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Virology DNA Viruses > Family: Herpesviridae, Subfamily: Alphaherpesvirinae > Flashcards

Family: Herpesviridae, Subfamily: Alphaherpesvirinae Flashcards

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1
Q

Virus morphology for family Herpesviridae

A

Eneveloped, spherical
Icosahedral capsid, T=16
Capsid consists of 162 capsomeres and is surrounded by a layer of globular material, known as tegument

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2
Q

Viral genome for family Herpesviridae

A

Monopartite (non-segmented), linear, double-stranded DNA genome

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3
Q

Herpesvirus genes fall into 3 categories

A
  1. those encoding proteins concerned with regulatory functions and virus replication (immediate early and early gnees)
  2. those encoding structural proteins (late genes)
  3. a heterologous set of “optional” genes; they are not found in all herpesviruses and are not required for replication
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4
Q

Viral replication of family Herpesviridae

A

DNA replication and encapsidation occur in the nucleus
Viral envelope is acquired by budding through the inner layer of the nuclear envelope (instead of cytoplasmic membrane like other viruses)
Mature virions accumulate within vacuoles in the cytoplasm and are released by exocytosis or cytolysis

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5
Q

Infection with Herpesviruses

A

Persistent infection with periodic or continuous shedding occurs in all herpesvirus infections
Sheddig of virus in nasal, oral, or genital secretions provides the source of infection for others
reactivation of latent herpesvirus infection is associated with stress

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6
Q

Inclusion bodies of Herpesviruses

A

Eosinophilic intranuclear inclusion bodies
Known as Type A Cowdry bodies
Inclusion bodies are composed of nucleic acid and protein

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7
Q

Bovine Herpesvirus 1 etiology

A 
Only one serotype of BHV-1 is recognized
3 subtypes of BHV-1:
BHV-1.1 = respiratory subtype
BHV-1.2 = genital subtype
BHV-1.3 = encephalitic subtype
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8
Q

Transmission of Bovine Herpesvirus 1

A

Respiratory disease and conjunctivitis result from droplet transmission
Genital disease may result from coitus or artificial insemination with infective semen

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9
Q

Pathogenesis of Bovine Herpesvirus 1

A

Dissemination from the initial focus of infection occurs via cell-associated viremia
In both genital and respiratory forms, the lesions are focal areas of epithelial cell necrosis in which there is ballooning of epithelial cells

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10
Q

Sites of Latency of Bovine Herpesvirus 1

A

Life-long infection with periodic shedding, source of new outbreaks
All seropositive animals are considered carriers

Trigeminal nerve = respiratory disease
Sciatic nerve = genital disease

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11
Q

Clinical signs of respiratory form of Bovine Herpesvirus 1

A

Red nose, Necrotic Rhinitis, Dust pneumonia
Inflamed nares give the appearance of having a “red nose” due to hyperemia
Nasal discharge becomes profuse and mucopurulent

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12
Q

Clinical signs of ocular form of IBR

A

Conjunctivitis is a common finding in “red nose”
Profuse ocular discharge
Do not misdiagnose as Pink Eye (Moraxella bovis) - IBR lesions are confined to the conjunctiva and no lesions on cornea except diffuse edema

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13
Q

Genital disease form of Bovine Herpesvirus 1

A

Infectious Pustular Vaginitis (IPV)
Frequent urination
Tail held in an elevated position and excessive tail switching
Balanoposthitis - inflammation and pustules in the mucosa of the penis and prepuce

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14
Q

Bovine Herpesvirus 2

Bovine ulcerative mammilitis

A

Direct contact and fomite mediate, through trauma to skin
Mechanical transmission by stable flies and other arthropods
Teat is swollen and painful, bluish skin, exudes serum, raw ulcers
High incidence of mastitis (reduction in milk yield)

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15
Q

Bovine Herpesvirus 2

Pseudo-lumpy Skin Disease

A

Mechanicla transmission by arthropods
Mild fever, followed by sudden appearance of skin nodules on the face, neck, back, and perineum
Shorter course of disease than Lumpy-skin diseae

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16
Q

Porcine Herpesvirus 1 common names

A

Pseudorabies

Aujeszky disease, Mad itch

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17
Q

Transmission of Porcine Herpesvirus 1 in primary host

A

Recovered pigs act as primary reservoirs and are latent carriers of the virus
Virus shed in saliva, nasal discharges, and milk of infected pigs
Transmission can occur by licking, biting, aerosol, ingestion of contaminated carcass, water, and feed

