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HerpesVirus Flashcards

1
Q

genome of herpes virus

A

double stranded DNA

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2
Q

herpes virus envelop?

A

yes, 10-12 structural protein in it

(can be deleted (marker))

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3
Q

3 family herpes viruse

A
  • Ortoherpesviridae
  • Alloherpesviridae
  • Malacoherpesviridae
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4
Q

Ortoherpesviridae sub family names

A
  • Alphaherpesvirinae
  • Betaherpesvirinae
  • Gammaherpesvirinae
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5
Q

Alloherpesviridae family infects which animals?

A

fish & frog

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6
Q

Malacoherpesviridae family infects which animals?

A

oyster

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7
Q
A
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8
Q

how long in the environment does Herpes virus survive for

A

few days to few weeks in excretions

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9
Q

which Herpes virus disease is eurixen

A
  • aujesky’s
  • malignant catarrhal fever
  • turkey herpes
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10
Q

Which Herpes virus is zoonotic

A

Monkey herpes B

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11
Q

viral latency

A

virus dormant in host cell, no rep, host is seronegatif for virus

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12
Q

persistent infection

A

virus is persisting in host cells, replication & production, anti-viral antibodies can be detected in host

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13
Q

how long can herpes virus infect the host

A

can be prolonged infection, life long

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14
Q

Herpes virus antigenicity

A
  • weak antigens
  • vaccine protection only for few months
  • cross reactions within genera

(rarely cross protection)

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15
Q

Herpes virus detection of infection

A

PCR, Isolation, antigen detection methods

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16
Q

Infectious Bovine Rhinotracheitis (IBR) causative agent

A

BHV1

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17
Q

BHV1 causes

A

IBR
IPV
IBP
abortion

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18
Q

BHV5 is found where

A

nervous tissue

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19
Q

What are the clinical signs of BoAHV in other ruminants like sheep, goat & wild ruminants

A

inapparent infection

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20
Q

introduction of Infectious Bovine Rhinotracheitis (IBR) in herd

A

intro of infected animal, or by semen

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21
Q

Infectious Bovine Rhinotracheitis (IBR) pathogenesis

A

PO, venereal
viraemia
multp in resp epithelial cells
inflammation

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22
Q

Infectious Bovine Rhinotracheitis (IBR) pathogenesis in calf

A

after viraemia OR ascending from nose along nerves: encephalitis

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23
Q

Infectious Bovine Rhinotracheitis (IBR) Pathogenesis in susceptible cattle

A

viraemia - resorption of foetus, abortion

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24
Q

Infectious Bovine Rhinotracheitis (IBR) Pathogenesis of the genital form

A

viraemia- vesicles on the mucosal membranes, inflammation, crusts, nodules

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25
Q

how long can the shedding last in Infectious Bovine Rhinotracheitis (IBR)

A

Long-term/life long

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26
Q

Where can we find the virus in cows that have been infected by Infectious Bovine Rhinotracheitis (IBR)

A

Latency in nervous tissue (reactivation)

Herpes virus BoAHV5

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27
Q

Can symptoms be different for animals?

A

yes, depends on age, amount of inoculum, pathogenicity, route of infection, immune status

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28
Q

Infectious Bovine Rhinotracheitis (IBR) clinical symptoms of respiratory form

Incubation period?

A

1-6months: fever, resp sympt, occasional diarrhoea
6months < : red nose disease, nasal discharge, conjunctivitis,decreased milk prod

Incubation: 2-5 days

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29
Q

what age does clinical symptoms appear in colostrum protected calves in Infectious Bovine Rhinotracheitis (IBR) Pathogenesis

A

from 6-8 weeks of age

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30
Q

what age does clinical symptoms appear in colostrum non-protected calves in Infectious Bovine Rhinotracheitis (IBR) Pathogenesis

A

1-2 weeks (+liver damage)

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31
Q

At what age do cows suffer from encephalitis in Infectious Bovine Rhinotracheitis (IBR) Pathogenesis

A

under 5 months

uncommon

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32
Q

Infectious Bovine Rhinotracheitis (IBR) clinical symptoms of encephalitis

A
  • Conjunctivitis, nasal discharge
  • lameness, tremor, opisthotonus

death after 5-7 days

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33
Q

When can abortion be seen in case of Infectious Bovine Rhinotracheitis (IBR)

A
  • acute phase of infection or few weeks later (with or after resp signs)
  • all phases of pregnancy
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34
Q
A
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35
Q

Infectious Bovine Rhinotracheitis (IBR)

What is IPV?

A

Infectious pustular vulvovaginitis

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36
Q

IPV clinical signs?

