Virology Flashcards

(153 cards)

1
Q

Poxvirus transmission

A

Resistant in environment (despite envelope)–>

Transmit via abraded skin, respiratory route (droplets), mechanical (fomites, insects, etc.)

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2
Q

Genus Capripoxvirus spp.

A

sheep pox
lumpy skin disease
goat pox
(all serologically identical)

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3
Q

Genus Caprivirus Epidemiology

A

endemic in SE Europe, Middle East, Africa, Asia
Generalized disease
Can spread between sheep/goats/cattle but often remain in respective host sp.
Mortality up to 50% in indigenous breeds, up to 100% in European breeds

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4
Q

Genus Caprivirus Pathogenesis and clinical signs

A

Infection by abrasion, aerosols, mechanical–> replicates locally in skin/lungs–> regional lymph nodes–> viremia–>shed from skin lesions and nasal/ocular discharge
Incubation ~ 1 week–> fever, edema of eyelids, conjunctivitis, nasal discharge, skin lesions, lung consolidation/hemorrhage

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5
Q

Genus Avipoxvirus spp., modes of transmission

A

Fowlpox virus, other avian poxviruses

Mechanical transmission by mosquitoes, aerosol transmission

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6
Q
Orf virus (scabby mouth, contagious ecthyma)
Transmission, pathogenesis, maintenance in population
A

= contagious pustular dermatitis (worldwide)
Transmitted by direct/indirect contact (abrasions)- infectious in scab for months
Epitheliotropic- proliferates locally in epidermal keratinocytes–> wart-like lesions near lips, muzzle, feet, genitalia, teats
papules–>vesicles–>pustules–>scabs
Primarily in young sheep, maintained by chronic carriers

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7
Q

Myxoma virus epidemiology and pathogenesis

A

Myxomatosis = poxvirus disease of rabbits
Benign fibromas in American wild rabbits, severely degenerative in European species
Mechanical transmission by mosquitoes and fleas (not contagious)–>listless and febrile–> often death w/in 48 hours (survivors have sub-Q gelatinous swellings)
Mortality rate ~99% in wild rabbits w/ virulent strain

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8
Q

African swine fever (asfarviridae) epidemiology, pathogenesis

A

Infects Suidae and soft ticks
Persistent tick infection–> 1) sylvatic cycle- viremia in juvenile warthogs (little-no dz in African breeds)
–> 2) domestic cycle- up to 100% mortality due to diffuse hemorrhage from platelet damage and complement activation, fever (European breeds)
Persists in meat for months–>pigs can become infected from carcass of dead infected pigs
No neutralizing Ab made, no vaccine, risk of international spread in pig products

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9
Q

Herpesvirus epidemiology/pathogenesis

A

Labile (enveloped)–> spread by close or mucosal contact (e.g. droplets)
Lifelong latent infection in neural or lymphatic tissue with continuous or periodic shedding (reactivated in times of stress)
Copies DNA in infected neurons, no viral gene expression except latency associated transcripts (LATs- inhibit apoptosis)
Can be shed while sub-clinical or recrudescent (reemerging clinical signs)

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10
Q

Bovine Herpesvirus 1 (infectious bovine rhinotracheitis)

Pathogenesis, clinical signs

A
Respiratory infection by aerosol route--> viremia (dissemination)--> rhinotracheitis, vulvovaginitis, balanoposthitis (virus shed in semen), conjunctivitis, abortion, enteritis, nasal discharge, hyperemic nasal mucosa, dyspnea, coughing, focal areas of epithelial necrosis and inflammation
Recovery 5-10 days
Intensive environments (e.g. feedlots) morbidity ~100%
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11
Q

Bovine herpesvirus 2

A

Bovine mammillitis virus/ pseudo-lumpy skin disease virus
2 forms:
Mammillitis (localized lesions on teats)
Generalized nodules and necrosis

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12
Q

Bovine herpesvirus 5

A

Bovine encephalitis virus

direct neural spread via trigeminal nerve from nasopharynx–> fatal meningoencephalitis in calves

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13
Q

Equine herpesvirus 1

epidemiology, pathogenesis

A

Most important viral cause of horse abortion worldwide
Infection via respiratory tract–> respiratory and neural dz–> viremia and systemic infection–> endothelium of endometrial vasculature–> vasculitis–> infarction–> abortion
Aborting mare infectious for 1-2 days from reproductive tract, 2 weeks from respiratory tract
Minimize risk by keeping pregnant mares separate from other horses and in small groups by foaling date
Reduce latent infection risk by minimizing stress

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14
Q

Equine Herpesvirus 4

A

Equine rhinopneumonitis- similar to EHV1 but only acute respiratory dz
nasal discharge and lymphadenopathy in foals (esp. weanlings and yearlings)
Only ELISA can differentiate EHV1/EHV4

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15
Q

Equine Herpesvirus 3

A

Equine coital exanthema
Veneral alphavirus
Lifelong latently infected carriers
Spread by mucosal contact

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16
Q

Feline Herpesvirus 1

clinical signs and prevention

A

Feline rhinotracheitis
Acute respiratory dz (similar signs to calicivirus)- nasal/ocular discharge, sneezing, dyspnea, oral ulcers
Lifelong latent carriers
Inactivated and live attenuated vaccines available
Live vaccine can cross placenta in pregnant queens

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17
Q

Gallid Herpesvirus 1

Clinical signs

A
Infectious laryngotracheitis (young chickens)
Acute respiratory dz- nasal/ocular discharge, sneezing, dyspnea, gasping/coughing
Often hemorrhagic exudate w/ diphtheritic pseudo-membrane occluding trachea
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18
Q

Canine adenovirus 1 pathogenesis

A

Infectious canine hepatitis (4-9 day incubation)
Contaminated urine/feces–> nasopharynx/mouth/conjunctiva–> tonsil crypts/peyer’s patches–> viremia–> vascular endothelial cells–> hemorrhage/necrosis of major organs (esp. liver- inflamm., hepatocellular damage, failure)
–> 1) virus shed in urine/feces/saliva
–> 2) shock–> death
–> 3) Neutralizing Ab response–> recovery