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18
Q

Transmission of Porcine Herpesvirus 1 in secondary host

A

Dogs and Cats = ingestion of infected pig carcass/meat, or rodents
Cattle = direct contact with infected pigs oral and nasal routes

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19
Q

Pathogenesis of Porcine Herpesvirus 1

A

Primary site of viral replication is the upper respiratory tract
Virus replicates in tonsils and nasopharynx
Brief viremia with virulent strains, with localization of virus in organs

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20
Q

Pathogenesis of Porcine Herpesvirus 1 in the CNS

A

Virus spreads to CNS via axons of cranial nerves with preference for neurons of the pons and medulla
CNS lesions - ganglioneuritis, nonsuppurative meningoencephalis, perivascular cuffing

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21
Q

Clinical signs of Porcine Herpesvirus 1

-sow, piglets, fattening pigs

A

Sows - poor fertility, abortion, stillbirth mummies, weak piglets, failure to farrow
Piglets - nervous signs, death
Fattening pigs - retarded growth

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22
Q

Clinical signs depending on age of Porcine Herpesvirus 1

A

Nonimmune piglets = 100% mortality
Nonimmune pregnant sows = 50% abortion rate
Older piglets, growers, and adults pigs = mild disease

A generalized febrile response, anorexia, and weight loss in infected pigs of all ages

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23
Q

Piglets born to nonimmune sows with Porcine Herpesvirus 1

A

Most susceptible

CNS disease signs - incoordination of hindlimbs, fitting, tremors, and paddling

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24
Q

Weaned pigs and growing pigs with Porcine Herpesvirus 1

A

CNS signs may be reduced and an increased in respiratory signs
Listlessness, depression, sneezing, coughing, fever, vomiting
Incoordination and pronounced muscle spasm