A

initially oedema of vulva and vagina (then pustules, that coalesce)
Mucosal membrane covered by yellowish white membrane
Painful: frequent urination & tail flapping

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37
Q

T/F

Abortion can be a clinical sign of Infectious pustular vulvovaginitis (IPV)

A

False

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38
Q

How long does it take for Infectious pustular vulvovaginitis (IPV) to heal

A

10-14 days

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39
Q

What is IBP?

A

Infectious pustular balanoposthitis (IBP)

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40
Q

Infectious pustular balanoposthitis (IBP) clinical symptom

A

Oedema of prepuce
painful: loss of libido

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41
Q

What can be observed during the histological examination of suspected Infectious Bovine Rhinotracheitis (IBR)

A

Acidophilic nuclear inclusion bodies:
- tracheitis
- multifocal necrosis in foetal organs
- lymphohistiocytic encephalitis

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42
Q

Infectious Bovine Rhinotracheitis (IBR) vaccines for control of epidemics :

A

live vaccines

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43
Q

Infectious Bovine Rhinotracheitis (IBR) vaccines for breeding animals

A

inactivated vaccines

(safer for the foetus)

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44
Q

calf immunisation from Infectious Bovine Rhinotracheitis (IBR)

A

at 4-6 months 2x in 2-3 wks, repeat every 6 months

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45
Q

Beef cattle vaccine immunisation from Infectious Bovine Rhinotracheitis (IBR)

A

2x in 2-3 wks, repeat every 6 months

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46
Q

How to raise a Infectious Bovine Rhinotracheitis (IBR) free generation

A
  • Immunisation of the whole herd
  • Separation of the suckling calves after 3 days of age (after consuming colostrum), isolated raising
  • Monitoring every 6 moths (ELISA ): free status if the herd negative in two consecutive tests

(time consuming)

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47
Q

What is the selection method to eradicate Infectious Bovine Rhinotracheitis (IBR) of a herd

A
  • Seropositivity below 10 %: removal of positive animals
  • Seropositivity above 10 %: selection by using marker vaccines
  1. Immunisation of the whole herd wit marker vaccine
  2. Repeating every 6 months: reduce the amount and frequency of virus shedding
  3. Repeated discriminative ELISA: gE positive animals are removed
  4. After 3-4 years the rate of infection below 10%: all positive animals removed
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48
Q

What is Bovine herpesmamillitis?

A

Oedema, pustules and erosions on the skin of the teats and the udder

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49
Q

Bovine herpesmamillitis causative agents

A

Bovid alfaherpesvirus 2 (BoAHV2, BHV2)

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50
Q

how is Bovine herpesmamillitis spread?

A
  • Spread by milking in herd (hand/machine), arthropods (mechanical vectors): more common in late summer and early fall
  • The virus can invade only through skin lesions; imunosuppression contributes to the disease
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51
Q

Bovine herpesmamillitis Pathogenesis?

A

Skin lesion contact infection: local multiplication → viremia → pustules (udder mainly) → inflammation, oedema → erosions → crusts

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52
Q

Bovine herpesmamillitis incubation time

A

3-7 days

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53
Q

clinical signs of Bovine herpesmamillitis in heifers

A

oedema, red discoloration, pustules, erosions, crusts

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54
Q

clinical signs of Bovine herpesmamillitis in suckling calves

A

pustules on mouth, oral cavity, face, ears

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55
Q

is Bovine herpesmamillitis economically important

A

decrease in milk production, blood in milk (confiscates), teats scab: difficulty in milking

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56
Q

Bovine herpesmamillitis differential diagnosis

A
  • Disease with pustules: FMD, vesicular stomatitis
  • Pox viruses (cowpox, pseudocowpox, papillomatosis, Lumpy skin disease): proliferative alterations (lump)
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57
Q

Description of Malignant catarrhal fever

A

Acute, usually lethal, febrile illness with general sings, kerato-conjunctivitis, encephalitis, haemorrhagic pneumonia, and enteritis mainly in cattle

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58
Q

Malignant catarrhal fever occurrence

A

worldwide

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59
Q

Malignant catarrhal fever causative agents

A

Ovid gammaherpesvirus 2 (OvGHV2, OHV2),
Alcelaphid gammaherpesvirus 1 (AlGHV1)

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60
Q

Difference between AlGHV1 and OvGHV2?

A

AlGHV1can be propagated in cell culture, OvGHV2 can not

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61
Q

AlGHV1 affects which animals?

A

Wild animals asymptomatic, only cattle is affected

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62
Q

OvGHV2 affects which animals?

A

sheep inapparent
affects: cattle, bison, deer, goat, swine, rarely buffalo

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63
Q

CpGHV2 affects which animals?

A

rarely affected: buffalo, deer, swine

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64
Q

What is the sheep associated MCF?