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19
Q

Canine adenovirus 1

clinical presentations, diagnosis, prevention

A

3 syndromes:

1) peracute dz- 3-4 hours, found dead
2) acute dz- fever, vomiting, dysentery, collapse, petechial gums, icterus, may be fatal
3) mild or inapparent dz

Dx: Ag detection in urine (virus isolation, PCR)
- Ab detection- ELISA, HAI

Prevention: vaccine part of C3 protocol, CAdV2 vaccine cross-protective and safer than CAdV1 (no risk of corneal edema)

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20
Q

Canine adenovirus 2

A

Infectious canine tracheobronchitis
Localized respiratory dz (part of kennel cough complex)- bronchitis/bronchiolitis
Not systemic, doesn’t affect wildlife
Vaccine provides complete homologous protection against CAdV1

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21
Q

Equine adenovirus 1 & 2

A

EAdV1: found in young horses w/ or w/o respiratory dz
EAdV2: in lymph nodes and feces of foals w/ respiratory disease and diarrhea
Mostly asymptomatic or mild
Could be fatal for Arabian foals with SCID

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22
Q

Family Papillomaviridae pathogenesis

A

Infections through skin abrasions–>infection of basal cells in squamous epithelium–> clonal proliferation (delayed maturation)–> papilloma formation (finger-like projections)–>viral shedding
Often in young animals, usually regress after several weeks

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23
Q

Bovine papillomavirus

pathogenesis, neoplastic transformation, diagnosis

A

Transmission via fomites, sexual (venereal warts)–> squamous papilloma in mucocutaneous areas–> fibropapillomas (pedunculated) on udder, teats, head, neck, genitalia–> spontaneous regression after 1-6 months
Neoplastic transformation: BoPV + bracken fern poisoning (enzootic hematuria)–> neoplasia (BoPV2= bladder cancer, BoPV4= alimentary cancer)
- UV + BoPV–> ocular squamous cell carcinoma in lateral esclero-corneal limbus, nictitating membrane, or lower eyelid
Dx: direct observation, histopathology, PCR

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24
Q

Equine sarcoid

Presentations, behavior, treatment

A

Papillomavirus (BoPV implicated)- most common equid skin tumor
Head, limbs, ventral abdomen of 4+ y.o. horses esp. at site of previous scarring
Locally aggressive but does not metastasize
Transmitted by fomites, possibly flies
Possible presentations: occult, verrucose, nodular, fibroblastic, malevolent, +/- pedunculated
Treatment (excision) ineffective- recurrence common

