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Herpesvirus Flashcards

1
Q

Herpesvirus

General Characteristics

A
  • dsDNA
  • Icosahedral
  • Enveloped
  • Replicates in nucleus-> Nuclear inclusion bodies!
  • Strongly immunosupressive , strong CPE
  • Weak antigenicity-> weak immune response-> Lifelong carriers and latency
  • Cross reaction withim the genera - cross protection
  • Weak resistance (exc. Marke’s disease virus)
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2
Q

Infectious Bovine Rhinotracheitis

Species affected

A

Ru

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3
Q

Infectious Bovine Rhinotracheitis

Most susceptible

A

All age groups

  • Respiratory form: 1-6mo
  • Calves encephalitis <5mo
  • Genital form: adults
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4
Q

Infectious Bovine Rhinotracheitis

Spread

A

Slow spread

  • Carrier animal introduction
  • Semen
  • contact
  • Airborne
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5
Q

Infectious Bovine Rhinotracheitis

Pathogenesis

A
  • Aerogenous: Respiratory Mucosa —> Inflammation —> Viraemia —> Other organs —> Encephalitis in calves and Abortion
  • Ascending inflammation in the nose —> nerves —> calf encephalitis
  • Genital form —> Degeneration and inflammation of the mucosal epithelium and nodule formation
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6
Q

Infectious Bovine Rhinotracheitis

Primary replication

A
  • Aerogenous: respiratory mucosa
  • Genital: genital mucosal epithelium
  • Incubation: 2-5d
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7
Q

Infectious Bovine Rhinotracheitis

Target organs

A

Respiratory & Genital organs

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8
Q

Infectious Bovine Rhinotracheitis

Clinical signs

A

Febrile disease!
*Respiratory form: conjunctivitis, coughing, nasal discharge, encephalitis, interstitial pneumonia, abortion(in resp form, not genital), red nose disease(necrotic mm), calf encephalitis (<5mo)

*Genital form: adults,
Vulvoginits& Balanoposthitis
Greyish yellow nodules, vaginal discharge

*no fertilization& abortion in acute

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9
Q

Infectious Bovine Rhinotracheitis

Pathology

A
  • Inflammation, hemorrhages and erosions in upper respiratory
  • Intranuclear inclusion bodies
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10
Q

Infectious Bovine Rhinotracheitis

Diagnosis

A

CS
PCR
ELISA

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11
Q

Infectious Bovine Rhinotracheitis

Treatment

A

No effective treatment

Ab

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12
Q

Infectious Bovine Rhinotracheitis

Prevention and immunity

A
  • AI tested bulls
  • closed groups according to age
  • Marker vaccines
  • Live&inactivated vaccine - inactivated- breeding, cow before parturition, 2-3mo calves, heifers in fertlization
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13
Q

Bovine Herpesmamillits

Species affected

A
  • Cattle, Buffalo (other ru might be seropositive)

* Humans —> Zoonotic!

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14
Q

Bovine Herpesmamillits

Most susceptible

A

Milking Cows

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15
Q

Bovine Herpesmamillits

Occurrence

A
  • Africa, Australia and USA

* Rare in Europe

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16
Q

Bovine Herpesmamillits

Spread

A
  • Infected animal
  • Spread within the herd via milking
  • Arthropod vectors
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17
Q

Bovine Herpesmamillits

Clinical Signs

A
  • After first parturition: teat edema, suffusion, pustules
  • Hu: lesions on the hands
  • Subclincial infection is common
  • Secondary infection -> mastitis
  • Reduced production
  • Teat scarring
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18
Q

Bovine Herpesmamillits

Primary Replication

A
  • Teat epithelium

* Incubation: 3-7d

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19
Q

Bovine Herpesmamillits

Target Organs

A

Teat

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20
Q

Bovine Herpesmamillits

Pathogenesis

A
  • Epithelial damage, inflammation —> pustules, scabs, lacerations, erosions —> recovery within 1-2 weeks
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21
Q

Bovine Herpesmamillits

Pathology & Histopathology

A

Intranuclear inclusion bodies

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22
Q

Bovine Herpesmamillits

Diagnosis

A

Histopathology
Virus isolation
PCR
Serology

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23
Q

Bovine Herpesmamillits

Treatment

A

Local, symptomatic treatment

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24
Q

Bovine Herpesmamillits

Prevention & Immunity

A

No vaccine available!

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25
Q

Malignant Catarrhal Fever

Species Affected

A
  • Reserviors: Wildbeest, Sheep (asymptomatic,the only oneswho can infect)
  • Ru - dead end hosts
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26
Q

Malignant Catarrhal Fever

Most susceptible

A

Elderly Animals!

