Herpesviridae (Ex2) Flashcards

1
Q

Morphology of Herpesviridae

A
  • enveloped, spherical to pleomorphic
  • icosahedral capsid, T=16
  • capsid surrounded by globular material called tegument
  • glycoproteins in lipid envelope
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2
Q

Describe the viral genome of Herpesviridae

A
  • non-segmented, linear, double-stranded DNA

- contains terminal and internal repeated sequences

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3
Q

Explain replication of Herpesviridae

A
  • DNA replication occurs in the nucleus
  • viral envelope acquired by bidding through inner layer of nuclear envelope
  • mature virions accumulate within vacuoles in the cytoplasm and are released by cytolysis
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4
Q

What are Type A Cowdry bodies?

A

eosinophilic intranuclear inclusion bodies that are characteristic of herpesvirus

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5
Q

General features of subfamily alphaherpesvirinae

A
  • highly cytopathic, lyse infected cells

- short replication cycle

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6
Q

Bovine Herpesvirus 1

subfamily, diseases caused

A
  • Alphaherpesvirinae
  • Infectious bovine rhinotracheitis (IBR)
  • Infectious pustular vulvovaginitis
  • Ocular form of IBR
  • abortion
  • Systemic disease of newborn calves
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7
Q

What are the 3 subtypes of BHV-1?

A
  • BHV-1.1 (respiratory)
  • BHV-1.2 (genital)
  • BHV-1.3 (encephalitic)
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8
Q

Transmission of BHV-1

A
  • respiratory disease and conjunctivitis from droplet transmission
  • genital disease from coitus or AI with infected semen
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9
Q

What are the sites of latency for BHV-1?

A
  • Trigeminal nerve (respiratory)

- Sciatic nerve (genital)

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10
Q

Clinical signs of the respiratory form of BHV-1

A
  • red nose: inflamed nares, hyperemia
  • rhinitis, laryngitis, tracheitis
  • anorexia, fever, depression, serous discharge
  • nasal lesions with numerous clusters of grayish necrotic foci on mucus membranes
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11
Q

Clinical signs of ocular form of IBR

A
  • conjunctivitis
  • ocular discharge
  • lesions confined to conjunctiva, inflamed, reddened, edematous
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12
Q

Clinical signs of Systemic Disease of Newborn Calves

A
  • severe in calves less than 10 days
  • generalized disease with pyrexia, diarrhea, respiratory distress, ocular discharge, incoordination, convulsions, and death
  • small ulcers in forestomachs, peritonitis
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13
Q

Clinical signs of genital form of BHV-1

IPV and Balanoposthitis

A
IPV: frequent urination
- vaginal mucosa red and swollen
- elevated tail position
- vaginal discharge
- swollen vulva, red spots, pustules
B: inflammation and pustules in mucosa of penis and prepuce
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14
Q

Bovine Herpesvirus-2

subfamily, diseases caused

A
  • Alphaherpesvirinae
  • Bovine Ulcerative Mammillitis
  • Pseudo Lumpy Skin Disease
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15
Q

Bovine Ulcerative Mammilitis Clinical signs and Transmission

A
  • teats swollen and painful, bluish skin, exudes serum
  • reduction in milk yield
  • mastitis
  • direct contact through damaged skin, and mechanical by arthropods
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16
Q

Pseudo-Lumpy Skin Disease clinical signs and transmission

A
  • mild fever
  • skin nodules with flat surface and depressed center on epidermis
  • mechanical by arthropods
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17
Q

Pseudorabies

subfamily, etiology, hosts

A
  • Alphaherpesvirinae
  • Porcine Herpesvirus 1/Suid Herpesvirus 1
  • disease of swine
  • wide range of secondary hosts
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18
Q

Transmission of Pseudorabies in primary and secondary hosts

A

Swine: recovered pigs are carriers
- transmitted by rodent reservoirs
- virus shed in saliva, nasal discharge, milk
- licking, biting, aerosol, ingestion of carcass, water, or feed
Dogs/Cats: ingestion of infected carcassas
Cattle: direct contact with infected pigs

