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Test 2- Herpesviridae Flashcards

1
Q

Herpesviridae

A
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2
Q

Family Herpesviridae

 Virus Morphology:

A

 Viruses are enveloped, spherical to pleomorphic in shape.

 150-200 nm in diameter.

 Icosahedral capsid, T=16.

Capsid consists of 162 capsomers and is surrounded by a layer of globular material, known as the tegument.

Glycoproteins complexes are embed in the lipid envelope.

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3
Q

Family Herpesviridae

 Viral Genome:

A

Monopartite (non-segmented), linear, double-stranded DNA genome of 120-220 kb.
 The genome contains terminal and internal reiterated (repeated) sequences.

Herpesvirus genes fall into three general categories:

(1) those encoding proteins concerned with regulatory functions and virus replication (immediate early and early genes).
(2) those encoding structural proteins (late genes).
(3) a heterologous set of “optional” genes, in the sense that they are not found in all herpesviruses and are not essential for replication in cultured cells.

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4
Q

Family Herpesviridae

Viral Replication

A

DNA replication and encapsidation occurs in the nucleus.

 The viral envelope is acquired by budding through the inner layer of the nuclear envelope.

 Mature virions accumulate within vacuoles in the cytoplasm and are released by exocytosis or cytolysis.

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5
Q

Family Herpesviridae

 General Characteristics:

A

Family Herpesviridae

Herpesviruses do not survive well outside of the host.

 General Characteristics:

 Transmission usually requires close contact, especially mucosal contact [coitus,licking, etc.], but droplet infection(less than 1 meter) is also common.

 Moist, cool environmental conditions promote extended survival of herpesviruses, and windy conditions can promote aerosol transmission over longer distances.

Latently infected animals serve as reservoir for transmission.

 Cell-to-cell fusion facilitates spread of infection and virus is not exposed to immune system.

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6
Q

Family Herpesviridae

general statements

A

Persistent infection with periodic or continuous shedding occurs in all herpesvirus infections.

 Some herpesviruses are oncogenic.

Shedding of virus in nasal, oral, or genital secretions provides the source of infection for other animals, including transfer from dam to offspring.

Reactivation of latent herpesvirus infection is usually associated with stress caused by intercurrent infections, shipping, cold, crowding, or by the administration of glucocorticoid drugs.

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7
Q
A

Cowdry type A intranuclear inclusion

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8
Q

Syncytium

A

Virus-specific proteins are also found in the host cell plasma membrane, where they are involved in cell fusion, resulting in formation of Syncytium, or multinucleated giant cells.

Can evade the immune system with these

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9
Q
A

Syncytium caused by HSV-1 infection in Vero cells

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10
Q

Subfamily: Alphaherpesvirinae

A

 Properties of alpha-Herpesviruses:

 Generally highly cytopathic in cell culture, lyse infected cells.

 Relatively short replication cycle.

 In alphaherpesvirus infections, multiple copies of viral DNA are demonstrable, either as episomes, or more rarely integrated into the chromosomal DNA of latently infected neurons.

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11
Q

Subfamily: Alphaherpesvirinae

 Properties of alpha-Herpesviruses:

A

 Some alphaherpesviruses, such as pseudorabies virus (suid herpesvirus 1), have a broad host range, whereas most are highly restricted in their natural host range

 Many alphaherpesviruses produce localized lesions, particularly in the skin or on the mucosae of the respiratory and genital tracts.

 Generalized infections characterized by foci of necrosis in almost any organ or tissue are typical of infection of very young or immunocompromised animals.

 In pregnant animals, a mononuclear-cell-associated viremia may result in the transfer of virus across the placenta, leading to abortion, characteristically with multifocal areas of necrosis in several fetal organs.

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12
Q
A

Focal necrosis seen in liver infected with Equine Herpesvirus 1

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13
Q

Subfamily: Alphaherpesvirinae

 Pattern of infection:

A

 Frequently cause latent infections in sensory ganglia.
 Virus is reactivated from latency by stress or immunosuppression.

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14
Q

Subfamily: Alphaherpesvirinae

Bovine herpesvirus 1

Etiology, Distribution, and Diseases

A

Diseases: Infectious bovine rhinotracheitis, Infectious pustular vulvovaginitis.
Bovine herpes virus 1 has been associated with rhinotracheitis, vulvovaginitis, balanoposthitis, conjunctivitis, abortion, enteritis, and a generalized disease of newborn calves.

Etiology:
 Bovine herpes virus 1 (BHV-1).
 Only a single serotype of BHV-1 is recognized.

 3 subtypes of BHV-1 have been described:

 BHV-1.1 (respiratory subtype)
 BHV-1.2 (genital subtype)
 BHV-1.3 (encephalitic subtype) [Now renamed as bovine herpesvirus 5]

Distribution: Worldwide

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15
Q

Transmission of Bovine herpesvirus 1

A

Transmission:

 Respiratory disease and conjunctivitis result from droplet transmission.

 Genital disease may result from coitus or artificial insemination with infective

semen.

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16
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Pathogenesis:

A

 Within the animal, dissemination of the virus from the initial focus of infection

probably occurs via a cell-associated viremia.

 In both the genital and the respiratory forms of the disease, the lesions are focal areas of epithelial cell necrosis in which there is ballooning of epithelial cells.

 Typical herpesvirus inclusions may be present in nuclei at the periphery of necrotic foci.

 Intense inflammatory response within the necrotic mucosa, frequently with formation of an overlying accumulation of fibrin and cellular debris (pseudomembrane).

 Life-long latent infection with periodic virus shedding occurs after BHV-1

infection.

 These animals are potential source of new outbreaks.

 All seropositive animals are considered as potential carriers.

 Virus can be reactivated from latency by corticosteroids or stress

Sites of Latency:

 Trigeminal nerve: Respiratory disease with BHV-1

 Sciatic nerve: Genital disease with BHV-1

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17
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

Ballooning of the epithelial cells

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18
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Clinical Signs:

A

 Respiratory form (Red Nose, Necrotic Rhinitis, Dust Pneumonia):

 Rhinitis, Laryngitis and Tracheitis.
 Morbidity and mortality are higher in feedlot cattle than in dairy herds.

 Anorexia, fever, depression, serous discharge from eyes and nose.
 Conjunctivitis may or may not be present.

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19
Q
A

Breathing through the mouth and salivation in a bovine affected with IBR.

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20
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Clinical signs:
 Respiratory form:

A

 Respiratory form:
 Inflamed nares give the appearance of having a “red nose”, due to hyperemia.

