Virology Test 2

Question 1

What is the purpose of PCR?

Answer 1

Amplification of viral genome/DNA

Question 2

What are the 3 steps of PCR?

Answer 2

Denaturation
Annealing
Extension/elongation

Question 3

What are real-time PCR or quantitative PCR (qPCR)?

Answer 3

Advanced form of PCR which allows monitoring and quantification of increasing accumulation of PCR products/nucleic acid load as the reaction progresses.

Useful to study virus load in patients

Question 4

What is DNA sequencing?

Answer 4

Process by which the sequence of bases in a DNA molecule is elucidated/can be obtained and read.

Question 5

What are advantages to using Next generation sequencing?

Answer 5

Significantly cheaper
Quicker
Needs less DNA
High throughput
More accurate and reliable than Sanger sequencing

Question 6

What is metagenomics?

Answer 6

The study of the collective set of microbial populations in a sample by analyzing the sample’s entire nucleotide sequence content, and is a powerful method for random detection of existing and new pathogens.

Question 7

What is phylogenetic analysis?

Answer 7

The use of virus genome sequence data to study evolution of viruses and genetic relationships among viruses.

Question 8

What is the advantage of microarrays in detection of pathogens in surveillance studies is?

Answer 8

Hundreds of pathogens can be screened for simultaneously using a single microarray chip.

Question 9

What happens in a microarray?

Answer 9

Several thousand of known DNAs (probes), amplified by PCRs/RT-PCRs, are spotted onto a glass or a silicon chip.

The target/sample DNA are fluorescently labeled and then hybridized/added to the chip containing DNA probes.

Positive reactions between probe-DNA and sample DNA (hybridization) generate a fluorscent signal from the spot where probe DNA is spotted in the chip.

Question 10

The study of virus evolution using genome sequence data is known as ______

Answer 10

Phylogenetics

Question 11

Antiviral drugs

Answer 11

Class of medication used specifically for treating viral infections.

Interfere with the ability of a virus to infiltrate a target cell or target different stages of replication/synthesis of components required for replication of the virus

Question 12

Immune system stimulation

Answer 12

Interferons, class of proteins that has antiviral effects and modulate functions of the immune system

Question 13

What are the 3 ways/purposes of treating viral diseases?

Answer 13

Administer antiviral drugs.
Immune system stimulation.
Synthesize antibodies or administration of natural antiserum (antibodies).

Question 14

Acyclovir antiviral activity is primarily restricted to________

Answer 14

Herpesviruses

Question 15

What is Acyclovir as?

Answer 15

A prodrug, inactive form

Question 16

What does acyclovir require in infected host cells to convert itself into active form and interfere with virus replication?

Answer 16

Virus enzymes

Question 17

What is Acyclovir used to treat?

Answer 17

Herpesvirus infections in humans
Feline herpesvirus 1 induced corneal ulcers
Equine herpesvirus-1 induced encephalomyelitis

Question 18

What is Acyclovir?

Answer 18

Synthetic nucleoside analog of deoxyguanosine.

Question 19

Two main steps of mechanism of antiviral effect of acyclovir

Answer 19

Herpes simplex’s DNA polymerase enzyme incorporates the acyclovir monophosphate into the growing DNA strand as if it were 2-deoxyguanosine monophosphate (a “G” base). Further elongation of the chain in now impossible. Viral DNA chain synthesis stops.

Competitive inhibition of viral DNA polymerase, as acyclovir-triphosphate compete with dGTP for viral DNA polymerase.

Question 20

Is acyclovir toxic to the uninfected host cell?

Answer 20

No

Question 21

Why is acyclovir non-toxic to the uninfected host cell?

Answer 21

Since the enzymes herpesvirus thymidine kinase and herpes virus DNA polymerase are viral enzymes and not found in uninfected host cells, acyclovir cannot be phosphorylated and incorporated into the host DNA.

Question 22

What does amantadine do?

Answer 22

Inhibits replication of most strains of influenza A viruses by blocking uncoating of the virus

Question 23

What is the antiviral MOA of amantadine?

Answer 23

The M2 ion channel is the target of the antiviral amantadine.

These compounds clog the channel and prevent it from pumping protons into the virion.

In the presence of amantadine, viral RNAs remain bound to M1 and cannot enter the nucleus. Viral replication is inhibited.

Question 24

Oseltamivir (Tamiflu) is what?

Answer 24

Inhibitor of neuraminidase (NA) enzyme synthesized by influenza A and B viruses.

Question 25

Blocking the function of _________ with __ inhibitors is an effective way to treat influenza

Answer 25

Neuroaminidase; NA

Question 26

Blocking the neuraminidase with NA inhibitors does what?

Answer 26

Prevents the release of virus and spread of infection, as the HA of virus is still bound/attached to the sialic acid containing receptors on the surface of already infected host cell.

Question 27

Inhibition of neuraminidase slows _____ ____, giving the immune system the opportunity to "catch up" and mediate virus clearance.

Answer 27

Virus spread

Question 28

What are two nucleoside analog reverse transcriptase inhibitors (NRTIs)

Answer 28

Zidovudine (ZDV) or AZT (Azidothymidine) | ddI (Didanosine)

Question 29

What are ZDV/AZT?

Answer 29

Nucleoside analog of thymine, i.e. Resembles the deoxyribonucleotide containing the base thymine

Question 30

What is the MOA of ZDV/AZT?

Answer 30

Competitive inhibition of reverse transcriptase activity: AZT-triphosphate competes with the thymine deoxyribonucleotide triphosphate for the reverse transcriptase. Insertion of AZT-monophosphate into cDNA blocks the growth of the cDNA being transcribed from the viral RNA by reverse transcriptase.

Question 31

AZT has been shown to reduce clinical signs of what when administered at a dose of 10mg/kg BID SQ for a period of 3 weeks?

Answer 31

FIV-positive cats

Question 32

True/False: Acyclovir is a pro-drug?

Answer 32

True

Question 33

_____ are required to cleave the HIV polyproteins into functional proteins

Answer 33

Proteases

Question 34

Easy question What inhibits the proteases?

Answer 34

Protease inhibitors

Question 35

With protease inhibitors, HIV polyproteins can/cannot be cleaved into functional proteins?

Answer 35

Cannot.

Question 36

How do protease inhibitors work?

Answer 36

Bind to the active site of the HIV protease and prevent the enzyme from cleaving HIV polyproteins into functional proteins. As a result, HIV can not mature and noninfectious viruses are produced

Question 37

How are live-attenuated virus vaccines created? (4 ways)

Answer 37

From naturally occurring attenuated viruses. Attenuation of virus by serial passage in cultured cells. Attenuation of viruses by serial passage in heterologous hosts. Attenuation of viruses by selection of cold-adapted mutations and reassortants.

Question 38

What are non-replicating viral vaccines made?

Answer 38

Inactive whole virions. | Purified native viral proteins.

Question 39

What is one more way/type of virus vaccines are made?

Answer 39

Produced by recombinant DNA and related technologies

Question 40

True/False: DIVA stands for Differentiating infected from vaccinated animals

Answer 40

True

Question 41

MOA of DIVA

Answer 41

Subunit 'marker vaccine' DIVA vaccines have only a portion (subunit) of the pathogen in the vaccine i.e. Has less antigens than natural strains. If antibodies to other parts/antigens of the pathogen no included in the vaccine are detected the animal has been infected with the pathogen. If only antibodies to the vaccine subunit/antigens are detected, the animal has not been infected. An accompanying diagnostic test allows us to actually make the differentiation.

Question 42

Isolation

Answer 42

Applies to animals/persons who are known to be ill with a contagious disease. Separate animal if they show clinical signs and/or test positive by diagnostic test.

Question 43

Quarantine

Answer 43

Applies to those who have been exposed to a contagious disease. Separate animal if exposed to a contagious disease, even if it does not show clinical signs, and/or animal test negative by diagnostic test.

Question 44

Quarantine and Culling

Answer 44

To separate and restrict the movement of animals. Culling of animals. Proper disposition of culled animals.

