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Virology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Basics & Clinical Features of Arboviruses

A
  • Arthropod borne viruses
  • usually RNA = mutation

Clinical Features
o Fever, encephalitis, hemorrhagic and reproductive diseases
o disease is typically seasonal

Defining Features
o Vector: usually a blood-feeding arthropod ->
o A well-adapted vertebrate reservoir host (enzootic host) ->
o Occasional spillover into epizootic hosts (diseased animals)

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2
Q

Arthropod Vectors of Arboviruses

A

o Mosquitos, ticks, etc
o Virus replicates & persists in
o Required for virus to exist in nature

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3
Q

Enzootic Hosts of Arboviruses

A

o Birds or small mammals
o Well adapted reservoir
o Non clinical or long survival w/ high viremia
o Must have many naïve & susceptible animals

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4
Q

Epizootic Hosts of Arboviruses

A 
o	Humans or domestic animals (horses)

o	“accidental” or “incidental” hosts

o	less well-adapted to virus = disease 
o	Do not typically have persistent infections 
o	Usually lower viremias
o	Frequently dead-end hosts
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5
Q

Enzootic Cycle for Arboviruses

A

o Virus is maintained in well- adapted vertebrate hosts (often birds or small mammals) ->
o Virus is transmitted between hosts by a blood-feeding arthropod vector ->
o Virus replicates in the vector, and is required = biologic vector
o Typically NO disease in enzootic host

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6
Q

Triggers for Epizootic Outbreaks

A 
o	Increased number of susceptible reservoirs 
o	Increased number of vectors
o	Vector feeding habits 
o	Change in vector distribution 
o	Enzootic habitat invasion 
o	Change in viral virulence 
o	Human interventions

o	Increased vector/susceptible host interaction
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7
Q

Important Arboviruses in Vet Med

A

Eastern/Western/Venezuelan Equine Encephalitis
• encephalitis

West Nile Virus
• encephalitis

Bluetongue Virus
• Endothelial hemorrhage & infarction

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8
Q

Equine Encephalitis Viruses Basics

A
  • arboviruses
  • EEV, WEV, VEV, WNV
  • 20-100% mortality
  • Eastern is most virulent
  • Venezuelan is the only transmitted btwn horse & human
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9
Q

Pathophysiology of Systemic Disease in Equine Encephalitus Viruses

A
  • Initial replication in dendritic cells and regional lymph node (near bite) = primary viremia ->
  • Amplification in central depot/amplifying organs = secondary viremia ->
  • seeds target organs = disease
  • Target organ (brain) 
is usually not source for shedding.
  • Portal of exit = blood
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10
Q

Clinical Signs of Equine Encephalitis Virus

A

Most common febrile illness
o Fever & malaise w/ or w/o infection of target organs
o Due to cytokines

Encephalitis
o Virus enters the brain
o Virus replicates in the brain/spinal cord
o CNS signs = virus usually not in blood or other tissue

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11
Q

Why has West Nile Spread so Quickly?

A
  • > 40 species of mosquito vectors
  • presence of suitable naive reservoir hosts
  • Many susceptible naïve epizootic hosts
  • Suitable environment
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12
Q

Clinical Features of West Nile

A

Subclinical
o 90% of cases

Infection w/o CNS Dz
o 9% of infections
o fever, non - specific “flu -like” clinical signs
o Most not brought to attention of the veterinarian

CNS Dz
o 1% of infections
o most severe in brainstem and spinal cord
o Ataxia, Hyperesthesia, Muscle tremors, Depression, Rarely seizures, Behavioral changes, Fever, Death in 33%

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13
Q

Diagnosis of West Nile

A
  • CSF: mononuclear pleocytosis, normal to increased protein
  • Titer for anti WNV IgM antibody by ELISA
  • Post mortem - detect virus in CNS by isolation, PCR, IHC
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14
Q

Control & Prevention of West Nile

A

Control
o Eliminate mosquito breeding sites (i.e. standing water)
o Control mosquito larvae
o Reduce exposure to biting mosquitos