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25
Feline Panleukemia virus | epidemiology, pathogenesis, clinical signs, prevention
``` Highly contagious generalized systemic/enteric dz worldwide (1 serotype) Enters cats (often young as maternal Ab wanes) via oropharynx--> replicates in pharyngeal lymphoid tissue--> viremia--> mitotically active cells (intestinal crypt, bone marrow, fetal cerebellum/retina)--> incubation ~5 days--> bone marrow suppression, GIT signs, cerebellar hypoplasia (in fetus via transplacental transmission)--> shed in saliva, urine, vomit, feces (several weeks) Inactivated and live vaccines available ```
26
Canine parvovirus 2 | Epidemiology and prevention
``` High morbidity and mortality in all Canidae 3 variants (2a, 2b, 2c) Vaccine protects against all variants but not 100% immunity- part of C3 given @ 6-8 weeks, 14-16 weeks, 1 year, every 3 years ```
27
Canine parvovirus 2 pathogenesis
Feco-oral transmission--> pharyngeal lymphoid tissue--> viremia--> replicates in intestinal crypt cells--> hemorrhagic gastroenteritis, vomiting--> virus shed in feces for 3-7 days after infection (persists in environment for months) Mucosal collapse w/ contraction/fusion of SI villi--> malabsorption, hemorrhage--> dysentery w/ fetid smell (usually enough to make presumptive Dx)
28
Porcine parvovirus | epidemiology, pathogenesis, diagnosis, prevention
Worldwide reproductive failure, 1 serotype, stable in environment Infection via oronasal route--> local replication in tonsillar lymphoid tissue--> viremia and transplacental transmission (takes ~15 days to reach fetus) - <30 days gestation--> resorption - 30-70 days gest.--> stillbirth & mummification - >70 days--> stillborn, abnormal, or normal fetus Dx: infected feti have high virus titer (PCR, HAI) Prevention: exposing guilt or vaccinating before pregnancy induces immunity
29
Psittacine beak and feather disease | pathogenesis and clinical signs
Cockatoos, parrots, budgerigars Replicates in basal epithelial layer--> basophilic intracytoplasmic inclusions, lymphoid depletion--> difficulty feeding and death Feather changes: stunted pin feathers, bloody/sheathed/fractured adult feathers Beak/claw deformities: broken, overgrown and shiny, delaminations, palatine necrosis
30
Porcine circovirus 2
Post-weaning multi systemic wasting syndrome | Progressive dz in 6-week old piglets- weight loss, enlarged lymph nodes, dyspnea
31
Chicken anemia virus
Shed in feces & feather dander--> transmitted by direct contact or fomites--> aplastic anemia, generalized lymphoid atrophy in 2-3 week old birds
32
Bluetongue epidemiology
Family Reoviridae, Genus Orbivirus Non-enveloped RNA virus with >25 serotypes of varying virulence Infects she, cattle, and goats in tropics/sub-tropics Arbovirus- replicates in arthropod (Culicoides spp.) salivary glands & has extrinsic (in arthropod) and intrinsic (in mammalian host) incubation periods
33
Bluetongue pathogenesis
Infection from arthropod--> incubation ~1 week--> replicates in lymphoid tissue and endothelial cells--> viremia for 14-28 days--> spread when bitten by Culicoides spp.
34
Bluetongue clinical signs
Various vascular lesions: hyperemia of oral cavity (frothy/salivation), nasal discharge (variable consistency), cyanosis of tongue, hyperemia of coronary bands, edema of head/neck Vary from sub-clinical to fatal (~2-8 up to 30% mortality), more severe in sheep than in goats Pregnant ewes may abort or have lambs with abnormalities (hydranencephaly)
35
Bluetongue diagnosis and control
Dx: presumptive based on clinical signs or post-moltem findings, isolation, PCR, serology (ELISA), neutralization assay Control: live attenuated vaccinations available (must know local prevalent serotypes), sentinel cattle herds
36
African Horse Sickness epidemiology
Same as Bluetongue but host species = horse | 9 serotypes
37
African Horse Sickness | clinical signs
3 forms of febrile dz: - Peracute pulmonary form (near 100% mortality): nasal discharge--> respiratory distress (pulmonary edema, pleural effusion) - Subacute cardiac form: conjunctivitis, abdominal pain & progressive dyspnea, sub-Q edema (infraorbital fossa, palpebral conjunctiva, intramandibular, hydropericardium) - Mild/sub-clinical dz in African donkeys and zebra
38
African Horse Sickness pathogenesis
Infection from arthropod vector-->incubation ~4-9 days--> replicates in regional & other lymphoid tissue--> blood cell-associated viremia w/ onset of fever--> heart, brain, lungs, endothelial cells
39
African Horse Sickness | diagnosis and control
Presumptive Dx based on clinical signs, rapid death, typical lesions (supraorbital edema, frothy nasal discharge, respiratory distress), seasonality Virus isolation or RT-PCR from washed RBCs Control: attenuated polyvalent vaccine available, predict outbreak through knowledge of vector life cycle
40
Genus Rotavirus pathogenesis
Feco-oral transmission (food, water, etc.) in 1-8 week old calves--> incubates ~12-24 hours--> capsid VP4 cleaved by chymotrypsin in epithelium of apical tips of SI villi--> severe enteritis, secretory diarrhea ("white scours"), inappetence, depression, dehydration (--> death)--> high titer shed in feces, persists for months, resistant to disinfection, small infective dose required
41
Rotavirus control
Improved hygiene IgG in colostrum/ lactogenic immunity (vaccinate dam) Prevent dehydration and electrolyte imbalance
42
Foot and Mouth Disease | epidemiology
Family Picornaviridae, Genus Aphthovirus Highly contagious dz of cloven-hooved farm animals (NOT horses) High morbidity, low mortality- huge production losses Multiple host spp. and modes of transmission 7 serotypes (O, A, C, SAT1, SAT3, Asia1) with little cross-tolerance Small infective dose, rapid replication Pigs = amplifier host, sheep often inapparent/persistent carriers
43
FMD pathogenesis
Oral transmission by aerosols or fomites--> incubation period 2-8 (up to 14) days--> shedding up to 4 days before onset of clinical signs
44
FMD control: | vaccination (inactivated) vs. slaughter
Vaccinated animals can be carriers- serologically identical to diseased FMD-free w/o vaccination = easier to trade than if vaccinated; serological test and slaughter (positive and in-contact animals) Endemic FMD- eradication campaign w/ ring or blanket vaccination
45
FMD clinical signs and diagnosis
Fever, inappetence, depression, decreased production, excessive salivation Vesicles on tongue and oral mucosa, interdigital region, coronary bands, teats, nasal mucosa/muzzle Vesicles coalesce/rupture--> large ulcers Myocarditis--> sudden death in calves and piglets Dx: sample from epithelium with vesicles, Ag detection by ELISA, culture, PCR
46
Eastern & Western Equine Encephalitis
Family Togaviridae, Genus Alphavirus- enveloped RNA viruses Maintained in mosquito-passerine bird cycles (neither show dz) Dz outbreaks when sufficient vectors spill over to horses and humans (dead-end hosts) Seasonal peak in late summer after heavy rainfall
