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Virology > Flaviviridae, Caliciviridae, Astroviridaex > Flashcards

Flaviviridae, Caliciviridae, Astroviridaex Flashcards

1
Q

Flavus =

A

yellow

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2
Q

Which viruses belong to the genus pestivirus?

A
  • Genus Pestivirus
    -Bovine viral diarrhea virus (BVDV)
    -Border Diseases virus of sheep
  • Classical swine fever virus (CSFV)
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3
Q

Which viruses belong to the genus flavivirus?
These viruses are all?

A

-West Nile Virus (WNV)
-Japanese Encephalitis virus (JEV)
-Dengue hemorrhagic fever virus (DHFV)
-Yellow fever virus (YFV)
-Tick-Borne Encephalitis virus (TBEV)
Arboviruses

Hepatitis C is apart of Flaviviridae

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4
Q

Flaviviridae have ___ genera and ___ species?

A

4, 89

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5
Q

What viruses belong to Flavivirus?

A

-WNV
-JEV
-DENV
-TBEV
YFV
-Bat flavivirus

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6
Q

What viruses belong to Pestivirus?

A

-BVDV-1
-BVDV-2
- Border DV
- Hagr DV

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7
Q

General Properties of family Flaviviridae
 Virion: ___ – __ nm in diameter,
 _____ in shape contains a lipid ________.
 _______ stranded (__ ve) sense ____ viruses with ____ ___-segmented genomes
 The virion RNA: infectious and serves as both the ______ and the viral ______ RNA.
 Replication takes place in the _________.

A

40, 60, Spherical, envelop, SS, +, RNA, linear, non, genome, messenger, cytoplasm

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8
Q

What virus is this?
What can you tell from this image?

A

Flaviviridae
SS (+ve) sense RNA viruses with linear
non-segmented genomes

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9
Q

What virus is this?

A

Flaviviridae

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10
Q

Describe the genome structure of Flaviviridae

A

Single stranded 5’ to 3’
At 5’ –> non coding region; plays an important role
Structural protein is closer to 5’ end. Non-structural region is closer to 3’ end.

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11
Q

Describe the replication cycle of Flaviviridae

A
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12
Q

What is the host range of Bovine viral diarrhea virus?

A

Infectious viral disease of a variety of domestic & wild
ruminants worldwide. Does not necessarily cause disease in all animals it infects.

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13
Q

How does BVDV contribute to reproductive loss?

A

BVDV and reproductive loss
* Low conception rates
* Abortion of early embryo
* Increase in return to service

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14
Q

What virus is pictured here? Label the image accordingly.

A
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15
Q

List the economic impacts of BVDV infection on dairy/beef industry

A
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16
Q

List the modes of transmission of BVDV

A
  1. Oro-nasal route
  2. Mechanical transmission of virus in blood
  3. Iatrogenic
  4. Endogenous: in utero* infections
  5. Semen
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17
Q

Explain the oro-nasal route of transmission of BVDV

A

I- Oro-nasal route: Saliva, nasal secretions and milk - lesser extent in feces

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18
Q

Explain the Mechanical transmission of virus in blood route of transmission of BVDV

A

II- Mechanical transmission: of virus in blood-
– via insect vectors

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19
Q

Explain the Iatrogenic route of transmission of BVDV

A

Iatrogenic methods relating to illness caused by medical examination or
treatment: [reused needles, nose tongs]

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20
Q

Explain the Endogenous:

A

in utero* infections route of transmission of BVDV

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21
Q

Explain the semen route of transmission of BVDV

A

from infected animal to susceptible animals

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22
Q

Immune tolerance is defined as?

A

state of unresponsiveness of the immune system to substances or tissues that have the potential to induce an immune response

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23
Q

Immunocompetent is defined as?

A

the host is capable of developing an immune response
following exposure to an antigen

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24
Q

Immunocompromised is defined as

A

the immune response attenuated by
administration of immunosuppressive drugs, by irradiation, by
malnutrition, or by certain disease processes such as the viral infection that
produces the acquired immunodeficiency syndrome (AIDS).

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25
Q

Persistent infection is defined as?

A

the virus is not cleared but remains in specific cells of infected individuals

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26
Q

Classification of BVDV is based on
Based on genomic characteristics and the severity of disease they produce in cattle,
BVD viruses are grouped into ____ genotypes?

  1. Each genotype is divided into two biotypes. List and explain.
    *** Cytopathogenicity does not correlate with the ______ of disease ____ ______.
  2. (Each biotype, cp and ncp contains ___ and ___ virulence strains. Cp and NCP are based on what?
A

two, : Type 1 and Type 2, severity, in vivo, high, low

cytopathic (cp) and non- cytopathic (ncp) based on how they replicate in cell culture.

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27
Q

Label accordingly.

A

PI animal means persistently infected animal

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28
Q
A
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29
Q

*** Important: Remember that BVDV biotype is only a _________ observation (in cell ______) and does not equate with virulence in ______ infections. Some cp strains are recovered from animals with _______ disease (MD), but most of the time ncp isolates are recovered from ________ animals.l

A

laboratory, culture, natural, mucosal, infected

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30
Q

BVDV Genotypes
 Classification based on the ________ of genomic ______ sequences
–> Difference in 5’ UTR sequence between types 1 and 2: The difference is based on the _______ on the __’ UTR (_________ region) between type 1 and 2
** Type-1 BVDV
 ______ BVD isolates
 Used in ________ tests
 Used in commercial _______ preparation
** Type -2 BVDV
 ______ and ________ BVD (_______ outbreaks)
 __________ and __________ syndrome

A

genotype, RNA, sequence, 5, untranslated, Classical, diagnostic, vaccines, Severe, hemorrhagic, recent, Thrombocytopenia, hemorrhagic

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31
Q
  • **Non-cytopathic recovered _____ of the times (more common form in ______).
    *** Cytopathic - recovered from animals with _______ disease.
    N.B: BVDV biotype is only a laboratory observation (in cell culture) and does
    not correlated with virulence in natural infections
    Non-cytopathogenic (NCP) Cytopathogenic (CP)
    Biotypes of BVDV
    BVDV
A

most, nature, mucosal

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32
Q

What can be seen in the image below?