Prevention
o	Killed virus vaccine, 
o	DNA vaccines, 
o	recombinant vaccine 
o	all require annual boosters
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15
Q

Orbiviruses

A
  • Bluetongue Virus (BTV)
  • Epizootic Hemorrhagic Disease Virus (EHDV)
  • African Horse Sickness (AHS)
  • Non-enveloped
  • RNA,
  • segmented genome (prone to reassortment)
  • transmitted by Biting Midge
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16
Q

Bluetongue Virus Tropisms

A

MACROPHAGES
• TNF and other vasoactive mediators -> increased vascular permeability -> EDEMA

ENDOTHELIAL CELLS
• direct injury -> thrombosis, infarction, and hemorrhage

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17
Q

Bluetongue Virus Clinical Syndromes

A

Vasculitic/Hemorrhagic Disease
• Sheep and wild ungulates/deer
• greatest clinical importance

Reproductive Disease 
•	Cattle
•	Abortion and reproductive failure 
•	 Hydranencephaly in offspring
•	mostly economically importance
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18
Q

Bluetongue Virus Diagnosis

A

o Symptoms in sheep

For cows
• PCR & Virus isolation from blood during viremic stage or tissues at post -mortem
• Serology of VP7 (inner capsid) & VP2 (outer capsid)

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19
Q

Bluetongue Virus Management

A

o Indoor housing during peak vector activity

Vaccination
• Modified -live vaccine available in California
• CAUTION: Use during vector season not recommended, may reassort with field virus
• PROBLEM: No/little cross -protection with other serotypes

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20
Q

Basics of Reproductive Viruses, ideal samples for diagnosis

A

o Most viral infections of the dam DO NOT cause abortion from fetal infection
o Teratogenic viruses = Developmental abnormalities
o Ex: Flaviviridae & Arteriviridae

Ideal sample for diagnosis
o Fetus
o Placenta
o Dam serum

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21
Q

Basics of Bovine Viral Diarrhea Virus (BVD)

A

o Flaviviridae = pestivirus
o Enveloped
o (+) RNA
o non-segmented
o mostly cattle but also sheep, goats, pigs, ruminats
o affects repro, GI, respiratory, neuro
o immunosuppression & secondary infections

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22
Q

2 Biotypes & 2 Genotypes of Bovine Viral Diarrhea Virus

A 
2 Biotypes
•	Non-cytopathic
•	90% of BVD
•	establish persistent infection
•	Cytopathic
•	No persistent infection

2 Genotypes
• type 1 & 2
• Both contain cytopathic and non biotypes 

• Based on genetic differences in the viral genome
• BVDV-2 associated w/ severe hemorrhagic disease

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23
Q

Pathogenesis of Transient (acute) Bovine Viral Diarrhea Virus infection in non-fetus

A
  • Tonsil & lymph node replication ->
  • Enters circulation & transported to lymph & subepithelial tissues of GI & skin ->
  • Spreads to epithelial cells ->
  • Lymphoid & epithelial necrosis ->
  • Shed in bodily fluids ->
  • Seroconversion & immunity
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24
Q

3 Outcomes of Transient (acute) Bovine Viral Diarrhea Virus infection in non-fetus

A

Mild
• Mild erosions of mucuous mebranes

Viral Induced Immunosuppression
•	Damage to lymphoid tissue

•	Lymphopenia and neutropenia 
•	Opportunistic infections 
•	Compenent of bovine respiratory dz complex

Peracute BVDV & hemorrhagic syndrome
• some BVDV-2 strains 

• High morbidity and mortality in all age groups 

• Sudden fever, death, diarrhea and pneumonia 

• Thrombocytopenia, neutropenia, myeloid 

• Highly fatal (death in 48 hrs)

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25
Q

Transient (acute) infections of BVD in reproduction

A
  • Seronegative pre-breeding or early bred cows
  • Compromised ovarian function

Transplacenta infection
• fetal infection leading to persistently infected (PI) calves