47
Venezuelan Equine Encephalitis epidemiology
Outbreaks when vectors spill over to horses and humans Viremia in infected horses = sufficient titer to be amplifying host for new vectors Enzootic/endemic cycle: between small mammals and Culex spp. Epizootic/epidemic cycle: virus mutates to enter cycle between mosquitoes and large mammals
48
Equine Encephlitidies pathogenesis
Mosquito bite--> replication in local cells--> regional lymph nodes--> primary viremia--> replicates in muscle, CT, endothelium--> secondary viremia--> CNS invasion--> neural necrosis, mononuclear infiltration, perivascular cuffing, interstitial edema (incubation up to 9 days)--> mild fever and depression to fatal encephalomyelitis with CNS signs (photophobia, head pressing, etc.)
49
Equine Encephalitidies diagnosis and control
Dx: viremia transient- difficult to isolate in blood - serology (IgM ELISA), neutralization on paired sera Control: vaccination available in endemic areas - Live VEE, inactivated WEE & EEE - Vector ctrl- insecticides, repellents, sentinel chickens
50
Japanese encephalitis epidemiology
Flavivirus endemic to SE Asia, India, China reservoir = water birds amplifying host = pigs (reproductive failure) Spillover to horses and humans (dead-end hosts)--> severe fatal encephalitis (fever, lethargy, hyperexcitability, recovery or death) Maintained in mosquito-pig life cycle Post-mortem serology for Dx
51
West Nile Virus | epidemiology, dz processes, prevention
Mediterranean, Asia, Africa, US (warm/wet climates) Urban bird-mosquito cycle Bird = amplifier--> blood titer sufficient to be picked up by more vectors Fatal encephalitis in horses, hemorrhagic fever in humans Vaccine: killed virus in 2 doses w/ annual booster - no IgM, high levels neutralizing Ab after 2nd dose
52
Murray Valley Encephalitis Virus epidemiology
Victoria and SA Arbovirus (vectors = Culex annulirostris, C. australicus) Maintained in herons, cormorants, darters Often sub-clinical (1 in 800 severe dz) Transient viremia- hard to detect (serological & virological)
53
Bovine viral diarrhea virus | different disease presentations (non-pregnant)
Acute- BVD Chronic- persistent mucosal dz (profuse watery diarrhea, ulcers, fatal w/in weeks) All ages susceptible Fever, immunosuppression, leukopenia, diarrhea, naso-ocular discharge, ulcerative stomatitis, decreased milk production
54
BVDV | pathogenesis (pregnant)
Transplacental transmission - <80 days: abort, resorb - 80-125 days: cytopathic strain--> lesions/weakened or dead calves, non-cytopathic strain--> tolerance to virus - >125 days: active immune response, develop Ab and survive
55
BVDV diagnosis, prevention, control
Dx: difficult- PCR, isolate virus/detect Ag, immunofluorescence, serology Killed and live vaccines available but not fully protective Must remove persistently infected animals to eradicate
56
Classical swine fever | epidemiology, pathogenesis, clinical signs, prevention
Contagious, exotic dz Virulent, moderate (chronic dz), and low virulence (decreased fertility) strains Ingestion/inhalation due to direct contact--> replicates in tonsils--> lymph & endothelial cells--> hemorrhages, DIC, thrombosis (2-10 day incubation)--> fever, hyperemia, purpura, convulsions, posterior paresis, paralysis, tremors, death wi/in weeks Effective live vaccine available
57
Influenza A pathogenesis
Aerosols (or feco-oral for birds)--> spread through respiratory tract in 1-3 days--> fever w/ necrosis of epithelial cells--> secondary bacterial infections may--> bronchopneumonia
58
Influenza A epidemiology
``` Orthomyxovirus- enveloped, RNA Subtypes: HA(16+) + NA(9) - external Ag^ do not cross-react - strains (usually geographical) w/in subtype may cross-react Seasonal Shed ~8-10 days (often sub-clinically) High morbidity, low mortality Common interspecies transmission (horse, human, bird, pigs) ```
59
Influenza A | common clinical signs
Cough, sneezing, nasal discharge, fever, loss of production (eg low virulence avian influenza)
60
Retrovirus | envelope & genome characteristics
``` Envelope has peplomers (glycoprotein spikes) (labile--> require close contact) Diploid RNA genome w/: - gag--> structural proteins - pol--> reverse transcriptase - env--> envelope protein ```
61
Rapid mutation of retroviruses
RT makes frequent errors--> inherent high rate of mutation Concurrent infection w/ 2 retroviruses--> high rate of recombination btwn viruses (partially due to diploidy)--> different peplomers = ability to bind new cell types--> potential for jumping species
62
Exogenous vs. endogenous retroviruses
``` Exogenous = can create infectious virions and transmit horizontally Endogenous = genetic element (provirus) w/in host genome that can replicate and insert into distant part of genome ```
63
``` Neoplastic dz (alpharetrovirus) in poultry 3 strains ```
Replication competent virus--> lymphoid leukosis, osteopetrosis, renal tumors Replication incompetent virus (carry onc gene)--> neoplasia of myeloid cells and sarcomas Replication competent rapidly transforming virus (w/ onc)--> Rous sarcoma virus
64
Neoplastic dz in poultry | pathogenesis
- If infected <5 days old--> immunological tolerance--> lifelong infection--> leukemia and other dz (constantly shedding) - If infected >5-6 days old--> transient viremia and neutralizing Ab production - DNA provirus insertion into germline--> genetic transmission - Horizontal transmission inefficient but facilitated by intensive conditions
65
Ovine pulmonary adenomatosis (Jaagsiekte- Betaretrovirus) | pathogenesis and control
Respiratory infection--> multiple small tumors (type II secretory epithelial cells) in lungs produce copious fluid w/ surfactant--> spasmodic coughing (no immune response) Incubates 1-3 years Transmission slow so removal of sick sheep/offspring is sufficient to control
66
Feline leukemia and sarcoma | dz processes
Gammaretrovirus Multicentric/thymic lymphoma, alimentary & lymphosarcoma of eye/skin/CNS, myeloproliferative dz w/ anemia, immune complex dz & immunodeficiency W/in 6 weeks will either: 1) persistent infection w/ viremia but no neutralizing Ab response 2) transient viremia w/ neutralizing (or anti-FOCMA) Ab response--> no dz signs (still contagious) Dx: clinical signs, post-mortem, test blood for Ag
67
``` Bovine Leukemia (BLV) presentation, diagnosis, control ```
Deltaretrovirus Mostly subclinical +/- leukocytosis, few develop lymphoid tumors Decreased productive life and condemned carcass Likely relies on proviral oncogenes targeting B cells Can detect Ab in serum or milk Natural transmission is slow- control by testing serum every 3 months and removing if Ab+
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Lentivirus behavior
slowly progressive acquired immunodeficiency | mutations in env gene--> Ag variation
69
Maedi/Visna | dz processes
= Ovine progressive pneumonia maedi = dyspnea- lung consolidation due to lymphocyte/macrophage infiltration visna = wasting- demyelinating leukoencephalomyelitis
