Herpesviridae Flashcards
Family: Herpesviridae
Enveloped, spherical to pleomorphic
Capsid surrounded by a layer of globular material- tegument
Double stranded DNA genome
Dont survive well outside host
Moist cool environmental conditions promote extended survival
Latently infected animals serve as reservoirs of transmission
Herpesviridae viral replication
DNA replication and encapsidation occur in nucleus
Viral envelope is acquired by budding through the inner layer of the nuclear envelope
Mature virions accumulate within vacuoles in cytoplasm and are released by exocytosis or cytolysis
Herpesviridae general characteristics
Persistent infection with periodic or continuous shedding occurs in all herpesvirus infections
Some are oncogenic
Reactivation of latent herpesvirus infection is usually associated with stress causes by intercurrent infections, shipping, cols, crowding, or by administration of glucocorticoid drugs
Eosinophilic intranuclear inclusion bodies- type A cowdry bodies
formation of syncytium
Subfamilies
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Alphaherpesvirinae
Generally highly cytopathic in cell culture
Relatively short replication cycle
Some (like pseudorabies) have a broad host range, whereas most are highly restricted in natural host range
Produce localized lesions- particularly in skin or mucosae of respiratory and genital racts
Generalized infections characterized by foci of necrosis in almost any organ or tissue are typical of infection of v young or immunocompromised animals
In preg- virus across placental- leading to abortion, with multifocal areas of necrosis in several fetal organs
Alphaherpesvirinae: examples
Bovine Herpesvirus 1 Bovine Herpesvirus 2 Equine Herpesvirus 1 Equine Herpesvirus 4 Porcine Herpesvirus 1 Feline Herpesvirus 1 Canine Herpesvirus 1 Gallid Herpesvirus 1 Gallid Herpesvirus 2
Bovine Herpesvirus 1
Disease: Infectious bovine rhinotracheitis, infectious pustular vulvovaginitis, infectious balanoposthitis, abortion, ocular form of IBR Systemic disease of newborn calves
Bovine Herpesvirus 2
Disease: bovine mammilitis,
pseudo-lumpy skin disease
Equine Herpesvirus 1
Disease: abortion,
respiratory disease,
encephalitis,
perinatal foal mortality
Equine Herpesvirus 4
Disease: Rhinopneumonitis
Porcine Herpesvirus 1
Disease: Pseudorabies,
Aujeszky’s disease
Feline Herpesvirus 1
Disease: Feline viral rhinotracheitis
Canine Herpesvirus 1
Disease: Hemorrhagic disease in puppies
Gallid Herpesvirus 1
Disease: Infectious laryngotracheitis of chickens
Gallid Herpesvirus 2
Disease: Marek’s disease of chicken (serotype 1)
Bovine Herpesvirus 1: etiology
3 subtypes:
BHV 1.1- respiratory
BHV 1.2- genital
BHV 1.3- encephalatic
Bovine Herpesvirus 1: transmission
Respiratory disease and conjunctivitis result from droplet transmission
Genital disease may result from coitus or artificial insemination with infective semen
Bovine Herpesvirus 1: pathogenesis
In both forms, 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 periphery of necrotic foci
Intense inflammatory response within necrotic mucosa, frequently with formation of an overlying accumulation of fibrin and cellular debris (pseudomembrane)
Lifelong latent infection with periodic virus shedding
All seropositive animals are considered potential carriers
Can be reactivated from latency by corticosteroids or stress
Bovine Herpesvirus 1: sites of latency
Trigeminal n: respiratory disease
Sciatic n: Genital disease
Bovine Herpesvirus 1: clinical signs- resp form
Respiratory form: (Red Nose, Necrotic Rhinitis, Dust Pneumonia)
Rhinitis, Laryngitis, Tracheitis
Inflamed nares give appearance of having red nose due to hyperemia. Grayish necrotic foci on mucous
Nasal discharge becomes more profuse and mucopurulent
Fibrinonecrotic rhinitis
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 result of secondary bronchopneumonia
Bovine Herpesvirus 1: Ocular form of IBR
Conjunctivitis is a common finding in typical red nose
Dont missjudge as pink eye- IBR lesions are confined to conjunctiva and no lesions on cornea except diffuse edema
Bovine Herpesvirus 1: Abortion
Occurs as a common sequel to natural infection
Result of some modified-live virus (MLV) vaccines being given to preg animals
Animals in contact with IBR susceptible pregnant animals
