Family Herpesviridae 2

Question 1

canine herpesvirus 1 within what subfamily?

aka what syndrome

Answer 1

subfamily: alphaherpesvirinae

Fading puppy syndrome - hemorrhagic disease of puppies

Question 2

hemorrhagic disease of puppies aka?
host

Answer 2

canine herpesvirus 1

dogs, coyotes, wolves, highly fatal, generalized hemorrhagic disease of puppies

Question 3

canine HV 1 transmission in neonates vs. older dogs

Answer 3

neonates: contact with infected oral, nasal or vaginal secretions of mom, contact with secretions of littermates, in utero transmission and from passage through birth canal, contact with fomites

older: veneral transmission and contact with saliva, nasal discharge and urine of infected dogs or puppies

Question 4

canine HV 1 - pathogen. in puppies
-in utero infection vs. systemic neonatal vs. CNS infection

Answer 4

in utero: abortion, stillbirth, infertility, if pup survives, will develop symptoms within 9 days from birth

systemic neonatal: pups less than 1 week are most susceptible, initial rep in nasal epith, tonsils and pharynx, mucosal invasion followed by leukocyte (macrophage) associated viremia, replication in endothelial cells, diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in several organs, thrombocytopenia and DIC

CNS infection: meningoencephalitis occurs in oro-nasally infected neonatal puppies, virus may travel up nerves to axons to CNS, puppies die from systemic illness before neuro signs are evident

Question 5

canine HV 1 - factors affecting systemic neonatal infection:

Answer 5

• body temp of puppies is critical: need to maintain ambient temp and maternal contact to maintain normal body temp, more severe the hypothermia, the more severe and rapid is the course of disease

-maternal immunity: maternal AB provide protection, pups born from seronegative bitches are highly vulnerable to severe form of disease

Question 6

canine HV 1 - CS in puppies

Answer 6

CS: painful crying, abdominal pain, anorexia, dyspnea, passing soft odorless greenish stool, no elevation in body temp
-animal that survive systemic disease, develop persistent neuro signs such as ataxia and blindness

Question 7

hemorrhagic disease of puppies: adult genital infection vs. adult respiratory infection vs ocular infection

Answer 7

adult bitches: asymptomatic or limited hyperemia, vesicular vaginitis with dishcarges, vesciular lesions, in utero infection may reuslt in abortion, still birth, mummified fetus and/or infertility
male dogs: balanoposthitis

adult resp. infection: older dogs - mild resp. infection

ocular infect: conjunctivitis

Question 8

hemorrhagic disease of puppies
control

Answer 8

reduce hypothermia by giving heated whelping box, heat lamp, low prevalence of severe illness in pups and not many CS in adult animals = lack of avail. vax

Question 9

feline herpesvirus 1 - what subfamily and infection

Answer 9

-alphaherpesvirinae
-feline rhinotracheitis

Question 10

feline rhinotracheitis
- 2 most common causes of resp infection in cats

Answer 10

feline herpesvirus 1 and feline calicivirus

Question 11

feline rhinotracheitis
transmission

Answer 11

FHV 1 is shed in ocular nasal and oral secretions, direct contact with infected cat, AEROSOL ROUTE IS NOT IMPORTANT, natural routes are infectino are nasal, oral and conjunctiva, all recovered cats become latent infected carriers, reactivation from stress may cause viral shedding

Question 12

feline rhinotracheitis
pathogenesis

Answer 12

-virus rep takes place in mucosa of nasal septum, turbinates, nasopharynx and tonsils
-viremia is rare, virus rep. restricted to areas of lower temp - URT
-infection leads to multifocal epithelial necrosis, inflammation and fibrinous exudation, secondary bacT infection = complication

Question 13

feline rhinotracheitis
CS in kittens, cats, pregnant queen

Answer 13

kittens: severe upper resp disease, extensive rhinotracheitis, fatal bronchopneumonia, hyperemia and serous ocular discharge, severe necrohemorrhagic rhinitis, multifocal necrohemorrhagic palatitis, conjunctivitis and ulcerative keratitis

cats: mild or subclinical disease in older kittens

pregnant queen: abortion, around 6th week of pregnancy, doesnt cross placenta, may be due to severe systemic illness and not direct effect of virus

Question 14

CS differentiation between FHV 1 and feline calicivirus (FCV)

Answer 14

calicivirus: TOUNGE ULCERS
oral ulcers are rare in FHV 1 infection

Question 15

feline rhinotracheitis
VAX for FCV and FHV

Answer 15

3 types avail.
-modified live parenterally, modified live intranasally, inactivated vaccine parenterally

Question 16

2 avian diseases within alphaherpesvirinae

Answer 16

infectious laryngotracheitis (Gallid herpesvirus 1)

Marek’s disease (gallid herpesvirus 2)

Question 17

infectious laryngotrach. host

transmission

Answer 17

highly contagious in chickens

INHALATION, droplets to conjunctiva, ingestion, recovered and vax. can serve as carriers of ILT and can shed the virus when they are subjected to stressful conditions (latent infection) through fomites, mechanical transmission (dogs, animals)

