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exam virology > 9. Herpesvirales > Flashcards

9. Herpesvirales Flashcards

1
Q

MEMBERS OF THE FAMILY HERPESVIRIDAE (3 subfamilies)

A
  1. ALPHAHERPESVIRINAE,
  2. BETAHERPESVIRINAE,
  3. GAMMAHERPESVIRINAE
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2
Q

Which viruses are:

Virions are enveloped and variably sized (approximately 200-300 nm in diameter), containing an icosahedral nucleocapsid of approximately 125 nm composed of 162 capsomers

Genome is linear dsDNA, 108-300 kbp in size Replication occurs in the nucleus, with sequential transcription and translation of immediate early (α), early (β), and late (γ) genes producing α, β, and γ proteins, respectively; the α proteins are mainly transcription factors regulating expression of β proteins involved in DNA replication and transcription and the structural γ proteins DNA replication and encapsidation occur in the nucleus; there are two envelopments.

The primary enveloped is acquired by budding through the inner layer of the nuclear envelope, which is lost by fusion with the outer nuclear membrane. Final envelopment occurs at Golgi or endosomal vesicles Infection results in characteristic eosinophilic intranuclear inclusion bodies Infection becomes latent, with recrudescence and intermittent virus shedding

A

Herpesviruses

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3
Q

Characteristics Common to Many HERPESVIRUS Infections

A
  • Transmission is generally associated with direct mucosal contact, but droplet and fomite infection is also common.
  • Moist, cool environmental conditions promote extended survival of herpesviruses, especially when the virus is not subject to exposure to ultraviolet light.
  • typically produce severe disease only in neonates, fetuses, immunocompromised individuals, or in nondefinitive (alternate) host species (species jumping)
  • In pregnant animals, a mononuclear-cell-associated viremia may result in the transfer of alphaherpesviruses across the placenta, leading to abortion, characteristically with multifocal areas of necrosis in several fetal organs.
  • Many alphaherpesviruses produce localized lesions, particularly in the skin or on the mucosae of the respiratory and genital tracts
  • Infections with the beta- and gammaherpesvirus are often clinically silent, (especially in mammals).
  • Persistent infection with periodic or continuous shedding
    *
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4
Q

Species of Avian Alphaherpesviruses (Fam. Herpesviridae, Subfamily Alphaherpesvirinae) (5)

A

ANATID HERPESVIRUS 1 (DUCK VIRAL ENTERITIS VIRUS OR DUCK PLAGUE VIRUS),

GALLID HERPESVIRUS 1 (AVIAN INFECTIOUS LARYNGOTRACHEITIS VIRUS),

PSITTACID HERPESVIRUS 1 (PACHECOíS DISEASE VIRUS),

GALLID HERPESVIRUS 2 (MAREK’S DISEASE VIRUS),

COLUMBID HERPESVIRUS 1 (PIGEON HERPESVIRUS)

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5
Q

Host range and geographical distribution of Duck Viral Enteritis or Duck Plague

A

Duck viral enteritis or duck plague, occurs worldwide among domestic and wild ducks, geese, swans, and other waterfowl.

Commercial duck operations in Europe and particularly Asia are affected.

Migratory waterfowl contribute to spread within and between continents. Major epizootics have occurred in duck farms in the United States and occasionally in wild waterfowl.

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6
Q

Method of transmission of duck viral enteritis or duck plague

A

Ingestion of contaminated water is believed to be the major mode of transmission, but the virus may also be transmitted by contact.

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7
Q

Clinical signs of duck viral enteritis or duck plague

A

The incubation period is 3-7 days.

  • There is anorexia, listlessness, nasal discharge, ruffled dull feathers, adherent eyelids, photophobia, extreme thirst, ataxia leading to recumbency with outstretched wings and with head extended forward, tremors, watery diarrhea, and soiled vents.
  • Most ducks that develop clinical signs die, and sick wild ducks often conceal themselves and die in vegetation at the water’s edge.
  • Commonly there is multifocal ulceration of mucosa of gastrointestinal tract and multiple pale foci of necrosis in spleen and liver.
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8
Q

Differential diagnosis of duck viral enteritis or duck plague

A

To be differentiated from hepatitis caused by picornavirus or astrovirus infections, and from Newcastle disease and avian influenza

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9
Q

Control of duck viral enteritis or duck plague

A

live-attenuated virus vaccines

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10
Q

Host range and geographic distribution of Avian infectious laryngotracheitis

A

Avian infectious laryngotracheitis, caused by gallid herpesvirus 1 (or infectious laryngotracheitis virus), occurs among chickens worldwide. (severe epizootic form has been a problem in some poultry-dense areas, particularly in the southern United States)

Chickens of all ages are susceptible, but disease is most common in those aged 4-18 months.

