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Virology > Canine, Equine, Avian Herpes > Flashcards

Canine, Equine, Avian Herpes Flashcards

1
Q

What viruses belong to the family Hepesviridae?

A
  • Canine herpesvirus
  • Equine herpesvirus
  • Avian herpesvirus
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2
Q

What is the structure of herpesviruses?

A
  • dsDNA
  • 200kb
  • enveloped - glycoproteins
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3
Q

How stable are herpes viruses?

A
  • known for ability to establish liflong infections, immune evasion and latency
  • sensitive to disinfectants, relatively unstable outside host
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4
Q

What is Canine Herpesvirus (CHV)?

A
  • 1965
  • Only canids suceptible
  • worldwide
  • high seroprevalence (20-98% depending on region)
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5
Q

How is CHV transmitted?

A
  • Direct oronasal contact with infected oral, nasal or vaginal secretions of shedding dogs
  • in utero or to neonatal puppies
    • immunologically naive pregnant bitches are at risk for acute infection and transmission to young
  • Shedding:
    • highest with primary systemic infection
    • lower with recrudescence after latent infection
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6
Q

What happens to fetuses/neonatal puppies infected with CHV?

A
  • Mortality rate of 100%
  • Puppies unable to regulate body temperature until 2-3 weeks of age
  • temp of <98.6 favorable for CHV replication
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7
Q

What happens to adult dogs infected with CHV?

A
  • Upper respiratory signs, ocular disease, vesicular vaginitis or posthitis, Subclinical
  • Recovery from clinical disease associated with lifelong latent infection
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8
Q

What is the clinical disease of puppies with CHV?

A
  • Sudden death (clin signs <24 hrs)
    • usually 1-3 wks
  • Lethargy, decreased suckling, crying, diarrhea, nasal discharge, conjunctivitis, corneal edema, abdominal pain, rarely oral or genital vesicles, erythematous rash
  • Notably No fever and leukocytosis
  • thoracic radiographs show diffuse interstitial pneumonia
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9
Q

What is the clinical disease of adult dogs with CHV?

A
  • Subclinical
  • Mild rhinitis, may contribute to infectious tracheobronchitis
  • Vesicular vaginitis or posthitis
  • Conjunctival and corneal ulcers
  • Abortions and stillbirths
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10
Q

What is the characteristic lesion associated with CHV?

A
  • Disseminated focal necrosis and hemorrhage
    • most pronounced in lungs, renal cortex, adrenal glands, liver and gastrointestinal tract
    • Mottled kidneys
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11
Q

What other lesions are seen in CHV?

A
  • enlarged hyperemic lymph nodes
  • enlarged/swollen spleen
  • Possible lesions in eyes and CNS
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12
Q

How is CHV diagnosed?

A
  • Hemagglutination, ELISA, IFA
  • Nucleic Acid: PCR - highly sensitive and specific when used on fresh tissue/fluid
  • VI, EM, IHC
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13
Q

What is the treatment for CHV?

A
  • Puppies - unsuccessful, poor prognosis
  • Adults - mild and self limiting
    • ophthalmic antiviral therapy
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14
Q

How can CHV be prevented?

A
  • No Vaccine
  • Prevent exposure by isolating pregnant bitches from other dogs during the last 3 weeks of gestation and first 3 weeks postpartum
  • Maternal antibodies protect puppies
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15
Q

What are the different forms of Equine herpesviruses (EHV)?

A
  • EHV-1 - Respiratory, abortions, neurologic, neonatal death
  • EHV-2 - ubiqiutous in horses, pathogenicity unknown
  • EHV-3 - coital exanthema (benign venereal disease)
  • EHV-4 Primarily respiratory
  • EHV 5 - associated with equine multinodular pulmonary fibrosis (EMPF)
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16
Q

Why are EHV 1 & 4 important?

A
  • Both ubiquitous worldwide
  • Both produce acute febrile respiratory disease (rhinopharyngitis, tracheobronchitis)
  • Horse in nature reservoir of both, most adults are latently infected
    • >80% of horses latently infected with EHV-1
    • Infection usually dormant
    • Stress/immunosuppression may contribute to recrudescence of disease
    • Infection can be subclinical or severe
      • less severe on re-infection or recrudescence
17
Q

How is EHV trasmitted?

A
  • Direct or indirect contact with:
    • Infectious nasal secretions
    • aborted fetuses
    • placentas
    • placental fluids
18
Q

What is the pathogenesis of EHV?

A

Oronasal exposure ⇢ nasopharynx, upper respiratory epithelium and lymphoreticular tissues of the respiratory tract (2-10 day incubation) ⇢ clinical or subclinical infection

19
Q

How are EHV 1 & 4 different?

A
  • 1: develops cell-associated viremia and infects the vascular endothelium of the nasal mucosa, lungs, placenta, adrenal gland, thyroid and CNS
  • 4: infection typically restricted to the respiratory tract epithelium and associated lymph nodes
20
Q

When does EHV-1 result in abortion

A
  • Viremia MUST occur
  • Mare abort 2-12 weeks after infection with most occurring approximately 30 days after exposure
    • usually occurs in late gestation (7-11 months)
    • Mares seldom display premonitory signs
    • Abortions may be sporadic or outbreaks
    • Aborted fetuses fresh or minimally autolyzed
    • no damage to reproductive tract and subsequent conception is NOT impaired
21
Q

What happens when mares with EHV-1 do NOT abort?

