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Veterinary Virology


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Main characteristics of prion

Main characteristics of prion
⬢ Neurological disease
⬢ Long incubation time
⬢ No immune response
⬢ No inflammation
⬢ Prion - protein infectious agent
⬢ Protein only - No nucleic acid detected
⬢ Resistant to heat, UV irradiation,
chemicals, proteases
⬢ Icelandic farmers - known for two
⬢ 1934 - sheep to sheep experimental
transmission by injection of infected brain
⬢ 1961 - sheep to mouse experimental
transmission by injection of infected brain
prion Brain lesions

Brain lesions
⬢ Astrocytosis
⬢ Vacuolization of neurons
scrapie Transmission and pathogenesis
Transmission and pathogenesis
• Horizontal
• Vertical - ewe to lamb
• IP. 1-5 years
• After infection, sequential spread into:
– Lymphoid tissues, tonsils, intestines, and
– Brain
⬢ "Mad cow disease"
⬢ Great Britain - 1986
⬢ Other countries - Ireland, France,
Germany, Switzerland, Japan
⬢ By 1997, over 172,000 confirmed cases in
the UK
Bovine Spongiform
Encephalopathy (BSE)
⬢ 1998 - 34 confirmed cases
⬢ Younger patients - 19-45 years
⬢ No risk factors
⬢ Longer course (mean 14 months vs.
standard 6 months)
⬢ Until 1989 ban - pooled homogenates of
bovine brains were used as binders in
Variant Creutzfeldt -Jakob Disease
⬢ Deer and elk
⬢ CO and WY endemic
⬢ Death within few months of clinical signs
Chronic Wasting Disease
Problems with antiviral therapy

Problems with antiviral therapy
⬢ Intracellular parasite
⬢ Stage of viral disease
⬢ Drug resistance
Drug targets in viral life cycle

Drug targets in viral life cycle
⬢ Attachment and penetration
⬢ Virus uncoating
⬢ Unique viral enzymes involved
⬢ Viral protein synthesis and processing
⬢ Assembly and release
⬢ Induced by
. 1.
⬢ 2.
⬢ 3.
⬢ _____________ specific
⬢ Not _______ specific
⬢ Induced by viral nucleic acids
⬢ Viral infected cells
⬢ Antigens
⬢ Species specific
⬢ Not viral specific
interferons Mechanism of action

Mechanism of action
⬢ Binding to cell surface receptor
⬢ Induction of antiviral effector molecules
⬢ Inhibition of viral mRNA translation
Interferon biological effects

Interferon biological effects
⬢ Initial viral defense
⬢ Important in recovery
⬢ Positive effects on T and B cells, Macrophages
⬢ Anticancer effects
Antiviral Drugs two types

Antiviral Drugs
⬢ Nucleoside analogs
⬢ Non-nucleoside analogs
⬢ Large 100-300 nm in
diameter, enveloped,
⬢ Linear, ds DNA
genome, 150 kb
⬢ Latency
⬢ Large family of
pathogens: mammals,
birds, fish, reptiles
and amphibians
Current Classification of
Current Classification of
⬢ Species, serial number
⬢ e.g., bovine herpesvirus 1 aka
infectious bovine rhinotracheitis
⬢ e.g., ranid herpesvirus 1 aka
Lucke frog herpesvirus
• ________________ (subfamily)
– Variable host range
– Rapid replication in cell culture
– Rapid cytopathic effect in cell culture
– Latency in sensory ganglia
• Example: Bovine herpesvirus 1(BHV-1)
⬢ Alphaherpesvirinae (subfamily)
– Restricted host range
– Slow replication
– Cytomegalia in cells
– Latency in secretory glands,
lymphoreticular cells, kidneys
• Examples: Porcine herpesvirus-2, aka
⬢ Betaherpesvirinae
⬢ Restricted host range
⬢ Replication in lymphoblastoid (T or
B) cells
⬢ Some lytic infections in epithelioid
and fibroblastic cells
⬢ Latency in lymphoid tissue
⬢ Example: alc
⬢ Gammaherpesvirinae
⬢ Enveloped, lipid,
⬢ Tegument,
⬢ Icosahedral
nucleocapsid, T=16
⬢ Fragile in the
⬢ Large ds DNA, 150 kbp
⬢ Linear in the virion
⬢ Circularizes in the infected cell
⬢ Encodes 70 to 200 proteins
⬢ Replication occurs in the nucleus
Latent Infection
⬢ Entry of herpesvirus into ________________
and transport of nucleocapsids to
______________ and _________
⬢ Viral DNA occurs as _________ (5-10) in
1% of ___________ in a __________
Latent Infection
⬢ Entry of herpesvirus into sensory nerve
endings and transport of nucleocapsids to
neuronal cell body and nucleus
⬢ Viral DNA occurs as episomes (5-10) in
1% of neurons in a ganglion
⬢ Latency-associated transcript (LAT) is
expressed during latency, but function is
not well understood
⬢ Stimulated by _______, _______, __________ associated with menstrual cycle,
⬢ Limited replication occurs in __________
⬢ Virions are transported down axons to
_______________ cell
⬢ Stimulated by stress, UV light, hormonal
changes associated with menstrual cycle,
⬢ Limited replication occurs in neurons
⬢ Virions are transported down axons to
epithelial cells
⬢ Lytic replication occurs in tissues
⬢ Limited by immune response