A
  • Sheep (and other ruminants) are asymptomatic carriers
  • Virus shedding of sheep is most intensive in 6-9 months of age, later low amount of virus shedding and only intermittent
  • Cattle get infected after prolonged (few months) contact with sheep
  • Cattle are not able to spread the virus

Outside of africa

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65
Q

MCF?

At which age are the animals more sensitive?

A

Elderly animals

(young animals can survive)

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66
Q

how can MCF appear in a herd?

A

only sporadic cases in a herd

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67
Q

Malignant catarrhal fever Pathogenesis

A
  • Not known in several aspects
  • Contribution of other latent virus infection in cattle?
  • Aerogene → cell-associated viraemia
  • Immunopathological process is responsible for the lesions: CD8+ lymphocytes-associated severe vasculitis and tissue necrosis
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68
Q

Malignant catarrhal fever incubation period

A

2 weeks to several months

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69
Q

Malignant catarrhal fever peracute CS

A

fever
inappetence
salivation
bloody diarrhea
tremor

(death within 1-2dys)

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70
Q

Acute Malignant catarrhal fever CS

A
  • Bilateral keratoconjunctivitis (beginning at the periphery)
  • Nasal discharge (containing necrotic tissue)
  • Salivation, bad breath
  • Loose of hoofs and horns
  • Bloody urine
  • Depression then excitement → convulsions → paralysis → death

lesions often only on the head

50% can survive: healing, or chronic disease

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71
Q

chronic Malignant catarrhal fever CS

A
  • fever
  • erosions in nasal and oral mucosal membranes (nasal discharge containing necrotic tissue)
  • bilateral uveitis
  • skin: hyperkeratosis, papular dermatitis

for weeks, CS can disappear then return : death

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72
Q

Malignant catarrhal fever dead animal pathology of peracute disease

A
  • Respiratory tract, intestines: reddened mucosal membranes, acute haemorrhages * Liver, kidney enlarged
  • Urinary bladder: oedema, reddened mucosal membranes, acute haemorrhages
  • Enlarged lymph nodes, and lymphoid follicles
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73
Q

Malignant catarrhal fever dead animal pathology of acute disease

A
  • Keratoconjunctivitis
  • Respiratory tract, intestines: reddened mucosal membranes, acute haemorrhages, erosions covered by fibrin
  • Enlarged lymph nodes, and lymphoid follicles
  • Small blood vessels: lymphocytic inflammation, fibrinoid necrosis, tissue necrosis
  • Lymphocytic encephalitis
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74
Q

Malignant catarrhal fever DD

A

IBR, BVD-MD, bluetongue virus, FMD, Rinderpest

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75
Q

Malignant catarrhal fever prevention

A

isolations from inapparent carriers (sheep)

Vaccine does not existe

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76
Q

Aujeszky’s disease description

A

Swine disease with febrile, general signs, abortion, respiratory and central nervous system signs. In other susceptible species manifests as severe, acute and lethal encephalitis.

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77
Q

Who found the Aujeszky’s disease vaccine

A

Bartha 1961: attenuated vaccine strain (K/61)

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78
Q

Aujeszky’s disease causative agents

A

Suis alfaherpesvirus 1 (SuAHV1)

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79
Q

Suis alphaherpesvirus is antigenically similar to which other virus

A

BoAHV1

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80
Q

SuAHV1 natural hosts and consequences

A

Swine & Wild Boars (carriers, can infect hunting dogs!)

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81
Q

for how long does a swine shedd the SuAHV1 virus for?

A

large amount in every excretions for 2-3 weeks after infection

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82
Q

Can SuAHV1 cross the placenta?

A

yes

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83
Q

how long does a swine carry SuAHV1 for?

A

life long

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84
Q

how can Aujeszky’s disease virus be reactivated?

A

Stress, pregnancy-lactation

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85
Q

can Aujeszky’s disease be detected in other animals than swine?

A

yes, dog, cat, cattle,etc
(limited viraemia and virus shedding : dead end for virus)

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86
Q

after how many days is the SuAH virus 1 inactivated in frozen meat?

A

40

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87
Q

Can SuAHV1 infect people

A

no, but there has been sporadic cases

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88
Q

Aujeszky’s disease pathogenesis in swine

A
  • Primer multiplication in the infection site: nasal and pharyngeal cavity, tonsils
  • Viraemia, spreading to the brain along the nerves as well
  • Secondary viral multiplication in large amount in organs * Adults: fever, respiratory symptoms
  • Suckling: encephalitis, mass-mortality
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89
Q

can piglets be protected from Aujeszky’s disease?