 Nasal lesions consist of numerous clusters of grayish necrotic foci on the mucous membrane of the septal mucosa.
 Nasal discharge becomes more profuse and mucopurulent.

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21
Q
A

Bovine herpesvirus 1- “red nose”

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22
Q
A

Hemorrhage and Congestion of the Muzzle on left

Fibrinonecrotic Rhinitis on right

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

Clinical signs:
 Respiratory form:

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23
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Clinical signs:
 Respiratory form:

Picture on the left: Hemorrhages and Erosions in the Buccal Mucosa and Gums

Pic on the right: Hemorrhage and Exudates in the Turbinates

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24
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Clinical signs:
 Respiratory form:

Diffuse hemorrhages (cut surface of turbinates)

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25
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

Necrotic Lesions in Epiglottis

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26
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Clinical signs:
 Respiratory form:

A

 Uncomplicated cases recover in 10-14 days
 Complications may result from secondary bacterial infection, such as

Mannheimia hemolytica and Pasteurella multocida (Shipping fever)  Death is usually the result of secondary bronchopneumonia.

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27
Q
A

Fibrinopurulent Bronchopneumonia

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

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28
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

Thrombotic Pneumonia

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29
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Ocular form of IBR:

A

 Ocular form of IBR:
 Conjunctivitis is a common finding in typical “red nose”.  Conjunctiva is inflamed, reddened and edematous.
 Profuse ocular discharge.
 May be unilateral or bilateral.

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30
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Ocular form of IBR:

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31
Q

You have to differentiate bovine herpes virus from…

A

Do not misdiagnose as Pink-Eye: Remember, IBR lesions are confined to the conjunctiva and no lesions on cornea except diffuse edema.

  • Gram-Negative Diplobacilli
  • Keratoconjunctivitis
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32
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Abortion:

A

 Abortion:
 Occurs as a common sequel to natural infection (can occur 100 days after

infection).
 Result of some modified-live virus (MLV) vaccines being given to pregnant animals  Animals in contact with IBR-susceptible pregnant animals.

 Fetuses in the second half of gestation have a higher incidence of abortion, but early embryonic death is also possible.

 Incidence of abortion does not correlate with the severity of disease in the dam, but is often preceded by pustular vulvovaginitis

in pic: Aborted bovine fetus, mid-gestation

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33
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Systemic Disease of Newborn Calves:

A

 Systemic Disease of Newborn Calves:

 Severe in calves less than 10 days of age. Often fatal.

Infected in-utero or right after birth.

 Calves develop a generalized disease with pyrexia, diarrhea, respiratory

distress, ocular discharge, incoordination, eventually convulsions and death.

 Small ulcers of the lining of the forestomachs, and peritonitis.

Hemorrhages in respiratory tract

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34
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Genital Disease:
 IPV (Infectious Pustular Vaginitis)

A

 Genital Disease:
 IPV (Infectious Pustular Vaginitis)

 May occur 1-3 days after coitus.
 Frequent urination
 Tail is usually held in an elevated position and excessive tail switching is noted  Vagina mucosa red and swollen
 Mild vaginal discharge
 Vulva swollen, red spots and discrete pustules may be noted

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35
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

Genital Disease:

A

 Balanoposthitis

Inflammation and pustules in the mucosa of the penis and prepuce

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36
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 1

 Control (Vaccination):

A

 Control (Vaccination):

 Modified live vaccines, subunit and inactivated vaccines are available.

 The subunit vaccines contain the major surface glycoproteins (gB, gC and gD) that

elicit antibody response.

 Combination or Multivalent vaccines containing other respiratory pathogens (BSRV,

BVDV) are also available.

 Parenteral and intranasal vaccine are available.

 Both stimulate the production of humoral antibodies

 The parenteral vaccine may cause abortion in pregnant cows.

 The intranasal vaccine is safe for use in pregnant cows.

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37
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 2

 Bovine Ulcerative Mammillitis

Etiology, distribution, host, transmission

A

 Bovine Ulcerative Mammillitis

 Etiology: BHV-2, rarely BHV-4

 Distribution: Worldwide

 Host: Cattle, heifers, usually within 2 weeks after calving. Large herds may have persistent disease.

 Transmission:
 Direct contact and fomite-mediated, through trauma to skin.

 Mechanical transmission by stable flies and other arthropods.

.

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38
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 2

 Bovine Ulcerative Mammillitis

 Clinical signs:

A

 Bovine Ulcerative Mammillitis  Clinical signs:

 In severe cases, teat is swollen and painful, skin is bluish, exudes serum, formation of raw ulcers.

 Vesicles occur, but not commonly seen.

 Reduction in milk yield.

 High incidence of mastitis.

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39
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 2

 Bovine Ulcerative Mammillitis

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40
Q

Subfamily: Alphaherpesvirinae Bovine herpesvirus 2

 Pseudo-Lumpy Skin Disease

A

 Pseudo-Lumpy Skin Disease

 Cattle are infected.
 Occurs most commonly in southern Africa.
 Mechanical transmission of the virus occurs by arthropods.

 Clinical signs:
 Mild fever, followed by the sudden appearance of skin nodules: a few, or many,

on the face, neck, back, and perineum.
 The nodules have a flat surface with a slightly depressed center, and involve

only the superficial layers of the epidermis, which undergo necrosis.  Shorter course of the disease than Lumpy-Skin Disease

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41
Q
A

Subfamily: Alphaherpesvirinae Bovine herpesvirus 2

 Pseudo-Lumpy Skin Disease

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42
Q

Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)

Etiology and host

A

 Etiology: Porcine herpesvirus 1/Suid herpesvirus 1

 Host:
 Primarily a disease of swine (pigs).
 Diverse range of secondary hosts, including horses, cattle, sheep, goats, dogs,

cats, and many feral species, can become infected and develop disease.

Humans are refractory(resistant) to infection.

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43
Q

Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)

 Transmission in Primary Host and secondary host:

A

Pseudorabies (Aujeszky disease, Mad itch)

Transmission in Primary Host:
 Recovered pigs act as primary reservoirs, and are latent carrier of virus for life.

 Rodents (Rats) can also act as reservoirs, and transmit disease from Farm-to-Farm.

Transmission Routes:
 Virus shed in saliva, nasal discharges and milk of infected pigs.

 Virus not shed in urine or feces.
 Transmission can occur by licking, biting, aerosol, ingestion of contaminated carcass, water and feed.

Transmission in Secondary Host:
 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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44
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

Pathogenesis and Spread of the Virus

A

 Pathogenesis:
After natural infection, the primary site of viral replication is upper respiratory tract.

 Spread of Virus:

 Following infection, virus replicates in tonsils and nasopharynx.