Alphaherpesviral Diseases

Alphaherpesviral Diseases
⬢ Host range: Bovidae, wild ruminants
⬢ Transmission: Aerosolized nasal
secretions, genital secretions, semen
⬢ Latent in trigeminal and sacral ganglia
⬢ Lifelong periodic shedding
⬢ Vaccines: inactivated and MLV IBR
Bovine Herpesvirus-1
bovine herpesvirus-1 Diseases
1. Infectious bovine rhinotracheitis (IBR),
“rednose”: respiratory disease/pneumonia
in feedlot and dairy calves
2. Conjunctivitis, “pinkeye”: keratitis,
corneal ulcers
3. Pustular vulvovaginitis, balanoposthitis:
venereal transmission, AI with
contaminated semen
4. Abortions: 4-7 months of gestation
following respiratory infection of dam
1. Rhinopneumonitis: fever, serous nasal
2. Subclinical infections are common
3. Outbreaks occur in young horses
4. Introduction of new stock, transport to
shows, racetrack or breeding facilities
5. Exposure to lat
Equine Herpesvirus-1&4
1. Abortions: dead foals, 4 to 11 months
2. Neonatal foal mortality: systemic
disease, interstitial pneumonia
3. Cell-associated viremia following
respiratory infection of the mare
4. Occurs 2 to 8 weeks post-infec
Equine Herpesvirus-1
1. Neurologic disease: ataxia, toe-dragging,
paralysis of bladder, tail, penis, paralysis
2. May/may not be preceded by respiratory signs
3. Can occur in outbreaks
4. Associated with specific strains
5. Pathogenesis: immune compl
Equine Herpesvirus-1
1. Coital exanthema
2. Transmission: venereal, iatrogenic
3. Vesicles, pustules, ulcers of the vaginal
mucosa, penis and prepuce
4. Depigmentation of vulva and perianal
5. Latent in sacral ganglion
6. Temperature
Equine Herpesvirus-3
1. Neonatal Mortality: systemic spread,
fever, abdominal pain, hemorrhagic
enteritis, shock, rapid progression to
2. Abortions: Focal necrosis of liver
3. Balanoposthitis: ulceration of preputial
mucosa, introduced via
Caprine Herpesvirus-1
1. PHV-1, Aujeszky’s disease
2. Abortions: embryonic death and
resorption, mummification, stillbirth,
weak pigs
3. Respiratory/generalized disease: fever,
sneezing, coughing, depression,
lethargy, anorexia, vomiting,
Pseudorabies - Pathogenesis
Pseudorabies - Pathogenesis
1. Ingestion/inhalation
2. Replication in oropharynx and
3. Viremia and spread to:
a. Reproductive tract and fetuses
b. Respiratory tract
4. Shedding via nasal and oral
secretions by recovered swine
5. Spread via cranial nerves to
ganglia via the axoplasm to the
6. Non-suppurative
meningoencephalitis and
7. Latent infection of ganglia
1. Decreasing mortality rates with
increasing age
2. Decreased growth rates in recovered
3. Eradication program in the U.S.
instituted in 1989
4. Currently, accelerated eradication
program in prog
1. “Mad itch”, disease in animals other
than swine, except tail-less apes
2. Virus in saliva of infected pigs,
transmission via ingestion, inhalation,
bites or wounds
3. Encephalitis, intense pruritus, selfmutilation,
1. Host Range: Felidae
2. Shedding by 30% of normal cats,
aerosol/contact transmission
3. Latent in trigeminal ganglion
4. Reactivated by parturition,
lactation, stress
Feline Herpesvirus-1
feline virus
1. Respiratory disease: sneezing,
serous to mucopurulent ocular and
nasal discharge, glossitis
2. Ocular disease: keratitis, corneal
3. Neonatal mortality: necrotizing
4. Vaccine reduc
Feline Herpesvirus-1
1. Host Range: Canidae
2. Seroprevalence: 20-30%
3. Transmission: oral-nasal route
4. Latent in sacral ganglia
5. Recrudescence at parturition and
infection of pups via vaginal secretions
6. Disease in puppies may or may not
Canine Herpesvirus-1
1. Neonatal mortality: systemic,
hemorrhagic disease
2. Puppies under 4 weeks of age
3. Abdominal pain, crying, dyspnea, rapid
progression to death
4. Viral replication at 33C, role of
hypothermia in generalized disease in
Canine Herpesvirus-1
Alphaherpesvirus infections of
avian species
Alphaherpesvirus infections of
avian species
1. Gallid herpesvirus 1 aka infectious
2. Gallid herpesvirus 2 aka Marek’s disease
3. Anatid herpesvirus aka duck plague aka
duck viral enteritis
4. Pacheco’s disease, psittacine herpesvirus-1
5. Great horned owl herpesvirus
• Host range: chickens
• Etiology: Gallid Herpesvirus-2
• Ubiquitous
• Serotypes:
– 1, oncogenic viruses in chickens
– 2, avirulent chicken viruses
– 3, avirulent turkey viruses
Marek’s Disease Virus
• Transmission: carrier birds
– Replicates in feather follicles
– Shed in feather dander
– Durable in the environment
• Affects chickens 12-24 weeks of age,
increased resistance with age
• Genetic resistance or s
Marek’s Disease Virus
• Lymphoproliferative disease, T
cell lymphoma
– Sciatic nerve: paralysis
– Liver, kidney, spleen: wasting,
hemorrhage due to rupture
– Iris: blindness
• Vaccines: live THV, attenuated
serotype I or serotype I
Marek’s Disease Virus
⬢ Outbreaks of
acute death in
wild and feral
⬢ High mortality
⬢ Enzootic in N.A.
⬢ A reportable
Duck Plague (Viral Enteritis)
Duck Plague
⬢ Host range: Anseriformes
⬢ Transmission:
⬢ Prevention/control:
Duck Plague
• Host range: Anseriformes
• Transmission:
– Direct contact with infected birds and
their secretions
– Contact with contaminated water
• Prevention/control:
– Separate domestic and wild waterfowl
– Carcass disposal, disinfection
– Vaccine is available under special
Clinical Presentation
⬢ Sudden death
⬢ Bloody or watery diarrhea
⬢ Dehydration
⬢ Oculonasal discharge
⬢ Photophobia
⬢ Drooping head and wings
⬢ Prolapsed penis
duck plague
Psittacine Herpesviruses
• Host range: ______________
• Etiologic agents:
– ______________ (PHV-1)
– PD-like disease viruses
• ______
• ______
• History of exposure to ________
Psittacine Herpesviruses
• Host range: psittacines
• Etiologic agents:
– Pacheco’s disease (PHV-1)
– PD-like disease viruses
• PHV-2
• PHV-3
• History of exposure to psittacines
PHV Clinical Presentation
1. Sudden death
2. GI: Anorexia, vomiting, bloody
diarrhea, increased thirst and
3. Respiratory: conjunctivitis
4. CNS: depression, tremors,
ataxia, opisthotonos, seizures
Other Avian Herpesviruses
• Raptors:
• Cranes:
• Passerines:
Other Avian Herpesviruses
• Raptors: owls, falcons
– Weakness, regurgitation, diarrhea
– Leukopenia, hepatosplenitis, hepatic
• Cranes: Inclusion body hepatitis
– Acute death
– Splenohepatomegaly, hemorrhagic
• Passerines:
– Conjunctivitis, respiratory disease
Betaherpesvirus infections
⬢ _____________________, porcine
cytomegalovirus, inclusion body rhinitis
⬢ Sneezing, coughing, serous to
mucopurulent nasal discharge, openmouth
⬢ Spread via aerosol/resp. secretio
Poricne herpesvirus 2
Gammaherpesvirus infections

Gammaherpesvirus infections
⬢ Alcelaphine herpesvirus 1,
Malignant catarrhal fever
⬢ Ovine herpesvirus 2, Malignant
catarrhal fever
⬢ Bovine herpesvirus-4
⬢ Equine herpesvirus-2, -5
⬢ Reservoir host: wildebeest, topi,
⬢ Affected species: cattle, deer, antelope
⬢ Etiologic agent can be grown in cell
⬢ Transmission: shed by wildebeest
particularly at calving
Alcelaphine herpesvirus 1
⬢ Reservoir host: domestic sheep
⬢ Affected species: cattle, deer, bison
⬢ Etiologic agent has not been isolated
⬢ Transmission: virus is shed by sheep,
increased transmission at lambing
⬢ Occurs in Nor
Ovine herpesvirus 2
⬢ Sporadic, fatal disease of cattle, deer,
bison and other ruminants
⬢ Characterized by profuse mucopurulent
nasal/ocular discharge
⬢ Keratoconjunctivitis with corneal opacity
⬢ Lymphadenopathy
⬢ V
Malignant Catarrhal Fever
Ovine herpesvirus 2
⬢ Non-enveloped,
icosahedral (T=25)
symmetry, 70-120
nm in diameter
⬢ Double-stranded,
linear DNA genome
36-44 kb
⬢ Pathogens of
mammals and birds
⬢ Discovered by Rowe (1953)
⬢ Explanted tonsillar tissue in culture
⬢ Highly host-specific and hostadapted
⬢ Persistent infections
⬢ Relatively stable in the environment
• ______________ (genus)
– Canine adenovirus-1, CAV-2
– Equine adenovirus
– Deer adenovirus
• ____________ (genus)
– Hemorrhagic enteritis in turkeys
– Marble spleen disease in pheasants
– Quail bronchit
• Mastadenovirus (genus)
– Canine adenovirus-1, CAV-2
– Equine adenovirus
– Deer adenovirus
• Avidadenovirus (genus)
– Hemorrhagic enteritis in turkeys
– Marble spleen disease in pheasants
– Quail bronchitis
• Atadenovirus (pending)
Adenoviridae Replication
⬢ Entry via endocytosis
⬢ DNA transport to
⬢ Early mRNA
⬢ Early protein
⬢ DNA genome synthesis
⬢ Late mRNA
⬢ Late protein translation
⬢ Assembly
1. Canine adenovirus 1
2. Canine adenovirus 2
3. Deer adenovirus
4. Equine adenoviruses
5. Miscellaneous adenoviruses
a. Etiology of infectious canine hepatitis
b. Host range: dogs, foxes, wolves,
coyotes, badgers, bears, skunks
c. Transmission: ingestion of virus in
urine, feces and saliva
d. Virus persists in kidneys and is shed
in the ur
Canine Adenovirus-1
1. Inapparent infections
2. Respiratory disease, component of
kennel cough
3. Peracute disease, sudden death
4. Acute disease: fulminant hepatitis,
enteritis +/- hemorrhage,
5. Immunopathologic diseases:
Infectious canine hepatitis
(Canine Adenovirus-1)
Infectious canine hepatitis
(Canine Adenovirus-1)
Clinical Presentation (Acute)
⬢ Fever
⬢ Leukopenia
⬢ Conjunctivitis, oculonasal discharge
⬢ Abdominal pain
⬢ Jaundice
⬢ Anemia, pale mucous membranes
⬢ Increased clotting time
⬢ Petechial hemorrhages
⬢ Disseminated intravascular coagulation
Pathogenesis of Infectious canine hepatitis
(Canine Adenovirus-1)
a. Ingestion
b. Replication in tonsils, Peyer’s patches
c. Viremia
d. Infects endothelial cells, DIC,
e. Infects liver, hepatitis, jaundice,
increased clotting time
f. Infects kidney, nephritis
Pathogenesis of “Blue-eye”
a. Immunopathologic consequence
observed in recovery phase 8 to 12 days
post-infection or vaccination with MLV
b. Virus-antibody complex formation
c. Deposition in capillaries in the ciliary
d. Impedes corneal fluid flow
e. Corneal edema
Canine Adenovirus-1 Prevention and Control
⬢ Vaccination, CAV-2
⬢ Rare disease in the U.S.
⬢ Occurs in unvaccinated puppies
⬢ Prolonged shedding of CAV-1 by
⬢ Lifelong immunity following natural
a. Etiologic agent: mild to inapparent
respiratory disease, tonsillitis,
pharyngitis, tracheitis, bronchitis
b. Host Range: Canidae
c. Antigenically similar to another dog virus, confers
cross-protective immunity and used as
Canine adenovirus-2
similar to CAV-1
a. Newly recognized (1993) hemorrhagic
disease in deer
b. Host Range: Black-tailed deer, muledeer,
white-tailed deer, moose,
c. Transmission: Direct contact
d. Described in captive fawns and freeranging
Adenovirus Hemorrhagic
Disease of Deer
a. 2 serotypes
b. Inapparent respiratory tract infections
in normal horses
c. Pneumonia, systemic spread to
pancreas, kidneys, bladder and GI tract
in immunocompromised hosts, e.g.,
severe combined immunodeficiency
Equine adenoviruses
Miscellaneous adenoviruses
a. Bovine – ___________
b. Swine – _________
c. Ovine – ________
d. Caprine – _________
e. Rabbits - __________
Miscellaneous adenoviruses
a. Bovine – inapparent or mild
respiratory disease
b. Swine – “
c. Ovine – “
d. Caprine – “
e. Rabbits - diarrhea
a. Ubiquitous viruses of birds
b. Host range: ___________
c. Serogroups based on group __________
1. Group I: ____________
2. Group II: ___________
3. Group III: _____________
d. _______ serotypes
a. Ubiquitous viruses of birds
b. Host range: domestic poultry,
pigeons, psittacines, ratites, raptors
c. Serogroups based on group antigen
1. Group I: quail bronchitis
2. Group II: turkey hemorrhagic
3. Group III: egg drop syndrome
d. Multiple serotypes
Clinical Presentation
a. Quail Bronchitis:_________
b. Hemorrhagic enteritis:__________
c. Marble spleen disease:_____________
d. Inclusion body hepatitis:_________
e. Egg drop syndrome: ______________
Clinical Presentation
a. Quail Bronchitis: respiratory
disease, rales, coughing, sneezing,
conjunctivitis, mortality 10-100%
b. Hemorrhagic enteritis: acute onset,
depression, bloody diarrhea, high
c. Marble spleen disease: sudden
death, dyspnea, bloody diarrhea
d.Inclusion body hepatitis: acute
onset of anemia, hepatitis, high
e. Egg drop syndrome: decreased
pigment, malformed shells,
decreased production
Aviadenoviruses Transmission
• Shed in the feces of healthy birds
• Ingestion
• Vertical transmission (?) IBH
• Persistent infection, reactivation
and intermittent shed
• Durable in the environment
• Strains tend to be more virulent for
species other than “normal” host
Aviadenoviruses Prevention and Control
• Vaccines:
– MSD for pheasants
– HE for turkeys
• Isolation, quarantine, all-in-all-out,
disinfection, sanitation
• Avoid feeding domestic poultry to
• Avoid contact with free-ranging
pigeons and other birds
⬢ ________________DNA
⬢ Ambisense or __________
⬢ Limited ______ and gene products
⬢ envelope +or-, shape:______
⬢ _______ in the environment
⬢ Single-stranded, circular DNA
⬢ Ambisense or positive-sense
⬢ Limited ORFs and gene products
⬢ Non-enveloped icosahedron, 17 - 22
nm in diameter
⬢ Durable in the environment
Circovirus Classification
• One genus:
– Chicken anemia virus
– Psittacine beak and feather
disease virus
– Porcine circovirus 1
– Porcine circovirus-2
• Host range: chickens
• Transmission:
– Horizontal: direct contact, fomites
– Vertical: hen to egg
• Age: young birds, 2-3 weeks of age
• Mortality: 10-50%
• Immunity: maternal Abs are
Chicken Anemia Virus