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Maedi/Visna pathogenesis
Spread by respiratory droplets or milk--> 2 year incubation--> present in blood/semen/bronchial secretions/tears/saliva/milk--> slow progression--> eventually fatal Detection by Ab in serum
71
``` Caprine arthritis (encephalomyelitis) dz processes, control, diagnosis ```
Progressive leukoencephalomyelitis (<4 m.o.) or arthritis (>1 y.o.) Transcolostral transmission- control by preventing suckling and supplementing kids with pasteurized colostrum Dx: history in flock, serum Ab
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Equine infectious anemia | pathogenesis, clinical signs, diagnosis
Transmission by mechanical vectors (stable flies, tabanids, mosquitoes, etc) or iatrogenic Incubates 7-21 days--> fever associated w/ macrophages and lymphocytes--> lifelong cell-associated viremia (sub-clinical or recurrent dz) Fever, weakness, anemia, jaundice, thrombocytopenia, IgM/IgG deposition on RBCs/platelets/endothelium Dx: serum Ab (Coggins test)
73
Feline immunodeficiency virus | epidemiology, pathogenesis, detection
Worldwide, many cat spp. Shed in saliva--> transmission through bites--> lifelong infection Early: fever & lymphadenopathy Terminal (months-years later): weight loss, CNS signs, leukopenia, secondary infections Detection by serum Ab, vaccine not widely used (only 2/5 serotypes)
74
Jembrana disease | pathogenesis, prognosis
Fatal dz in Balinese cattle (high morbidity and mortality) 5-12-day incubation--> hemorrhages & splenomegaly--> fever, lethargy, anorexia, swollen lymph nodes, panleukemia Rapidly progressive, recovered animals clear the virus (unique for Lentivirus)
75
Oncogenic Retroviruses & major genes
FeLV, BLV, avian leukosis virus, porcine lymphosarcoma, murine leukemia, koala retrovirus RNA genome: gag = core nucleocapsid structural protein pol = reverse transcriptase env = envelope proteins +/- v-onc = induce cancer
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Replication incompetent exogenous retroviruses
gag_pol__v-onc | Require co-infection w/ other virus to induce cancer
77
Replication competent exogenous retroviruses (2 types)
1. gag_pol_env - insert provirus near c-onc or TSG to alter expression - chance event-->longer incubation period 2. gag_pol_env_v-onc - cancer after short incubation (short as 2 weeks) - e.g. Rous sarcoma virus of chickens
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Oncogenic Flaviviruses
Hepatitis C virus can--> late stage hepatocellular carcinoma (humans)
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Oncogenic Poxvirus mechanism
Replicate entirely in cytoplasm (DNA genome) | Early viral protein homologous to epidermal growth factor--> cell proliferation--> local benign tumor-like lesions
80
Hepadnavirus oncogenesis
Associated w/ natural hepatic carcinomas | e.g. duck hepatitis B + mycotoxin ingestion--> malignancy
81
Marek's dz oncogenesis
Herpesvirus in chickens w/ many v-onc genes - meq- activates signal transduction pathways - vTR- encodes subunit of telomerase to maintain telomere length
82
Coronavirus characteristics
Enveloped (labile but can survive in GIT) RNA genome Replicate in cytoplasm Glycoprotein spike "crown" for attachment- determines tropism, antigenicity, target for neutralization ( S "spike" protein)
83
Coronavirus pathogenesis
Aerosol, feco-oral, or close contact transmission--> GIT and URT of birds and mammals Clinical infections often in young animals as maternal Ab wanes Can spread to LI (unlike rotaviruses, which also infect apical enterocytes) Enteric dz: 20-100% morbidity, 1-2% mortality Good at jumping species
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Bovine Coronavirus | enteric infection
Calf diarrhea from <3 weeks-3 months old (maternal Ab) Destroys mature absorptive enterocytes of SI and LI villi--> malabsorption--> water and electrolyte loss--> circulatory failure and death (calves) or intestinal hemorrhage/necrosis (adults)--> explosive dysentery, decreased milk production
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Bovine Coronavirus respiratory infection
Mild dz- coughing and rhinitis More severe- pneumonia in 2-6 m.o. calves Part of shipping fever complex Cattle arriving at feedlot w/ high BoCV Ab titer are less likely to contract/spread dz Found in URT and LRT
86
Transmissible gastroenteritis virus (TGEV) | pathogenesis, reasons it targets young animals
= highly contagious coronavirus w/ severe clinical signs in piglets - Feco-oral transmission--> mature enterocytes of SI--> vomiting, watery diarrhea, weight loss, dehydration, death w/in days Young more susceptible b/c less gastric acid and milk diet protect virus in GIT, slower turnover of enterocytes than adults, immature immune system, more vulnerable to electrolyte/fluid loss than adults
87
Porcine respiratory coronavirus
Variant of TGEV w/ partial deletion of S protein gene--> altered tropism (strong cross-immunity to TGEV) Aerosols--> mild to no respiratory signs
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Porcine epidemic diarrhea virus (PEDV)
Clinically/pathogenically similar to TGEV, but different Ag/genome/serological properties
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Porcine hemagglutinating encephalomyelitis virus (PHEV)
Aerosol transmission--> primary replication in nasal mucosa/tonsils/lung/SI--> CNS via peripheral nerves--> vagal sensory ganglia/gastric myenteric plexus--> vomiting/wasting dz in piglets (<3 w.o.) Passive protection from maternal Ab
90
Canine coronavirus
Enteric dz: worldwide in domestic & wild dogs, single serotype, similar path. to other spp. Resp. dz: associated w/ "kennel cough" complex - genetically distinct from enteric virus - aerosol spread--> mild dz- dyspnea, pneumonia, occasionally death
91
Feline coronavirus | 2 biotypes
2 biotypes of same virus (only difference is dz induced): 1) Feline enteric coronavirus (FECV)- mild enteric disease 2) Feline infectious peritonitis (FIP)- fatal systemic pyogranulomatous dz
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FIP | clinical signs and 2 forms
Clinical signs depend on vasculitis and extent of organ damage from loss of blood supply Wet form: many vessels affected--> exudation into body cavities--> viscous/clear ascites--> abdominal dissension/thoracic effusion Dry form: signs vary depending on which organs damaged by granulomas Both forms: white/grey nodules around vessel walls in omentum, liver, peritoneum, etc.
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FIP | pathogenesis
Virulent mutant emerges with strong tropism for macrophages and monocytes--> productive infection--> perivascular aggregations--> macrophage activation and release of inflamm. mediators--> increased vascular permeability and chemotaxis--> further inflamm. cascade Kittens prone as maternal Ab wanes, other Ab not protective Likely maintained in population by sub-clinically shedding cats
