Final: Virology Lab

Front 1

FIV
family / genus

Back 1

feline immunodeficiency virus
retroviridae / lentivirus

Front 2

Distemper
family / genus

Back 2

canine distemper virus
paramyxoviridae / morbiliivirus

Front 3

What are the reservoirs of rabies in the united states?

how are they infected by the virus?

Back 3

skunk, fox, racooon, bat, coyote

rabies virus infects these mammals and that it will eventually kill them – however, they take longer to develop the clinical signs
They transmit the virus amongst the species and maintain the virus

Front 4

Pathogenesis of rabies replication

Back 4

virus replicates locally at bite wound specifically in muscle fibers in the vicinity of the neuromuscular junction. enters nerve endings and migrates up nerve by axoplasm flow. reaches the cns and infects neurons. virus then spreads centripetally to salivary glands and to other organs via nerve cells. in the salivary glands, rabies virus replicates in the acinar cells and is excreted in the saliva. there is no viremia. virus may be present in the saliva before clinical signs of rabies are seen

Front 5

EIA / swamp fever
family / genus

Back 5

retroviridae / lentivirus

Front 6

presenting clinical signs of rabies in the dog

Back 6

most common form is the furious form: loose fear of humans, abnormal aggressive behavior, attack moving objects without provocation, change in voice-laryngeal paralysis. peculiar howling, salivation due to paralysis of the pharyngeal muscles. abnormal sexual behavior

Front 7

what other viruses can cause CNS disease in dogs?

Back 7

distemper, pseudorabies, infectious canine hepatitis (CAV-1), non resp parainfluenza virus infection, EEE/VEE, powassan, st louis encephalitis, la crosse virus

Front 8

Equine viral arteritis
family / genus

Back 8

equine arteritis virus
arteriviridae / arterivirus

Front 9

what vaccines are available to prevent rabies infection in dogs?

Back 9

killed, attenuated

Front 10

presenting clinical signs of rabies in cats

Back 10

most common form is the furious form: loose fear of humans, abnormal aggressive behavior, attack moving objects without provocation, change in voice-laryngeal paralysis. peculiar howling, salivation due to paralysis of the pharyngeal muscles. abnormal sexual behavior. Cats are often anxious, staring, with a blank look on their eyes, spooky

Front 11

viruses that cause CNS dz in cats

Back 11

pseudorabies, panleuk, FIP, FeLV, FIV, FSE

Front 12

BVDV
family / genus

Back 12

bovine viral diarrhea virus
flaviviridae / pestivirus

Front 13

presenting clinical signs of rabies in cattle

Back 13

aggression, bellowing, abnormal sexual behavior, tenesmus with paralysis of the tail and anal sphincter muscles, etc

Front 14

viruses that cause CNS dz in cattle

Back 14

pseudorabies, BSE, BHV-5,, MCF, EEE/VEE, BTV, BVDV, Akabane

Front 15

blue tongue
family / genus

Back 15

bluetongue virus
reoviridae / orbivirus

Front 16

presenting clinical signs of rabies in horses

Back 16

lameness!

Front 17

differentials for CNS dz in horses

Back 17

EEE/WEE/VEE, West Nile, pseudorabies, EHV-1, powassan, main drain virus, st louis encephalitis, la crosse virus

Front 18

when are reservoirs most likely to transmit rabies?

Back 18

when they become clinically ill

Front 19

most telling sign of rabies infection in wild mammals?

Back 19

behavioral changes

Front 20

pathognomonic sign for rabies

Back 20

negri bodies (in all but 15-20% of cases)

Front 21

scrapie

Back 21

a non febrile chronic and fatal dz of sheep and goats, characterized clinically by pruritis, which is manifested by rubbing affected parts against objects and biting the flank

Front 22

Which animals has CWD been diagnosed in?

Back 22

mule deer, elk, moose

Front 23

clinical signs of CWD

Back 23

teeth grinding, abnormal behavior, excressive drinking, marked weight loss

Front 24

If thoracocentesis is performed on a cat with a thymic lymphosarcoma, what cells would you expcet to see in this fluid?

Back 24

large lymphocytes/lymphoblasts

Front 25

what affect has vaccination had on thymic lymphosarcomas?

Back 25

decreased incidence

Front 26

which cats are more prone to mediastinal or thymic lymphomas?

Back 26

cats less than 3 years of age. 80-90% of all cases are FELV associated

Front 27

signs of thymic lymphoma

Back 27

pleural effusion, dyspnea, occasional regurgitation (from esophageal pressure)

Front 28

which cats are more prone to alimentary lymphosarcoma?

Back 28

older cats, often test negative by the SNAP test

Front 29

if you wanted to detect the presence of felv in the cells on a blood smear, what test would you use?

Back 29

IFA test

Front 30

IFA procedure for Felv testing

Back 30

1st ab is mouse ab specific for p27, and second ab is a rabbit antimouse ab tagged with fluorescent molecule

Front 31

what kind of leukemia does felv cause?

Back 31

acute lymphoblastic leukemia

Front 32

felv vaccination?

Back 32

recombinant poxvirus, given ID

Front 33

are gingivitis and stomatitis more often associated with FeLV or FIV?

Back 33

FIV

Front 34

primary cuase of gingivitis and stomatitis in FIV

Back 34

FCV that starts to replicate in the mucosal epithelium and causes the lesions

Front 35

how will a high percentage of cats with FIP present?

Back 35

anorexic and icteric

Front 36

what organ is frequently involved with FIP

Back 36

liver

Front 37

what type of fluid is typically seen with the wet form of FIP?

Back 37

clear, straw colored, clots on standing, slimy to the touch. cellularity is low (predominantly macrophages, some neutrophils). AG ratio <.45; total protein >3.5

Front 38

What affect does FIP have on the eyes?

Back 38

fibrin deposition/precipitates
retinal hemorrhate, cuffing, color change of iris, keratic precipitates

Front 39

What affect does FIP have on the eyes?

Back 39

fibrin deposition/precipitates
retinal hemorrhate, cuffing, color change of iris, iritis/keratic precipitates
anterior uveitis

Front 40

What clinical signs would you expect to observe in cats with the dry form of FIP?

Back 40

pyogranulomas in liver, spleen, lungs, kidneys, lymph nodes, and eyes.

Front 41

histologic lesions of FIP (dry form)

Back 41

perivascular granulomas or pyogranulomas with systemic vasculitis or thrombovasculitis

Front 42

Ovine progressive pneumonia/Visna
family / genus

Back 42

OPPV
retroviridae / lentivirus

Front 43

composition of FIP pyogranuloma?

Back 43

macrophages predominate and are accompanied by some neutrophils, lymphocytes and plasma cells

Front 44

what is the typical posture of cats with feline panleukopenia virus?

Back 44

head over water bowl, hunched posture

Front 45

what type of dz in FPV?