This virus also causes disease in pheasants, and infections have been identified rarely in peafowl, turkeys, and ducks. After

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11
Q

Clinical symptoms of Avian Infectious Laryngotracheitis

A

Incubation 6-12 days.

  • Most common: Mild coughing and sneezing followed by nasal and ocular discharge, dyspnea, loud gasping and coughing, and depression.
  • Low virulence: conjunctivitis, ocular discharge, swollen infraorbital and nasal sinuses, decreased egg production.
  • Severe cases: neck is raised and head extended during inspiration: ‘pump handle respiration’.
    • Head shaking with coughing is characteristic. Expectoration of bloody mucus and frank blook that appear on the beak, face and feathers.
      *
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12
Q

Morbidity and mortality of avian Infectious laryngotracheitis

A

Morbidity ~100%

Mortality: 50-70% (virulent strains)

~20% (low virulence strains)

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13
Q

Another term for Avian infectious laryngotracheitis

A

‘Fowl diphtheria’ because of formation of diphtheritic membranes which can plug the airway resulting in death from axphysia.

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14
Q

Methods of transmission of avian Infectious laryngotracheitis

A

Infectious laryngotracheitis virus is introduced into a flock via carrier birds.

It is transmitted by:

  • droplet and inhalation,
  • droplet to conjunctiva or
  • by ingestion (exposure to the nasal epithelium through the choanal slit)
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15
Q

Methods of control of avian infectious laryngotracheitis and risks

A
  • Vaccination for breeding and egg prodution flocks.
    • Live-attenuated virus vaccine or vectored recombinant turkey herpesvirus or fowl poxvirus vaccine with infectious laryngotracheitis virus glycoprotein I inserts.
  • Vaccination protects birds against disease but not against infection with virulent virus or the development of a latent carrier status.
  • Outbreaks of acute disease have occurred in broilers as a result of reversion to virulence of live-attenuated chicken embryo origin vaccine virus strains.
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16
Q

Major reservoir of avian infectious laryngotracheitis virus

A

Backyard poultry

17
Q

Species of Bovine Alphaherpesviruses (Fam. Herpesviridae, Subfamily Alphaherpesvirinae) (3)

A
  • BOVINE HERPESVIRUS 1 (INFECTIOUS BOVINE RHINOTRACHEITIS / INFECTIOUS PUSTULAR VULVOVAGINITIS VIRUS),
  • BOVINE HERPESVIRUS 2 (MAMMILLITIS/PSEUDOLUMPY SKIN DISEASE VIRUS),
  • BOVINE HERPESVIRUS 5 (BOVINE ENCEPHALITIS VIRUS)
18
Q

Species of Equine Alphaherpesviruses (Fam. Herpesviridae, Subfamily Alphaherpesvirinae) (4)

A
  • EQUID HERPESVIRUS 1 (EQUINE ABORTION VIRUS),
  • EQUID HERPESVIRUS 3 (EQUINE COITAL EXANTHEMA VIRUS),
  • EQUID HERPESVIRUS 4 (EQUINE RHINOPNEUMONITIS VIRUS),
  • EQUID HERPESVIRUSES 6, 8, AND 9
19
Q

Species of Betaherpesviruses in pigs (Fam. Herpesviridae, Subfamily Betaherpesvirinae) (1)

A

SUID HERPESVIRUS 2 (PORCINE CYTOMEGALOVIRUS VIRUS)

20
Q

Species in Subfamily GAMMAHERPESVIRINAE (Fam. Herpesviridae) (cattle, horse, primates)

A

MALIGNANT CATARRHAL FEVER:

  1. ALCELAPHINE HERPESVIRUS 1 (cattle),
  2. OVINE HERPESVIRUS 2 (sheep)

BOVINE HERPESVIRUSES 4 (Movar Virus)

EQUID HERPESVIRUSES 2, 5, AND 7 (ASININE HERPESVIRUS 2)

PRIMATE HERPESVIRUSES:

  • Human Herpesvirus 4 (Epstein-Barr - mononucleosis),
  • Human Herpesvirus 8 (Kaposi’s sarcoma)
21
Q

Species of Primate Alphaherpesviruses (Fam. Herpesviridae, Subfamily Alphaherpesvirinae) (3)