Question 45

Decontamination

Answer 45

Term used to describe a process or treatment that renders a medical device, instrument, or environmental surface safe to handle.

Question 46

Sterilization

Answer 46

A process that destroys or eliminates all forms of microbial life/pathogens, including highly resistant pathogens, such as bacteria with spores.

Question 47

Disinfection

Answer 47

A process that eliminates many or all pathogenic microorganisms, except bacterial spores, on inanimate objects. Less effective than sterilization, does not necessarily kill all microorganisms.

Question 48

Antisepsis

Answer 48

Application of a liquid antimicrobial chemical to skin or living tissue to inhibit or destroy microorganisms.

Question 49

What are the sterilization methods?

Answer 49

Moist heat: autoclave. Dry heat: hot air oven Chemical methods: gases like ethylene oxide, ozone Radiation: non-ionizing - UV radiation; ionizing - gamma rays, x-rays Sterile filtration: microfiltration using membrane filters

Question 50

Vaccines produced by serial passage of viruses in heterologous hosts is a ______

Answer 50

Live-attenuated vaccine

Question 51

True/False: Quarantine and isolation have the same meaning

Answer 51

False

Question 52

Autoclave is a method of _________

Answer 52

Sterilization

Question 53

What is the family of poxviruses?

Answer 53

Poxviridae

Question 54

What is the subfamily of Poxviridae?

Answer 54

Chordopoxvirinae

Question 55

How many genera are there for the pox virus?

Answer 55

8

Question 56

What are the 6 genera important for our class on pox virus?

Answer 56

``` Orthopoxvirus Parapoxvirus Avipoxvirus Capripoxvirus Leporipoxvirus Suipoxvirus ```

Question 57

Properties of Poxviruses

Answer 57

Large, sometimes enveloped, DNA viruses with complex structure. Most are pleomorphic, typically brick-shaped. Possess an irregular surface of projecting tubular or globular structures. Members of the genus Parapoxvirus are ovoid, covered with long thread-like surface tubules, which appear to be arranged in crisscross fashion, resembling a ball of yarn.

Question 58

What are the two distinct infectious poxvirus particles that exist?

Answer 58

Intracellular mature virus (IMV) | Extracellular enveloped virus (EEV)

Question 59

T/F: both IMV and EEV are infectious

Answer 59

True

Question 60

EEV contains 2 membranes:

Answer 60

Envelope | Inner membrane

Question 61

How do virions acquire the extra envelope?

Answer 61

Cells released by budding. The envelope contains virus encoded-proteins from host cell membrane.

Question 62

IMV have how many membranes?

Answer 62

1 Only inner membrane; come out by disruption of host cells.

Question 63

T/F: Poxviruses conform to the icosahedral or helical symmetry.

Answer 63

False Complex symmetry

Question 64

The virion outer layer encloses a ________-shaped core and two lateral bodies

Answer 64

Dumbbell

Question 65

What is contained in the core of a poxvirus?

Answer 65

Viral DNA with several proteins May have more than 200 genes in their genome, and as many as 100 of these encode proteins that are contained in virions

Question 66

The genome of poxviruses consists of

Answer 66

Single molecule of linear ds DNA

Question 67

Many proteins encoded by the poxvirus are enzymes involved in ______ _____ synthesis and virion structural components

Answer 67

Nucleic acid Also encode proteins that specifically counteract host adaptive and innate immune responses

Question 68

Where does replication of the poxvirus occur?

Answer 68

Predominantly in the cytoplasm

Question 69

How is it possible that the poxvirus replicates in the cytoplasm?

Answer 69

Have evolved to encode the enzymes required for transcription and replication of the viral genome.

Question 70

How are poxviruses released after replication?

Answer 70

Budding Exocytosis Cell lysis

Question 71

Most virions are not enveloped and are released by ____ _______

Answer 71

Cell lysis

Question 72

T/F: Enveloped virions are taken up by cells more readily and appear to be more important in the spread of virions through the body of the animal

Answer 72

True

Question 73

Stability of poxviruses

Answer 73

Virion is enveloped particle. High environmental stability, remain infectious over a period of several months in ambient environment. Low lipid content - less sensitive to organic solvents/disinfectants. High resistance to drying Can survive many years in dried scabs or other virus-laden material.

Question 74

Poxvirus transmission

Answer 74

Skin: cannot infect intact skin. Contact of infectious material with broken or lacerated skin is a common route of poxvirus transmission. Respiratory route: some by aerosol route (sheeppox) Mechanically: arthropods (Myxoma virus and avipoxviruses

Question 75

Pathogenesis and Immunity to poxvirus

Answer 75

Epitheliotropic causing cutaneous lesions Sometimes cause systemic diseases in birds and wild animals Many are host specific Orthopoxviruses infect a wide range of species

Question 76

Spread of poxvirus

Answer 76

Following introduction into the body, poxvirus usually gains access to the systemic circulation via the lymphatic system. A secondary viremia disseminates the virus back to the skin and to other target organs.

Question 77

What is the pathway of skin lesions in poxvirus infection?

Answer 77

Macule-> papule -> vesicle -> pustule -> scab -> scar

Question 78

What is a macule

Answer 78

Flat and red. Local inflammation immune response infiltrating leukocytes

Question 79

What is a papule?

Answer 79

Raised and red. More marked inflammation (invasion of neighboring tissue)

Question 80

What is a vesicle?

Answer 80

Small blister: microbe invades epithelium

Question 81

T/F: Ulceration will never develop with poxvirus lesions

Answer 81

False | They are possible

Question 82

Rupture of the ______ from poxvirus can predispose to secondary bacterial infections

Answer 82

Pustules

Question 83

Distribution of cowpox

Answer 83

Endemic only in Europe and Asia

Question 84

Hosts of cowpox

Answer 84

Cattle Wild and domestic cats Humans Zoo animals

Question 85

Reservoir host of cowpox

Answer 85

Rodents

Question 86

Transmission of cowpox in cattle

Answer 86

Infected milker's hands or teat cups Infected farm cats Rodents

Question 87

Economic importance of cowpox in cattle

Answer 87

Losses to farmers due to inconvenience in milking b/c of soreness of teats and mastitis resulting from secondary bacterial infections

Question 88

Clinical findings with cowpox in cattle

Answer 88

Mildly febrile, papule appear on teats and udders Sucking calves may develop lesions in mouth Vesicles may not be evident or may rupture readily leaving ulcerated areas that form scabs

Question 89

Transmission of cowpox in cats

Answer 89

Skin inoculation - bit or skin wound Rodents Oro-nasal route Pneumonia in exotic felids

Question 90

Primary lesions of cowpox in cats

Answer 90

Primary skin lesion - head, neck or forelimb | May form small, stabbed wound to large abscess

Question 91

Secondary lesions of cowpox in cats

Answer 91

After primary, widespread secondary appears. 2-4 days - discrete, circular, ulcerated papules that are .5-1 cm in diameter. Ulcers covered by scabs and healing is usually complete by 6 weeks. Many cats show no signs other than skin lesions, ~20% develop mild coryza or conjunctivitis. Complications fro secondary bacterial infection

Question 92

Transmission of cowpox in humans

Answer 92

Cuddly cats Rarely from rodents and zoo animals Less likely from cattle

Question 93

Clinical signs of cowpox in humans

Answer 93

``` Macropapular lesions on hands and face -> vesicular and ulcerative lesions. Enlarged painful local lymph nodes Fever Vomiting Sore throat ```

Question 94

Monkeypox in humans

Answer 94

Viral zoonosis with symptoms in humans similar to those seen in the past in smallpox patients

Question 95

Transmission of monkeypox in humans

Answer 95

Primary - direct contact with blood, bodily fluids, or rashes of infected animals. In Africa, human infections have been documented through the handling of infected monkeys, Gambian rats or squirrels. Secondary- human to human. Close contact with infected respiratory tract excretions, with the skin lesions of an infected person or with recently contaminated objects

Question 96

Pseudocowpox: que es?

Answer 96

Viral skin disease that causes mild sores on the teats and udders of cattle. Can also infect humans and condition is commonly referred to as milker's nodules.