⬢ Acute infection
⬢ Anorexia, lethargy, depression
⬢ Decreased hematopoiesis: anemia,
pale birds
⬢ Hemorrhages:
⬢ Immunosuppression: atrophy of
lymphoid organs/tissues, bone
marrow, thymu
Chicken Anemia Virus

⬢ Host Range: Cockatoos, parrots and
budgerigars, etc.
⬢ Transmission: Shed in feather
follicular epithelium
⬢ Age: Fledglings and young birds
Psittacine Beak and Feather
• Dystrophic feathers
– Necrosis
– annular constrictions
– shaft hemorrhage,
– feather loss
• Beak dystrophy, reduced growth
• Abnormal plumage or color
Psittacine Beak and Feather
⬢ Canaries:
⬢ Canaries: Black spot
avian Circoviruses
Transmission and Control
• Shed in feather dander and feces
• Durable in the environment, resistant to
many disinfectants
– Clean up organic material
– 1:30 solution of bleach
– Environmental testing, PCR
• Maternal antibodies are protective
against disease but not infection
• Survivors are immune
• No vaccines available
Porcine Circoviruses
• Host species: ________
• Etiologic agents:
– _________________
(pathogenicity unknown)
– ________________
• Disease:_________________________
Porcine Circoviruses
• Host species: domestic swine
• Etiologic agents:
– Porcine circovirus-1
(pathogenicity unknown)
– Porcine circovirus –2
• Disease: Porcine post-weaning
wasting syndrome (PMWS)
Porcine Circoviruses Clinical Presentation
⬢ Specific pathogen-free herds
⬢ Piglets 6 weeks of age
⬢ Weight loss, lymphadenopathy,
dyspnea, diarrhea
⬢ 10% mortality
⬢ Disease is dependent on multiple
factors and etiologic agents
⬢ envelope+or- shape
⬢ ____________genome, 5kb
⬢ Pathogens of
humans and animals
⬢ Small (18-26 nm in
⬢ Non-enveloped,
icosahedral virus
⬢ Single-stranded
DNA genome, 5kb
⬢ Pathogens of
humans and animals
• T=1 icosahedron, 60 molecules of VP2
• Hollow cylinder at 5-fold axis of
• “________” surrounding 5-fold axis
• “__________” at the 3-fold axis is the viral
attachment pro
• T=1 icosahedron, 60 molecules of VP2
• Hollow cylinder at 5-fold axis of
• “Canyon” surrounding 5-fold axis
• “Spike” at the 3-fold axis is the viral
attachment protein which determines
tissue tropism and host range
• “Dimple” at 2-fold axis
• Parvovirinae (subfamily)
– __________ (genera)
– __________
– ___________
• Densovirinae (subfamily)
– ____________
– ____________
– ____________
• Parvovirinae (subfamily)
– Parvovirus (genera)
– Erythrovirus
– Dependovirus
• Densovirinae (subfamily)
– Densovirus
– Iteravirus
– Brevidensovirus
parvo Replication
• No viral polymerase encoded
• Requires host cell functions of late S or
early G2 phase of cell cycle
• Cellular DNA polymerase II extends ss
vDNA using the hairpin and free 3’-OH
as primer to make ds DNA intermediate
• Cellular transcriptases synthesize mRNA
• Alternate splicing generates multiple
parvo Target tissues
⬢ Stem cells in bone marrow and
lymphoid organs: erythroid
precursors, lymphocytes,
neutrophils, monocytes & platelets
⬢ Stem cells in the crypts of
⬢ Cells in the external granular layer
of the cerebellum
⬢ Emerged in 1978
⬢ Virgin-soil pandemics, high morbidity
and mortality rates
⬢ Host Range: Canidae, felidae
⬢ Transmission: acquired by ingestion,
shed in feces
⬢ Durable in the environment
Canine parvovirus-2
⬢ Hemorrhagic enteritis: 8 to 12 weeks
of age: leukopenia, lymphopenia,
fever, vomiting, anorexia, lethargy,
depression, bloody diarrhea,
dehydration, secondary septicemia,
⬢ Neonatal infections: 4 to 8 w
Canine parvovirus-2
• Etiologic agent: feline panleukopenia
virus, feline distemper virus, feline
enteritis, “cat fever”, feline ataxia
• Host range: Felidae, some canids
• Transmission: highly contagious,
shed in feces, vomit, urine, sali
Feline Parvovirus
• Acute infection: fever (>104oF),
lethargy, depression, anorexia,
mucopurulent oculonasal discharge
– Panleukopenia: leukopenia,
– Enteritis: bloody diarrhea,
– Peracute death
Feline Parvovirus
• Fetal or neonatal infection: in utero
to 4 weeks of age
– cerebellar hypoplasia, ataxia,
– Hydrocephalus, circling
– Microphthalmia, blindness
• Early gestation: abortion, resorption
Feline Parvovirus
parvo Prevention and Control
⬢ Vaccination: MLV vaccines
⬢ Maternal antibody: 6 to 16 weeks
of age, protects, interferes with
⬢ Sanitation/disinfection: 1:10-1:30
dilution of hypochlorite/bleach,
⬢ Isolation: Separation of infected
cats, duration of virus shed =
months post-recovery
Aleutian Disease of Mink
⬢ Host range:_______________
⬢ Etiologic agent: _________
⬢ Diseases:_______________________________________________________
Aleutian Disease of Mink
• Host range: Mink, ferrets, skunks,
• Etiologic agent: Aleutian Mink
Disease virus
• Diseases:
– Neonates: acute, fatal interstitial
– Adults: persistent infection,
chronic immune complexmediated
Aleutian Mink
Disease virus:Immune-complex disease
• Aleutian coat color homozygous
mutants with a defect of ____________________
• Failure of antibody to neutralize ____
and “__________” phagocytosis of
immune compl
Immune-complex disease
• Aleutian coat color homozygous
mutants with a defect of lysosomal
membranes (Chediak-Higashi)
• Failure of antibody to neutralize ADV
and “frustrated” phagocytosis of
immune complexes by macrophages
• Chronic plasmacytosis, hypergammaglobulinemia,
lymphadenopathy, vasculitis,
glomerulonephritis, arteritis, anemia
⬢ Ubiquitous virus of swine
⬢ Etiologic agent: SMEDI, reproductive
⬢ Host range: swine
⬢ Transmission: Oral-nasal, venereal,
virus crosses the placenta
Porcine Parvovirus
Porcine Parvovirus
Clinical Presentation
⬢ Infertility: < 30 days, fetal death and
⬢ Abortions: 30-70 days, fetal death,
mummification, stillbirths
⬢ Weak pigs: > 70 days, stunting,
immune response, immunotolerance
Porcine Parvovirus Prevention and Control
⬢ Persistent infection (immunotolerant)
occurs in pigs infected >70 days of
gestation, chronic shedders
⬢ Durable in the environment up to 20
weeks, resistant to many disinfectants
⬢ Vaccination: inactivated vaccines,
immunity 4-6 months
⬢ Natural infection: exposure of gilts,
lifelong immunity
• Aka the minute virus of dogs
• Disease:
– interstitial pneumonia of
neonatal puppies, mild enteritis
– Fetal death, abortions,
• Approximately 50% of adult dogs
have antibodies
Canine Parvovirus-1
⬢ Genetically distinct from CPV-2
⬢ Mink enteritis virus
⬢ Kilham virus of rats
⬢ H-1 virus of rats
⬢ Minute virus of mice
⬢ Enveloped +/-, size
⬢ _____________________________genome 30kb
⬢ Pathogens of __________
and ____________
⬢ Enveloped, large
peplomers, helical
⬢ Single-stranded,
positive-sense, linear
RNA genome 30kb
⬢ Pathogens of avian
and mammalian
• Coronavirus (genus)
– Group I:
– Group II:
– Group III:
– Unclassified:
• Torovirus:
• Coronavirus (genus)
– Group I: (mammalian) TGE,
– Group II: (mammalian, avian)
– Group III: (avian) IBV
– Unclassified: rabbit
• Torovirus: Breda, Berne
1. Enteritis (diarrhea):
2. Respiratory:
3. Systemic:
Pathophysiologic Classification
1. Enteritis (diarrhea):
2. Respiratory: IBV, PHEV,
3. Systemic: FIPV, MHV

