Other Topics Flashcards
- Foetopathy of swine caused by parvoviruses (SMEDI).
o Parvoviridae family, Parvovirinae subfamily, Protoparvovirus
o Porcine parvovirus disease – PPV1:
– 5 biotypes/strains: eg. classical PPV1 is SMEDI in suscept. sows, coinfection with PCV2 - PMWS or PRDC, apathogen strain for vaccine
- Almost all females are infected before their 2nd pregnancy & develop a life-long immunity,
preventing transplacental infection of offspring → Disease of first parity pigs!
(o Reproductive problems may return every 3-4 years
o Abortus is atypical)
– SMEDI = stillbirth, mummification, embryonic death, infertility
– PO, aerogen. Feces, saliva, semen, fomites
– Replication: macrophages, monocytes, no cross placenta if seropos. sow, maternal immunity 6 months, antibodies max prod. 14 days – up to 10 months
– Signs: return to estrus, abortion, smaller size litter, unlikely if 8 piglets or more. Resorption, mummification, death, calcification, myoclonia congenita(shaking piglets).
- Adult: resp or vesicular. Neonate: systemic
– Endemic, may return every 3-4 years
– Path: not unique. Piglets diff. stages, mummification
– Histopath: not unique. lymphoid infiltration, hepatitis, nephritis
– Diagnostic: serology: VN, HAI, ELISA. Direct: IF, PCR, HA, CPE in isolation
– Diff: PRRS, PCV2
– Vaccines: good, longlasting, every 1 year, inactivated (live), monovalent, combined
- Canine enteritis caused by parvoviruses.
o Parvoviridae, Parvovirinae, Protoparvovirus, Carnivore protoparvovirus-1, Canine parvovirus 2(!)
Hele denne linja er en
- Subtypes 2a, b, cat ́s only with a subtype (10% of panleukopenia cases!)
o Worldwide. Dog, wolf, fox
o PO à repl. lymphoid tissue around throat à viremia à organs rapid cell division (BM,
spleen, thymus, lnn, crypt cells SI, myocardium young dogs)àmassive shedding
o Signs: not specific. 3-8 weeks: sudden death, myocardial damage. High mortality!
Above 8: enteritis, stinky grey persistent diarrhea, hemorrhagic form or subclinical. Mortality 10%
o Path: damaged basal layer, intestinal villi, inflamed, desquamation, hemorrhages, basophilic
nuclear inclusion bodies in intest. cells. Myocarditis with necrosis, lymphoid infiltration and
plasma cells. Decr. lymph cells in mesent. lnn.
o Diagnosis: feces – HA swine RBC ́s, PCR, sandwich ELISA, EM (see dividing vir), rapid test,
antibodies (already immunised, think about ab ́s)
o Diff.: coronavirus (watery), herpesvirus (mostly resp.), rotavirus (milder)
o Treat: symptomatic, ab for 2ndary infections, quarantine, hyperimmune serum (in FP too, helps if given within 2w, best before serious…
o Vaccines: inactivated (live atten), maternal abs (3-4 months), hyperimmune serum (help 2w)
- -> If vaxed too young -> maternal will block the ag, dont vax under 4m! Do rapid test to see if seropos!
- -> If exposed unvaxed young dog we usually give hyperimmune sera!
7 - Feline panleukopaenia.
Parvoviridae, Parvovirinae, Protoparvovirus, Feline panleukopenia virus (CPV-2a)
o Infectious gastroenteritis
o Cats and Felidae. Worldwide
o Feces, secretions àPOà repl. lymphoid tissue in throatà viremia, macrophages and
lymphocytesàorgans rapid cell division (lacking polymerase enzyme)àblood organs anemia, lymphoid cells – leukopenia, crypt cells SI, myocard in young, cross placenta – cerebellar hypoplasiaàshedding virus in feces
o Signs: acute enteritis, diarrhea, vomit, exsiccosis.
- Adult: subclinical, outcome depend on age
o Patho: cerebellar hypoplasia,
̈feline ataxia syndrome ̈ - lysing purkinje fibers,
edema intestinal wall and hemorrhages
o Diagnosis: vacc status, feces – IF, PCR, sandwich ELISA, VN
o Diff.: Herpesvirus – infectious rhinotracheitis (conjunctivitis), coronavirus – FIP, calicivirus
(oral ulcers)
o Vaccines: inactivated (live attenuated), maternal abs 3-4 months (don’t give vacc too early), hyperimmune serum (before very sick), combo – parvo, herpes, calicivirus, chlamydia
o Treat: symptomatic, ab for 2ndary, quarantine (mothers hyperimmune sera - cant buy like in dog.. use before serious signs)
8 - Parvovirus diseases of the mink.
Mink parvovirus enteritis
– Protoparvovirus, Mink enteritis virus
– Canada, Europe
– Similar to dog and cat – fever, no special symptoms, diarrhea
- incubation 5-7 days, outcome depends on age and immunity
– Clinical signs + patho same as dog and cat
– High mortality (up to 80%!)
– Vaccine: inactivated from 2 months, Botulism + Pseudomonas
Aleutian mink disease – plasmacytosis
– Amdoparvovirus, Aleutian mink disease (AMDV)
– Worldwide. Mink, Mustelidae, ferret. Mink of Auletian genotype more susc.
– pathogenesis like other parvo
–> Difference is NO virus neutralising antibodies –> immune complexes!! Type 3 hypersensitivity
Forms:
young: interstitial pneumonia.
Old(mainly aleutian): hypergammaglobulinemia, glomerulonephritis
Signs:
Chronic appearance, incubation 4-6 weeks, bleeding nose and mouth, anorexia, bloody feces, CNS signs, maintained for weeks
- Bleeding from nose and mouth
- Anorexia, bloody faeces, nervous signs
- Signs maintained for weeks
- Lethality: link btw color and antigen presenting cells! – Auletian 50%, other 5%
– Patho: incr. plasma cell count, swollen liver, spleen, lnn., lymphoid foci. Bleeding mm., glomerulonephritis, arteritis
– Diagnosis: PCR, isolation. Antibodies: gammaglobulin, specific ab ́s, immune complex
– Treat: no vaccine, no treatment. Vaccineàmore immunoglobulins prod!! Dont vax!! Will induce disease
10 - Circoviral disease of swine (PMWS, PDNS).
