Test 2- Herpesviridae Flashcards
1
Q
Herpesviridae
A
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.
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.
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.
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.
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.
7
Q
A
Cowdry type A intranuclear inclusion
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
9
Q
A
Syncytium caused by HSV-1 infection in Vero cells
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.
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.
12
Q
A
Focal necrosis seen in liver infected with Equine Herpesvirus 1
13
Q
Subfamily: Alphaherpesvirinae
Pattern of infection:
A
Frequently cause latent infections in sensory ganglia.
Virus is reactivated from latency by stress or immunosuppression.
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
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.
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
17
Q
A
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Ballooning of the epithelial cells
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.
19
Q
A
Breathing through the mouth and salivation in a bovine affected with IBR.
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.
21
Q
A
Bovine herpesvirus 1- “red nose”
22
Q
A
Hemorrhage and Congestion of the Muzzle on left
Fibrinonecrotic Rhinitis on right
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Clinical signs:
Respiratory form:
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
24
Q
A
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Clinical signs:
Respiratory form:
Diffuse hemorrhages (cut surface of turbinates)
25
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Necrotic Lesions in Epiglottis
26
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Clinical signs:
Respiratory form:
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.
27
Fibrinopurulent Bronchopneumonia
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
28
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Thrombotic Pneumonia
29
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Ocular form of IBR:
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.
30
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Ocular form of IBR:
31
You have to differentiate bovine herpes virus from...
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
32
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Abortion:
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
33
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Systemic Disease of Newborn Calves:
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**
34
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Genital Disease:
IPV (Infectious Pustular Vaginitis)
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
35
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Genital Disease:
Balanoposthitis
Inflammation and pustules in the mucosa of the penis and prepuce
36
Subfamily: Alphaherpesvirinae Bovine herpesvirus 1
Control (Vaccination):
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.
37
Subfamily: Alphaherpesvirinae Bovine herpesvirus 2
Bovine Ulcerative Mammillitis
Etiology, distribution, host, transmission
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.
.
38
Subfamily: Alphaherpesvirinae Bovine herpesvirus 2
Bovine Ulcerative Mammillitis
Clinical signs:
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.
39
Subfamily: Alphaherpesvirinae Bovine herpesvirus 2
Bovine Ulcerative Mammillitis
40
Subfamily: Alphaherpesvirinae Bovine herpesvirus 2
Pseudo-Lumpy Skin Disease
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
41
Subfamily: Alphaherpesvirinae Bovine herpesvirus 2
Pseudo-Lumpy Skin Disease
42
Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)
Etiology and host
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.**
43
Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)
Transmission in Primary Host and secondary host:
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.
44
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Pathogenesis and Spread of the Virus
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.
45
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Virus spread in the CNS and the lesions in the CNS
**_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
46
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
CNS lesion
47
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Clinical Signs
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%
48
Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)
Clinical Signs:
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.
49
Piglet with outstretched forelimb
Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch)
50
Signs of CNS disease
Subfamily: Alphaherpesvirinae Pseudorabies (Aujeszky disease, Mad itch
51
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Clinical signs
Weaned pigs and growing pigs:
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.
52
Weaned pig showing signs of severe depression. The animal also presented with pneumonia and head pressing
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
53
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Clinical Signs:
Nonimmune Pregnant Sows:
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.
54
Mummified pigs, a symptom of Pseudorabies
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Clinical Signs:
Nonimmune Pregnant Sows:
55
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Necropsy Findings:
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.
56
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Necropsy Findings:
Necrotizing Tonsillitis
57
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Rhinitis in snout of pig with Pseudorabies
58
Secondary Hosts
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Secondary Hosts
Ruminants
Dogs
Cats
Goats, Sheep, Horses
Intense pruritus
Hyperacute, Rapid progress, High mortality
59
Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts
Cattle (Mad Itch):
Cattle (Mad Itch):
Intense pruritus (Itching).
Cattle may become frenzied.
Progressive involvement of CNS, stage of paralysis, ataxia.
Death from respiratory failure.