Question 97

Etiology of pseudocowpox

Answer 97

Member of the genus parapoxvirus

Question 98

Epidemiology of pseudocowpox

Answer 98

Reported from most countries

Question 99

Transmission of pseudocowpox

Answer 99

``` Infected cattle Contaminated milker's hands, teat cups Biting insects Calves get during suckling Semen of bulls ```

Question 100

Pathogenesis of pseudocowpox

Answer 100

Hyperplasia of squamous epithelium

Question 101

Clinical signs of pseudocowpox

Answer 101

General mild

Question 102

Acute lesions of pseudocowpox

Answer 102

Erythema -> papules -> vesicle or pustule -> rupture -> thick scab ``` Thick scab (.5 to 25 cm) becomes elevated due to accumulation of granulation tissue. 7-10, scab falls off leaving horseshoe-shaped ring of small scabs surrounding a small wart-like granuloma ```

Question 103

Chronic lesions of pseudocowpox

Answer 103

``` Starts as erythema Yellow-gray, soft scurfy scabs which are rubbed off during milking Skin is corrugated No pain Lesions may persist for months ```

Question 104

Diagnosis of pseudocowpox

Answer 104

Horseshoe-shaped ring like lesions are pathognomonic. | Isolation and detection of the virus by various diagnostic lab methods from vesicular fluid or from teat skin.

Question 105

Differential diagnosis of pseudocowpox

Answer 105

``` Cowpox virus Bovine herpesvirus ulcerative mammalitis Vesicular stomatitis Udder impetigo (bacterial dermatitis characterized by the development of small pustules on the skin of the udder and teats) Teat chaps and frostbite Black spot (a form of hyperkeratosis) ```

Question 106

Treatment of pseudocowpox

Answer 106

Removal of scabs Burn the scabs to prevent environmental contamination Application of emollient ointment before milking Application of astringent preparation after milking

Question 107

Prevention of pseudocowpox

Answer 107

Disinfection - use iodophor teat dip Isolation and treatment of infected cows Reduce teat trauma, as injuries to skin of teat predisposes to infection

Question 108

Pseudocowpox in humans or Milker's nodules

Answer 108

Causes a mild skin lesion known as Milker's Nodules Lesions on the hands of dairy farmers milking teats or vets treating infected cows Lesions may vary from multiple vesicles to a single, indurated nodule

Question 109

What is the etiology of Contagious ecthyma, ORF?

Answer 109

Orf virus, Genus Parapoxvirus

Question 110

Who is the host of ORF?

Answer 110

Sheep and goat. Primarily in lambs and goat kids

Question 111

What is the distribution of ORF?

Answer 111

Worldwide

Question 112

Transmission of ORF?

Answer 112

Scabs that fall off from the healing lesions contain virus. Virus are stable in the environment, i.e remains highly infectious for long periods under dry conditions. Contaminated instruments, like docking instruments or ear-tagging plier can transmit virus. Spread in flock in rapid. Virus infects healthy animals primarily through damaged skin. Oral lesions in lambs or kids result from nursing dams with teat lesions, and vice-versa.

Question 113

Pathogenesis of contagious ecthyma (ORF)

Answer 113

Damage of skin is essential to establish infection. The skin reaction to viral infection consists of a cellular response with necrosis and sloughing of the affected epidermis and underlying stratum papillary of the dermis. The cutaneous response to infection includes a delayed-type hypersensitivity reaction and an influx of inflammatory cells. The lesions evolve from macule -> papule -> vesicle -> pustule ->ulcers -> scab formation.

Question 114

Clinical signs of orf

Answer 114

First lesions develop in the mucocutaneous junction and are accompanied by swelling of the lips. From there, lesions spread to the muzzle and nostrils, surrounding hairy skin and the buccal mucosa. Animals may find it difficult to take food because of oral lesions: anorexia and weight loss Infected lambs or kids sucking ewes or goats may result in lesions on teats. They may predispose to secondary bacterial infection = mastitis.

Question 115

Severe cases show what clinical signs of ORF?

Answer 115

May show in genitals, coronets (feet), and ears. Lesions in feet result in lameness. Lesions in scrotum leads to infertility.

Question 116

The scabs from orf drop off and the underlying tissues heal. But what can happen to the skin after?

Answer 116

Complications from secondary infection, or from invasion of lesions by fly larvae. A malignant form of the disease has also been observed in sheep.

Question 117

Vaccination of ORF

Answer 117

Prepared from suspension of scabs in glycerol saline and is painted onto a small area of scarified skin inside the thigh, where a localized lesion develops. The vaccine should NEVER be used on farms that do not have a problem with orf. Inspect the lamb 1 week after vaccination for local reactions, which indicates the viability of the vaccine. Vax do not offer long-lasting immunity, ~1-2 years

Question 118

T/F: in problem flocks/herds, the lambs/kids may need to be vaccinated

Answer 118

True

Question 119

Pregnant ewes should be vaccinated before/after lambing

Answer 119

Before

Question 120

ORF in humans

Answer 120

Macro-popular lesions and large nodular lesions in finger, hand, arm, face and even the penis. Secondary bacterial infections of lesions may cause complications

Question 121

Etiology and distribution of sheeppox and goatpox

Answer 121

E: members of the Genus Capripoxvirus D: Endemic in Africa, Asia and parts of Europe

Question 122

Sheep pox virus (SPV) and goat pox virus (GPV) were once believed to be strains of the same virus, but ____ ________ has now demonstrated them to be separate viruses

Answer 122

Genetic sequencing

Question 123

T/f: most strains of sheep and goat pox are host specific and cause severe clinical disease in either sheep or goats, while some strains have equal virulence in both species

Answer 123

True

Question 124

Can SPV and GPV be distinguished from each other with serological techniques, including viral neutralization

Answer 124

No sir they cannot

Question 125

SPV and GPV are closely related to what viral disease of cattle? Is there evidence of this virus infecting sheep and goats?

Answer 125

Lumpy skin disease virus (LSDV) No

Question 126

Transmission of sheeppox and goatpox

Answer 126

Highly contagious Enters by respiratory tract - aerosol route*** Through mucous membrane or abraded skin, especially by direct contact with contaminated iatrogenic materials Virus is present in nasal and oral secretions for several weeks after infection Can survive in dry scabs for months Evidence of mechanical transmission by biting arthropods

Question 127

Pathogenesis of sheeppox

Answer 127

Systemic disease**** Incubation period is followed by a leukocyte-associated viremia. Localizes in skin and other internal organs

Question 128

Deposition of the immune-complexes (of sheeppox) results in what and where does it develop?

Answer 128

Severe necrotizing vasculitis develops in arterioles and postcapillary venules of skin. Results in ischemic necrosis of dermis and overlying epidermis

Question 129

What are the two forms of sheeppox

Answer 129

Malignant | Benign

Question 130

Malignant form from sheeppox

Answer 130

In lambs and susceptible nonnative breeds. Pox lesions develop on skin and buccal, respiratory, digestive and urinary tract mucosa. Cutaneous nodules are distributed widely over body- occasionally become vesicular, pustular and finally scabs. Lesions heal leaving star-shaped scar free of hair or wool

Question 131

The lesions from malignant sheeppox can spread from primary regions to?

Answer 131

``` Pharynx Larynx Lungs Vagina Abomasum Spleen ``` Secondary pneumonia common Abortion rare

Question 132

The mortality and case fatality rate of malignant sheeppox is high/low.

Answer 132

High

Question 133

Benign form of sheeppox

Answer 133

More common in adults and resistant breeds Only skin lesions occur None to mild systemic reactions

Question 134

Prevention and control of sheeppox

Answer 134

Notifiable disease in most countries of the world

Question 135

Are vaccines available for sheeppox?

Answer 135

Yes, a large variety of commercial vaccines are available including subunit vaccines. Killed vaccines elicit temporary protection at best. Live attenuated vaccines offer excellent protection >1 year

Question 136

Where is Goatpox found?

Answer 136

Africa Asia parts of Europe

Question 137

Is goatpox reportable?

Answer 137

Yes

Question 138

Goatpox disease is clinically similar to?

