometimes mild diarrhoea, o Diagnose: culture, PCR o Treatment not necessary o Lying hens: campylobacter-hepatitis o Prevention: all-in-all-out, vaccines can reduce the rate of carriage o Public health: poultry - zoonotic! MAIN HUMAN SOURCE OF INFECTION!!! Eggs, meat CAMPYLOBACTER HEPATITIS of laying hens! - jejuni sometimes cause, in laying hens only! Typically backyard farms. - predisposing! Coccidiosis, mycotoxins, hygiene, physiological - beginning of laying!! From gut may enter blood -> liver, acute multifocal necrosis (but lesions ONLY in liver) SIGNS o Drop of egg production (5-15%) o Slight diarrhoea o Recovery within a few weeks! PM Normally dont die If they do then in beginning of egg prod - just a few percent --> Slight enteritis (small intestine), haemorrhages, enlarged liver, focal necrosis, fibrinous perihepatitis Detection of the agent: bacterium isolation (blood agar, 42C(!), acid) - Differential diagnosis: fowl typhoid, fowl paratyphoid, yersiniosis (focal inflamm and necrosis, but here only in liver!!) Treatment: tetracycline, erythromycin 4-5 days Dog/cat: - diarrhoea, young. C. Jejuni

Answer 44

LYME Zoonosis, ND! Lyme borreliosis is a vector-borne(biological-survive winter) zoonotic disease transmitted by ticks. MAINLY A HUMAN DISEASE = why its imp bc animals imp spread eg dog!!, animals asympt usually. Affected dogs typicall'y present with intermittent, lameness, fever, inappetance, lethargy, and renal failure, polyarhtitis. Diagnosis starts with screening test(serology). Treatment consists of an extended (eg, 30-day) course of antibiotics, supportive measures including analgesia, and immunosuppressive therapy in the case of autoimmune reaction. VENERAL DISEASE transmitted by breeding and from the doe to offspring. Only rabbit and hare. The incubation period is 3–6 weeks. Small vesicles or ulcers are formed, which ultimately become covered with a heavy scab. These lesions usually are confined to the genital region, but the lips and eyelids may be involved. Infected rabbits should not be bred. Diagnosis is based on the lesions and observation of the spirochete’s corkscrew motility under darkfield microscopy. Serologic tests used to diagnose T pallidum, such as the VDRL slide test and the rapid-plasma regain card test, are widely available and can be used to diagnose T paraluiscuniculi. Careful rabbit flora ab!

Answer 45

Swine dysentery Infection of weaners after maternal with FECES(indirect, rodent, bird). Damage mm in large intestines causing damage to epithelium, incr goblet cell mucous prod, necrosis, incr perm of bc, decr abs - but wont destroy mm completely so can regerate! First we see watery then mucoid haemorrhagic - TYPICAL!! General signs. Can heal or die. = no stamp out. We treat thirsty animals with ab in water! (Swine)B. Pilosicoli: growers (younger than dysentery). Watery gray, mortar like (no blood) (Avian) b. Alvinipulli: layers. Local but!! Bloody diarrhoea(necrosis), arthitis secundary to spoiled bedding, poor nutrient abs so egg dropo ecundary to this.

Answer 46

V imp, economical impact - LOVES ABORTION, two su spp maintaining(pomona, tarssovi). Pomona spreads past, while tarassovi slower - huge management importance. Strong foetopathogenic and nephropathogenic effect in sows, blood signs are seen. Other adults and gilts nem preg flu like signs! Vs other lepto spp young worse here not, sows is where we see it. MAT for detection. After detection of cases, metaphylaxis of sows to stop abortion!!! Isolate age groups (older may carry)- eradicaation program in europe. Generation shift - Should isolate vaxed sows after weaning! Vax of sows! Boars should have uniform immunity! --> now rare due to eradication

Answer 47

M. mycoides subsp. mycoides (SC) free from 1999 in europe. Obl pathogen - asympt infect new herds. No avirulent vax available. (Large BO, small ru carry, wild ru other than bo not susc). Mostly resp infection - slow spread bc intracanalicular spread in lung - 1-4m incubation. Repl in bronchioli - intracanalicular spread slowly --> diff lobe diff phase, marble like! (Actinobac pleuropneum of swine). Contagious! 100% infected, around 50% die. Thrombus formation. Localized lesions - sequesters, cough bact can exit.extrapulm lesions in young. Chronic - arthtitis, edema (thrombus) one of easiest m to diagnose/culture! Chronic worse, no treatment or vax - only endemic, eu we stamp out.