PCV-2
Porcine circoviruses:
- PCV1 – non-pathogenic, PCV2 – responsible for disease (immune supp + 2ndary), PCV3 – commonly detected together with circoviral diseases! fetus or resp, PCV4 – similar to mink circovirus
The virus is constantly changing – mutating (vaccine not efficient against some strains) DNA Virus but b/c doesn’t have replicase enzymes/repair enzymes – easy to mutate
PMWS
- porcine multisystemic wasting syndrome
- usually seen 1.5-4m
- The disease is caused by PCV-2. Huge variations clinically btw induviduals and farms. After weaning we see poor growth, anorexic, weight loss. Often seen with either resp or diarrhoea. Sudden death also occur. Huge economic losses. Important feature is the immunosuppression, so co-infections are common.
o Endemic worldwide, spreading. Domestic pig + reservoirs (wild boar rodent)
Oronasal -> viraemia -> lung -> lymphoid organs, liver, kidney, heart, brain, (monocytes, macroph, dendrites, lymphocytes) —> IMMUNOSUPPRRESSION!
Ab from 2nd week. Maternal last up to 3m, persistent infection up to 6m! (Loads of ab!)
Any immune activation may help develope the disease due to immunosuprressive! (Vax, viral infections). Activated immune system –> incr immunosuppression!
(Enteritis, hepatitis, pneumonia, lymphoid organs, blood cells)
o Signs: morbidity 20-30%, weight loss, anemia, resp (cyanosis, tachypnea, jaundice), diarrhea, CNS, fever, rough hair!! + 2ndary
o Patho: enlarged lnn. (inguinal, mesenteric), hemorrhages,
lung: heavy, tan color, red areas, pulm and interstit edema, pneumonia, flaccid myocardium, strawberry heart, ascites, anemia, jaundice, gastric ulceration(peyer??), enters fetus (myocard repl)
o Histo: lymphocyte depletion
o Diagnosis: PM, histo, check protein of virus, PCR, IF, ELISA, in situ hybrid, IH. Ab ́s: VN, ELISA
(IgG/IgM – M to see if first infection or older). Find virus in macrophag, giant cell, dendritic, tubular, Kupffer, brain cell, heart endothel
PDNS
- porcine dermatitis nephropathic syndrome
- usually seen over 1.5m
Complex stay in caps -> ig bind in wall of cap – NG cant phagocy. –> thrombosis.
Tries to phagocytise but very big so NG not able but tries. They degranulate causing problems with cap cells too -> petechiae
o Skin, kidney
o IComplex deposition > skin, kidney, blood vessels (thrombosis)
o Signs: weight loss, heavy breath, pale, multifocal circular red skin lesions, hemorr, edema
o Patho: large grey kidney + hemorrhages, necrotic area, large lnn., hemorrhages in skin, edema, mesenteric edema
o Histo: thrombosis capillaries, lymphohistiocytic vasculitis, fibrinoid necrosis of skin, exudative
glomerulonephritis, interstitial nephritis
o Diagnosis: PMWS also present or may be without PCV-2 at all (mycoplasm, bact - immune complexes!). Similar ln lesion (huge!)
2 criteria
1) Characteristic pathological lesions: skin infarcts. Enlarged kidneys with haemorrhages on the surface
2) Characteristic histology findings: systemic necrotizing vasculitis, glomerulonephritis
o Diff: any immune complex disease, ASF, CSF (redness skin)
PRDC
– porcine respiratory disease complex
- usually seen OVER 4m (ddx. PMWD)
o More frequent. America, coming to Europe
o Others involved: PRRSV, swine influenza, mycoplasma hyopneumoniae, Actinobacillus
pleuropneumoniae, Pasteurella multocida
o Not very characteristic symptoms
o Diagnosis(!): Ab resistant resp disease, histo lesions of lung, PCV2 detected in lesion, exclude
other things. PCR, ELISA, IF, in situ hybrid, IH
11 - Avian diseases caused by circoviruses, chicken infectious anaemia.
o 1) BFDV – Psittacine beak and feather disease
o 2) PiCV,- Pigeon circovirus
o 3) GoCV Goose circovirus
Immunosuppression, dividing –> weak animal, may die easy of secundary!
o Commons: Circovirus genus. Clinical signs, pathology & histology as in PMWS
o Cytoplasmic inclusion bodies in infected cells (macrophage, lymphocyte), lymphocyte depletion
o High morbidity, low mortality, growing resistance with age, immune suppression, secondary infections - often cause of death!!
BFD - Psittacine beak and feather disease
- under 3yrs, old, new parrots, cockatoos etc. type of birds
o Horizontal & vertical transmission
o In dividing cells: feather follicles, cell division areas of beak & claws
o ACUTE: lethargy, anorexia, rep signs, weight loss, vomit, diarrhoea
Death w/in 2-4 weeks b/v of secondary infections
Frequently before the typical feather & beak deformities
o CHRONIC: typical lesions sometimes obvious only after molting, loss of feather, feather & beak
deformities. Can go on for years or die within 1 year b/c of secondary infections
- Surviving birds are persistent carriers & shedders!
2) Pigeon circovirus (PiCV)
- pigeon 1-12m
- decr performance, beak/feather/claw abn
- acute like beak and feather, in young mort can be even 100%!
- spleen, thymus & bursa: cells are destroyed
3) goose CV
- from 1w old even! More commonly see retarded growth here. Higher mortality, decr production, feather.
- lymphocyte depletion, bursa atrophy
Anelloviridae, gyrovirus genus, CAV - chicken infectious anemia!
- one serotype, only chicken!
- vertical (Egg, sperm), horizontal (direct contact, faeces, fomites)
- Infection: below 3 weeks:
disease/severe immunosuppression, over 3 weeks: no disease/mild immunosuppression
Widespread disease, we usually see asymptomatic - we see decr productivity… then we should think of this. Po - resp/gi - blood - bm - (myeloid & lymphoid cells destroy) anemia, immunosuppression!