A

NCP BVDV

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33
Q

What virus can be seen below?

A

CP - BVDV

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34
Q

BVDV Pathogenesis
** BVDV has a tropism for rapidly _______ cells e.g. ?
** BVDV replicates in ______ cells and has a predilection for the ______
– depletion of CD__+ and CD__+ T lymphocytes
  immunosuppression
 **—> Bone _______ and intestinal _____ are often infected, the lymphoid tissue of the ________ ______ is frequently depleted.
 ** –> Tissue distribution varies between strains and highly virulent strains are associated with ______ tissue distribution *** highest concentrations in the ?

A

dividing, Lymphocytes, mononuclear phagocytes and epithelial cells

epithelial, tonsil, 4, 8, marrow, mucosa, Peyer’s patches, wider

tonsil, thymus and ileum

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35
Q

BVDV infection causes?

A

Respiratory syndromes
Immuno-suppression
Reproductive syndromes
Enteric Syndrome

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36
Q

Bovine viral diarrhea Virus (BVDV) - Three forms (syndromes)

Type I

A
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37
Q

Bovine viral diarrhea Virus (BVDV) - Three forms (syndromes)

Type 2

A
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38
Q

Bovine viral diarrhea Virus (BVDV) - Three forms (syndromes)

Type 3

A
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39
Q

**Mucosal disease : is clinicopathologic syndrome occurs when PI animals become infected with a closely related ____ strain of _____

A

CP, BVDV

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40
Q

NPC and CP behave differently in pregnant animal.

NCP vs CP
NCP = from 0-120, _______ and _____ infection occurs, if happens after 120, will __ affect pregnant animal and calf = ______.

CP = more severe action. If infection happens around 90-100 days = ______ , _______, _______ can occur; 100-150 = __________, 150-200 = ______.

Calf born seroposiitve produces ? (see image)

A

tolerance, persistent, not, normal, abortion, resorption, mummification, malformation, normal

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41
Q

***BVDV immune evasion strategies have effects on both the _______ and __________ immune system. Describe the effects on innate immune response:
-Reduction in ___ and ___ receptor expression on phagocytes.
-Suppress ___-inflammatory cytokines
-Suppress ______ production

A

innate, adaptive, Fc, C3, pro, interferon

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42
Q

***BVDV immune evasion strategies have effects on both the innate and adaptive immune system. Describe the effects on adaptive immune response
-Depletion of CD__+ and CD__+ T cells
-Decrease in MHC__ and MHC __
production
BVDV immune evasion strategies
Effects on innate immune response
-Reduction in ___ and __ receptor expression
on phagocytes.
-Suppress pro-inflammatory cytokines
-Suppress interferon production

A

8, 4, I , II, Fc, C3

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43
Q

Fc: protein found on the surface of certain cells – including, among others, ___ lymphocytes, follicular ______ cells, natural killer
* C3: Complement receptors type-3

A

B, dendritic

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44
Q
A

Virus enters calf.
Inhibits t cell function, plasma cell, b cell. No antibodies or cytotoxic t cells? Hyjacks immune system to ensure replication.

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45
Q
A

Study table.

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46
Q

BVDV Persistent Infected carrier development:
*****PI animal: produced when _____ heifer/cow is infected between ____-____ days of pregnancy and the foetus survives
* PI calf is a ______ of BVDV for _____
* ___ animal is a virus factory
* PI animals are poor doer animals: grow at ______ rate than other calves

A

naïve, 30-125, carrier, life, PI, slower

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47
Q

***Persistent infected carriers will produce ________ ______% of the time.

A

PI’s, 100

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48
Q

Mechanism of BVDV persistence

A
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49
Q

****Acute MD
Onset of clinical symptoms within ___-____ days post- infection.
* ________ fever, ________, __________, _________,
* Nasal-ocular _________, corneal ________,
hypersalivation,
* Decreased ____ production
* ____ diarrhea. Diarrhea is often characterized by the
presence
* of mucosal shreds, fibrinous casts, blood and foul
odor.
* Erosions and ulcers - on the tongue, palate, and gingiva
* Epithelial erosions may be pronounced in the
interdigital regions,
* coronary bands, teats, vulva, and prepuce.
* Cattle with acute MD become progressively dehydrated
and usually die within 3-10 days. Although mortality
usually approaches 100%, a few animals may survive
the acute MD but are prone to develop the chronic MD.

A

10-14, Biphasic, anorexia, tachycardia, polypnea, discharge, opacity, milk, Watery

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50
Q

****Chronic MD
Affected cattle are “poor _____” and may
have ________ diarrhea, chronic ___,
decreased ______, and weight __.
* ________-________ __________ is commonly
seen.
* Cattle with chronic MD rarely survive
past ___ months and are usually _____
due to low performance or die of severe ___________.

A

doers, intermittent, bloat, appetite, loss, Nasal-ocular discharge, 18, culled, debilitation

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51
Q

Infection in
immunocompetent
non-pregnant cattle
(subclinical infections)
(acute infections)

 Sub-clinical
 Mild fever, leukopenia,
decreased milk production
 Mild BVD - mild erosive
lesions, ulcerative stomatitis,
diarrhea, respiratory
 Severe disease - lesions
mimic MD,
thrombocytopenia,
hemorrhagic syndrome,
hyphemia

A
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52
Q

Infection in
immunocompetent
pregnant cattle
(fetal infections)
All syndromes described above
 Embryonic death
 Abortions
 Birth defects
 Persistently infected calves

A
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53
Q

Infection
In persistently infected-
immunotolerant
cattle
(mucosal disease)
 Continuously shed
millions of virus all its
life from all its secretions
- Feces - urine - saliva -
nasal
- milk - semen - uterine
secretions
- aborted membranes, fluids,
fetus - Across fences.
-Virus survives in
environment up to 7 days

