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Virology > Herpes & Parvo > Flashcards

Herpes & Parvo Flashcards

1
Q

The greek word Herpein means?

A

To creep

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2
Q

Herpesvirales is no longer considered a family but an?

A

Order

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3
Q

Order: Herpesvirales
accommodates
* __ Families
* ____ Subfamilies
* ____ Genera
* ____ Species

A

3, 3, 17, 90

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4
Q
A

Herepesviridae subfamily - alpha, beta, gamma
Within alpha, beta, and gamma several viruses higlighted -> know names

Alpha, beta, gamma = subfamily
Alpha = highlighted viruses

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5
Q
A

Examples of viruses here; we select which ones we want to study

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6
Q

Does he want us to know this?

A

Allo = fish
Mala= oysters

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7
Q

Describe the size and characteristics of the herpesvirus virion.

A

Know the size

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8
Q

Define the term tegument

A
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9
Q

Describe the herpesvirus envelope.

A
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10
Q

Describe the herpesvirus capsid.

A
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11
Q

Describe the herpesvirus core

A
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12
Q

Label accordingly

A
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13
Q

Label accordingly

A

Viral capsid

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14
Q

General properties of of Herpesvirus
Structure and Composition
 Spherical ______, ___-____ nm
 _____-stranded ___, linear
 More than ___ proteins
 Enveloped or non-enveloped?
 Replication from _____ (______)

A

iscoahedron, 150, 200, Double, DNA, 35, Enveloped, nucleus, budding

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15
Q

What are the important features of Herpesvirus
–> Important features
 Encode many _____
 Establish ____ infections
 Lifelong ______
 A significant cause of death in ________ hosts
 Some can cause ____

A

enzymes, latent, persistence, immunocompromised, cancers

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16
Q

Label accordingly

A

Herpesvirus

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17
Q

Label accordingly

A

Herpesvirus

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18
Q

Label accordingly

A
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19
Q

Label accordingly

A

Herpesvirus
Envelope

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20
Q

Label accordingly

A

Herpesvirus
Tegument

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21
Q

Label accordingly

A

Herpesvirus
Capsid

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22
Q

Label accordingly

A

Herpesvirus
DNA

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23
Q

Describe the herpesvirus genome

A

Genome: monopartite, linear, dsDNA
genome of 120-240 kb

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24
Q

The herpesvirus genome contains?

A

terminal and internal repeated sequences

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25
Q

The herpesvirus genome contains unique ____ (UL)
and unique ____ (US) regions bounded by ______ ______ (ITR) which allow _________ of unique
regions

A

long, short, inverted repeats, rearrangement

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26
Q

Most vertebrates carry ________ ______ species

A

multiple herpesvirus

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27
Q

The herpesvirus encodes a large number of enzymes involved in ____ metabolism and ______ processing

A

Nucleic Acid, protein

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28
Q

Herpesvirus
DNA synthesis and viral assembly occur in the ?

A

nucleus (IP)

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29
Q

Herpesvirus
 Production of progeny virus resulted in ?

A

host cell distortion
Production of large number of viruses in cell –> expands cell size

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30
Q

Herpesvirus
Persistent infection with ______ or ______ shedding

A

periodic, continuous

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31
Q

 Herpesvirus can remain _____ in the host cell
-Alpha: ______
-Beta: ______
-Gamma: _______

A

latent, neurons, monocytes, lymphocytes

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32
Q

 ____ & ______ herpesvirus infections often clinically silent in mammals

A

Beta, gamma

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33
Q

 Herpesviruses highly _____ to their hosts, and severe infection is usually observed only in the very ____.

A

adapted, young

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34
Q

 Most Herpesviruses establish a ______ infection, a cell-associated _____ being detectable during primary infection.

A

systemic, viremia

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35
Q

Herpesvirus replication cycle
Simple

A
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36
Q

Herpesvirus replication cycle
Complex

A

Nucleus = transcription
mRNA produced
translation
released from host cell

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37
Q

What can be seen here?

A

Herpesvirus - Formation of capsid; Budding through a nuclear envelope

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38
Q

What can be seen here?

A

Infected cells with intranuclear inclusion bodies

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39
Q

What can be seen here?

A

“Owl eye” Herpesvirus intranuclear inclusion

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40
Q

Latent replication of Herpesvirus:
Replication of circular viral episome in
tandem with the host cell DNA using the host cell replication machinery
“_____ ____” Herpesvirus ______ inclusion

A

owl eye, intranuclear

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41
Q

Why Herpesviruses are difficult to be controlled?
1- Some infect _____ target tissues: ___ and maternal _____. If virus affecting placenta –> _____
2-All become _____ (as circular DNA in the nuclei of ganglia of lymphocytes) of
recovered animals
Subsequent reactivation during _____ causes disease or tumors
3- All are ____-associated and can spread between cells by cell ______.

A

crucial, brain, placenta, abortion, latent, stress, cell, fusion

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42
Q

What are the outcomes of Herpesvirus infected cells?
 Lytic Herpesviruses: ______ of the infected cells due to alteration in the _____ and ______ process in the cell
 Non-lytic Herpesviruses: integrated in the host cell _____ resulted in changes in the cells
-distortion or change in the cell _____
-change in the appearance of cell _____
- appearance of viral ____ (___) in the cell membrane

A

destruction, biochemical, biological, genome, nucleus, membrane, proteingD

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43
Q

Human herpesvirus = ?
Equine herpesvirus = ?
Bovine herpesvirus = ?
Caprine herpesvirus = ?
Avian herpesvirus = ?
Feline herpesvirus = ?
Canine herpesvirus = ?
Swine herpesvirus = ?
Fish herpesvirus = ?

A

HSV
EHV-1,2,3,4,5,9
Caprine Herpevirus
MDV, ILTV, DVE
FeHV
Canid Herpesvirus-1
Suid HV’s, Pseudorabies, Aujeszky’s
Salmonid Herpesvirus 1,2,3

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44
Q

HSV is involved in a variety of clinical
manifestations which includes?

A
  1. Acute gingivostomatitis
  2. Herpes Labialis (cold sore)
  3. Ocular Herpes
  4. Herpes Genitalis
  5. Other forms of cutaneous herpes
  6. Meningitis
  7. Encephalitis
  8. Neonatal herpes
  9. Keratoconjunctivitis (corneal ulcers)
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45
Q

What can be seen here?

A

Herpes Labialis aka cold sore

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46
Q

What can be seen here?

A

Keratoconjunctivitis (corneal ulcers) caused by Herpesvirus

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47
Q

What can be seen here?

A

Meningitis due to Herpesvirus infection

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48
Q

What can be seen here?

A

CPE of HSV in cell culture: Note ballooning
of cells

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49
Q

What can be seen here?