A
  • Foals have Fulminating viral pneumonitis
  • May refuse to nurse, become febrile, have severe respiratory distress and weakness
  • May die shortly after birth or demonstrate rapid deterioration within days, typically developing secondary bacterial infections
22
Q

What are the fetal lesions seen with EHV-1 induced viral abortion?

A
  • Interlobular lung edema and pleural fluid
  • Multifocal hepatic necrosis
  • Petechiation of myocardium, adrenal gland, and spleen
  • Thymic necrosis
  • Intranuclear inclusions in lung, liver, adrenal gland, and lymphoreticular tissues
23
Q

What lesions are seen with viral rhinopneumonitis (EHV)?

A
  • Hyperemia and ulceration of the respiratory epithelium
  • Multifocal, pinpoint plum-colored foci in lungs
  • Inflammation, necrosis ad intranuclear inclusions in the respiratory epithelium and germinal centers of associated lymph nodes
  • Lung lesions characterized by:
    • Neutrophilic infiltration of terminal bronchioles
    • Peribronchiolar and perivascular mononuclear cell infiltrate
    • Serofibrinous exudate in alveoli
24
Q

What is neuropathic EHV-1?

A
  • specific strains resulting in neurologic disease
  • increased morbidity and mortality
  • viremia 10-100x greater
  • acute disease
  • Reportable in most states
25
Q

What is Equine Herpesvirus myeloencephalopathy (EHM)?

A
  • Clinical signs vary from mild incoordination/ataxia and posterior paresis to severe posterior paralysis with recumbency, loss of bladder and tail function, urinary incontinence, loss of skin sensation in the perineal and inguinal areas
  • Rarely progresses to quadriplegia
26
Q

How can EHV-1 cause neurologic disease?

A
  • Viremia must occur
  • to infect the CNS: vasculitis ⇢ ischemic condition
27
Q

What lesions are seen with neurologic EHV-1?

A
  • May have no gross lesions or minimal evidence of hemorrhage in the meninges, brain and spinal cord parenchyma
  • Microscopic lesions in brain or spinal cord:
    • vasculitis with endothelial cell damage an perivascular cuffing
    • Thrombus formation and hemorrhage
    • Malacia in advanced cases
28
Q

How are the different manifestations of EHV diagnosed?

A
  • Respiratory: PCR or virus isolation from nasopharyngeal swab or buffy coat blood samples
  • Abortion: PCR, virus isolation, ICH, and IFA of lung, liver, adrenal gland, and lymphoreticular tissue samples from aborted fetus
    • serologic testing of mares has little dx value
  • Neurologic: PCR on samples obtained form nasal secretions, cerebral spinal fluid or neural tissue
29
Q

What is the treatment for EHV?

A
  • Nonspecific and supportive
    • Antibiotic if evidence of secondary bacterial infection
    • antipyretics if fever >104F
    • Potentially antivirals during outbreaks
    • Intensive nursing care
30
Q

How can EHV be prevented?

A
  • Minimize exposure
    • new or returning horses should be isolated for 21 days prior to comingling with resident horses
  • Minimize stress
  • Maintain pregnant mares separate from other horses
  • During outbreaks:
    • isolate affected horses
    • decontaminated premises (reduce fomite transmission)
    • change PPE between horses
    • Restrict movement
    • implement quarantine
31
Q

What EHV vaccinations exist?

A
  • EHV1&4:
    • inactivated vaccine
    • foals first at 4-6 months, 2nd 4-6wks later, 3rd at 10-12 months
    • Booster up to every 6 months until maturity
    • Mares vaccinated 4-6 wks prior to foaling
  • EHV 1-abortion
    • inactivated vaccine
    • during months 5, 7, and 9 of gestation
  • EEHV-1 respiratory
    • modified live vaccine
  • NONE for neurologic
32
Q

What are the Avian herpesviruses?

A
  • Infectious laryngotracheitis
  • Marek’s disease
33
Q

What is Infectious laryngotracheitis?

A
  • Gallid herpesvirus 1
  • infects chickens and phesants
  • Reported in most areas of US
  • highly contagious
  • latent infections
34
Q

What are the clinical signs of Infectious laryngotracheitis?

A
  • severe dyspnea
  • gasping
  • coughing
  • sneezing
  • hemorrhagic exudate
  • rales
  • nasal and ocular discharge
  • conjunctivitis
35
Q

How is Infectious laryngotracheitis prevented

A

biosecurity and vaccination

36
Q

What is Marek’s Disease

A
  • Gallid herpesvirus 2
  • chickens most important natural host
    • ubiquitous infection, worldwide distribution
  • highly contagious, readily transmitted
  • Neoplastic transformation in latenlty infected T cells (characteristic lymphoid neoplasia)
  • 4 forms cutaneous, neural, ocular, visceral

Virology (37 decks)

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