If signs then under 3w from horizontal or infection at hatching, anemia-dermatitis
Pm
- Anaemia, oedema, haemorrhages (also in gizzard & proventriculus), thymus atrophy, bursa atrophy
(mild/medium – btwn 10-14d of age, after vertical transmission), BM yellowish, liver necrotic areas
Inact vax: parenteral only, no mucosal immunity
Live: can use in drink/feed! May infect younger tho (need mucosal immunity)
12 - Papillomatoses
Have to infect in str. Basale to replicate
=need opening
Detected virions in str corneum -> movement fom here
(Primary infection stratum basale > str. granulos prod. viral capsid > str. corneum shed virus. NO viremia, only in skin)
1-2month incubationperiod bc longer process
Spread to lesions - mainly direct contact or mechanic vector eg fly, mosquito. Iatrogenic spread.
Bovine papillomatosis:
6 types:
o 1,2,3: skin tumors (1,2: also horses), 4: intest, 5,6: skin udder
o Signs: nodules near eye, horn base, abdomen, neck, withers, rare other. Benign and can heal
o Histo: epithelial cell hyperplasia, fibroblasts, enlarge str. gran and corneum
o Treat: cut, burn, freeze, autovaccine
Horse papillomatosis:
EPV-2, BPaV-1 and BPaV-2 (bovine 1 and 2 – Horse sarcoid)
o Head and neck, rare others
o Iatrogen
o Horse sarcoid: most common horse skin tumor! look serious, fibroblasts, head/abd/hoof, aggressive, but no metastas/asympt, though freq. Grow back if removed. Genetic, mech vector (fly) from cattle (BPaV 1/2 –> cant spread further!)
Dog, cat:
o Young animals, oral cavity (boxer), genitalia, immunosupp –>whole body, spontan healing (months)
–> Doesnt need treatment
Can remove tumors if struggle to eat, drink, breathe
Wild animals:
o Human – 16 and 18, vaccine, persistent, asymptomatic, precancerous lesions, warts
o Incr risk cancer cervix, vulva, vagina, penis, anus, throat
13 - Haemorrhagic nephritis and enteritis of geese.
Goose hemorrhagic polyomavirus (GHPV)
First seen in hungary, one of the major diseases of geese
High mortality! Up to 80%, in young geese 3-10w
PO -> throat lymphoid tisse -> endothel, bursa(b-cells), kidney, intestines, –> edema, diarrhoea, death!
Ddx derzy! (Primary repl in SI = diarrhoea, secundary in liver =CNS and heart - ascites - fibrin!!)
o Duck can be seropositive and carry, Muscovy duck, hybrids and wild goose
o Signs: (CNS, DIARRHOEA!)
- few hours before death, shaking head and neck, lethargy, diarrhea, coma, depends on
age (can be 100% mortality, gosling).
- Chronic: uric acid crystals, or asymptomatic in elderly
o Patho:
edema under skin, ascites, hemorrhages
hemorrhagic nephritis, necrosis tubular epithelia, gout,
necrotic hemorrhagic enteritis,
o Histo: interstit nephritis, epithel necrosis kidney, necrotic enteritis, hepatitis
o Diagn: IF, PCR, hard to isolate. ELISA, HAG, sera
o Diff: Derzy ́s, goose Circovirus(mortality, decr growth), Marek
o Vaccine, inactivated
Budgerigar fledgling disease virus - BFDV
o Parrots, falcons, finch
o Edema, ascites, nephritis, hepatitis, hemorrhage, stop growth and feather
- can be used for vax of GHPV!
14 - Pneumoenteritis of ruminants caused by adenoviruses.
Part of complexes (brdc, diarrhoea, not much alone!). Urolithiasis rams.
Part of complexes (brdc, diarrhoea, not much alone!). Urolithiasis rams. (Adeno is primarily a DOG disease)
o Adenoviruses alone are not important - become important when part of a syndrome
o Immune suppression is the first step, then usually virus (adeno, parainfluenza, herpes, rio, etc.)
which damage the resp epith surface, then secondary bacterial (mannheimia, pasteurella,
histophilus etc.)
- the problem turns chronic due to the bacteria phase
o Mild disease of 1-4m old calves with nasal discharge, coughing and diarrhea
Causative agents:
Mastadenovirus genus:
“Subgroup I.” - Replication in bovine kidney cells (BAdV- 1, 3, 10)
Atadenovirus genus
“Subgroup II” - Replication in bovine testicle cells (BAdV- 4-8)
Epizootiology
Intro to a farm with carrier calves
Usually in large farms (crowding) - pretty much all large farms are infected
Fattening farms which are purchasing young calves from many sources
Poor colostrum uptake
In adult cattle subclinical
Role of co-infections BRDC:(BVD, IBR, PI-3, Pasteurella, etc.)
PO/air -> tonsilla -> viraemia -> resp, GI
Clinical signs
From 6-8w (without colostrum from 3-4w). Mild resp and diarrhoea
Secundary viral: interst pneumonia, secundary bact: bronchopneumonia
Pm: lung, gi, kidney
BAdV-10 in N-ireland - haemorrhagic enteritis, nephritis!
Pneumoviral enteritis of lambs - like calves…
Resp and enteric disease usually in intensively raised lambs
Also haemorrh enteritis in lambs - OAdV-4!
Urolithiasis in rams
Causative agents: Mastadenovirus genus, Atadenovirus (like calves..)
15 - Canine infectious hepatitis and infectious laryngotracheitis.
CAV-1 and 2 crossprotection! One serogroup.
CANINE INFECTIOUS HEPATITIS - one of the most imp dog diseases!
(Disteper, rabies, CAV-1, parvo)
Acute disease.
Po -> lymphoid -> ln -> viraemia in lymphoid cells -> hepatitis, brain (kills animal), kidney - glomruloneph. Chronic (immunocomplexes) eyes - blue eye disease!
Mortalities 3-6m - mortalities, after maternal!