Question 18

infectious laryngotracheitis pathogenesis

Answer 18

severe laryngotracheitis in affected birds - necrosis, hemorrhage, ulceration and formation of diphtheritic membranes, extensive dipther. membrane formation = forms second tube for length of trachea (tracheal plug), blocking air passage = death from asphyxia!!
ILT can persist in infected birds, TRIGEMINAL GANGLION is target for ILT viral latency

Question 19

ILT CS severe form

Answer 19

resp distress, head shaking with coughing, neck is raised and head extended - “pump handle respiration”, cough may be bloody and blood may stain beak and neck
-strains of low virulence associated with conjunctivitis, ocular discharge, swollen infraorbital and nasal sinuses and decreased egg production, mild enzootic form is most common now, severe epizootic form is uncommon

Question 20

ILT diagnosis

Answer 20

necropsy finidngs: tracheal plug
-detection of intranuclear inclusions in resp. tissues
virus isolated in nasal mucosa, virus grows well in CAM of embryonated eggs

Question 21

ILT control, vax

Answer 21

outbreak: complete depopulation (slaughter of infected birds) and disinfect premises

VAX: 3 types
1. chicken embryo origin (CEO) - better immunity but can revert to virulence
2. tissue culture origin (TCO) - limited immunity but does not revert to virulence, BETTER CHOICE BECAUSE SAFER
3. pox vectored recombinant vax
-applied via eye drop, mass vax by water or spray
+ farm biosecurity

Question 22

Mareks disease - what subfamily and herpes virus?
-hosts

Answer 22

alphaherpesvirinae, gallid herpesvirus 2
-chickens most impt. natural host, turkeys, quails, pheasants

Question 23

mareks disease transmission

Answer 23

-highly contagious
-inhalation of infectious feather debris, chicken dander or dust
-cell free viruses release from the feather follicles are highly infectious, but labile
-viruses in desquamated cells (dander) are less infectious, but can survive in poultry house, dust or litter for several months

Question 24

mareks disease 4 pathotypes

Answer 24

-mild (mMDV): neural MD, disease is preventable with vax
-virulent (vMDV): high indicence of neural and visceral lymphomas (lesions in organs), disease is preventable with vax
-very virulent (vvMDV): high incidence of neural and visceral lymphomas, viruses are oncogenic HVT vaxxed chickens, preventable with bivalent vax
-very virulent plus (vv+MDV): high incidence of neural and visceral lymphomas, viruses are oncogenic in chickens vaxxed with bivalent vax

Question 25

mareks disease pathogenesis

Answer 25

1. inhalation of virus
2. first round of rep in URT epithelial cells
3. macrophage associated viremia
4. virus detectable in spleen, bursa and thymus
5. a. productive restrictive infection: cytolytic replication primarily in B cells and later activated CD4T cells
   b. non productive latent infection: in T cells
   c. non productive neoplastic transformation: some latently infected CD4 T cells
6. a. Fully productive infection: production of enveloped virions and cell death (lysis) occurs in feather follicle epithelium, infected T cells have ‘trojan horse’ by which MDV enters the feather follicle epithelium
   b. productive restrictive infection: production of naked virions (not infectious) and viral antigens, cell death due to lysis, occurs in B cells and activated T cells, immunosuppression
   c. non productive infection: viral genome persists in T cells, no AG expressed
   d. non productive neoplastic transformation: some latently infected T cells undergo neoplastic transformation, new AG (MATSA - Mareks disease associated tumor specific antigen) appears in transformed T cells

Question 26

mareks disease pathogeneiss - speed of repl.

Answer 26

virus is slowly cytopathic and remains associated with cells, cell free infectious viruses are almost impossible to obtain, except in dander from feather follicles
-lesions in mareks disease result from infiltration and in situ proliferation of transformed T lympthocytes
-cell lysis also results in marked inflammatory response

Question 27

mareks disease clinical features - 4 main ones

Answer 27

1. neurolymphomatosis: enlargement of nerve trunks, lose striations and are grey or yellow in appearance = lameness, droopy wings, paresis of legs, incoordination
2. visceral lymphomatosis = diffuse or nodular lymphoid tumors on diff. organs, in liver, spleen, gonads, heart, lung, bursa is ATROPHIC = absence of bursal tumors helps distinguish it is mareks
3. ocular lymphomatosis: graying of the iris (gray eye), interference with normal pupilar constriction and dilation, partial or total blindness
4. cutanous lymphomatosis: plucking of feathers reveal nodular lesions on skin, enlarged feather follicles (skin leukosis)

Question 28

mareks disease control

Answer 28

-REPORTABLE DISEASE!!!!
-most widely used vax consists of turkey herpesvirus (HVT)
-bivalent vax consists of HVT and either SB-1 or 301B/1 strains of gallid herpesvirus 3 (serotype 2, avirulent strain)
-most protective vax is CV1988/Rispens, attenuated mareks disease virus strain that is commonly mixed with HVT at vax.