Back 45

acute dz characterized by vomiting and dehydration. NOT DIARRHEA IF ACUTE

Front 46

blood results of FPV?

Back 46

severe leukopenia, primarily neutropenia

Front 47

what cells does FPV infect?

Back 47

crypt cells leading to secondary bacterial infection

Front 48

clinical signs of panleuk

Back 48

seen primarily in <6mo old kittens. peracute dz: overhwelming infection with no clinical signs and death within 24hrs
acute- fever, depression, anorexia, and vomiting. extreme dehydration, hunched posture, tender abdomens.
cerebellar hypoplasia

Front 49

clinical signs of CPV-2

Back 49

frequent, bloody diarrhea, anorexia, dehydration

Front 50

what does the CPV SNAP test detect and how?

Back 50

solid phase ELISA that uses a CPV2 MAb to capture the virus on a membrane. performed on fecal or intestinal material

Front 51

Clinical signs of CDV infection?

Back 51

copious mucopurulent nasal discharge, sunken eyes, dehydration,
cough
GI form- vomiting, diarrhea
CNS signs- seizures, ataxia, myoclonus, chorea, ascending paralysis
hyperkeratosis of pads

Front 52

what wild animals does CDV frequently infect?

Back 52

raccoons

Front 53

what symptom can CDV cause in young, growing, animals?

Back 53

enamel hypoplasia

Front 54

when are CNS signs of CDV seen?

Back 54

1-3 weeks after infection or 2-4 weeks after dog seemingly recovers from a mild respiratory dz

Front 55

CDV is aka

Back 55

hard pad disease

Front 56

CDV inclusions

Back 56

histopath- both IN and IC inclusions can be seen.
generally only see IC inclusions except in brain and bladder wall where both are seen

Front 57

signs of ICH

Back 57

echymotic hemorrhages in the mucosa, pale mucosa from anemia. enlarged tonsils

Front 58

what does ICH/CAV1 cause in the fox?

Back 58

CNS disease

Front 59

most common form of CAV-1 in the dog?

Back 59

hepatitis

Front 60

ICH/CAV1 is aka

Back 60

blue eye

Front 61

what is blue eye?

Back 61

a keretatisis caused by Ab binding the cells of the cornea, on the descemet membrane. Transient lesion that does not cause blindness

Front 62

caprine arthritis encephalitis
family / genus

Back 62

retroviridae / lentivirus

Front 63

Why do we vaccinate with CAV2 not CAV1?

Back 63

CAV1 vaccine can cause blue eye lesions

Front 64

typical lesion of canine herpesvirus that are seen at necropsy?

Back 64

mottled kidneys with focal disseminated echymotic hemorrhages

Front 65

how can you prevent CHV1 infections in a litter?

Back 65

hyperimmune serum, increase body temp

Front 66

EIA family / genus

Back 66

retroviridae, lentivirus

Front 67

signs of acute EIA infection

Back 67

After an incubation period of 7-21 days, infected horses develop a high fever, severe anemia, anorexia, ataxia, profound weakness, and thrombocytopenia with resultant petechial hemorrhages on the mucosal surface particularly the conjunctiva and under the tongue
Rapid weight loss and dependent edema of the abdomen and legs are also notedduring this acute episode
Signs will last for about a week during which time the horse may die or recover from the infection and become a healthy carrier capable of transmitting the virus – a persistent EIA virus carrier

Front 68

signs of recurrent EIA infection

Back 68

Seen in infected horses weeks to months after the initial acute attack
The recurrent attacks of fever is what characterizes this disease
The recurrent attacks are characterized by fever, anemia, weakness (wobbly, tired), emaciation, ventral edema, thrombocytopenia, and hypergammaglobulinemia
The horse may die during the recurrent attack, recover to undergo more recurrent attacks, or may remain healthy for the rest of its life without undergoing any more recurrent attacks

Front 69

necropsy of an EIA horse

Back 69

Depends upon the stage of infection. If death occurs during acute disease, see widespread hemorrhage, splenomegaly, emaciation, anemia, and enlarged reddish‑brown liver caused by liver necrosis and hemosiderin deposition. During the chronic stages of disease, see evidence of hematopoiesis - yellow marrow of long bone being replaced by red marrow.

Front 70

what do the c-ELISA and AGID detect?

Back 70

circulating serum ab to the core p26 protein

Front 71

what is the anemia of EIA due to?

Back 71

hemolysis and erythrophagocytosis of complement coated RBC

Front 72

Hypergammaglobulinemia seen during each recurrent episode of EIA is due to

Back 72

Ab production during clonal expansion of memory/plasma cells brought on by the high degree of virus replication and viremia

Front 73

Understand the pathogenesis of EIA ventral edema

Back 73

p26ag/ab complexes in vasculature

Front 74

pathogenesis of EIA anemia

Back 74

erythrophagocytosis

Front 75

when are abortions due to EHV1 commonly seen?

Back 75

after the 6th month of pregnancy

Front 76

symptoms of EHV1

Back 76

myeloencephalopathy
ataxia
posterior paresis
eventually quadiplegia

Front 77

what animals are susceptible to the respiratory form of EHV1

Back 77

weaned foals, a few weeks preceding the outbreak of abortion storms

Front 78

respiratory dz due to EHV-1

Back 78

EHV-1 spreads naturally from older infected horses to susceptible younger horses by aerosol droplets and by close contact (mucosa-to-mucosa)
A mild respiratory tract disease may spread amongst young horses at weaning, or a few months later; this is characterized by fever, and nasal catarrhal that becomes mucopurulent. This respiratory infection coincides with period when mares are 6-11 months pregnant
However, most EHV-1 respiratory infections are subclinical and go undetected – seroconversion is the only evidence of infection
More severe respiratory disease associated with EHV-1 has been observed in foals from birth to a few months old, sometimes coinciding with myeloencephalopathy in mares

Front 79

EHV-1 myeloencephalopathy is observed

Back 79

adult horses usually where horses congregate
It is observed in adult mares (1) during and following abortion storms, (2) 1-3 months after foaling, and (3) a few weeks after a respiratory disease outbreak in either mares and in foals

Front 80

signs of EHV1 myeloencephalopathy

Back 80

Signs include incoordination, ataxia, posterior paresis (weakness in the hind quarters), paraplegia leading to quadriplegia, recumbency, and sometimes death

Front 81

paralytic or myeloencephalitic form of EHV-1 infection is caused by the

Back 81

neuropathogenic EHV-1 which can be differentiate from the respiratory virus by a mutation in the DNA polymerase gene; however, the respiratory virus can cause CNS disease and the neuropathogenic virus is transmitted via the respiratory route and can cause severe pneumonia in young foals