Coronaviral Diseases

Coronaviral Diseases
Coronaviruses of Swine
Coronaviruses of Swine
1. Transmissible gastroenteritis virus
2. Porcine respiratory coronavirus (PRC)
3. Vomiting and wasting disease, porcine
hemagglutinating encephalomyelitis
virus (PHEV)
4. Porcine epidemic diarrhea (PEDV)
⬢ Host range: Domestic swine
⬢ Etiologic agent family: cornaviridae
⬢ Disease: Highly contagious diarrhea of
piglets, occurs in explosive epidemics
⬢ Transmission: fecal-oral route
⬢ Infection is restricted to the
Transmissible Gastroenteritis
⬢ Severe disease in piglets <3weeks of age
⬢ Vomiting, profuse diarrhea, dehydration
⬢ Weight loss, gaunt pigs
⬢ Death in 2 to 5 days
⬢ High mortality (up to 100%) in piglets <2
weeks of age
Transmissible Gastroenteritis
(TGEV) cornaviridae
Transmissible Gastroenteritis
(TGEV) cornaviridae
⬢ Gastric pH is relatively neutral in
neonates and is buffered by milk
⬢ Virus replicates rapidly in mature
enterocytes at the villous tips
⬢ Villi are blunted and replenished with
immature enterocytes
⬢ Decreased digestive enzyme expression
and absorption of nutrients leads to
increased osmolarity of intestinal
contents and efflux of water into the
Transmissible Gastroenteritis
(TGEV) cornaviridae
Prevention and Control
⬢ _________ antibodies (________ immunity)
play an important role in the severity of the
⬢ ___________(colostrum, milk) is protective
Prevention and Control
⬢ Maternal antibodies (lactogenic immunity)
play an important role in the severity of the
⬢ Mucosal IgA (colostrum, milk) is protective
⬢ Systemic IgG is not protective
⬢ Maternal lymphocyte trafficking from the
gut to mammary gland results in IgA
secretion in colostrum/milk
⬢ Oral inoculation of sows with dead piglets
stimulates production of TGEV-specific
IgA in milk
⬢ Host range: Domestic swine
⬢ Etiologic agent: Deletion mutant of
TGEV lacking a single epitope of the E2
(Spike) protein
⬢ Transmission: respiratory secretions
⬢ Disease: subclinical respiratory infection
Porcine respiratory coronavirus
⬢ Host range: domestic swine
⬢ Etiologic agent: __________
⬢ Transmission: inhalation of aerosolized
respiratory secretions
⬢ Diseases: acute vomiting and wasting of
young pigs < 3weeks of age, neurologic
Porcine hemagglutinating
encephalomyelitis virus (HEV
⬢ Vomiting, wasting and acute
encephalomyelitis in young pigs
⬢ Anorexia, hyperesthesia, muscle tremors,
⬢ Vomiting, depression, emaciation
⬢ Mortality: up to 100%
⬢ Must be distinguished from porcine
Porcine hemagglutinating
encephalomyelitis virus (HEV
⬢ Etiologic agent: a porcine coronavirus
unrelated to TGEV
⬢ Geographic range: Europe and Asia
⬢ Clinical presentation: similar to TGE but
usually less severe
⬢ Mortality = 50 to 90%
Porcine epidemic diarrhea
⬢ Ubiquitous infection of cattle
⬢ Host range: domestic cattle, elk
⬢ Transmission: fecal-oral route
⬢ Disease: Malabsorptive diarrhea
⬢ Prevention/Control: maternal immunity
Bovine coronavirus enteritis
Etiologic agent: bovine coronavirus
⬢ Major cause of diarrhea in calves
⬢ Occurs 4 to 5 days post-ingestion
⬢ Affects calves 3 to 21 days of age with a
peak age of 1 week
⬢ Profuse liquid diarrhea, hypoglycemia,
lactic acidosis, hypovolemia, shock,
Bovine coronavirus enteritis
Winter dysentery
⬢ Sporadic disease of adult cattle
⬢ Etiologic agent: not determined,
coronaviruses implicated, BVDVassociated
with severe disease
⬢ Clinical Presentation: Profuse watery to
bloody diarrhea, depression, anorexia,
respiratory signs, decreased milk
• Clinical presentation: isolated from
“summer” pneumonia cases, epidemics of
respiratory disease in feedlot calves
• Other factors/agents involved in severe
disease, e.g., BVDV
Bovine respiratory coronavirus
⬢ Etiologic agent: indistinguishable from
bovine enteric coronaviruses
• Host range: chickens
• Transmission: aerosolized respiratory
secretions, highly contagious
• Diseases: strain dependent, multiple
– Acute respiratory disease
– Nephritis
⬢ Etiologic agent: Infectious bronchitis
virus (IBV)
• Infectious bronchitis:
– High morbidity, low mortality
– Sneezing, coughing, oculonasal discharge,
• Decreased egg production: to <50%, egg &
shell quality, egg yolk peritonitis, permanent
damage to
Avian Infectious Bronchitis
Avian Infectious Bronchitis
Prevention and Control
⬢ Shedding by carriers for months after
⬢ IBV can persist up to 4 weeks outside the
⬢ Vaccination with attenuated or
inactivated virus
⬢ A sporadic, fatal disease of cats
⬢ Host range: Felidae