A

yes, from convalescent or vaccinated sows by colostrum until 8-14 wks

(they can contract inapparent infection during that time)

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90
Q

Aujeszky’s disease pathogenesis in other species than swine

A

Direct access to the brain from the oral mucosa along the nerves (limited viraemia, and virus shedding): Encephalomyelitis, death

* Except lambs: they can excrete the virus in large amount

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91
Q

Aujeszky’s disease clinical symptoms in swine in new born?

A

sudden death

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92
Q

Aujeszky’s disease incubation period in swine

A

1-8 days

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93
Q

Aujeszky’s disease clinical symptoms in swine in suckling?

A

Fever, vesicles, tremor, swallowing disorders, ataxia, convuslion

100% mortality

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94
Q

Aujeszky’s disease clinical symptoms in swine in 3-6 weeks old pigs?

A

Neuro pb (4-5dys)
50% mortality

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95
Q

Aujeszky’s disease clinical symptoms in swine in growing pigs

A

inappetence, fever, nasal discharge, sneezing, trembling nasal & facial muscles
healing after 5-7 days residual sympt: head shaling & tremor on head

5% mortality

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96
Q

how long does it take a growing pig to heal from Aujeszky’s disease

A

5-7 days

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97
Q

Aujeszky’s disease clinical symptoms in swine in adults

A

often none, mild resp
pregnant sows:
* Repeated breading, abortion, mummification, stillbirth, weak new-borns
* Necrotic placentitis, endometritis

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98
Q

Aujeszky’s disease clinincal symptoms in cattle, sheep & goat?

A

fever, inappetence, reduced milk prod
convulsion, sitting, laying, pharyngeal paralysis, meteorism

death withon 1-2 days

99
Q

Aujeszky’s disease incubation time in cattle, sheep & goat

100
Q

Aujeszky’s disease clinincal signs in carnivores

A

dep then excitement, itching, salivation, convulsions, paralysis & death

101
Q

Aujeszky’s disease diagnosis from live swine

A

PCR, isolation from secretions
serology:
*gE blocking ELISA in pigs vaccinated with gE deleted vaccine: positive in case of wild virus infection
*gB competitive ELISA detects both vaccine and wild virus strains: for controlling free status

102
Q

Patho of Aujeszky’s disease in suckling

A

multiple necrotic foci in tonsils, liver, spleen

103
Q

Aujeszky’s disease patho in adult

A

lung oedema

104
Q

Aujeszky’s disease patho in aborted foetus

A

multiple necrotic foci in organs, splenomegaly

105
Q

histopath findings in Aujeszky’s disease

A
  • Multifocal acute necrosis associated with acidophilic intranuclear inclusion
    bodies
  • Lymphohistiocytic meningoencephalitis
  • Interstit. pneumonia
106
Q

DD of Aujeszky’s disease in other species than swine

A

disease presenting neuro symptoms: rabies, CSF, Teschen disease

107
Q

Aujeszky’s disease prevention

A

not feed raw pork
vaccination (attenuated/inactivated)

108
Q

Aujeszky’s disease vaccine protections

A

after 7-10 days until 3-4 months

109
Q

Aujeszky’s disease vaccine first vaccination

A

10-12th wk, repeat vaccine in 2 wks

110
Q

Aujeszky’s disease vaccination of gilts

A

at 6 mth, at fertilization & at 70th-90th day of prego

a

111
Q

Aujeszky’s disease vaccination of older sows

A

at fertilization

112
Q

how to eradicate Aujeszky’s disease

A

virus can maintain in vaccinated pig herds…
need to raise virus free generation, selection with help of marker vaccines

113
Q

Swine Inclusion Body Rhinitis causative agent

A

Suis betaherpes virus 2 (SuBHV2)

114
Q

Swine Inclusion Body Rhinitis infections in world & in herds

A

worldwide & 100% of infected animals within a herd

115
Q

Swine Inclusion Body Rhinitis affects which animals

116
Q

Swine Inclusion Body Rhinitis spread types

A

horizantal & vertical

117
Q

Swine Inclusion Body Rhinitis horizantal spread pathogenesis

A

Contact, aerogene (saliva, nasal discharge) → multiplication in nose, lacrimal gland → cell-associated viraemia → seconder multiplication mainly in lymphocytes, lung macrophages

118
Q

Swine Inclusion Body Rhinitis vertical spread pathogenesis

A

Pregnant sows: foetuses get infected → abortion, stillbirth, weak new-borns

119
Q

Swine Inclusion Body Rhinitis incubation time

A

10-20 days

120
Q

Swine Inclusion Body Rhinitis CS

A

until 3 wks: infection in utero or during delivery
sudden death, fever, rarely bloody discharge

10-50% mortality

121
Q

Swine Inclusion Body Rhinitis diagnosis in live animals

A

nasal swab, unclotted blood: PCR

122
Q

Swine Inclusion Body Rhinitis DD

A

SMEDI, PRRS, Aujeszky’s disease, PCV-2, classical swine fever

123
Q

How many equine herpesvirus is there in domesticated horses?