A

Positive
immunofluorescence test
for HSV antigen in
epithelial cell

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50
Q

What can be seen here?

A
  • Stained smear of materials from
    Herpesvirus simple lesion
  • Multinucleated giant cell and
    intramuscular inclusion bodies
  • Pink areas within the epithelial
    cell nuclei are intranuclear IB.
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51
Q

List the various alpha herpesviruses

A

EHV-1, 3,4,9

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52
Q

EHV-1 leads to?

A
  1. Abortion
  2. Respiratory issues
  3. Neurological issues
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53
Q

EHV-3 leads to?

A

Coital exanthema

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54
Q

EHV-9 leads to?

A

Fatal encephalitis of gazelle, giraffe, and polar bear

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55
Q

EHV-4 leads to?

A

Respiratory diseases in young foals

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56
Q

List the various beta herpesvirus

A

EHV 2, 5

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57
Q

EHV-2 leads to?

A

Suppression of horse’s immunity

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58
Q

EHV-5 leads to?

A

Pulmonary fibrosis

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59
Q

EHV-1 causes? Equine _______ virus
What are the clinical signs of EHV-1?
Respiratory, abortions, encephalomyelitis
Can cause four manifestations of disease in horses, including ________ form, ______ disease, ____ and neonatal _____

A

abortion
neurological, respiratory, abortion, death

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60
Q

What are the clinical signs of EHV-2?

A

Granulomatous dermatitis

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61
Q

What are the clinical signs of EHV-3?
Genital lesions (______ ______ ______ Virus)
Causes a ______ disease called _____ _____ that affects the ____ genitalia but has not been shown to affect ______.

A

Equine Coital Exanthema, venereal, coital exanthema, external, fertility

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62
Q

What are the clinical signs of EHV-4?

A

Equine Rhino pneumonitis syndrome
Causes a nonfatal upper respiratory tract disease in foals and is uncommonly associated with abortion and rarely with neurological disease

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63
Q

What are the clinical signs of EHV-5?

A

Equine multinodular pulmonary fibrosis (EMNPF)

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64
Q

What are the clinical signs of EHV-8?

A

Rhinitis

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65
Q

What are the clinical signs of EHV-9?

A

Asymptomatic in equids, severe disease in other species

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66
Q

Epidemiology of EHV
 _______ distribution
 Transmission: ____ or _____ contact with infectious ____ secretions, ____
fetuses, ______, or ______ fluids
 Horses may become ____ carriers of EHV; virus may be reactivated after ____
 Horse is the only known _____ for the virus
 The usual mode of transmission is _____
–> The pathogenic mechanisms of EHV-1 and EHV-4 differ significantly:
 EHV-1 strains have a predilection for _______ ______, especially the nasal
mucosa, lungs, adrenal, thyroid, and CNS
 EHV-1 gains access to peripheral tissues via cell-associated viremia, which may
manifest as _____ or _____ disease
 EHV-4 infection is restricted to ______ _____ epithelium and associated
lymph nodes

A

Worldwide, direct, indirect, nasal, aborted, placentas, placental, latent, stress, reservoir, venereal, vascular endothelium, abortion, neurologic, respiratory tract

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67
Q

Clinical signs of EHV
 _____ commonly precedes the development of other clinical signs
 Respiratory disease: fever, coughing, and nasal discharge
 Other equine respiratory diseases, such as influenza, and differential laboratory diagnosis is required
 _____ typically occur late in pregnancy (greater than eight months, although earlier cases are reported)
 ______ disease associated with EHV-1 can range from mild incoordination to severe posterior paralysis
* Severely affected horses may become ____ and unable to rise-Incoordination -Lower leg swelling -Weakness in hind limbs
 Inability to pass urine or manure
* Neurological problems (not by direct neuronal infection but indirectly via endothelial infection) –
 ________ –> _______ –> resulting in: an ______ condition in the spinal cord –> neuronal _______ –> neuronal ______

A

Fever, Abortions, Neurological, recumbent, Vasculitis, thrombosis, ischemic, anoxia, necrosis

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68
Q
A

EHV-1
Neurological signs

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69
Q

Pathogenesis of EHV -1
EHV-1 infects the ______ cells of the ?
* EHV-1 ______ and ____
* Dissemination through the ________ ____
* Virus reach _____ _____ (PBMC) will be infected
* Virus circulate and infect _____
* Dissemination of the virus to distant such as the _____ &
________ _____, MALT= _____ associated lymphoid tissue, NALT= _____ associated lymphoid tissues
-> EHV-1 transmission from mare to fetus:
* EHV-1 spreads by cell-to-cell contact to the fetus through ______ endothelium
* EHV-1 can also infect ______ cells causing uterine pathology leading to premature placental ______ and fetus ____ (inadequate _______ of the mother)

A

epithelial, upper respiratory
tract
replicates, sheds
respiratory tract
lymph nodes
leucocytes
CNS
reproductive tract
mucosal
nasal
capillary, endometrial, separation, anoxi, oxygenation

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70
Q

Describe how EHV-1 can cause abortion

A

Endothelial cells and leukocytes –> Endometrial vessels –> fight CD4+ and CD8+ –> inflammation, vasculitis –> affects fetus.

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71
Q

EHV-1 and abortion

A

Umbilical cord has blood vessels, lymph supplies, etc. and connects fetus to mother. Fetus is an obligate parasite of the mother b/c has no way to function on its own.
Viremia leads to endometrial endothelial cell infection –> Endometrial vasculitis and thrombosis (blood clot) –> Extensive infarction: virus negative fetus

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72
Q

What are some complications of EHV-1 infection in pregnant mares?

A
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73
Q

What are some complications of EHV-1 infection in full term foals?

A

FULL TERM FOALS
l -General weakness
l -Pneumonia
l -Death

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74
Q

What are some complications of EHV-1 infection in infected fetuses?

A

Infected fetuses aborted in late pregnancy
are often fresh- death due to suffocation
following rapid placental separation

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75
Q

EHV-4 may rarely cause isolated abortions but not ?

A

abortion storms

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76
Q

General pathogenesis of EHV1&4

A
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77
Q

General pathogenesis of EHV1&4

A
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78
Q

Equine Viral Rhinopheumonitis
1. What species is effected by this disease? Age range?
2. What is this disease caused by?
3. EHV-4 replication is restricted to?
4. EHV-1 infection extends to what parts of the body?