60
Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts
Pruritus—self trauma
Swollen eyelid due to intense rubbing. Profuse salivation
61
Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts
Dogs and cats
**_ 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.
62
Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts
Dog with pseudorabies and self- mutilation injuries
63
Subfamily: Alphaherpesvirinae Pseudorabies in Secondary Hosts
Paralysis of the Jaws and Pharynx, Profuse Salivation
64
65
Subfamily: Alphaherpesvirinae Pseudorabies
Dx
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
66
Subfamily: Alphaherpesvirinae Pseudorabies in Pigs
Vaccination:
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.
67
Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)
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.
68
Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)
Latency:
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.
69
Outcomes of Equine Herpes Virus- 1
70
Life Cycle of Equine Herpes Virus
71
Cell-associated viremia (macrophages, other leukocytes) protects
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
72
Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)
Pathogenesis:
Immunosuppression
**EVS -1 codes a protein that inhibits TAP protein, thereby blocking delivery of antigen to class I MHC molecules.**
73
Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)
Pathogenesis:
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.
74
Pulmonary Consolidation
Subfamily: Alphaherpesvirinae Equine herpes virus 4 (EHV-4)
75
Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)
Respiratory Disease
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
76
Subfamily: Alphaherpesvirinae EHV-1 and EHV-4
Vaccination digram
77
ubfamily: Alphaherpesvirinae
Equine herpes virus 1 (EHV-1)
Encephalomyelopathy (EHM, equine herpesvirus myeloencephalopathy)
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
Subfamily: Alphaherpesvirinae Equine herpes virus 1 (EHV-1)
Reproductive form:
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
Subfamily: Alphaherpesvirinae
Equine herpes virus 4 (EHV-4)
Disease, Transmission, distribution
**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
Subfamily: Alphaherpesvirinae Equine herpes virus 4 (EHV-4)
Pathogenesis and clinical signs
**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
Subfamily: Alphaherpesvirinae EHV-1 and EHV-4
Vaccination:
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
Human herpesvirus 1
Cold sores
83
Human herpesvirus 2
Human herpesvirus 2
Genital infections
84
Human herpesvirus 3 (Varicella Zoster virus)
Chickenpox & Shingles
85
Bovine herpesvirus 1
Infectious bovine rhinotracheitis, infectious pustular vulvovaginitis, infectious balanoposthitis, abortion
86
Bovine herpesvirus 2
Bovine mammilitis, pseudo-lumpy skin disease
87
bovine herpesvirus 3
Encephalitis
88
Equine herpesvirus 1
Abortion, respiratory disease, encephalitis, perinatal foal mortality
89
Equine herpesvirus 3
Coital exanthema
90
Equine herpesvirus 4
Rhinopneumonitis
91
Porcine herpesvirus 1
Pseudorabies, Aujeszky’s disease
92
Feline herpesvirus 1
Feline viral rhinotracheitis
93
Canine herpesvirus 1
Hemorrhagic disease in puppies
94
Caprine herpesvirus 1
Conjunctivitis, respiratory & enteric disease
95
Gallid herpesvirus 1
Infectious laryngotracheitis of chickens
96
Gallid herpesvirus 2
Marek’s disease of chicken (serotype 1)
97
Gallid herpesvirus 3
Nonpathogenic Marek’s disease (serotype 2)
98
Meleagrid herpesvirus 1
Nonpathogenic turkey herpesvirus
99
100
Subfamily: Alphaherpesvirinae Canine herpesvirus 1 (CHV-1)
Hemorrhagic Disease of Puppies (Fading Puppy Syndrome)
101
Hemorrhagic Disease of Puppies
Etiology, Host, Transmission
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
Hemorrhagic Disease of Puppies:
Pathology
103
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.
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
Hemorrhagic Disease of Puppies
Pathogenesis in Puppies:
Factors Governing Systemic Neonatal infection:
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
Hemorrhagic Disease of Puppies Clinical signs in Puppies:
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
Hemorrhagic Disease of Puppies Clinical signs in Puppies:
Animals that survive systemic disease
Animals that survive systemic disease develop persistent neurological signs, such as ataxia, blindness.