Front 82

what is responsible for the ataxia, paresis and paralysis seen with EHV1

Back 82

hemorrhage and necrosis in various parts o the spinal cord

Front 83

two most important viruses associated with abortion in mares

Back 83

EHV-1 is most important
also EVA

Front 84

histopath to diagnoses EHV1 abortion

Back 84

lesions in aborted fetal liver and spinal cord. multiple focal areas of necrosis in the liver with IN inclusions in infected cells

Front 85

Vaccination protocols for EHV1

Back 85

Many vaccines available, but none are completely satisfactory
MLV vaccines given IM are not very immunogenic; 2 doses induce immunity in mares and foals, but does not protect fully against abortions.
Inactivated vaccines provide good immunity, but must be given frequently.
Vaccinate at weaning, a month later, 6 months later and then annually.
Pregnant mares should be vaccinated with the inactivated virus vaccine at 5th, 7th and 9th months of pregnancy

Front 86

equine viral arteritis:
system affected
AKA
clinical signs
viral pathogenesis

Back 86

A respiratory disease primarily
Common name is pinkeye because it causes severe conjunctivitis
Depressed horse with ventral edema, nasal and occular discharges
Virus replicates in endothelial cells of blood vessels and causes arteritis, hence the fluid effusion (edema) and the name of the disease
An important virus that causes abortions in mares

Front 87

EVA family / genus

Back 87

arteriviridae / arterivirus

Front 88

EVA transmission
role of the stallion?
types of horses most susceptible?

Back 88

Transmission is by (1) aerosol transmission during outbreaks of respiratory disease and (2) venereally through infected semen
Transmission can also take place via mucosal contact with aborted foals/placenta


Of all the various means of transmission, the most important means of transmission on breeding farms is through infected semen venereally. Stallions can shed virus in semen for up to 2 years post-infection. Frozen semen used in AI is a very important source of EAV and an important way to introduce the virus onto a breeding farm
STB's most susceptible

Front 89

two viral diseases associated with ventral edema in horses

Back 89

EVA and EIA

Front 90

most common way EVA is introduced onto a farm

Back 90

via infected semen from stallions who are carriers (natural service or AI)

Front 91

another name for infectious bovine rhinotracheitis

virus that causes IBR

What does IBR cause?

Back 91

red nose

BHV-1

necrosis of nasal epithelium and turbinates

Front 92

An intense inflammation is observed in the nasal cavity:
hyperaemia, edema, pseudomembranes and ulcers.

Back 92

BHV-1

Front 93

two viruses that cause open mouth breathing in cattle

Back 93

IBR-BHV1 and BRSV

Front 94

bovine dz that causes frequent urination, tail switching and slight vaginal discharge in cows. small pustules and small white necrtotic areas and ulcers can be seen on the vulva and vaginal mucosa

Back 94

Infectious Pustular vulvovaginitis
BHV-1 genital form-

Front 95

When are BHV1 abortions commonly seen?

What lesions are seen at necropsy?

Diagnose by?

Back 95

Commonly seen in last trimester of pregnancy in animals that have not been vaccinated
Typically see multifocal disseminated necrosis in liver and lungs with intranuclear inculsions
Dx by IPX and PCR

Front 96

Family/ genus?

Transmission?

Back 96

Bovine leukemia virus

family Retroviridae and is a deltaretrovirus

BLV Transmission
PRIMARILY via blood inoculation
Insect vectors may play a role in transmission (Tabanids and Stomoxys)
Blood transfusion, dirty needles, vaccination, traumatic injuries, tattooing, all can transmit the disease if blood infected leukocytes are present on the instruments.
Cattle are the only animal that are naturally infected… sheep are highly susceptible to lymphoma when experimentally infected

Front 97

what cells are infected and transformed with BLV?

Is there viremia?

Back 97

B-cells are infected and transformed
No free virus in blood

Front 98

clinical signs associated with BLV lesions

Back 98

All cases of LSA are characterized by decreased appetite, decreased milk production, WEIGHT LOSS, and anemia. Additional signs are seen with LSA in certain specific organs:
Diarrhea and melena are observed with abomasal LSA
Hydropericard, hydrothorax, and edema of brisket with cardiac LSA

Front 99

BVD infection of pregnant cattle and fetal infection

Back 99

Exposure of cattle to virus at estrus may lead to failure of conception. Insemination of seronegative cattle with BVD infected semen can lead to poor conception initially. However, after the animal has seroconverted, conception is normal and calf is born healthy. Infection during 0-45 days leads to decreased conception rate and return to estrus.
Infection of fetus 45-125 days can lead to death of the fetus (mummification or abortion), congenital abnormalities, or persistent infection. Persistent infection occurs when the fetus is infected during 45-125 days with a NCP strain. The fetus recognizes the virus as self. It is born normal except that it secretes the virus consistently.
PI calves will develop mucosal disease when the (1) NCP virus mutates into a CP virus, or (2) infected with a CP virus that is homologous (antigenically similar) to the NCP virus. Mucosal disease can occur within the first 2 years of life.
PI calves will develop a normal immune response to other strains of BVDV that are antigenically different to the one they are persistently infected with. They can even respond well to vaccines!!!
Infection of the fetus during the period 125-175 days of gestation will result in congenital defects.
Infection of the fetus after 180 days of gestation results in a fully competent immune response by the fetus, with elimination of the virus. Calf is born with antibodies to the virus and is virus free.

Front 100

BVD family / genus

how do you diagnose BVD?

Back 100

family Flaviviridae and genus pestivirus

Lekopenia in acute mucosal disease (< 50% of normal)
Erosive lesions (NOT VESICULAR)
Virus Isolation. Virus can easily be grown on TC. Virus in TC is identified as BVDV by FA test or IPX. Approximately 5-7 days required for identification. NCP BVD does not cause CPE!! A whole blood sample is the best sample for virus isolation (virus in lymphocytes). Nasal swabs can be submitted. Feces is not a good sample.
Direct virus identification in tissues. This can be by FA, IHC , or PCR. Ear notch sample is a sample that is easily obtained and on which IHC or PCR is performed.
Serology can be performed on paired samples taken 3-4 weeks apart. The antibody titer is determined by the SNT. Screening of herds for BVD can be done using single serum samples.

Front 101

Note the erosions on the tongue (upper), and the erosive/ulcerative lesions in the esophagus (lower)

What diseases can cause these lesions?

Back 101

MCF and BVD mucosal dz
BHV-1 in very young calves
Rinderpest

Front 102

transmission of BVDV

Back 102

is primarily through PI animals excreting the NCP BVDV in all secretions

Front 103

when can a bovine fetus be infected with BVDV to cause cerebellar hypoplasia?

Back 103

125-175d

Front 104

what can occur with BVDV fetal infections?

Back 104

Cerebellar hypoplasia and hydranencephaly is common and calves are unable to stand and walk normally after birth. Retinal atrophy and dysplasia, optic neuritis, microphthalmia, can lead to various degrees of blindness.

