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3. Food Animal 2 > Mucosal Diseases (with diarrhea) > Flashcards

Mucosal Diseases (with diarrhea) Flashcards

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1
Q

important mucosal diseases with diarrhea

A

 Bovine Viral Diarrhea
 Malignant Catarrhal Fever
 Jejunal Hemorrhagic Syndrome
 Rinderpest

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2
Q

BVDV family, genus, structure

A

Family: Flaviviridae
 Genus: Pestivirus
 Small single stranded positive sense RNA virus

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3
Q

BVDV is closely related to:

A

 Border Disease virus: sheep
 Classical Hog Cholera (Swine Fever) virus

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4
Q

does BVDV affect non-domesticated animals?

A

Serology and virus isolation evidence of BVDV replication in wild ruminants:
 Antelope, giraffe, African buffalo, bison (European and American), big horn sheep, mountain goats, and various Cervidae (reindeer, kudu, roe deer, red deer, fallow deer, mule deer, white-tailed deer, and caribou)

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5
Q

BVDV; how common? what body systems does it affect?

A

 Common
 Multi-systemic viral disease

Can affect:
 Enteric system
 Respiratory system
 Reproductive system
 Immune system

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6
Q

Possible BVDV symptoms:

A
  • neurological defects in calves
  • nasal discharge
  • oral ulcers
  • immunotolerance vs immunosuppression
  • GI ulcers
  • Erosions
  • Genital ulcers
  • Infertility, abortions

> BRD (immunosuppression), reproductive disorders, BVDV, acute mucosal disease, chronic mucosal disease

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7
Q

biotypes of BVDV: what are they, what are they based on?

A

Based on their effects when grown in tissue culture
 Non-cytopathic (NCP)
 Cytopathic (CP)

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8
Q

Non-cytopathic BVDV; culture properties, virulence, prevalence in the wild, how it affects the fetus,, how it remains in a population

A

 Do NOT harm cells when grown in tissue culture
 The most VIRULENT strains of BVDV in vivo are non-
cytopathic (NCP) in vitro
 85-99% of naturally acquired BVDV field isolates are non-
cytopathic
 Crosses the placentome to establish BVDV in the fetus
 NCP-BVDV maintained in population by production of persistently infected cattle

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9
Q

Cytopathic BVDV; properties in vitro, how it arises, how it establishes PIs, easy to isolate?

A

 Produces cellular damage in vitro
 Arise as mutations of NCP-BVDV
 More easily isolated than NCP-BVDV
 Do NOT establish persistent infections

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10
Q

BVDV strains; how many, how they vary

A

 To date at least 25 BVDV- and BVDB-2 subtypes described
 Many strains of BVDV
> BVDV-1: 21 subtypes (1a to 1u) ; BVDV-2: 4 subtypes (2a to 2d)
 Vary in virulence
 Genetic and antigenic variation
 BVDV strains have distinguishable antigenic diversity

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11
Q

Two GENOTYPES of BVDV; what are they, uses, symptoms

A

 Type 1:
> the older “classic” BVD viruses
> used in vaccines, diagnostic tests

 Type 2:
> more virulent than Type 1
> Hemorrhagic syndrome, thrombocytopenia, death.

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12
Q

prevalence of BVDV, geographic spread, and PI prevalence

A

 Many countries throughout the world
 Herds: 20-90%
 General prevalence of PI <2%.
 Some individual herds may be higher

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13
Q

BVDV transmission overview; methods

A

 Direct OR Indirect transmission
 Highly infectious agent
 Inhalation OR ingestion of BVD virus
 PI animals:
> main source of virus: high amounts/long period
 Acute infected:
> Low amounts/short period (4-10 days)

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14
Q

How is a BVDV PI calf created?

A
  1. Pregnant BVDV-PI female
    > less common route (<10%)
    >PI calf

-BVD shed from infected animals

  1. Pregnant female (non-PI) infected with BVD virus during first half of gestation
    > most common route (>90%)
    > PI calf
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15
Q

viral shedding rate of non-PI vs PI calf? Why do PI calves affect so many others?