 The virus spreads via the lymphatics to regional lymph nodes, where replication

continues.

 A brief viremia is associated with virulent strains, with localization of virus in

different organs.

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45
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

Virus spread in the CNS and the lesions in the CNS

A

Virus spread in CNS:

 Virus also spreads to CNS via axons of cranial nerves.

 Virus continues to spread within the CNS.

 Preference for neurons of the pons and medulla.

CNS Lesions:

 Ganglioneuritis

 Nonsuppurative meningoencephalitis

 Perivascular cuffing

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46
Q
A

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

CNS lesion

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47
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

Clinical Signs

A

Clinical Signs:

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

The clinical signs in pigs depend on the age of the affected animal.

Nonimmune piglets:
 ~100% mortality rate

Nonimmune pregnant sows:

 ~50% abortion rate

Older piglets, growers, and adult pigs:

 Mild disease; mortality rate < 2%

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48
Q

Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)

Clinical Signs:

A

Clinical Signs:

 A generalized febrile response (41°–42°C [105.8°–107.6°F]), anorexia, and weight loss are seen in infected pigs of all ages.

Pruritus (Itching), a dominant feature in secondary hosts, is rare in Pigs. It is mostly found in secondary hosts!

 Piglets born to nonimmune sows:
Most susceptible. Signs of CNS disease (incoordination of hindlimbs, fitting, tremors and paddling) are more commonly seen.

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49
Q
A

Piglet with outstretched forelimb

Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)

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50
Q
A

Signs of CNS disease

Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch

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51
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

Clinical signs

Weaned pigs and growing pigs:

A

 Weaned pigs and growing pigs:
 Central nervous signs may be reduced and an increase in respiratory signs.
 Respiratory diseases often associated with secondary infections.
 Listlessness, depression, sneezing, coughing, and moderate fever (40°C), vomiting.
 Incoordination and pronounced muscle spasm, circling, and intermittent convulsions.

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52
Q
A

Weaned pig showing signs of severe depression. The animal also presented with pneumonia and head pressing

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

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53
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

 Clinical Signs:

 Nonimmune Pregnant Sows:

A

 Clinical Signs:

 Nonimmune Pregnant Sows:
 Infection before 30th day of gestation result in death and resorption of embryo.  Infection in late pregnancy may result in mummified, macerated, stillborn, weak,

or normal swine.
 Up to 20% of sows aborting are infertile on next breeding, but eventually

conceive.

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54
Q
A

Mummified pigs, a symptom of Pseudorabies

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

 Clinical Signs:

 Nonimmune Pregnant Sows:

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55
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

 Necropsy Findings:

A

 Necropsy Findings:
 Gross lesions are often absent or minimal
 Serous to fibrinous rhinitis is common and a necrotic tonsillitis.
 Liver and spleen typically have yellow-white necrotic foci (2-3 mm)  Necrotic placentitis and endometritis may be observed.

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56
Q
A

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

 Necropsy Findings:

Necrotizing Tonsillitis

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57
Q
A

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

Rhinitis in snout of pig with Pseudorabies

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58
Q

Secondary Hosts

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

A

Secondary Hosts

Ruminants

Dogs

Cats

Goats, Sheep, Horses

Intense pruritus

Hyperacute, Rapid progress, High mortality

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59
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts

 Cattle (Mad Itch):

A

 Cattle (Mad Itch):
 Intense pruritus (Itching).
 Cattle may become frenzied.
 Progressive involvement of CNS, stage of paralysis, ataxia.

 Death from respiratory failure.

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60
Q
A

Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts

 Pruritus—self trauma
 Swollen eyelid due to intense rubbing.  Profuse salivation

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61
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts

Dogs and cats

A

 Dogs:
 Frenzy associated with pruritus. Self-mutilation.
 Paralysis of jaws and pharynx with drooling of saliva  Plaintive howling
 Unlike rabies, the dogs do not tend to attack

 Cats:
 Disease progress so rapidly that pruritus may not be observed.

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62
Q
A

Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts

Dog with pseudorabies and self- mutilation injuries

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63
Q
A

Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts

Paralysis of the Jaws and Pharynx, Profuse Salivation

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64
Q
A
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65
Q

Subfamily: Alphaherpesvirinae Pseudorabies

Dx

A

 Diagnosis:

The history and clinical signs

 Histopathology: Intranuclear eosinophilic inclusion bodies, CNS lesions (perivascular cuffing)

 Serology: Serum neutralization, ELISA, Immunohistochemistry or fluorescent antibody staining of frozen tissue sections

 Nucleic acid detection by PCR

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66
Q

Subfamily: Alphaherpesvirinae Pseudorabies in Pigs

 Vaccination:

A

 Vaccination:

 Vaccination of swine in enzootic areas reduce losses.

 Vaccination do not prevent infection, or establishment of latent infection by wild-

type virus, but can alleviate clinical signs in pigs of certain ages.

 Recombinant DNA, deletion-mutant, live-attenuated, and inactivated vaccines are

available.

 A pseudorabies vaccine from which both the thymidine kinase and a glycoprotein

gene have been deleted is available.

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67
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

A

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

Most virulent equine herpesvirus

 Distribution: EHV-1 is endemic in horse populations around the world

 Transmission: Inhalation of infected aerosols, direct or indirect contact with nasal discharges, aborted fetuses, placenta or placental fluids.

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68
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

Latency:

A

 Latency of EHV-1 maintains the virus:
 Latency of EHV-1 allow the virus to survive and spread within the equine population.

 A latent EHV-1 can reside in tissues of the CNS (neuron cell bodies, specifically the trigeminal ganglia) and lymph system (leukocytes, more specifically lymphocytes) without causing any clinical symptoms of disease.

 When host is immunosuppressed; the virus is then reactivated, causing disease, or shedding of virus once again.

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69
Q

Outcomes of Equine Herpes Virus- 1

A
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70
Q

Life Cycle of Equine Herpes Virus

A
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71
Q

Cell-associated viremia (macrophages, other leukocytes) protects

A

Cell-associated viremia (macrophages, other leukocytes) protects EHV-1 from immune system, allow spread into endothelial lining of blood vessels in the CNS and pregnant uterus

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72
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

 Pathogenesis:
 Immunosuppression

A

EVS -1 codes a protein that inhibits TAP protein, thereby blocking delivery of antigen to class I MHC molecules.

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73
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

 Pathogenesis:

A

 Pathogenesis:

 The principal route of EHV-1 infection is via the respiratory tract.

 Following infection of epithelial cells, EHV-1 infects endothelial cells in the lamina propria.