A
  • A disease of young horses (up to 2 years), and older animals – mild clinical signs
  • Caused by 4 Herpesviruses (EHV-1 (subtype-1, subtype-2), EHV-2, EHV-3, EHV-4)
  • EHV-4 replication is mainly restricted to URT
  • EHV-1 infection extends beyond the respiratory tract (Cell associated viremia) lung pneumonia, placenta endometritis, abortion.
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79
Q
A

Equine Viral Rhinopheumonitis

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80
Q
A

Equine Viral Rhinopheumonitis

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81
Q
A

Equine herpesvirus 2-associated granulomatous dermatitis; Multifocal to coalescing areas of necrosis marked by histiocytic cell

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82
Q
A

Equine herpesvirus 2-associated granulomatous dermatitis

Multifocal to coalescing areas of necrosis marked by histiocytic cell
infiltration and the presence of giant cells.
* Intranuclear and intracytoplasmic viral particles consistent with
Herpesvirus

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83
Q
A

Equine Herpesvirus-3 (EHV-3)(Equine Coital Exanthema

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84
Q

Equine Herpesvirus-3 (EHV-3)(Equine Coital Exanthema)
1. Acute ______ transmitted disease –> ? (4) penis and prepuce of stallions -
external genitalia and peripheral skin of mares
- lips, external nares, nasal mucosa, and conjunctiva:
lesions heal after 14 days l, leaving depigmented
patches on the vulva -erosions and ulcers on prepuce
and penis of the male cacauseorse genital herpes
infection
- white depigmented spots on vulva, penis, prepuce
develop and stay for life – helps in identifying
previously infected animals or carriers
* EHV3 exhibits no cross-reactivity with other
Herpesviruses
* High antibody incidence >50%
* Experimental inoculation in the uterus – abortion
occurs
* Subclinical respiratory infection in yearling horses

A

sexually, papules, vesicles,
pustules, and ulcers

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85
Q

What diagnostic tests would you run if you suspect your patient has EHV?

A

Case history
 Clinical signs
 Virus isolation from aborted foetus using cell culture
 PCR (nasal, rectal, vaginal, placental fluid)
 Serology: -Serum Neutralization test (SNT)
-Complement fixation test (CFT)
 Haematology: Leukopenia

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86
Q

How can you control the spread of EHV?

A

Vaccination
-an early age
- periodically depending on management factors
- recommended to reduce the incidence and severity of disease

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87
Q

What types of vaccines are available for EHV-1?

A
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88
Q

Psuedorabies Virus (PRV)-(Aujeszky’s Disease, Mad Itch)
1. What is the cause of Mad Itch disease?
2. Genus name?
3. How many serotypes does this virus possess?
4. What species are affected?
5. Which species are dead end hosts?
6. Morbidity?
7. Mortality?

A

Alphaherpesvirus (Porcine herpesvirus-1)
 Genus: Varicellovirus
 Single serotype
 Disease of pigs (natural host) that is fatal for most
other animals
 Dead end host (dogs, cats, cattle etc.)
 Morbidity
 Up to 100% in piglets,
mild or no signs in adults
 Up to 20% abortions
 Mortality
 Highest in younger
animals
 Decreases with age
 Always fatal in other
species

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89
Q
A

-Aujeszky first identifies
ADV in cattle and dogs
-Determines swine are
natural hosts

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90
Q

Describe the modes of transmission of Psuedorabies Virus (PRV)

A

Most common
 Respiratory
 Oral
 Nose-to-nose contact
 Aerosol
 Fomites
 Contaminated bedding and water
 Meat products or carcasses
 Latent carriers possible
 Contact with infected pigs
 Ingestion of contaminated raw meat
 Rarely lateral transmission
 Pig bite—uncommon

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91
Q

What are the clinical signs seen in pigs affected by Mad itch?

A

** Incubation period: 2 to 6 days
 < 1 week old piglets
 Fever, listlessness, anorexia
 Neurological signs
 Tremors, paddling, seizures, dog-sitting
 High mortality within 24 to 36 hours
** Older piglets/weaned pigs
 Similar signs
 Respiratory, neurological, vomiting
 Lower mortality
** Adult pigs
− Mild or subclinical infection
− Respiratory and neurological signs
− Pregnant sows: reproductive signs

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92
Q

Describe the pathogenesis of Pseudorabies in pigs.

A

Pigs
 Replicates in tonsils and oral pharyngeal epithelium
 Mild respiratory signs - follows trigeminal nerve to the TG- latent infection,
in rare cases CNS invasion.
 Can cross placenta
 Systemic infection in fetuses and neonates (CNS invasion)

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93
Q

Describe the pathogenesis of Pseudorabies in other animals (_____ _____ hosts).

–> Entry by ____ routes/______
 Virus follows ______ nerves to spinal cord –> brain
 ____ signs, rapid death (sometimes found dead), ______ .
–> Entry by ____ wounds
 Follows nerves to spinal cord and CNS
 Intense pruritus (____ ____) with self mutilation at site of bite
 Death

A

dead end, oral, ingestion, autonomic, CNS, pruritus, bite, mad itch

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94
Q

What are the clinical signs of pseudo rabies in cattle and sheep

A

Cattle and sheep
Intense pruritus
 Licking, rubbing,
gnawing, self-mutilation
 Neurological signs

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95
Q

What are the clinical signs of pseudo rabies in dogs and cats

A

Dogs and cats
 Similar to cattle and sheep
Resembles rabies
 Sudden death

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96
Q

Hosts other than pigs diagnosed with pseudo rabies live for how long?

A

1-2 days

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97
Q
A

Pseudo rabies
Top image = swayback?

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98
Q
A

Some Necropsy and histology findings of Psuedorabies Virus (PRV)

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99
Q

Describe what you would find on necropsy in pigs and other hosts diagnosed with pseudorabies.

A

Pigs
-Neurological
Nonsuppurative meningoencephalitis
-Respiratory
Necrotic tonsillitis, bronchitis,
bronchiolitis, alveolitis
-Focal necrosis
Other species
-Spinal cord lesions

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100
Q
A

PRV

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101
Q

What vaccines exist against PRV in swine species

A
  • Inactivated vaccines
  • Modified live virus vaccine
  • Deletion mutant vaccines
  • Sub-unit vaccine plus some immune stimulating complex called (ISCOMs)
  • Vaccination prevents/minimize diseases but not the infection
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102
Q

How do you control PRV?

A

 IMMEDIATELY notify authorities
 Federal
 Area Veterinarian in Charge (AVIC)
www.aphis.usda.gov/animal_health/area_offices/
 State
 State Animal Health Officials
www.usaha.org/Portals/6/StateAnimalHealthOfficials.pdf
 Quarantine Isolation and testing of new animals
Test and slaughter approach: UK eradication
 Biosecurity measures
 Prevent entry
 Double fencing
 Disinfection
 Phenols, quaternary ammonium compounds
 Inactivated by heat, sunlight

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103
Q

What can be seen clinically in a patient diagnosed with BHV-1.1?

A

Implicated in respiratory diseases; may cause abortion

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104
Q

What can be seen clinically in a patient diagnosed with BHV-1.2a?