A
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54
Q

***PI animals shed the virus throughout life and are a main source of infection for other animals in a herd

A
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55
Q

Spot the PI among this group of heifers
Two calves in the picture are persistently infected.
* One of them is indistinguishable from the other healthy calves.
* Usually there is notable variation in weaning weight of
persistently infected calves

A
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56
Q

BVDV Disease – Acute (TI)
 Incubation 5-7 days
 Viremia (virus in blood circulation)
4-5 d after infection (up to 15 d)
 Seroconversion 2-4 wk later
 Virus shedding for 1-2 weeks
 Low concentrations compared to PI
 Diarrhea, slobbering, fever
 Ulcers - lips, gums, esophagus, etc.
 Immune suppression
 Fetal infections
 Most infections are not noticed -
estimate 70-90% are subclinical but
can be severe (death) if virulent
strain

A
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57
Q

Severe BVD type 1: Clinical Manifestations
Severe, diffuse _____ erosions
Effects on _____ stock
(3-12 months of age)
 Unthrifty/Rough ______
 Diarrhea
 Coughing
 Ulcers in mouth (sometimes!!)
 Lameness
 ** ________
 _______
 ** _____ /____ discharge
 ______
** Oral _________
 Immunosuppression
 Often confused with parasitism
 High morbidity
 Low mortality

A

gingival, young, coats, Leukopenia, Depression, Ocular, nasal, Pneumonia, ulcerations

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58
Q

BVD Type 1

A
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59
Q

The Hemorrhagic Syndrome associated with BVDV-type 2
* Fever
* Bloody diarrhea
* Epistaxis
* petechiae & ecchymoses
* Hyphema
bleeding from injection sites
* Marked thrombocytopenia
and leukopenia
* IHC staining of infected
megakaryocytes from bone
marrow aspirates of BVDV
type II calf expressing BVDV
antigens

A
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60
Q
A

BVDV-Type 2

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61
Q
A
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62
Q

***BVDV in-utero infections and reproductive outcomes

  1. ___________ defects
  2. ____________ in calf with BVDV
  3. _________/____________
  4. Cerebellar __________
    ___________-difficulty getting up and is with broad stance
A

Congenital, Arthrogryposis, Alopecia, hypotrichosis, hypoplasia, Hypermetric

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63
Q

***Some congenital defects associated with BVDV Infection

Nervous system
Immune system
Musculosketal system
Respiratory system
Eye

 Embryonic death -Abortions
 Congenital defects -Stillbirths
 Normal calves born seropositive to BVDV
 Calves born immunotolerant & persistently
infected (PI )

A
64
Q

–> Outcomes of BVDV infection in immun-tolernat cattle
1. PI animals may appear normal but go through cycles of clinical diseases marked by ______ and ____
**2. Mortality of PI calves prior to weaning is high
- Congenital defects
- Secondary infections: enteritis, pneumonia, arthritis
** PI animals are the primary _______ for & _____ of BVD virus
** Shedding large amounts of virus in the _____
* Shedding BVDV for life
– Est. in general US cattle population
that prevalence of PI animals is 0.13-
2.0%

A

anorexia, edema, reservoir, source, environment

65
Q

Virus Isolation in Cell Culture
**1. Sample types:
 WBCS Whole blood Urine
 Scrapings from affected gum lesions
 Post-mortem tissues (Tonsil, thymus)
* Identification: FA, IHC, RT-PCR
 Persistent infection (PI): elevated virus titer
** Rapid tests:
 -IHC (ear notch initially)
 -Antigen Capture ELISA, RT-PCR
 -RT-PCR- Whole blood
 Further Confirmatory tests (not rapid)
 virus isolation from body fluids, whole
blood

A
66
Q

What can be seen in this image?

A
67
Q

Diagnosis of BVDV infection
 Acute Infection (typically clear infection by 2-3 wks
post-infection)
* Rapid Tests:
* EDTA blood - Buffy coat (RT-PCR)
 IFA/IHC on buffy coat cells
 After necropsy – tonsil, thymus – RT-
PCR,FA,IHC,
Further Confirmatory - Isolate virus from buffy
coat or affected tissues and ID by _____-____ or ____/_____ (Takes long but considered most reliable test - gold standard)
_______ - (60-85% of cattle have BVDV titers)
**Must know ______ status
– Paired samples: sero-conversion (Four-fold or more)
 Submit both samples to same lab at the same time

A

RT-PCR, IFA/IHC, Serology, vaccination

68
Q

 By blood or milk testing
 By skin testing
 Testing tissues of a dead
animal
 Virus isolation
 Small numbers
 Herd screening -
microtitre
 Antigen capture ELISA
 Herd screening
 Serology
 VN
 ELISA
 PCR
 Genotyping
 Pooled samples

A
69
Q

_______ _______ samples in the diagnosis of BVDV. This becomes the tissue of choice for screening for PI animals because
1) ____ to collect
2) Equipment requirements are _____
3) **They are not affected by presence of _______ __________
4) They can be used as the sample for a wide variety of tests
-immunohistochemistry,
-real-time polymerase chain reaction and
-antigen-capture ELISA.
Pooling of ear notch samples has been proposed for reducing the cost of surveillance programs

A

Easy, Ear notch, minimal, passive, antibodies

70
Q

***BVDV-PI -Diagnostic Tests

A
71
Q

PI Management: identification & elimination of PI carriers (Beef feedlots)
** Determine if BVD is active in a herd
– Serology on ________ sentinel animals
* Identify ___ animals
 Pooled ear notch/serum samples, then RT-PCR detection
 *****a single PI animal can be detected in pools of ___-__ negative samples
 Individual skin IHC (ear notch)
 Micro plate virus isolation
 Any positive test for PI in valuable animals can be confirmed by segregating the animal
then retesting with serum ELISA or whole blood VI/PCR at least 3 weeks later to
eliminate TIs and false positives.
**BVDV Serum Neutralization Test- ________ and ________ antibodies.
**Differentiation of titers due to ________ or ____ virus exposure is difficult

