Exam 3 Flashcards
(79 cards)
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)
2
Q
Arthropod Vectors of Arboviruses
A
o Mosquitos, ticks, etc
o Virus replicates & persists in
o Required for virus to exist in nature
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
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
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
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
7
Q
Important Arboviruses in Vet Med
A
Eastern/Western/Venezuelan Equine Encephalitis
• encephalitis
West Nile Virus
• encephalitis
Bluetongue Virus
• Endothelial hemorrhage & infarction
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
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
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
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
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%
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
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
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
16
Q
Bluetongue Virus Tropisms
A
MACROPHAGES
• TNF and other vasoactive mediators -> increased vascular permeability -> EDEMA
ENDOTHELIAL CELLS
• direct injury -> thrombosis, infarction, and hemorrhage
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
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)
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
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
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
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
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
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)
25
Transient (acute) infections of BVD in reproduction
* Seronegative pre-breeding or early bred cows
* Compromised ovarian function
Transplacenta infection
• fetal infection leading to persistently infected (PI) calves
26
Non Cytopathic BVD & Transplacental BVDV Infection
```
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
```
27
Immunotolerence due to BVD & Outcomes
* 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
28
Character of PI Calves
* Clinically small/unthrifty or normal
* More susceptible to other diseases
* constant source of virus
* susceptible to fatal mucosal disease
29
Mucosal Dz associated w/ BVD
* 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
30
Transmission of BVD
* 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
31
Control of BVD
* Biosecurity
* Elimination of PIs
Vaccination
• Prevention of acute disease
• Prevention of reproductive losses
• Prevention of creating PIs
32
Diagnostics for BVD
* 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
Rabies Basics
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
Rabies Hosts, Human Infection, & Control
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
Rabies Transmission
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
Rabies Diagnosis, Shedding Sites/Time
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
Clinical Features of Rabies, incubation, classic presentation, morbidity/mortality
```
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
Border Disease Virus Basics
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
Border Disease Virus Pathogenesis, Diagnosis, Transmission, Prevention
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
Equine Arteritis Virus (EAV); basics, related dz, transmission
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
Equine Arteritis Virus (EAV); Pathogenesis, Target Systems, Clinical Signs
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
Pathogenesis of Equine Arteritis Virus (EAV) Abortion
* Leukocyte viremia ->
* Infection of uterine endothelium & myometrium ->
* Placental damage -> abortion
OR
* Leukocyte viremia ->
* High virus in fetus ->
* Stress ->
* Abortion
43
Maintenance of Equine Arteritis Virus (EAV) in population
* 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
Control & Diagnosis of Equine Arteritis Virus (EAV)
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
Equine Herpesvirus & Reproductive Dz
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
Exotic Vesicular Dz Viruses; basics, example Dz's, DfDx
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
Foot & Mouth Dz features & basics
* 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
Foot & Mouth Dz; Clinical Signs & how it Affects calves, pigs, sheep, camelids
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
Foot & Mouth Dz; Prevention/Control & Disadvantages of Vx
```
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
Horse, Cow, Pig Susceptibility to Vesicular Dz
Horses
• vesicular stomatitis
Cows
• Foot & mouth
• Vesicular stomatitis
```
Pigs
• Foot & mouth
• Vesicular stomatitis
• Vesicular exanthema
• Swine Vesicular Dz
• Seneca Valley Virus
```
51
Vesicular Exanthema of Swine
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
Seneca Valley Virus
```
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
Swine Vesicular Dz
```
o Picornavirus
o Looks like FMD
o Exotic
o Endemic in Italy
o Transmitted by feeding undercooked infected meat
```
54
Vesicular Stomatitis Virus; Basics & Transmission
```
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
Vesicular Stomatitis Virus; Symptoms, Diagnosis, Treatment, Control
```
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
Rinderpest; Basics & Symptoms
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
Goat Plague; Basics, Transmission, Symptoms
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
Basics of African Swine Fever, type of virus, Hosts, & sources of virus
* 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
Peracute, Acute, Subacute, & Chronic Clinical Signs of African Swine Fever
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
African Swine Fever Pathogenesis & Gross Lesions
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
African Swine Fever Diagnosis & Control
Diagnosis
• Ab ELISA of serum
• PCR on blood/tissue
• others
Control
• Import control
• Slaughter
• disinfection
62
Basics of Classical Swine Fever
* Pestivirus
* Enveloped RNA virus
* transmission through placenta is possible
63
Basic, Acute, Chronic, In Utero, & transient Clinical Signs of Classical Swine Fever
* 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
Control & Diagnosis of Classical Swine Fever
Control
• Surveilence (test tonsils)
• Slaughter
Diagnosis
• Ab ELISA on serum
• PCR on blood/tissue
• Others
65
Basics of African Horse Sickness
* 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
Clinical Signs & Key Lesions of African Horse Sickness
```
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
Diagnosis & Control of African Horse Sickness
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
Basics of Papillomaviruses & lesions
```
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
Papillomaviruses; clinical features & Pathophysiology
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
Bovine Papilloma Virus; features of different serotypes
• 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
Equine Paipilloma Virus; 3 lesions
Cutaneous & benign
• Head & nose
Invasive warts
• Usually sarcoids
• Associated w/bovine papillomavirus
Aural Papillomas
• Rarely regress
• Black flies are mechanical vector
72
Canine Papillomavirus
* 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
Basics of Poxviruses
```
o Mild localized or severe systemic
o Brick-shaped virion
o Enveloped but highly resistant
o dsDNA genoma
o show cytoplasmic inclusions
```
74
Lesions of Poxviruses
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
Orthopoxvirus; 3 types
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
Parapoxviruses; 2 types
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
Control & Treatment of Orf
Control of Orf
• Live virus Vx
• Disinfection
Treatment
• Ab for secondary infections
78
Capripoxviruses
* Sheep pox, goat pox, bovine lumpy skin dz
* severe, systemic diseases
* High morbidity and up to 50% mortality.
* All are currently exotic
79
Avipoxviruses
* 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