A

Implicated in infectious balanoposthitis/infectious pustular
vulvovaginitis syndrome and may cause abortion

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105
Q

What can be seen clinically in a patient diagnosed with BHV-1.2b?

A

Implicated in infectious balanoposthitis/infectious pustular
vulvovaginitis syndrome and has not been associated with abortion

106
Q

What can be seen clinically in a patient diagnosed with BHV-2?

A

Bovine Ulcerative Mamillitis (Bovine Herpesvirus II)
(Allerton virus)

107
Q

Bovine Herpesvirus-1-IBRV may present as ?

A

ocular, genital , respiratory and neurologic diseases

108
Q

Bovine Herpesvirus-1-IBRV is what type of disease?

A

Respiratory disease :(infectious bovine rhinotracheitis, IBRV) lead to sever
fatal bronchopneumonia

109
Q

Bovine Herpesvirus-1 results in?

A

Genitalia resulting in
- Abortion and vulvovaginitis (infectious pustular vulvovaginitis, (IPVV))
-Infectious balanoposthitis (infection of the penis, (IBPV))
 Meningoencephalitis in young calves occurs infrequently with BHV-1

110
Q

Describe the pathogenesis of Bovine Herpevirus-1-IBRV.

A

Pathogenesis:
-Virus replicates in the upper respiratory tract
-Spread via lacrimal ducts
-Virus can be recovered from nasal secretion for almost 2 wks PI
- Genital infections are most likely venereal transmission

111
Q

Describe the pathogenesis of Bovine Herpevirus-1-IBRV.

112
Q

How do BHV-1 lesions develop?

A

Immunosuppression- animal susceptible to other disease.
Staph, strep, etc.

113
Q

Describe what can be seen here from left to right.

114
Q

Describe what can be seen here

A

Clinical signs and lesion of IBRV infection in cattle.

115
Q

What can be seen here?

A

Clinical signs and lesion of IBRV infection in cattle.

116
Q

Describe what can be seen here

A

Clinical signs and lesion of IBRV infection in cattle.

117
Q

What can be seen here?

A

Clinical signs and lesion of IBRV infection in cattle

118
Q

What can be seen here?

A

Clinical signs and lesion of IBRV infection in cattle

119
Q

What can be seen here?

A

Clinical signs and lesion of IBRV infection in cattle

120
Q

How do you diagnose IBRV? Control?

A

Case history, clinical signs, PM lesions
 Proper sampling (Feces, fecal swabs, nasal swabs, etc)
 Detection of the viral particles by EM
 Viral isolation from the conjunctival swabs and placenta
 IFA, immunoperoxidase
 PCR : for the conformation of diagnosis
 Serology: virus neutralization: ELISA
 Vaccine is available in the form of injection and
intranasal
 Modified-live (attenuated)
 intra nasal
 intra muscular
 Inactivated
 intra muscular

121
Q

What can be seen here?

A

IBRV - nasal discharge

122
Q

Bovine Herpesvirus-2 (BHV-2)
1. Alternative name?
2. How can BHV-2 be isolated?
3. How is this virus transmitted?
4. How can you diagnose a patient with BHV-2?

A
  1. (Pseudolumpy skin disease)
    Bovine Viral Mammillitis, Allerton virus )
  2. Isolated from cattle with generalized skin
    disease mammilitis and stomatitis
  3. Virus may be transmitted by biting flies
  4. Diagnosis: based on
  5. Clinical sings
    -Viral isolation in tissue culture
    -Serology in paired samples will
    demonstrate an increase in Abs
123
Q

What can be seen here?

A

BHV-2
Facial skin lesions
A: Mild alopecia with crust above
the left eye and one of he left ear
B: Severe alopecia of the dorsum
of ear bilaterally

124
Q

Malignant Catarrhal Fever Virus (MCFV) is a clinically dramatic and often _____ infection
of many species of ______ and ______ caused by
a member of the MCF virus (MCFV) group. Belongs to the genus _____ in the subfamily _________.
* Very high _____ rate (>95%)

A

lethal, Bovidae, Cervidae, Macavirus, Gammaherpesvirinae, mortality

125
Q

Malignant Catarrhal Fever is categorized by?

What happens if your patient is diagnosed with MCFV?

A
  1. Acute, high fever, catarrhal inflammation,
    corneal edema, enlarged nodes, skin
    lesions, +/- diarrhea
  2. Notifiable diseases to the OIE
126
Q

Malignant Catarrhal Fever exist in nature as in ______ infections as well as in _____ hosts

A

apparent, adapted

127
Q

What can be seen grossly in a patient suffering from Malignant Catarrhal Fever?

A

Severe inflammatory lesions of the muzzle, eye,
respiratory and digestive tract with swollen lymph
nodes and terminal encephalitis

128
Q

What is an important clinical sign of Malignant Catarrhal Fever?

A

Peripheral (centripetal) corneal opacity is an
important clinical sign suggestive of MCF in cattle

129
Q

What can be seen here?

A

MCFV
Bottom left = urinary bladder
Bottom right = tongue

130
Q

What can be seen here?

A

MCF Virus Transmission between Carrier and Clinically
Susceptible Hosts

131
Q
A

Number of ? each year

132
Q

CpHV-1 in goats
1. This viral disease can be isolated in which species? In which region(s) in the world?
2. What can be seen upon necropsy?
3. What may this disease cause?
4. CpHV-1 may cross react with which virus serologically? Explain why.
5. How does this disease present itself in adults?

A
  1. Isolated from young goats (1 week) dying in North
    America
  2. Enteric signs and necrosis and ulceration in the
    rumen, cecum, and colon
  3. It may cause abortion, vulvovaginitis, balanoposthitis
  4. It may cross react with BVH-1 serologically: they may have common ancestors
  5. Infection in adults, usually in-apparent, and genital
    disease may occur as vulvitis
133
Q

What can be seen in the images below?

A

CpHV-2 in captive sika deer
a- nasal discharges
b- oral vesicles on the muzzle and tongue
c- growth lesions on the kidney
d- growth lesions on the lung

134
Q

Canid Herpesvirus-1
1. This disease causes?
2. In cases of Canid Herpesvirus-1, patients that seem healthy often?
3. Canid Herpesvirus-1 maybe apart of?
4. Is there a vaccine available?
5. What should you consider if you diagnose a patient with Canid Herpesvirus-1?

A
  1. Neonatal deaths, abortion and mummification as
    well as fatal systemic infection in newborn pups. Induce genital lesions in male and female dogs
  2. Affected animals appear healthy but often
    present a history of infertility
  3. Could be a part of the canine respiratory disease
    complex (kennel cough syndrome)
  4. No vaccine is available
  5. Removal or separation of infected animals
    should be considered
135
Q

What can be seen here?