A

unvaccinated, PI, 10-25, detects, quantifies, vaccination, field

72
Q

***Controlling BVDV infections
Biosecurity program for Dairy cattle herds

A
73
Q

Management and control of BVD
* _____ and ______ PI animals
* Test all new born calves for ___ months
 For 9-12 months segregate age groups
** ____________ replacements
Vaccination with _____-_______
 BVD infections may persist for some time after removal
of PI animals
* Vaccinate calves after __ months of age
Modified Live: __ dose is protective; ___ doses best
 Killed: ___ shots, __-____ weeks apart is required
 Best if done at least two weeks before anticipated _____ (weaning/transport/commingling)
 ***___ months protection against clinical disease

A

Test, remove, 9 months, Vaccination, MLV-BVDV, 4, 1, 2, Two, 3 - 4 , stress, 12

74
Q

Border Disease of Sheep
**_________ in sheep, and also is known as “_______ ______ disease” or “____ lamb syndrome.”
* _______ syndrome characterized by ____ birth weight and poor _____, poor _______, tremors because of
delayed _____ of the central nervous
system, and an excessively ____ birth coat
resulting from ___-_____ infection with a _________
*** Note ___ rather than wool
* This lamb trembles and ataxic

A

Worldwide, hairy shaker, fuzzy, Congenital, low, viability, conformation, myelination, hairy, in-utero, pestivirus, hair

75
Q

What disease are these lambs suffering from?

A

Border disease - sheep

76
Q

Transmission of Border disease of sheep

A

Transmission typically by direct contact between sheep, and persistently infected
carrier animals

77
Q

Classical swine fever virus (CSFV)
**Highly contagious viral disease of pigs
(domestic and feral) replicates in ____ ticks (__________ spp)
** Varies in virulence
**** Environmentally ____
**- In tissues (_____)
** - ____ temperatures
* Hog Cholera,
* Peste du Porc,
* Colera Porcina
**** First confirmed in US, 1833
* Endemic in late 19th and 20th century
* Eradicated by late 20th
* Reported in the UK, 1864
**** Recognized in 36 countries
* Eradication
* Australia, Canada, New
Zealand, and the US
* **US last outbreak in 1976
* 1978 US declared Hog
Cholera free

A

soft, Ornithodoros, stable, meat, Cold

78
Q

Classical swine fever virus (CSFV)- Hog Cholera
_____ fever (105oF)________, weakness
 Anorexia, Conjunctivitis, Diarrhea
 Staggering Cyanosis Skin hemorrhages Death
_________: Similar to acute form, but symptoms ___ severe
 Pigs ____ survive
 Subacute and chronic forms
 Chronic: Anorexia, depression, fever, diarrheal; Poor reproductive performance including abortions, stillbirths, and deformities
 Persistently infected piglets
 Highly variable
 Hemorrhage
 Necrotic foci in tonsils
 Petechiae/ecchymoses on serosal and mucosal surfaces
 Kidney, larynx, trachea,
intestines, spleen, lungs
 *****________ ____ (“_______ ulcers”)

A

High, Huddling, Subacute, less, may Necrotic foci, button

79
Q
A

Classical swine fever - cold

80
Q

CSV - Morbidity and Morality
Age and immune status important
 Varies with viral strain
**Acute
** ______mortality (up to 100%)
 ****Subacute
 **Lower morbidity and mortality rates
**Chronic
 **** _____ animals affected – always fatal
 **Some cases are asymptomatic

A

High, Few

81
Q

Animal Transmission - Class Swine Fever

* ______ contagious
* Infection via contact with?
* Transmission: Ingestion of contaminated ____ or ___ products, ___ or _____ contact (______)
* Less common: ?
 Congenital
 Infected pigs are the only reservoir
 CSFV only infects pigs

A

Highly, Blood, saliva, urine, feces, tissues,
garbage, meat, Direct, indirect, fomites

aerosol, semen,
vectors

82
Q

Clinical Signs Varies: Acutely fatal to asymptomatic
 ***Acute Disease
 Incubation period: __ to __ days
 ____ fever (___oF)
 ______, weakness
 Anorexia -Conjunctivitis
 Diarrhea - _______
 ____
 Skin ______ -Death
**Subacute
 Similar to acute form, but symptoms less
severe
 Pigs may survive
**Chronic
 Anorexia, depression, fever, diarrhea
 Poor reproductive performance including
abortions, stillbirths, and deformities

A

2, 14, High, 105, Huddling, Staggering, Cyanosis, hemorrhages

83
Q

Congenital Forms of CSF
**Weak “______” piglets
**_______, ________, ________,
 ***born dead, or congenital tremors.
 Persistently infected (immunotolerance) –
become persistent _____ to maintain CSF in ______ herd;
 Viremic - seronegative piglets
 Highly variable
 Hemorrhage
 Necrotic foci in tonsils
 Petechiae/ecchymoses on serosal and
mucosal surfaces
 Kidney, larynx, trachea,
intestines, spleen, lungs

A

Shaker, Stillbirths, deformities, mummies, shedders, breeding

84
Q

CSF-Post Mortem Lesions: Chronic Disease
**________ foci (“ ______ ulcers”)
 Intestinal mucosa
 Epiglottis
 Larynx
* Congenital infection
− Cerebellar hypoplasia,
− Thymic atrophy, hemorrhages
− deformities
* ***CSFV can survive long periods in ____ or body ___, particularly if _____ or ______, therefore, feeding of ______ swill should be avoided.