- sudden death
- general signs, icterus, vomiting and bloody diarrhoea, abd pain (hepatitis), coagulopathy (haemorrhages, edema - mm, CNS -> death!)
- chronic - blue eye (recovery but immunocomplexes still being made)
>1yr mild/asympt!!
HP: edema, hemorrhages
o Enlarged, yellow liver
o Centrolobular hepatocyte necrosis, hepatitis, icterus
o Serosa hemorrhages, nephritis, hall bladder oedema
o Nuclear inclusion bodies (Cowdry A)
o Liver parenchymal cell degeneration
o Invasion of indlammatory cells
Icterus and hepatic problems - leptospira, babesia - 2 most important infections of dogs which cause very similar lesions and symptoms, and they are much more imp in the DD because those can be lethal, and one is zoonotic.
(Rabies, parvo)
(Fox encephalitis - CAV-1, CNS more imp - rabies, distemper! Ca are susceptible
Vax (laryngotrach) part of basic immunization 2-3m.. symptomatic treatment.
Kennel cough: (dbpp)
- CAV-2 + distemper, PI-2, herpes, b. Bronchiseptica, p. Multocida = kennel cough SYNDROME!
- upper resp mm only!!! DRY cough
- young, aerosol, alone rare signs.., kennels!! Must improve keeping conditions.
16 - Adenoviral diseases in poultry.
PO -> Repl in intestines in all! (+germ in seroptype 1 and 3)
Serogr 1: aviadenovirus genus:
- germinative(!)/PO -> viraemia -> gut, LIVER, kideneys -> trachea
- we see after yolk immunity - 1m
FAdV-1, -7, & -8 (fowl adenov) - inclusion body hepatitis
- (growers, petecchie) in broilers
- edema, diarrhoea
FAdV-4 - hydropericardium syndrome of geese
- (hepatitis and hydropericard)
- sitting, 5-6h…
- geese - ddx derzy!
Serogr 2 - Sia: (s=spleen) - turkey haemorrh enteritis (like marble spleen)
- big losses!
- PO -> GI -> viraemia -> anemia(bv damage), immunosuppressive, enteritis
- thirsty, bloody feces, anemia, depressed
- pm: splenomegaly mottled, haemorrh, fluid in body cav
Serogr 3 - Atadeno: (avian and mammal!)
DAdV-1 (duck atadenovirus, but this is mainly a chicken disease!)
- egg drop syndrome of chicken imp, enteric disease, decr egg prod a lot bc incr oviduct motility. No time for calcification. Vertical spread but horizontal when laying starts make it spread like crazy!
- presumibly first spread with mareks vax from ducks into chicken farms and became chicken disease!
- pm: oviduct edema
- epi: must eradicate from primary breeding flocks and disinfect egg shells! Hygiene! Yolk immunity - vax!
17 - Characteristics of herpesviruses, groups, epidemiological features.
See general…
20 - Bovine herpesmamillitis, inclusion body rhinitis of swine.
BoHV-2 - alphaherpes
Bovine herpesmamillitis:
Local pustules, erosions if more serious on udder, spread with milking, arbo through skin damages. Common subclinical (heifers!)
- aka pseudoLSD
- rare in europe! (AAU - africa, australia, USA)
- signs in cattle and bo, other ru seropos
introduction with infected animal, then spread via milking (hand/machine), arthropod vectors
(mechanic) –> infection through skin damages
Common subclinical, if signs usuallt only on teats, recover within 2w. Predispose for bacterial mastitis…
Spread: perineal region, lips of calves
Can turn generalized, nodules everywhere (pseudoLSD)
Reduced milk prod, bloody mild and scars on teats
HP: in ib (dna..), syncytia
Just sympt treatment…. disinfection to avoid secudnary!
inclusion body rhinitis of swine: SuHV-2 - betaherpes
Mostly no signs are seen where herd immunity present… may occur in nonimmunized piglets..
There is no vax, meaning, 50yrs ago this disease was a problem, so immunity developed. (Rhinitis signs piglet, abortion)
Only pig! Latency in lacrimal gland.
Before signs were:
Under 3w: general signs, bloody/serous nasal discharge, with even 25% mortality!
Pm: haemorrh, edema under skin, pharynx and lungs. Hydrothorax, hydropericardium.
21 - Malignant catarrhal fever.
Ovine herpesvirus 2 (OHV-2) - gamma
- ovine - sheep associated!
- The wildebeast associated in africa is caused by alcelaphine herpesvirus-1. (AIHV-1)
Sheep associated, endothel damage, goblet cell - all mm show signs(purulent), older more severe
Only cattle give clinical signs, sporadic infection, sometimes endemic. Other ru asymptomatic. Sporadic su infection.
- Direct infection of cattle from sheep – after long term (a few months) contact
- The cattle does not transmit further the virus
- OLDER are MORE susceptible than young! Old usually lethal, young may recover!
Aerogenic -> cell associated viramia -> immunopathoglogical processes… unclear pathogenesis!
SIGNS:
o Catarrhal: produced by goblet cells in mucus membrane - all mucous membranes will show signs
o Peracute: high fever (!!!), unappetite, depression, salivation, hemorrhagic enteritis, tremor, convulsions, death
(Deer, bison)
o Subacute: (endothel damage..)
- fever, depression, rumen paralysis, agalactia,
- peripheral keratitis (periph corneal thinning), purulent conjuncitivitis,
- nasal discharge (serous -> purulent with necrotized tissue), nasal mucosa suffusion, epithelial necrosis, crouposal membranes (labored breathing), laminitis (loose of hoofs, horns),
- swollen LN, edema under skin (mainly on head),
- abdominal pain, obstipation (severe, hemorrhagic enteritis),
- hemorrhages and necrosis in genital mucosa and skin,
- meningitis, encephalitis (excitement, convulsions, restlessness, paralysis > death),
- abortive or mild form may occur in young, but they can get sick again in a few months
Recap:
(Either we see v high fever, cns and death, or:
General signs, discharge (purulent!) eyes, nose, mm necrosis, laminitis, head edema, abdominal pain, haemorrh genital mucosa, CNS and death!!
