Herpesviridae (Ex2) Flashcards
Morphology of Herpesviridae
- enveloped, spherical to pleomorphic
- icosahedral capsid, T=16
- capsid surrounded by globular material called tegument
- glycoproteins in lipid envelope
Describe the viral genome of Herpesviridae
- non-segmented, linear, double-stranded DNA
- contains terminal and internal repeated sequences
Explain replication of Herpesviridae
- DNA replication occurs in the nucleus
- viral envelope acquired by bidding through inner layer of nuclear envelope
- mature virions accumulate within vacuoles in the cytoplasm and are released by cytolysis
What are Type A Cowdry bodies?
eosinophilic intranuclear inclusion bodies that are characteristic of herpesvirus
General features of subfamily alphaherpesvirinae
- highly cytopathic, lyse infected cells
- short replication cycle
Bovine Herpesvirus 1
subfamily, diseases caused
- Alphaherpesvirinae
- Infectious bovine rhinotracheitis (IBR)
- Infectious pustular vulvovaginitis
- Ocular form of IBR
- abortion
- Systemic disease of newborn calves
What are the 3 subtypes of BHV-1?
- BHV-1.1 (respiratory)
- BHV-1.2 (genital)
- BHV-1.3 (encephalitic)
Transmission of BHV-1
- respiratory disease and conjunctivitis from droplet transmission
- genital disease from coitus or AI with infected semen
What are the sites of latency for BHV-1?
- Trigeminal nerve (respiratory)
- Sciatic nerve (genital)
Clinical signs of the respiratory form of BHV-1
- red nose: inflamed nares, hyperemia
- rhinitis, laryngitis, tracheitis
- anorexia, fever, depression, serous discharge
- nasal lesions with numerous clusters of grayish necrotic foci on mucus membranes
Clinical signs of ocular form of IBR
- conjunctivitis
- ocular discharge
- lesions confined to conjunctiva, inflamed, reddened, edematous
Clinical signs of Systemic Disease of Newborn Calves
- severe in calves less than 10 days
- generalized disease with pyrexia, diarrhea, respiratory distress, ocular discharge, incoordination, convulsions, and death
- small ulcers in forestomachs, peritonitis
Clinical signs of genital form of BHV-1
IPV and Balanoposthitis
IPV: frequent urination - vaginal mucosa red and swollen - elevated tail position - vaginal discharge - swollen vulva, red spots, pustules B: inflammation and pustules in mucosa of penis and prepuce
Bovine Herpesvirus-2
subfamily, diseases caused
- Alphaherpesvirinae
- Bovine Ulcerative Mammillitis
- Pseudo Lumpy Skin Disease
Bovine Ulcerative Mammilitis Clinical signs and Transmission
- teats swollen and painful, bluish skin, exudes serum
- reduction in milk yield
- mastitis
- direct contact through damaged skin, and mechanical by arthropods
Pseudo-Lumpy Skin Disease clinical signs and transmission
- mild fever
- skin nodules with flat surface and depressed center on epidermis
- mechanical by arthropods
Pseudorabies
subfamily, etiology, hosts
- Alphaherpesvirinae
- Porcine Herpesvirus 1/Suid Herpesvirus 1
- disease of swine
- wide range of secondary hosts
Transmission of Pseudorabies in primary and secondary hosts
Swine: recovered pigs are carriers
- transmitted by rodent reservoirs
- virus shed in saliva, nasal discharge, milk
- licking, biting, aerosol, ingestion of carcass, water, or feed
Dogs/Cats: ingestion of infected carcassas
Cattle: direct contact with infected pigs
Pathogenesis of Pseudorabies in Swine
site of replication, spread
- site of replication is upper respiratory tract
- spreads via lymphatics to lymph nodes
- virema spreads to other organs
- spreads to CNS via cranial nerves
Pseudorabies clinical signs in swine
- febrile response, anorexia, weight loss
- piglets: 100% mortality, CNS disease
- pregnant sows: 50% abortion, before 30th day, death and reabsorption, later, stillborn, weak, or normal piglets
- older piglets: mild disease, respiratory signs, CNS signs
Describe the necropsy findings of a pig with pseudorabies
- serous to fibrinous rhinitis
- necrotic tonsilitis
- liver and spleen with yellow-white necrotic foci
- necrotic placentitis and endometritis
- CNS: perivascular cuffing
Clinical Signs of Pseudorabies in secondary hosts
Cattle: intense pruritis, frenzy - progressive CNS signs - death from respiratory failure Dogs: pruritis frenzy, self-mutilation - paralysis of jaw and pharynx - plaintive howling Cats: rapid development so possibly no pruritis
Equine Herpesvirus 1 transmission and latency sites
- inhalation of infected aerosols, direct or indirect contact with nasal discharges, aborted fetuses, or placental fluids
- sites of latency: tissues of CNS (trigeminal ganglia), and lymph system
Equine Herpesvirus 1 pathogenesis
- route of infection is the respiratory tract
- infects endothelial cells of lamina propria
- infected phagocytes drain in lymph and enter circulation
- main lesion: infection of endothelial cells, leading to vascular necrosis, thrombus formation, and death to tissues
How does EHV-1 cause immunosuppression?