A

Necrotic, button, meat, fluid, chilled, frozen, uncooked

85
Q

Diagnostic Tests - Classic Swine Fever Virus
* Detect virus, antigens, nucleic acids
** Tissue samples (?)- Frozen/cryosections for
IHC/FA, Nucleic acids for RT-PCR
 Whole blood/buffy coat
 ***____-PCR
**_____, ____) or direct immunofluorescence,
 Serology: ELISA
 Diagnostic testing can only be performed @ ?
(FADDL), Plum Island
 Differential diagnosis

A

tonsils, spleen, kidneys, distal ileum

RT, ELISA, IHC, foreign animal disease diagnostic lab

86
Q

Prevention and control
 Do not feed uncooked garbage or meat
products to swine
 Minimize visitors on the farm
 Especially those who have traveled
internationally in the last 5 days
 Implement biosecurity measures
 ***Clean/disinfect boots
**Clean coveralls
Vaccines for CSF
 Available in endemic countries
 Protects from disease
 Does not eliminate infection
 Helpful in outbreak control

A
87
Q

**Differential Diagnosis
 African swine fever
 Acute PRRS
 Porcine dermatitis and
nephropathy syndrome
Recommended actions
IMMEDIATELY notify
authorities
Federal Area Veterinarian in
Charge (AVIC)

A
88
Q

West Nile Virus (WNV)
* First identified in 1937 in ____ in
the eastern region of Africa;
*****Outbreaks spread to ?
* Virus is spread when a _____
bites an infected ____ and then bites a ___
* Mosquitoes carry highest amount of
the virus during ____ fall (late August to early September).

A

Uganda, Europe, Asia, and the Middle East

mosquito, bird, person, early

89
Q

Human infection with WNV
 Most asymptomatic
 Fever, “flu” like symptoms
(fatigue, anorexia, nausea,
vomiting, arthralgia, rash,
lymphadenopathy)
 Encephalitis, meningoencephalitis
- ataxia, painful eyes, seizures,
change in mental status
(confusion)
 Case fatality rate in hospitalized
patients - 10-12% risk factor for
severe disease (age 50-60 yr are
10 times and >80 yr are more than
40 times likely)
 Most people infected with WNV have
no signs or symptoms.
 Common signs and symptoms of West
Nile fever include:
 Fever
 Headache
 Muscle aches
 Backache
 Lack of appetite
 Nausea, vomiting and diarrhea
 Skin rash
 Swollen lymph glands
 At risk group of people
 Adults over 50 years old.
 People with immune systems weakened
by long-term steroid use, chemotherapy
drugs or anti-rejection drugs following
transplant surgery.
 Pregnant women.
 People with certain genetic mutations.

A

skipped this

90
Q

know this

A
91
Q

Biological transmission of WNV-in the mosquito

A

know this

92
Q

Phases of WNV infection

A

know this

93
Q

Replication cycle of WNV-In mammals

A

know this

94
Q

WNV Neurological disease in horses
 Ataxia 86% Depression 51%
 Hind limb weakness 49%
 Difficulty or inability to rise 46%
 Muscle tremors 41% Fever only 24%
 Differentials: Rabies, EHV 1, EEE, WEE, botulism
10% to 50% of horses with neurological signs die

A
95
Q

What disease is this horse suffering from?

A

West Nile Virus

96
Q

Transmission cycle of WNV
 Reservoir: ____ (Jays and
Crows)
 Transmission vector: Mosquitoes from
the genus ____
 Incubation period: ___-___ days

A

Birds, Culex, 3-14

97
Q

WNV and JEV transmission cycles
* Enzootic cycles are maintained by ___________ vectors host
* WNV-predominantly ____
* JEV- ___ and ____
* Both _______, _______ and other _____ are considered dead-end hosts: incapable of participating in enzootic cycle

A

mosquitoes, birds, birds, swine, Humans, horses, mammals

98
Q

Some common causes of Stumbling in horses
None infectious causes
* Long toes are commonly known to cause
stumbling
* Foot pain can lead to stumbling
* Osteoarthritis, such as ringbone (high or low)
or arthritis in the carpus (knee)
* None infectious Neurological problems
(trauma trauma to the spine in the back or
neck)
* A “Wobbler“ diseases in horses (horse with a
damaged spinal cord)
* Some liver diseases

A

skipped

99
Q

Infectious Neurological problems
* Equine Protozoal Myloencephalitis (EPM)
* Verminous encephalitis
* West Nile virus (WNV)
* Equine Herpesviruses (EHV-1)
* Eastern Equine Encephalitis (EEE)
* Western Equine Encephalitis (WEE)
* Venezuelan Equine Encephalitis (VEE)
* Rabies virus
* Tetanus

A

skipped

100
Q

Mortality rates:
EEE, 90%
WEE, 50%
Tetanus, 75%
West Nile, 33%
Rabies, 100%

A

skipped

101
Q

know this

A
102
Q

WNV-Vaccines
* No TBEV licensed vaccines available
in __
* Two _________ cell culture derived
TBEV vaccine are available in Europe

A

US, inactivated

103
Q

Japanese Encephalitis virus (JEV)
 1870s: Japan “_______ encephalitis” epidemics
 1924: Great epidemic in Japan
 6,125 human cases; 3,797 deaths
 1935: Virus first isolated
 Fatal human encephalitis case
 1938: Virus isolated from mosquito ____ tritaeniorhynchus
 Ecconomic impact
 Porcine: high mortality in piglets
 Equine: up to 5% mortality rate
 Humans: -Cost for immunization and medical treatment
-Vector control measures

A

Summer, Culex

104
Q

JEV - Horses
* IP: 8 to 10 days
* Usually subclinical
Fever, impaired ________, _____, teeth _____ Blindness, coma, death (rare)
* PM lesions
Horses
Non-specific
Nonsuppurative
meningoencephalitis

A

locomotion, stupor, grinding

105
Q

JEV - Pigs
IP unclear
Exposure _____ in pregnancy more harmful
Birth of _____ or ________ fetuses
Piglets: _______ signs, death
Boars: _______, _____ testicles
Swine (fetuses)
Mummified
Hydrocephalus, cerebellar hypoplasia
Spinal hypomyelinogenesis