Fetuses in the second half of gestation have a higher incidence of abortion- early death also possible
Often preceded by pustular vulvovaginitis
Bovine Herpesvirus 1: Systemic disease in newborn calves
Severe in calves less than 10 d- often fatal
Infected in-utero or right after birth
Bovine Herpesvirus 1: Genetal disease
IPV (infectious pustular vaginitis)
After coitus
Freq urination
Tail is usually held in an elevated position and excessive switching noted
Vaginal mucosa red and swollen
Mild Vaginal discharge
Vulva swollen, red spots, discrete pustules may be notes
Balanoposthitis: inflammation and pustules in teh mucosa of penis and prepuce
Bovine Herpesvirus 1: Control (Vxn)
Modified live vxns, subunit and inactivated vxns available
Parenteral and intranasal vxn avail
Both stimulate production of humoral Abs
Parenteral vxn may cause abortion in preg cows
Intranasal safe for preg cows
Bovine Herpesvirus 2: Bovine Ulcerative Mammilitis Host
Cattle, heifers, usually within 2 weeks of calving
Persistent disease
Bovine Herpesvirus 2: Bovine Ulcerative Mammilitis Transmission
Direct contact and fomite-mediated, through trauma to skin
Mechanical transmission by stable flies and other arthropods
Bovine Herpesvirus 2: Bovine Ulcerative Mammilitis Clinical signs
In severe cases, teat is swollen and painful, skin is bluish, exudes serum, formation of raw ulcers
High incidence of mastitis
Bovine Herpesvirus 2: Pseudo-lumpy skin disease
Cattle infected
Occurs most commonly in southern Africa
Mechanical transmission of virus occurs by arthropods
CS: mild fever, followed by sudden appearance of skin nodules: a few or many, on face, neck, back, and perineum
Porcine Herpesvirus 1: Pseudorabies
Primarily disease of swine
Diverse range of secondary hosts- horses, cattle, sheep, goats, dogs, cats, etc can become infected and develop disease
Humans are refractory to infection
Porcine Herpesvirus 1: Pseudorabies- transmission in primary host
Recovered in pigs act as primary reservoirs and are latent carrier for life
Rodents can also act as reservoirs and transmit farm to farm
Virus shed in saliva, nasal discharges and milk of infected pigs
Not shed in urine or feces
Transmission by licking, biting, aerosol, ingestion of contaminated carcass, water and feed
Porcine Herpesvirus 1: Pseudorabies- 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
Porcine Herpesvirus 1: Pseudorabies- pathogenesis
Primary site of viral replication is upper respiratory tract
Porcine Herpesvirus 1: Pseudorabies- spread of virus
Replicated in tonsils and nasopharynx
Spreads via lymphatics to regional lymph nodes, where replication continues
Brief viremia associated with virulent strains, with localization of virus in different organs
Porcine Herpesvirus 1: Pseudorabies- virus spread in CNS
Spreads to CNS via axons of cranial nerves
Continues to spread within CNS
Preference for neurons of pons and medulla
Porcine Herpesvirus 1: Pseudorabies- CNS lesions
Ganglioneuritis
Nonsuppurative meningoencephalitis
Perivascular cuffing
Porcine Herpesvirus 1: Pseudorabies- Clinical signs
Non immune piglets: 100% mortality rate
Nonimmune pregnant sows: 50% abortion rate
Older piglets, growers, and adult pigs: mild disease; mortality <2%
Prutitus (itching) a dominant feature in secondary hosts- rare in pigs
Porcine Herpesvirus 1: Pseudorabies- Clinical signs-Piglets born to nonimmune sows
most susceptible- signs of CNS disease (incoordination of hindlimbs, fitting, tremors and paddling)
Porcine Herpesvirus 1: Pseudorabies- Clinical signs- weaned pigs and growing pigs
Central nervous signs may be reduced and an increase in respiratory signs
Porcine Herpesvirus 1: Pseudorabies- 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- eventually conceive
Porcine Herpesvirus 1: Pseudorabies- necropsy findings
Gross lesions are often absent or minimal
Serous to fibrinous rhinitis is common and a necrotic tonsilitis
Porcine Herpesvirus 1: Pseudorabies- Secondary hosts
Ruminants, Dogs Cats Goats, sheep horses Intense pruritus Hyperacute, rapid progress, high mortality
Porcine Herpesvirus 1: Pseudorabies- Cattle
Intense prutitus
Cattle may become frenzied
Progressive involvement of CNS, stage of paralysis, ataxia
Death from respiratory failure
Porcine Herpesvirus 1: Pseudorabies- Dogs
Frenzy associated with pruritus. Self mutilation
Paralysis of jaws and pharynx with drooling of saliva