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Poultry coronavirus | pathogenesis
= infectious bronchitis virus - Respiratory +/- systemic dz of chickens spread via aerosols and fecal-contaminated feed - ciliated resp. cell infection--> viremia (18-48 hour incubation)--> damage to URT/LRT +/- ovary, kidney, oviduct 1-4 week old chicks: - virulent strain- gasping, coughing, dyspnea, mortality 25-30% (up to 75%) - less virulent strain- milder signs, lower morbidity/mortality Laying hens- decreased productivity
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Poultry coronavirus | control and diagnosis
Both Ab and CMI required for protection- vaccinate 1-day chicks extensively - can have vaccine breaks when poor match to endemic serotype Dx: sample tissues, RT-PCR
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Lyssavirus genotype I (Rabies) epidemiology
Worldwide except Japan, UK, Australia, NZ, Antarctica, parts of Europe Maintained in given region within particular mammalian host in 1 of 2 cycles: 1) Urban rabies in dogs (dog population > 4.5 dogs/km^2) 2) Sylvatic (wildlife)- in US 36.5% in raccoons, 23.5% in skunks, 23.2% in bats
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Lyssavirus genotype I (Rabies) pathogenesis
Transmission primarily through bites (saliva) - -> replicates in local muscle cells - -> variable incubation (weeks-years) - -> binds ACh receptors @ NMJ - -> climbs peripheral nerves to CNS via retrograde axonal transport - -> up spinal cord to brain - -> lymbic system (loss of behavioral ctrl = "Furious" rabies) - -> neocortex ("Dumb" rabies) - -> centrifugal spread down nerves to non-nervous tissue (e.g. salivary glands) - -> death due to respiratory depression
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Lyssavirus genotype I (Rabies) control
``` 1 vaccine (inactivated or attenuated) prevents disease from all strains In areas with epidemic urban rabies in dogs vaccination (+/- spay/neuter) >>> culling Vaccination coverage must be 60-80% of dog population to significantly reduce risk in local human populations ```
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Vesicular stomatitis | Pathogenesis, clinical signs, similar dz
- Febrile dz of horse, cattle, pig (exotic to Australia) - Clinically indistinguishable from FMD- main difference being that horses can get infected - Mechanically transmitted by arthropod vectors (black flies) - Vesicular lesions on oral mucosa, teats, coronary band, snout, tongue for 7-10 days
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Bovine Ephemeral Fever (BEF) epidemiology
- Arbovirus spread by Culicoides and mosquitos - Outbreaks follow conditions favorable for vectors - Tropics: outbreak after rainfall - Temperate: outbreaks in summer - High morbidity, low mortality
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Bovine Ephemeral Fever (BEF) pathogenesis
Transmission via Culicoides or mosquito - -> primary site of replication unknown - -> 3-4 day viremia, 4-7 day incubation - -> sudden onset fever, decreased milk production, depression, lameness, recumbency - associated w/ neutrophilic, polyserositis & hypocalcemia, neutralizing Ab (day 3 of clinical signs) - -> recover w/in 3 days - -> strong immunity post-infection
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Bovine Ephemeral Fever (BEF) diagnosis and treatment
Dx: typical clinical signs (affecting majority of herd) Tx: anti-inflammatory drugs effective, inactivated vaccine available
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Bunyavirus Akabane | epidemiology
- Arbovirus spread by Culicoides brevitarsis and mosquitos in tropics/subtropics of Middle East, Asia, Australia, and Africa - Sporadic epidemics correspond to vector movement - Infects sheep and cattle (+ goats and deer)
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Bunyavirus Akabane | pathogenesis
Susceptible dam bitten by infected vector - ->crosses placenta w/o causing disease in mother - ->variable signs in fetus depending on stage of development - Primary fetal infection = encephalomyelitis, polymyositis - Survivors have cerebral cavitations, hydranencephaly, arthrogryposis, torticolis/scoliosis/kyphosis
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Bunyavirus Akabane | diagnosis and prevention
Dx: usually by gross pathological findings, serological findings (neutralizing Ab fetal/newborn sample, paired maternal sera) Inactivated vaccine available in Japan and Australia
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Family Paramyxoviridae | 2 major glycoprotein peplomers
1) Hemagglutinin/Neuraminidase (H/N) protein- involved in attachment - Neutralizing Ab directed against HN 2) Fusion (F) protein- cleavage essential for infectivity (esp. Newcastle Disease) - (similarly, G protein in Hendra and Nipah viruses necessary to infect)
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Avian paramyxovirus 1 (Newcastle Disease- NDV) | epidemiology
- Highly contagious resp/GI/neural dz in poultry worldwide - Varying virulence and tropism between strains - Many avian species susceptible (turkeys, pigeons, chickens, etc.); wild birds = reservoir - Excreted in feces or respiratory tract, persist in environment or carcass for weeks, transmit via aerosols or contaminated feed/water
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Newcastle Disease Virus | pathogenesis
Feco-oral or aerosol transmission - -> replicates in respiratory or GI epithelium - ->primary viremia - ->spleen and bone marrow - ->secondary viremia - -> lungs, intestines, CNS - -> (5-day incubation) clinical signs depend on strain virulence, tissue tropism, host factors
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Newcastle Disease Virus | virulence of strains and associated clinical signs
- Velogenic = high virulence--> sudden high mortality (~100%) - Mesogenic = intermediate--> mild dz (coughing, production losses), mortality only in young - Lentogenic = mild dz or inapparent infection (F protein only cleaved in RT or GIT) - virulence associated w/ cleavability/activation of F protein in different tissues - Viscerotropic vs. neurotropic - viscerotropic velogenic isolates: severe fatal dz w/ intestinal hemorrhage & bright green diarrhea - neurotropic velogenic: respiratory signs--> neurological signs (tremors, paralysis)
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Newcastle Disease Virus | diagnosis and control
Dx: virus isolation from swabs in embryonate eggs, HA/HAI Pathogenicity test: mean death time for eggs, sequence F protein, RT-PCR Ctrl: - NDV-free countries: test and slaughter - NDV-endemic countries: attenuated live vaccination strains
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Morbillivirus Rinderpest | epidemiology