Answer 138

Sheeppox

Question 139

Age group affected by goatpox systemic disease

Answer 139

Young kids

Question 140

Age group affected by mild forms of goatpox

Answer 140

Adults

Question 141

Etiology of lumpy skin disease

Answer 141

Members of genus Capripoxvirus

Question 142

Distribution of lumpy skin disease

Answer 142

Enzootic in sub-Saharan Africa and Middle East with recent incursion in Iraq

Question 143

Transmission of lumpy skin disease

Answer 143

Arthropod vector | Direct contact

Question 144

Host of lumpy skin disease

Answer 144

Cattle All ages and types susceptible

Question 145

Clinical findings of lumpy skin disease

Answer 145

Fever Multiple nodular lesions on skin and mucus membranes Lymphadenopathy

Question 146

Etiology of swinepox

Answer 146

Members of genus Suipoxvirus

Question 147

Distribution of swinepox

Answer 147

Worldwide | Widespread, sporadic disease

Question 148

Hosts of swinepox

Answer 148

Cattle JK, making sure you're paying attention. Pigs Benign with low mortality and morbidity in older. High case fatality in congenitally infected and very young sucking piglets

Question 149

Transmission of swinepox

Answer 149

Direct contact associated with skin injury, can live in scab for years. Mechanical transmission - pig louse or Haematopinus suis. Lice can carry virus for weeks-months. Also flies and insects.

Question 150

For swinepox, there is evidence of ________ infection in neonatal pigs

Answer 150

Transplacental

Question 151

What are the typical pox lesions of swinepox?

Answer 151

``` Skin lesions occur anywhere, most obvious on abdomen and inner thighs. Exudative epidermitis (greasy pig disease) and secondary bacterial dermatitis occasionally follow swine pox. Severe infections, especially in congenitally-acquired pox infections can have lesions occur in upper respiratory and digestive tracts ```

Question 152

Control of swinepox

Answer 152

Eradication of lice from piggery | No commercially available vaccine

Question 153

Etiology of fowlpox

Answer 153

Genus Avipoxvirus *first virus grown in embryonated eggs

Question 154

Hosts of fowlpox

Answer 154

Poultry and turkeys Are turkeys not poultry?

Question 155

Distribution of fowlpox

Answer 155

Worldwide

Question 156

Transmission of fowlpox

Answer 156

Extremely resistant to desiccation Can survive in exfoliated scabs for long time. Transmitted within flocks through minor wounds and abrasions of mouth, comb, wattles, or skin from fighting or pecking each other. Mechanically by mosquitoes, lice and ticks. Possibly aerosol

Question 157

What are the 3 forms of fowlpox disease

Answer 157

Cutaneous (dry) Diphtheritic (wet) Ocular

Question 158

The cutaneous or dry form of fowlpox

Answer 158

Most common Low mortality Results from biting arthropods or mechanical transmission to injured or lacerated skin Small papules on comb, wattles and around beak Occasionally lesions on legs, feet and cloaca Nodules become yellowish and thick scab Sharp fall in egg production

Question 159

T/F: in uncomplicated cases of cutaneous form of fowlpox, the affected birds recover

Answer 159

True

Question 160

Diphtheritic (wet) form of fowlpox

Answer 160

Probably caused by droplet infection. Involves infection of mucous membranes of mouth, pharynx, larynx, and sometimes trachea. Coalescing lesions result in necrotic pseudomembrane -> death by asphyxiation. Prognosis is poor.

Question 161

Ocular form of fowlpox

Answer 161

Conjuntivitis | Cheesy exudate accumulates under eyelids

Question 162

What are Bollinger bodies of avipoxvirus?

Answer 162

Eosinophilic granular intracytoplasmic inclusion bodies.

Question 163

What are Borrel bodies of avipoxvirus?

Answer 163

Occur inside Bollinger bodies. Are minute spherical bodies obtained by tryptic digestion of Bollinger bodies.

Question 164

Vaccination for fowlpox control

Answer 164

Modified live fowlpox or pigeon pox virus vaccines of chicken embryo or avian cell culture origin are available commercially. Recombinant fowlpox vectored vaccines have been developed.

Question 165

Other than vaccines, what's another method of fowlpox control?

Answer 165

Control mosquito population and other biting insects

Question 166

Transmission of ulcerative dermatosis of sheep (unclassified poxvirus)

Answer 166

Infection through damaged skin or by coitus

Question 167

Clinical forms of ulcerative dermatosis of sheep

Answer 167

Usually ulcers with raw crater that bleeds easily

Question 168

Ulcerative dermatosis of sheep manifests in what two clinical forms?

Answer 168

Lip and les ulceration Venereal form: ulceration of the prepuce and penis or vulva. Ram becomes unfit for natural breeding.

Question 169

How do we diagnose poxviruses?

Answer 169

Clinical signs Sample material: scrapings from skin lesions, vesicular fluid, crusts, scabs Electron microscopy: characteristic morphology and size of poxviruses. Orthopoxviruses are brick shaped. Parapoxviruses are ovoid. ``` Serological assays (ELISA) Detection of poxvirus nucleic acid by PCR ```

Question 170

How do we use histopathology to diagnose poxvirus?

Answer 170

To see presence of characteristic intracytoplasmic inclusion bodies. Type-A Type-B Bollinger and Borrel bodies

Question 171

What are Type-B (Guanrnierei) inclusion bodies?

Answer 171

Induced by most poxviruses. Slightly basophilic Composed of viral particles and protein aggregates.

Question 172

What are Type-A (ATI) inclusion bodies

Answer 172

Induced by some poxviruses - cowpox and ectromelia virus. | Strongly eosinophilic

Question 173

Can we inoculate embryonated eggs to diagnose poxviruses?

Answer 173

Yes Chorioallantoic membrane -> pock lesions. *Parapoxviruses do NOT multiply in chicken embryo

Question 174

What two viruses are we talking about under the family Circoviridae, genus Circovirus?

Answer 174

Porcine circovirus type-1 (non-pathogenic) Porcine circovirus type-2 (post-weaning multisystemic wasting syndrome [PMWS])

Question 175

What virus is under the family Circoviridae, genus Gyrovirus?

Answer 175

Chicken infectious anemia virus

Question 176

What are the viruses with circular single-stranded DNA genomes? What are the differences?

Answer 176

Circovirus: ambisense DNA Gyrovirus: negative sense DNA

Question 177

What virus has 12 trumpet-like structures that are less obvious in the other circoviruses?

Answer 177

Chicken infectious anemia virus

Question 178

Virus replication occurs in what type of cells for Circoviridae?

Answer 178

Actively dividing cells

Question 179

Where does DNA replication occur?

Answer 179

Nucleus

Question 180

T/F: Circoviridae virions are not very stable

Answer 180

False

Question 181

Etiology of post-weaning multisystemic wasting syndrome (PMWS)

Answer 181

Porcine circovirus 2 (PCV2)

Question 182

Hosts of PMWS

Answer 182

Pigs | Most common 4-6 weeks or 2-3 weeks post-weaning

Question 183

Transmission of PMWS

Answer 183

Wide-spread Fecal-oral: most common method Vertical transmission (transplacental infection)

Question 184

Pathogenesis of PMWS

Answer 184

Individual coalescing foci of granulomatous inflammation in lymphoid tissue, lungs, liver, kidney, heart and intestines; sometimes with prominent "botryoid" (grape-like) intra-cytoplasmic inclusion bodies in virus infected macrophages

Question 185

What is lymphoid depletion?

Answer 185

Loss of B-cells and T-cells

Question 186

Transplacental infection of PMWS

Answer 186

Infection during the first and second trimesters results in fetal death and resorption or aborted fetuses with severe cardiac congestion. Infection during last trimester has minimal effect of fetuses

Question 187

Clinical signs of PMWS

Answer 187

``` Subclinical infection most common. Lethargy Progressive weight loss Cough Dyspnea Slow growth Lymphadenopathy Diarrhea Skin discoloration Congenital tremors Icterus (less common ```

Question 188

PMWS commonly gets a co-infection with which viruses?