–> Mild in young but reinfection! Herpes poor ag…)
PM
- peracute; inflamed mm, haemorrhages, large and pale liver/kidney, bladder wall edema/haemorrh
- subacute: eye lesions, hemorrhagic pneumonia and enteritis, fibrinaceous membranes,
hemorrhages, necrosis, swollen LN and follicles, arteritis, capillary and vein fibrinoid necrosis,
infarcts, lymphocytic polio- and leucoencephalomyelitis (mainly cortical)
No treatment or vax - must isolate from sheep!!! Will be re-infected if survive!!
25 - Diseases caused by EHV-2, EHV-3 and EHV-5 viruses in horses.
2 and 5: gamma
- widespread, often asympt, low virulence
- mild resp in some w old foal, recovery within a week.
- may predispose to r. Equi
- EHV-5 is suspected to have a role in the background of horse multinodulary pulmonary fibrosis
- prevent with hyperimmune serum, lasts 6w!
EHV-3: alpha - coital exanthema of horses
- worldwide, often asymp
- veneral disease of both sexes
- coital exanthema. Beningn only erosions, papules on vagina, penis and prepuce.
- latency, stress, recurrance
- may spread to udder -> lips of foal
- (BENIGN ONLY EPITH DAMAGE)
- no mating during signs and 1 month after
26 - Canine herpesviral disease.
CaHV-1 - alphaherpes
- worldwide, common in kennels
- Ca are susceptible
- disease of young!
- Thermosensitive - Winter cold - incr repl!!! Cold puppies.
Transmission from parturition, fomites, mother, sublings
Latency in ggl, re-activation, eg pregnancy!! New born weak immunity and cold facilitates!
In utero infection -> viraemia in wbc -> DIC, haemorrh, necrosis -> stillborn/abortion!
< 2w -> PO/aerogenic -> mm –> viraemia –> same as in utero! Or like below if good immunity, body temp, maternal ab.
< 2w -> PO/aerogenic -> local infection in resp –> viraemia -> repro tract mucosa -> latency (RE-ACTIVATION!)
Signs;
- puppies die one after the other…, abortion at different ages
- general signs newborn, mild resp, gi, haemorrhages, edema, rash, cns -> death or permanent cns lesion…
- adult asympt or mild resp, repro disorder of bitch
If death already occured among puppies, its hard to treat… should inform owner rest will probably die
PM (puppies)
Generalised haemorrhages, oedema, necrosis (liver, spleen, brain, lungs)
Ddx fading puppies: parvo 1/2, general: distemper, CAdV-1
Can try hyperimmune sera but rare use..
Inactivated vax of bitch!! Maternal ab + avoid infection!!
27 - Feline infectious rhinotracheitis.
FeHV-1, alphaherpes
Similar to last! Secundary infections more imp as death of young, abortion rare. Sneezing, coughing, conjunctivitis typical here!
- woldwide, common
- VN crossreactions with BHV-1 and SuHV-1! (IBR, aujeszky)
- Felines susceptible, winter, under 6m
Upper resp, conjunctivitis common, abortion rare! Very infectious, among young/other predisposing 100% will be infected and many die due to secundary infections.
Po/aerogenic -> upper resp -> viraemia -> foetus
General signs, lacrimation, conjunctivitis, nasal discharge, nasal mucosa edema –> discharges turn purulent closing eyes and blocking nose.
coughing, sneezing(!)
After some days secundary infection and empyema (bordetella, stept)
- -> face eyes nose sticky dirty (KCS), cats not cleaning themselves! Owner will notice this.
- -> if survive lacrimal duct and nasal and sinus tissue damage - predisposing to chronic bacterial infections…
Most imp ddx is calici! Sneezing, eye lesions.
(Chlamydia, b. Bronchiseptica)
Treatment:
- Cleaning face, AB, treat eye lesions, food/rehydration, hyperimmune sera
- will survive probably with treatment!!
VAX! Basic immunisation (attenuated or inactivated)
28 - Infectious laryngotracheitis of chicken.
ILT
- GaHV-1 (gallid), iltovirus, alphaherpesvirus
- worldwide, first poultry vax was made against it!
- 1 serotype, several virulence var
- mostly chicken is susceptible!
o Air-borne infection - upper airways, conjunctiva (NOT in bronchi & parenchyma of lungs)
o Local multiplication - no viraemia!
o No germinative infection
o Convalescent birds are long-term carriers & shedders
o Very contagious - quick spread in the population
o Virus multiplication in the mucosa of the upper third of the resp tract EPITHEL & ENDOTHEL! damage - exudates, oedema, haemorrhages
SIGNS
- mainly in GROWERS, ADULTS!
- typical form: Dyspnoea (gasping), rattling, extension of the neck during inspiration. The mouth & beak may be blood-stained from the tracheal exudate
Eyelid oedema, conjunctivitis, haemorrhages, exudate
Eye lesions!
Anorexia, inactivity, red egg prod
Haemorrhage & fibrin precipitation in the trachea -> cheesy plugs -> occlusion -> Mortality in adults 10-20 (50-70)%, recovery w/in 2-6 weeks
- mild form: mild resp… 5% mortality, production loss
Cause of death:
Necrotising MM inflammation, formation of pseudomembranes is typical - form fibrinous plaque which gets into the pharynx & obturating it -> chicken cant cough so cant remove the plug (suffocate)
PM
o Trachea mucosa swollen, red, bleeding, pseudomembrane, cheesy plug
o Desquamative, necrotising tracheitis: cilia disappear, cellular infiltration, degeneration of the capillary walls, nuclear inclusion bodies
Typical, dont need aetiological. Mild form needs aetiologial.
Ddx AI and Newcastle - but here its only local so…
PREVENTION
–> Sporadic: slaughtering and replacement
–> enzootic: immunisation
- Eye drop w/ attenuated vaccine (Drinking, aerosol is less efficient) broilers and layers!
(Attenuated vaccines are shed by the birds neem)
30 - Duck plague, herpesviral disease of pigeons.
Duck plague - ND!