A

CEROPITHECINE HERPESVIRUS 9 (SIMIAN VARICELLA VIRUS),

MACACINE HERPESVIRUS 1 (B Virus),

HERPES SIMPLEX VIRUS 1 in Animals

22
Q

Species of Alphaherpesviruses in pigs (Fam. Herpesviridae, Subfamily Alphaherpesvirinae) (1)

A

SUID HERPESVIRUS 1 (PSEUDORABIES OR AUJESZKY’S DISEASE VIRUS)

23
Q

Species of Alphaherpesviruses in dogs (Fam. Herpesviridae, Subfamily Alphaherpesvirinae) (1)

A

CANID HERPESVIRUS 1

24
Q

Species of Alphaherpesvirus in Cats (1)

A

FELID HERPESVIRUS 1 (FELINE VIRAL RHINOTRACHEITIS VIRUS)

25
Q

Importance of Marek’s disease

A

Marek’s disease remains an important disease of chickens because of continuing losses from disease and the costs of vaccination.

Before vaccination in 1970, Marek’s disease was the most common lymphproliferative disease of chickens (substantial economic losses worldwide)

26
Q

Clinical symptoms of Marek’s disease

A

Marek’s disease is a progressive disease, variable signs and overlapping pathologic syndromes.

Can resemble avian leukosis; key differences: Lymphoproliferative syndromes are most frequent with Marek’s disease, lymphoma being most common, in several visceral organs and paralysis of one or both legs or wings. Incoordination (common early sign): one leg is held forward and the other backward when the bird is stationary, (unilateral paralysis, usually sciatic nerve). Wing dropping and lowering of the head and neck are common. If the vagus nerve is involved, there may be dilation of the crop and gasping. Marek’s disease lymphoma may occur without neurologic signs, (only depression and comatose state with lymphomas).

  • Acute Marek’s disease or fowl paralysis occurs in explosive outbreaks in young chickens. Depression followed by ataxia and paralysis of some birds. Significant mortality occurs without localizing neurologic signs. Visceral lymphomas absent but nerve lesions are prominent.
  • Ocular lymphomatosis (rare syndrome) that leads to graying of the iris of one or both eyes as a result of infiltration of transformed (neoplastic) lymphocytes; the pupil is irregular and eccentric, and there is partial or total blindness. Mortality is rare and usually older birds are infected.
  • Cutaneous Marek’s disease is recognized after plucking, when round, nodular lesions (up to 1 cm in diameter), at feather follicles of young birds. The nonfeathered area of the legs may have a distinct red coloration, and Marek’s disease is therefore sometimes called “redleg syndrome.”
  • Other:
    • immunosuppression: relatively common with newer and more virulent virus strains and regularly result in full clinical Marek’s disease after several weeks and in death of the animals.
    • Transient paralysis is associated with specific genotypes of chickens linked to specific haplotypes of the major histocompatibility complex (MHC) genes.
27
Q

Methods of transmission of Marek’s disease

A

Inhalation of virus in the dust and dander shed from infected feather follicles that is present in chicken houses, regardless of the vaccination status (virus is also shed by vaccinated birds)

28
Q

Morbidity and mortality of Marek’s virus

A

Epizootics of Marek’s disease usually involve nonvaccinated and sexually immature birds and result in high mortality (about 80%)

29
Q

Method of control of Marek’s disease and threats

A
  • Virtually all commercial layer chickens in the United States are vaccinated against Marek’s disease in ovo at day 18 of embyronation, or at hatching.
    • heterotypic lyophilized cell-free preparation (herpesvirus of turkeys)
    • cell-associated preparation (gallid herpesvirus 3)
    • live-attenuated Marek’s disease virus
  • Also: flocks built up with birds with increased genetic resistance.
  • However,
    • broilers are not regularly vaccinated in Europe and
    • appearance of new “vaccination resistant” virus strains has resulted in the evolution of ever more virulent strains
30
Q

Method of transmission of Marek’s disease virus

A

Inhalation of contaminated dust and dander.

31
Q

Pathogenesis and Pathology of Marek’s disease virus

A
  • Marek’s disease virus is slowly cytopathic and remains highly cell-associated, so that cell-free infectious virus is only produced in the feather follicle epithelium from which it is shed into the environment.
  • Subclinical infection with virus shedding
    is the rule.
  • Infection of lymphoid cells in primary lymphoid organs including the thymus, cloacal bursa (bursa of Fabricius) and spleen results in virus amplification and immunosuppression.
  • From about 4 days after infection, viremia followed by a proliferation of CD4+ T cells. Deaths
  • A subset of CD4+ T lymphocytes is transformed by the virus to produce T-cell lymphomas,
  • Unilateral enlargement of one or more peripheral nerve trunks

exam virology (26 decks)

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