A

early, stillborn, mummified, Neurological, Infertility, swollen

106
Q

JEV - Human
Acute _________
Headache, high ____, ____ neck, stupor
May progress to ?
Neuropsychiatric sequelae ___ to ___% of survivors. In ___ infection possible, Abortion of fetus
PM lesions
Pan- _________
Infected ______ throughout CNS
Occasional microscopic ________ __
___________ generally severely affected

A

encephalitis, fever, stiff

paralysis, seizures, convulsions, coma, and death
45, 70, utero, encephalitis, neurons, necrotic foci, Thalamus

107
Q

Diagnosis of JEV
 Laboratory diagnosis required
 Tentative diagnosis
 Antibody titer: HI, IFA, CF, ELISA
 JE-specific IgM in serum or CSF
 Definitive diagnosis
 Virus isolation: CSF, brain
 No specific treatment
 Supportive care

A

nothing specific or special; taking right samples, looking at antigens, Ab

108
Q

Dengue Hemorrhagic fever virus (DHFV)Virus-General criteria
Grade 1
- ______ and _________ constitutional symptoms
-Positive _________ test is only __________ manifestation
Grade 2
-Grade 1 manifestations + ___________ bleeding
Grade 3
-Signs of circulatory ______ (rapid/weak pulse, narrow pulse pressure, hypotension,
cold/clammy skin)
Grade 4
-Profound _____ (________ pulse and BP)

A

fever, nonspecific, tourniquet, hemorrhagic

spontaneous, failure

shock, undetectable

109
Q

Transmission and pathogenesis of Dengue virus
The most common epidemic vector of dengue in
the world is the _______ ________ ________. It can be identified by the white _____ or ____ patterns on its legs and thorax

A

Aedes aegypti mosquito, bands, scale

110
Q

Pathogenesis of DHFV

A

Aedes aegypti - see bottom right

111
Q

DHFV clinical profile

A
112
Q

Diagnosis and control of DHFV
* Virus isolation
** Increased IgM as a marker
* Detection of the viral Ag
* IHC
* IFA
* ELISA
* PCR
* ***CBC: __________ and ________
*Reduce vector density to a level below
which epidemic vector transmission will not
occur

A

Leucopenia, thrompocytopenia

113
Q

Tick borne encephalitis virus (TBEV)
Louping-ill virus (LIV)

A

Ticks bite human, incubation period, first phase = uncharacteristic phase, 28 days, curve up again and is in neurological phase.

114
Q

Pathogenesis and control of TBEV

A

went through this

115
Q

Transmission and pathogenesis of TBEV

A

went through this

116
Q

TBEV diagnosis

A

went through this

117
Q

Yellow fever virus (YFV)
** Caused by __________ that is spread by the _____ ____ or ________ mosquito
*** Cause _______ in patients due to liver damage

Jungle cycle - Between monkeys and forest mosquitoes.
Humans can only get infection occasionally during their ____ visits.
Urban cycle - Occurs between humans and ____ mosquitoes (Aedes aegypti

A

Flavivirus, Aedes egypti, Haemagogus, jaundice, forest, urban

118
Q
A

yellowish coloration of mucous membrane = liver dysfunction
albumin produced by liver

119
Q

Clinical signs - (YFV)

A

Muscle aches, hepatomegaly, etc.

120
Q

*Wesselsbron disease
Acute, ________-borne _______ infection of
mainly which species?
* ________ lambs and goat ___ are most
susceptible, and mortality may occur
* Occasional abortion in ewes, together with congenital malformation of the CNS with arthrogryposis of the ovine (and also the bovine) fetus and hydrops amnii in ewes
* (Incidental spillover occurs to ____, causing a ______, _____-like disease
* Moderate to severe icterus and hepatomegaly, the liver is yellowish to orange brown

A

arthropod, flavivirus, sheep, cattle, and goats

Newborn, kids, people, nonfatal, influenza

121
Q

General properties of the family Caliciviridae
* **Calici: latin word ___ or __ (small _____ structures viruses)
* **Virions: non-________, 27-40 nm in diameter, ________
* Some virions have characteristic shape with 32 cup-shaped depressions on their surface
***** Genome: ____ molecule of ____ (__ Ve) sense ___ RNA, 7.4- 8.3 kb in size
* Genomic RNA is polyadenylated
* ________ replication

A

chalice, Cup, round, enveloped, icosahedral, single, linear, +, SS, Cytoplasmic

122
Q

insert photo of calici virus here

A
123
Q

Caliciviridae- Phylogenetic tree
Four genera:
1- Vesivirus,** = feline callicivirus, swine?, others
2- Lagovirus (rabbit) and
Two genera contain
human caliciviruses
3- Norovirus
4- Sapovirus

A
124
Q

Genome structure and organization of Caliciviridae
* Genome organization of human noroviruses into three overlapping open reading frames (ORF1–ORF3).
*** ORF1, -2, and -3 encode for ?
Classification
-VP-1
-RdRp

A

ORF-1: polyprotein,
ORF-2: major capsid protein VP1
ORF-3: minor capsid protein viral protein 2

125
Q

Diseases caused by Caliciviruses affecting various species of animals

Good table!

