C19 Gastrointestinal Pathology IV Flashcards

1
Q

what we need to differentiate vesicular viruses

A
  • Many look clinically and grossly identical
    o Need virus isolation or antigen detection to differentiate
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2
Q

vesicular viruses
* Most have multiple serotypes that vary in pathogenicity and virulence
- can we protect against one serotype with a vaccine for another?
- what if you get infected with two serotypes at once?

A

o Infection or vaccination for one serotype usually does not protect against others o Simultaneous infection with >1 tends to make the problem worse

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3
Q

vesicular viruses
- speed of disease course

A
  • The virus often gets in, wreaks havoc, and gets out very quickly
    o An animal may not be shedding virus anymore within days of developing signs
    o This is a feature of many viruses, not just vesicular diseases!
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4
Q

Foot and mouth disease
- species?
- genus, family, serotypes
- environmental survival? spread?

A
  • Highly contagious disease of all cloven-hoofed animals, serious economic impact
  • Genus Apthovirus, Family Picornaviridae, 7 serotypes
  • Virulence and host tropism vary between strains (ex. some are specific to pigs)
    <><><><>
  • Excellent survival in carcasses
  • Spread by animal movement, contaminated products
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5
Q

FMD
- pathogenesis
- when does shedding decrease? why?

A

1) Entry through pharynx, lung
2) Replication in epithelium
3) Dissemination
4) Acute fever, lesions in epithelium prone to mechanical stress
5) By day 11 of clinical disease, shedding decreases due to antibody

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6
Q

FMD
- what type of hosts are pigs, cattle?

A

Pigs are amplifiers, ruminants can sometimes remain carriers post-infection

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7
Q

FMD
- morbidity, mortality’
- lesions
> how they spread disease

A
  • High morbidity but low mortality – lesions in mouth, on feet, teats
  • Profuse salivation in cows
  • Vesicles quickly rupture, leaving raw, red ulcers > Secondary infections common
  • Vesicle fluid contains lots of virus
  • Also exhaled by infected animals
  • Interdigital or coronary band lesions present in most animals
  • Myocarditis can occur without ulcers in youngstock, sometimes adults
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8
Q

Vesicular stomatitis
- genus, family, serotypes
- how does the virus enter the body?
- pethogenesis?
- length of infection
- temperature & transmission

A
  • Genus Vesiculovirus, Family Rhabdoviridae, RNA virus, multiple serotypes
  • Intact epithelium resists infection, but damaged epithelium allows virus in
    <><>
    1) Replicates at site of inoculation
    2) Brief viremia
    3) Reaches lymph nodes
    <><>
    Infection is transient – virus is gone by 6 days
    <><>
  • Absent in cold weather and present when warm – insect vector feeding on lesions?
  • Also transmitted by contact
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9
Q

Vesicular stomatitis
- species
- looks like?
- lesions?

A
  • Affects horses, cattle (especially dairy), pigs, some wildlife (deer, rodents, raccoons)
    o The only vesicular disease of horses but does not affect small ruminants!
    <><>
  • Identical to foot and mouth disease, economic cost from lost production
    <><>
  • Affected cows may not salivate much
  • Mouth lesions > feet (most common in pigs)
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10
Q

Swine vesicular disease
- genus, family
- lesions
- contagious? production impact
- spread
- shedding, carriers

A

Swine vesicular disease: Genus Enterovirus, Family Picornaviridae
o Lesions mostly on feet (10% in mouth), present in tonsil for 7 days, viremia 2-3 days
o Highly contagious but milder loss of production (impact due to resembling FMD)
o Very resistant to inactivation, spread by contaminated pork and close contact
o May have carrier state with reactivation of shedding under stress

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11
Q

Senecavirus A
- genus, family
- species
- history

A

Senecavirus A: Genus Senecavirus, Family Picornaviridae
- swine vesicular disease
o Recently described, sporadic outbreaks in Canada and the US