124
Q

How many equine herpes virus is there in wild horses

125
Q

diseases caused be equine herpesvirus

A
  • Equine epizootic abortion and rhinopneumonitis: EqAHV1, 4 (EHV1,
    4)
  • Encephalomyelopathia: EqAHV1 (EHV1)
  • Coital exanthema: EqAHV3 (EHV3)
  • EqGHV2 (EHV2), EqGHV5 (EHV5): subclinical infection in 60-100% of horses
126
Q

EqAHV1 has 2 types of genotype

A

neurotropic & non-neurotropic

127
Q

EHV1 neurotropic genotype

A

causes encephalomyelopathy
rarely abortion and resp signs

128
Q

EqAHV1 non-neurotropic genotype

A

causes abortion and resp signs
rarely can cause encephalomyelopathy

129
Q

Equine rhinopneumonitis and Epizootic abortion occurence

A

world wide
One of most important equine viral pathogen

130
Q

Equine rhinopneumonitis causative agent

A

Equid alfaherpesvirus 1 (EqAHV1, EHV1)
Equid alfaherpesvirus 4 (EqAHV4, EHV4)

131
Q

Epizootic abortion causative agent

A

Equid alfaherpesvirus 1 (EqAHV1, EHV1)
Equid alfaherpesvirus 4 (EqAHV4, EHV4)

132
Q

Equid alfaherpesvirus 4 (EqAHV4, EHV4)

A
  • Preferred cells: respiratory epithelial cells, endothelial cells,
    (rarely: neurocytes, lymphoid cells) * Respiratory disease, rarely abortion
133
Q
  • Equid alfaherpesvirus 1 (EqAHV1, EHV1)
A
  • Preferred cells: respiratory epithelial cells, endothelial cells,
    neurocytes, lymphoid cells
  • Respiratory disease, abortion, nervous symptoms
134
Q

Equine rhinopneumonitis and Epizootic abortion
Pathogens lytic cycle

A

Lytic cycle: multiplication induces cell damage, necrosis

135
Q

T/F

EqAHV1, 4 have different strains all showing the same pathogenicity

A

false, strains with different pathogenicity

136
Q

EqAHV1, 4 route of infection

A

PO, Aerogene

137
Q

EqAHV1, 4 viral secretion can last up to

A

21 days, 56 days in mares

138
Q

can EqAHV1, 4 be reactivated

A

yes, mainly without clinical symptoms, by stress

139
Q

what is EqAHV1, 4 local reactivation

A

within the blood vessels of uterus, placenta or CNS -> thromboischemia -> tissue damage -> abortion

140
Q

how long does the protection lasts following infection from EqAHV1, 4

A

3-6 months

no CS, no viral excretion, but can be infected

141
Q

will mares that were infected by EqAHV1, 4 and aborted, abort again in the following years

142
Q

How long does colostral immunity protect from EqAHV1, 4

143
Q

EqAHV1 (EHV1) pathogenesis in the respiratory system

A
  • Primary multiplication in respiratory epithelial cells: viral secretion in aerosol
  • Cell necrosis, mucosal erosions
  • Parallel latent cycle
  • T cell associated viraemia → systemic infection of endothelial cells
144
Q

EqAHV1 (EHV1) pathogenesis in the uterus

A

infection following viremia
* Placenta: virus multiplication in vascular branches of blood vessels located in the base of microcotyledons in the second part of pregnancy → vasculitis, thrombosis, necrosis
* If large number of microcotyledons is affected: abortion before reaching the virus of the foetus
* In other cases, the virus reach the foetus and induced tissue damage: abortion at the end of pregnancy

145
Q

EqAHV1 (EHV1) pathogenesis in the nervous system

A

virus multiplication in blood vessels (endothelial cells) following viremia → vasculitis, thrombosis → tissue degeneration and necrosis: encephalomyelopathy (mainly without inflammation)

* Clinical symptoms according to the location of the damage

146
Q

EqAHV4 (EHV4) pathogenesis

A
  • Primary multiplication in respiratory epithelial cells * Lytic cycle → cell necrosis, mucosal erosions
  • Parallel latent cycle
  • Viraemia rarely, mainly reached the respiratory lymph
    nodes only
  • Rarely induced abortion
  • Pathogenesis is not known: it is supposed the occurrence of virulent strains able to multiplicate in endothelial cells → vasculitis, thrombosis, abortion
147
Q

Equine rhinopneumonitis CS

A

Serous/mucous nasal discharge, (coughing), conjunctivitis, enlarged submandibular lymph nods
* Foals with damaged immune system: seconder bacterial infection and severe pneumonia*