107
Hemorrhagic areas with necrotic foci in kidney of puppy
Hemorrhagic Disease of Puppies Clinical signs in Puppies:
108
Diffuse hemorrhages in abdomen and spleen
109
Mummified fetuses
Hemorrhagic Disease of Puppies
110
Liver—Multifocal Necrosis and Petechiae
Hemorrhagic Disease of Puppies
111
Hemorrhagic Disease of Puppies
Adult Genital Infection:
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
Hemorrhagic Disease of Puppies
Diagnosis:
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
Inclusion Body in Endothelial Cell
Hemorrhagic Disease of Puppies
Diagnosis:
114
Hemorrhagic Disease of Puppies
Diagnosis:
FAT (Nasal turbinate epithelium)
115
Hemorrhagic Disease of Puppies
Control:
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
Subfamily: Alphaherpesvirinae
Feline herpesvirus 1 Feline Rhinotracheitis
Distribution, host, transmission
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
Feline herpesvirus 1 Feline Rhinotracheitis
Pathogenesis:
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
Feline herpesvirus 1 Feline Rhinotracheitis
Clinical Signs- Kittens
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
Feline herpesvirus 1 Feline Rhinotracheitis
Clinical Signs:
Pregnant Queen
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
Feline Rhinotracheitis
Conjunctivitis; Hyperemia
and Serous Ocular Discharge
121
Feline Rhinotracheitis
Ulcerative Keratitis
122
Detection of Corneal ulcers using Fluorescein Ophthalmic Strips
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
Difference between Feline calicivirus and FHV?
Ulcers on tongue of cat are common in Feline Calicivirus (FCV) infection.
Oral ulcers are rare in cats with FHV-1 infection.
124
Feline herpesvirus 1 Feline Rhinotracheitis
Diagnosis:
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
Lungs: The arrow points to a syncytial cell containing multiple nuclei. These nuclei contain characteristic viral inclusion bodies
126
Necropsy photos of pneumonic lungs of a kitten suffering from feline herpes virus.
127
Feline Rhinotracheitis
Cross-Section of Nasal Turbinates
Severe necrohemorrhagic rhinitis
128
Soft and Hard Palates
Feline Rhinotracheitis
Multifocal necrohemorrhagic
palatitis
129
Feline herpesvirus 1 Feline Rhinotracheitis
Vaccination
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
Infectious Laryngotracheitis (ILT)
Etiology and host
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
ILT
Transmission:
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
Infectious Laryngotracheitis (ILT)
Pathogenesis:
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
Diphtheric membrane forming a second tube and blocking trachea
Infectious Laryngotracheitis (ILT)
134
Infectious Laryngotracheitis
- Hemorrhagic Tracheitis
- Necrotizing Hemorrhagic Tracheitis
- Tracheal plug
135
Infectious Laryngotracheitis (ILT)
Clinical signs:
severe form
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
Pump handle respiration
137
Expectoration of bloody mucus
138
Low virulent strains of ILT are associated with
Clinical signs:
conjutivigitis, ocular discharge, swollen infraorbital and nasal sinuses, and decreased egg production.
.
139
What is the most common form of ILT?
The mild enzootic form is most common in modern poultry production, and the severe epizootic form is uncommon.
140
Bird infected with ILT have swollen eyelids, reddened conjugativa, and watery eyes
141
Conjunctivitis with nasal discharge
ILT
142
Infectious Laryngotracheitis (ILT)
Diagnosis:
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
What do you inoculate ILT in?
Virus inoculation in embryonated eggs
144
Expanding the nuclei of sloughed epithelial cells and syncytial cells, marginating the chromatin are eosinophilic inclusion bodies (arrows).