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12
Q

Rinderpest
- genus, family
- species, contagious?
- environmental survival, vaccine
- pathogenesis, shedding

A
  • Genus Morbillivirus, Family Paramyxoviridae, RNA virus
  • Highly contagious, acute disease of even-toed ungulates (variable pathogenicity)
  • Poor survival outside host – eradicated by vaccination and movement restrictions in 2001
    <><><><>
    1) Enter nasopharynx
    2) Replicate in tonsils and local LNs (8-11 days incubation)
    3) Viremia and fever (lasts 2-3 days)
    4) Replication in all lymphoid tissues, mucosa: secretions virus +++
    5) No further virus shedding after ~day 9 of clinical disease
    <><><><>
    Outbreaks more severe than endemic disease
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13
Q

Rinderpest
- lesions
- signs
- similar to?
- immunity?

A
  • Erosive or hemorrhagic lesions of all mucous membranes, secondary infections common
  • Diarrhea +/- blood, abdominal pain, oculonasal discharge, dehydration, emaciation
  • Severe intestinal lesions associated with lymphoid tissue
  • Similar lesions to BVD mucosal disease and malignant catarrhal fever
  • Vaccine or recovery produces permanent immunity
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14
Q

Peste des petits ruminants (PPR)
- genus, family, relative
- course of disease
- species and dead-ends
- immunity?
- leasions

A
  • Genus Morbillivirus, Family Paramyxoviridae, closely related to rinderpest * Similar clinical course and lesions, but more acute and faster course
  • Disease in small ruminants, pigs and cattle are dead-end hosts
  • Vaccination or recovery cause permanent immunity: target for eradication
    <><><><>
  • Oral necrotic pseudomembranes and secondary infections are common
  • Hemorrhagic colitis
  • Marked respiratory involvement (cough, dyspnea) Interstitial pneumonia like distemper in dogs
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15
Q

Bluetongue
- genus, familu
- serotypes
- species, presentations
- wildlife
- geography
- spread

A

Bluetongue: Genus Orbivirus, Family Reoviridae
o Multiple serotypes, not all pathogenic
o Most severe in sheep, goats usually subclinical, disease in cattle rare and mild
o Most North American wild ungulates susceptible except elk and bison
o Sporadic disease in Okanagan valley
* replicate in and spread by Culicoides spp. midges

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16
Q

Epizootic hemorrhagic disease
- serogroup
- species
- disease in sheep
- spread

A

Epizootic hemorrhagic disease: different serogroup of Orbivirus
o Major pathogen of white-tailed deer
o Mostly subclinical in sheep but can have mild disease
* replicate in and spread by Culicoides spp. midges

17
Q

Bluetongue and Epizootic hemorrhagic disease
- pathogenesis
- rule outs

A

Replicates in LNs, spleen
> Viremia 4-6 days post-infection > Infects endothelial cells > Fever, leukopenia
> ~1 week post-infection Microthrombi, increased permeability
> Widespread ischemic necrosis > Edema, hemorrhage, DIC
<><>
Rule outs: contagious ecthyma, photosensitization and vesicular diseases!

18
Q

Bluetongue and Epizootic hemorrhagic disease
- lesions
- signs

A

Inapparent to fulminant disease in sheep with bluetongue
<><><>
- Hyperemic oronasal mucosa
- Eyelid, ear, lip, and submandibular edema
- Drooling
<><>
- Swelling and hemorrhages of coronet band
- Survivors may be reluctant to move
<><>
- Congested, edematous, cyanotic tongue (hence name)
- Hemorrhages on lips, gums
- Erosion and ulcers of infarcted epithelium
<><>
- May have pulmonary artery hemorrhage, ventricular papillary muscle necrosis +/- pulmonary edema due to heart failure, endothelial damage

19
Q

Bluetongue and Epizootic hemorrhagic disease in cattle
- sings?
- lesions
- repro issues?