A

Canid Herpesvirus-1
Hemorrhagic infarcts of the
kidneys

136
Q
A

Acyclovir –> cream on eye or blisters OR injection

137
Q

Feline Herpesvirus-1 (Feline viral rhinotracheitis)
1. This virus causes?
2. Describe the behavior of a patient suffering from Feline Herpesvirus-1.
3. What is this disease associated with?
4. Describe the transmission route.
5. How often should a cat be vaccinated against Feline Herpesvirus-1? How long does immunity against this virus last?

A
  1. Cause feline viral rhinotracheitis (FVR) along
    with the upper respiratory disease
  2. The hunched-up appearance of a cat with its head on the floor. The third eyelid is prominent
  3. Associated with conjunctivitis, ulcerative
    keratitis, ulcerative stomatitis, abortions, and
    pneumonia
  4. Spreads by direct cat-to-cat contact through
    infectious discharges and aerosolized
    microdroplets
  5. Vaccination every 6-12 months is recommended. Protective immunity is relatively short.
138
Q

What can be seen here?

A

Feline Herpesvirus-1 (Feline viral rhinotracheitis)

139
Q

FeHV-1:Transmission, Pathogenesis and Clinical Signs
1. How is FeHV-1 shed?
2. How is FeHV-1 transmitted?
3. FeHV-1 results in?

A
  1. Virus is shed in discharges from the nose, eyes, throat
  2. Transmitted through direct/indirect contact
  3. Conjunctivitis and conjunctival edema, Possible dyspnea (open mouth breathing) as a result of
    blockage of nasal passages, Keratitis, Dendritic ulcers in the cornea with possible perforation (more common as a result of reactivation-
    see below)    , Stromal keratitis
    Vascularisation and hazy infiltrate at the leading edge of the vascularization, Intestinal loop flaccid and hemorrhage
140
Q
141
Q

Marek`s Disease Virus-MDV
is a ________ & _____ diseases of which species?
It is _____ contagious viral infection mainly affects _____.
It can also affect ?

A

Lymphoproliferative, neuropathic, chickens, highly, chickens, Pheasants, Quails, and Turkeys

142
Q

Name the serotypes of Marek’s Disease Virus (MDV).

A

There are three serotypes of the virus
 **Serotype 1: pathogenic and oncogenic strains
Strains of serotype 1 divided into
-Mildly virulent -Virulent -Very virulent
 **Serotype 2: avirulent and non-oncogenic strains
 **Serotype 3 (HVT): avirulent in turkey only (acts as vaccine strains - heterologous vaccine that can protect against one of the chicken viruses within the same family)

143
Q

How long does it take for clinical signs to manifest after the onset of infection?

A

Clinical signs from 6 – 16 weeks

144
Q

In cases of MDV, the majority of neoplastic changes occur in?

A

broiler chickens

145
Q

In cases of MDV, there is _______ (_______) infiltration in peripheral nerves and other organs.

A

Mononuclear, lymphoblasts

146
Q

MDV causes?
Clinical signs?

A

Lymphomas in gonads, hearth, lungs, seldom in BF, skin, muscles
 Ataxy, paralysis, macroscopic thickening of peripheral nerves

147
Q

Describe the clincal signs of MDV.

A

 Neurolymphomatosis – classical
MD, loss of coordination,
asymmetric paresis and paralysis
 Acute MD – expansive burst in
the flock, depression, ataxy,
paralysis in some animals.
Significant mortality without
neurologicchanges
 Lymphomatosis of the eye –
lymphoblastoid infiltration of
pupil, blindness
 Skin form – round, nodular
lesions in feather follicles

148
Q

Describe the pathogenesis of MDV

A
  1. Viral entry
  2. Viral replication
  3. B cell and T cell = cell death
    transformation and tumor of T cells
  4. Latency (most herpes virus induce latency and then spread)
  5. Replication and shedding rom hair follicle (this is one of the most important samples that you can collect, especially the shaft b/c filled with fluids).
149
Q

How is MDV transmitted?

A

**Transmission: highly contagious, concentrates in feather follicles and spreads by bird-to-bird contact, by contact with infected dust and dander

150
Q

MDV particles can survive for months in chicken-house dust and litter

151
Q

MDV not transmitted through the egg, chicks are born free of the disease

152
Q

The infectious virus matures in the epithelium of ______ ______ and
infects other birds by inhalation of infected dust or dander

A

feather follicles

153
Q

MDV: usually occur in the form of
- ______ form (classical form): _____ nerves mainly affected.

A

neural, sciatic

154
Q

Visceral form of MDV
-Visceral form is also observed
 **Enlargement of _______ nerves up to ____ times the normal size
 Birds are unable to _____, become paralysed (a typical leg-paralysis victim will have one leg extended _____ and one leg extended _____)
 ______ and ____ due to an inability to reach feed and water
 Wings or neck may be involved

A

peripheral, three, stand, forward, back, Starvation, death

155
Q
A

MDV
? position
On necropsy –> size of sciatic nerve is GIANT.

156
Q

**In the visceral form of MDV, where do tumors form?
When does infection form?
What are the side effects of the visceral form?

A

Tumors form in various internal organs usually occurs between 16-35 wks
Infection occur at very young age, but birds can die of
MDV near the onset of egg production
 Visceral form: signs are less specific and include:
-Depression Loss of appetite Loss of weight Anaemia
(pale combs)
-Dehydration (shrunken combs) Diarrhoea
-Tumours internal organs including bursa of Fabricius,
ovary, liver & lungs
-Death without any clinical signs being noticed
Clinical Sings and PM
Multiple lymphomas in the lung and heart

157
Q
A

Visceral form MDV

158
Q

**Cutaneous form of MDV

A
  • Cutaneous form: Proliferating lymphocytes deposited in
    skin producing nodular type lesion
  • Ulcers in the feather follicles
159
Q

**Ocular form MDV

A

Iris may be involved and associated with blindness
-Left: normal eye (sharply defined pupil and well pigmented iris)
-Right: MDV infected: discoloured iris and very irregular pupil as
a result of mononuclear infiltration

160
Q
A
  • Perivascular cuffing in the brain
161
Q

How do you diagnose MDV?

A

 **Proper sampling (Feather follicle)
 Detection of viral antigens
 FAT of tissues or smears
 Electron microscopic examination of species
 Detection of viral : PCR
 Detection of viral antibodies using ELISA, virus neutralization etc.
 Four fold increase in antibody titer – seroconversion
 Virus isolation – Herpesviruses can be grown in embryonated eggs or in cell
cultures derived form their natural host
 Gross and histopathology
-Intra-nuclear inclusion bodies
-Syncytia (giant cell formation)

162
Q

In cases of MDV, Vaccinate all chicks at ____ ____ old; keep chicks from exposure until
immunity has developed, about seven days
 An avirulent turkey herpesvirus – ______ vaccine: HVT may be used
as a vaccine: antigenic relationship
 An attenuated serotype-1 vaccine is also available

A

one day, heterologous

163
Q

In cases of MDV, the preferred vaccine is the ______ ______ _____
VACCINE because the virus infects birds productively, yielding a high antigenic dose.