A
  • Normal Calf (non- PI) with a BVDV infection sheds 10,000 viral particles per day and recovers in 10–14 days.
  • PI calf sheds 10 million viral particles EVERY DAY (1000 x non-PI).
  • This is why one calf that is
    persistently infected can affect so
    many other cattle.
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16
Q

BVDV
Direct transmission:
PI animals continuously shed large amounts of NCP-BVD virus in:

A

 ocular discharge
 nasal discharge
 saliva
 semen
 feces
 urine
 milk

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17
Q

BVDV
Indirect transmission:

A

Indirect contact with fomites
 clothing, boots
 cattle equipment
 blood, hypodermic needles, surgical instruments, oral dosing guns
 visitors
 transport trucks

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18
Q

BVD Pathogenesis: how cows get infected, what cells?

A

 Inhalation or ingestion of BVDV
 Multiplication of BVD virus at mucosal surfaces
> within the epithelial cells of the oro-nasal mucosa (palatine tonsil)
 Viremia
<><><><>
 BVDV has tropism for actively-dividing cells:  Reproductive tissues
 Fetal tissues
 Gastrointestinal tract mucosa
 Intestinal crypts
 Peripheral lymphoid tissue  Bone marrow
 Pituitary gland
 Pancreas

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19
Q

what does a subclinical BVDV infection look like? how common?

A

 Mild fever
 Leukopenia
 Serum neutralizing antibodies
 70-90% of BVDV infections occur without manifestations of clinical signs

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20
Q

what animals are generally acutely ill with BVDV? incubation time and signs?

A

 Immuno-competent cattle of 6-24 month of age
 Incubation: 5-7 days
 Fever, leukopenia, depression, ocular discharge, oral erosions/ulcerations, drop milk production, diarrhea.

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21
Q

when do we see severe acute BVDV? what types produce this syndrome? clincal signs?

A

 Post-natal infection of immuno-competent cattle with virulent NCP-BVDV
 BOTH type 2 and type 1 BVDV can produce this syndrome
 Clinical signs: fever, pneumonia, sudden deaths

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22
Q

what is hemorrhagic syndrome? what are the signs? associated with what type of BVDV? Ddx?

A

 Bloody diarrhea, epitaxis, hemorrhage on mucosal surfaces, bleeding from injection sites, hyphema, pyrexia, death
 Thrombocytopenia and leukopenia
 Associated with non-cythopathic isolates, type II
 Experimentally induced in calves
 DDx: DIC, sweet clover and bracken fern poisoning

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23
Q

Hemorrhagic syndrome pathogenesis? in what cells has BVDV antigen been found?

A

 Pathogenesis in not clear
 Virus induces thrombocytopenia:
> Virus appeared to be associated with platelets
> Altered platelets function
 BVDV antigen has been demonstrated in megakaryocytes

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24
Q

BVDV - Acute infections and respiratory disease - associations?

A

 Associated with bovine respiratory disease syndrome (BRD)
 Synergistic affects with: Manhemia haemolytica, bovine herpesvirus type I, and bovine syncytial virus
 The contribution to BRD may be related to immunosuppressive effects

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25
Q

how can immunosuppression arise from BVDV? coinfections with what other pathogens are common?

A

 Acute infection and modified live vaccines induced immunosuppression
 Co-infections with: M. haemolytica, bovine herpesvirus type I, and bovine syncytial virus
 Co-infections with: E. coli, bovine papular stomatitis, rotavirus, coronavirus

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26
Q

Acute infections and immunosuppression
- BVDV pathogenesis for this effect

A

 BVDV targets lymphocytes and macrophages
 Lymphopenia with lymphoid depletion
 decreased CD 4+ and CD8+, and B lymphocytes and neutrophils
<><>
 Reasons for immunosuppression:
 decreased Production of interferon, monocyte IL-1, IL-2, TNF-α and
decreased chemotactic response
 Impaired: neutrophil-mediated; antibody dependent, cell mediated cytotoxicity
 Prostaglandin production of infected cells

27
Q

BVDV infection and reproductive outcomes based on month of gestation infected

A

0: infertility
0-2: EED
1.5-4.5: immunotolerance/PI
2-9: abortion
3-6: congenital defects
4-9: normal/abnormal and seropositive

28
Q

venereal spread of BVDV? effects?

A

 Semen of acutely infected or PI bulls may contain virus → source of
infection
 Virus shedding in semen extend beyond period of viremia
 Can affect fertility (decreased conception)
 Oophoritis

29
Q

In-utero transmission of BVDV to fetus can cause:

A

 Early embryonic losses
 Severe congenital abnormalities
 Life-long persistent infections

30
Q

Reproductive Consequences of BVDV - when do we see abortions and why?