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26
Q

Non Cytopathic BVD & Transplacental BVDV Infection

A 
Early gestation (0-45 days)
•	Abort/embryonic death

Early-mid gestation (45-125 days)
• immunotolerance

• persistent infection

Mid-late gestation (125-175 days)
• Congenital abnormalities 
(microphthalmia, cataracts)
• Or normal 


Late gestation (175 days to term)
•	Normal
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27
Q

Immunotolerence due to BVD & Outcomes

A
  • Recognize virus as “self”
  • high viral load (Ag positive) but no measurable specific Ab response
  • PI cows give birth to PI calves (100% vertical transmission)

Outcomes
• weak and succumbs to disease by 1 year of life
• normal, grows and has babies

• death within hours/days

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28
Q

Character of PI Calves

A
  • Clinically small/unthrifty or normal
  • More susceptible to other diseases
  • constant source of virus
  • susceptible to fatal mucosal disease
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29
Q

Mucosal Dz associated w/ BVD

A
  • Only affects PI animals
  • Uncommon and typically 6-12 months of age
  • Superinfection with CP-BVDV Or
  • NCP-BVDV viral mutation (common)
  • HIGH mortality rate (almost 100%) w/in 2 weeks
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30
Q

Transmission of BVD

A
  • active for days- wks under ideal conditions
  • Biologic AI material derived from PI animal
  • Breeding
  • Fomites or iatrogenic
  • Introducing new PI animal
  • Aerosol transfer from neighbor farm

Transient infection
• Shedding for 1-2 wks

Persistent infection
• Shedding for life

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31
Q

Control of BVD

A
  • Biosecurity
  • Elimination of PIs

Vaccination
• Prevention of acute disease
• Prevention of reproductive losses 

• Prevention of creating PIs 


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32
Q

Diagnostics for BVD

A
  • Viral Ag found in serum, milk, ear notches
  • Ab in serum
  • Herd screening thru bulk milk testing
  • PCR
  • Ag ELISA

Immunohistochemistry on skin
• Highly sensitive & false (+) from transient infections

33
Q

Rabies Basics

A

o Rhabdoviridae
o Enveloped
o (-)RNA

Envelope Causes:
o Transmission and epidemiology are usually based on direct contact (bite)
o Topical wound (bite) treatment can be of significant benefit
o Glycoprotein G – ligand & target of neutralizing antibodies

34
Q

Rabies Hosts, Human Infection, & Control

A

Hosts
o Cats, cows, dogs, horses
o Raccoons, skunks, bats, foxes

Human Infections
o 59,000 annual deaths
o predominant source worldwide = dogs
o predominant source US = raccoons, skunks, bats

Control
o Wound treatment immediately

Vaccination
• All inactivated accept recombinant canarypox for cats
• Viral vectored Vx in bait for wildlife

35
Q

Rabies Transmission

A

o Bite wounds ->
o Replicates in muscle cells at site ->
o Quiescent stage in muscle (5days – wks) (time to treat) ->
o Entry into peripheral nerves at motor end-plate ->
o Migrates centripetally, towards CNS (1 inch / day) ->
o Dorsal root ganglion ->
o Spinal cord ->
o In CNS - minor inflammation, neuronal replication & damage, widespread inclusions ->
o Centrifugal spread back to nerves
o NO VIREMIA

36
Q

Rabies Diagnosis, Shedding Sites/Time

A

Diagnosis
o Negri bodies in purkinje cells (Inclusion bodies)
o Post mortem
o Direct fluorescent antibody (DFA) test 

o PCR (not a public health approved test)


Shedding Sites & Time
o Urine
o SALIVA
o Saliva (+) for virus no more than 10-13 days before signs

37
Q

Clinical Features of Rabies, incubation, classic presentation, morbidity/mortality

A 
Variable incubation determined by 
•	Location of bites
•	Severity of trauma
•	Dose
•	Viral variant

Classic Presentations
• Furious – excitability & aggressiveness
• Dumb – paralysis & depression