AnHV-1 (anatid) - unassigned herpesvirus
- 1 serotype, several virulence factors
- anatidae susceptible: duck, goose, swan
- duck plague bc associated with mass mortality in ducks
- Convalescent birds are lifelong carriers
- Domestic ducks usually get infected on open waters (lakes) via the contact w/ wild ducks (long term spread!)
- Virus is shed through nasal discharge & faeces –> contaminates the water
- The virulence of the strain, the sp. & density of the hosts, the weather & food availability influences the severity of the outbreak
- LAYER DUCKS, ADULTS are more sensitive
- Morbidity: ~100%, mortality: 15-25% (5-100%)
- Mainly oral(water!) infection -> primary replication (bloody diarrhoea, rhinitis, conjunctivitis) -> viraemia ->
endothel damage of the BVs -> necrosis, haemorrhage, fibrin precipitation on the mucosa
SIGNS (sudden mass mortality, endothel signs)
o Incubation period: 3-7 days
o Sudden & persistent increase in flock mortality
o Photophobia, conjunctivitis, eyelid oedema
o Loss of appetite, nasal discharge, increased thirst?
o Droopiness, ataxia, tremors, spoiled vents, watery or bloody diarrhoea
o Inactivity, floating on the water
o Adult ducks may die in good flesh
o Ducklings: dehydration, weight loss, blue beaks, blood-stained vents, changed voice
o Decreased egg production
o Dead males, prolapsed penis
o Death w/in 4-6 days
PM
- blood in body cavities and tissues
- petechiae and ecchymotic on heart (paint brush like) and other PO
- Specific mucosal eruptions (in the oral cavity, oesophagus, ceca, rectum & cloaca): elevated yellowish crusted plaques –> green supf scabs -> large patchy diphteric membranes (yellow, green - duck colors :-))
- mucosal lesions align parallel w/ the longitudinal folds in the oesophagus & with the annular bands in the intestines (follicles).
- liver enlarges, brass colour w/ greyish pattern (dystrophy) & haemorrhage
- Clear, yellow fluid infiltrates & discolours the SC tissues from the thoracic inlet to the upper 3rd of
the neck
- Ruptured yolk & free blood in the abdominal cavity of laying ducks
DIAGNOSIS
- tissue culture
- acute - no serology
Ddx. Duck viral hepatitis, fowl cholera (more common diseases of duck than ND, AI!)
CONTROL
- wild, water
- sporadic: stamp out and clean
- epizootic: vax and lifelong quarantine
PIGEON HERPES
CoHV-1 (columbid), mardivirus genus, alphaherpes
- worldwide
- signs in YOUNG! Older are carriers
- Infection from mother PO, during maternal Ab protection -> no clinical signs
- Infection from other birds, later (i.e. during race) -> airborne infection
- Simultaneous infections (chlamydia, E. coli, mycoplasma, pasteurella) make the pigeons more vulnerable
- Convalescent birds are latently infected -> periodic shedders (~stress)
SIGNS (similar to plague but here fewer die and not so sudden, here young)
- 2-6m old
- serious conjunctivits! Fat eye
- rhinitis, pharyngitis, diarrhoea
- Death w/in 3-4 days (~10% mortality)
- may turn chronic: sinusitis, dyspnoea, concomitant infections (Trichomonas columbae, mycoplasma, pasteurella, salmonella)
PM (- similar to before but milder)
- Conjunctiva: oedema, suffusions
- Liver: enlarged, haemorrhages, greyish foci
- Pancreas: enlarged, oedematic
- SI: watery-bloody content, red mucosa
- Trachea, pharynx: croupous inflammation, necrotic foci, erosions, pseudomembranes
- Pancreas, brain: acute inflammatory processes
Ddx: Newcastle disease CNS signs, lab testing, pigeon pox: skin lesions
Vax
32 - Contagious pustular dermatitis of sheep and goat. Swine pox.
Orf virus, parapox,
- Acute dermatitis of sheep and goats (similar to bovine papular stomatitis?)
- This disease occurs worldwide and is zoonotic(para!), not a rare disease.
Enter flock by carriers or fomites - super resistant! And spread by contact.
After parturition see lesions on teats then mass disease in suckling (mouth lesions).
Immunity max 6m - repeat infections.
Economic losses due to weight loss as the mouth lesions are painful - anorexia,
Teat lesions painful - wont let them suckle.
Lesions on the reproductive mucosa: reproductive problems (no mating)
Lesions on limbs - lameness, complications with panaritium - footrot!
–> recovery within 4-6w
High morbidity, mortality <10% due to bacterial complications
Hu: pocks on skin
Ddx FMD
Treatment: clean, remove scabs (contain virus), local and systemic AB
Prevention:
Vax in places with a lot of sheep..
Swinepox, suipox genus
- rare, in poor management, 2-8w mostly, older subclinical
- only pig susceptible
- mechanical vector: lice, fleas
- Direct contact transmission - skin lesions, poor keeping conditions
- Long-term immunity after convalescence
- Maternally derived antibodies can protect piglets
Pathogenesis, signs
o Usually benign, but may cause mortality in piglets
o 1-3 weeks incubation
o Febrile general signs
o Wet nodules - pustules - scabs (within ~ 1 week)
o LONG LASTING illness, lesions in different stages, bacterial complications –> death!
o Inner ear lesions - meningitis (severe)
Ddx. S. Hyicus
Ab for secundary
34 - Myxomatosis
Myxoma virus, leporipox genus, ND!
- myxoma: tumor of CT embedded in mucous
- cotton tail rabbit - subclinical, domestic - severe. Australia biological control for rural rabbit
- reduced virulence, 90% -> 40% mortality), development of herd immunity
- now present worldwide, europe too!
- european rabbit is susc, european brown hare is NOT
o ARTHRPOD TRANSMISSION (mosquitoes, fleas, flies) - mechanical vectors, carry for months
o Seasonality - autumn; epizootics in few-year intervals
o Direct and iatrogenic transmission may occur
- 2 serotypes wth virulence variants
- Attenuated and wild virulent strain present in europe
Skin primary replication -> hydropic degeneration of epith cells, vesicles filled with serous fluid -> covering skin necrosis!