Plaintive howling
Unlike rabies, dogs don’t attack
Porcine Herpesvirus 1: Pseudorabies- Cats
Disease progress so rapidly that prutitus may not be observed
Porcine Herpesvirus 1: Pseudorabies- Vaccination
Of swine in enzootic areas reduce losses
Does not prevent infection, or establishment of latent infection by wild type virus, but can alleviate CS in pigs of certain ages
Recombinant DNA, deletion-mutant, live attenuated, and inactivated vaccines are available
Equine Herpes virus 1: distribution
Endemic in horse populations around the world
Equine Herpes virus 1: Transmission
Inhalation of infected aerosols direct or indirect contact with nasal discharges, aborted fetuses, placenta or placental fluids
Equine Herpes virus 1: Latency
Latent virus can reside in tissues of the CNS (neuron cell bodies, specificaly trigeminal ganglia) and lymph system (leikocytes, more specifically lymphocytes) without causing any clinical symptoms of disease
When host is immunosuppressed virus reactivated causing disease or shedding again
Equine Herpes virus 1: Pathogenesis
Principal route is via resp tract
Following infection of epithelial cells, it infects endothelial cells in lamina propria
Virus-infected mononuclear cells and T lymphocytes subsequently appear in drainage lymph nodes and are released into 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
Central lesion caused by it responsible for the 3 types of conditions seen (resp, repro, CNS) is an infection of endothelial cells, leading to vascular necrosis, thrombus formation, subsequent death to tissues serviced by blood vessels (ischemia)
Cell-associated viremia confers protection from body’s immune defenses and allow virus to spread to endothelial cells lining blood vessels in CNS and preg uterus= CNS signs or abortion
Equine Herpes virus 1: Respiratory Disease
Affects mostly younger horses
Rhinopneumonitis
Equine Herpes virus 1: Encephalomyelopathy
May affect horses of any age or breed
Equine Herpes virus 1: Reproductive Form
Although abortions may occur early in gestation, majority occur in last trimester (8-10 m)
Reproductive efficiency is not compromised
Cases of abortion are usually sporadic
If large numbers susceptible mares are exposed to aborted conceptus, extensive outbreaks of abortion occur
Natural immunity to EHV may last 2-3 yrs- abortion storms have 3 year cycles
Equine Herpes virus 4: Equine Viral Rhinopneumonitis- transmission
Antigenically related to EHV-1
Most infections sporadic
Mostly observed in horses under 2 yrs
Often causes life long latent infection which can be reactivated
Droplet infection from infected horses and older horses in `which inapparent viral shedding occurs
Equine Herpes virus 4: Equine Viral Rhinopneumonitis- Pathogenesis
Causes less severe tissue destruction than 1
Rarely causes abortion when infects preg mares
rarely results in viremia
Death is rare
Equine Herpes virus 4: Equine Viral Rhinopneumonitis- Clinical signs
Infection results primarily in upper respiratory tract disease (rhinopharyngitis and tracheobronchitis)
EHV-1 and EHV 4- Vaccination
Ideal Vxn should prevent early infection of suckling foals as well as latency of infection in preg mares
Live attenuated and inactivated commercial EHV-1 vxns available including combined products that include 1 and 4
Immunity short lived
Alphaherpesvirinae
Canine Herpesvirus 1 (CHV-1)
Hemorrhagic disease of Puppies (fading puppy syndrome)
Feline herpesvirus 1
Feline Rhinotracheitis
Avian: Infectious Laryngotracheitis; Mareks disease
Hemorrhagic disease of Puppies: etiology
Canine herpesvirus 1
Alphaherpesvirinae
Hemorrhagic disease of Puppies: Hosts
Dogs, wild canidae
Highly fatal, generalized hemorrhagic disease of puppies
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)
Hemorrhagic disease of Puppies: Transmission (older dogs)
Venereal transmission
Contact with saliva, nasal discharge, or urine of infected dogs or puppies
Hemorrhagic disease of Puppies: Pathogenesis in Puppies (In-utero infection)
Abortion, stillbirth, infertility
If survives, most pups develop systemic CHV-1 infections within 9 days from birth
Hemorrhagic disease of Puppies: Pathogenesis in Puppies (Systemic Neonatal infection)
Pups less than 1 wk are most susceptible to fatal generalized infection
Initial replication occurs in nasal epithelium, tonsils, and pharynx