A
126
Q

Lagovirus- Rabbit Hemorrhagic Diseases virus

RHDV: belongs to genus Lagovirus
* **RHDV: a deadly disease that can infect rabbits affecting the _____ & blood _________-
* **RHDV: remain in the environment for up to ____ months, making it resilient
* RHDV: capable of surviving both ______ and very ____ temperatures
* RHDV: original strain emerged in China in 1984
* RHDV: second strain called RDHV2 found in France in 2010
* ***RHDV: Rabbits under ____ months of age are not susceptible
*
** RHDV: It is a mutant form of a non-pathogenic virus, termed rabbit ________
* RDHV2: continued to spread throughout Europe and now the US & Western Canada

A

liver, vessels, 3.5, freezing, hot, two, calicivirus

127
Q

*******RHDV-Clinical Signs
* Fever
* Shortness of breath
* Loss of appetite
* Listlessness
* Neurological signs such
paddling, seizures, and
paralysis
* Jaundice
* Blood spots in eyes
* Sudden death
* Bleeding from nose at time of
death
 Diagnosis of RHDV
-History, clinical signs, PM
-Detection of viral NA by RT-
PCR
-Detection of viral Abs

A
128
Q

Feline Calicivirus (FCV)- clinical syndromes

** ______ contagious pathogen with a
widespread distribution in the feline
population
** Belongs to the _______ family,
genus _______; caliciviruses
** Cats can be infected with FCV via the
(3) routes
*** The _________ is the primary site of
replication
* Transient viraemia occurs 3 to 4 days after
infection
* FCV: induces necrosis of epithelial cells:
vesicles, typically on the tongue, develop
into ulcers; in the affected regions, the
mucosa is infiltrated with neutrophils

A

Highly, Caliciviridae, Vesivirus, nasal, oral or conjunctival

oropharynx

129
Q

addd photo of ansal and ocular conjunctiva

A
130
Q

Feline Calicivirus (FCV)- clinical syndromes
_____ and ____ disease
Erosive lesions on the _______
* FCV infection is ubiquitous and can induce severe disease.
* Feline chronic gingivostomatitis (FCGS)
* Limping syndrome
*
Virulent systemic feline calicivirus (VS-FCV) infection

A

Paw, mouth, tongue

131
Q

Diagnosis of FCV
* History, clinical signs, PM lesions
* Viruses in modified live virus vaccines are occasionally shed post-vaccination
* PCR (RT-PCR)-positive result because of the poor correlation between the presence
of virus and clinical signs
* cat that has typical clinical signs and a positive RT-PCR result, a causal relationship
is likely
* Conventional, nested and real-time RT-PCR assays to detect FCV RNA in
conjunctival and oral swabs, blood, cutaneous scrapings or lung tissue
* Virus isolation : FCV replicates in cell lines of feline origin; Virus can be isolated
from nasal, conjunctival or oro-pharyngeal swabs
* Detection of FCV antibodies : ELISA

A
132
Q

Therapeutic trials for the FCV

curve of virus goes down post treatment

A
133
Q

Feline Calicivirus Prevention
* Both modified live and inactivated parenteral vaccines are available
** __________ ___ intranasal vaccines are still current in the USA
** There is currently no vaccine available that protects equally well against ____ FCV field strains
 Modified live (I/M, nasal, conjunctival routes)
 Potential hazards
 Not in kittens <12 wks. (clinical signs and
persistence)
 ***Potential for post-vaccination infections
 Killed (parental)
 Pregnant queens
 (Induce only relative not absolute protection)
 IN administration of an experimental inactivated, non-
adjuvanted FCV vaccine has been shown to be better than a
S/C vaccine in terms of reducing clinical scores and virus
shedding following exposure

A

Modified, live, all

134
Q

3- Noroviruses
* Nonenveloped viruses belonging to the Caliciviridae family
* According ICTV the genus Norovirus has one species, which is called “ _________ virus” named after ______, _____, USA
* Outbreak of acute gastroenteritis occurred among children at Bronson
Elementary School in Nov-1968
* ***Responsible for approximately 90% of epidemic non-________ outbreaks of _________ around the world
* Cause of 50% of all foodborne outbreaks of gastroenteritis
* Able to survive freezing and high temperatures
** Transmitted by ____ contaminated food or water, by person- to-person
contact, and via ______ of the virus and subsequent contamination of
surfaces
* Norovirus are Diverse Group Norovirus (NoV): genetically diverse group of
single stranded RNA

A

Norwalk, Norwalk, Ohio, bacterial, gastroenteritis, faecal, aerosolization

135
Q

Noroviruses
* **Noroviruses are a diverse group of viruses in the family _________
* Named after the original Norwalk virus that caused an
outbreak of gastroenteritis in a school in Norwalk, Ohio,
in 1968.
* >25 different types of norovirus strains have been
identified within these groups and new strains continue
to emerge.
** It is possible to develop immunity to ________ types, but we don’t know how ____ that immunity lasts

A

Caliciviridae, specific, long

136
Q

ECM picture of Norovirus

A
137
Q

Classification of Norovirus

A

Because..

138
Q

Food Handlers and Norovirus
* **Persons working with food who are sick with Norovirus gastroenteritis are a particular risk to others because they handle the food and drink many other people will consume
* Transmission:
* -Oral-fecal‖ route: Food (39%)
* -Hands, person-to- person (12%)
* -Water (3%)
** Indirect contact with the virus on contaminated surfaces
* Via contaminated food and water
** Shellfish from sewage contaminated water

A
139
Q

Norovirus Signs and symptoms

Acute gastroenteritis (inflammation of the stomach and intestines)
diarrhea, vomiting, nausea, stomach pain
Fever, body aches, fatigue
* Dehydration (because of having diarrhea and vomiting many times per
day)
-Less urination -Dry mouth or throat -Dizziness
** When someone gets infected with norovirus, they may say they
have ‘food _________’ or ‘stomach ____’.
Food poisoning can be caused by _________, but other germs and
chemicals can also cause food poisoning.
* ***People can get infected by:
-Eating ___ or drinking ____ contaminated with norovirus
-Touching ______/______ have norovirus on them then putting fingers in ____
-Having direct contact with someone infected with norovirus caring for, or sharing food, drinks, or eating utensils with an infected person

A

poisoning, flu, noroviruses, food, liquids, surfaces, objects, mouth

140
Q

Why are norovirus are difficult to deal with?
Noroviruses are a public health problem.
 They are _______ contagious.
 ***People with norovirus illness shed _______ of virus particles in their ____ and ______, but it only takes a very ___ amount of them (<100 particles) to make someone sick.
 They spread easily and ______, especially in closed places like daycare settings, nursing homes, schools, and cruise ships.
 They are hard to get rid of because they:
1. stay on objects and surfaces and still infect people after days or weeks
 survive both freezing and heating (although not thorough cooking)
and even some disinfectants
2. They are constantly evolving. difficult to develop a vaccine

A

highly, billions, stool, vomit, small, quickly

141
Q

Foods commonly involved in norovirus outbreaks

** _____ or _______ foods: such as ___ greens, fresh ____, or _____.
-Any food served raw or handled after being cooked can get contaminated with
noroviruses.
-Fresh produce: may be handled at several different points, including harvesting, processing, and preparing, before it is eaten.
-Water: used to ________ crops can cause norovirus contamination, which will persist
on raw food.
-Raw or undercooked shellfish: like _______, can be problematic when they are
harvested from contaminated water.
-** ___-to-eat foods: like sandwiches and salads.

