HERPESVIRALES Flashcards
1
Q
Herpesviridae are non-enveloped. True or False?
A
False
2
Q
Herpesviridae acquire its envelope from?
A
Nuclear membrane through budding
3
Q
Herpesviridae establish short infections. True or False?
A
False, life-long infections or persistent viral infeciton
4
Q
Latency is common for Herpesviridae. True or False?
A
True
5
Q
Reactivation of Herpesviridae infection is associated with _____ and _____.
A
stress; immunosuppresion
6
Q
Gallid herpesvirus 1 causes what disease?
A
Infectious laryngotracheitis virus
7
Q
Give the pathogenesis of Avian infectious laryngotracheitis. (also considered as clinical signs)
A
- 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.
- In severe cases, neck is raised and the head extended during inspiration - “pump handle respiration”.
- Head shaking with coughing is characteristic, and may be associated with expectoration of bloody mucus and frank blood that appear on the beak, face and feathers.
— Strains of low virulence are associated with conjunctivitis, ocular discharge, swollen infraorbital and nasal sinuses, and decreased egg production.
8
Q
Give the characteristics of severe laryngotracheitis caused by Avian infectious laryngotracheitis.
A
- Necrosis, hemorrhage, ulceration, and the formation of diphtheritic membranes
- Extensive diphtheritic membrane formation can plug the airway at the tracheal bifurcation; resulting in death from asphyxia - “fowl diphtheria”.
9
Q
Give the transmission mode of Avian Infectious laryngotracheitis (Gallid).
A
— Usually introduced into a flock via carrier birds
- Droplet and inhalation to respiratory tract
- Droplets to conjunctiva
- Less commonly ingestion - still requires exposure to the nasal epithelium through the choanal slit which communicates between the oral cavity and middle nasal chamber
10
Q
What is the causative agent of Marek’s disease?
A
Gallid Herpesvirus 2
11
Q
Give the clinical signs of Marek’s Disease.
A
- Lymphoproliferative syndromes such as lymphoma of several visceral organs
- Paralysis of one or both legs or wings
- Incoordination is a common early sign: one leg is held forward and the other backward when the bird is stationary, because of unilateral paresis or paralysis, usually involving the sciatic nerve.
- Wing dropping and lowering of the head and neck
- If vagus nerve is involved, dilation of the crop and gasping
— May occur without neurologic signs; present only as depression and comatose state, with visceral lymphomas
12
Q
Give the 3 main syndromes induced by Marek’s Disease Virus and describe them.
A
- Acute Marek’s Disease or Fowl paralysis
- Occurs in explosive outbreaks in young chickens
- Depression followed by ataxia and paralysis
- Significant mortality occurs without localizing neurologic signs
- Visceral lymphomas are typically absent, nerve lesions are prominent - Ocular lymphomatosis
- Graying of the iris of one or both eyes as a result of infiltration of transformed (neoplastic) lymphocytes
- Pupil is irregular and eccentric
- Partial or total blindness
- Mortality is rare and usually older birds are infected - Cutaneous Marek’s Disease
- Recognized readily after plucking, when round, nodular lesions up to 1 cm in diameter occur particularly at feather follicles of young birds
- The nonfeathered area of the legs may have a distinct red coloration; therefore called as “redleg syndrome”
— Other syndromes include immunosuppression and transient paralysis from brain edema
13
Q
Give the transmission mode of Marek’s Disease Virus.
A
Typically infected by inhalation of virus in the dust and dander shed from infected feather follicles that is present in chicken houses
14
Q
Give the pathogenesis of Marek’s disease.
A
- Entry via inhalation of contaminated dust and dander
- Target dendritic cells and macrophages
- Productive infection of lymphoid cells in primary lymphoid organs including the thymus, cloacal bursa, and spleen
- Virus amplification and immunosuppression
- 4 days after infection: there is a persistent cell-associated viremia followed by a proliferation of CD4 + T cells.
- Deaths can occur within a week of infection but usually start within the flock between 3 and 4 weeks, although regression may also occur.
15
Q
What is the cause of both Infectious bovine rhinotracheitis and Infectious pustular vulvovaginitis ?
A
Bovine Herpesvirus 1
16
Q
What are the clinical signs of Infectious bovine rhinotracheitis?
A
INITIAL SIGNS
* Fever, depression, inappetence, profuse nasal discharge - initially serous and later mucopurulent
* Nasal mucosa is hyperemic; progress from focal necrosis with associated purulent inflammation to large areas of shallow, hemorrhagic, ulcerated mucosa covered by a cream-colored diphtheritic membrane
* Breath may be fetid
* Dyspnea, mouth breathing, salivation, deep bronchial cough are common
- Unilateral or bilateral conjunctivitis, often with profuse lacrimation
- Gastroenteritis may occur in adult cattle
- Abortion
17
Q
What are the clinical signs of Infectious pustular vulvovaginitis?