A

avirulent TURKEY HERPESVIRUS

164
Q

 1. Herpesvirus of turkeys- heterotypic lyophilized cell-free preparation
 2. Cell-associated vaccine using Gallid Herpesvirus-3 (does not interfere
with maternal ab)
 3. live-attenuated Marek’s disease virus - Gallid Herpesvirus 2 – interferes
with Mab

165
Q

How do you control MDV?

A

 Production of chicken on (all-in-all-out) principle is highly recommended
 General sanitation and hygiene measures

166
Q

Differences between Marek’s Virus and Avian Leukosis

167
Q

Infectious Larygotracheitis Virus
–ILTV is an ____, ____ contagious disease of ____

A

acute, highly, chickens

168
Q

What does ILTV cause?

A

Severe dyspnea, coughing and rales

169
Q

When was ILTV detected in the USA?

170
Q

Where in the world can ILTV be found?

171
Q

Name the hosts of ILTV

A

Chickens, pheasants

172
Q

What is the etiologic agent of ILTV?

A

Etiologic agent – gallid herpesvirus 1, one serotype
although strains of virus differ significantly in virulence

173
Q

How is ILTV transmitted?

A

Introduced into a flock by carrier birds. Mostly via inhalation – occasionally via ingestion

174
Q

Describe the pathogenesis of ILTV

A

Pathogenesis – severe laryngotracheitis characterized by necrosis, hemorrhage, ulceration and the formation of diphtheritic membranes

175
Q

In cases of ILTV,
Diphtheritic membrane – may form a tube the length of trachea – _____ air flow –> death by _________.

A

occluding, asphyxiation

176
Q

How do ILTV die?

A

Death occurs from asphyxiation

177
Q
178
Q

What are the clinical features of ILTV

A

Marked respiratory disease – extension
and slinging of the neck during
inspiration
 Head pressing, resting on breast during
exhalation, coughing, rattling
 **Birds may cough up blood mucus that
stains walls and posts (expectoration of
mucous tinged blood)
 **Morbidity – 100%, mortality 20-70% -
depending on virulence of the strain

179
Q

**When do clinical signs develop in a patient with ILTV?

A

2-8 days.
Most common in chickens 4-18 months.

180
Q
A

Necropsy: hemorrhagic mucosa, diptheric membrane

181
Q
A

ILTV
Cheesy like material
This is why animals are asphyxiated.

182
Q

L- normal) (C- hyperemic) (R - fibrin)

183
Q

How do you diagnose patients with ILTV?

A
  • History, Clinical Signs, PM lesions
  • Proper sampling
  • FAT staining of smears and tissues
  • Virus isolation – nasal mucosa
    -Chorioallantoic membrane of ECE
    stunted embryos which die 2-12 days PI
    -GHV-1 grows well in various cultures
  • Serology – detection of neutralizing antibody using pock or plaque reduction
    assays
  • PCR
184
Q

How do you control ILTV?

A
  • Vaccines
    -Live attenuated ILTV vaccines (cell culture or ECE origin)
    -Viral vector recombinant vaccines
  • Administration of vaccines; eye drops, spray, or through drinking water
185
Q
A

ILTV produces intranuclear inclusion bodies

186
Q

Duck viral Enteritis (DVE)
(Anatid Herpesvirus-1) affects which species? Of what age range?

A

Severe disease of both wild and domestic waterfowl
induced by Anatid alphaherpesvirus 1

187
Q

Duck viral Enteritis (DVE)
(Anatid Herpesvirus-1)
* Anorexia, listlessness, nasal discharge, ruffled dull
feathers, adherent eyelids, ______, extreme thirst, ataxia leading to recumbency with outstretched
wings and with head extended forward, tremors, watery diarrhea, and soiled vents
* Multifocal _____ in the intestinal mucosa
* Enlarged mottles ____
* Mottled thymus with petechial _____
* Inflammation and hemorrhage of the proventriculus and gizzards
* Hemorrhagic intestine: _____ _____
* Diffuse petechial hemorrhage in liver
* isolation: 1-day-old Muscovy or white Peking ducks, inoculation of CAM of 9-14 day-old embryonating duck eggs
* Confirmation: herpesvirus inclusion bodies in tissues
* Contact between susceptible captive waterfowl with
wild, free-flying waterfowl should be avoided

A

photophobia, ulceration, spleen, hemorrhage, annular band

188
Q
A

Animal experiences photophobia
Multifocal ulcertaion in ? Why mucosa is hemorrhagic.
Annular band = when open carcass, see this. Intestine seems to be intact but then open and see band.

189
Q

Psittacid Herpesvirus-1
(Pacheco’s Disease Virus)
is an acute, contagious and lethal in psittacine birds.

190
Q

Psittacid Herpesvirus-1 effects which species?

A

macaws, amazon parrots, monk, parakeets, and conures
* Old world parrots (Africa/Asia/Europe) - resistant to disease and carrier state

191
Q

What are the main sources of contraction for Psittacid Herpesvirus-1?

A

through the faeces, oral and pharyngeal secretions of carrier birds where the virus has shed

192
Q

Psittacid Herpesvirus-1 causes ?

A

splenic and liver necrosis with typical intranuclear
herpesvirus inclusions

193
Q

What treatment is available for Psittacid Herpesvirus-1?

A

There is no effective vaccine that completely cures
Pacheco’s disease in infected birds

194
Q
A

Blue-fronted Amazon
parrot: susceptible and
transmit the diseases

195
Q
A

**Psittacid Herpesvirus 1
Hepatomegaly, splenomegaly, petechial hemorrhages in pericardium can be found

196
Q

Inclusion body disease of falcons (IBDF)

  • The virus is pathogenic for American kestrels
    (Falco sparverius) and great horned owls (Bubo virginianus) in which typical lesions of IBDF are
    reproduced.
  • Caused by a Herpesvirus (Falconid HV-1)
  • The clinical course is short, 24 to 72 hours in duration, and is characterized by mild to severe depression and weakness often accompanied by
    anorexia.
  • The disease is invariably fatal.
  • The virus has a marked affinity for the
    __________ system and __________,
    producing focal to diffuse necrosis of infected
    tissues accompanied by the formation of
    ?
A

reticuloendothelial, hepatocytes, intranuclear inclusion bodies

197
Q
A

Inclusion body disease of falcons (IBDF)
Inclusion bodies

198
Q

Elephant Endotheliotropic Herpesviruses (EEHVs)
* Elephant endotheliotropic herpesviruses 1A and
1B - cause ~20% mortality in newborn
* Asian elephants: vague signs like lethargy and
inappetence – death in 24h
* Massive and generalized hemorrhages
(hemorrhagic diathesis) due to replication in
_____________ __________.
* Intermittent shedding observed in elephant
trunk washes

A

vascular endothelium

199
Q
A

Lesions on trunk of elephant in bottom right.
Intranuclear inclusion bodies

200
Q

Channel Catfish Virus Disease (CCVD)
CCVD infection resulted in the presence of ______ inclusions and extensive _______ formation.