 Virus-infected mononuclear cells and T lymphocytes subsequently appear in the drainage lymph nodes and are released into the circulation producing viremia.

 Following infection of respiratory epithelium, latent infections are established in circulating T lymphocytes and trigeminal ganglionic neurons.

 Reactivation results in shedding of virus from nasal epithelium and probably uterine infection.

 The central lesion caused by EHV-1 responsible for the three types of conditions seen (Respiratory, reproductive & CNS) is an infection of endothelial cells, leading to vascular necrosis, thrombus formation and subsequent death to the tissues serviced by these blood vessels (Ischemia).

 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 respectively.

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74
Q
A

Pulmonary Consolidation

Subfamily: Alphaherpesvirinae Equine herpes virus 4 (EHV-4)

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75
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

Respiratory Disease

A

Respiratory Disease:

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

 Affects mostly younger horses
 Rhinopneumonitis
 Fever (38.9-41.7 °c), bilateral nasal discharge, coughing, inappetence and depression  Secondary bacterial infections

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76
Q

Subfamily: Alphaherpesvirinae EHV-1 and EHV-4

 Vaccination digram

A
77
Q

ubfamily: Alphaherpesvirinae

Equine herpes virus 1 (EHV-1)

Encephalomyelopathy (EHM, equine herpesvirus myeloencephalopathy)

A

 Encephalomyelopathy (EHM, equine herpesvirus myeloencephalopathy)

 May affect horses of any age or breed.

 Characterized by immune-mediated vasculitis leading to infarction and hemorrhage

within the brain and spinal cord.

 May or may not be preceded by respiratory disease or abortion.

 Severity may range from slight hind limb incoordination of a transient nature to

quadriplegia and recumbency resulting in death.

78
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)

 Reproductive form:

A

 Reproductive form:

 Although abortions may occur early in gestation, the majority occur in the last trimester

(between 8-10 months) of gestation.

 Reproductive efficiency is not compromised.

 Cases of abortion are usually sporadic.

 If large numbers of susceptible mares are exposed to the aborted conceptus, extensive

outbreaks of abortion (abortion storms) occur.

 Natural immunity to the EHV-1 may last 2 to 3 years, thus explaining why “abortion

storms” tend to display 3 year cycles.

79
Q

Subfamily: Alphaherpesvirinae

Equine herpes virus 4 (EHV-4)

Disease, Transmission, distribution

A

Disease: Equine Viral Rhinopneumonitis: EHV-4 antigenically related to EHV-1

Distribution: Worldwide

Transmission:

 Most infections with EHV-4 are sporadic

 Mostly observed in horses under two years of age.

 EHV-4 often causes a lifelong latent infection, which can be reactivated.

 Droplet infection from infected horses and older horses in which inapparent viral

shedding occurs.

80
Q

Subfamily: Alphaherpesvirinae Equine herpes virus 4 (EHV-4)

 Pathogenesis and clinical signs

A

Pathogenesis:

 EHV-4 causes less severe tissue destruction than EHV-1.

 EHV-4 rarely causes abortion when it infects pregnant mares.

 EHV-4 rarely results in viremia.

 Death is rare.

Clinical Signs:

 Infection results primarily in upper respiratory tract disease (rhinopharyngitis and

tracheobronchitis).

 Clinical signs may include nasal discharge that may progress into a mucoid or

mucopurulent discharge, increased lung sounds, mild coughing, fever, and occasionally abortion.

81
Q

Subfamily: Alphaherpesvirinae EHV-1 and EHV-4

 Vaccination:

A

 Vaccination:
The ideal vaccine should prevent early infection of suckling foals as well as latency of infection in pregnant mares.

 Live-attenuated and inactivated commercial EHV-1 vaccines are available, including combined products that include both EHV-1 and EHV-4.

 Immunity is short-lived

82
Q

Human herpesvirus 1

A

Cold sores

83
Q

Human herpesvirus 2

A

Human herpesvirus 2

Genital infections

84
Q

Human herpesvirus 3 (Varicella Zoster virus)

A

Chickenpox & Shingles

85
Q

Bovine herpesvirus 1

A

Infectious bovine rhinotracheitis, infectious pustular vulvovaginitis, infectious balanoposthitis, abortion

86
Q

Bovine herpesvirus 2

A

Bovine mammilitis, pseudo-lumpy skin disease

87
Q

bovine herpesvirus 3

A

Encephalitis

88
Q

Equine herpesvirus 1

A

Abortion, respiratory disease, encephalitis, perinatal foal mortality

89
Q

Equine herpesvirus 3

A

Coital exanthema

90
Q

Equine herpesvirus 4

A

Rhinopneumonitis

91
Q

Porcine herpesvirus 1

A

Pseudorabies, Aujeszky’s disease

92
Q

Feline herpesvirus 1

A

Feline viral rhinotracheitis

93
Q

Canine herpesvirus 1

A

Hemorrhagic disease in puppies

94
Q

Caprine herpesvirus 1

A

Conjunctivitis, respiratory & enteric disease

95
Q

Gallid herpesvirus 1

A

Infectious laryngotracheitis of chickens

96
Q

Gallid herpesvirus 2

A

Marek’s disease of chicken (serotype 1)

97
Q

Gallid herpesvirus 3

A

Nonpathogenic Marek’s disease (serotype 2)

98
Q

Meleagrid herpesvirus 1

A

Nonpathogenic turkey herpesvirus

99
Q
A
100
Q

Subfamily: Alphaherpesvirinae Canine herpesvirus 1 (CHV-1)

A

Hemorrhagic Disease of Puppies (Fading Puppy Syndrome)

101
Q

Hemorrhagic Disease of Puppies

Etiology, Host, Transmission

A

First identified in USA in 1965

 Etiology: Canine herpes virus 1, Subfamily: Alphaherpesvirinae

 Host: Dogs, also wild Canidae [Wolves, Coyote]. Highly fatal, generalized hemorrhagic disease of puppies

 Transmission:

 Neonates:

 Contact with infected oral, nasal, or vaginal secretions of dam (mother).

 Contact with secretions of littermates.

 In-Utero transmission

 From passage through birth canal

 Contact with infected fomites (rare).

 Older dogs:

 Venereal transmission

 Contact with saliva, nasal discharge, or urine of infected dogs or puppies.

102
Q

Hemorrhagic Disease of Puppies:

Pathology

A
103
Q

Hemorrhagic Disease of Puppies  Pathogenesis in Puppies:

A

 In-Utero infection:
Abortion, stillbirth, infertility.
If survives, most pups develop systemic CHV- 1 infections within 9 days from birth.