–> viraemia -> endothelial damage -> serous infiltration of corium, tumor-like myxoma cell proliferation and serous infiltration => moist nodules in skin
Signs
- incubation 1w, death 2w PI
- typical form - 100% mortality, myxomas, lion head, resp signs
- nodular form - 20-90%, firm nodules, benign (slow progression)
- conjunctival/resp/atypical form - 80%, resp signs, no or mild swellings
PM
- myxomas in corium
- Epithelial necrosis, corium oedema, proliferation of mesenchymal cells
- Lymph nodes, spleen: reticulum cell hyperplasia, lymphocyte damages
Typical form can diagnose from that, other need aetiological: HP, PCR
Prevention, control
- closed farm, arthropods
- stamp out infected + vax in protection zone if outbreak
35 - Fowl pox.
Fowl pox, many different viruses, avipoxgenus
- Canarypox virus, Fowlpox virus, Juncopox virus, Mynahpox virus, Pigeonpox virus, Psittacinepox
virus, Quailpox virus, Sparrowpox virus, Starlingpox virus, Turkeypox virus
- worldwide
- many pox species cause it - cross reactions, partial cross protection.
- We see milder infection in heterologous host, eg turkey transmit to pheasant.
- Important in pheasant, turkey, chicken, pigeon
- Introduction with carrier bird, wild birds may play a role, btw farms with fomites! (Good resistance!)
- spread in herd with arthropods (mechanical), direct contact, feces, food, water!
- Mainly in chicken!!! Mortality may occur
- Wild birds and pigeons more commonly infected in wet, rainly weather (more mosq)
- Turkey, fowl(chicken): more severe in autumn, winter (decr immunity: a-avitaminosis, viral/mycopl)
PO/inhalation/skin lesion -> primary asympt replication -> viraemia -> organs, skin, mm —> secund viraemia –> skin replication - flourising!
- heterologus strain - only primary repl (swelling)
- DRY (cutaneus) form: skin lesions (warty on non-featherd areas)
- WET (mm) (diphteroid) form: more severe, more generalized, (anorexia, lethargy, coryza, conjunctivitis),
mm nodules on resp and oral - converge and cover with fibrin - anorexia) diphteric lesions in resp tract, may cause mortality! (Raised yellowish lesion in mouth)
Mixed form
Acute haemorrhagic/septicemic form -> sudden death
Fowl: mainly diphteric, immunized only resp signs
Turkey: diphteric form, infertile eggs
Pheasant: resp signs
Pigeon: diphteric in young
o Cutaneous form PM
Proliferative nodules at the larynx - may be obstructive
Tracheitis, diphtheric membranes
Body condition loss, degeneration of visceral organs, pulmonary oedema, enteritis
Epithel-proliferation, oedema, cytoplasmic inclusion bodies
Ddx: ILT! Mycoplasma common complication so may find, marek skin lesions, a-hypovitaminosis (milder, mm lesion)
Ab for mycoplasma co-infection
39 - Avian encephalomyelitis.
Picrona - termorvirus genus, Avian encephalomyelitis virus
- Aka epidemic tremor, affecting the CNS of esp chicken, phaesant, turkey, quail.
- worldwide
- Good antigen, widespread seropositivity -> clinical signs are quite rare
- maternal protection 3-6w
- mainly see signs from 1-5w!
- spread from feces (Direct, indirect), germinative if fresh infection (reach ovarium, will infect eggs for 3w!), embryos infected NOT damaged. If not fresh infection will have maternal protection.
- 50% morbidity, high mortality in young!
PO -> gut -> viraemia -> PO, ovary, CNS (inflammation, necrosis)
After some days see signs, CNS signs, most characteristically is the tremor - constant tremor of head and neck -> paralysis -> closed fingers … -> death
(tremors, ataxia, and weakness that progresses to paralysis.)
No gross pm, only HP CNS (lymphocytoc infiltr, degeneration)
Ddx other neurological
Active infection - no hatching for 1 month, then yolk immunity is seen when not fresh anymore!
40 - Duck viral hepatitises.
There are 4 viruses that might cause DVH, but the most widespread is duck hepatitis A
Type 1-4:
1: duck hepatitis A (picorna, avihepatogenus, most virulent, v resistant, ducklings under 6w)
2,3: astroviruses: duck astrovirus type 1 and 2. milder disease
4: duck hepatitis B in china, older ducks too..(hepadna, dsDNA, circular, enveloped)
PO: faeces, tracheal discharge, no germinative infection -> GI 1st repl -> viraemia -> PO, liver repliation(!2nd repl), liver dystrophy, necrosis of hepatocytes, death
- long immunity, yolk immunity!
o FAST spreading within the flock
o Day-old ducklings
- Explosive, 90% mortality
- If there is yolk immunity: slower (till the age of 2-3 weeks) -> 50% mortality
Clinical signs in young ducklings (0-4 weeks)
- most dead within 1w, many peracute, acute: general, ataxia, SPASMODIC PADDLING (opisthotonus, hunched back)
- Mycotoxins, complications can make more severe
Pathology
o Liver: enlarged, yellow, liver dystrophy, haemorrhages with sharp edges
o Spleen: enlarged, mottled
o Kidney: swollen, plethoric, nephrosis
Ddx duck hepatitis by astro! (Hepadna in china), duck plague
No treatment
Prevention: strict isolation in the first 4 weeks of age, infection after hatching…
Vax Layers, day old ducklings - homogenous protection important!
41 - Encephalomyocarditis
Encephalomyocarditis virus, cardiogenus, picorna
- widespread, europe too, but clinical form of the disease is NOT widespread! Maternal!!
- wide host range. Rodent virus, swine and human are important (other mammals susc too)
- rodents shed in urine, feces, infection by contaminated water/feed
- (msd: pigs shed in nasal disch 3d, direct transmission to other pig, also in environment, resistant)
- Mortality: newborn animals 25-50%, growers/fattening: 5-25%
- SLOW SPREAD
2 strains
EMCV-1, type A, widespread, reproductive issue
EMCV-2, type B, germany, myocarditis
- some strains cause A and B!