codes a protein that inhibits TAP protein, thereby blocking delivery of the antigen to class 1 MHC molecules
Clinical Signs of respiratory disease caused by EHV-1
- in younger horses
- rhinopneumonitis
- fever, bilateral nasal discharge, coughing, inappetence, and depression
- secondary bacterial infections
Clinical Signs of encephalomyeopathy caused by EHV-1
- immune-mediated vasculitis leading to infarction and hemorrhage within the brain and spinal cord
- severity ranges from hind limb incoordination to quadriplegia resulting in death
Clinical Signs of reproductive form of EHV-1
- abortions occur in last trimester
- reproductive efficiency not compromised
- abortion storms
What disease is caused by Equine Herpesvirus 4?
- What subfamily?
Equine Viral Rhinopneumonitis
- alphaherpesvirus
Clinical signs of Equine Viral Rhinopneumonitis
- rarely causes abortion
- upper respiratory tract disease
- nasal discharge, coughing, fever, increased lung sounds
What disease is caused by Canine Herpesvirus 1?
What subfamily is it?
Hemorrhagic Disease of Puppies
“Fading Puppy Syndrome”
- alphaherpesvirus
Transmission of CHV-1
Neonates: contact with infected oral, nasal, or vaginal secretions of mom or littermates
- in-utero transmission
- passage through birth canal
- fomites
Older dogs: venereal
- contact with saliva, nasal discharge, or urine of infected dogs
Pathogenesis of CHV-1 systemic neonatal infection
- replication in nasal epithelium, tonsils, and pharynx
- leukocyte associated viremia
- replication in endothelial cells
- diffuse necrotizing vasculitis, hemorrhagic necrosis in several organs
- thrombocytopenia, DIC
- temp of puppy is critical
Clinical Signs of Fading Puppy Syndrome
- painful crying
- abdominal pain
- anorexia
- dyspnea
- soft, odorless, green stool
- no elevation in body temp
Clinical signs of Fading Puppy Syndrome in bitches
- generally asymptomatic
- vaginal hyperemia, vesicular vaginitis with discharge
- in-utero infection may result in abortion, stillbirth, mummified fetus, or infertility
What disease is caused by Feline Herpesvirus 1?
What subfamily is it?
Feline Rhinotracheitis
- infectious respiratory disease
- alphaherpesvirus
Transmission of Feline Rhinotracheitis
- shed in ocular, nasal, and oral secretions
- spread by direct contact with infected cat
- routes: nasal, oral, conjunctival
- all recovered cats become carriers
Pathogenesis of Feline Rhinotracheitis
- replication in mucosa of the nasal septum, turbinates, nasopharynx, and tonsils
- viremia is rare, replication restricted to low temperature
- areas of multifocal epithelial necrosis, inflammation, and fibrinous exudation
- secondary bacterial infections
Clinical Signs of Feline Rhinotracheitis
Kittens: severe upper resp disease
- rhinotracheitis, fatal bronchopneumonia
- conjunctivitis and ulcerative keratitis
Adults: mild or subclinical
Pregnant: abortion
Explain the use of Fluorescein Ophthalamic Strips
- detection of corneal ulcers
- intact corneal epithelium has high lipid content, and resists the penetration of fluroescein
- a break in the corneal epithelium allows fluorescein to be absorbed, therefore dying the ulcer
What types of vaccines are available for Feline Rhinotracheitis?
- modified live parenterally
- modified live intranasally
- inactivated parenterally
What avian diseases are caused by Alphaherpesviruses?
- Infectious Laryngotracheitis
- Marek’s Disease
Infectious Laryngotracheitis
subfamily, etiology, hosts
- Alphaherpesvirus
- Gallid herpesvirus 1
- contagious infection of chickens
Transmission of Infectious Laryngotracheitis
- mostly by inhalation
- droplets to conjunctiva
- possible by ingestion
- recovered chickens can become carriers
- fomites
- mechanical via scavengers
Pathogenesis of Infectious Laryngotracheitis
- characterized by necrosis, hemorrhage, ulceration, and formation of diphtheritic membranes
- diphtheritic membranes can block trachea, resulting in asphyxia
- latency in trigeminal ganglion
Clinical Signs of Infectious Laryngotracheitis
- mild coughing, sneezing, nasal/ocular discharge, dsypnea, gasping, depression
- head shaking with cough, pump handle respiration, coughing up blood
What types of vaccines are available for Infectious Laryngotracheitis
- chick embryo origin: induce better immunity, but can revert to virulence
- tissue culture origin: eye drop, does not revert to virulence, limited immunity
- a pox-vectored recombinant vaccine
Marek’s Disease
subfamily, etiology, other names, hosts
- alphaherpesvirus
- Gallid herpesvirus 2
- fowl paralysis, range paralysis, polyneuritis
- chickens mainly
- turkeys, quail, pheasants
Transmission of Marek’s disease
- highly contagious (reportable)
- inhalation of feather debris, dander, dust
What are the 4 pathotypes of Gallid Herpesvirus 2?