Answer 48

Mycoplasma pneumonia of Swine, hyopneumoniae Naturally in mm - management disease of (only) su. Slow spread, common asympt - eg in herd may only see reduced gain and not so much signs, see at slaughterhouse. High morbidity but low mortality! Mostly seen after maternal - 3-6m. Cytotoxic; resp epith(ciliated!), alveoli -> damage alv macroph -> cytokine release, immune response is peribronchial infeiltraion of immune cells, and the we see epith proliferation. If see signs, then dry cough with increasing intensity and poor gain typical, and gen signs only with secundary really. Atelectasia in cranial lobes. Diagnosis may be tricky, and path changes must be present (slow.. signs hard to rec, part of resp complex so other pathogens..). Tricky to treat - mass repeated ab treatment (wont be allowed soon), and really hard to eradicate... allinall out ... mission impossible Hyorhinis: lower economic impact, but emerging disease. May see signs in weaners, polyserositis, arthritis (glassers!!) Hyosynoviae: also milder, growers, fatteners joint inflammation!

Answer 49

C. Abortus: enzootic abortion of sheep is a v important disease causing the most frequent infectious abortions. Found in europe and mostly affecting the newly introduced first time preggo ewe, due to long prescence in the flock. C. pecorum cause pneumoniac form of some weeks old lambs exposed to predisposing! Also arthritis, conjunctivitis and tenteritis form can occur. Importance of not mixing animals, and vaccinating them! C. Psittaci sometimes

Answer 50

Ornithosis - c. Psittacis An avian disease affecting many bird spp. Aerogenic dust inhal is mostly the way of infection, causing repl and inflammation of resp and gut mm, then entering blood where it can affect different organs. Shedding with feces and nasal discharge, intermittently and affected by the stress and laying period (resistance, lower more shedding). A commonly asymptomatic disease, but generalized disease does happen, eg turkey duck and goose see resp signs, enteritis and geese may see cns signs too. Hens have a milder course, and we see resp and diarrhoea. Pigeons look exhausted after flying. Paired sera can be usedul in diagnosis an active infection, and PCR for id of agent.

Answer 51

Q comes from query fever, meaning unknown fever. Occurance is underest. Often, asympt frewuently but infection widespread in ru herds! Aetiology similar to chlamydia (small(infectiouus) cell variant, and large (met. Active) - inside phagolysosomes ic it inhibits maturation of phagolysosome - cant be lysed! Has a wide host range, but mainly signs in ru, and humans are imp too bc zoonosis (susceptible!). We see a natural focal infection, where we have maintaining host (ru most imp) + ticks - disease circulate btw them (like lyme disease!) the tick has a special characteristic as a biological vector, the virulence can incr in next gen. spread by discharges are aerosolized, dust, ticks. humans most imp is excretions, milk. Dogs can eat. Repl --> blood to lung, liver(this repl lead to death), lymphoid tissue, udder, uterus. The immune system kicks the bacteria out of blood, hides in gut and udder and foetus. Typiical pm lesion is haemorrh necrotic placentitis in foetus. (We dont see lesions in cow) Most imp sign is the abortion, seen most in small ru, not so often in cow (dog).

Answer 52

Ca Ehrlichiosis: Mideterranina (warmer), only dogs (german shepard most!), brown dog tick. Dog carry 1-2yrs! Damage lymphoid and endothelial cells. Local breeds less susceptible. Immunoblot to ddx rickettsia fam. Anaplasma phagocyticum Tick borne/pasture fever of ruminants Gb, scandinavia and central europe. Infected on pasture when ticks present (spring-summer) (=pasture fever/tick born fever), we see immunosupression due to the repl in lymphoid cells, and as result secundary infection are more common. Generali signs, abortion, decr. Mild prod and long carriage is typical. There is no vax. Equine granulocytic anaplasmosis Switzerland, sweden, GB - tick vectors may infect horse, dog, llama, rodents. Replicate in vacoules of granulocytes. We see vasculitis causing thrombus formation. Signs dep on age. Over 1yr general signs, edema, ataxia, maybe myocarditis. Younger milder version and jaundice. POTOMAC Weird gang! Neorickettsia risticii - potomac fever - typically on pastures near rivers - potomac river first detected (fluke vector!!) . wide host range. Repl in monocytes mainly. Fluke is vector, intermed hosts are snails and flies. The infected flies and early stage of fluke can also transmit the infection! Also the feces of infected horse! First we see repl in gut enterocytes, monocytes, macrophages, then the bacteria enters blood causing septicemia. We see general signs, diarrhoea, laminitis, belly edema and abortion later. We see gut lesions mostly!!! Avoid pastures near rivers!!! The mortality can be up to 30%!

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