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25
Nonimmune pregnant sows with Porcine Herpesvirus 1
Infection before 30th day of gestation = death and resorption of embryo Infection in late pregnancy = mummified, macerated, stillborn, weak, or normal swine Sows can be infertile on next breeding, but eventually conceive
26
Pseudorabies in secondary hosts
Cattle Dogs Cats
27
Pseudorabies in Cattle
``` Maditche intense pruritis cattle may become frenzied progressive involvement of CNS, paralyssi, ataxia death from respiratory failure ```
28
Pseudorabies in Dogs
frenzy associated with pruritis, self-mutilation paralysis of jaws and pharynx with drooling of saliva plaintive howling unlike rabies, dogs do not tend to attack
29
Pseudorabies in Cats
disease progresses so rapidly that pruritis may not be observed
30
Vaccination for Porcine Herpesvirus 1
Do not prevent infection, but can alleviate clinical signs
31
Transmission of Equine Herpesvirus 1
Inhalation of infected aerosols, direct or indirect contact with nasal discharges, aborted fetuses, placenta, or placental fluids
32
Latent EHV-1
Latency of EHV-1 allows the virus to survive and spread Latent EHV-1 can reside in tissues of the CNS (trigeminal ganglia) and lymph system without causing any clinical symptoms
33
Pathogenesis of EHV-1
Principal route of EHV-1 transmission is the respiratory tract Virus infected mononuclear cells and T lymphocytes are released into circulation causing viremia Reactivation results in shedding of virus from nasal epithelium and uterine infection Cell-associated viremia confers protection from the body's immune defenses and allows the virus to spread to endothelial cells lining blood vessels in the CNS and pregnant uterus, resulting in CNS signs or abortion
34
Central lesion caused by EHV-1
An infection of endothelial cells, leading to vascular necrosis, thrombus formation and death to the tissues serviced by these blood vessels (ischemia) is responsible for the three types of conditions seen - respiratory, reproductive, and CNS
35
Immunosuppression of EHV-1
EHV-1 codes a protein that inhibits TAP protein, thereby blocking delivery of antigen to class 1 MHC molecules
36
3 types of conditons of EHV-1
Respiratory disease Encephalomyelopathy Reproductive form
37
Respiratorydisease of EHV-1
Mostly younger horses Rhinopneumonitis Fever, bilateral nasal discharge, coughing, inappetence, and depression
38
Encephalomyelopathy (EHM) of EHV-1
Horses of any age or breed Characterized by immune-mediated vasculitis leading to infarction and hemorrhage within brain and spinal cord Range from hindlimb incoordinatiion to quadriplegia and recumbency resulting in death
39
Reproductive form of EHV-1
Majority of abortions occur in the last trimester Reproductive efficiency is not compromised If susceptible mares are exposed to the aborted conceptus the abortion outbreaks can Natural immunity to EHV-1 about 2-3 years, thus abortion storms are in 3 year cycles
40
Transmission of EHV-4
Sporadic infections Mostly in horses under 2 years of age Causes a lifelong latent infection Droplet infection from infected horses and older horses in which viral shedding occurs
41
Pathogenesis of EHV-4
Less severe tissue destruction Rarely causes abortion Rarely results in viremia Rarely results in death
42
Clinical signs of EHV-4
Upper respiratory tract diseae (rhinopharyngitis and tracheobronchitis) Nasal discharge that may progress into a mucoid or mucopurulent discharge, increased lung sounds, mild coughing, fever
43
Vaccination of EHV-4
Ideal vaccine prevents early infection of suckling foals as well as latency of infection in pregnant mares Infected mare passes EHV-4 to foal = target for vaccination to limit viral infection of foal from shedding by infected mares Infected foal sheds the virus acting as a source of infection for other pregnant mares = target for vaccination limiting transmission from infected foals to pregnant mares
44
Common name of Canine Herpesvirus 1
Hemorrhagic disease of puppies | Fading puppy syndrome
45
CHV-1 Transmission
Neonates - contact with infected oral, nasal, or vaginal secretions of dam; in-utero transmission; from passage through birth canal; contact with secretions of littermates Older dogs - veneral transmission; contact with saliva, nasal discharge, or urine
46
In-utero infection pathogenesis of CHV-1
Abortion, stillbirth, infertility | If the pup survives, it will most likely develop systemic CHV-1 infections
47
Systemic neonatal infection pathogenesis of CHV-1
Initial replication in nasal epithelium, tonsils, and pharynx Mucosal invasion is followed by leukocyte (macrophage)-associated viremia Diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in organs Thrombocytopenia, DIC
48
CNS infection pathogenesis of CHV-1
Meningoencephalitis occurs in oro-nasally infected neonatal puppies Virus may travel up nerve axons to CNS Puppies die from systemic infection before neurologic signs are seen
49
Factors governing systemic neonatal infection of CHV-1
1. Body temperature of puppies: CHV-1 replicates at 33 C, the temperature of the outer genital and upper respiratory tracts the more sever the hypothermia, the more severe and rapid the course of disease 2. Maternal immunity: maternal Abs provide protection pups born from seronegative bitches are highly vulnerable to severe disease
50
Clinical signs of CHV-1 in puppies
Painful crying, abdominal pain, anorexia, dyspnea Passing soft, odorless, greenish stool No elevation in body temperature Those that survive systemic disease develop persistent neurologic signs, such as ataxia, blindness
51
Pathogenesis of CHV-1 in adults
1. Genital infections Female: asymptomatic; vesicular vaginitis with discharges; abortion, stillorn, mummified fetuses Male: balanoposthitis 2. Respiratory infections (rhinitis and pharyngitis) 3. Ocular infection (conjunctivitis)
52
Control of CHV-1
Reduce hypothermia by providing heated whelping boxes, or placing puppies under an infrared lamp Isolated of infected bitch and her litter Low prevalence of severe illness in pups and paucity of clinical signs in adult animals has resulted in lack of availability of vaccines