Front 105

An animal that is transiently viremic with BVDV (undergoing acute infection) will be ICH _____ if ear notch sample is tested

Back 105

negative

Front 106

how cna BVDV PI animals be diagnosed?

Back 106

IHC on ear notch samples

Front 107

MCF virus reservoirs / specific viruses

2 forms:

Back 107

MCF Reserviors
The virus that causes MCF belongs to the virus family Herpesviridae and is a gamma-herpesvirus.
Alcelaphine herpesvirus type 1 (AHV-1) is a virus that infects wildebeest naturally
Ovine herpesvirus type 2 (OHV-2) is a virus that infects sheep naturally
2 Forms of MCF are recognized.
(1) The African form of MCF is associated with AHV-1 in wildebeest. The disease is endemic in Africa but also occurs in the US in zoos and on exotic animal farms that show and breed wilderbeest.
(2) The Sheep-associated or US‑European form of MCF is caused by OHV-2 of sheep and is endemic in the US. OHV-2 is transmitted from sheep to cattle, bison, and deer in the US.

Front 108

describe the eye lesions seen with MCF

Back 108

Corneal opacity starts at the limbus and progresses towards the center
Interstitial keratitis

Front 109

most common form of MCF seen

clinical signs

Back 109

The head and eye from is the form most commonly seen:
It is characterized by sudden onset of high fever (106-107 F), extreme depression, anorexia, photophobia with blepharospasm, profuse mucopurulent nasal and ocular discharges, bilateral corneal opacity, and diarrhea. There is a generalized lymphadenopathy and lymph nodes are unusually large. Lamness is often noted due to coronitis
Corneal opacity, described as chronic bilateral stromal keratitis, begins at limbus and progresses centrally, and is accompanied by blepharospasm and congestion of scleral vessels
Examination of the mouth will reveal erosions on the soft palate, tongue and gums. The nasal mucosa and nasal passages are deep red, necrotic, and covered with fibrinopurulent exudates
CNS signs may appear and is characterized by incoordination, muscle tremor, and head pressing
Death occurs in 7-10 days after onset of signs

Front 110

two other forms of MCF and their clinical signs

Back 110

The peracute and alimentary tract form is common in deer and characterized by high fever, dyspnea and acute gastroenteritis. The typical head and eye from may not be present. Death occurs in 1-3 days
The mild from is characterized by transient fever and mild erosion.

Front 111

pathognomonic lesion in cattle with MCF

where does virus replicate?


what does MCF cause?

Back 111

Necrotic vasculitis is the pathognomonic lesion in cattle with MCF
Virus replicates in vascular endothelial cells and CD8+ cells kill these viral infected cells
Lymphoproliferation in various tissues, with widespread perivascular lymphoplasmacytic infiltration

Front 112

what species does MCF cause high mortaliity in?

Back 112

deer

Front 113

what vector transmits Bluetongue Virus?

seasonality of BTV?

Back 113

cullicoides

late summer/fall

Front 114

pathognomic lesion for BTV

Back 114

BTV

Hemorrhage at the base of the pulmonary artery
This is a pathognomonic lesion of BT in sheep

Front 115

Two viruses that cause hydranencephaly in sheep

Back 115

Bluetongue virus
akabane virus

Front 116

define hydranencephaly

define hydrocephalus

Back 116

Hydranencephaly is accumulation of fluid within the white matter as a result of virus induced necrosis


Hydrocephalus is fluid accumulation in ventricles

Front 117

Congenital infections with BTV

Back 117

Dumb calf
BTV, particularly the attenuated vaccine virus, will cross the placenta and infect calves and lambs
Brain lesions include hydranencephaly and arthrogryposis

Front 118

BTV in cattle

cattle act as _____ of BTV

clinical signs

Back 118

BT infection in cattle is usually sub-clinical or inapparent
Cattle act as amplifiers of BTV
Clinically, it is characterized by lameness, erosions in the nostril, and by peeling of the skin of the nasal septum

Front 119

how transmitted?

mortality?
Seasonality?

lesions at necropsy

Back 119

Epizootic hemorrhagic Dz

seasonal disease – transmitted by Cullicoides
Mortality may be high in deer and it is observed in late summer/fall
Carcass of dead deer will show extensive hemorrhages

Front 120

One form of this dz is ____ and deer die as a result of ___________. __________________ is commonly observed with this form

Back 120

epizootic hemorrhagic dz


One of the forms of EHD in deer is the pulmonary form
Deer die as a result of acute lung edema
Frothing at the mouth/nostril is commonly observed in this form
Observe the prominent lung edema - interlobular fluid accumulation is evident in this lung

Front 121

how does this dz get its name?

Back 121

EPIZOOTIC HEMORRHAGIC DISEASE GETS ITS NAME FROM THE FACT THAT THERE ARE HEMORRHAGES EVERYWHERE PARTICULARLY IN THE MUSCLES

Front 122

three diseases that cause high mortality in wild and farmed deer

Back 122

EHD, BT, MCF
MCF- presumably acquired from contact with sheep. sporadic and highly fatal in deer!

Front 123

four vesicular dzs

Back 123

vesicular stomatitis
vesicular exanthema of swine
foot and mouth dz
swine vesicular dz

Front 124

Vesicular stomatitis
incubation period
clinical signs
recovery, morbiidty, mortality

Back 124

Incubation period is average – about a week.
Fever, anorexia, and excess salivation are the first signs usually – mild fever with profuse "ropy" saliva. In horses and cattle see vesicles on dorsum of tongue, dental pads, buccal mucosa, teats, coronary bands. When vesicle rupture, it leaves a small shallow erosion/ulcer. Lamness is often noted. In swine vesicle on the snout and feet causing lameness. In horses, tongue lesions are most pronounced. Confusion arises when there are no vesicles present. Vesicle may dehydrate by fluid seepage resulting in an eroding rough area or dry necrotic lesion. Difficult to diagnose in this case.
Recovery in 3 - 4 days Morbidity = 10-80% Mortality = 0%

Front 125

Vesicular exanthema of swine
incubation period
clinical signs
recovery, morbiidty, mortality

what type of virus causes?

Back 125

An acute, febrile, contagious disease of swine characterized by the formation of vesicles on the snout, in the mouth, and on the feet. Incubation period: 18 ‑ 72 hours.
Morbidity is high, mortality low

. Importance is that it is clinically indistinguishable from F&M, swine vesicular disease, and vesicular stomatitis.

Caused by a calicivirus.

Apart from outbreaks in Iceland and Hawaii, VESV has only been diagnosed in the US.