Answer 188

Porcine parvovirus (PPV) Porcine reproductive and respiratory virus (PRRSV) SIV Mycoplasma hyopneumonea Other opportunistic bacteria that may cause severe disease and more pronounced lesions

Question 189

Diagnosis of PMWS

Answer 189

Serological assays: most pigs are seropositive so antigen detection is not of much value

Question 190

Vaccines for PMWS

Answer 190

Chimeric vaccines: use non-pathogenic porcine circovirus 1 (PCV-1) as a genetic backbone for expression of the immunogenicity capsid protein of PCV-2. Inactivated or baculovirus-expressed vaccines: virus-like particles include the capsid protein of PCV-2 Sow vaccination antepartum

Question 191

Porcine dermatitis and nephropathy syndrome (PDNS)

Answer 191

Associated with PCV2 Sporadic Reported in older piglets Findings: Necrotizing skin lesions Necrotizing vasculitis Necrotizing and fibrinous glomerulonephritis

Question 192

What is Gyrovirus cause?

Answer 192

Chicken infectious anemia

Question 193

Host of chicken infectious anemia

Answer 193

Highly contagious disease of young chickens (2-4 wo) | Older chickens more resistant

Question 194

Transmission of chicken infectious anemia

Answer 194

Virus is shed in feces and feather dander Horizontal transmission is through inhalation or oral exposure Virus is also transmitted vertically through egg

Question 195

Pathogenesis of chicken infectious anemia

Answer 195

Replication in hemocytoblasts in bone marrow, precursor T cells in the cortex of the thymus, and dividing CD4 and CD8 cells in spleen Apoptin protein of CAV virus induce apoptosis Immunosuppression and aplastic anemia Vulnerable to secondary bacterial and fungal infections Replication in oviduct regulated by estrogen allowing more efficient vertical transmission

Question 196

Clinical signs and lesions of chicken infectious anemia

Answer 196

``` Anorectic Lethargic Depressed Reduced body weight gain Pale Thrombocytopenia: watery blood with slow clot PCV low SQ hemorrhages and skeletal hemorrhages Pale muscles ```

Question 197

Differences in anatomy with chicken infectious anemia

Answer 197

CAV-induced thymic atrophy Pale, aplastic bone marrow Pale carcass Atrophied bursa

Question 198

Diagnosis of chicken infectious anemia

Answer 198

Examination of blood: low PCV Examine blood for total erythrocytic count will reveal anemia Thrombocytopenia Blood watery with slow clot

Question 199

Vaccination for chicken infectious anemia

Answer 199

Presence of antibodies in breeders greatly reduced vertical and horizontal transmission Protect progeny from vaccinated breeders from early infections by means of maternally derived antibodies Live vaccines available: antibody-negative breeder flocks before the start of egg production

Question 200

T/F: Herpesviridae are enveloped, spherical to pleomorphic viruses

Answer 200

True

Question 201

Do Herpesviridae have ss or ds DNA?

Answer 201

ds

Question 202

Viral replication of Herpesviridae

Answer 202

DNA replication and encapsidation occur in nucleus Viral envelope is acquired by budding through the inner layer of nuclear envelope Mature virions accumulate within vacuoles in cytoplasm and are released by exocytosis or cytolysis

Question 203

Do Herpesviruses survive well outside of the host cell?

Answer 203

Nope to the nope nope Moist, cool environmental conditions promote extended survival of herpesviruses. Latently infected animals serve as a reservoir for transmission

Question 204

T/F: Persistent infection with periodic or continuous shedding occurs in only a few herpesvirus infections

Answer 204

False, all of them

Question 205

T/F: herpesviruses are oncogenic

Answer 205

True

Question 206

Reactivation of latent herpesvirus infection is usually associated with _____ caused by intercurrent infections, shipping, cold, crowding or by the administration of __________ drugs

Answer 206

Stress; glucocorticoid

Question 207

What type of inclusion bodies belong to Herpesviruses?

Answer 207

Eosinophilic intranuclear | Known as type A Cowdry bodies

Question 208

T/F: Herpesviruses can cause syncytium

Answer 208

True

Question 209

What are the properties of Alphaherpesvirinae?

Answer 209

Generally highly cytopathic in cell culture | Relatively short replication cycle

Question 210

T/F: some alphaherpesviruses, like pseudorabies virus) have a narrow host range, whereas most are highly restricted in their natural host range.

Answer 210

False, broad host range

Question 211

Where do most localized lesions occur from alphaherpesviruses?

Answer 211

Skin | Mucosa of the respiratory and genital tracts

Question 212

(Alphaherpesviruses) Generalized infections characterized by foci of necrosis in almost any organ or tissue are typical of infection of ______ or ______ animals.

Answer 212

Very young; immunocompromised

Question 213

In pregnant animals, alphaherpesvirus cross the placenta, leading to ______, characteristically with multifocal areas of necrosis in several fetal organs.

Answer 213

Abortion

Question 214

There are 3 subtypes of bovine herpesvirus 1 (BHV-1) but what are the 2 important ones for this class?

Answer 214

BHV-1.1 (respiratory subtype) | BHV-1.2 (genital subtype)

Question 215

Transmission of BHV

Answer 215

Respiratory disease and conjunctivitis result from droplet transmission Genital disease may result from coitus or AI with infective semen.

Question 216

Pathogenesis of BHV

Answer 216

In both genital and respiratory forms of the disease, lesions are focal areas of epithelial cell necrosis in which there is ballooning of epithelial cells. Typical herpesvirus inclusions may be present in the nuclei at the periphery of necrotic foci. Intense inflammatory response within the necrotic mucosa, frequently with formation of an overlying accumulation of fibrin and cellular debris (pseudomembrane)

Question 217

T/F: life-long latent infection with periodic virus shedding occurs after BHV-1 infection

Answer 217

True

Question 218

T/F: All seropositive animals are considered as potential carriers.

Answer 218

True

Question 219

T/F: BHV cannot be reactivated from latency by corticosteroids or stress

Answer 219

False, they can be

Question 220

Where are the sites of latency for BHV?

Answer 220

Trigeminal nerve: respiratory disease with BHV-1. | Sciatic nerve: genital disease with BHV-1

Question 221

Clinical signs of BHV

Answer 221

Respiratory form (red nose, necrotic rhinitis, dust pneumonia): Rhinitis Laryngitis Tracheitis

Question 222

Clinical signs for the respiratory BHV form

Answer 222

Inflamed nares gives the appearance of having a "red nose" due to hyperemia Grayish necrotic foci on the mucous membrane Nasal discharge becomes more profuse and mucopurulent Uncomplicated cases recover in 10-14 days

Question 223

Respiratory BHV may result from secondary bacterial infections such as? Death is usually a result of?

Answer 223

Mannheimia hemolytica and Pasteurella multocida (shipping fever) Secondary bronchopneumonia

Question 224

Ocular form of IBR

Answer 224

Conjunctivits is a common finding in typical "red nose"

Question 225

Do not misdiagnose BHV as what?

Answer 225

Pink-eye or infectious bovine keratoconjunctivitis. IBR lesions are confined to the conjunctiva and no lesions on cornea except diffuse edema.

Question 226

Abortion caused by BHV-1

Answer 226

Occurs as a common sequel to natural infection Result of some modified-live virus (MLV) vax being given to pregnant animals. Animals in contact with IBR-susceptible pregnant animals. Fetuses in second half of gestation have a higher incidence of abortion but early embryonic death is possible Often preceded by pustular vulvovaginitis

Question 227

BHV-1 causing systemic disease of newborn calves

Answer 227

Severe in calves less than 10 days of age Often fatal Infected in-utero or right after birth

Question 228

Genital disease from BHV-1: IPV (infectious pustular vaginitis)

Answer 228

After coitus Frequent urination Tail is usually held in an elevated position and excessive tail switching is noted Vagina mucosa red and swollen Mild vaginal discharge Vulva swollen, red spots and discrete pustules may be noted

Question 229

BHV-1 genital disease: balanoposthitis

Answer 229

Inflammation and pustules in the mucosa of the penis and prepuce

Question 230

Control (vaccination) of BHV

Answer 230

Modified live vax, subunit and inactivated vax are available Parenteral and intranasal vax available Both stimulate the production of humoral antibodies The parenteral vax may cause abortion in pregnant cows. Intranasal vax is safe for use in pregnant cows

Question 231

What two diseases are caused by BHV-2

Answer 231

Bovine ulcerative mammalitits | Pseudo-lumpy skin disease

Question 232

Host of bovine ulcerative mammalitis

Answer 232

Cattle Heifers Usually within 2 weeks after calving (persistent disease)

Question 233

Transmission of Bovine ulcerative mammilitis

Answer 233

Direct contact and fomite-mediated, through skin trauma | Mechanical transmission by stable flies and other arthropods

Question 234

Clinical signs of bovine ulcerative mammilitis

Answer 234