Morbidity / Mortality
• IF disease signs appear, usually fatal
• Post-exposure prophylaxis (PEP) is very effective if done properly (humans only)

38
Q

Border Disease Virus Basics

A

o Closely related to BVDV
o Western US
o Subclinical & transient infections in adults
o Barren ewes, abortions, stillbirths, small weak lambs
o PI lambs: BDV infection day 30-70 of gestation
o Hair replaces wool due to thyroid dysfunction

39
Q

Border Disease Virus Pathogenesis, Diagnosis, Transmission, Prevention

A

Pathogenesis
• BDV destroys schwann cells & infects thyroid ->
• Low T3 & T4
• Low cyclic nucleotide phosphodiesterase (CNP) ->
• Hypomyelination

Diagnosis
• Ag in tissue,
• PCR for virus,
• no Ab

Transmission
• Body fluids
• Close contact w/ PI animal

Prevention & Control
• Test & removal

40
Q

Equine Arteritis Virus (EAV); basics, related dz, transmission

A

o Arterivirus
o Enveloped, (+) RNA
o Infection common but Dz uncommon

Related Dz
• Porcine reproductive and respiratory syndrome virus (PRRSV)

Transmission
• From acutely infected horses

41
Q

Equine Arteritis Virus (EAV); Pathogenesis, Target Systems, Clinical Signs

A

Pathogenesis
• enters via respiratory or venereal route ->

• Infects macrophages and endothelial cells ->
• Spreads to regional and central lymphoid organs ->
• Infection of endothelium of blood and lymphatic vessels ->
• Generalized vasculitis and leakage of fluid

Target Systems
• Respiratory
• Vascular
• Reproductive

Clinical Signs
• Fever, depression, anorexia, lymphopenia
• Edema - limbs, prepuce, scrotum 

• Periorbital swelling and conjunctivitis 

• Abortion
• Neonates: pneumonia & enteritis

42
Q

Pathogenesis of Equine Arteritis Virus (EAV) Abortion

A
  • Leukocyte viremia ->
  • Infection of uterine endothelium & myometrium ->
  • Placental damage -> abortion

OR

  • Leukocyte viremia ->
  • High virus in fetus ->
  • Stress ->
  • Abortion
43
Q

Maintenance of Equine Arteritis Virus (EAV) in population

A
  • 30-70% of exposed stallions/colts become carriers
  • Asymptomatic carriage, weeks to life-long 

  • Virus persists in genital tract and shed in semen
  • Persistence is testosterone-dependent
  • Source of venereal transmission of virus to mares
  • Restrictions on international movement of horses and semen
44
Q

Control & Diagnosis of Equine Arteritis Virus (EAV)

A

Control
• Non-stallion clears virus ~28 days

Vx
• Modified live and inactivated
• long-lasting immunity for stallions & non-pregnant mares
• Complicated by import/export regulations regarding seropositive horses

Breeding

• Breed (+) stallions to (+) mares
• Breed (-) stallions to (-) mares

Diagnosis
• Need both virology and serology
• Serum Ab detected by neutralization assay or ELISA
• Virus isolation and/or RT-PCR

45
Q

Equine Herpesvirus & Reproductive Dz

A

EHV-3 - Coital exanthema (genital disease)

• Similar to genital disease from BHV-1
• Pustules & ulcers on vagina, penis, prepuce
• Localized infection
• No abortion or infertility
• Loss of libido

46
Q

Exotic Vesicular Dz Viruses; basics, example Dz’s, DfDx

A

o Eradicated from US but endemic in other countries
o Must control import
o Vets responsible for detection/surveillance

Viruses
o	Foot and mouth disease (most important)
o	Vesicular exanthema of swine
o	Swine vesicular disease

o	Vesicular stomatitis (not exotic)
o	Seneca Valley Virus (not exotic)

DfDx
• Autoimmune diseases 

• Chemical, thermal burn or frictional trauma 

• Drug reactions (secondary autoimmune) 