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27
Q

Malignant Catarrhal Fever

Occurrence

A
  • Africa —> Wildebeest associated MCF

* Rest of World —> Sheep associated MCF

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28
Q

Malignant Catarrhal Fever

Spread

A
  • Carrier animal introduction, thier secretion (respiratory)

* Cattle are unable to shed and transmit the virus

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29
Q

Malignant Catarrhal Fever

Pathogenesis

A

Aerogenous Infection —> Cell associated viraemia —>immunopathological process

  • Lifelong infection in surviving animals
  • Systemic febrile disease
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30
Q

Malignant Catarrhal Fever

Primary Replication

A

Latent infection -Incubation: 2w-couple of months

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31
Q

Malignant Catarrhal Fever

Target Organs

A
  • All organs
  • Lifelong infection in surviving animals
  • Systemic febrile disease
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32
Q

Malignant Catarrhal Fever

Clinical Signs

A
  • Peracute: fever, hemorrhagic enteritis, convulsions, Urinary bladder wall oedema death.
  • Acute: keratitis, conjuctivitis, laboured breathing, laminitis, odema, severe hemorrhagic enteritis, CNS
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33
Q

Malignant Catarrhal Fever

Pathology & Histopathology

A

Peracute:

  • Inflamed mucosa, haemorrhages, without erosions
  • Urinary bladder wall oedema

Subacute:

  • Eye lesions, *Hemorrhagic pneumonia and enteritis
  • Arteritis
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34
Q

Malignant Catarrhal
Fever

Diagnosis

A

History, CS, PM, histopathology, PCR, ELISA

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35
Q

Malignant Catarrhal Fever

Treatment

A

Poor prognosis

No effective treatment

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36
Q

Malignant Catarrhal Fever

Prevention & Immunity

A

No vaccine available!

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37
Q

Aujeszky’s Disease (Pseudorabies)

Species Affected

A

Pigs: natural hosts&reservoir

Other mammals - dead end hosts

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38
Q

Aujeszky’s Disease (Pseudorabies)

Most susceptible

A

All age groups

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39
Q

Aujeszky’s Disease (Pseudorabies)

Spread

A

*infected swine, semen (vertical transmission), fomites, mechanical vectors (rodents), raw pork!!

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40
Q

Aujeszky’s Disease (Pseudorabies)

Pathogenesis

A

PO/inhalational-> haemolymph->nerves->encephalitis> Secondary lung multiplication->fever& respiratory

Pigs may be lifelong carriers& shedders

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41
Q

Aujeszky’s Disease (Pseudorabies )

Primary Replication

A

Tonsils, Nasal & Pharyngeal mucosa
2-8d incubation
Placental crossing!

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42
Q

Aujeszky’s Disease (Pseudorabies)

Target Organs

A

All organs (lungs, brain)

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43
Q

Aujeszky’s Disease (Pseudorabies)

Clinical Signs

A

*Febrile& systemic
*Vertically infected piglets will be asymptomatic
*Piglets usually have febrile general disease, CNS (~100% mortality), sometimes die without CNS cs
*Gilts mostly recover after 5-6d(resp& CNS symp)
*Pregnant: abortion, stillbirth, infertility
*Adults are usually subclinical
*Ru- mad itch disease, acute lethal encephalitis, death in 1-2s, recovery is rare
Ca- febrile& general, acute lethal encephalitis

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44
Q

Aujeszky’s Disease (Pseudorabies)

Pathology & Histopathology

A
  • Lung edema
  • suckling piglets- necrotic foci on pharyngeal mucosa& tonsils, spleen and liver
  • hemorrhages in Ln
  • Nuclear inclusion bodies
  • Meningitis
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45
Q

Aujeszky’s Disease (Pseudorabies)

Treatment

A

No effective treatment

Ab

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46
Q

Aujeszky’s Disease (Pseudorabies )

Prevention & Immunity

A

Epidemiology measures

  • No feeding with raw pork to carnivores
  • Maternal protection until 8-14w
  • modified live vaccine at 10-121wo, 6mo, at fertilization and 70-904 pregnant
  • The virus can maintain in vaccinated pigs!
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47
Q

Inclusion Body Rhinitis

Most susceptible

A

Nestlings/newly weaned/ pregnant

48
Q

Inclusion Body Rhinitis

Spread

A

Airbonre/direct contact

49
Q

Inclusion Body Rhinitis

Pathogenesis

A

PO/Inhalational Infection —> Viraemia —> Lymphocytes & alveolar macrophages —> latency in lacrimal gland, nasal mucosa & kidney

*Shed in nasal&ocular secretion, urine, aerosol

50
Q

Inclusion Body Rhinitis

Target organ

A

Upper Respiratory Tract

Placental Crossing!