A
- Fever, depression, anorexia, and stand apart, often with the tail held away from contact with the vulva
- Micturition is frequent and painful
- Vulval labial are swollen; slight vulval discharge
- Vestibular mucosa is reddened and contains many small pustules - usually coalesce to form a fibrinous pseudomembrane that covers an ulcerated mucosa
18
Q
What are the transmission mode of Infectious bovine rhinotracheitis and Infectious bovine vulvovaginitis?
A
- Transport and introduction to a feedlot of young, fully susceptible cattle from diverse sources
- Droplet or smear transmission
- Coitus or artificial insemination
19
Q
Give the pathogenesis of both Infectious bovine rhinotracheitis and Infectious bovine vulvovaginitis.
A
- Entry via coitus or droplet or smear transmission
- Lesions are focal areas of epithelial cells necrosis in which there is ballooning of epithelial cells; typically herpesvirus inclusion may be present in nuclei at the periphery of necrotic foci
- Intense inflammatory responses within the necrotic mucosa, frequently with formation of an overlying accumulation of fibrin and cellular debris
- Microscopic foci of necrosis are present in most tissues and the liver and adrenal glands are affected most consistently.
20
Q
What causes Mammillitis and Pseudo-Lumpy skin disease?
A
Bovine herpesvirus 2
21
Q
Distinguish Mammillitis from Pseudo-Lumpy.
A
Mammillitis - localized to the teats, occasionally spreading to the udder
Pseudo-Lumpy - more generalized skin disease
22
Q
Give the clinical signs of Pseudo-lumpy skin disease.
A
- Mild fever, followed by the sudden appearance of skin nodules: a few or many on the face, neck, back, and perineum
- Characteristic central depression on the surface of the skin nodules
- Superficial necrosis of the epidermis
- Shorter course of the disease compared to true lumpy disease.
23
Q
Give the clinical signs of Mammillitis.
A
- Lesions occur only on the teats but in severe cases most of the skin of the udder may be affected
- Occasionally, heifers may develop fever, coinciding with the appearance of lesions
- Milk yield may be reduced by as much a 10% as a result of difficulty in milking the affected cows, and concurrent mastitis
24
Q
What are the transmission modes of Mammillitis and Pseudo-lumpy?
A
- Mechanical transmission via arthropods
- Miking machines (rarely the case)
25
Give the pathogenesis of Mammillitis and Pseudo-lumpy.
Mammillits - restricted and local spread
Pseudo-lumpy - viremic spread
(infos were lacking)
26
Bovine encephalitis virus is caused by ?
Bovine herpesvirus 5
27
Give the pathogenesis and clinical signs of Bovine encephalitis virus.
** Direct neural spread from the nasal cavity, pharynx, and tonsils via the maxillary and mandibular branches of the trigeminal nerve
** Lesions occasionally in the midbrain and later involve the entire brain
28
Give the transmission mode of Bovine encephalitis virus.
** Possibly the same as rhinotracheitis and vulvovaginitis since Bovine HV 1 is closely related to 5
1. Transport and introduction to a feedlot of young, fully susceptible cattle from diverse sources
2. Droplet or smear transmission
29
Equine abortion virus is caused by ?
Equid herpesvirus 1
30
What are the clinical signs of Equine abortion virus?
--- Principal route is via the respiratory tract
* Abortion
* Encephalomyelitis
* Respiratory disease
* (?) Lesion within the CNS; ranging from mild ataxia and urinary incontinence to limb paralysis and death
31
Give the pathogenesis of Equine abortion virus.
* Fetus is aborted without the evidence of autolysis.
* Fetus aborted before 6 months of gestation may exhibit autolysis
* Aborted fetuses: icterus, meconium staining of the integument, edema in body cavities, lung distension, splenomegaly with prominent lymphoid follicles, and numerous pale foci of necrosis that are evident on the capsular or cut surfaces of the liver and kidney
* Bronchiolitis and interstitial pneumonitis, severe necrosis of splenic white pulp, and focal necrosis of the liver and adrenal glands
32
What is the transmission mode of Equine abortion virus?
1. Possibly inhalation
2. Direct contact through nasal secretions, reproductive tract discharge, placenta or the aborted fetus
33
What causes Equine coital exanthema virus?
Equid herpesvirus 3
34
What are the clinical signs of Equine coital exanthema virus?