• Photosensitization 


47
Q

Foot & Mouth Dz features & basics

A
  • World’s most economically important dz
  • country is required to notify the World Organization for Animal Health (OIE) of an outbreak within 24
  • endemic in Africa, south Asia, south America

Features
• Highly contagious picorna virus
• non-enveloped RNA virus
• survives well in environment
• dz of cloven hooved animals (some wildlife)
• virus shed in all bodily fluids before clinical signs

48
Q

Foot & Mouth Dz; Clinical Signs & how it Affects calves, pigs, sheep, camelids

A

Clinical Signs
• 2-14 day incubation
• fever lameness, anorexia, salivation, decreased milk
• ulcers/vesicles in mouth, nares, muzzle, feet, teats
• best location = coronary band of hoof
• high morbidity
• prolonged recovery & shed of virus after recovery

Who does it affect
• Neonates & calves – myocardial infection
• Pigs – most severe lesions in feet
• Sheep/goats/camelids – asymptomatic to mild

49
Q

Foot & Mouth Dz; Prevention/Control & Disadvantages of Vx

A 
Prevention/Control
•	Vx (serotype must match)
•	Heat treatment of swill
•	Quarantine
•	Disinfection
•	Euthanasia
•	Wildlife control

Disadvantages to Vx
• Loss of OIE status
• Vx not cross-protective for 7 serotypes
• Immunity short

50
Q

Horse, Cow, Pig Susceptibility to Vesicular Dz

A

Horses
• vesicular stomatitis

Cows
• Foot & mouth
• Vesicular stomatitis

Pigs 
•	Foot & mouth
•	Vesicular stomatitis
•	Vesicular exanthema
•	Swine Vesicular Dz
•	Seneca Valley Virus
51
Q

Vesicular Exanthema of Swine

A

o Calicivirus
o Exotic but affects feral US swine & sea lions
o Indistinguishable form foot and mouth
o Transmitted by feeding undercooked infected meat

52
Q

Seneca Valley Virus

A 
o	Picornavirus
o	Looks like FMD
o	Present in the US
o	Symptoms = Ds, Lethargy, fever
o	30-70% morbidity & mortality
o	resolves w/in 7-10 days
53
Q

Swine Vesicular Dz

A 
o	Picornavirus
o	Looks like FMD
o	Exotic
o	Endemic in Italy
o	Transmitted by feeding undercooked infected meat
54
Q

Vesicular Stomatitis Virus; Basics & Transmission

A 
o	Rhabdovirus
o	Serotypes from New Jersey & Indiana
o	Endemic in SE US
o	Vesicles -> ulcers on & around mouth
o	Looks like FMD
o	Affects horses
o	Zoonotic (flu-like in humans)
o	Reportable
Transmission
•	Arthropods
•	Transmucosal & transcutaneous
•	Animal to animal thru direct contact w/ vesicle fluid, saliva, nasal secretions
•	Plants & soil
•	Spreads during summer
55
Q

Vesicular Stomatitis Virus; Symptoms, Diagnosis, Treatment, Control

A 
Symptoms
•	Mortality rare
•	Fever
•	Vesicles, ulcers, crusting of muzzle, lips
•	Excess salivation
•	Can involve coronary band, interdigital space, teats
•	Quick healing
•	Sheep/goats rarely have signs
Diagnosis
•	Contact state vet
•	VSV Ag test of vesicular fluid
•	Virus isolation
•	PCR of vesicular fluid & tissue

Ab serology
• Complement fixation = recent infection

Treatment
• Supportive care

Control/Prevention
• Quarantine
• Disinfection
• Control insects

56
Q

Rinderpest; Basics & Symptoms

A

o Highly contagious morbilivirus
o Africa & Asia
o High morbidity & mortality
o Similar to distemper minus CNS signs

Symptoms
•	Nasal, lacrimal secretions
•	Salivation
•	Severe bloody Ds
•	Necrosis & ulceration in GI
57
Q