= "cattle plague" (eradicated in 2011) - Acute fatal dz w/ pyrexia, inflammation, necrosis of mucous membranes - High morbidity, high mortality - 1 serotype, different strains (one vaccination protects against all strains) - Virus shed in feces, urine, respiratory secretions (often before clinical signs) - Labile in environment (requires close contact) - No carrier state (difference from FMD)
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Morbillivirus Rinderpest | pathogenesis
Transmission by inhalation - ->replication in tonsils and local URT lymph nodes - ->viremia - ->other lymphoid tissue, respiratory/GIT mucosae - -> leukopenia from lymphoid necrosis
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``` Morbillivirus Rinderpest clinical signs (progression) ```
3-5 day incubation--> rapid pyrexia (prodromal phase) - ->mucosal phase (necrotic foci in nasal, oral, urogenital mucosa) = mucopurulent nasal/ocular discharge - -> necrotic foci--> erosions (fever regresses when ulcers appear) - -> hemorrhagic diarrhea - -> death w/in 12 days (dehydration, wasting, etc)
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Rinderpest | diagnosis and control
Dx: viral Ag in spleen, lymph nodes, or secretions Ctr: quarantine, widespread attenuated vaccination (-->eradication in 2011)
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Pest de Petit Ruminants
= "goat plague" in Africa - acute, contagious dz in small ruminants - spread by aerosols, direct contact - similar signs to rinderpest, up to 70% mortality - ctrl with rinderpest vaccine (PPRV vax now also available)
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Morbillivirus Canine Distemper | epidemiology
- highly contagious dz of dogs/carnivores worldwide - outbreaks in dogs, foxes, skunks, raccoons, ferrets, lions - labile in environment- aerosol or direct contact transmission - urban dogs: young dogs as maternal Ab wanes (maintained in population through infecting susceptible animals) - rural dogs: lower population pressure, more unvaccinated dogs--> outbreaks among various ages
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Canine distemper | pathogenesis
Transmission via aerosols or direct contact - ->initial replication in URT - ->lymphocyte-associated viremia - ->reticuloendothelial system - ->secondary viremia - ->mucosal epithelium of GIT, RT, CNS (neurons & glia) - ->incubates 3-6 days - ->dz of variable severity/duration
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Canine distemper | clinical signs
- incubates 3-6 days - biphasic pyrexia- 2nd peak w/ oculonasal discharge, pharyngitis, tonsillar enlargement - +/-skin rash & pustules - hyperkeratosis of nose & footpads - acute: cough, vomiting, diarrhea; followed by either recovery or --> - CNS dz: (grave prognosis) myoclonic contractions, ataxia, paresis, seizures, often death
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Canine distemper | diagnosis and control
Dx: presumptive, IHC on smears from discharges | Vaccination (part of C3) effective as maternal Ab wanes
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Hendra virus epidemiology
- acute respiratory dz, sporadic outbreaks in horses (+/-humans) in NE Australia since 1994 (usually late winter/spring) - reservoir = pteroid flying fox fruit bats (Pteropus alecto, P. conspicillatus) - seroprevalence 2-50% in bat colonies (suggests non-lethal to bats) - 80% case fatality rate in horses, 57% in humans
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Hendra virus | clinical signs/findings
- similar signs to African Horse Sickness: horses tachypneic, tachycardia, ataxic, frothy nasal discharge, collapse (many die in 12-24 hours) - congested, firm, fluid-filled lungs w/ dilated lymphatics, thick/foamy/bloody exudate in airway - other possible signs: shifting weight/uneasiness, neurological signs, congested mucous membranes, weakness
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Hendra virus control
Killed/inactivated vaccine available for horses (boosters and adjuvants required) Ab-mediated response Vaccinating horses important for human safety (all human cases associated with contact with infected horses)
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Equine Viral arteritis | epidemiology
- Worldwide - Usually asymptomatic (rare clinical outbreaks- mostly in trotters and pacers) - Susceptibility: horses > mules > donkeys - SBs more seropositive than TBs - Transmission via respiratory tract (aerosols), genital tract (35% of infected stallions shed in semen), transplacentally
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Equine viral arteritis | clinical signs
3-14 day incubation--> fever, excessive lacrimation, conjunctivitis, rhinitis, nasal discharge, stiff gait, ventral edema, urticaria on head/neck, abortion - worse in very young and very old
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Equine viral arteritis | pathogenesis
Aerosols -->replication in alveolar macrophages -->bronchial lymph nodes -->viremia (free and macrophage-associated) -->primary targets = macrophages & endothelium (-->edema, congestion, etc.) -->secondary targets = kidneys, liver, seminiferous tubules (carrier stallions= reservoir), etc. -->after acute infection virus eliminated from mares, geldings, and 65% of stallions - abortions follow viremia and transplacental spread
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Equine viral arteritis | diagnosis and control
Dx: RT-PCR, virus isolation from semen or respiratory secretions, serology (ELISA, neutralization) Vaccine available
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Porcine Respiratory and Reproductive Syndrome Virus (PRRSV) | clinical signs and dz processes
- reproductive failure in sows - pneumonia in young pigs- respiratory distress and cyanosis of skin (ears, vulva, etc.) exacerbated by Mycoplasma spp. or Streptococcus suis infection
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Porcine Respiratory and Reproductive Syndrome Virus (PRRSV) | epidemiology, diagnosis, control
- exotic to Australia (North America and Europe only) - infects pigs only - Dx: serology (ELISA, neutralization) or isolation - Ctrl: quarantine, vaccination
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Infectious bursal dz of chickens (IBDV) | epidemiology
- Worldwide - In naive flock morbidity up to 100%, mortality up to 90% (20-30% in endemic flocks) - Usually infects 3-6 week-old chicks - No effective vaccine - Very stable in environment- resistant to detergents and disinfection
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Infectious bursal dz of chickens (IBDV) | pathogenesis
Feco-oral transmission - -> replicates in gut-associated macrophages - -> portal system - -> viremia - -> preferential location in bursal lymphoid cells (destruction of Bursa of Fabricius--> immunodeficiency) - -> excreted in feces (highly contagious)
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Vesivirus: Vesicular exanthema of swine