Front 126

Foot and Mouth Dz
incubation period
clinical signs

Back 126

Incubation period is short: 2‑4 days
In Cattle: starts with lameness, smacking of lips and salivation. Vesicles may appear in mouth (gums, tongue, lips, dental pad), on muzzle, on feet (interdigital space, dew claw), on teats and udder. Vesicles starts as blanched areas, rupture, with complete healing after 2 weeks. In calves, death may occur from myocarditis. In Pigs: lameness and vesicles on snout are prominent signs.

Front 127

swine vesicular dz
clinical signs

Back 127

- It is a disease of pigs characterized by vesicular lesions in the mouth and on the feet ‑ minimal loss of condition and lesions heal rapidly.

Front 128

Name the 2 viruses that cause vesicular disease in cattle
How is the virus transmitted with each of these viruses
What samples would you collect in clinically affected cattle

Back 128

Two viruses that cause vesicular disease in cattle
Vesicular Stomatitis Virus
Foot and Mouth Disease Virus (An aphtovirus belonging to the virus family Picornaviridae.)
Virus Transmission of Vesicular Stomatitis
Transmitted primarily by the sand flies (eye gnats) and blackflies. See outbreak along river drainages. Wild life species in Central America act as reservoir, where VSV is enzootic. Outbreaks in the US is believed to be windborne, initiated by infected carrier insects blown up from Central America. Many animals are infected asymptomatically and serve as amplifiers of VSV.
Transmission during an outbreak is through mucosa or broken skin. Saliva and vesicular fluid from infected animals are highly infectious. Virus remains viable in envionment
Virus Transmission of Foot and Mouth
Transmission: In acutely ill animals, virus in saliva and most body fluids (also in semen). Spread by direct contact with infected animals and fomites, by inhalation (aerosols), by ingestion (garbage feeding).
What samples would you collect in clinically infected animals
Vesicular Stomatitis: Samples include vesicular fluid and paired serum samples on which RT-PCR and virus isolation are performed
Foot and Mouth: Vesicular fluid** and epithelial covering

Front 129

Name the 2 vesicular viruses that can cause vesicles on the teat of cows

One other dz that can cause vesicules on teats

Back 129

Vesicular Stomatitis Virus
Foot and Mouth Disease Virus
Bluetongue Virus

Front 130

Name the 4 viruses that cause vesicular disease in Pigs
How is the virus transmitted with each of these viruses
What samples would you collect in clinically affected pigs

Back 130

4 vesicular disease viruses
Vesicular Stomatitis Virus
Vesicular Exanthema of Swine
Foot and Mouth Disease Virus
Swine Vesicular Disease (an enterovirus in the virus family Picornaviridae )

Virus Transmission
Transmitted primarily by the sand flies (eye gnats) and blackflies. See outbreak along river drainages. Wild life species in Central America act as reservoir of the virus where VSV is enzootic in low-lying areas receiving heavy rainfall with high vector population. Outbreaks in the US is believed to be windborne, initiated by infected carrier insects blown up from Central America. Many animals are infected asymptomatically and serve as amplifiers of VSV.
Feeding of infected meat (garbage)
Transmission: In acutely ill animals, virus in saliva and most body fluids (also in semen). Spread by direct contact with infected animals and fomites, by inhalation (aerosols form milk trucks, wind), by ingestion (garbage feeding).
Not listed in the notes…

Samples to collect
Samples include vesicular fluid and paired serum samples on which RT-PCR and virus isolation are performed
Virus is diagnosed in fluid from vesicles – RT-PCR and virus isolation
Vesicular fluid and epithelial covering

Front 131

vesicular stomatitis
virus family / genus

Back 131

Caused by a vesiculovirus in the virus family Rhabdoviridae

(bullet shaped virion)

Front 132

what arthropod transmits vesciular stomatitis?

Back 132

primarily by the sand flies (eye gnats) and blackflies.

Front 133

only vesicular dz that affects horses

Back 133

vesicular stomatitis

Front 134

vesicular dz


Know the vesicular diseases and the clinical signs in each species
What would you expect to observe if you examined the mouth of this animal?

Back 134

Foot and Mouth dz
Clinical Signs
- In Cattle: starts with lameness, smacking of lips and salivation. Vesicles may appear in mouth (gums, tongue, lips, dental pad), on muzzle, on feet (interdigital space, dew claw), on teats and udder. Vesicles starts as blanched areas, rupture, with complete healing after 2 weeks. In calves, death may occur from myocarditis.
- In Pigs: lameness and vesicles on snout are prominent signs.

Front 135

most important consequence of suid herpesvirus 1 in sows

Back 135

SMEDI

Front 136

pseudorabies in cattle is AKA

symptoms

Back 136

Mad itch

intense pruritis (flank/hind legs) leading to frenzy. eventual pharnygeal paralysis, salivation, mania, bellowing and convulsions. death within 48 hours

Front 137

Pseudorabies in dogs and cats
clinical signs

Back 137

intense pruritis (head region). scratching, violent rubbing. Bulbar paralysis, salivation. frantic, frenzy. generalized convulsions. NO aggression. Howling, mewling, vomting and diarrhea are common

Front 138

how is encephalomyocarditis virus transmitted?

what does EMV cause in piglets?

Back 138

by rodents, especially rats


in piglets- convulsions and acute heart failure

Front 139

what type of virus is this?

Back 139

coronavirus

Front 140

TGE is caused by a ____virus

clinical signs in young piglets

what cell types are affected? what is the result of this?

vaccinate protocol for sows?

Back 140

coronavirus

100% mortality in piglets less than 10d old- severe diarrhea, vomiting, dehydration, death

infects and kills columnar epithelial cells resulting in villous atrophy- reduces digestive and absorptive capacity

vaccinate sows 3 weeks prior to farrowing with MLV

Front 141

this virus is also referred to as ______

what cell types are infected?

mortality?

Back 141

Rotavirus diarrhea is often referred to as “white scours” or “milk scours”
Rotavirus infects and destroys the terminally differentiated enterocytes
lining the tips of the intestinal villi causing intestinal malabsorption and maldigestion
Mortality due to rotavirus is < 20 % amongst suckling pigs
It is a major factor in post-weaning diarrhea resulting in poor weight gain

Front 142

what causes porcine postwearning multisystemic wasting syndrome?

where does the virus replicate?
why does it cause substantial mortality?

Back 142

porcine circovirus-2

Replicates in lymphoid tissues causing swollen lymph nodes
It can cause substantial mortality in young pigs because of its immunosuppressive properties

Front 143

what does porcine repro resp syndrome cause

Back 143

respiratory disease in growing pigs and SMEDI in adult sows

Front 144

clinical signs?

Back 144

SWINE INFLUENZA CAUSED BY H1N1 AND H3N2

Clinically see sudden onset of fever, anorexia, followed by extreme prostration
(do not want to move, muscle pain, stiffness), labored breathing, "thumps",
deep cough, watery discharge from eyes and nose.
Disease looks bad, but most recovery rapid after few days
Mortality 1-4%.