53
Feline herpesvirus 1 commone name and common cause of....
Feline Rhinotracheitis | One of the two most common causes of infectious respiratory diseases in cats, the other is feline calicivirus (FCV)
54
Transmission of FHV-1
Shed primarily in ocular, nasal, and oral secretions Spread largely by direct contact with an infected cat All recovered cats become latently infected carriers
55
Pathogenesis of FHV-1
Virus replication takes place in the mucosae of nasal septum, tubinates, nasopharynx, and tonsils Viremia is rare as virus replication is restricted to areas of low temperature, upper respiratory tract
56
Clinical signs of FHV-1 in kittens
Sever upper respiratory disease Extensive rhinotracheitis Fatal bronchopneumonia (from secondary bacterial infection) Conjunctivitis and ulcerative keratitis
57
Clinical signs of FHV-1 in pregnant queens
Abortion around 6th week of pregnancy No evidence that virus crosses the placenta May be due to severe systemic effects of illness, and not direct effect of virus
58
Diagnosis of FHV-1
Detection of corneal ulcers using Fluorescin Ophthalmic Strips An intact corneal epithelium has a high lipid contect that resists the penetration of fluorescein and so is not colored by it A break in corneal epithelium allows water-soluble fluorescein to be absorbed by the hydrophilic corneal stroma
59
Vaccinations for FHV-1
3 types of FHV-1 and FCV vaccines are avaiable: Modified live virus (MLV) parenterally MLV intranasally Inactivated vaccine parenterally
60
Gallid Herpesvirus 1 common name and host
Infectious Laryngotracheitis | Highly contagious infection of chickens
61
Transmission of GHV-1
Mostly by inhalation Droplets to conjunctiva Recovered and vaccinated chickens can serve as carriers Mechanical transmission through scavengers like vultures, crows, domestic dogs
62
Pathogenesis of GHV-1
Severe laryngotracheitis in affected birds, characteried by necrosis, hemorrhage, ulceration, and the formation of diphtheritic membranes Diphtheritic membrane formation can form a second tube in the trachea, blocking air passage, result in death from asphyxia Trigeminal ganglion is target for viral latency
63
Clinical signs of severe form of GHV-1
Respiratory distress, head shaking and coughing Neck is raised and head is extended during inspiration -> pump handle respiration Cough can result in explosion of bloody mucous
64
Clinical signs of less virulent GHV-1
Low virulent strains are associated with conjunctivitis, ocular discharge, swollen infraorbital and nasal sinuses, and decreased egg production
65
Clinical signs of mild enzootic form of GHV-1
The mild enzootic form is the most common in modern poultry production Severe epizootic form is uncommon
66
Diagnosis of GHV-1
Necropsy findings - tracheal plug (diphtheric membrane)
67
Vaccination of GHV-1
1. Chick embryo origin (CEO) - vaccines have the capability of reverting to virulence and causing ILT signs; induce better immunity 2. Tissue culture origin (TCO) - vaccines are given by eye drop and does not spread or revert to virulence; level of induced immunity is limited 3. A pox-vectored recombinant vaccine
68
Gallid Herpesvirus 2 common name and hosts
Marek's Disease Very important disease of poultry Chickens are the most important natural host
69
Transmission of GHV-2
Inhalation of infectious feather debris, chicken dander, or dust Cell free viruses release from feather follicles are highly infectious, but labile Viruses in desquamated cells (dander) are less infectious, but can survive in poultry house dust or litter
70
4 pathotypes of GHV-2
1. Mild (mMDV) - neural MD; preventable with HVT (turkey herpesvirus vaccine) 2. Virulent (vMDV) - neural and visceral lymphomas; preventable with HVT 3. Very virulent (vvMDV) - neural and visceral lymphomas; oncogenic in HVT vaccinated chickens; preventable with bivalent vaccines 4. Very virulent plus (vv+MDV) - neural and visceral lymphomas; oncogenic in chickens vaccinated with bivalent vaccines
71
Pathogenesis of fully productive infection of GHV-2
Production of enveloped virions and cell death (lysis) Occurs only in feather follicle epithelium Infected T cells are the 'Trojan Horse' by which MDV enters the feather follicle epithelium
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Pathogenesis of productive-restrictive infection of GHV-2
Production of naked virions (not infectious) and viral antigens Cell death (lysis) Occurs in B ells and activated T cells Profound immunosuppression
73
Pathogenesis of non-productive infection of GHV-2
Viral genome persists in T cells | No antigens expressed
74
Pathogenesis of non-productive neoplastic transformation of GHV-2
Latently infected T cells undergo neoplastic transformation | New antigen, MATSA (Marek's diseae associated tumor specific antigen), appears in transformed T cells
75
Genetic susceptibility of GHV-2
Susceptibility varies depending on different MHC II halotypes B19 halotype chickens are highly susceptible to MD B21 halotype chickens are genetically resistant to MD
76
Neuolymphomatosis of GHV-2
Enlargement of nerve trunks Peripheral nerves become enlarged and lose their striations Edematous, grey or yellowish appearance Lameness, droopy wings ,paresis of legs (one leg forward and the other backward, limberneck, torticollis, incoordination
77
Visceral lymphomatosis of GHV-2
Diffuse or nodular lymphoid tumors in organs (liver, spleen, gonads, heart, lung, kidney, muscle, proventriculus) Bursa is rarely tumerous and frequently atrophic Absence fo bursal tumors helps distinguish the diseae from lymphoid leukosis
78
Ocular lymphomatosis of GHV-2
Graying of the iris Interference with normal pupular constriction and dilation Due to T cell infiltration Partial or total blindness
79
Cutaneous lymphomatosis of GHV-2
Plucking of feathers reveal nodular lesions on skin | Enlarged feather follicles (skin leukosis)
80
Control of GHV-2
Reportable disease Most widely used vaccine consists of turkey herpesvirus (HVT) Bivalent vaccines consist of HVT and either SB-1 or 301B/1 strains of GHV-3

Virology DNA Viruses (11 decks)

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