``` Severe cases: teats swollen and painful Skin is bluish Exudes serum Formation of raw ulcers High incidence of mastitis ```

Question 235

Pseudo-lumpy skin disease

Answer 235

Cattle are infected Occurs most commonly in Southern Africa Mechanical transmission of the virus occurs by arthropods

Question 236

Clinical signs of pseudo-lumpy skin disease

Answer 236

Mild fever followed by sudden appearance of skin nodules: few or many, on face, neck, back, and perineum

Question 237

What disease is caused by Porcine herpesvirus 1/Suid herpesvirus 1 (belong to subfamily Alphaherpesvirus)

Answer 237

Pseudorabies (Aujeszky disease, Mad itch)

Question 238

Etiology of Pseudorabies

Answer 238

Porcine herpesvirus 1/Suid herpesvirus 1

Question 239

Hosts of pseudorabies

Answer 239

Primarily swine ``` Secondary: Horse Cattle Sheep Goats Dogs Cats Many feral species ``` Humans are refractory to infection

Question 240

Transmission of pseudorabies in primary hosts

Answer 240

Recovered pigs act as primary reservoirs, and are latent carriers for life. Rodents can be reservoirs and transmit disease from farm to farm. Routes: She'd in saliva, nasal discharges and milk of infected pigs Not shed in urine or feces Licking, biting, aerosol, ingestion of contaminated carcass, water and feed.

Question 241

Transmission of pseaudorabies in secondary hosts

Answer 241

Dogs and cats: ingestion of infected pig carcass/meat, or rodents Cattle: direct contact with infected pigs, oral and nasal routes

Question 242

Pathogenesis of pseudorabies

Answer 242

Primary site of viral replication is upper respiratory tract

Question 243

Spread of pseudorabies

Answer 243

Virus replicates in tonsils and nasopharynx Spreads via the lymphatics to regional lymph nodes, where replication continues A brief viremia is associated with virulent strains, with localization of virus in different organs

Question 244

Pseudorabies virus spread in CNS

Answer 244

Via axons of cranial nerves | Preference for neurons and the pons and medulla

Question 245

CNS lesions due to pseudorabies

Answer 245

Ganglioneuritis Nonsuppurative meningoencephalitis Perivascular cuffing

Question 246

Clinical signs of pseudorabies

Answer 246

Nonimmune piglets: 100% mortality rates Nonimmune pregnant sows: ~50% abortion rate Older piglets, growers, and adult pigs: mild disease, mortality <2% Pruritus (itching), a dominant feature in secondary hosts, is rare in pigs

Question 247

Piglets born to nonimmune sows with pseudorabies

Answer 247

Most susceptible | Signs of CNS disease (in coordination of hindlimbs, fitting, tremors, and paddling) are more commonly seen

Question 248

Weaned pigs and growing pigs with pseudorabies

Answer 248

CNS signs may be reduced and an increase in respiratory signs

Question 249

Nonimmune pregnant sows with pseudorabies

Answer 249

Infection before 30 days of gestation result in death and resorption of embryo. Infection in late pregnancy may result in mummified, macerated, stillborn, weak or normal swine. Up to 20% of sows aborting are infertile on next breeding, but eventually conceive

Question 250

Necropsy findings of swine with pseudorabies

Answer 250

Gross lesions are often absent or minimal | Serous to fibrinous rhinitis is common and a necrotic tonsillitis

Question 251

Clinical signs of pseudorabies in secondary hosts

Answer 251

(Ruminants, dogs, cats, horses) Intense pruritus Hyperacute Rapid progress High mortality

Question 252

Cattle with pseudorabies

Answer 252

``` Aka Mad itch Intense pruritus Cattle may become frenzied Progressive involvement of CNS, stage of paralysis, ataxia Death from respiratory failure ```

Question 253

Dogs and cats with pseudorabies

Answer 253

Dogs: Frenzy associated with pruritus, self-mutilation Paralysis of jaws and pharynx with drooling Plaintive howling Dogs do not tend to attack Cats: Progress is so rapid that pruritus may not be observed

Question 254

Vaccination of pseudorabies

Answer 254

Vax of swine in enzootic areas reduce losses. Vax do not prevent infection, or establishment of latent infection by wild-type virus, but can alleviate clinical signs in pigs of certain ages Recombinant DNA, deletion-mutation, live-attenuated, and inactivated vaccines are available

Question 255

What are the two important Equine herpesviruses?

Answer 255

Equine herpes virus 1 (EHV-1) | Equine herpes virus 4 (EHV-4)

Question 256

Distribution of EHV-1

Answer 256

Endemic in horse populations around the world

Question 257

Transmission of EHV-1

Answer 257

Inhalation of infected aerosols Direct or indirect contact with nasal discharges Aborted fetuses, placenta or placental fluids

Question 258

Latency of EHV-1

Answer 258

Can reside in tissues of CNS (specifically the trigeminal ganglia) and lymph system (leukocytes or lymphocytes) without causing any clinical symptoms When host is immunosuppressed; the virus is then reactivated, causing disease, or shedding of virus once again

Question 259

T/F: cell-associated viremia protects EHV-1 from the immune system, allows spread into endothelial lining of blood vessels int he CNS and pregnant uterus

Answer 259

True

Question 260

The principal route of EHV-1 infection is via the _______ tract

Answer 260

Respiratory

Question 261

T/F: following infection of epithelial cells, EHV-1 infects endothelial cells of the lamina propria

Answer 261

True

Question 262

Virus-infected _________cells and _ __________ subsequently appear in the drainage lymph nodes and are released into the circulation producing viremia

Answer 262

Mononuclear; T lymphocytes

Question 263

T/F: Following infection of respiratory epithelium (EHV-1), latent infections are established in circulating T lymphocytes and trigeminal ganglionic neurons

Answer 263

True

Question 264

Reactivation of BHV-1 results in shedding of virus from ______ epithelium and probably ______ infection

Answer 264

Nasal; uterine

Question 265

Central lesion caused by EHV-1 is responsible for three types of conditions seen is an infection of endothelial cells. What does this lead to?

Answer 265

Vascular necrosis Thrombus formation Subsequent death to the tissues serviced by these blood vessels

Question 266

Cell-associated viremia confers protection from the body's immune defenses and allows the virus to spread to endothelial cells lining blood vessels in the CNS and pregnant uterus, resulting in ___ signs or ____.

Answer 266

CNS; abortion

Question 267

Pathogenesis of EHV-1

Answer 267

Immunosuppression

Question 268

EHV-1 Respiratory disease

Answer 268

Affects mostly younger horses | Rhinopneumonitis

Question 269

EHV-1 Encephalomyelopathy (EHM, equine herpesvirus myeloencephalopathy) affects what group?

Answer 269

May affect horses of any age or breed

Question 270

EHV-1 Reproductive form

Answer 270

Abortions may occur early in gestation, the majority occur in the last trimester Repro efficiency is not compromised Cases of abortion are usually sporadic If large numbers of susceptible mares are exposed to the aborted conceptus, extensive outbreaks of abortion (abortion storms) occur Natural immunity may last 2-3 years, which is why abortion storms tend to show after 3 year cycles

Question 271

Equine viral Rhinophneumonitis

Answer 271

EHV-4 antigenically related to EHV-1

Question 272

Transmission of Equine viral rhinopneumonitis

Answer 272

Most infections with EHV-4 are sporadic Mostly observed in horses under 2 yo EHV-4 often causes a lifelong latent infection, which can be reactivated Droplet infection from infected horses and older horses in which inapparent viral shedding occurs

Question 273

Pathogenesis of EHV-4

Answer 273

Causes less severe tissue destruction than EHV-1 Rarely causes abortion when it infects pregnant mares Rarely results in viremia Death is rare

Question 274

Clinical signs for EHV-4

Answer 274

Infection results primarily in upper respiratory tract disease (rhinopharyngitis and tracheobronchitis)

Question 275

Vaccination of EHV-1 and EHV-4

Answer 275

Ideally should prevent infection of suckling foals as well as latency of infection in pregnant mares Live-attenuated and inactivated commercial EHV-1 vax are available, including combined products that include both EHV-1 and EHV-4 Immunity is short-lived

Question 276

What does Canine herpesvirus 1 (CHV-1) cause?

Answer 276

Hemorrhagic disease of puppies (fading puppy syndrome)

Question 277

Etiology of Hemorrhagic disease of puppies

Answer 277

Canine herpes virus 1, subfamily: Alphaherpesvirinae

Question 278

Hosts of CHV-1

Answer 278

Dogs Wild canids Highly fatal Generalized hemorrhagic disease of puppies

Question 279

Transmission of CHV-1 in neonates

Answer 279