ubiquitous coronavirus
⬢ Transmission: Fecal-oral or respiratory
⬢ Age distribution: Disease of cats < 1
year old or >13 years
⬢ Target cell is
Feline infectious peritonitis
____________is a mutation of
an enteric feline coronavirus (FECV), a
ubiquitous coronavirus, type I and II
Risks associated with FIP
• Age of initial infection with FECV:
– ______________
– ______________
• High dose of ______
• Defects of ____
– _________________, e.g., FeLV,
FIV or prior FPV infection
Risks associated with FIP
• Age of initial infection with FECV:
– <16 weeks of age
– >13 years of age
• High dose of FECV
• Defects of CMI
– Immunosuppression, e.g., FeLV,
FIV or prior FPV infection
– Genetic predisposition, e.g.,
Persian cats, cheetahs
⬢ Mutation in _____ yields ____ that
replicates in macrophages
⬢ Systemic spread in _______
⬢ Defective _____ leads to persistent FIPV
⬢ ________________ stimulation leads to
⬢ Mutation in FECV yields FIPV that
replicates in macrophages
⬢ Systemic spread in macrophages
⬢ Defective CMI leads to persistent FIPV
⬢ Chronic antigenic stimulation leads to
production of binding Abs
⬢ FIPV + Ab = immune-complex formation
⬢ Immune-mediated vasculitis (Type III/IV)
Clinical Presentation
1. Wet or effusive form: __________________
– Abdominal or thoracic ______, with
elevated ________ content, >35 g/dl
– Hyper________
– Hypo_________
• Chronic fever of ______ origin<
Clinical Presentation
1. Wet or effusive form: severe vasculitis
and leakage
– Abdominal or thoracic effusion, with
elevated protein content, >35 g/dl
– Hypergammaglobulinemia
– Hypoalbuminemia
• Chronic fever of unknown origin
• Anorexia, depression, anemia, weight loss
• Dyspnea with thoracic effusion
Clinical Presentation
2. Dry or non-effusive form:
• ______ fever, wasting
• Renal disease, ________
• Hepatic disease, _______
• Anterior _______
• Neurologic signs
• Pathologic lesions:
– _
Clinical Presentation
2. Dry or non-effusive form:
• Chronic fever, wasting
• Renal disease, dehydration
• Hepatic disease, icterus
• Anterior uveitis
• Neurologic signs
• Pathologic lesions:
– Moderate vasculitis
– Granuloma formation
Control and Prevention
Control and Prevention
⬢ FeCV infections usually occur very early
in life; test new introductions
⬢ FeCV is transmitted from cat to cat;
reinfection occurs; persistent shedders
maintain the infection in multiple cat
⬢ FIPV is not transmitted from cat to cat
⬢ FIP has an immunopathologic component
⬢ FIP vaccination may enhance the risk of
⬢ Host range: Canidae
⬢antigenically related to FECV
⬢ Transmission: fecal-oral
⬢ Disease: Acute diarrhea of dogs, more
severe in puppies, subclinical infections
⬢ Most infections occur by 4 to 12 wks of age
⬢ Co
Canine coronavirus enteritis
⬢ Etiologic agent: Canine coronavirus
⬢ Nonfatal, self-limiting diarrhea
⬢ Frequently inapparent
⬢ Incubation period of 1 to 4 days
⬢ Acid-stable, remain infective following
passage through gastric acid
⬢ Replicates in mature enterocytes of villou
Canine coronavirus enteritis
⬢ Etiologic agent: Canine coronavirus
⬢ Host range: mice
multiple strains
⬢ Diseases: Enteritis, hepatitis, demyelinating
encephalomyelitis, nephritis
⬢ Transmission: introduction of carriers,
fomites, wild mice
⬢ Clinical: diarrhea with high mortality,<
⬢ Etiologic agent: mouse hepatitis virus
a coranavirus
⬢ Host range: rats
⬢ Disease: inflammation of the salivary and
nasolacrimal glands, self-limiting
⬢ Transmission: direct contact, fomites,
aerosolized ocular secretions
⬢ Clinical: lacrimation, exophthalmus,
⬢ Etiologic agent: sialodacryadenitis virus
a coronavirus
⬢ Host range:
⬢ Transmission:
⬢ Disease:
⬢ Replication:
⬢ Host range: Horses, humans, cattle, pigs,
⬢ Transmission: presumed fecal-oral
⬢ Disease: diarrhea in humans, cattle, pigs
and turkeys; inapparent infections in
⬢ Replication: difficult to culture or
⬢ Distribution: >80% seroprevalence
⬢ Mild to moderate diarrhea in calves up to
10 months of age
⬢ Infects infects the mid- and lower parts of
intestinal villi, including the crypt cells, of
small and large intestines
Torovirus diarrhea of cattle
⬢ Emerged in Nov. 2002,
Guangdong, China
⬢ Reservoir host: unknown,
civet cats, raccoon dogs
⬢ Clinical disease in
humans: severe, acute
interstitial pneumonia,
pulmonary edema,
hypoxia, respiratory
Severe Acute Respiratory Syndrome
Innate Immunity
1. Anatomic: _________
2. Physiologic: ____________
3. ________ and _______ cells

4. Interferons and cytokines
5. Complement
6. Presence of receptors, enzymes,
etc. to support virus replication
Innate Immunity
1. Anatomic: skin, mucosa
2. Physiologic: gastric acid,
lysozymes in tears
3. Natural Killer (NK) cells, and
4. Interferons and cytokines
5. Complement
6. Presence of receptors, enzymes,
etc. to support virus replication
Characteristics of Innate
⬢ No antigen specificity
⬢ No memory
⬢ No MHC class restriction
⬢ No antibody dependence
⬢ Target cells, infected by viruses, viral Ag
presented in the context of ____
⬢ Perform ______________
⬢ Antigen presenting cells, viral Ag presented
in the cleft of _________
⬢ Release __________ involv
⬢ Target cells, infected by viruses, viral Ag
presented in the context of MHC I
⬢ Perform phagocytosis
⬢ Antigen presenting cells, viral Ag presented
in the cleft of MHC II
⬢ Release cytokines involved in macrophage
and T cell activation: IL-1, IL-2, TNF, IFNs
⬢ Cause tissue injury: lysosomal enzymes,
reactive oxygen, NO, prostaglandins,
⬢ Release growth factors involved in
angiogenesis, fibrosis, healing.


⬢ No _________ specificity
⬢ __________ specific
⬢ Produced ________ in the course of
⬢ Protect ___________ cells
⬢ Inhibit _________ spread of virus
⬢ Production/treatment correlates w
⬢ No viral specificity
⬢ Species specific
⬢ Produced early in the course of
⬢ Protect neighboring cells
⬢ Inhibit early spread of virus
⬢ Production/treatment correlates with
⬢ Inhibition of production leads to
severe disease

Antiviral activities of IFN

Antiviral activities of IFN
• ________ and _______ proteins
• Activation results in amplification of
products that:
• Serum and membrane proteins
• Activation results in amplification of
products that:
–Form pores in membranes
(membrane attack complex)
–Mediate inflammation
–Act as opsonins [C3b]
–Solubilize immune complexes

what happens to the mice

type of immunity
Acquired Immunity
⬢ Inducible protection against
infection, disease or death
⬢ Requires time to develop
⬢ Specific for antigen
⬢ Responds to many antigens
⬢ Memory
⬢ Humoral vs cell-mediated
Anti-Viral Actions of Antibodies
Anti-Viral Actions of Antibodies
1. Neutralization
– Prevents virus from binding to receptor
– Prevents virus from uncoating
2. Opsonization
3. Antibody dependent cell-mediated
– Macrophages, neutrophils, K cells
4. Complement activation
Cell-Mediated Immunity
Cell-Mediated Immunity
1.T helper cells (CD4+)
a.Th1 (inflammatory)
b.Th2 (helper)
2.T cytotoxic (CD8+)
3.T suppressor (CD8+)
4.T delayed type hypersensitivity
Endogenous Pathway
⬢ Proteins made in the cytosol are
digested by __________ into
⬢ _____ transports the peptides to
the ____
⬢ _______ molecules associate with
the peptides
⬢ MHC I + p
Endogenous Pathway
• Proteins made in the cytosol are
digested by proteosomes into
• TAP transports the peptides to
the ER
• MHC I molecules associate with
the peptides
• MHC I + peptide complex is
exported to the cell’s surface
Exogenous Pathway
⬢ _________ of extracellular
⬢ __________ enzyme
digestion produces peptides
⬢ ______ molecules are
transported to the endosomes and
pick up the peptides
⬢ MHC II + pepti
Exogenous Pathway
• Endocytosis of extracellular
• Endosomal/lysosomal enzyme
digestion produces peptides
• MHC II molecules are
transported to the endosomes and
pick up the peptides
• MHC II + peptide complex is
exported to the cell’s surface

MHC Restriction

MHC Restriction

fill in the chart

out come of viral infection
Gell-Coombs Classification of
⬢ Type I, Anaphylaxis
⬢ Type II, Cytotoxic
⬢ Type III, Immune complex,
Arthus reaction
⬢ Type IV, Cell-mediated, delayed
type of hypersensitivity?
⬢ IgE + viral antigen release of granules
from mast cells containing histamine,
heparin, serotonin and plasma kinins
⬢ May account for erythema,
congestion, swelling in upper
respiratory tract p
Type I, Anaphylaxis
Type of hypersensitivity?
⬢ IgM/IgG + viral antigen on the cell
surface results in cell destruction
⬢ May account for hemolysis during
acute infection with EIAV leading
to anemia
⬢ May account for liver necrosis in
Type II, Cytotoxic
Type of hypersensitivity?
⬢ IgG + viral antigen leads to immune
complex formation
⬢ Lattice formation dependent on relative
amounts of IgG and antigen
⬢ Dependent on Ig affinity, presence of
complement, abilit
Type III, Immune Complex
Type III, Immune Complex
⬢ e.g., Aleutian disease of _____
⬢ ____virus
⬢ _________ infection
⬢ Immune complex formation
⬢ Deposition in ________,
__________, ______, ________
Type III, Immune Complex
⬢ e.g., Aleutian disease of mink
⬢ Parvovirus
⬢ Persistent infection
⬢ Immune complex formation
⬢ Deposition in renal glomeruli,
skin, synovium, choroid plexus
Type of hypersensitivity?
⬢ Virus-specific T lymphocytes +
viral antigens presented in the
context of MHC
⬢ Inflammation in an unfortunate
⬢ E.g., CTLs and encephalitis in
LCMV infection in adult mice, or
Type IV, Cell-mediated
⬢ An immune response directed
against normal host components
which results in tissue injury
⬢ Can be primarily a humoral immune
⬢ Can be primarily a cell-mediated
immune response
⬢ Vaccine-induced suspe
Viral Diagnostics
⬢ Infectious virus
⬢ Whole virions
⬢ Viral proteins
⬢ Viral RNA/DNA
⬢ Serology
Virus Isolation