Mainly EqAHV4 (EHV4) detected

148
Q

Equine rhinopneumonitis incubation time

149
Q

Epizootic abortion CS

A

early as 2wks, mostly last third of prego & unexpectedly

mainly EqAHV1 (EHV1), rarely EqAHV4 (EHV4) is detected

150
Q

Epizootic abortion CS in stallions

A

Scrotal enlargement, decreased libido, bed quality of sperm for few days

151
Q

Equine rhinopneumonitis and Epizootic abortion CS of nervous form

A
  • above 20yo usually
  • CS at end of viraemia
  • hindlimbs affected
  • rarely cerebral symptoms
152
Q

Equine rhinopneumonitis and Epizootic abortion Diagnosis pathology of abortion

A
  • Placenta not ruptured
  • Yellow discoloration and oedema in the foetal connective tissues, petechial haemorrhages on the mucosal membranes and serosa
153
Q

gold standard to diagnose Epizootic abortion

A

Isolation
(IHC is more sensitive than iso)
detection of pathogen in foetal lung

154
Q

DD of Equine rhinopneumonitis and Epizootic abortion Resp form

A
  • Equine influenza
  • Rhino-, Adeno-, Reovirus
155
Q

DD of Equine rhinopneumonitis and Epizootic abortion Abortion

A
  • Equine arteritis virus
  • Bakteria, fungi, parasites
156
Q

DD of Equine rhinopneumonitis and Epizootic abortion Nervous form

A
  • Rabies, West-Nile fever, Borna disease
157
Q

Vaccination against Equine rhinopneumonitis and Epizootic abortion

A
  • Attenuated and inactivated vaccines
  • Decrease the severity of clinical symptoms and the amount
    of secreted virus
  • Weak protection: mainly against respiratory disease, do not protect against abortion and nervous form
158
Q

Why is it hard to make a vaccine against EqAHV1, 4 (EV1, 4)

A

based equally on mucosal, humoral, and cell associated immunity: production of effective vaccines is difficult

159
Q

Equine rhinopneumonitis and Epizootic abortion

How long should we seperate Aborted and incoming mares for?

160
Q

Equine rhinopneumonitis and Epizootic abortion

how long should we seperate new incoming horses for?

161
Q

Coital exanthema of horses
causative agent

A

Equid alfaherpesvirus 3 (EqAHV3)

162
Q

Coital exanthema of horses spreading

A

breading, insemination, iatrogenic, contact

163
Q

Coital exanthema of horses how long does the infection and protection lasts

A

persistant infection
short lived protection (repeatedly occuring disease)

164
Q

Coital exanthema of horses incubation time

165
Q

Coital exanthema of horses where does the viral multiplication take place

A

genital mucosa and skin (vesicles, ruptered, erosions)

166
Q

Coital exanthema of horses CS

A

genital mucosa and skin: vesicles (1-1,5 cm diameter), ruptured, erosions
* Painful
* Healing within 2-3 weeks, loss of
pigmentation can remain
* Prolonged healing in case of secondary bacterial infection
* Udder can be affected: lesions on the mouth of foal
* Lesions on the mouth of stallions

167
Q

Canine herpes virus (CHV) occurance

A

WOrldwide, 30-100% of dog pop is infected

168
Q

where can be found a latent infection of Canine herpes virus (CHV)

A

ganglions, optic nerve, bulbus olphactorius, corneal epithelia

169
Q

Optimal temperature for Canine herpes virus (CHV)

A

low temp, 33-35°C

170
Q

Canine herpes virus (CHV) pathogenesis

A
  • Route of infection: intrauterine, P.O., aerogene
  • Cell associated viraemia
  • Pregnant bitch: acute infection or reactivation * Embryo death, abortion, infected newborn
  • Puppies: infected from bitch, or from littermate * Disease in puppies of seronegative bitches
  • Until 3 weeks of age:
  • Local lesions, and subclinical infection
  • Systemic disease: mostly fatal
  • From 3 weeks of age: mature thermoregulation, only
    subclinical infection
171
Q

Canine herpes virus (CHV) adult infection

A

subclinical (resp, ocular, repro)

172
Q

Canine herpes virus (CHV) incubation time

173
Q

Canine herpes virus (CHV) CS of puppies

A

no suckling, vesicles, nasal discharge
(survivors have mouvement disorder, visual impairment)

< 3wks old

174
Q

Canine herpes virus (CHV) CS adults

> 3wks old

A

resp signs (agent of kennel cough)
vesicles on genital mucosa
keratoconjunctivitis
abortion

175
Q

Canine herpes virus (CHV) therapy

A

no time
antiviral treatment of littermates (acyclovir) decrease the severity of CS