``` Contact with infected oral, nasal or vaginal secretions of dam Contact with secretions of litter mates In-utero transmission From passage through birth canal Contact with infected fomites (rare) ```

Question 280

Transmission of CHV-1 in older dogs

Answer 280

Venereal transmission | Contact with saliva, nasal discharge, or urine of infected dogs or puppies

Question 281

Pathogenesis of In utero CHV-1 infection in puppies

Answer 281

Abortion Still birth Infertility If they survive, most pups develop systemic CHV-1 infections within 9 days from birth

Question 282

Pathogenesis of systemic neonatal infection

Answer 282

Pups less than 1 week old are most susceptible to fatal generalized infection Initial replication occurs in nasal epithelium, tonsils and pharynx Mucosal invasion is followed by leukocyte (macrophage)-associated viremia Virus replication in endothelial cells Diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in several organs Thrombocytopenia, DIC

Question 283

Pathogenesis of CNS infection of CHV-1

Answer 283

Meningoencephalitis commonly occurs in oro-nasally infected neonatal puppies. Virus may travel up the nerve axons to CNS. However, puppies die from systemic illness before neurologic signs are evident

Question 284

What are the two main factors governing systemic neonatal infection?

Answer 284

Body temperature of puppies is critical | Maternal immunity

Question 285

Why is the body temp of puppies critical when it comes to CHV-1?

Answer 285

Replicates at 33C - temp of the outer genital and upper respiratory tracts Hypothalamic thermoregulatory centers of the pup are not fully operative until 2-3 weeks of age Pup is critically dependent on ambient temp and maternal contact for the maintanence of it's normal body temp The more severe the hypothermia, the more severe and rapid is the course of the disease

Question 286

Why is maternal immunity important?

Answer 286

Maternal antibodies provide protection. | Pups born from seronegative bitches are highly vulnerable to severe form of disease

Question 287

Clinical signs of CHV-1 in puppies

Answer 287

``` Painful crying Abdominal pain Anorexia Dyspnea Passing soft, odorless greenish stool No elevation in body temp ``` Survivors develop persistent neurolgical signs, such as ataxia, blindness

Question 288

CHV-1 Adult genital infection

Answer 288

Bitches: Generally asymptomatic or limited to vaginal hyperemia Vesicular vaginitis with discharges, vesicular lesions. In-utero infection may result in abortion, stillbirth, mummified fetus, and/or infertility Male: Balanoposthitis

Question 289

CHV-1 Adult respiratory infection

Answer 289

Older dogs: | Mild respiratory infection (rhinitis and pharyngitis)

Question 290

Ocular infection from CHV-1

Answer 290

Conjunctivitis

Question 291

CHV-1 Control

Answer 291

Reduce hypothermia by providing heated whelping boxes, or placing puppies under infrared lamp Low prevalence of severe illness in pups and paucity of clinical signs in adult animals has resulted in lack of availability of vaccines

Question 292

Feline herpesvirus 1 causes what?

Answer 292

Feline Rhinotracheitis

Question 293

What are the two main causes of infectious respiratory disease of cats?

Answer 293

``` Feline herpes virus 1 Feline calicivirus (FCV) (family Caliciviridae) ```

Question 294

Transmission of Feline herpesvirus 1

Answer 294

FHV-1 is shed primarily in ocular, nasal and oral secretions Spread is largely by direct contact with an infected cat Aerosol route in not considered important Natural routes of infection are nasal, oral and conjunctiva All recovered cats become latently infected carriers Reactivation may cause viral shedding in organs all and conjunctival secretions

Question 295

Pathogenesis of FHV-1

Answer 295

Replication takes place predominantly in the mucosa of the nasal septum, turbinates, nasopharynx and tonsils. Viremia is rare, as virus replication is restricted to areas of low temperature, upper respiratory tract Infection leads to areas of multifocal epithelial necrosis, inflammation and fibrinous exudation Secondary bacterial infection can cause complications

Question 296

Clinical signs of FHV-1

Answer 296

``` Kittens (up to 4 weeks): Severe upper respiratory disease Extensive rhinotracheitis Fatal bronchopneumonia may develop Conjunctivitis and ulcerative keratitis ``` Cats (6 months or older): Mild or subclinical disease in older kittens

Question 297

What are the clinical signs of FHV-1 in pregnant queens?

Answer 297

Abortion around the 6th week of pregnancy No evidence that the virus crosses the placenta May be due to severe systemic effects of illness, and not direct effect of virus

Question 298

What are the 2 things that are common with feline rhinotracheitis?

Answer 298

Conjunctivitis with hyperemia and serous ocular discharge | Ulcerative keratitis

Question 299

Are ulcers on the tongue common with feline calicivirus (FCV)infection?

Answer 299

Yes

Question 300

Are oral ulcers common in cats with FHV-1 infections?

Answer 300

No, rare

Question 301

T/F: you can have severe necrohemorrhagic rhinitis and multifocal necrohemorragic palatitis with feline rhinotracheitis

Answer 301

True

Question 302

Vax of FHV-1

Answer 302

Three types of FHV-1 and FCV are available: MLV (modified live virus) parenterally MLV intranasal Inactivated vaccine parenterally

Question 303

What are the two avian diseases we are worried about in the herpesvirus world?

Answer 303

``` Infectious laryngotracheitis (Gallid herpesvirus 1) Marek's disease (Gallid herpesvirus 2) ```

Question 304

Etiology of infectious laryngotracheitis (ILT)

Answer 304

Gallid herpesvirus 1

Question 305

Hosts of ILT

Answer 305

Highly contagious infection of chickens

Question 306

Transmission of ILT

Answer 306

Inhalation**** Droplets by conjunctiva Occasionally by ingestion Recovered and vax chickens can also serve as carriers of ILT and can shed the virus when they are subjected to stressful conditions Transmission can occur through fomites such as contaminated litter, and/or farm workers Mechanical transmission, especially through scavengers like vultures, crow, domestic dogs and wild animal that feed on improperly disposed dead birds

Question 307

Pathogenesis of ILT

Answer 307

Severe laryngotracheitis in affected birds Extensive diphtheritic membrane formation can form a second tube for the length of trachea, blocking the air passage. This can result in death from asphyxia ILT virus can persist in the infected birds. The trigeminal ganglion is the target for ILT viral latency

Question 308

T/F: with ILT, birds can have hemorrhagic tracheitis, necrotizing hemorrhagic tracheitis, and tracheal plugs

Answer 308

True

Question 309

Severe form of ILT

Answer 309

Severe respiratory distress. Head shaking with cough is characteristic. Raised neck and extended head during inspiration - pump hardly respiration Cough may result in expulsion of bloody mucous which may stain beak and neck feathers

Question 310

Clinical signs of ILT

Answer 310

Strains of low virulence are associated with conjunctivitis, ocular discharge, swollen infraorbital and nasal sinuses, and decreased egg production. The mild enzootic form in most common in modern poultry production, and the severe epizootic form in uncommon

Question 311

Diagnosis of ILT

Answer 311

Necropsy findings: tracheal plug (diphtheria membrane) Detection of typical intranuclear inclusions in respiratory tissues Virus isolation: nasal mucosa Virus grows well in CAM of embryonated eggs

Question 312

Control of ILT

Answer 312

In an outbreak, complete depopulation (slaughter) of infected birds, and disinfection of infected premises

Question 313

3 types of vaccines for ILT

Answer 313

1. Chick embryo origin (CEO) - have the capability of reverting to virulence and causing full-blow ILT signs, induces better immunity. 2. Tissue culture origin (TCO) - only given by eye drop and does not spread significantly or revert to virulence. Level of induced immunity is limited 3. Pox-vectored recombinant vax * These are applied via eye drop, or through mass vax by water or spray

Question 314

Farm biosecturity of ILT

Answer 314

Implementation of farm biosecurity measures

Question 315

What is Marek's Disease?