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19
Q

Pathogenesis of Pseudorabies in Swine

site of replication, spread

A
  • site of replication is upper respiratory tract
  • spreads via lymphatics to lymph nodes
  • virema spreads to other organs
  • spreads to CNS via cranial nerves
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20
Q

Pseudorabies clinical signs in swine

A
  • febrile response, anorexia, weight loss
  • piglets: 100% mortality, CNS disease
  • pregnant sows: 50% abortion, before 30th day, death and reabsorption, later, stillborn, weak, or normal piglets
  • older piglets: mild disease, respiratory signs, CNS signs
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21
Q

Describe the necropsy findings of a pig with pseudorabies

A
  • serous to fibrinous rhinitis
  • necrotic tonsilitis
  • liver and spleen with yellow-white necrotic foci
  • necrotic placentitis and endometritis
  • CNS: perivascular cuffing
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22
Q

Clinical Signs of Pseudorabies in secondary hosts

A
Cattle: intense pruritis, frenzy
- progressive CNS signs
- death from respiratory failure
Dogs: pruritis frenzy, self-mutilation
- paralysis of jaw and pharynx
- plaintive howling
Cats: rapid development so possibly no pruritis
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23
Q

Equine Herpesvirus 1 transmission and latency sites

A
  • inhalation of infected aerosols, direct or indirect contact with nasal discharges, aborted fetuses, or placental fluids
  • sites of latency: tissues of CNS (trigeminal ganglia), and lymph system
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24
Q

Equine Herpesvirus 1 pathogenesis

A
  • route of infection is the respiratory tract
  • infects endothelial cells of lamina propria
  • infected phagocytes drain in lymph and enter circulation
  • main lesion: infection of endothelial cells, leading to vascular necrosis, thrombus formation, and death to tissues
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25
Q

How does EHV-1 cause immunosuppression?

A

codes a protein that inhibits TAP protein, thereby blocking delivery of the antigen to class 1 MHC molecules

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26
Q

Clinical Signs of respiratory disease caused by EHV-1

A
  • in younger horses
  • rhinopneumonitis
  • fever, bilateral nasal discharge, coughing, inappetence, and depression
  • secondary bacterial infections
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27
Q

Clinical Signs of encephalomyeopathy caused by EHV-1

A
  • immune-mediated vasculitis leading to infarction and hemorrhage within the brain and spinal cord
  • severity ranges from hind limb incoordination to quadriplegia resulting in death
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28
Q

Clinical Signs of reproductive form of EHV-1

A
  • abortions occur in last trimester
  • reproductive efficiency not compromised
  • abortion storms
29
Q

What disease is caused by Equine Herpesvirus 4?

- What subfamily?

A

Equine Viral Rhinopneumonitis

- alphaherpesvirus

30
Q

Clinical signs of Equine Viral Rhinopneumonitis

A
  • rarely causes abortion
  • upper respiratory tract disease
  • nasal discharge, coughing, fever, increased lung sounds
31
Q

What disease is caused by Canine Herpesvirus 1?

What subfamily is it?

A

Hemorrhagic Disease of Puppies
“Fading Puppy Syndrome”
- alphaherpesvirus

32
Q

Transmission of CHV-1

A

Neonates: contact with infected oral, nasal, or vaginal secretions of mom or littermates
- in-utero transmission
- passage through birth canal
- fomites
Older dogs: venereal
- contact with saliva, nasal discharge, or urine of infected dogs

33
Q

Pathogenesis of CHV-1 systemic neonatal infection

A
  • replication in nasal epithelium, tonsils, and pharynx
  • leukocyte associated viremia
  • replication in endothelial cells
  • diffuse necrotizing vasculitis, hemorrhagic necrosis in several organs
  • thrombocytopenia, DIC
  • temp of puppy is critical
34
Q

Clinical Signs of Fading Puppy Syndrome

A
  • painful crying
  • abdominal pain
  • anorexia
  • dyspnea
  • soft, odorless, green stool
  • no elevation in body temp
35
Q

Clinical signs of Fading Puppy Syndrome in bitches

A
  • generally asymptomatic
  • vaginal hyperemia, vesicular vaginitis with discharge
  • in-utero infection may result in abortion, stillbirth, mummified fetus, or infertility
36
Q

What disease is caused by Feline Herpesvirus 1?