Front 145

Five viruses that have been associated with SMEDI in sows

What does SMEDI stand for and why is it so important?

Pathogenesis of SMEDI?

Back 145

Know the 5 viruses that cause SMEDI
Pseudorabies (Suid Herpesvirus-1)
Encephalomyocarditis Virus
Porcine Postweaning Multisystemic Wasting Syndrome (Porcine Circovirus type-2)
Porcine Reproductive and Respiratory Syndrome Virus (Caused by an arterivirus – Prototype virus is called the Leylytstad virus)
Porcine Parvovirus
Porcine Teschovirus types 2-7 and 11-13
Classical Swine Fever (CSF virus is a Pestivirus belonging to the virus family Flaviviridae.)

SMEDI- stillbirth, mummification, embryonic death and infertility

SMEDI Pathogenesis
- Sows infected in later part of pregnancy will abort premature piglets, stillborn piglets, and mummified fetuses

Front 146

what do classical and african swine fever cause?

how can these viruses be transmitted?

most important necropsy lesions?

Back 146

Hog Cholera and African Swine fever cause very high mortality in pigs
The viruses causing these diseases remain in meat products and will be transmitted to pigs fed the garbage containing the virus tainted meat
During an outbreak the virus is easily spread between pigs through contact with infected secretion – feces, saliva, etc..
Most important necropsy lesion is wide spread hemorrhages throughout the body
Both are exotic viruses in the US and are reportable diseases

Front 147

clinical signs include by high fever, depression, conjunctivitis, diffuse purplish discoloration (hyperemia) of skin,and Nervous signs (circling, convulsions)

Back 147

hog cholera - clasical swine fever

Front 148

Enlarged haemorrhagic mesenteric lymph nodes

Enlarged hemorrhagic gastro-hepatic lymph node

Enlarged hemorrhagic renal lymph nodes
with petechiation of the renal cortex

Back 148

african swine fever

Front 149

how is ASF transmitted, and what animals can serve as as reservoir?

Back 149

argasid ticks
wild hogs

Front 150

very important virus of chickens with 100% mortality.
Characterized by various clinical signs including sneezing, coughing, edema of the face and head, diarrhea, and CNS signs
Widespread hemorrhages at necropsy

Back 150

Highly pathogenic avian influenza

Front 151

what disease can cause a very similar clinical presentation to HPAI and is indistinguishable?

Back 151

Newcastle dz- avian paramyxovirus-1

Front 152

what clinical signs are seen with both HPAI and NCD

Back 152

open mouth breathing.
80% mortality not uncommon
virus spreads quickly
other signs inlucde CNS dz (tremors, torticollis, weird postures) and diarrhea

Front 153

signs of HPAI in ducks?

Back 153

generally no clinical signs, but may see CNS signs

Front 154

HPAI and VVND
what are these pictures showing

what is pathognomic for these diseases?

Back 154

Echymotic hemorrages in the heart muscle and in the fat around the heart.
Hemorrage in the proventriculus - this is almost pathognomonic for HPAI and VVND viruses
Echymotoc hemorrages are also seen in the intestinal tract and respiratory tracts

Front 155

what can the viscerotropic velogenic pathotype cause?

Back 155

100% mortality with no accompanying clinical signs.

When clinical signs are present, it usually starts with respiratory disease characterized by fever (43 C), dullness, thirst, ruffled feathers, hemorrhagic comb, edema of the head, respiratory distress (open mouth breathing and gasping for air, coughing) and death

Front 156

in the US what maintains the ND virus

what species has NDV affected?

Back 156

domestic birds and cormorants

ND outbreaks have been diagnosed in chickens, guinea fowl, turkeys, pheasants, ducks, geese, pigeons, and wild birds

Front 157

pathogenesis of avian paramyxovirus-1

Back 157

Like influenzavirus, the insertion of multiple basic AA, e.g. lysine and arginine, just before the cleavage site of the F protein results in increased virulence
The F protein of the lentogenic pathotypes are cleaved by trypsin-like enzymes present on the epithelial cells of the respiratory and gastro-intestinal tracts, and the virus cannot go systemic
The F protein of the velogenic pathotypes, on the other hand, can be cleaved by furin-like proteases within cells. Intracellular cleavage means that virus leaves the cells as infectious particles and in that way can go viremic and infect cells in all organs of the body

Front 158

how has VVND been introduced into the country?

Back 158

through smuggling of exotic birds, or through illegal trade of poultry and poultry products.

Front 159

early signs of NCD?

Back 159

typically include a dramatic drop in egg production. In layers that produce brown eggs, eggs that are laid may be discolored. The light eggs in this image are abnormal. This discoloration is caused by abnormal pigment deposition of the egg while in the oviduct of infected chickens.

Front 160

infectious laryngotracheitis
caused by?

common symptom? pathogenesis?

Back 160

Caused by Gallid herpesvirus 1
Open mouth breathing is common because of the necrosis in the tracheal epithelium and the accumulation of caseous exudate in the trachea and larynx

Front 161

infectious bronchitis
caused by?
causes?
what cells are infected?
what does this result in?

Back 161

Caused by a coronavirus – it causes mild respiratory disease in adult chickens
This respiratory virus (like other respiratory viruses!) also infects the epithelial cells of the oviducts
Because of the inflammation, calcium deposition in the egg shell is interfered with causing abnormal misshapen eggs with thin egg shells
Albumin is also watery

Front 162

Differentials for egg deformities and decline in egg production:

Back 162

Infectious Bronchitis (decline in #’s for layers, deformed)
Lentogenic Newcastle Disease Virus (deformed) – Low Pathogenic Avian Influenza (decline in #’s)
Mesogenic NDV (deformed, decline in #’s)

Front 163

what is infectious bronchitis virus associated with in young chicks?

Back 163

Associated with very high morbidity, but low mortality in young chicks - (explosive) respiratory infection characterized by sneezing, coughing, and gasping for air.

Front 164

infectious bronchitis virus in layers

Back 164

Although IBV infection in layers, is often subclinical, it is accompanied by a marked drop in egg production, with many soft‑shelled and malformed eggs with watery albumin

Front 165

Mareks dz
caused by?

where does virus replicate?
transmission?
pathogenesis?

Back 165

Marek’s disease is caused by Gallid herpesvirus 2
During the acute infection, the virus replicated in the cells lining the feather follicles and are transmitted when the feathers fall out
The virus is inhaled by susceptible birds and this is how the infection spreads

Pathogenesis
Virus is inhaled and reaches the lungs where it is taken up by lung macrophages.
Infects lymphocytes disseminates throughout the body via infected lymphocytes
Virus reaches the follicles in the skin and infects epithelial cells lining the feather follicles
Replication in the epithelial cells of the feather follicles allows the virus to be released into the environment as “dry skin aerosol” when the feather “fall off”
After the infected chicken mounts an immune response, the virus goes latent in T‑cells
These T-cells can eventually be transformed into cancer cells by the virus.