Mucosal invasion is followed by leukocyte (macrophage)-associated viemia
Virus replication in endothelial cells
Diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in several organs
Thrombocytopenia, DIC
Hemorrhagic disease of Puppies: Pathogenesis in Puppies (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 neurological signs are evident
Hemorrhagic disease of Puppies: Pathogenesis in Puppies- Factors Governing Systemic Neonatal infection
Body temp of puppies is critical:
-CHV-1 replicates optimally at 33C- which is the temp of the outer genital and upper resp tracts
-The hypothalamic thermoregulatory centers of the pup are not fully operative until 2-3 wks old
-Pup is critically dependent on ambient temp and maternal contact for the maintenance of normal body temp
-The more sever 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
Hemorrhagic disease of Puppies: Clinical signs
Painful crying, abdominal pain, anorexia, dyspnea, passing soft, odorless, greenish stool, no elevation in body temp
Animals that survive systemic disease develop persistent neurological signs- ataxia, blindness
Hemorrhagic disease of Puppies: 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
Males: Balanoposthitis
Hemorrhagic disease of Puppies: Adult respiratory infection
Older dogs: mild respiratory infection (rhinitis and pharyngitis)
Hemorrhagic disease of Puppies: Ocular infection
Conjunctivitis
Hemorrhagic disease of Puppies: Control
Reduce hypothermia by providing heated whelping boxes, or placing puppies under infrared lamp
Isolation of infected bitch and litter
Low prevalence of severe illness in pups (<20%) and paucity of CS in adult animals has resulted in lack of availability of vaccines
Feline Rhinotracheitis
One of the two most common causes of infectious respiratory disease of cats:
- FHV-1
- Feline calicivirus (FCV)
Feline Rhinotracheitis: Transmission
FHV-1 shed primarily in ocular, nasal, and oral secretions
Spread is largely by direct contact with 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
Feline Rhinotracheitis: 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
Feline Rhinotracheitis: Clinical signs (kittens up to 4 wks)
More common Severe upper respiratory disease Extensive rhinotracheitis Fatal bronchopneumonia (from secondary bacterial infection) may develop Conjunctivitis, and ulcerative keratitis
Feline Rhinotracheitis: Clinical signs (Cats >6 months)
Mild or subclinical disease in older kittens
Feline Rhinotracheitis: 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 the illness, and not direct effect of virus
Feline Rhinotracheitis
Conjunctiviti; hyperemia and serous ocular discharge
Ulcerative keratitis
Oral ulcers rare
(Ulcers on tongue common in FCV infections)
Severe necrohemorrhagic rhinitis
Multifocal necrohemorrhagic palatitis
Feline Rhinotracheitis: Vaccination
Three types of FHV-1 and FCV vaccines are available:
- MLV- modified live virus- parenterally
- MLV intranasally
- Inactivated vaccine parenterally
Infectious Laryngotracheitis: Etiology
Gallid herpesvirus 1
Infectious Laryngotracheitis: Hosts
Highly contagious infection of chickens
Infectious Laryngotracheitis: 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, esp through scavengers like vultures, crow, domestic dogs and wild animals that feed on improperly disposed dead birds
Infectious Laryngotracheitis: Pathogenesis
there is severe laryngotracheitis in affected birds (necrosis, hemorrhage, ulceration)
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 infected birds. The trigeminal ganglion is the target for ILT viral latency
Infectious Laryngotracheitis
Hemorrhagic Tracheitis
Necrotizing Hemorrhagic Tracheitis
Tracheal plus
Infectious Laryngotracheitis: severe form
Severe respiratroy 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
Infectious Laryngotracheitis: Clinical Signs
Strains of low virulence are associated with conjunctivits, occular discharge, swollen infraorbital and nasal sinuses, and decreased egg production
The mild enzootic form is most common in modern poultry production, and severe epizootic form is uncommon
Infectious Laryngotracheitis: Diagnosis
Necropsy findings: tracheal plug (diphtheric membrane)
Detection of typical intranuclear inclusions in respiratory tissues
Virus isolation: nasal mucosa