-The _______ (popeye) is accompanied by hemorrhaging of
the ____ and ventral _____.
-Swelling of abdominal cavity contains fluid contaminants.
-Dark and enlarged spleen.
-Pale and enlarged kidney.
-Large numbers of fish aggregate around the edges of hatching
troughs or pools, remaining motionless in a head-up, tail-down
position.

A

intranuclear, syncytium, exophthalmos, fins, abdomen

201
Q

What is the first sign of CCVD?

A

-Reduced feeding activity most likely the first sign and in high
mortality for fry and juvenile with severe infection.

202
Q
A

Channel Catfish Virus Disease (CCVD)
Intranuclear inclusion bodies in center picture
Distended abdomen

203
Q

Family Alloherpesviridae affects which species?
Morphologically similar to other _______, distinct genome sequences.
High level of host ______, modulates host ______, long-term _____, epiteliotrophic.

Makes salmon?

A

Salmon, Herpesviruses, specificity, defenses, latency

lethargic

204
Q
A

Look at eyes and gills during examination.
Eyes = clear
Gills = rose in color

205
Q
A

Eye is protruding/bulging out.

206
Q

2- Family: Parvoviridae-General properties
 Parvoviridae includes the _____ known DNA viruses

207
Q

 Parvoviruses : small (___-___nm), non_______, _______ viruses that
contains a _____ _____-stranded DNA genome

A

18-28, enveloped, icosahedral, linear, single

208
Q
  • VirusFive genera (Parvovirus, Dependovirus, Amdovirus, and Bocavirus)
209
Q
  • Virions: icosahedral, 25 nm in diameter composed of 60 protein subunits
210
Q
  • Genome: ss-DNA virus (4-6kb) in size
211
Q
  • Virus replication: nucleus causing ?
212
Q
  • stable at pH (3-9) and resist 60C for 60 min
213
Q
  • Virus hemagglutinates some RBCs
214
Q
A

Icosahedral symmetry
EM picture of virus on far right. Machine gives you diameter of virus = 18-28 nm.

215
Q

Parvovirus genome structure and organization
* Terminal ______ sequence
-enable ends to make hairpin
-facilitate packaging of virions
* __’ capped and ___’ polyadenylated
* VP-__ and VP-__ produced in large amounts
* Nonstructure protein? _____
facilitates
-binding to DNA
-serve as helicase
-serve as endonuclease
-interfere with cellular DNA
replication__

A

palindromic, 5, 3, 1, 2 , NSP1

216
Q

Replication of Parvovirus
 Attachment and entry
 _______ of viral DNA into nucleus
 Transcription and translation
of viral nonstructural protein
and nucleocapsid
 DNA replication
 Virus assembly (____)
 Release from the cell through _____

A

Translocation, nucleus, lysis

217
Q

Replication of Parvovirus

218
Q

Classification of the family Parvoviridae

219
Q

Which viruses belong to the genus Protoparvovirus ?

A

-Feline Panleukopenia virus
-Mink enteritis virus
-Canine parvovirus-2
-Porcine Parvovirus
-Parvovris of rodents
-Rabbit Lapine parvovirus

220
Q

Which viruses belong to the genus Amdoparvovirus ?

A

Aleutian mink disease virus

221
Q

Which viruses belong to the genus Aveparvovirus ?

A

-Chicken and turkey parvovirus

222
Q

Which viruses belong to the genus Bocaparvovirus ?

A

-Bovine parvovirus
-**Canine minute virus (Canine parvovirus-1)
Canine Bocavirus-1

223
Q

Which viruses belong to the genus Dependovirus ?

A

Goose Parvovirus
-Duck Parvovirus

224
Q

Which viruses belong to the genus Erythroparvovirus ?

A

Parvovirus of nonhuman primates

225
Q

Feline Panleukopenia Virus (Feline Distemper virus) is a Highly contagious viral disease of cats: sudden onset, fever, in appetence
(loss of _____), dehydration, depression, vomiting, decreased numbers of
circulating white blood cells (______), and often a high mortality rate

A

appetite, leukopenia

226
Q

Feline Distemper causes ?

A

Intrauterine (within the uterus) infection: abortions, stillbirths, early
neonatal deaths, and cerebellar hypoplasia (underdevelopment of the
cerebellum)

227
Q

Which species are most susceptible to FDV?

A

All members of the cat family (Felidae) are susceptiblle

228
Q
A

Feline Distemper Virus
Cat vomiting

229
Q

How is FPV transmitted?

A

direct contact with infected
cats or their excretions

230
Q

Describe the early stages of FPV

A

The early stages of the infection, virus is
shed in feces, urine, saliva, and vomitus

231
Q

FPV results in?

A

 Flaccid small intestine with hemorrhage
and mucosal sloughing
 Villi are blunted and fused
 Cerebellar atrophy and hydrocephalus

232
Q
A

Feline panleukopenia virus

233
Q
A

FPV
Hemorrhage in right picture.
Black tar in intestine –>

234
Q

Diagnosis and treatment of Feline Panleukopenia Virus

A

Hematology: CBC: sharp decrease in the WBCs count
* Fecal ELISA test: for the detection of parvovirus
* Serology is not recommended due to the non discrimination
between the infected and vaccinated animals (None DIVA)
* Intensive car of the infected cats

235
Q

Canine Parvovirus (CPV)
It is infectious disease of dogs worldwide, caused by Parvo’ is a highly contagious disease characterized by ______ that is often _____.
 CPV: can survive for long periods (over 1 year) in
the environment
Prior to 1980, the most canine parvovirus-caused
disease was Type __ (CPV-2)
* After 1980, CPV-2 was replaced by CPV-__ became more common, and in 1986, another variation called CPV-__ appeared
* Today, CPV-___ has largely replaced the previous strains as the most common parvovirus-causing
disease in the dog
* In the past few years, a new strain, CPV-__, has
been detected.

A

diarrhea, bloody, 2, 2a, 2b, 2b, 2c

236
Q

CPV- Clinical signs, host range and transmission

Host range of CPV
 Dogs, especially less than ____ weeks
of age. But, can also occur in _____ or _______ vaccinated ____ dogs.