Virus Isolation
Animal Inoculation
⬢ Some viruses do
not replicate in
cell culture and
only grow by this
⬢ Expensive
⬢ Slow
⬢ Cumbersome
Inoculation of embryonated eggs
⬢ Growth of
unknowns especially
avian viruses &
⬢ Sensitive
⬢ Expensive
⬢ Slow
⬢ Technical expertise
and equipment
Inoculation of cell culture
⬢ Sensitive
⬢ Allows identification
of unknown agents
⬢ Allows recovery of
viruses for further
⬢ Expensive
⬢ Slow
⬢ Cytoplasmic vacuolation
⬢ Changes in cell shape
⬢ Cell death
⬢ Syncytia formation
⬢ Transformation
Electron Microscopy viral detection
⬢ Based on viral
⬢ Used to detect whole
virions in feces
⬢ Sensitive
⬢ Rapid
⬢ Expensive, equipment
and technical time
⬢ Technically difficult
Polymerase Chain Reaction (PCR) for viral dection
Samples Samples MW MW
POS POS 1 2 3 1 2 3
⬢Applicable to bulk or pooled
⬢Technical considerations
⬢Subject to false positives due
to DNA contamination
⬢Subject to false negatives due
to inhibitors of reagents
⬢Requires knowing the viral
genetic sequence

type of viral test?
types of Serology for viral testing
⬢ Immunological footprints
⬢ Serum neutralization (SN, VN)
⬢ Enzyme-linked immunosorbent assay
⬢ Agar gel immunodiffusion (AGID)
⬢ Hemagglutination inhibition (HI)
⬢ Acute vs convalescent samples
⬢ IgM vs IgG
⬢envelope +/-
⬢ ____________________
⬢ __________
and __________
⬢ Non-enveloped,
double capsid, 80 nm
icosahedral virus
⬢ Double-stranded, 10-
12 segmented RNA
⬢ Arthropod-borne
and enteric
1. __________(genus): African horse sickness,
bluetongue viruses, epizootic hemorrhagic
disease of deer, Ibaraki virus
2. ____________: rotaviruses of many species
3. ____________: mammalian and avian
1. Orbivirus (genus): African horse sickness,
bluetongue viruses, epizootic hemorrhagic
disease of deer, Ibaraki virus
2. Rotavirus: rotaviruses of many species
3. Orthoreovirus: mammalian and avian
4. Coltivirus: Colorado tick fever virus
5. Aquareovirus: viruses of fish and
⬢ Arthropod-borne, Culicoides spp.
⬢ Tropism: reticuloendothelial cells,
endothelial cells
⬢ Pathogenesis: vasculitis, vascular
⬢ Pathologic lesions: edema,
⬢ Host range: Equidae, dogs, elephants,
zebras, camels, (humans)
⬢ Etiologic agent: (1-9 serotypes), multiple strains
⬢ Exotic to the U.S.
⬢ Disease: Highly lethal disease of horses,
90-95% mortality
⬢ Transmission
African Horse Sickness
African Horse Sickness (Orbiviruses)Clinical Presentation-Horses
1. Pulmonary form: fully susceptible horses
⬢ Fever for 1 to 2 days
⬢ Dyspnea, coughing, frothy nasal
discharge, peracute death
⬢ Mortality rate approaches 100%
2. Cardiac form: donkeys, vaccinated horses
⬢ Fever for 5 to 8 days
⬢ Edema of supraorbital fossae, head
⬢ Colic, subacute course
⬢ Mortality rate = 50-70%
African Horse Sickness (Orbiviruses)Pathogenesis
⬢ Culicoides bite
⬢ Replication in local lymph nodes
⬢ Primary viremia
⬢ Infection of reticuloendothelial cells
⬢ Secondary viremia
⬢ Replication in endothelial cells
⬢ Vasculitis, damage to blood vessels
⬢ Pulmonary edema, petechial
hemorrhages in pericardium
⬢ Host range: sheep, camelids, bighorn
sheep, goats, cattle, deer, bison, elk,
pronghorn, other wild ruminants, (dogs)
⬢1-25 serotypes
⬢ Disease: clinical disease in sheep, subclinical
infections in cattle
• Fever, “wool break”
• Salivation, hyperemia of oral mucosa,
oral ulcers, frothing of the mouth
• Cyanosis of tongue
• Nasal discharge, serous to
• Edema of muzzle, ears, head, neck
• Coron
bluetongue Reproductive effects - sheep
⬢ Fetal infection
⬢ Congenital defects: hydrocephalus,
hydrancephaly, porencephaly,
mummification, arthrogryposis
⬢ Abortion
⬢ Transient infertility in rams
⬢ Reduced lamb crop
Culicoides varipennis and blue tongue virus
• “no-see-ums”, midges
• Late summer to fall
• Breed in damp
organic material
• Virus is acquired in a
blood meal from
viremic animal
• Replicates in midge
• Shed in saliva during
every blood meal
bluetongue Prevention and Control
⬢ Found throughout W. & S.E. U.S.
⬢ Reservoirs: Maintained on RBCs of
infected cattle and sheep for
prolonged intervals
⬢ Non-tariff trade barrier: restriction to
trade with New York, Canada and
other countries
⬢ Control of Culicoides breeding
⬢ Host range: WTD, mule deer,
pronghorn, reservoir host?
⬢ found in the western
and S.E. U.S.
⬢ Disease: acute hemorrhagic fever
⬢ Transmission: Culicoides spp.
Epizootic Hemorrhagic Disease
of Deer
⬢ Deer carcasses in creeks, late
⬢ Fever, anorexia, ataxia
⬢ Lethargy, weakness
⬢ Salivation, oral ulcers
⬢ Hyperemia of mucous membranes, skin
⬢ Edema of conjunctiva, head and neck
⬢ Lameness,
Epizootic Hemorrhagic Disease
of Deer
⬢ shape:________
⬢______________________ genome
⬢ Stable in the
⬢ Stable at __ pH
⬢ Resistant to ________
⬢ Double-shelled
icosahedron (80 nm)
⬢ ds RNA, 10-12
segmented genome
⬢ Stable in the
⬢ Stable at low pH
⬢ Resistant to lipid
• Rotavirus diarrhea, “milk scours”
• Host range: cattle, sheep, pigs,
horses, rabbits, rodents, humans
• Transmission: fecal-oral route
• Disease: malabsorptive diarrheas,
dehydration, acid-base imbalance
Rotavirus enteritis
Rotavirus Classification
⬢ Based on genotype and group-specific viral
antigen (VP6)
⬢ Group A:
⬢ Group B:
⬢ Group c:
⬢ Group D:
⬢ Group E:
⬢ Group F:
⬢ Based on genotype and group-specific viral
antigen (VP6)
⬢ Group A: humans, cattle, other species
⬢ Group B: humans
⬢ Group C: swine
⬢ Group D: fowl
⬢ Group E: swine
⬢ Group F: fowl
Rotavirus enteritis Pathogenesis
⬢ Infection and cytolysis of mature
enterocytes at the tips of the villi
⬢ Exposure of the basement membrane
⬢ Migration of immature enterocytes
⬢ Blunting & fusion of adjacent villi
⬢ Reduced absorptive surface/function
⬢ Transient malabsorption
⬢ Rotavirus infection specifically and
selectively decreases ________
expression on the ___________
⬢ A functional __________
peptide secreted from rotavirusinfected
⬢ Rotavirus infection specifically and
selectively decreases sucraseisomaltase
expression on the apical
brush border
⬢ A functional NSP4 enterotoxin
peptide secreted from rotavirusinfected
Rotavirus enteritis
Factors influencing disease
⬢ Proteases:____________________________________________
⬢ Milk:_____________________________
⬢ Age:________________________________________
⬢ Immunity:____________________
Factors influencing disease
⬢ Proteases: VP4 cleavage is necessary
for penetration of the host cell
⬢ Milk: Osmotic pressure of proteins
and saccharides
⬢ Age: Age-dependent expression of
receptors on enterocytes
⬢ Immunity: colostrum and milk
Rotavirus enteritis Clinical Presentation
⬢ Neonatal animals: 1 to 8 weeks of age
⬢ Incubation period: 12 hours to 6 days
⬢ Watery diarrhea, dehydration
⬢ Anorexia, depression, vomiting
⬢ Death is due to severe dehydration
secondary to fluid loss
Rotavirus enteritis Clinical considerations
⬢ Shed in large amounts, 109 to 1012
virions/gram of feces
⬢ Virus shedding: up to 14 days p.i.
⬢ Spread on milk buckets, utensils,
boots, hands
⬢ Not inactivated by chlorination
Rotavirus enteritis Contributing factors
⬢ Lack of maternal immunity, not
necessarily failure of passive transfer
⬢ Exacerbated by milk ingestion
⬢ Chilling, overcrowding
⬢ Lack of sanitation
⬢ Other pathogens: E. coli, coronavirus,
⬢ Zoonotic disease
⬢ Fever, myalgia, headache,
hemorrhagic fever
⬢ Tick-borne, D. andersonii
⬢ Virus is transmitted
⬢ Virus overwinters in nymphs
and adults
⬢ Pro
Colorado Tick Fever
⬢ Envelope +/-
⬢ genome:_________
⬢ _________ and
⬢ Enveloped, helical
virus (80-120 nm)
⬢ Single-stranded,
negative or
ambisense, 3 RNA
⬢ Rodent- and
family Bunyaviridae
Classification (genera)
1. ________: Rift Valley fever virus
2. ________: Nairobi sheep disease,
Crimean-Congo hemorrhagic fever
3. __________: Akabane, Cache Valley,
La Crosse (California encephalitis)
Classification (genera)
1. Phlebovirus: Rift Valley fever virus
2. Nairovirus: Nairobi sheep disease,
Crimean-Congo hemorrhagic fever
3. Bunyavirus: Akabane, Cache Valley,
La Crosse (California encephalitis)
4. Hantavirus: Sin Nombre, Prospect
Hill, etc.
• Host range: cattle, sheep, humans,
wildlife species
• Diseases: hemorrhagic fever, hepatitis,
abortion, encephalitis
• Mortality:
– 90% in lambs
– 20-60% in adult sheep
– 90-100% abortion rate in ewes, cow
Rift Valley Fever
Rift Valley Fever Transmission
• Mosquito-borne, Culex, Aedes spp.
– transmitted transovarially
– eggs survive for extended periods
• Ingestion of contaminated meat
• Handling of contaminated carcasses
⬢ Host range: cattle, sheep, humans,
wildlife species
⬢ Entry via mosquito bite or oropharynx
⬢ Incubation of 30 to 72 hours during which
virus replicates to high titers
⬢ Virus spreads to the liver and
Rift Valley Fever
⬢ Host range: sheep and goats
⬢ Vertebrate reservoir host: ?
⬢ Transmission: Rhipicephalus appendiculatus,
transstadial/transovarial transmission,
persistent infection of adult ticks
⬢ Disease: Fever, hemorrhagic enteriti
Nairobi sheep disease
• Host range: humans
• Disease: severe hemorrhagic fever,
necrotizing hepatitis, myocarditis,
• Reservoir hosts:
– Small mammals and birds
– Wild and domestic ruminants, sheep,
goats, cattle
Crimean-Congo Hemorrhagic
Crimean-Congo Hemorrhagic
Fever Transmission
⬢ Tick-borne, Hyalomma spp.,
⬢ Direct contact with infected animals
⬢ Human to human contact, e.g.,
nosocomial infections
⬢ Host range: cattle, sheep, goats