What subfamily is it?

A

Feline Rhinotracheitis

  • infectious respiratory disease
  • alphaherpesvirus
37
Q

Transmission of Feline Rhinotracheitis

A
  • shed in ocular, nasal, and oral secretions
  • spread by direct contact with infected cat
  • routes: nasal, oral, conjunctival
  • all recovered cats become carriers
38
Q

Pathogenesis of Feline Rhinotracheitis

A
  • replication in mucosa of the nasal septum, turbinates, nasopharynx, and tonsils
  • viremia is rare, replication restricted to low temperature
  • areas of multifocal epithelial necrosis, inflammation, and fibrinous exudation
  • secondary bacterial infections
39
Q

Clinical Signs of Feline Rhinotracheitis

A

Kittens: severe upper resp disease
- rhinotracheitis, fatal bronchopneumonia
- conjunctivitis and ulcerative keratitis
Adults: mild or subclinical
Pregnant: abortion

40
Q

Explain the use of Fluorescein Ophthalamic Strips

A
  • detection of corneal ulcers
  • intact corneal epithelium has high lipid content, and resists the penetration of fluroescein
  • a break in the corneal epithelium allows fluorescein to be absorbed, therefore dying the ulcer
41
Q

What types of vaccines are available for Feline Rhinotracheitis?

A
  • modified live parenterally
  • modified live intranasally
  • inactivated parenterally
42
Q

What avian diseases are caused by Alphaherpesviruses?

A
  • Infectious Laryngotracheitis

- Marek’s Disease

43
Q

Infectious Laryngotracheitis

subfamily, etiology, hosts

A
  • Alphaherpesvirus
  • Gallid herpesvirus 1
  • contagious infection of chickens
44
Q

Transmission of Infectious Laryngotracheitis

A
  • mostly by inhalation
  • droplets to conjunctiva
  • possible by ingestion
  • recovered chickens can become carriers
  • fomites
  • mechanical via scavengers
45
Q

Pathogenesis of Infectious Laryngotracheitis

A
  • characterized by necrosis, hemorrhage, ulceration, and formation of diphtheritic membranes
  • diphtheritic membranes can block trachea, resulting in asphyxia
  • latency in trigeminal ganglion
46
Q

Clinical Signs of Infectious Laryngotracheitis

A
  • mild coughing, sneezing, nasal/ocular discharge, dsypnea, gasping, depression
  • head shaking with cough, pump handle respiration, coughing up blood
47
Q

What types of vaccines are available for Infectious Laryngotracheitis

A
  • chick embryo origin: induce better immunity, but can revert to virulence
  • tissue culture origin: eye drop, does not revert to virulence, limited immunity
  • a pox-vectored recombinant vaccine
48
Q

Marek’s Disease

subfamily, etiology, other names, hosts

A
  • alphaherpesvirus
  • Gallid herpesvirus 2
  • fowl paralysis, range paralysis, polyneuritis
  • chickens mainly
  • turkeys, quail, pheasants
49
Q

Transmission of Marek’s disease

A
  • highly contagious (reportable)

- inhalation of feather debris, dander, dust

50
Q

What are the 4 pathotypes of Gallid Herpesvirus 2?

A
  • mild: associated with neural MD, preventable with HVT
  • virulent: high incidence of neural and visceral lymphomas, preventable with HVT
  • very virulent: high incidence of neural and visceral lymphomas, oncogenic with HVT, preventable with bivalent vaccines
  • very virulent plus: high incidence of neural and visceral lymphomas, oncogenic with bivalent vaccines
51
Q

Pathogenesis of a fully productive infection of Marek’s Disease

A
  • production of enveloped virions and cell death
  • only in feather follicle epithelium
  • infected T cells act as Trojan horse for virus to enter follicle epithelium
52
Q

Pathogenesis of a productive-restrictive infection of Marek’s Disease

A
  • production of naked virions and viral antigens
  • cell death due to lysis
  • occurs in B cells and activated T cells
  • immunosuppression
53
Q

Pathogenesis of a non-productive infection of Marek’s Disease

A
  • viral genome persists in T cells

- no antigens expressed

54
Q

Pathogenesis of a non-productive neoplastic transformation of Marek’s Disease

A
  • some latently infected T cells undergo neoplastic transformation
  • a new antigen, MATSA, appears in transformed T cells
55
Q

Which haplotype chickens are susceptible to Marek’s, and which are not?