Mode of transmission of CPV
____-____ route and virus that persists
on fomites.
Virus is shed for a ___ ____ before the
onset of clinical signs

A

12, unvaccinated, improperly, adult, Fecal-oral, few, days

237
Q
A

Canine parvovirus

238
Q

Describe the life cycle of canine parvovirus

239
Q

Describe the pathogenesis of CPV

240
Q

Canine Parvovirus (CPV)
 Highly contagious virus of dogs
affect intestines and causes
sloughing of the inner layers of the
intestine
 “Intestinal form”: –>
 “Cardiac form”: very ___ pups
(less than __ wks of age) affect the
heart ____, often resulting in ____ death

A

vomiting and diarrhea, young, 8, muscle, sudden

241
Q
A

CPV
Severe hemorrhagic
diarrhea in dogs

242
Q
A

CPV
Pale streaking of the myocardium

243
Q
  • Tropism for intestinal epithelium
    leads to the collapse of intestinal
    villi, epithelial necrosis, and
    hemorrhagic diarrhea—clinical signs
    of gastroenteritis
    Depletion of lymphocytes and
    compromised gastrointestinal system
    may lead to bacteremia by normal
    gut flora, i.e. Escherichia coli, which
    can be
    fatal
244
Q
A

**A: Normal intestinal villus showing cellular
differentiation
**B: CPV infected villus showing collapse and necrosis of the intestinal villi

**Villi responsible for absorption of food –> animal will not benefit from food that is ingested.

245
Q

CPV infection risk associated factors
The severity of clinical signs
depends on:
* Virus strain
* Host immunity, is affected by
stressors such as weaning and
overcrowding, maternal
antibody, and the presence of
concurrent infections such as
other enteric viral and parasitic
infections

246
Q

CPV
***Mechanism of Death

A
  1. Diarrhea and vomiting, extreme
    dehydration: SHOCK
  2. Loss of intestinal barrier:
    bacterial invasion: SEPTIC SHOCK
247
Q
A

CPV, replicate and destroy crypt epithelial cells

249
Q

Some necropsy and histopathology findings - CPV

A
  • Small intestine of dog died suddenly of enteritis
  • Note: discoloration of intestinal wall and fibrin on the
    serous surface
  • Pathology of small intestine of dog died due to CPV
    infection showing
    -Villi collapse
    -Crypt lamina are dilated and filled with
    necrotic debris
252
Q

How do you diagnose CPV?
Clinical signs and symptoms: the sudden onset of foul-smelling, bloody diarrhea in a
young dog (under 2 years of age) is often considered indicative of CPV infection
**Laboratory tests
**CBC (leukopenia, neutropenia, and lymphopenia)
Abnormal coagulation test
Cardiac troponin I is a plasma marker for myocardial
damage.
Biochemical tests (often shows hypoproteinemia, hypoalbuminemia, and hypoglycemia)
***Virus detection
Fecal ELISA antigen tests(specific but less sensitive)
PCR methods.
Antibody Detection
Serology is not the best method to diagnose CPV infection because most dogs are
vaccinated against it or have been previously exposed to the virus

253
Q

Name the biomarkers of Canine Parvovirus

254
Q

Diagnosis & control of Parvoviruses

A

 Clinical Signs and PM
 Laboratory diagnosis
-Fecal enzyme immunoassays
-HA test (pig, cat, monkey) RBCs
-Detection of virus by EM
-PCR: amplification of viral DNA
-Serology: ELISA
Control: various types of vaccines are
commercially available

255
Q

Prevention of CPV - Vaccines
Both attenuated live and inactivated CPV vaccines are available
**Attenuated live vaccines: should never be administered to pregnant bitches
because they may cause disease in the developing fetus
**Monovalent CPV vaccines: administered by the intranasal route and
commercially available
The age at which a pup should be vaccinated successfully can be predicted
through the determination of the MDA titters by serologic tests
Pups from a bitch with a low protective titer of antibody to CPV can be
successfully immunized by six weeks of age, but in pups from a bitch with a
very high titer to CPV, MDA may persist much longer
Pups of unknown immune status can be vaccinated with a high-titer-attenuated
live CPV vaccine at 6, 9, and 12 weeks of age
Prevention of CPV-Vaccines

256
Q

Porcine parvovirus (PPV)
* The virus is lymphotropic and live/persists in B
and T cells for a long time
* If the infection occurs in the first month of
pregnancy, the fetal pigs will die and be ______
* From day 30-70 of the pregnancy- fetal pigs _____ and are ______
* After 70 days, the growing pigs may be able to
fight off the infection
* SMEDI =

A

absorbed, die, mummified
Stillbirth
Mummification
Embryonic death
Infertility

257
Q
258
Q

Differential diagnosis of Porcine Parvovirus (PPV) infection
*Aujeszky’s disease
*Leptospirosis
*Foot-and-mouth disease
*Classical swine fever
*Japanese encephalitis
*Porcine brucellosis
*Porcine reproductive and respiratory syndrome (PRRSV)
*Porcine enterovirus infection
*Vesicular stomatitis

259
Q

Aleutian mink disease virus (AMDV)
* Aleutian disease (AD) is known to produce clinical
signs in mink and ferrets only
* In adult mink, AD is a persistent, slowly progressive
AMDV infection in which a dysregulated immune
system
* a postinfectious antibody response cause an immune
complex–mediated vasculitis
* Perivascular and glomerular immune complexes
causing membranoproliferative glomerulonephritis
* Mononuclear cells may surround the vessel, and
connective tissue proliferation and necrosis in the
tunica elastica media narrow the lumen
* Serum protein electrophoretic patterns
* The serum of infected animals shows a polyclonal _______: the gamma globulin accounts for
62.4% of serum proteins
* The normal level is 14.3%

A

gammopathy

260
Q

Equine parvovirus, named equine parvovirus hepatitis (EqPV-H)- & _______ Disease
* EqPV-H is hepatotropic and pathogenic but the great majority of recently infected horses (within 4-12 weeks) have non-clinical hepatitis with 2 or more weeks of elevated serum liver enzymes
* Two modes of transmission are recognized in horses:
* **Biologic transmission: occurs through the administration of biologic
products containing _______. To date, EqPV-H has been identified in
tetanus antitoxin (TAT), botulinum antitoxin, Streptococcus equi antiserum,
pregnant mare’s serum, allogenic stem cell preparations and equine plasma
products. Cases generally present 4-13 weeks after receiving equine
biologic products
**Non-biologic transmission occurs _______ in horses with no history of
receiving biologic products.
**Clinical forms:
* Asymptomatic infection: Most horses infected with EqPV-H remain
asymptomatic.
Clinical hepatitis: It is estimated that approximately 2% of infected horses
will develop clinical liver disease, ranging from mild illness to acute
fulminant liver failure

A

Theiler’s, EqPV-H, sporadically

Virology (17 decks)

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