⬢ Diseases: developmental defects of the
spine, joints, e.g., arthrogryposis,
neurologic defects, e.g., hydranencephaly,
abortions, fetal death
⬢ Transmission: mosquito- & Culico
⬢ Etiologic agent: Akabane virus
⬢ Host range: sheep, goats
⬢ Disease: fetal defects, similar to
Akabane, following maternal
infection 30 to 60 days of gestation
⬢ Transmission: mosquito-borne
⬢ Reservoir host: deer
⬢ Geographic range: U.S.
Cache Valley virus
• Host range: humans zoonotic disease
• Reservoir hosts: Apodemus agrarius,
Peromyscus spp., voles, mice, rats
• Persistent, inapparent infection in
• Transmission:
– virus is shed in saliva, urine, feces (
Hantavirus diseases
1. Hemorrhagic fever with renal syndrome:

2. Hantavirus pulmonary syndrome:

Hantavirus diseases
1. Hemorrhagic fever with renal syndrome:
⬢ Fever, headache
⬢ Hemorrhages in multiple organs
⬢ Acute renal failure with shock
2. Hantavirus pulmonary syndrome:
⬢ Acute respiratory distress syndrome
⬢ Fever, myalgia, headache
⬢ Nonproductive cough, shortness of
⬢ Pleomorphic,
envelope +/-
⬢ 50-300 nm
⬢ _______________genome,
⬢ __________ reservoirs
⬢ Zoonoses
⬢ Pleomorphic,
⬢ 50-300 nm
⬢ Single-stranded
RNA genome,
⬢ Rodent reservoirs
⬢ Zoonoses
⬢ Pleomorphic
⬢ Envelope containing glycoproteins
⬢ 2 single-stranded, ambisense RNA
segments, L, S
⬢ Circularized nucleocapsids
⬢ Contains host cell ribosomes
• Lymphocytic
choriomeningitis virus
• ______________
– Lassa fever virus
• _____________
– Junin, Machupo, Sabia,
Guanarito, Tacaribe, etc.
• Lymphocytic
choriomeningitis virus
• Old World
– Lassa fever virus
• New World
– Junin, Machupo, Sabia,
Guanarito, Tacaribe, etc.
• Highly host-adapted
• Usually inapparent infection in
• Vertical transmission
• Persistent infection
• Shed virus in urine, saliva, feces
• Important infection in laboratory
rodents and “pocket p
Arenavirus infections in rodents
• Host species: mice, hamsters
• Clinical presentation:
– Usually asymptomatic
– Runting, failure to thrive
–Immunopathologic disease,
Lymphocytic choriomeningitis
Lymphocytic choriomeningitis
virus Zoonosis
• Clinical disease
• At risk:
• Clinical disease
– “flu-like” illness, fever, headache
– Aseptic meningitis
– Severe encephalomyelitis
– Intrauterine infections leading to fetal
death and congenital defects of brain
• At risk:
– children handling hamsters as pets
– laboratory animal workers
⬢ envelope +/-,
stable at __ C for __
min and pH ______
⬢ Genome:
⬢ Pathogens of ______, ____ and __________
⬢ Non-enveloped, icosahedral virus (60
nm in diameter); stable at 60 C for 60
min and pH 3-9
⬢ 2 linear, double-stranded, RNA
segments, 6 kb in length
⬢ Pathogens of birds, fish and shellfish
Birnaviridae Classification
1. _____________ (genus)
– Infectious bursal disease virus
2. ______________ (genus)
– Infectious pancreatic necrosis
3. _____________ (genus)
1. Avibirnavirus (genus)
– Infectious bursal disease virus
2. Aquabirnavirus (genus)
– Infectious pancreatic necrosis
3. Entomobirnavirus (genus)
⬢ aka Gumboro disease
⬢ Host range: variety of avian species,
chickens, turkeys, penguins
, 2 serotypes
⬢ Diseases: acute diarrheal disease of
young chicks, immunosuppression
in poultry
⬢ Geographic distribution
⬢ Etiologic agent: Infectious bursal disease virus
Infectious bursal disease virus
Clinical Presentation
⬢ Morbidity up to 100%
⬢ 3 to 6 weeks of age
⬢ Mortality from 0 to 30%
⬢ Vent picking, soiled vent feathers
⬢ Anorexia, depression
⬢ Diarrhea, dehydration
⬢ Trembling, prostration
Infectious bursal disease virus Pathogenesis
⬢ Following _______ inoculation, IBDV infects
_________ and ______ cells in the
⬢ Replicates in the ______
⬢ Results in primary viremia and spread to
the ________
⬢ Following oral inoculation, IBDV infects
macrophages and lymphoid cells in the
⬢ Replicates in the liver
⬢ Results in primary viremia and spread to
the bursa of Fabricius,
⬢ Lymphotropic for B cells
⬢ Secondary massive viremia and spread to
other organs
⬢ Immunosuppression due to reduced
humoral immune responsiveness
Infectious Bursal Disease Pathology
⬢ Bursal edema, hemorrhages,
necrosis, atrophy
⬢ Watery to bloody diarrhea,
dehydrated carcass
⬢ Splenomegaly; necrosis of lymphoid
tissues including thymus, spleen,
cecal tonsils, bone marrow;
hemorrhages in the proventriculus
and gizzard
Infectious Bursal Disease Transmission
⬢ Highly contagious viral infection
⬢ Fecal-oral route
⬢ Virus persists in the environment
up to 4 months
⬢ Harbored in meal worms for weeks
⬢ Resistant to most disinfectants
Infectious Bursal Disease
prevention and control
⬢ Maternal immunity is important in
reducing susceptibility of chicks
⬢ Vaccination of breeders is the most
effective method of preventing the
disease in chicks
⬢ Vaccination of chicks
⬢ Sanitation is difficult
⬢ Good husbandry, e.g., environmental
⬢ ____________ symmetry,
envelope +/-
⬢ _____________________
genome 19.1 kb
⬢ Pathogens of
⬢ Helical symmetry,
enveloped, 80 x 800
to 1000 nm
⬢ Single-stranded,
negative-sense, RNA
genome 19.1 kb
⬢ Pathogens of
hemorrhagic fevers
• Marburg-like virus (genus)
• Ebola-like virus
– Zaire (subtype)
– Côte d’Ivoire
– Reston
Ebola Hemorrhagic Fever
⬢ Host species:
⬢ Reservoir:
⬢ Etiologic agent:
⬢ Diseases:
⬢ Transmission:
Ebola Hemorrhagic Fever
• Host species: primates
• Reservoir: unknown
• Etiologic agent: Ebola-like viruses
• Diseases: hemorrhagic fever
• Transmission:
– Blood, secretions
⬢ Envelope +/- , shape:
⬢ 90 nm in diameter
⬢ _____________________ genome, 8.9kb
⬢ host range ________
⬢ Enveloped, spherical virus
⬢ 90 nm in diameter
⬢ Single-stranded, negative-stranded
RNA genome, 8.9kb
⬢ Wide host range
Bornaviridae Classification
• Mononegavirales (order)
– Bornaviridae (family)
• Bornavirus (genus)
⬢ Species affected: horses, sheep, cattle,
cats, rabbits, ostriches, dogs
⬢ Reservoir: birds?, rodents?