Goat Plague; Basics, Transmission, Symptoms

A

o Rinderpest of sheep & goats
o Morbilivirus
o Africa & Middle East
o Abs to Goat Plague & Riderpest are corss-reactive

Transmission
• Close contact & inhalation

Symptoms
•	Fever
•	Inappetence
•	Depression
•	Nasal/ocular discharge
•	Oral hyperemia & erosion
•	Watery or bloody Ds
•	Abortion
•	Dyspnea
•	cough
58
Q

Basics of African Swine Fever, type of virus, Hosts, & sources of virus

A
  • Asfivirus
  • Enveloped DNA virus
  • Multiplies in soft ticks
  • Incubation = 5-14 days

Hosts
• Reservoirs – African wild pigs
• Clinical – domestic & wild European pigs

Sources of virus
• Persistently infected animals
• Arthropods
• Environment/fomites

59
Q

Peracute, Acute, Subacute, & Chronic Clinical Signs of African Swine Fever

A

Peracute
o sudden death

Acute
o fever, red skin, anorexia, V & Ds, incoordination, abortion,
o 100% death

Subacute
o Less intense
o Fever, anorexia
o 30-70% death

Chronic
o Weight loss, intermittent fever, red skin, respiratory signs, arthritis
o Low death

60
Q

African Swine Fever Pathogenesis & Gross Lesions

A

Pathogenesis
• Inhalation, ingestion, or tick bite ->
• Replication in macrophages of of tonsils & LNs ->
• Downregulation of cytokines & immunosuppression ->
• Apoptosis of T & B cells & endothelial cells ->
• Lymphoid necrosis & hemorrhage

Gross Pathology
•	ENLARGED SPLEEN (important marker)
•	Cutaneous Ecchymosis (reddening)
•	Petechial mucus membranes & viscera
•	Hemorrhagic lymph nodes
•	Petechial kidneys (turkey egg)
61
Q

African Swine Fever Diagnosis & Control

A

Diagnosis
• Ab ELISA of serum
• PCR on blood/tissue
• others

Control
• Import control
• Slaughter
• disinfection

62
Q

Basics of Classical Swine Fever

A
  • Pestivirus
  • Enveloped RNA virus
  • transmission through placenta is possible
63
Q

Basic, Acute, Chronic, In Utero, & transient Clinical Signs of Classical Swine Fever

A
  • Infarcts on margin of SPLEEN
  • Hemorrhage of skin, tonsils, kidneys, spleen, LNs
  • Fluid in body cavities

Acute
o fever, huddling, lethargy, hyperemia and hemorrhagic skin, lymphadenomegaly, V & Ds, conjunctivitis, incoordination, cyanosis, convulsions
o death of young in 1-3 weeks

Chronic
o Persistent Fever, Ds, poor growth,
o Button ulcers in cecum & large intestine
o apparent recover with eventual relapse
o death w/in 3 months, any age animal 


In Utero Transmission
o CNS deformities
o abortion

Transient
o Older animals
o Transient like BVD

64
Q

Control & Diagnosis of Classical Swine Fever

A

Control
• Surveilence (test tonsils)
• Slaughter

Diagnosis
• Ab ELISA on serum
• PCR on blood/tissue
• Others

65
Q

Basics of African Horse Sickness

A
  • 70-95% death
  • orbivirus (retrovirus)
  • transmitted by biting midges (not contagious)
  • zebras & donkeys are subclinical reservoirs
  • causes vasculitis -> severe edema & hemorrhage
  • can rarely be zoonotic
66
Q

Clinical Signs & Key Lesions of African Horse Sickness

A 
Clinical signs
•	Fever 

•	Edema of face and neck 
•	sweating 

•	Respiratory signs 

•	Cardiac failure 

•	Death 

Key Lesions
•	Peracute dz w/ high death rate
•	Respiratory distress (froth coming form nares)
•	Edema of supraorbital fossa
•	Pulmonary edema
67
Q

Diagnosis & Control of African Horse Sickness

A

Diagnosis
• ELISA on serum
• PCR on blood, spleen, lung, LN
• gelatinous edema around nucal ligament on necropsy