 Systemic Neonatal infection:
 Pups less than 1 week are most susceptible to fatal generalized infection.

 Initial replication occurs in nasal epithelium, tonsils and pharynx.
 Mucosal invasion is followed by leukocyte (macrophage)-associated viremia.  Virus replication in endothelial cells
 Diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in several organs.  Thrombocytopenia, DIC (Disseminated Intravascular Coagulation)

 CNS infection:
 Meningoencephalitis commonly occurs in oro-nasally infected neonatal puppies.  Virus may travel up the nerve axons to CNS.
 However, puppies die from systemic illness before neurologic signs are evident.

104
Q

Hemorrhagic Disease of Puppies

 Pathogenesis in Puppies:
 Factors Governing Systemic Neonatal infection:

A

 Pathogenesis in Puppies:
 Factors Governing Systemic Neonatal infection:

Body temperature of puppies is critical:

 CHV-1 replicates optimally at 330C—that is, the temperature of the outer genital and upper respiratory tracts.

 The hypothalamic thermoregulatory centers of the pup are not fully operative until 2-3 weeks of age.

 The pup is critically dependent on ambient temperature and maternal contact for the maintenance of its normal body temperature.

 The more severe the hypothermia, the more severe and rapid is the course of the disease.

Maternal Immunity:

Maternal antibodies provide protection. Pups born from seronegative bitches are highly vulnerable to severe form of disease.

105
Q

Hemorrhagic Disease of Puppies  Clinical signs in Puppies:

A

Painful crying, abdominal pain, anorexia, dyspnea, passing soft, odorless, greenish stool, no elevation in body temperature.

Hemorrhages in Multiple Organs

Necrotic lesions in lung and liver

106
Q

Hemorrhagic Disease of Puppies  Clinical signs in Puppies:

Animals that survive systemic disease

A

Animals that survive systemic disease develop persistent neurological signs, such as ataxia, blindness.

107
Q
A

Hemorrhagic areas with necrotic foci in kidney of puppy

Hemorrhagic Disease of Puppies  Clinical signs in Puppies:

108
Q
A

Diffuse hemorrhages in abdomen and spleen

109
Q
A

Mummified fetuses

Hemorrhagic Disease of Puppies

110
Q
A

Liver—Multifocal Necrosis and Petechiae

Hemorrhagic Disease of Puppies

111
Q

Hemorrhagic Disease of Puppies

 Adult Genital Infection:

A

 Adult Genital Infection:

 Bitches:
 Generally asymptomatic or limited to vaginal hyperemia.
 Vesicular vaginitis with discharges. Vesicular lesions.
 In-utero infection may result in abortion, stillbirth, mummified fetus, and/or infertility.

 Male dogs: Balanoposthitis  Adult Respiratory Infection:

 Older dogs: Mild respiratory infection (rhinitis and pharyngitis)  Ocular infection: Conjunctivitis

112
Q

Hemorrhagic Disease of Puppies

 Diagnosis:

A

 Diagnosis:
 Focal areas of necrosis and hemorrhages in multiple organs.  Intranuclear inclusion bodies may be present.
 Causative virus can be isolated readily in canine cell cultures  Nucleic acid detection
 Serology like FAT.

113
Q
A

Inclusion Body in Endothelial Cell

Hemorrhagic Disease of Puppies

 Diagnosis:

114
Q
A

Hemorrhagic Disease of Puppies

 Diagnosis:

FAT (Nasal turbinate epithelium)

115
Q

Hemorrhagic Disease of Puppies

 Control:

A

 Reduce hypothermia by providing heated whelping boxes, or placing puppies under infrared lamp.

 Isolation of infected bitch and her litter.

 Low prevalence of severe illness in pups (<20%) and paucity of clinical signs in

adult animals has resulted in lack of availability of vaccines.

Heated whelping box

116
Q

Subfamily: Alphaherpesvirinae

Feline herpesvirus 1  Feline Rhinotracheitis

Distribution, host, transmission

A

One of the two most common causes of infectious respiratory disease of cats:

Feline herpes virus 1 (FHV-1)

The other being feline calicivirus (FCV) (Family: Caliciviridae)

 Distribution: FHV-1 is distributed worldwide

 Host: All members of felidae appear to be susceptible

 Transmission:

 FHV-1 is shed primarily in ocular, nasal and oral secretions.

 Spread is largely by direct contact with an infected cat.

 Aerosol route is not considered important.

 Natural routes of infection are nasal, oral and conjunctiva.

 Virtually, all recovered cats become latently infected carriers.

 Reactivation (from stress, steroids) may cause viral shedding in oronasal and

conjunctival secretions.

117
Q

Feline herpesvirus 1 Feline Rhinotracheitis

 Pathogenesis:

A

 Pathogenesis:

 Virus replication takes place predominantly in the mucosae of nasal septum,

turbinates, nasopharynx and tonsils.

 Viremia is rare, as virus replication is restricted to areas of low temperature, upper

respiratory tract.

 Infection leads to areas of multifocal epithelial necrosis, inflammation and fibrinous

exudation.

 Secondary bacterial infection can cause complications.

118
Q

Feline herpesvirus 1 Feline Rhinotracheitis

Clinical Signs- Kittens

A

 Clinical Signs:

Feline herpesvirus 1 Feline Rhinotracheitis

 Kittens (up to 4 weeks):
 Severe upper respiratory disease.
 Extensive rhinotracheitis
 Fatal bronchopneumonia (from secondary bacterial infection) may develop.  Conjunctivitis, and ulcerative keratitis.

 Cats (> 6 months ):
Mild or subclinical disease in older kittens ( > 6 months )

119
Q

Feline herpesvirus 1 Feline Rhinotracheitis

 Clinical Signs:

 Pregnant Queen

A

 Clinical Signs:

 Pregnant Queen
 Abortion, around 6th week of pregnancy.
 No evidence that the virus crosses the placenta
 May be due to severe systemic effects of illness, and not direct effect of virus.

120
Q
A

Feline Rhinotracheitis

Conjunctivitis; Hyperemia
and Serous Ocular Discharge

121
Q
A

Feline Rhinotracheitis

Ulcerative Keratitis

122
Q

Detection of Corneal ulcers using Fluorescein Ophthalmic Strips

A

 An intact corneal epithelium has a high lipid content that resists the penetration of fluorescein and so is not colored by it.

 A break in the corneal epithelium allows water-soluble fluorescein to be absorbed by the hydrophilic corneal stroma. The exposed, and now stained, corneal stroma will therefore fluoresce.

123
Q

Difference between Feline calicivirus and FHV?