* Formation of pustular and ulcerative lesions on the vaginal and vestibular mucosae and adjacent perineal skin of affected mares, and on the penis and prepuce of affected stallions
* Lesions are occasionally present on the teats, lips, and respiratory mucosa
* Where the skin of the vulva, penis, and prepuce is black, white depigmented spots mark for life the site of earlier lesions and identify potential carries
35
What is the transmission mode of Equine coital exanthema virus?
1. Sexual intercourse
2. Direct contact with contaminated objects
(as per the web)
36
What causes Pseudorabies/Aujeszky's disease?
Suid herpesvirus 1
37
What is the transmission mode of Pseudorabies in swine?
* Licking, biting, and aerosols
* Contamination of livestock feed
* Ingestion of the infected carcasses by swine
* Ingestion of contaminated material
* Rats may contribute to farm-to-farm transfer
--- Virus is shed in the saliva and nasal discharges
38
What are the clinical signs of Pseudorabies in swine?
PREGNANT SOWS
* 50% of pregnant sows may abort over a short period of time
* Infection of a sow before the 30th day of gestation results in death and resorption of embryos (embryonic loss); whereas infection after that time can result in abortion
* In late pregnancy, delivery of a mixture of mummified, macerated, stillborn, weak, and normal swine
WEANED, GROWING, AND MATURE
* Sneezing, coughing, moderate fever - 40 - 42 C
* Constipation during fever; feces are hard and dry, vomiting may occur
* Listless, depressed, tent to remain recumbent
* By the 5th day, incoordination and pronounced muscle spasm, circling, an intermittent convulsions accompanied by excess salivations
* By the 6th day, moribund and death
39
What are the clinical signs of Pseudorabies in cattle?
* Intense pruritus; often on the flanks or hind limbs - licked incessantly - gnawing an rubbing such that the area becomes abraded
* CNS involvement
* Death
40
What are the clinical signs of Pseudorabies in dogs?
* Frenzy associated with intense pruritus
* Paralysis of the jaws and pharynx, accompanied by drooling of saliva and plaintive howling - simulates the rabies
* THERE IS NO TENDENCY FOR DOGS TO ATTACK OTHER ANIMALS
41
What are the clinical signs of Pseudorabies in cats?
* The disease may progress rapidly that frenzy is not observed.
42
What is the pathogenesis of Pseudorabies?
1. After primary oral or intranasal infection of swine, virus replicates in the oropharynx
2. Within 24h, virus can be isolated from various cranial nerve ganglia and the medulla and the pons, to which virions have traveled via the axoplasm of the cranial nerves
3. Virus continues to spread within the CNS; there is ganglioneuritis at many sites, including those controlling viral functions
4. Tonsillitis, pharyngitis, tracheitis, rhinitis, and esophagitis may be occasionally evident, with formation of a diphtheritic pseudomembrane overlying the affected mucosa
5. Similarly, discrete small white or yellow foci of necrosis may sometimes be present in the liver and spleen
6. Diffuse nonsuppurative (predominantly lymphocyttic) meningoencephalitis and ganglioneuritis, marked perivascular cuffing, and focal gliosis associated with extensive necrosis of neuronal and glial cells.
43
What agent causes Porcine cytomegalovirus?
Suid herpesvirus 2
44
What are the clinical signs of Porcine cytomegalovirus?
* Rhinitis may occur in affected swine up to 10 weeks of age
* Sneezing, coughing, serous nasal and ocular discharge, depression
* Subsequent mucopurulent discharges blocking nasal passages; interferes with suckling; piglets lose weight and dies
* Fetal death upon crossing the placenta
--- Large basophilic intranuclear inclusion thus the name "inclusion body rhinitis"
45
What are the transmission modes of Porcine cytomegalovirus?
1. Transplacentally
2. Horizontally
46
Malignant catarrhal fever herpesviruses targets what type of animal?
Even-toed ungulates (cattle, deer, antelope, giraffe, and swine)
47
What are the clinical signs MCFH induce?
* Fever, depression, leukopenia, profuse nasal, and ocular discharges
* Bilateral corneal opacity that can progress to blindness
* Generalized lymphadenopathy
* Extensive mucosal erosions
* CNS signs that are characteristic of "head and eye" form of the disease
48
MCFH is induced by what herpesvirus?
Closely-related gammaherpesviruses
49
What is/are the transmission modes of MCFH?
1. Inoculation of cattle or bison with blood from a clinically affected animal
2. By aerosol to cattle or bison with nasal secretions from sheep experiencing a virus-shedding episode
50
What is the pathogenesis of MCFH?
*** Basically same as that of the clinical signs but include:
- Hemorrhage of GIT, oral cavity, urinary bladder (hemorrhagic cystitis), mucosa of nasal turbinates, larynx, trachea
- Multiple foci of interstitial inflammation in the kidney