- eradicated in 1956 - clinically indistinguishable from FMD - Lab Dx essential- isolate from vesicles - closely related to San Miguel Sea Lion Virus (swill?)
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3 diseases with same clinical presentation as FMD:
- Vesicular stomatitis- difference = seen in horses - Swine vesicular dz (picornaviridae- enterovirus) - Vesicular exanthema of swine (eradicated in 1956)
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Agents that cause feline URT dz
Feline herpesvirus Feline calicivirus Chlamidophyla
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Feline calicivirus | epidemiology
- URT pathogen in large/domestic cats - all ages susceptible but most common in kittens 2-6 m.o. (maternal Ab) - large titers of virus remain in oronasal secretions for months-years - persistent infection possible post-recovery or sub-clinical infection - maintained in population in small proportion of infected animals (not in latency)
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Feline calicivirus | pathogenesis
Transmission by aerosol or direct contact via oronasal or ocular routes - -> rapid spread through URT/conjunctiva - -> transient viremia - -> variable clinical signs (dependent on strain virulence)
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Feline calicivirus | clinical signs
Incubates ~5 days - -> conjunctivitis, rhinitis, tracheitis, pneumonia - -> gesticulation & ulceration of tongue/oral mucosa, shifting lameness
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Feline calicivirus | diagnosis and control
Dx: RT-PCR on swab material, paired sera Ctrl: inactivated & attenuated (not if pregnant or immunocompromised) vaccines available
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Feline core 3 vaccines
Feline herpesvirus Feline calicivirus Feline panleukemia
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Rabbit hemorrhagic dz | epidemiology
- Highly contagious/potentially fatal dz in European rabbits (>2 m.o.) - Virus shed in excretions, persists in environment - Transmission: deco-oral, inhalation, conjunctiva, mechanical (fleas, mosquitos, etc.) - Similar to myxomatosis, except contagious - High morbidity, high mortality
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Rabbit hemorrhagic dz | pathogenesis and clinical signs
Replicates in mononuclear phagocytic cells - -> acute hepatic necrosis, DIC - -> 3-day incubation - -> fever, depression, dyspnea, serosanguineous nasal discharge, hematuria, neurological signs - -> death w/in 36 hours of onset of clinical signs
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Rabbit hemorrhagic dz | diagnosis and prevention
Dx: many dead rabbits w/ characteristic gross lesions; RT-PCR Inactivated vaccination available (may cause local alopecia)
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Scrapie prion hypothesis
Scrapie = variant of host's PrP protein (PrPsc) that alters host PrP structure -->takes on structure of infectious prion -->prion propagated through altered protein folding (misfolded protein unable to be degraded-->accumulates) Support for hypothesis: - no nucleic acid structure IDed so far - deletion of PrP gene in mice protects against Scrapie - protease-resistant PrPsc demonstrated to alter PrP conformation in vitro
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Scrapie pathogenesis
Likely horizontal (+ iatrogenic) spread of unknown mechanism - -> agent first appears in tonsils, spleen, lymph nodes (likely after replication in follicular DCs) - -> 3-5 year incubation while it spreads to/through CNS - -> lipid- (myelin-) associated infection resulting in deposition of rods/fibrils (scrapie associated fibrils- SAFs) in brain - vacuolation and degeneration of CNS neurons, astrocyte hypertrophy
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Scrapie epidemiology
- likely horizontal (+ iatrogenic) spread) - may be significant population of sub-clinically infected sheep resistant to clinical dz - PrPsc found in macrophages of mammary tissue during mastitis- suggestive of transmammary transmission
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Scrapie diagnosis and control
Dx: not cultivable or detectable other than by animal inoculation (only possible with some strains) - usually diagnosed based on histopathology Ctrl: only successfully eradicated from NZ and Australia by aggressive slaughter campaigns and quarantine/import regulations from endemic areas
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Bovine Spongiform Encephalopathy (BSE) | pathogenesis and dz characteristics
Cattle likely infected via contaminated feed (most cases related to ingestion of meat meal) - -> incubates for several years - -> hyperesthesia, apprehension/nervousness, frenzy - -> ataxia - -> debility, recumbency, death (wks-mos) - spongiform lesions found in brains - concurrent natural SEs seen in felid spp. and some zoo antelope - agent may be scrapie or some other amplified agent normally found in low levels in cattle
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BSE epidemiology
- Primarily occurred in British dairy cattle after changes in meat processing protocols (decreased temperature and lipid solvents used during processing--> reduced inactivation of scrapie-like agents) - Most cases related to ingestion of meat meal - Dramatic reduction in cases since 1988 ban on feeding meat meal to animals - Recently new strain has arisen- Bovine Amyloidotic Spongiform Encephalopathy (BASE)- assoc. w/ amyloid plaque deposition
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BSE diagnosis and ctrl
Dx: histopathology of brain through foramen magnum - PrP detection w/ ELISA Ctrl: ban on feeding meat meal to animals since 1988
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Transmissible Mink Encephalopathy
- prevalent in mink farms in US | - possibly from feeding them scrapie-infected sheep or BSE-infected cows
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Chronic wasting dz (TSE)
- mule deer, white-tailed deer, Rocky Mountain elk in US - progressive weight loss, behavioral changes, salivation, PU/PD - infectivity found in muscle- potential risk of eating infected venison
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Kuru (TSE)
- progressive paralysis in Fore people (mostly women and children) of New Guinea - association with ritual cannibalism of dead relatives - women and children eat viscera (higher dose)
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Creutzfeldt-Jacob Dz (CJD)
``` Rare presenile demential in humans 3 epidemiological patterns: - familial - sporadic - iatrogenic- GH administration from pooled pituitary glands, instrument contamination ```
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BSE zoonotic potential
- no increased risk in farmers - affected people have specific polymorphism in PrP gene (encoding methionine residue @ position 129) - ~80 cases SE per year in UK (~1/4 due to CJD)