176
Q

Canine herpes virus (CHV) vaccine

A

Inactivated vaccine (2x during prego), weak protection
only in breeding kennels with reccurent disease

177
Q

Canine herpes virus (CHV) prevention

A

new-borns in a 39°C environment for 2 wks

178
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) occurance

A

Worldwide, 2-40% of infected cats

179
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) is very similar genetically to which other disease

180
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) predisposing factor

A

winter
younger than 6 months old

181
Q

how long does colostrum protect from Felid alfaherpesvirus 1 (FeAHV1, FHV1)

A

7-10 wks of age

182
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) route of infection

A

PO, contact, fomites

183
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) pathogenesis

A

Viral multiplication in conjunctiva, nasal cavity, and trachea: epithelial cell necrosis
* Viraemia rarely: generalised disease in weak kitten, pregnant cat → infection of the foetus → abortus
* Latent infection in tonsilla, trigeminal ganglion
* Reactivation: stress, lactation, immunosuppression

184
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) CS

A

lacrimation, nasal discharge, conjunctival erosion (painful, eyelids stuck together)
* New-borns panophtalmitis → blindness
* Chronic rhinitis can cause permanent deformation of nasal cavity → laboured breathing

185
Q

Felid alfaherpesvirus 1 (FeAHV1, FHV1) incubation period

186
Q

DD of Felid alfaherpesvirus 1

A

Calicivirus, Chlamydia felis, Bordetella
bronchiseptica

187
Q

which Felid alfaherpesvirus 1 vaccine is given S.C.?

A

inactivated

188
Q

Which Felid alfaherpesvirus 1 can be given I.M, S.C.?

A

attenuated

189
Q

What are the diseases caused by herpes virus in poultry

A
  • marek’s disease
  • Infectious laryngotracheitis of poultry
  • duck viral enteritis
  • pigeon herpes
190
Q

in poultry Marek’s disease can be seen 2 different symptoms

A

proliferation of lympjoid tissue (mainly)
enlargement peripheral nerves (rarely)

191
Q

Marek’s disease occurence

192
Q

Marek’s disease causative agents

A

Gallid herpesvirus-2 (GaAHV2), (previously serotype 1)
Gallid herpesvirus-3 (GaAHV3), (previously serotype 2)

193
Q

Which closely related virus is important in the vaccine development for marek’s disease

A

Turkey Herpesvirus (Meleagrid herpesvirus-1, HVT, MeAHV1)

194
Q

Marek’s disease virus resistancy

A

high in feather follicular cells (mixed with dust more than 1 year!)

195
Q

Marek’s disease virus envelopped?

196
Q

What is effective against enceloped virus?

A

formaldehyde & chlorine

197
Q

How virulent can Gallid herpesvirus-2 (GaAHV2), (previously serotype 1) be?

A

Very virulent plus
Very virulent = Tumors
Virulent = Tumors and transient paralysis
Moderately virulent= Neurological form
Avirulent= No clinical signs

198
Q

Marek’s disease most susceptible birds

A

1-2 wks old

199
Q

infected after 8 wks of Marek’s disease what happens?

A

no CS, but virus shedding

200
Q

Marek’s disease infection route

A

airborn, rarely PO

201
Q

Marek’s disease Horizantal and/or vertical?

A

no germinative infection, but can be infected in the hatchery

202
Q

Marek’s disease classical (neuro) form age, frequency and duration?

A
  • growers and young hens
  • sporadic
  • long lasting, recovery after 1 year of age
203
Q

Marek’s disease transient paralysis age, frequency and duration

A
  • 4-7 wk old non vaccinated broiler
  • sporadic
  • transient recovery -> visceral form
204
Q

Marek’s disease acute Lymphoproliferative form age, frequency and duration

A
  • Non vaccinated: from 6 wks (Vacinnated: growers)
  • frequent (non vacc) & sporadic in vacc
  • long lasting in the flock, may lead to CNS symptoms
205
Q

Marek’s disease pathogenesis

A

Airborne
Macrophages (cell associated viraemia)
Lymphoid tissue
Cytolysis, early immune supp.
lymphoid proliferation
massive cytolysis, long lasting immune supp.
Free virion only in feather follicles

206
Q

pathogenesis of how Marek’s disease virus spreads in animal

A

from cell to cell directly, no free virions, hiding from the Ab

207
Q

Marek’s disease incubation time

A

wide range:
acute: 4-6wks
Chronic 0.5-1 year

208
Q

Marek’s disease CS

A

grey iris/ misshapen pupil
neck paralysis
collapsed crop
leg paralysis
weight loss
wing paralysis
lumps on skin

