Canine, Equine, Avian Herpes Flashcards
1
Q
What viruses belong to the family Hepesviridae?
A
- Canine herpesvirus
- Equine herpesvirus
- Avian herpesvirus
2
Q
What is the structure of herpesviruses?
A
- dsDNA
- 200kb
- enveloped - glycoproteins
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
4
Q
What is Canine Herpesvirus (CHV)?
A
- 1965
- Only canids suceptible
- worldwide
- high seroprevalence (20-98% depending on region)
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
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
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
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
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
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
11
Q
What other lesions are seen in CHV?
A
- enlarged hyperemic lymph nodes
- enlarged/swollen spleen
- Possible lesions in eyes and CNS
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
13
Q
What is the treatment for CHV?
A
- Puppies - unsuccessful, poor prognosis
- Adults - mild and self limiting
- ophthalmic antiviral therapy
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
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)
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