A

 Ulcers on tongue of cat are common in Feline Calicivirus (FCV) infection.

 Oral ulcers are rare in cats with FHV-1 infection.

124
Q

Feline herpesvirus 1 Feline Rhinotracheitis

 Diagnosis:

A

 Diagnosis:

 History & Clinical signs

 Histopathology: Characteristic histological lesions of feline rhinotracheitis include

necrosis of epithelia of the nasal cavity, pharynx, epiglottis, tonsils, larynx, and trachea

and, in extreme cases, in young kittens, a bronchopneumonia.

 Virus isolation: Ocular or pharyngeal swab

 Serology

 PCR, Real-time PCR

125
Q
A

Lungs: The arrow points to a syncytial cell containing multiple nuclei. These nuclei contain characteristic viral inclusion bodies

126
Q
A

Necropsy photos of pneumonic lungs of a kitten suffering from feline herpes virus.

127
Q
A

Feline Rhinotracheitis

Cross-Section of Nasal Turbinates

Severe necrohemorrhagic rhinitis

128
Q
A

Soft and Hard Palates

Feline Rhinotracheitis

Multifocal necrohemorrhagic

palatitis

129
Q

Feline herpesvirus 1 Feline Rhinotracheitis

Vaccination

A

 Vaccination:

Feline herpesvirus 1 Feline Rhinotracheitis

 Three types of FHV-1 and FCV vaccines are available:  MLV (modified live virus) parenterally
 MLV intranasally
 Inactivated vaccine parenterally

 Genetic engineered vaccine composed of a gene deletion mutant of FHV-1 into which capsid protein encoding gene of FCV has been inserted is being developed.

130
Q

Infectious Laryngotracheitis (ILT)

Etiology and host

A

 Etiology:
Gallid herpesvirus 1
It is not possible to identify different strains of ILT virus by serological methods

 Host:

 Highly contagious infection of chickens. Most common in those aged 4–18

months.

 It can also affect pheasants, partridges and peafowl.

 Distribution:

 Worldwide

 First identified in chickens in USA in 1925.

131
Q

ILT

 Transmission:

A

 Transmission:

 Mostly by Inhalation

 Droplets to conjunctiva

 Occasionally by ingestion

 Recovered and vaccinated chickens can also serve as carriers of ILT and can shed the virus when they are subjected to stressful conditions.

 Transmission can occur through fomites, such as contaminated litter, and/or farm workers.

 Mechanical transmission, especially through scavengers like vultures, crow, domestic dogs and wild animals that feed on improperly disposed dead birds.

132
Q

Infectious Laryngotracheitis (ILT)

 Pathogenesis:

A

 There is severe laryngotracheitis in affected birds, characterized by necrosis,

hemorrhage, ulceration, and the formation of diphtheritic membranes.

 Extensive diphtheritic membrane formation can form a second tube for the length of trachea, blocking the air passage. This can result in death from asphyxia.

 ILT virus can persist in the infected birds. The trigeminal ganglion is the target for ILT viral latency.

133
Q
A

Diphtheric membrane forming a second tube and blocking trachea

Infectious Laryngotracheitis (ILT)

134
Q

Infectious Laryngotracheitis

A
  • Hemorrhagic Tracheitis
  • Necrotizing Hemorrhagic Tracheitis
  • Tracheal plug
135
Q

Infectious Laryngotracheitis (ILT)

 Clinical signs:

severe form

A

 Clinical signs:
After an incubation period of 6–12 days, mild coughing and sneezing are followed by

nasal and ocular discharge, dyspnea, loud gasping and coughing, and depression.

 Severe form:

 Severe respiratory distress. Head shaking with coughing is characteristic.

 The neck is raised and the head extended during inspiration—“pump handle

respiration.”

 Cough may result in expulsion of bloody mucous. Blood may stain beak and neck

feathers.

 Morbidity approaches 100%; the mortality for virulent strains may be 50–70%.

136
Q
A

Pump handle respiration

137
Q
A

Expectoration of bloody mucus

138
Q

Low virulent strains of ILT are associated with

A

Clinical signs:
conjutivigitis, ocular discharge, swollen infraorbital and nasal sinuses, and decreased egg production.

.

139
Q

What is the most common form of ILT?

A

The mild enzootic form is most common in modern poultry production, and the severe epizootic form is uncommon.

140
Q
A

Bird infected with ILT have swollen eyelids, reddened conjugativa, and watery eyes

141
Q
A

Conjunctivitis with nasal discharge

ILT

142
Q

Infectious Laryngotracheitis (ILT)

 Diagnosis:

A

 History & Clinical signs

 Necropsy findings: Tracheal plug (diphtheric membrane).

 Histopathology: Detection of typical intranuclear inclusions in respiratory tissues

 Virus isolation: Nasal mucosa.

 Virus grows well in CAM of embryonated eggs (stunted embryos that die 2-12 days postinculoation)

 Serology (FAT), PCR assays.

143
Q

What do you inoculate ILT in?

A

Virus inoculation in embryonated eggs

144
Q
A

Expanding the nuclei of sloughed epithelial cells and syncytial cells, marginating the chromatin are eosinophilic inclusion bodies (arrows).

ILT

145
Q

Infectious Laryngotracheitis (ILT)

Control and Vaccine

A

 Control:

 In event of an outbreak, complete depopulation (slaughter) of infected birds, and

disinfection of infected premises.

 Vaccination:
3 types of vaccine available:

1) chick embryo origin (CEO), 2) tissue culture origin (TCO), and 3) a pox-vectored recombinant vaccine.

 CEO vaccines have the capability of reverting to virulence and causing full-blown

ILT signs. Induce better immunity.

 TCO vaccine is only given by eye drop and does not spread significantly or revert to

virulence. Level of induced immunity is limited
These are applied via eye drop, or through mass vaccination by water or spray.

 Farm biosecurity:
Implementation of farm biosecurity measures.

146
Q

Subfamily: Alphaherpesvirinae Marek’s Disease (Gallid herpesvirus 2)

Etiology, hosts, Distribution, Transmission

A

 Very important disease of poultry
 Synonyms: Fowl paralysis, range paralysis, polyneuritis, neurolymphomatosis  Etiology: Gallid herpesvirus 2

 Hosts:
 Chickens are the most important natural host.  Turkeys, quails, pheasants are susceptible.

 Distribution: Worldwide.

 Transmission:

 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.

147
Q

Subfamily: Alphaherpesvirinae Marek’s Disease (MD)

 4 pathotypes of gallid herpes virus 2 are currently recognized:

A

 Mild [mMDV]: Mostly associated with neural MD.