Front 166

marek's dz

what is the bottom picture showing

Back 166

Note the swollen sciatic nerve on the left and how different it is from its pair on the right – the nerve is infiltrated with virus infected lymphocytes and causes nerve swelling resulting in paralysis
Marek’s disease is caused by Gallid herpesvirus 2

Front 167

how is marek's dz transmitted and acquired?

Back 167

MDV is transmitted via virus replication in the epithelial cells of the feather follicles, and being aerosolized when the feathers are shed
Therefore, MDV is a acquired through the respiratory system

Front 168

the top is a typical clinical picture of what disease?

what is the pathogenesis of this disease that leads to the lesion seen in the bottom picture?

Back 168

Mareks DZ

MDV eventually transforms the lymphocytes in some infected birds and the transformed lymphocytes infiltrate the nerves and causes paralysis of the legs (Sciatic nerve) or wings (brachial nerve)
Sciatic nerve is enlarged (unilaterally) and looses whiteness and striation

Front 169

these lesions are typical of what dz?

what are the nerves infiltrated with?

Back 169

Mareks Dz

Sciatic and brachial nerves are enlarged and loose their typical striation patterns

These nerves are infiltrated with herpesvirus transformed T-cells

Front 170

what dz is causing this pheasant to show neuro signs?

Back 170

EEE

Front 171

Infection causes swelling, edema, hyperemia and sub-serosal hemorrhages in the gland

what disease is this?

what is the BF?

Back 171

Infectious Bursal Dz
BF= bursa fabricius (Where chicken manufactures b-cells)

Front 172

what is Pacheco's dz? what birds are most affected?

Back 172

Pacheco's Disease is a highly contagious and highly fatal disease of all psittacine birds and affects all ages. Amazon parrots account for the majority of cases, followed by African grey parrots, macaws, and cockatoos

Front 173

what virus causes pacheco's dz?
how is it transmitted?
clinical signs?

Back 173

Psittacine herpesvirus-1
Healthy birds that have recovered from the disease are carriers and can excrete virus in feces during time of stress (breeding, loss of mate, change in environment, pet shops!)
Very often, parrots are described as normal one day and dead the next!
Signs include lethargy, anorexia, regurgitation, diarrhea, ruffled feathers, and neurological signs characterized by tremors of neck, wings, and legs

Front 174

Birds die of massive liver necrosis characterized by enlarged liver, spleen, and kidneys
See multifocal hepatic and splenic necrosis with eosinophilic intranuclear inclusion bodies

Back 174

Pacheco's Dz

Front 175

what virus causes this high contagious dz of parrots (electus spp, african greys and cockatoos)

Back 175

psittacine beak and feather dz
psittacine circovirus

Front 176

name the viruses that can cause infectious tracheobronchitis

Back 176

Canine Parainfluenza virus
Canine Influenza virus
Canine Adenovirus type-2 (Infectious canine laryngotracheitis)
Canine Adenovirus-1
Canine Distemper virus
Canine Herpesvirus-1
Canine Reoviruses

Front 177

what bacterial pathogen is associated with ITB

Back 177

Bordatella Bronchiseptica
mycoplasma

Front 178

this virus causes severe eye lesions that includes keratitis and corneal ulceration
It may also cause oral erosions or ulcerations
Sneezing, nasal discharge, anorexia, fever, are the other commonly seen clinical signs
This virus infects young kittens usually and they remain latently infected after they recover

Back 178

feline viral rhinotracheitis
caused by feline herpesvirus-1

Adults = conjunctivits only
Causes oral ulcerations when nasal passages are infected
Can recrudesce

Front 179

what are the most importan diseases that cause bovine respiratory dz?

Back 179

bhv-1
PI-3
BRSV

Front 180

what three viruses are associated with bovine interstitial pneumonai

Back 180

PI-3
BRSV
Bovine adenovirus

Front 181

what two virses are most frequently associated with bovine enzootic pneumonia of young calves and veal calves

Back 181

PI-3
BRSV

Front 182

pathogenesis of Jaagseikte sheep retrovirus

Back 182

Virus transforms the pneumocytes of the lungs which secrete excessive amounts of fluid that fill up the alveolar space
This fluid pours out of the nostril when the sheep’s head is down or when you hold up the animals like a wheelbarrow!

Front 183

Ovine progressive pneumonia pathogenesis

Back 183

Virus transforms macrophages which inflitrate the lungs and other tissues including the udder and brain
Lungs are heavy and infiltrated with macrophages

Front 184

viruses that can cause equine respiratory dz

Back 184

EHV-1
EHV-4
Equine Influenza
EVA
Equine Rhinitis A Virus
Equine Adenovirus
Equine Reovirus
EHV-2
Hendra virus

Front 185

What is the common names for EHV-4?
What are the clinical signs associated with infection with EHV-4 and the age group of horses?
What samples to submit for a diagnosis of equine herpesvirus 4?
What type of vaccines are available to protect against EHV-4 infection and what is the recommended vaccination program?

Back 185

Equine viral rhinopneumonitis
Foals & yearlings – fever, mucopurulent nasal catarrh & conjunctivitis
Nasal secretions for PCR & virus isolation
MLV – 2 doses
Inactivated – frequently
Pregnant mares – 5, 7 & 9 months

Front 186

Influenza and Rhinitis A

What are the most important clinical signs associated with these 2 viral infection and what clinical signs might help differentiate between these 2 infections?
Are vaccines available? If so, what type are available and the vaccination routine followed.
What sample would you submit to the diagnostic laboratory for diagnosis of these infections

Back 186

Equine Influenza - fever, dry hacking coughing, slight nasal discharge, depression, inappentance
Equine Rhinitis A – copious nasal discharge that becomes mucopurulent & coughing for 2-3 weeks

2. Equine influenza – bivalent inactivated vaccine – foals at 6 months and again 3-8 weeks later; booster 6 months post 2nd dose; revaccinated biannually in April & October

Equine Rhinitis A – no vaccine

Equine influenza – deep nasal or pharyngeal swabs & paired serum samples

Front 187

common virus of horses that rarely causes clinical dz

however, in certain arab foals, it can be fatal

Back 187

Equine adenovirus is a common virus of horses that rarely causes clinical disease in normal horses
It spreads easily between horses and cause subclinical infections
However, in Arab foals that are born with combined immunodeficiency, this virus will infect the foals and cause a fatal disease
These foals usually start to show clinical disease after the first month or two and respiratory disease is the most common disease associated with this condition
They will normally die by the time they reach 4-6 months of age

Front 188

extensive hemorrhage in the cortex and perivascular cuffing

only lesion seen with this dz- there are no systemic lesions

Back 188

EEE

Front 189

Perivascular cuffs are commonly seen in the CNS of animals ________

Back 189

infected with all types of “viral encephalitides”

Front 190

two most important viruses that cause diarrhea in calves?

how are calves infected?