A
  • Rarely clinical in cows, low mortality (if fatal, it’s usually due to secondary infections)
    o Fever, anorexia, leukopenia, milk drop
    o If lesions form, look similar to sheep
    o Can also cause abortion and congenital defects (hydranencephaly, arthrogryposis,
    enlarged tongue)
20
Q

Vesicular disease
- we can’t tell them apart easily
If in doubt……

A

….report and do virus isolation or antigen retrieval to find out!

21
Q

Vesicular diseases summary
- which are reportable?

A

ALL REPORTABLE
<><>
Foot and mouth
Picornavirus
7 serotypes
ruminants
pigs
<><>
Vesicular stomatitis
Rhabdovirus
Multiple serotypes
ruminants (cattle ++)
pigs
horses
<><>
Swine vesicular disease
Enterovirus
pigs
<><>
Rinderpest (eradicated)
Morbillivirus
1 serotype
ruminants (cattle ++)
<><>
Peste des petitis ruminants
Morbillivirus
1 serotype
ruminnats (sheep ++)
<><>
Bluetongue
Orbivirus
Multiple serotypes
ruminants (sheep ++)
horses (mules +)
<><>

22
Q

Bovine viral diarrhea
- genus, family
- 4 species in genus
<><>
- species
- which virus (1 or 2) more severe
<><>
- mutations
<><>
- immune impact

A
  • Genus Pestivirus, Family Flaviviridae, RNA virus
    o 4 species in the genus: BVD-1, BVD-2, classical swine fever, border disease
    <><>
  • BVD is widespread in cattle and can infect most even-toed ungulates
    o Range of virulence in both BVD-1 and BVD-2
    o BVD-2 often causes more significant external hemorrhage
    <><>
  • Readily mutates via recombination to adapt to host responses
    o Can shift from noncytopathic to cytopathic
    <><>
  • BVD suppresses interferon
    o Impaired immune function therefore prone to secondary diseases
23
Q

Bovine viral diarrhea
- pathogenesis
- outcome options

A

1) Inhaled or ingested
2) Replication in oropharyngeal lymphoid tissues
3) Viremia
4) Outcome depends on status of cow
* Option 1: Immunocompetent, naïve, and nonpregnant or late pregnancy
* Option 2: Immunocompetent, naïve, early pregnancy or pregnant persistently infected (PI) cow
* Option 3: Mucosal disease in PIs

24
Q

BVDV - naïve, immunocompetent cases
> (including late gestation feti >135 days capable of antibody response)
- signs
- morbidity, mortality
- looks like?

A
  • Subclinical or mild disease in most naïve, immunocompetent cases (including late gestation feti >135 days capable of antibody response)
    <><>
  • Sometimes high morbidity and low mortality syndrome in animals > 6 months
    o Fever, leukopenia, lethargy, oculonasal discharge, decreased milk production
    o Sometimes mild oral ulcers and diarrhea
    <><>
  • Severe acute BVD causes high morbidity and mortality in all ages o Fever, profuse bloody diarrhea, pneumonia, sudden death
    o Sometimes thrombocytopenia
    o Resembles rinderpest and mucosal disease of PI animals
25
Q

BVDV - In the first 4 months of pregnancy
- fetus response to virus
- outcomes?
- PI calf signs
- PI offspring
- source in herd
<><>
- lesions, signs
- where to look

A
  • In the first 4 months of pregnancy, feti cannot respond to the virus
    o Infection of naïve dam leads to pregnancy loss, congenital anomalies (especially 90-
    120 days), or birth of persistently infected (PI) calf
    o PI calves are always viremic because they are immunotolerant to the virus
    o May be normal or weak and unthrifty with a rough or curly coat
    o All offspring of female PIs will also be PIs (virus is always present)
    o THE MOST IMPORTANT SOURCE OF VIRUS IN HERDS!!!
    <><>
  • Look for antigen – present in many tissues including skin (R/O acute infection)
  • Eye defects: microphthalmia, cataracts
  • Brain defects: cerebellar hypoplasia, hydrocephalus, hydranencephaly, microcephaly
26
Q