Disease is preventable with HVT (turkey herpesvirus vaccine).

 Virulent [vMDV]: Associated with high incidence of neural and visceral lymphomas. Disease is preventable with HVT (turkey herpesvirus vaccine).

 Very Virulent [vvMDV]: Associated with high incidence of neural and visceral lymphomas. Viruses are oncogenic in HVT vaccinated chickens. Disease preventable with bivalent vaccines.

 Very virulent plus [vv+MDV]: Associated with high incidence of neural and visceral lymphomas. Viruses are oncogenic in chickens vaccinated with bivalent vaccines.

148
Q

Marek’s Disease (MD)

 Pathogenesis:
Various overlapping virus-cell interactions have been observed:

A

 Fully productive infection:

 Production of enveloped virions and cell death (lysis).

 Occurs only in feather follicle epithelium.

 Infected T cells appear to be the ‘Trojan horse’ by which MDV enters the

feather-follicle epithelium

 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 (primarily CD4+ cells).
 Profound immunosuppression.

 Non-productive infection:
 Viral genome persists in T cells (primarily CD4+).  No antigens expressed.

 Non-productive neoplastic transformation:

 Some latently infected T cells undergo neoplastic transformation.

 A new antigen, MATSA (Marek’s disease Associated Tumor Specific Antigen),

appears in transformed T-cells.

149
Q

Marek’s Disease (MD)

 Pathogenesis:

A

 Subclinical infection with virus shedding is more common.

Virusisslowlycytopathicandremainassociatedwithcells. Cell-freeinfectious viruses are almost impossible to obtain, except in dander from feather follicles.

 Lesions in Marek’s disease result from infiltration and in situ proliferation of transformed T lymphocytes.

Cell lysis also results in marked inflammatory response.

150
Q

Marek’s Disease (MD)

 Genetic susceptibility:

A 
 Genetic susceptibility:
Susceptibility varies depending on different MHC class II haplotypes.

 B19 haplotype chickens are highly susceptible to MD.  B21 haplotype chickens are genetically resistant to MD.

151
Q

Clinical Features of Marek’s Disease

A
  • Neurolymphomatosis
  • Visceral lymphomatosis
  • Ocular lymphomatosis
  • Cutaneous lymphomatosis
152
Q

Marek’s Disease (MD)

 Clinical signs:

A

 Neurolymphomatosis:

 Enlargement of nerve trunks.

 Various peripheral nerves, but particularly the vagus, brachial, and sciatic,

become enlarged and lose their striations.

 Edematous, grey, or yellowish in appearance.

 Enlargement of nerves in usually unilateral

 Neurolymphomatosis:
Lameness, droopy wings, paresis (partial paralysis) of legs (one leg forward and other backward], limberneck, torticollis, incoordination.

 Visceral lymphomatosis

 Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lung, kidney, muscle, and proventriculus.

 The bursa is only rarely tumorous and more frequently is atrophic. The absence of bursal tumors helps distinguish this disease from lymphoid leukosis.

 Ocular lymphomatosis

 Graying of the iris (also known as “gray eye”, “cat’s eye”, “pearl eye”) of one or both eyes.

 Interference with normal pupilar constriction and dilation

 Due to T-cell infiltration.

 Partial or total blindness.

Cutaneous lymphandits

 Plucking of feathers reveal nodular lesions on skin.

 Enlarged feather follicles (commonly termed skin leukosis)

153
Q
A

Marek’s Disease (MD)

 Clinical signs:

 Neurolymphomatosis:

enlarged sciatic nerve trunks

154
Q
A

paresis of legs-

 Clinical signs:

 Neurolymphomatosis:

155
Q
A

 Clinical signs:

 Visceral lymphomatosis

 Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lung, kidney, muscle, and proventriculus.

 The bursa is only rarely tumorous and more frequently is atrophic. The absence of bursal tumors helps distinguish this disease from lymphoid leukosis.

156
Q
A

 Visceral lymphomatosis

157
Q
A

 Ocular lymphomatosis

158
Q

 Diagnosis: of Marek’s disease

A

 Diagnosis:
 History
 Clinical signs
 Necropsy
 Histopathology
 Serology: AGID, IFA, Neutralization test
 Nucleic acid detection: PCR, Real-time PCR  Cell culture, CAM inoculation

159
Q

Marek’s Disease (MD)

 Control:

A

 Control: Reportable disease

 Vaccination:
 The most widely used vaccine consists of turkey herpesvirus (HVT).

 Bivalent vaccines consisting of HVT and either the SB-1 or 301B/1 strains of Gallid herpesvirus 3 (Serotype 2, avirulent strain).

 Most protective commercial vaccine currently available appears to be CVI988/Rispens, an attenuated Marek’s disease virus strain that is also commonly mixed with HVT at vaccination

160
Q

Subfamily: Betaherpesvirinae

A

General properties:

 Slow replicating viruses

 Associated with chronic infections

 Infected cells are often enlarged (cytomegaly)

 Maintained in latent form in secretory glands (salivary glands) and

lymphoreticular cells (macrophages, lymphocytes)

 Often associated with continuous viral excretion

161
Q

Inclusion Body Rhinitis

Etiology, host, transmission, distribution

A

 Etiology: Porcine herpesvirus 2
Also known as Porcine cytomegalovirus (PCMV)

subfamily: Betaherpesvirinae

 Host: Pigs
 Seen in pigs 2 to 10 weeks old.
 Severe disease in piglets less than 3 weeks.

 Distribution: Worldwide

 Transmission:
 Primarily inhalation
 Transplacental transmission

162
Q

Inclusion Body Rhinitis

 Pathogenesis:

A

 Pathogenesis:

 Widespread petechiae and edema
 Most common in thoracic cavity and subcutaneous tissues

163
Q
A

Inclusion Body Rhinitis

Infected cells are enlarged and posses intranuclear inclusion bodies [Arrow], especially in nasal glands. Hence, known as Inclusion Body Rhinitis

164
Q

Inclusion Body Rhinitis

 Clinical signs:

A

 In suckling pigs < 3weeks old, mucopurulent rhinitis accompanied by violent sneezing, respiratory distress, conjunctivitis, shivering, perhaps mouth breathing, and a variable death loss.

 Infected neonatal piglets appear weak, anemic or stunted and there may be edema around the throat and tarsal joints.

 Fetal mummification, stillbirths, neonatal deaths and failure of piglets to thrive

have been associated with infection of naïve, pregnant sows.  Subclinical disease in older animals.

165
Q

Subfamily: Gammaherpesvirinae

Genearal Properties

A

 General properties:

 Lymphotropic (replicate in B or T lymphocytes)

 Slowly cytopathic for epithelial and fibroblastic cells, causing death without virion production.