51
Q

Inclusion Body Rhinitis

Clinical Signs

A

Piglets < 3weeks of age:

  • Fever, appetite loss, sneezing, serous or bloody nasal discharge
  • Up to 25% mortality

Piglets > 6 weeks of age: Inapparent

*Infection of foetus weak, SMEDI

52
Q

Inclusion Body Rhinitis

Pathology & Histopathology

A
  • Mucopurulent exudate in nasal passages
  • SC odema & in larynx, pharynx , lungs
  • serum accumulation in body cavities , pleura, pericardium
  • Intranuclear inclusion bodies in mucous
  • cytomegaly
53
Q

Inclusion Body Rhinitis

Treatment

A

No effective treatment

54
Q

Inclusion Body Rhinitis

Prevention & Immunity

A

Maternal immunity up to 4wo

55
Q

Equine Rhinopneumonitis / Epizootic Abortion

Species Affected

A

Equids are the hosts & reservoirs

56
Q

Equine Rhinopneumonitis / Epizootic Abortion

Most susceptible

A

Foals (<2yo) , pregnant mares

57
Q

Equine Rhinopneumonitis / Epizootic Abortion

Spread

A

quick, aerosols, direct contact, ingestion, semen, aborted fetus ,placenta - infective sources

58
Q

Equine Rhinopneumonitis / Epizootic Abortion

Pathogenesis

A

PO/inahalational -> viraemia via lymphoid cells

59
Q

Equine Rhinopneumonitis / Epizootic Abortion

Replication& Target Organs

A

Respiratory mucosa
3-5d incubation
placental crossing!

60
Q

Equine Rhinopneumonitis / Epizootic Abortion

Clinical Signs

A
  1. interstitial pneumonia: <2yo foals- ,fever (risk of co-infection with R.equi - laminitis)
  2. abortion:(weak, dying foals) , usually >5m of pregnancy, abortion storm (30-40%). After recovery, mares return cycling and fertility
  3. CNS: neural degeneration- paresis(lysis) tail& anus paralysis - euthanasia
61
Q

Equine Rhinopneumonitis / Epizootic Abortion

Pathology

A
  • Pneumonia

* aborted fetus: yellow, SC edema, lung edema and necrotic foci, hemorrhages in mm and brain

62
Q

Equine Rhinopneumonitis / Epizootic Abortion

Treatment

A

Rest, supportive therapy

*Prevent abortion: hyperimmune serum and acycloguanosine

63
Q

Equine Rhinopneumonitis / Epizootic Abortion

Prevention & Immunity

A

Early dx.- > vaccination

  • ongoing abortion storms are difficult to eradicate
  • maternal immunity until 3-6mo
  • vaccination with weak Ag - only effective for respratory form, foals from 3mo and 5m pregnant mare, new horses in quarantine
64
Q

Equine Multinodulary Pulmonary Fibrosis

Most susceptible

A

Few week old foals

65
Q

Equine Multinodulary Pulmonary Fibrosis

Clinical Signs

A
  • Fever
  • Mild respiratory symptoms (serous nasal discharge, coughing) - recovery after 1 week/ secondary bacterial infection (R.equi!)
  • Keratoconjunctivitis,
  • swollen lymph nodes
  • Can also be isolated from clinically healthy horses!
66
Q

Equine Multinodulary Pulmonary Fibrosis

Prevention & Immunity

A

Hyperimmune serum

67
Q

Coital Exanthema of Horses

Pathogenesis

A

Mating , iatrogenically (rectal/genital exam.)

foals - from teat suckling

68
Q

Coital Exanthema of Horses

Clinical Signs

A
  • venereal->nodule, vesicle and pustule formation on epithelium of vagina,
  • prepuce and penis -> erupts to become erosions -> scab
  • Recovery usually within 2-3 weeks but unpigmented spots and scars will remain
  • DOESN’T affect pregnancy!
  • No viraemia
  • Lifelong latency&persistant
69
Q

Coital Exanthema of Horses

Primary Replication

A

Genital mucosa

6-8d incubation

70
Q

Coital Exanthema of Horses

Histopathology

A

Intranuclear inclusion bodies

71
Q

Coital Exanthema of Horses

Prevention & Immunity

A

No mating during signs and one month thereafter

72
Q

Canine Herpes

Most susceptible

A

All age groups

73
Q

Canine Herpes

Spread

A

Close contact with secretion and infected animals, replicates in leukocytes->generalized infection