Virus grows will in CAM of embryonated eggs
Infectious Laryngotracheitis: Control
In event of outbreak, complete depopulation (slaughter) of infected birds, and disinfection of infected premises
Infectious Laryngotracheitis: Vaccination
3 types:
Chick embryo origin- have capability of reverting to virulence and causing full blown ILT signs. Induce better immunity
Tissue culture origin- only given by eye drop and does not spread significantly or revert to virulence. Level of induced immunity is limited- Better choice as its safe to use
Pox-vectored recombinant Vaccine
These are applied via eye drop or mass vaccination by water or spray
Infectious Laryngotracheitis: farm biosecurity
Implementation of farm biosecurity measures
Marek’s Disease
Gallid herpesvirus 2
Very important disease of poultry
Marek’s Disease: Hosts
Chickens are most important natural host
Turkeys, quails, pheasants are susceptible
Marek’s Disease: 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
Marek’s Disease: Pathotypes
Mild mMDV
Virulent vMDV
Very Virulent vvMDV
Very Virulent Plus vv+MDV
Marek’s Disease: Pathotypes- Mild
Mostly associated with neural MD
Disease is preventable with HVT (turkey herpesvirus vaccine)
Marek’s Disease: Pathotypes- virulent
Associated with high incidence of neural and visceral lymphomas. Disease is preventable with HVT
Marek’s Disease: Pathotypes- Very Virulent
Associated with high incidence of neural and visceral lymphomas.
Viruses are oncogenic in HVT vaccinated chickens
Disease preventable with bivalent vaccines
Marek’s Disease: Pathotypes- very virulent plus
Associated with high incidence of neural and visceral lymphomas
Viruses are oncogenic in chickens vaccinated with bivalent vaccines
Marek’s Disease: Pathogenesis
Inhalation of the virus
Initial round of replication in epithelial cells
Macrophage associated viremia
Virus is detectable in the spleen, thymus, and bursa of fabricius
Productive restrictive infection: Cytolytic replication primarily in B cells and later activated CD4+ T cells
Non productive latent infection in CD4+ T cells
Non-productive neoplastic transformation: some latently infected CD4+T cells
Fully productive infection: Occurs in feather follicle epithelium. Infected T cells appear to be the trojan horse by which MDV enters the feather follicle epithelium
Marek’s Disease: Pathogenesis- 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
Marek’s Disease: Pathogenesis-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
Marek’s Disease: Pathogenesis- non productive infection
Viral genome persists in T cells (primarily CD4+)
No antigens expressed
Marek’s Disease: Pathogenesis- non productive neoplastic infection
Some latently infected T cells undergo neoplastic transformation
A new antigen, MATSA (Mareks disease associated tumor specific antigen) appears in transformed T cells
Marek’s Disease: Pathogenesis- more
Virus is slowly cytopathic and remain associated with cells
Cell free infectious viruses are almost impossible to obtain, except in dander from feather follicles
Lesions in Mareks disease result from infiltration and in situ proliferation of transformed T lymphocytes
Cell lysis also results in marked inflammatory response
Marek’s Disease: Clinical features
Neurolymphomatosis
Visceral lymphomatosis
Ocular lymphomatosis
Cutneous lymphomatosis
Marek’s Disease: Neurolymphomatosis
Enlargement of nerve trunks
Lose their striations
Edematous, grey, or yellowish in appearance
Lameness, droopy wings, paresis (partial paralysis) of legs (one leg forward and other backward), limberneck, torticollic, incoordination
Marek’s Disease: Visceral lymphomatosis
Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lung, kidney, muscle, and parventriculus
The bursa is only rarely tumorous and more frequently is atrophic. The absence of bursal tumors helps distinguish this disease from lymphoid leukosis
Marek’s Disease: Ocular lymphomatosis
Graying of the iris (also known as gray eye, cat’s eye, or pearl eye) of one or both eyes
Interference with normal pupilar constriction and dilation
Partial or total blindness
Marek’s Disease: Cutneous lymphomatosis
Plucking of feathers reveal nodular lesions on skin
Enlarged feather follicles (commonly termed skin leukosis)
Marek’s Disease: Vaccination
The most widely used vaccine consists of turkey herpesvirus