Control
• Vx in endemic areas
• Quarantine & testing of imported animals

68
Q

Basics of Papillomaviruses & lesions

A 
o	Papoviridae
o	Small dsDNA
o	Non enveloped
o	Environmentally resistant
o	Often seen in young

Cutaneous & mucosal neoplastic lesions (warts)
• Usually benign
• Can become malignant
• Can involve fibroblasts -> fibropapilloma
• Highly species specific

69
Q

Papillomaviruses; clinical features & Pathophysiology

A

Clinical Features
• Localized infections
• Slow process (6-8 wks)
• Proliferating/thickened stratum basale and spinosum (acanthosis) -> hyperkeratosis

Pathophysiology
• Basal epithelium through abrasion ->
• Clonal expansion & continued S phase ->
• Differentiation and viral shedding at/near surface ->
• In healthy animals, immune response controls & wart regresses

70
Q

Bovine Papilloma Virus; features of different serotypes

A

• Many serotypes

Serotypes 2 & 4
• bladder & GI warts
• can become malignant w/ co-factors such as brackenfern
• “enzootic hematuria”

Serotype 1 & 2
• Associated w/ equine sarcoid
• Locally aggressive fibroblastic tumor
• Not malignant

71
Q

Equine Paipilloma Virus; 3 lesions

A

Cutaneous & benign
• Head & nose

Invasive warts
• Usually sarcoids
• Associated w/bovine papillomavirus

Aural Papillomas
• Rarely regress
• Black flies are mechanical vector

72
Q

Canine Papillomavirus

A
  • Cutaneous/mucosal warts on/around oral cavity, pharynx 

  • Sometimes on other parts of the body (digits) 

  • Pigmented plaques on ventrum and limbs in pugs and min schnauzers 

73
Q

Basics of Poxviruses

A 
o	Mild localized or severe systemic
o	Brick-shaped virion
o	Enveloped but highly resistant
o	dsDNA genoma
o	show cytoplasmic inclusions
74
Q

Lesions of Poxviruses

A

o can be both

Proliferative Lesions
• Induces hyperplasia of epithelial cells 

• raised edges and depressed center, the classic “pock” nodule 


Vesicular Lesions
• Replication, necrosis in deeper epidermal cells, with overlying cells intact ->
• fluid, exudate accumulate in the space, leading to vesicle initially, pustule later ->
• After rupture, exudate forms a crust ->
• Macule -> papule -> vesicle -> pustule -> ulcer -> crust -> scar

75
Q

Orthopoxvirus; 3 types

A

Variola (smallpox)
• Systemic dz of humans

Cowpox
• Cutaneous poxviral disease of cattle with lesions on teats, udder 

• Rodents -> cow or cat -> human

Monkeypox (exotic)
• Systemic dz of rodents & monkeys in Africa
• Zoonotic

76
Q

Parapoxviruses; 2 types

A

Orf & Bovine Papular Stomatitis Virus
• zoonotic
• Very Contagious ecthyma
• Localized infections on lips, mouth (lambs, calves usually) and udders (ewes, cows) 

• Interferes with nursing/eating 

• Weight loss, trauma (can predispose to secondary infections)

Pseudocowpox (Milker’s Nodules)
• Teat lesions
• Zoonotic
• Causes painless itchy red nodules on humans

77
Q

Control & Treatment of Orf

A

Control of Orf
• Live virus Vx
• Disinfection

Treatment
• Ab for secondary infections

78
Q

Capripoxviruses

A
  • Sheep pox, goat pox, bovine lumpy skin dz
  • severe, systemic diseases
  • High morbidity and up to 50% mortality. 

  • All are currently exotic
79
Q

Avipoxviruses

A
  • Many
  • Highly host-specific
  • Systemic or localized infections
  • lesions on non-feathered areas of legs/face
  • Some cause mucosal lesions 
(pigeon pox)
  • Interfere with eating, predator avoidance, secondary infections

Virology (2 decks)

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