A

Raw, undercooked, leafy, fruits, shellfish, irrigate, oysters, Ready

142
Q

***Clinical signs of Norovirus infection
* Signs and symptoms include:
* Acute gastroenteritis (inflammation of the
stomach and intestines)
* diarrhea, vomiting, nausea, stomach pain
* Fever, body aches, fatigue
* Dehydration (because of having diarrhea and
vomiting many times per day)
* Less urination
* Dry mouth or throat
* Dizziness
* When someone gets infected with norovirus,
they may say they have ‘food poisoning’ or
‘stomach flu’.

A
143
Q

How are Noroviruses spread?
* People with norovirus illness shed billions of virus
particles in their stool and vomit.
* People can get infected by:
* eating food or drinking liquids contaminated
with norovirus
* touching surfaces or objects that have norovirus
on them then putting fingers in mouth
* having direct contact with someone infected
with norovirus
* caring for, or sharing food, drinks, or
eating utensils with an infected person

A
144
Q

Diagnosis of Norovirus
Specific diagnosis (PCR) assays or real-
time PCR assays, which give results
within a few hrs
* These assays are very sensitive and can
detect concentrations as low as 10 virus
particles
* Molecular detection of Norovirus
Specimen Processing (Faeces)
* RT-PCR Amplify by real-time PCR
Norovirus Genogroup I or II identified
Sequencing Genotyping

A
145
Q

*******How to protect ourselves from Norovirus infection?
First: always wash your hands carefully with soap and water after using
toilet and changing diapers and before eating, preparing, or handling food.
 Second: wash your fruits and vegetables thoroughly, and cook oysters and
other shellfish thoroughly before eating them.
 Third: do not handle or prepare food for others when you are sick.
 Fourth: clean and disinfect contaminated surfaces after throwing up or
having diarrhea.
 Finally: wash any soiled laundry thoroughly after throwing up or having
diarrhea.

A
146
Q

Control of Norovirus outbreak
* Secondary spread via aerosols and vomit is a major problem
* Isolation of patients, staff, and infected areas
* Staff may execrate NOV for up to 14 days (should be checked for clearance)
* Surface cleaning (benches, taps, fomites, fur natures, floors, etc)
* Good hand washing practices: some disinfectants are not effective
* Refer specimens for viral analysis and genotyping to help track movement
of epidemic strains

A
147
Q
  • Vesicular exanthema of swine (VE)
    San Miguel Sea Lion Viral Disease (SMSL)
  • An acute, contagious disease characterized by
    vesicles on the feet, snout, mucous membranes of
    the mouth and tongue, and non-haired skin
  • The disease in sea lions causes vesicles on the
    flippers
  • VE is quite contagious among swine and spreads by
    direct contact and fomites
  • VE is transmitted by eating uncooked garbage
    containing infectious meat scraps from swine or
    certain fish
A
148
Q

Vesicles on the flipper of an
affected animal
Histological appearance of
the vesicle, with
fluid accumulation within the
epidermis.

A
149
Q

Family:
Astroviridae
104
Astroviridae: 2 genera, 22 species
:
Genus: Avastrovirus:
Genus: Mamastrovirus
Virion: non-enveloped, icosahedral
28-33 nm in diameter
Genome:
-ss linwar (+Ve) sense RNA
-Poly adenylated at 3’ end and it is infectious
-6-7 Kb in size
-A subgenomic RNA is developed during replication
-6 principle ORFs encoding at least 6 proteins (P, X,
M, G, & RdRp)
* Persistent infection reported in cell culture and
animals
* Virions are resistant to
-Heating at 50 °C for 1 h or 60 °C for 5 min

A
150
Q

Classification of Astroviridae

A
151
Q

Genome structure and organization of Astroviruses
106
* The astrovirus genome is arranged in three ORFs: ORF1__ and ORF1__ at the 5’ end encoding the ____-structural proteins, and ORF__ at the 3′ end encoding the ________ proteins

A

a, b, non, 2, structural

152
Q

Replication cycle of Astroviruses

A
153
Q

Transmission of Astroviruses

A
154
Q

Pathogenesis of TAstV in turkey poults
Intestinal villi of turkey poults
* A: Control poults showing normal crypts
(3dpi)
* B: Infected poults showing significant _________ in the crypt ____
* C: : Control poults showing normal crypts
(7dpi)
* D: Infected poults showing epithelial _______ and multiple prominent _____

A

increase, depth, hyperplasia, nucleoli

155
Q

Pathogenesis of TAstV in turkey poults

Ileum of turkey poults inoculated with TAstV
A:Ileum: cells containing aggregates of _________ inclusion bodies
B: aggregates of intracytoplasmic inclusion bodies
with few free in the cytoplasm
C: Aggregation of astrovirus in the lumen of the distal
ileum adjacent to the enterocytes

A

intracytoplasmic

156
Q

Diagnosis & control
 History, clinical signs
 Sampling: fecal samples , intestine, blood
 Detection of virus by EM
 Detection of viral nucleic acids by PCR
 Detection of viral antibodies by ELISA, SNT etc
 Control: adoption of hygienic measures

A
157
Q
A

Virology (17 decks)

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