 Some gammaherpesviruses are shed continuously from epithelial surfaces.

 Latency occurs in lymphoid tissue

 Some members cause lymphoid tumors.

166
Q

Malignant Catarrhal Fever (MCF)

Host, Etiology

A

Synonyms: Bovine Malignant Catarrh, Malignant Head Catarrh

 Host: Highly fatal disease of cattle and some wild ruminants (deer, bison, antelope)  Etiology:

 Malignant catarrhal fever is caused by viruses in subfamily Gammaherpesvirinae.

 At least ten MCF viruses have been recognized.

 The two most important MCF viruses are:

Alcephaline herpesvirus-1 (AHV-1)

Known as Wildebeest-associated MCF

Ovine herpesvirus-2 (OvHV-2)

Known as Sheep-associated MCF

167
Q

Malignant Catarrhal Fever (MCF)
 Wildebeest-associated MCF

[Alcephaline herpesvirus-1 (AHV-1)]:

A

 AHV-1 is transmitted to cattle from wildebeest.

 Wildebeest-associated MCF occurs in most African countries, where cattle

commingle with infected normal wildebeest

AHV-1 doses not cause any disease in the principal host, the wildebeest.

 Wildebeest-associated MCF is Epizootic and Seasonal (during the wildebeest calving season).

168
Q

Malignant Catarrhal Fever (MCF)  Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:

A

 Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:

 Occurs worldwide.
 OvHV-2 is transmitted from sheep to cattle.
 Goats also can act as a source of infection to cattle.
 Occurs year-round in cattle, with moderate increase during lambing season.

 Usually sporadic, occasionally outbreaks.

169
Q

Malignant Catarrhal Fever (MCF)

In Africa, MCF is predominantly found where

A

In Africa, MCF is predominantly found where cattle are in close contact with blue- or black wildebeest, while outside Africa, it is usually associated with contact between sheep and susceptible species

170
Q

Malignant Catarrhal Fever (MCF)
 Transmission of Wildebeest-associated MCF [Alcephaline herpesvirus-1 (AHV-1)]:

 Between Wildebeest:

A

 Between Wildebeest:
 Horizontal and occasional intrauterine transmission in wildebeest. Inapparent infection.

Transmission from Wildebeest to Cattle:
 AHV-1 is present in nasal and ocular secretions of young wildebeest in a cell-free state.
 Ingestion of pasture contaminated with nasal or ocular secretions from young wildebeest.

 Direct or close contact, inhalation of aerosol with young wildebeest.
 Direct or close contact with wildebeest during calving (virus in cell-free state in young).
 Virus in cell-associated form in adult wildebeest, so rarely transmitted from adults.

171
Q

Malignant Catarrhal Fever (MCF)
 Transmission of Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:

 Between sheep:

A

 Between sheep:
 Respiratory (aerosol)
 Transplacental rare
 Contact with nasal secretions

172
Q

Transmission from Sheep to Cattle:

 Transmission of Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:

A

 Transmission from Sheep to Cattle:

 Not known

 Presumably by inhalation or ingestion

173
Q

Malignant Catarrhal Fever (MCF)

 Transmission of MCF viruses [AHV-1 and OvHV-2]:

A

 Wildebeest and Sheep:
 Inapparent infection in Wildebeest and Sheep.
 Virus transmitted from Wildebeest-to-Wildebeest and Sheep-to-Sheep.

 Cattle:

 Cattle are dead-end hosts, i.e. No evidence for transmission of virus from Cattle-to-Cattle.

 Cattle have cell-associated virus, but not cell-free virus, in secretions.

 This may explain the noncontagious nature of MCF when contact occurs with MCF affected cattle.

174
Q

Malignant Catarrhal Fever (MCF)

Pathogenesis:

A

 Infection followed by cell-associated viremia.

 Lymphoid proliferation and infiltration.

 Necrotizing Vasculitis.

 CD8+ T cells are predominant cells associated with vascular lesions.

 Disease may be immunologically mediated.

 Vascular lesions accounts for development of gross lesions, such as epithelial erosions and keratoconjunctivitis.

175
Q

Malignant Catarrhal Fever (MCF)

 Clinical Signs:

A

 Clinical Signs:

 Peracute form: Sudden death

 Head and eye form: Majority of cattle cases

 Alimentary/Intestinal form: Initially like head and eye form, but death occurs from severe diarrhea. Diarrhoea is rarely observed in wildebeest derived MCF, but is more common in sheep associated MCF.

 Mild form: Inoculated animals; recovery expected

176
Q

Malignant Catarrhal Fever (MCF)

 Peracute form:

A

 Peracute form:
Sudden, Characteristic clinical signs of “head and eye” form may not appear. High fever, acute gastroenteritis.

ALL OF A SUDDEN

177
Q

Malignant Catarrhal Fever (MCF)

 Head and Eye Form:
 Early Stages:

A

 Reddened eyelids
 Bilateral corneal opacity

 Crusty muzzle, nares
 Nasal discharge

 Salivation

MOST COMMON FORM

178
Q

Malignant Catarrhal Fever (MCF)

 Head and Eye Form:

 Other Clinical signs:

A

 Other Clinical signs:
 Joints, superficial lymph nodes swell

 Horn, hoof coverings slough
 Nervous signs

 Incoordination,

 head pressing,

 nystagmus,
 hyperesthesia

179
Q
A

ZEBRA STRIPING: Bovine, colon. Severe longitudinal linear congestion of the mucosa

Malignant Catarrhal Fever (MCF)

Necropsy findings

THIS IS A CHARACTERISITIC SIGN

180
Q
A

Mucoid exudate multifocally covers the nasal and pharyngeal mucosa.

MCF necropsy findings

181
Q
A

Multifocal lymphoid infiltration in the renal cortex

MCF- necropsy findings

182
Q
A

Enlarged prescapular lymph node

MCF necropsy findings

183
Q
A

Multiple coalescing mucosal erosions in hard palate

MCF necropsy findings

184
Q
A

Hemorrhage (and necrosis) in prescapular lymph node

MCF necropsy findings

185
Q
A

Multiple pale foci of necrosis & ulcers in omasum

MCF necropsy findings

186
Q
A

Bovine, kidney. Multiple pale foci in the cortex are foci of interstitial nephritis.

MCF necropsy findings

187
Q

Malignant Catarrhal Fever (MCF)

Control:

A

Control:

 Separation of cattle from wildebeest and sheep.
 Incidence too low to justify development of a vaccine.

188
Q
A

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