⬢ Disease: encephalomyelitis
⬢ Endemic: Germany, Iran, Israel,
Japan, Sweden, Switzerland, U.K.
⬢ Exotic
⬢ Etiologic agent: Borna disease virus
Borna disease virus
Clinical presentation-Equine
• Prodromal phase:
• Neurologic phase:
– Limbic system:
– Opthalmologic:
Clinical presentation-Equine
• Prodromal phase: fatigue, colic, fever,
coughing icterus
• Neurologic phase:
– Limbic system: excitability ,
somnolence, ataxia, hyperesthesia
– Motor system: paresis, paralysis
– Opthalmologic: nystagmus,
pupillary reflex dysfunction,
⬢ Mononegavirales (order) horses
⬢ Usually fatal
⬢ Progression to death in 3 days to 3
⬢ Survivors have permanent
neurologic deficits
Borna Disease
Borna Disease Pathogenesis
⬢ Acquired by intranasal route
⬢ Passes into the CNS via olfactory
⬢ Replicates in neurons, astrocytes and
⬢ Severe encephalomyelitis
Borna Disease Pathology
⬢ Lesions in the gray matter of the
olfactory bulb, basal cortex, caudate
nucleus and hippocampus
⬢ Lymphocytic perivascular cuffing
⬢ Intranuclear, eosinophilic inclusions
(Joest-Degen bodies)
⬢ Necrosis leading to hydrocephalus,
cortical atrophy
Borna Disease Immunity
⬢ Cell-mediated immune response in
immunocompetent adults
contributes to the immunopathology
of disease
⬢ Humoral immune response is not
⬢ Vaccine is not available
⬢ Envelope+/- shape/size:
⬢ _________________ genome, 13-15 kb
⬢ Pathogens of _______,
______, ______,
⬢ Macrophage,
⬢ Enveloped, icosahedral
virus, 50-70 nm in
⬢ Single-stranded,
positive-sense, RNA
genome, 13-15 kb
⬢ Pathogens of swine,
horses, primates,
⬢ Macrophage,
Arteriviridae Classification
• Arterivirus (genus)
– Equine arteritis virus
– Porcine respiratory and
reproductive syndrome virus
– Lactate dehydrogenase
elevating virus
– Simian hemorrhagic fever
• Contagious viral disease of Equidae
• Etiologic agent: isolated from an
outbreak of respiratory disease and
abortions in Bucyrus, OH (1953)
• Diseases: respiratory disease, abortions
• Transmission:
– Aerosolized
Equine viral arteritis
Equine viral arteritis
• Worldwide ______________
• Variation in seroprevalence between _______
and ______________
– 70 to 90% seroprevalence in
– 2 to 3 % seroprevalence in
• Worldwide distribution
• Variation in seroprevalence between breeds
and geographic regions
– 70 to 90% seroprevalence in
– 2 to 3 % seroprevalence in
• Increased prevalence due to increased
surveillance & testing; international trade in
horses and semen
⬢ Usually sub-clinical and rarely fatal
⬢ Fever up to 41oC (106oF) 3 to 14 days
post-exposure, lasts 2 to 9 days
⬢ Depression, anorexia
⬢ Leukopenia
⬢ Limb edema
⬢ Stiffness of gait
Equine viral arteritis
⬢ Nasal and/or lacrimal discharge
⬢ Conjunctivitis and/or rhinitis
⬢ Periorbital/supraorbital edema
⬢ Edema of prepuce or mammary glands
⬢ Urticaria, papules & erosions on
mucous membranes
⬢ Death
Equine viral arteritis
Equine viral arteritis
Pathogenesis, general
⬢ Virus replication in _____________
⬢ Systemic spread via _______
⬢ Infection of multiple __________ and _________
⬢ Damage to endothelium leads to ________,
________ and
Pathogenesis, general
⬢ Virus replication in alveolar
⬢ Systemic spread via viremia
⬢ Infection of multiple organs and
endothelial cells
⬢ Damage to endothelium leads to edema,
congestion and hemorrhage
⬢ Infarction of multiple organs following
segmental necrosis of small arteries
⬢ Hypovolemic, hypotensive shock
Equine viral arteritis Clinical presentation, abortions
⬢ Mares infected via respiratory tract
⬢ Occurs with/without clinical signs in
the mare
⬢ Abortions occur 10 to 30 days postinfection
⬢ Occurs 3 to 10 months of gestation
⬢ Abortion rates of 10 to 60% of mares
Equine viral arteritis Pathogenesis, abortions
⬢ Mares bred to infected stallions or
inseminated with infected semen do not
experience any virus-related fertility
⬢ Pyrexia 6 to 8 days after venereal
⬢ Spread of virus to the respiratory tract
⬢ Shed the virus to other horses via
respiratory secretions up to 16 days
⬢ Systemic spread via viremia
⬢ Fetal infection
⬢ Endothelial infection and damage
leads to edema, fluid accumulation in
peritoneal and pleural cavities, and
⬢ Fetuses are frequently autolysed
Equine viral arteritis Pathogenesis, stallions
⬢ Spreads to seminiferous tubules
⬢ Persistence of virus in the accessory sex
glands and vas deferens of stallions
⬢ Chronic carrier state and shed of virus
in semen of infected stallions
⬢ Only a transient effect on semen quality
or fertility
⬢ Virus survives in chilled or frozen
Equine viral arteritis Immunity
• Serum neutralizing antibodies detected
1 week post-infection
• Long duration of immunity following
• Colostral antibodies are protective for
• Vaccination protects against disease and
establishment of carrier state in stallions
• Vaccination does not “cure” persistently
infected stallions
Equine viral arteritis prevention and control
1. Biosecurity
2. Isolation of broodmares from young
stock and new introductions
3. Restrict movement of exposed horses
4. Quarantine infected horses
5. Serologic testing of stallions
6. Vaccination – inactivated or MLV
vaccine to prevent persistent infections
in stallions
Equine viral arteritis Differential Diagnosis
⬢ Equine influenza A viruses
⬢ Equine herpesvirus-1, -4
⬢ Equine infectious anemia virus
⬢ Exotic viruses: African horse
sickness, Getah virus
⬢ Purpura hemorrhagica
• Blue ear, mystery pig disease
• Host range: Domestic swine
• Etiologic agent:
– first recognized in the U.S.
and Canada (1987)
– North American and European
Porcine reproductive and
respiratory syndrome (PRRS)
Porcine reproductive and
respiratory syndrome (PRRS) Clinical Presentation
Clinical Presentation
1. Transient anorexia, fever in growers,
cyanosis of ears, snout, tail, vulva
2. Respiratory disease in young pigs:
dyspnea, “thumping”, increased
bacterial pneumonia, pre-weaning
3. Reproductive disease: delayed estrus
cycles, agalactia, late term abortions,
weak pigs, premature births, stillbirths,
mummified fetuses
Porcine reproductive and
respiratory syndrome (PRRS)Pathogenesis and Transmission
⬢ Tropism: ______________________________________
⬢ Shed in ___________________________________________________
⬢ Virus persists in ________
Pathogenesis and Transmission
⬢ Tropism: alveolar macrophages,
antibody-enhanced uptake of virus
⬢ Shed in saliva, nasal secretions, urine,
semen, mammary secretion, feces
⬢ Virus persists in tonsils
⬢ Transmission: direct contact,
aerosolized respiratory secretions, AI
with virus-positive semen
• Host range: Mice, Mus musculus
• Transmission: via saliva, contact, biting
• Disease:
– Inapparent, persistent infections
– Elevation of LDH levels
– Influences immune response of mice
to other agents
Lactate dehydrogenaseelevating
virus (LDHV)
⬢ Host species: macaques, Macaca
⬢ Disease: acute, febrile hemorrhagic fever
⬢ Transmission: aerosolized respiratory
secretions, direct contact
⬢ Mortality rate: approaches 100% in
⬢ Rese
Simian hemorrhagic fever

Deck Info