ILT
145
Infectious Laryngotracheitis (ILT)
Control and Vaccine
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
Subfamily: Alphaherpesvirinae Marek’s Disease (Gallid herpesvirus 2)
Etiology, hosts, Distribution, Transmission
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
Subfamily: Alphaherpesvirinae Marek’s Disease (MD)
4 pathotypes of gallid herpes virus 2 are currently recognized:
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
Marek’s Disease (MD)
Pathogenesis:
Various overlapping virus-cell interactions have been observed:
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
Marek’s Disease (MD)
Pathogenesis:
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
Marek’s Disease (MD)
Genetic susceptibility:
```
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
Clinical Features of Marek's Disease
* Neurolymphomatosis
* Visceral lymphomatosis
* Ocular lymphomatosis
* Cutaneous lymphomatosis
152
Marek’s Disease (MD)
Clinical signs:
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
Marek’s Disease (MD)
Clinical signs:
Neurolymphomatosis:
enlarged sciatic nerve trunks
154
paresis of legs-
Clinical signs:
Neurolymphomatosis:
155
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
Visceral lymphomatosis
157
Ocular lymphomatosis
158
Diagnosis: of Marek's disease
Diagnosis:
History
Clinical signs
Necropsy
Histopathology
Serology: AGID, IFA, Neutralization test
Nucleic acid detection: PCR, Real-time PCR Cell culture, CAM inoculation
159
Marek’s Disease (MD)
Control:
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
Subfamily: Betaherpesvirinae
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
Inclusion Body Rhinitis
Etiology, host, transmission, distribution
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
Inclusion Body Rhinitis
Pathogenesis:
Pathogenesis:
Widespread petechiae and edema
Most common in thoracic cavity and subcutaneous tissues
163
Inclusion Body Rhinitis
Infected cells are enlarged and posses intranuclear inclusion bodies [Arrow], especially in nasal glands. Hence, known as Inclusion Body Rhinitis
164
Inclusion Body Rhinitis
Clinical signs:
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
Subfamily: Gammaherpesvirinae
Genearal Properties
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
Malignant Catarrhal Fever (MCF)
Host, Etiology
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
Malignant Catarrhal Fever (MCF)
Wildebeest-associated MCF
[Alcephaline herpesvirus-1 (AHV-1)]:
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
Malignant Catarrhal Fever (MCF) Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:
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
Malignant Catarrhal Fever (MCF)
In Africa, MCF is predominantly found where
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
Malignant Catarrhal Fever (MCF)
Transmission of Wildebeest-associated MCF [Alcephaline herpesvirus-1 (AHV-1)]:
Between Wildebeest:
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
Malignant Catarrhal Fever (MCF)
Transmission of Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:
Between sheep:
Between sheep:
Respiratory (aerosol)
Transplacental rare
Contact with nasal secretions
172
Transmission from Sheep to Cattle:
Transmission of Sheep-associated MCF [Ovine herpesvirus-2 (OvHV-2)]:
Transmission from Sheep to Cattle:
Not known
Presumably by inhalation or ingestion
173
Malignant Catarrhal Fever (MCF)
Transmission of MCF viruses [AHV-1 and OvHV-2]:
_ 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
Malignant Catarrhal Fever (MCF)
Pathogenesis:
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
Malignant Catarrhal Fever (MCF)
Clinical Signs:
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
Malignant Catarrhal Fever (MCF)
Peracute form:
Peracute form:
Sudden, Characteristic clinical signs of “head and eye” form may not appear. High fever, acute gastroenteritis.
ALL OF A SUDDEN
177
Malignant Catarrhal Fever (MCF)
Head and Eye Form:
Early Stages:
Reddened eyelids
Bilateral corneal opacity
Crusty muzzle, nares
Nasal discharge
Salivation
MOST COMMON FORM
178
Malignant Catarrhal Fever (MCF)
Head and Eye Form:
Other Clinical signs:
Other Clinical signs:
Joints, superficial lymph nodes swell
Horn, hoof coverings slough
_ Nervous signs_
Incoordination,
head pressing,
nystagmus,
hyperesthesia
179
**_ZEBRA STRIPING_**: Bovine, colon. Severe longitudinal linear congestion of the mucosa
Malignant Catarrhal Fever (MCF)
Necropsy findings
**_THIS IS A CHARACTERISITIC SIGN_**
180
Mucoid exudate multifocally covers the nasal and pharyngeal mucosa.
MCF necropsy findings
181
Multifocal lymphoid infiltration in the renal cortex
MCF- necropsy findings
182
Enlarged prescapular lymph node
MCF necropsy findings
183
Multiple coalescing mucosal erosions in hard palate
MCF necropsy findings
184
Hemorrhage (and necrosis) in prescapular lymph node
MCF necropsy findings
185
Multiple pale foci of necrosis & ulcers in omasum
MCF necropsy findings
186
Bovine, kidney. Multiple pale foci in the cortex are foci of interstitial nephritis.
MCF necropsy findings
187
Malignant Catarrhal Fever (MCF)
Control:
Control:
Separation of cattle from wildebeest and sheep.
Incidence too low to justify development of a vaccine.
188