Back 190

The 2 most important viruses that cause diarrhea in calves is Bovine Rotavirus and Bovine Coronavirus
Adults secrete both viruses in their feces just before and at time of calving – they are asymptomatic carriers and contaminate the environment

Front 191

what cells do bovine rotavirus and coronavirus infect?
what does this result in?

treatment?

vaccination?

Back 191

Bovine Rotavirus and Bovine Coronavirus infect the epithelial cells of the small intestine and replicate and destroy the mature columnar cells lining the villi
Decrease ability to digest and adsorb nutrients
Very voluminous watery diarrhea with severe dehydration
Must cut off milk for 2 days and give lots of electrolytes by mouth, or sub cut or IV
Explosive outbreaks may occur on farms that do not have good hygiene or management
Vaccinate dam with inactivated vaccine before calving both IM and Intramammary

Front 192

this dz is caused by a type B coronavirus.

The most significant clinical sign is profuse and watery diarrhea, which is greenish to brownish with occasional blood streaks
Persists for about 5 days
Anorexia, depression, and drastic decrease in milk production is also noted

Back 192

Winter Dysentery

Front 193

this dz is caused by a morbiliivirus
causes very high morbidity and mortalitiy
Profuse watery diarrhea erosive with mucosal lesions throughout the gastro intestinal tract

Back 193

rinderpest

Front 194

causes warts most often in young cattle on the face/neck.

Virus?
how is it spread?
treatment?
vaccine?

Back 194

bovine papilloma

Spread via rubbing on posts and leaving the virus on the wood or metal
Will eventually regress by themselves
Vaccine is available – Killed vaccine given intradermally
Efficacy of vaccine difficult to judge because warts go away by themselves anyway

Front 195

two types of papillomas

pathogenesis

Back 195

Papilloma are either epithelial papilloma or fibropapillomas
All warts have similar structural features
Papilloma virus stimulates the cells of the basal layer to replicate – this is through one viral protein translated in the viral infected cells
These infected cells do not contain any structural viral proteins or infectious virus
Infectious virus present in dead cells overlaying the wart

Front 196

where are papillomas most often seen in cows?
transmission?
control?

Back 196

Papilloma are often seen on the teat of milking cows
Easily transmitted between cattle via milking machine if not careful
“Rice grain” or “frond like” warts are described
Difficult to control and get rid of!

Front 197

proliferative lesion on the teat of a cow that progresses to a scab
caused by a parapoxvirus and is zoonotic

Back 197

pseudocowpox

Front 198

what type of virus causes this dz?
what samples need to be taken to confirm?

the lesions are proliferative, but not erosive or ulcerative

Back 198

Bovine papular stomatitis, caused by a parapoxvirus

samples to confirm: EM exam of lesion scraping or saliva

Front 199

Viruses that can cause teat lesions

Back 199

Bovine Papallomavirus (BPV-1 and BPV-6)
Psuedocowpox (parapoxvirus)
Cowpox/Buffalopox (orthopoxvirus)
Bovine Herpesvirus-2/ Bovine Herpes Mammillitis Virus
Vaccina Virus

Front 200

painful, ulcerative lesions on teat and udder

Back 200

bovine herpes mammillitis virus
(BHV-2)

Front 201

Typical proliferative lesions on the lips of sheep – young lambs especially
Human infection with the virus – starts as a vesicular lesion, progresses to a pustule, and then forms a firm adherent scab
Shearers commonly infected

Back 201

contagious ecthyma

Front 202

proliferative/scabby lesions caused by a parapoxvirus

age affected?vaccination?

Back 202

contagious ecthyma

Disease of in young lambs 2-6 months old
Must vaccinate the lambs at 2 months for protection
Vaccinating the ewe is useless for protecting the lambs

Front 203

know the three diseases caused by a parapoxvirus

are they all zoonotic?

Back 203

pseudocowpox
bovine papular stomatitis
contagious ecthyma

all are zoonotic

Front 204

pseudocowpox lesions

Back 204

Lesions start with small papule, which quickly grows into a vesicle or pustule, which ruptures after 48 hours forming a thick scab. Scab is elevated with granulation tissue underneath. After 7-10 days, scab drops off leaving behind an area of 0.5‑2.5 cm diameter. This area is encircled by small scabs giving it the appearance of a "horseshoe-shaped ring" - crusty reddish raised border with a wart like granulomatous lesion in the middle

Front 205

bovine papular stomatitis?
importance?

Back 205

Characterized by raised and not depressed lesions - raised hyperemic areas, which rapidly become roughened plaque-like with irregular borders. Occurs on lips, dental pads, muzzle, buccal mucosa. Not economically important. Importance in that it must be differentiated from the vesicular diseases.

Front 206

contagious ecthyma lesions

Back 206

characterized by cutaneous vesiculo-papular eruptions followed by development of pustule and thick friable crusts. Commonly affects young lambs ‑ lesions most common on muzzle, lips, occasionally in mouth, on the feet, face. In ewes, see lesions primarily on the udder. Morbidity is high, but case fatality is low. Lambs loose weight due to suckling difficulties.

Front 207

when are papillomas most frequently seen in dogs?
treatment?

Back 207

Most frequently seen in younger dogs
Not cause for alarm – will regress normally in 6-8 weeks
May remove surgically if interferes with eating or collects bacteria and gets infected

Front 208

solitary lesions that are proliferative in nature

why lesions on the face and leg?
zoonotic?

Back 208

Cowpox

Lesion associated with cowpox virus that cats pick up from rodents (mice, rats) – lesions on face/leg because that is what contacts the rodent!

it is zoonotic

Front 209

when will these lesions be seen on cats?

lesions are solitary, proliferative lesions that can occur anyway. they resemble raised plaques.

Back 209

feline papilloma

occur in older cats that are immunodeficient as a result of FIV infection

Front 210

Inflammation of the synovial membrane resulting in painful joint swelling
Adults become progressively more lame and looses weight

Back 210

caprine arthritis encephalitis
aka Big knee

Front 211

venereal dz of horses

Lesions consist of vesicular or pustular eruptions on the vulva and perineum of mares and on the penis of stallions. Lesions may occur on the teats and on muzzle of suckling foals.

Back 211

equine coital exanthema
EHV-3

Front 212

dz caused by a lentivirus

what cells are transformed?
what does this cause?

Back 212

caprine arthritis encephalitis

transforms monocytes which then infiltrates joints, CNS, and Udder
Chronic progressive lameness in adult goats

Front 213

many goats affected with CAE develop ____ and the virus spreads through the ____

Back 213

mastitis
milk

Front 214

lamb has hair, rahter than wool and presents as ataxia and trembling

Back 214

hairy shaker / border disease