- mild: associated with neural MD, preventable with HVT
- virulent: high incidence of neural and visceral lymphomas, preventable with HVT
- very virulent: high incidence of neural and visceral lymphomas, oncogenic with HVT, preventable with bivalent vaccines
- very virulent plus: high incidence of neural and visceral lymphomas, oncogenic with bivalent vaccines
Pathogenesis of a fully productive infection of Marek’s Disease
- production of enveloped virions and cell death
- only in feather follicle epithelium
- infected T cells act as Trojan horse for virus to enter follicle epithelium
Pathogenesis of a productive-restrictive infection of Marek’s Disease
- production of naked virions and viral antigens
- cell death due to lysis
- occurs in B cells and activated T cells
- immunosuppression
Pathogenesis of a non-productive infection of Marek’s Disease
- viral genome persists in T cells
- no antigens expressed
Pathogenesis of a non-productive neoplastic transformation of Marek’s Disease
- some latently infected T cells undergo neoplastic transformation
- a new antigen, MATSA, appears in transformed T cells
Which haplotype chickens are susceptible to Marek’s, and which are not?
- B19 susceptible
- B21 resistant
Clinical Signs of Marek’s Disease
- neurolymphomatosis: enlargement of nerve trunks, edematous grey yellow, lameness, droopy wings, paresis of legs, limberneck
- visceral lymphomatosis: lymphoid tumors is various organs
- ocular lymphomatosis: graying of iris, abnormal pupil constrict/dilate, blindness
- cutaneous lymphomatosis: large nodular lesions on skin, enlarged feather follicles
General Features of subfamily Betaherpesvirus
- slow replication
- associated with chronic infections
- infected cells often enlarged
- latent form in secretory glands and lymphoreticular cells
- continuous viral excretion
Inclusion Body Rhinitis
subfamily, etiology, host
- Betaherpesvirinae
- Porcine Herpesvirus 2: Porcine cytomegalovirus
- pigs 2-10 weeks old
Pathogenesis of Inclusion Body Rhinitis
- widespread petechiae and edema
- common in thoracic cavity and SQ tissues
- replication in nasal mucosal glands and epithelial cells of upper resp tract
- viremia
- infected cells are enlarged and possess intranuclear inclusion bodies
Clinical Signs of Inclusion Body Rhinitis
- mucopurulent rhinitis with violent sneezing, resp distress, conjunctivitis, shivering, mouth breathing
- neonates appear weak, anemic, or stunted
- fetal mummification, stillbirths, neonatal deaths
- subclinical disease in older animals
General Features of Subfamily: Gammaherpesvirinae
- replicate in B or T lymphocytes
- slowly cytopathic for epithelial and fibroblastic cells
- latency in lymphoid tissue
Malignant Catarrhal Fever
subfamily, etiologies, host
- gammaherpesvirinae
- alcephaline herpesvirus 1 (wildebeest), ovine herpesvirus 2 (sheep)
- highly fatal disease of cattle and some wild ruminants
Wildebeest-Associated MCF
distribution and transmission
- African countries
- present in nasal and ocular secretions of young wildebeest in cell-free state
- ingestion of contaminated pasture
- direct or close contact, inhalation, or aerosol
- rarely transmitted from adults
Sheep-Associated MCF
distribution, transmission
- worldwide
- between sheep: respiratory, nasal secretions
- sheep to cattle: unknown, by inhalation or ingestion
Transmission of MCF viruses in cattle
- cattle are dead-end hosts
- no transmission between cattle
- have cell-associated virus, no cell-free virus, in secretions
Pathogenesis of MCF
- cell-associated viremia
- lymphoid proliferation and infiltration
- necrotizing vasculitis
- CD8 T cells associated with vascular lesions
Clinical Signs of MCF in cattle
Peracute: sudden death
- high fever, acute gastroenteritis
Head and Eye: majority of cattle
- reddened eyelids, corneal opacity, crusty muzzle, nasal discharge, salivation
- erosions of tongue, hard palate, and buccal papillae
- joints, swollen lymph nodes
- incoordination, head pressing, nystagmis
Necropsy findings of MCF in cattle
- enlarge prescapular lymph node
- mucoid exudate over nasal mucosa
- zebra striping: severe longitudinal linear congestion of mucosa
- multiple pale foci of necrosis and ulcers in omasum
- lymphoid infiltration in renal cortex