  • Venereal
  • Intrauterine
  • optimal temp for the virus: 33-35c
74
Q

Canine Herpes

Clinical Signs

A
  • Intrauterine infection: generalized& fatal death/recovery with CNS
  • <2wo: death/recovery with CNS signs( vision and motion) necrotising vasculitis, fever, rash, death if opisthotonus
  • > 2wo+adults: localized infection in respiratory/reproductive tract-> latency, reactivation in stress.
  • adults are usually asymptomatic/ vesicular vaginitis or posthitis, abortion, transient infertility
75
Q

Canine Herpes

Pathology & Histopathology

A
  • Generalized haemprrhages&odema
  • Necrosis in spleen, liver, brain, lungs
  • Nuclear inclusion bodies
76
Q

Canine Herpes

Treatment

A

Hyperimmune sera IP, antivirals

77
Q

Canine Herpes

Prevention & Immunity

A

keep warm, vaccinate 2x in pregnancy

78
Q

Infectious Rhinotracheitis of Cats

Most susceptible

A

all age groups

predisposing factors: <6mo, old, pregnant , weak

79
Q

Infectious Rhinotracheitis of Cats

Spread

A

very contagious, contact, airborne, vertical

shed in nasal discharge

80
Q

Infectious Rhinotracheitis of Cats

Pathogenesis

A

PO/Inhalational —> Replicates in respiratory mucosa (necrosis& inflammation) —> Viraemia —> foetus —> Abortion

81
Q

Infectious Rhinotracheitis of Cats

Primary Replication

A

Respiratory mucosa
3-6d incubation
*Latency in pharynx lymp and trigiminal ggl.

82
Q

Infectious Rhinotracheitis of Cats

Clinical Signs

A
  • Serous->mucopurulent conjuctival &nasal discharge, *Corneal ulcers,KCS, epiphora.
  • In young age: permanent damage to nasal and sinus tissue - disruption of cillary clearance -> chronic bacterial infection
  • Abortion in 6th week
83
Q

Infectious Rhinotracheitis of Cats

Histopathology

A

intranuclear inclusion bodies

84
Q

Infectious Rhinotracheitis of Cats

Treatment

A

Symptomatic treatment: IV, feeding tube, oxygen ,hyperimmune serum

85
Q

Infectious Rhinotracheitis of Cats

Prevention & Immunity

A
  • Attenuated (intranasal) or inactivated vaccines in 7wo, 2x, then yearly only protects from CS, doesn’t prevent infection
  • Maternal immunity 7-10wo
86
Q

Infectious Laryngotracheitis of Chicken

Species Affected

A

Mainly Chicken.

But also Pheasant, Turkey, Peacock, Quail

87
Q

Infectious Laryngotracheitis of Chicken

Most susceptible

A

Growers and Adults

88
Q

Infectious Laryngotracheitis of Chicken

Spread

A

Very contagious , Airborne

89
Q

Infectious Laryngotracheitis of Chicken

Pathogenesis

A

Airborne —> Upper airways, conjunctiva —> Local multiplication in the upper respiratory epithelium —> endothelium damage —> exudates, oedema, haemorrhage

  • No viraemia
  • Lifelong carriers & shedders
90
Q

Infectious Laryngotracheitis of Chicken

Clinical Signs

A
  • Mild form: mild respiratory symptoms, seconday bacterial infection
  • Classic virulent form: dyspnoea, conjuctivitis, almond shaped eyes, cheesy plugs in trachea recovery in 2-6w
91
Q

Infectious Laryngotracheitis of Chicken

Pathology & Histopathology

A
  • inflammed, necrotised tracheal mucosa, pseudomembrane , bleeding, cheesy plugs
  • Nuclear inclusion bodies
92
Q

Infectious Laryngotracheitis of Chicken

Treatment

A

No effective treatment

Slaughter affected birds if sporaic

93
Q

Infectious Laryngotracheitis of Chicken

Prevention and Immunity

A

Eye drop with attenuated vaccine

*Broilers 2-4wo, 12-16wo, protected for 1 laying period, doesn’t last long

94
Q

Duck Plague / Duck Viral Enteritis

Most susceptible

A

Layer ducks
Adults
Wild ducks are main reservoirs
Notifiable!

95
Q

Duck Plague / Duck Viral Enteritis

Spread

A

Contact with wild duck& thier secretion

Notifiable!