A

 Abortions
> Transplacental infections is common
> Fetal infection (50-100 days of gestation) → fetal death → fetal expulsion→days or months later
 Late term infections usually do not result in abortions but have been reported
> Incidence is low (immune herds) but may be high in non-immune herds
> Incidence is high in acute infections with type II BVDV

31
Q

BVDV During Late Gestation - what do we see?

A

 Calves infected transplacentally can be born normal
 Born seropositive
 Serum should be tested before
colostrum ingestion in order to detect these animals
 Weak calves

32
Q

Outcomes of Fetal Infection with BVDV

A

 Between 45 and 110-120 days gestation
 From the end of embryonic stage -to- the development of immune competence of the fetus to BVDV antigens
> immunotolerance / PI
<><>
 Transplacental infection of the fetus between 100-150 days gestation
 Numerous **congenital defects **
 BVDV is an important teratogen
<><>
 Over 175 days gestation to term:
 Fetus is immunologically competent to BVDV
 Calf eliminates BVDV
 Calf is born BVD virus-free and with BVD antibodies

33
Q

Teratogenic effects of BVDV?

A

 Nervous system - many
 Ocular effects - many
 Thymic aplasia
 Growth retardation
 Hypotrichosis
<><>

34
Q

when do the cerebellum and retina develop in the bovine fetus?

A

 Organs being developed between 80-150 days gestation

35
Q

possible nervous system effects of fetal BVDV? signs?

A

 Cerebellar hypoplasia
 Hydranencephaly
> (absent cerebral hemispheres)
 Hydrocephalus
> (water on the brain)
 Hypomyelinogenesis
> (inadequate synthesis of myelin)
<><>
 Ataxic, uncoordinated
 Reluctant or unable to stand
 “Wide-based” stance
 Unable to walk, suckle
 Intention tremors

36
Q

BVDV fetal infection possible ocular system effects?

A

 Retinal atrophy and dysplasia
 Cataracts
 Microphthalmia
 Hypoplasia of optic tract

37
Q

fetal BVDV infection possible immune system effect

A

 Immune system: thymic hypoplasia

38
Q

fetal BVDV infection possible skin effect

A

 Skin: hypotrichosis, alopecia

39
Q

fetal BVDV infection possible musculoskeletal system effect

A

 Growth retardation
 Brachygnathism

40
Q

when do we get a persistent infection with BVDV? what is the nature of this infection? what type of virus?

A

 Fetal infection with NCP-BVDV before development of immune competency
 Immuno-tolerance and PI with BVDV
 Immuno-tolerance is rare after 100 day but can occur up to 125
days of gestation
 Viremic, continuously shed virus and appear healthy
 Immuno-tolerance is specific to NCP-B VDV → immune response to heterologous isolates can occur→seropositive for BVDV

41
Q

BVDV PI prevalence? how do PI family lines arise? significance?

A

 Prevalence is low (1 in every 100 to 1000 births)
 PI females produced PI offspring → may result in PI family lines
 May be the way BVDV is maintained in the cattle population

42
Q

PI survival rate

A

 50% survival rate in the 1st year

43
Q

PI animals are at risk of:

A

mucosal disease, other diseases and
survivorship

44
Q

what % of PI heifers reach lactating herd?

A

 Low % of PI heifers (10%) reach
lactating herd

45
Q

characteristics of PI calves?

A

 Undersized, slow growth, predisposed to infections (enteritis, pneumonia), unresponsive to treatments
 Alteration of immune response
> neutrophil and lymphocyte function

46
Q

Diseases of PI cattle - mucosal disease pathogenesis?

A

 Immuno-tolerant and PI animal (NCP- biotype)→infected with a CP biotype of close homology with the persistently infecting NCP
 Not every NCP-CP combination result in MD
 Source of CP virus:
 External (modified live virus)
 Internal (molecular rearrangement of NCP infecting biotype)

47
Q

mucosal disease clinical presentation options? why is there clinical variation?

A

 Acute MD
 Chronic MD
 MD with recovery
 NCP-CP biotypes relatedness may be responsible for the difference in clinical variations

48
Q

acute MD characteristics - mortality, incubation, clinical signs, lesions

A

 Sporadic (5%)
 High mortality (close to 100%)
 Incubation period: 10-14 days
 Clinical signs: biphasic fever, anorexia, tachycardia, polypnea, decreased milk production, diarrhea (frank blood, fibrinous casts, foul smell)
 Blunted papilla, ulcers of tongue palate, buccal surfaces and pharynx.