Bivalent vaccines consisting of HVT and either 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
Subfamily Betaherpesvirinae
Slow replicating viruses
Associated with chronic infections
Infected cells are often enlarges (cytomegaly)
Maintained in latent form in secretory glands (salivary glands) and lymphoreticular cells (macrophages, lymphocytes)
Often associated with continuous viral excretion
Inclusion body rhinitis: etiology
Porcine herpesvirus 2
Also known as Porcine cytomegalovirus (PCMV)
Inclusion body rhinitis: Host
Pigs
Severe disease in piglets
Inclusion body rhinitis: Transmission
Primarily inhalation
transplacental transmission
Inclusion body rhinitis: Pathogenesis
Widespread petechiae and edema
Most common in thoracic cavity and subcutaneous tissues
Cross placenta: stillbirth, mummification, neonatal death
Primary site of viral replication: nasal mucous glands; Epithelial cells of URT
Endothelial cell damage and necrosis: petechial hemorrhages and edema
In some neonates, bone marrow damage, anemia
Inclusion body rhinitis:
Infected cells are enlarged and posses intranuclear inclusion bodies, especially in nasal glands. Hence known as inclusion body rhinitis
Inclusion body rhinitis: Clinical signs
In suckling pigs < 3wks old, mucopurulent rhinitis
Infected neonatal piglets appear weak, anemic or stunted- may have edema around the throat and tarsal joints
Fetal mummification, stillbirths, neonatal deaths, and failure of piglets to thrive have been associated with infection of naive, pregnant sows
Subclinical disease in older animals
Subfamily: Gammaherpesvirinae
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
Malignant Cararrhal Fever:
Bovine malignant catarrh, Malignant head catarrh
Malignant Cararrhal Fever: host
Highly fatal disease of cattle and some wild ruminants (deer, bison, antelope)
Malignant Cararrhal Fever: etiology
Caused by viruses in subfamily gammaherpesvirinae
At least ten MCF viruses have been recognized
The 2 most important: Alcelaphin herpesvirus-1 (Wildebeest associated MCF)
Ovine herpesvirus-2 (Sheep associated MCF)
Wildebeest-associated MCF:
Transmitted to cattle from wildebeest
Occurs in most African countries, where cattle commingle with infected normal wildebeest
Does not cause any disease in the principal host, the wildebeest.
Epizootic and seasonal (during wildebeest calving season)
Sheep-associated MCF
Occurs worldwide
Transmitted from sheep to cattle
Goats can also act as source of infection to cattle
Occurs year-round in cattle, with moderate increase during lambing season
Usually sporadic, occasionally outbreaks
Malignant Cararrhal Fever:
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
Wildebeest-associated MCF: Transmission between wildebeest
Horizontal and occasional intrauterine transmission
Inapparent infection
Wildebeest-associated MCF: Transmission to cattle
Present in nasal and ocular secretions of young wildebeest in cell-free state
Ingestion of pasture contaminated with nasal or ocular secretions from young wildebeest
Direct or close contact, inhalation or 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
Sheep-associated MCF: Transmission between sheep
Respiratory (aerosol)
Transplacental rare
Contact with nasal secretions
Sheep-associated MCF: Transmission from sheep to cattle
Not known
Presumably or inhalation or ingestion
Malignant Cararrhal Fever: Transmission
Wildebeest and sheep: inapparent infection
-virus transmitted from W-W or S-S
Cattle: dead end hosts- no C-C transmission
- 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
Malignant Cararrhal Fever: pathogenesis
Necrotizing vasculitis
Vascular lesions accounts for development of gross lesions, such as epithelial erosions and keratoconjunctivitis
Malignant Cararrhal Fever: Clinical signs
Peracute form: Sudden death
Head and eye form: majority of cattle cases (erosions on tongue)
Alimentary/intestinal form: initially like head and eye form, but death occurs from severe diarrhea. Diarrhea is rarely observed in Wildebeest MCF but is more common in sheep MCF
Mild form: inoculated animals; recovery expected
Malignant Cararrhal Fever: Necropsy findings
Zebra stripingL bovine colon. Severe longitudinal linear congestion of mucosa
Malignant Cararrhal Fever: control
Separation of cattle from wildebeest and sheep
Incidence too low to justify development of vaccine