96
Q

Duck Plague / Duck Viral Enteritis

Pathogenesis

A

PO —> primary replication –>viraemia —> endothelia damage of blood—> necrosis, haemorrhage, fibrin precipitation in mucosa

*lifelong carriers and shedders
Notifiable!

97
Q

Duck Plague / Duck Viral Enteritis

Primary Replication

A

*Intestines —> Bloody diarrhoea
*Upper Respiratory Tract —> Rhinitis
*Eye —> Conjunctivitis
*Incubation 3-7 day
Notifiable!

98
Q

Duck Plague / Duck Viral Enteritis

Target Organs

A

Blood Vessel Walls

Notifiable!

99
Q

Duck Plague / Duck Viral Enteritis

Clinical Signs

A

*Bloody diarrhea, rhinitis, conjuctivitis death within 4-6d(15-25%)
*Eye: photophobia, eyelid edema
*CNS signs: ataxia, tremors, droopiness, floating on water
*Ducklings: blue beaks, blood-stained vents, changed voice.
*adult may die while appear healthy or with prolapsed penis blood in cavities,
*paint brush heart,
*large patchy diphteric membrane hepatomegaly, brass, gray and hemorrhagic.
Notifiable!

100
Q

Duck Plague / Duck Viral Enteritis

Treatment

A

No effective treatment
Slaughter affected birds if sporadic

Notifiable!

101
Q

Duck Plague / Duck Viral Enteritis

Prevention & Immunity

A
  • Avoid contact with wild waterfowl

* Modified live virus vaccine available >3wo, 2x , immunize layers 2x before laying season

102
Q

Pigeon Herpes

Most susceptible

A

2-6 month old

103
Q

Pigeon Herpes

Pathogenesis

A

Airborne/ PO from mother

104
Q

Pigeon Herpes

Clinical Signs

A
  • Adults are asymptomatic
  • Young are asymptomatic when maternal ab protection
  • co-infection with chlamydia, E. coli mycoplasma, pasteurella
  • Acute: conjuctivits, pharyngitis, rhinitis, diarrhoea, death(10%)
  • Chronic: sinusitis, dyspnoea, co-infection
  • latent infection and periodic shed
105
Q

Pigeon Herpes

Pathology & Histopathology

A
  • Hepatomegaly, bloody intestine, conjunctival edema, enlarged pancreas
  • Nuclear inclusion bodies
106
Q

Pigeon Herpes

Treatment

A

No effective treatment

107
Q

Pigeon Herpes

Prevention & Immunity

A

Attenuated or inactivated vaccines (may be with other viruses- polyvalent) 50do&2w after

108
Q

Marek’s Disease

Species Affected

109
Q

Marek’s Disease

Most susceptible

A

1-2 weeks old, hens are more susceptible

110
Q

Marek’s Disease

Spread

A

very resistant virus, airborne, quick spread

  • In feather follicular epithelial cells and in dust —> Over 1 year
  • In litter for about 4 months
111
Q

Marek’s Disease

Clinical Signs

A

*Severity is strain dependant

    1. Neurological form: the classical, chronic, low virulence, long lasting, recovery >1yo. growers &young hens, one sided leg paralysis, wing and claw paralysis, convulsions, Grey eye disease, blindness , enlarged plexus brachialis and ischiadicus
      1. Transient paralysis: more virulent, quick (24h), may lead to visceral form. 6-7wo &unvaccinated
    1. Visceral form: acute, CNS in vax, 100% morbidity in unvaccinated, high mortality! tumours in all parenchymal organs, red leg disease, T cell tumour, MATSA
      1. Peracute/anaemia: 4-6 yo
112
Q

Marek’s Disease

Pathology & Histopathology

A
  • microtumours in skin, CNS signs, small focal tumours in organs, grey eye disease, in very virulent -> mononuclrar cell tumours(T)
  • Neurological: Enlarged plexuss brachialis&Ischiadicus
113
Q

Marek’s Disease

Diagnosis

A

*No differentiation between Avian Leucosis and Marek’s
disease based on clinical signs!
*PM, histo, PCR

114
Q

Marek’s Disease

Prevention and immunity

A

*Prevent early infection:
• Frequent egg collection, shell disinfection, hatching hygiene
• Cleaning, disinfection of stables and ventilators
• Overpressure ventilation, filtered air, separate stuff
• Cleaning and disinfection and destroying fomites
• Breeding genetically resistant
chicken lines
*Immunisation
• In ovo vaccination - 18do embryo
• Vaccinate the day of hatching
• Vaccine does not protect from infection

115
Q

Marek’s Disease

Treatment

A

No effective treatment

Epidemiology (16 decks)

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