49
Q

diagnostic testing for BVDV for subclinical dz

A

Samples:
1.Paired serology
2.Buffy coat
3.Serum
<><>
Tests:
1. SN test
2. Virus isolation
3. PCR
<><>
Serology for both types (1&2)
Viremia may be transient

50
Q

diagnostic testing for BVDV for acute dz

A

Samples:
1.Paired serology
2.Buffy coat
3.Serum
4. PM tissues
<><>
Tests:
1. SN test
2. Virus isolation
3. PCR
4. FA, IHC, PCR
<><>
Serology for 1&2. Type 2 more associated with
mortality

51
Q

diagnostic testing for BVDV for abortion / mummification

A

Samples:
1. Paired serology
2. Fetal fluid
3. Fetal organs
<><>
Tests:
1. SN test
2. SN, Virus isolation
3. PCR
4. FA, IHC, PCR
<><>
Antibody detection suggest
B VD V induced-abortion but not definitive

52
Q

diagnostic testing for BVDV for PI

A

Samples:
1. Serum or Buffy coat
2. Serum
3. Skin biopsy (ear notch)
<><>
Tests:
1. Virus isolation
2. PCR
3. IHC
<><>
SN repeat 3-4 weeks for PI. Buffy coat in young calves (<4w)

53
Q

diagnostic testing for BVDV for MD

A

Samples:
1. Serum or Buffy coat
2. Serum
3. PM tissues
<><>
Tests:
1. Virus isolation
2. PCR
3. FA, IHC, PCR, virus isolation
<><>
Isolation of types 1&2

54
Q

diagnostic testing for BVDV for repeat breeding

A

Paired serum, SN test

55
Q

BVDV Treatment/Prognosis

A

 No specific therapy
 Supportive care
 Prevention of secondary bacterial infections  Broad spectrum antibiotics
 Fluid therapy and electrolytes
 Severely ill animal may have MD (usually fatal)

56
Q

BVDV Prevention/Control

A

 Vaccinate after 6 months-of-age due to maternal antibodies
 Vaccinate ALL young females (6-14 months old) just prior to breeding
 Aim is to ensure maximum protection of fetus before 120 days gestation

57
Q

BVDV vaccination schedule, reasoning

A

 Vaccination of all breeding females to protect cattle that are NOT persistently infected
 To ensure that cattle are immune to B VDV BEFORE service or insemination
 To prevent infection of fetus with B VDV

58
Q

Reason for variation in efficacy in BVDV vaccine:

A

Antigenic composition of BVD viruses in vaccine
Type 1 or Type 2 strains of BVDV?
Number of doses of vaccine required?
 Adjuvants used?
Methods used for viral inactivation?
Cell types used to grow virus?
Fetal calf serum used?
 What constitutes a protective dose?

59
Q

Inactivated (killed) vaccines limitations and schedule: (BVDV)

A

 Limited immune response
 Response to 1st vaccination is weak
 Need 2 doses at 14-28 days intervals
 Preferably 3 doses prior to breeding

60
Q

BVDV killed vaccines availability in Canada? immunity duration?

A

 Type 1 and Type 2 killed vaccines available in Canada
 Duration of immunity is short
 Yearly boosters required

61
Q

BVDV killed vaccines safety profile? use in pregnancy?

A

 SAFE vaccines
 Can be used in pregnant animals
 Do NO T cause immunosuppression
 Do NOT replicate in host tissue
 NO reports of post-vaccinial disease
 Cost: low

62
Q

BVDV modified live vaccines for what strain?

A

 Contain Type-1 cytopathic strains of B VDV
 Attenuation through repeated passage Either NADL, Singer, Oregon C24V strains
 MLV vaccines available since 1959

63
Q

BVDV modified live vaccines admin schedule and immune response?

A

 Only need to administer ONCE by intramuscular or subcutaneous injection
 Rapid immune response
 Rapidly induces B VD VN antibodies in 90-95% of animals within 3 weeks

64
Q

BVDV modified live vaccine limitations

A

 Sporadic reports of post-vaccinial outbreaks of Mucosal Disease
 Reports of reproductive failure following MLV vaccination
MLV vaccine contaminated with NCP-BVDV
> (contaminated cell lines, fetal calf serum)

3. Food Animal 2 (20 decks)

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