209
Q

Marek’s disease neuro form patho findings

A

Plexus brachialis/ plexus ischiadicus and other peripheral nerves are enlarged
grey eye

less frequent, longer lasting

210
Q

Marek’s disease acute visceral form patho findings

A

spleen, liver, kidneys, ovaries, testies: infiltrated with tumors (walnut sized)

212
Q

Marek’s disease diagnosis according to age

A
  • acute visceral form from 6 wks (frequent)
  • neuro form from 6 mnths (rare)
213
Q

what is MATSA

A

Marek’s disease associated tumor surface antigen

214
Q

Very important DD with Marek’s disease

A

Reticuloendotheliosis ! virology/serology is needed

215
Q

Marek’s disease vaccination

A

at hatching
in hatchery 18 dy old embryo, in ovo

216
Q

Marek’s disease vaccine type and name

A
  • attenuated serotype 1 (Rispens)
  • (serotype 2)
217
Q

Infectious laryngotracheitis of Poultry - ILT description

A

upper resp illness & conjunctivitis in chickens

218
Q

Infectious laryngotracheitis of Poultry - ILT susceptible animals

A

pheasant, turkey, peacock

219
Q

Infectious laryngotracheitis of Poultry - ILT causative agents

A

Gallid herpesvirus 1

220
Q

how can Infectious laryngotracheitis of Poultry - ILTpropagate in cell culture

A

on chorio-allantoic membrane (CAM) in chicken cell culture

221
Q

Infectious laryngotracheitis of Poultry - ILT pathogenesis

A

Airborne
local multiplication (no viraemia)
No germinative INFECTION
long term carriers and shedders (resp secretion)
EXTREMELY contagious

virus rep in upper third of resp tract

222
Q

Infectious laryngotracheitis of Poultry - ILT incubation time

A

6-12dys

(lol my BDay)

223
Q

Infectious laryngotracheitis of Poultry - ILT CS

A

dyspnea, fibrin precipitation in trachea
Conjunctivitis, almond shaped eyes
mouth & beak stained with blood from tracheal exsudates

224
Q

Infectious laryngotracheitis of Poultry - ILT vaccine

A

eye drop with attenuated vaccine

vaccine are shed by the birds

225
Q

Infectious laryngotracheitis of Poultry Differential diag

A

newcastle disease
fowlpox
infectious coryza
swollen head syndrome
mycoplasmosis
infectious bronchitis

226
Q

Duck viral enteritis (duck plague) description

A

Acute haemorrhagic disease of duck and other waterfowl

227
Q

Duck viral enteritis (duck plague) causative agents

A

Anatid-herpesvirus-1

228
Q

Duck viral enteritis (duck plague) susceptible animals, infection route, shedding, infection time

A
  • wild ducks
  • PO
  • shedding through nasal discharge & faeces (contaminated water)
  • lifelong carriers
229
Q

Duck viral enteritis (duck plague) pathogenesis

A

PO
primary rep: mucosal epithelium of GI tract
viraemia
endothel damage of blood vessels
necrosis & haemorrages

230
Q

Duck viral enteritis (duck plague) CS

A

sudden and persistant flock mortality
nasal discharge
watery/bloody diarrhea
conjunctivitis, eyelid oedema
ducklings: blue beaks, change of voice

231
Q

Duck viral enteritis (duck plague) patho findings

A

Haemorrhages, Oedema (neck), diphteric pseudomembranes, enlarged liver

232
Q

Duck viral enteritis (duck plague) differential diagnosis

A

Newcastle disease
avian influenza
duck viral hepatitis
pasteurellosis
necrotic & hemorrhagic enteritis

233
Q

Duck viral enteritis (duck plague) vaccination

A

inactivated, oil adjuvated vaccine (lower efficacy)

234
Q

Pigeon herpes description

A

in young pigeon liver, pancreas and intestinal disease and conjunctivits

235
Q

Pigeon herpes causative agent

A

Columbid herpes virus 1

236
Q

Pigeon herpes pathogenesis

A

PO (from mother), airborne (CS)
periodic shedding (stress)
no virus entry in the eggs

237
Q

CS of adult pigeon with Pigeon herpes

A

non-symptomatic carriers

238
Q

acute Pigeon herpes CS

A

serous conjunctivits
diphteric, yellow plaques on beak, oropharynx, oesophagus & trachea

(2-6 mths old)

239
Q

pahto findings in Pigeon herpes

A

liver: enlarged, haemorrages, greyish foci

240
Q

Pigeon herpes diagnostic

A

PCR

(pharyngeal swab, liver)

241
Q

Pigeon herpes DD

A

Newcastle disease
Pigeon Pox

242
Q

Pigeon herpes vaccine

A

attenuated, live vaccine
inactivated vaccines

Epi MT (16 decks)

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