PO infection -> SI shed -> replicate in tonsils -> Viraemia:
Heart: necrosis in heart muscle (necrotic myocarditis)
Liver, kidney, spleen, lungs
CNS: encephalomyelitis
Foetus: abortion, weak piglets
o Immune response
SIGNS
- any age but more severe in young, 4-5w
- Heart muscles failure, anorexia, depression, 41C fever
- Shaking, paralysis, dyspnoea (oedema in the lungs)
- In PIGS: Viremia cross placenta - reproductive failure, abortion, SMEDI
PM
o Death of acute myocarditis -> some epicardial haemorrhage
o Heart: enlarged (compensating), soft, pale, necrotic foci, hydropericardium, hydrothorax, pulm. oedema
o Foetus: no gross lesions, sometimes oedema, haemorrhages
o Histology: IHC - positive myocardial cells, non-purulent encephalitis
–> Myocarditis: interstitial infiltration of lymphocytes & neutrophil granulocytes
Rodent control!! Seroconversion (paired to see active)
Human: infection from rodent, swine, rare signs
44 - Feline calicivirus infections.
Catteries! Cat FMD + resp :-) (systemic - lethal) basic vax w/ herpes!
Feline calicivirus - vesivirus
- Fe susceptible
- 1 serotype, significant differences in virulence variants (vax might not protect all, esp high virulence) - highly pathogenic strains!!
- woldwide
- catteries! Direct, indirect, aerogenic
- long carriage, some lifelong!!, continous shedding in ocular/nasal/oral disch (lower immunity, eg FIV, longer shedding)
- vax only lower signs, wont stop shedding!
Oronasal infection -> pharynx -> viraemia -> lungs, mouth, throat, joint synovial membranes, pads, visceral organs (very virulent strains -> hemorhages and edema)
o Oral mucosa, pads: blisters, epithelia necrosis -> erosions, neutrophil infiltration
o Lungs: alveolitis, exudative pneumonia, proliferative interstitiall pneumonia
o Joints: acute synovitis, thickened synovial membrane, liquid accumulation
First fever then second fever and signs are seen
- erosions: oral cavity- mainly on the margin of the tongue, lips, nose, pads, rarely skin
- Mild conjunctival & resp signs
- Lameness & fever (limping syndrome), Can be independent from the oral & resp signs
Virulent strains!
- severe systemic syndrome!
- Vasculitis, face & pad (50%), fever (90%), resp signs (50%), icterus (20%), nose & intestinal bleeding (30-40%), up to 60% lethality!
- MORE SEVERE IN ADULTS; in vaccinated cats too!
Chronic stomatitis may occur
Pathology, histopathology
o Erosions in the oral cavity, at the margin of the tongue
o Very virulent strains: vasculitis, enlarged liver, pneumonia, pancreatitis, pericarditis
Secundary infections make it tricky - secundary or the main cause? (Fe rhinotracheitis(herpes), b. Bronchiseptica, chlamydia)
Supportive, ab, vaccine! Vax too early - infection! Problem with breeders vax too early. Potects from signs but not infection or becoming carrier. (Live vs. Killed), live gives faster protection - good in shelters eg.
Hygiene, managemend, ID shedders!
NOT FINISHED FROM HERE
46 - Diseases of farm animals caused by hepatitis E virus.
Petras favorite virus :-) hepevirus family - Orthohepevirus A & C
Hu, pig imp (avian hep E confused farmer)
47 - Diseases caused by astroviruses.
Winter gastroenteritis: mamastrovirus genus (ho, bo, su, fe)
Avastrovirus genus
- Avian nephritis is the major disease
- duck astroviruses, duck hepatitis minor causative agents, other topic
- turkey astrovirus - diarrhoea
49 - Equine infectious arteritis.
Abortion, resp! Carrier stallion!
51 - Louping ill and tick-borne encephalitis (Zoon.)
These are pestivirus genus FLAVI, so the strongest of the weak.. nonarbo possible (po, aerogenic!)
Louping ill: sheep, biphasic fever(flu-cns) louping = ataxia, permanent lesions
Tick borne enceph - hu mostly, small mammal - rodent - tick cycle may reach human (raw goat milk). Biphasic fever like louping, permanent lesions
54 - Border disease of sheep.
Similar to BVD(should ddx, can infect sheep too), foetopathogenic, abortion! Aust/new zealand: hairy shaker disease!
58 - Porcine epidemic diarrhoea, haemagglutinating encephalomyelitis of pigs.
PED
Now more imp than TGE. #2 less pathogenic, same ancestor, can use for vax for both (2) - presence in herd influence TGE!
Haemagglutinating enceph
- Periph nerve to cns from ent/resp –> stim vomiting from brain, nasal disch shedding. Vomiting/wasting or CNS form! (2 forms)
- Coronaviral diarrhoea of cattle and dogs.
Cattle: calf diarrhoea –> BRDC –> winter dysentery (dairy mostly. Decr milk prod) - heating!
Dog: mild, heating! Pantropic!! (Dysentery, pneumonia, cns - generalized,
- Diseases of cats caused by coronaviruses
FIP: infectious yet not contagious, has 100% mortality, virtually no diagnostic test to confirm it, and no effective treatment :-)
- Diseases of cats caused by coronaviruses
FIP: infectious yet not contagious, has 100% mortality, virtually no diagnostic test to confirm it, and no effective treatment :-)
61. Infectious bronchitis of chicken, coronaviral enteritis of turkey.
Chicken
- Below 6w: caseous pllug,perm oviduct damage
Grower/layer: mild resp, transient oviduct damage (egg drop)
Nephropathogenic - PD, wet litter
Use several vax!
Turkey - like BoCV.. mortality can go up to 50% if young/bad management! B fabricii affected! Egg drop, no vax! Eradication!!
- Diseases of farm animals caused by orthoreoviruses and rotaviruses
Orthoreo
Ru pneumoenteritis young mainly… (BRDC)
Rota
Maternal!! 1-2w
- Reoviral diseases of poultry.
HEMHRIT - orthoreoviruses!
Helicopter, enteric, malabs, hydropericardium, resp, immunsuppr (bursa), tenosynovitis