A
  • B19 susceptible

- B21 resistant

56
Q

Clinical Signs of Marek’s Disease

A
  • neurolymphomatosis: enlargement of nerve trunks, edematous grey yellow, lameness, droopy wings, paresis of legs, limberneck
  • visceral lymphomatosis: lymphoid tumors is various organs
  • ocular lymphomatosis: graying of iris, abnormal pupil constrict/dilate, blindness
  • cutaneous lymphomatosis: large nodular lesions on skin, enlarged feather follicles
57
Q

General Features of subfamily Betaherpesvirus

A
  • slow replication
  • associated with chronic infections
  • infected cells often enlarged
  • latent form in secretory glands and lymphoreticular cells
  • continuous viral excretion
58
Q

Inclusion Body Rhinitis

subfamily, etiology, host

A
  • Betaherpesvirinae
  • Porcine Herpesvirus 2: Porcine cytomegalovirus
  • pigs 2-10 weeks old
59
Q

Pathogenesis of Inclusion Body Rhinitis

A
  • widespread petechiae and edema
  • common in thoracic cavity and SQ tissues
  • replication in nasal mucosal glands and epithelial cells of upper resp tract
  • viremia
  • infected cells are enlarged and possess intranuclear inclusion bodies
60
Q

Clinical Signs of Inclusion Body Rhinitis

A
  • mucopurulent rhinitis with violent sneezing, resp distress, conjunctivitis, shivering, mouth breathing
  • neonates appear weak, anemic, or stunted
  • fetal mummification, stillbirths, neonatal deaths
  • subclinical disease in older animals
61
Q

General Features of Subfamily: Gammaherpesvirinae

A
  • replicate in B or T lymphocytes
  • slowly cytopathic for epithelial and fibroblastic cells
  • latency in lymphoid tissue
62
Q

Malignant Catarrhal Fever

subfamily, etiologies, host

A
  • gammaherpesvirinae
  • alcephaline herpesvirus 1 (wildebeest), ovine herpesvirus 2 (sheep)
  • highly fatal disease of cattle and some wild ruminants
63
Q

Wildebeest-Associated MCF

distribution and transmission

A
  • African countries
  • present in nasal and ocular secretions of young wildebeest in cell-free state
  • ingestion of contaminated pasture
  • direct or close contact, inhalation, or aerosol
  • rarely transmitted from adults
64
Q

Sheep-Associated MCF

distribution, transmission

A
  • worldwide
  • between sheep: respiratory, nasal secretions
  • sheep to cattle: unknown, by inhalation or ingestion
65
Q

Transmission of MCF viruses in cattle

A
  • cattle are dead-end hosts
  • no transmission between cattle
  • have cell-associated virus, no cell-free virus, in secretions
66
Q

Pathogenesis of MCF

A
  • cell-associated viremia
  • lymphoid proliferation and infiltration
  • necrotizing vasculitis
  • CD8 T cells associated with vascular lesions
67
Q

Clinical Signs of MCF in cattle

A

Peracute: sudden death
- high fever, acute gastroenteritis
Head and Eye: majority of cattle
- reddened eyelids, corneal opacity, crusty muzzle, nasal discharge, salivation
- erosions of tongue, hard palate, and buccal papillae
- joints, swollen lymph nodes
- incoordination, head pressing, nystagmis

68
Q

Necropsy findings of MCF in cattle

A
  • enlarge prescapular lymph node
  • mucoid exudate over nasal mucosa
  • zebra striping: severe longitudinal linear congestion of mucosa
  • multiple pale foci of necrosis and ulcers in omasum
  • lymphoid infiltration in renal cortex