BVD - mucosal disease
- who affected, when
- how
- disease course
- signs, lesions

A
  • PIs usually die of mucosal disease at 6-24 months old
    o Superinfected by another strain or mutation of congenital strain boosts virulence
    o Overwhelming infection because incapable of response
    o Low morbidity but very high mortality, death usually within 2 weeks
    o Different epidemiology than severe acute disease, antigen isolation best differentiator
    <><>
  • Drooling, ulcers and crusts on nose and mouth
  • Febrile, nasal discharge, buccal papilla erosion
  • Peyer’s patch necrosis
  • Severe diarrhea and tenesmus > May contain blood
27
Q

Border disease
- like what disease? species?
- +BVD?

A
  • Equivalent virus to BVD in small ruminants
    o Naïve dam infected before 80 days gestation = congenital infection
    o PIs are called ‘hairy shakers’ (long fleece, tremors, unthrifty)
    o Can be superinfected with BVD – chronic diarrhea
28
Q

Malignant catarrhal fever
- genus, family
- mortality?
<><>
- viral strains and species
- signs in species, spread

A
  • Genus Macavirus, Family Herpesviridae, Subfamily gammaherpesvirinae
  • Result of infection by herpesvirus adapted to another ruminant species
  • Sporadic disease with nearly 100% mortality
    <><><><>
    Ovine herpesvirus 2 - sheep
  • Ubiquitous
  • Asymptomatic carriers
  • Shed intermittently
  • Spread from adults to lambs in early life
  • aerosol to other species
    <><>
    Alcelaphine herpesvirus 1 - wildebeest
  • Asymptomatic carriers
  • Shed intermittently
  • aerosol to other species
    <><>
    MCF - Cattle, bison, deer
  • get disease from aerosol
  • high exposure needed for cattle
  • deer very susceptible
  • Disease but little virus shed
  • No transmission
  • Antibodies are not protective
29
Q

Malignant catarrhal fever
- pathogenesis
- major lesions
- signs

A

1) Entry via tonsils and upper respiratory mucosa
2) Incubation period 2-10 weeks
3) Viremia starts ~7 days before clinical signs and persists through clinical course
<><><><>
- Major lesions: T lymphocyte proliferation, vasculitis, mucosal ulceration
- Clinical signs vary, hard to isolate virus due to lymphotropism
- Some cases develop neurological signs due to vasculitis
<><>
- Ocular and oral lesions common
- Conjunctivitis, corneal opacity
- Mucosal edema, ulcers, congestion
- Skin lesions around horns and hooves common but overlooked
<><>
- May have gastroenteritis
- Diarrhea +/- blood (negative prognostic indicator)

30
Q

Malignant catarrhal fever
Cattle:
- disease course, mortality
- where do leasions start
- survivor lesions
<><>
Bison
- death and signs?
- lesions?
<><>
DEER
- typical presentation
<><>
common kidney lesion

A

CATTLE:
* Death in 1-3 days (rare cases live 9-10 days)
* Oral lesions start at mucocutaneous junctions and progress into mouth
* Rare survivors will have persistent ocular lesions and vasculitis
<><>
BISON
* Often die before clinical signs have time to manifest
* More subtle and localized lesions
<><>
DEER
* Hemorrhagic colitis typical
<><>
Mottled kidneys due to interstitial lymphocytes

31
Q

Malignant catarrhal fever
- how can we tell the difference between this and mucosal disease?

A

MCF sounds a lot like mucosal disease – how can we tell them apart???
o Lymphoproliferation rather than lymphoid atrophy/necrosis
o MCF usually involves at least one system that BVD doesn’t (liver, kidneys, eyes, brain)