Answer 315

Caused by Gallid herpesvirus 2 | Important disease of poultry

Question 316

Hosts of Marek's disease

Answer 316

Chickens are the most important natural host | Turkeys, quails, pheasants are susceptible

Question 317

Transmission of Marek's disease

Answer 317

Highly contagious Inhalation of infectious feather debris, chicken dander, or dust Cell free viruses release from the feather follicles are highly infectious, but labile Viruses in desquamated cells (dander) are less infectious, but can survive in poultry house dust or litter for several months

Question 318

What are the 4 pathotypes of Gallid herpes virus 2?

Answer 318

Mild [mMDV] Virulent [vMDV] Very virulent [vvMDV] Very virulent plus [vv+MDV]

Question 319

Mild [mMdv]

Answer 319

Mostly associated with neural MD. | Disease is preventable with HVT (turkey herpesvirus vaccine)

Question 320

Virulent [vMDV]

Answer 320

Associated with high incidence of neural and visceral lymphomas. Disease is preventable with HVT

Question 321

Very virulent [vvMDV]

Answer 321

Associated with high incidence of neural and visceral lymphomas Viruses are oncogenic in HVT vaccinated chickens. Disease preventable with bivalent vaccines

Question 322

Very virulent plus [vv+MDV]

Answer 322

Associated with high incidence of neural and visceral lymphomas. Viruses are oncogenic in chicken vaccinated with bivalent vaccines

Question 323

Marek's disease pathogenesis

Answer 323

Fully productive infection: occurs in feather follicle epithelium. Infected T cells appear to be the 'Trojan horse' by which MDV enters the feather follicle epithelium Inhalation of virus -> initial round of replication in epithelial cells -> macrophage associated viremia -> virus is detectable in the spleen, thymus and the bursa of Fabricius -> productive restrictive infection: cytolytic replication primarily in B cells and later activated CD4+ T cells -> non-productive latent infection in CD4+ T cells -> non-productive neoplastic transformation: some latently infected CD4+ T cells

Question 324

For MD, what is a fully productive infection?

Answer 324

Production of enveloped virions and cell death (lysis) Occurs only in feather follicle epithelium. Infected T cells appear to be the 'Trojan horse' by which MDV enters the feather-follicle epithelium

Question 325

Productive-restrictive infection for MD

Answer 325

Production of naked virions (not infectious) and viral antigens Cell death due to lysis Occurs in B-cells and activated T cells (primarily CD4+ cells) Profound immunosuppression

Question 326

Non-productive infection of MD

Answer 326

Viral genome persists in T cells (primary CD4+) | No antigens expressed

Question 327

Non-productive neoplastic transformation of MD

Answer 327

Some latently infected T cells undergo neoplastic transformation A new antigen, MATSA (MD associated tumor specific antigen), appears in transformed T-cells

Question 328

MD virus is slowly _____ and remain associated with cells. Cell-free infectious viruses are almost impossible to obtain, except in dander from _______ _________.

Answer 328

Cytopathic; feather follicles

Question 329

Lesions in MD result from infiltration and in situ proliferation of transformed _ __________. Cell lysis also results in marked inflammatory response

Answer 329

T lymphocytes

Question 330

Clinical features of MD

Answer 330

Neurolymphomatosis Visceral lymphomatosis Ocular lymphomatosis Cutaneous lymphomatosis

Question 331

Neurolymphomatosis

Answer 331

Enlargement of nerve trunks. Nerves lose their striations Edematous, grey, or yellowish in appearance. ``` Lameness Droopy wings Paresis of legs Limberneck Torticollis Incoordination ```

Question 332

Visceral lymphomatosis

Answer 332

Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lung, kidney, muscle, and proventriculus. The bursa is only rarely tumorous and more frequently is atrophic. The absence of burial tumors helps distinguish this disease from lymphoid leukosis

Question 333

Ocular lymphomatosis

Answer 333

Grading of the iris (aka gray eye, cats eye, or pearl eye) of one or both eyes. Interference with normal pupil are constriction and dilation. Partial or total blindness

Question 334

Cutaneous lymphomatosis

Answer 334

Plucking of feathers reveal nodular lesions on skin | Enlarged feather follicles (commonly termed skin leukosis)

Question 335

Vaccination for MD

Answer 335

Most widely used consists of turkey herpesvirus (HVT) Bivalent vax consisting of HVT and either the SB-1 or 301B/1 strains of Gallid herpesvirus 3 (serotype 2, avirulent strain) Most protective commercial vax available appears to be CVI988/Rispens, an attenuated MD virus strain that is also commonly mixed with HVT at vaccination

Question 336

General properties of the subfamily Betaherpesvirinae

Answer 336

Slow replication Associated with chronic infections Infected cells are often enlarged (cytomegaly) Maintained in latent form in secretory glands (salivary glands) and lymphoreticular cells (macrophages, lymphocytes) Often associated with continuous viral excretions

Question 337

Etiology of Inclusion Body Rhinitis

Answer 337

Porcine herpesvirus 2 aka Porcine cytomegalovirus (PCVM) subfamily Betaherpesvirinae

Question 338

Hosts of Inclusion Body Rhinitis

Answer 338

Pigs | Severe disease in piglets

Question 339

Transmission of Inclusion Body Rhinitis

Answer 339

Primarily inhalation | Transplacental transmission

Question 340

Pathogenesis of Inclusion Body Rhinitis

Answer 340

Widespread petechiae and edema Most common in thoracic cavity and SQ tissues Primary site of viral replication: nasal mucus glands, epithelial cells of upper respiratory tract In some neonates, bone marrow damage and anemia Still birth, mummification, neonatal death Endothelial cell damage and necrosis: petechial hemorrhages and edema

Question 341

With Inclusion Body Rhinitis, infected cells are enlarged and posses _______ inclusion bodies, especially in ______ glands. Hence, known as Inclusion Body Rhinitis

Answer 341

Intranuclear; nasal

Question 342

Clinical signs of Inclusion Body Rhinitis

Answer 342

In suckling pigs <3wo, mucopurulent rhinitis Infected neonatal piglets appear weak, anemic or stunted with edema around the throat and tarsal joints Fetal mummification, stillbirths, neonatal deaths and failure of piglets to thrive have been associated with infection of naive, pregnant sows Subclinical disease in older animals

Question 343

Subfamily Gammaherpesvirinae general properties

Answer 343

Lymphotropic (replicate in B or T lymphocytes) Slowly cytopathic for epithelial and fibroblastic cells, causing death without virion production Some gammaherpesviruses are shed continuously from epithelial surfaces Latency occurs in lymphoid tissues Some members cause lymphoid tumors

Question 344

Etiology of Malignant Catarrhal Fever (MCF) aka Bovine Malignant Catarrh

Answer 344

Viruses in subfamily Gammaherpesvirinae At least 10 viruses have been recognized Two most important MCF viruses are: Alcephaline herpesvirus-1 (AHV-1) aka Wildebeest-associated MCF Ovine herpesvirus-2 (OvHV-2) aka Sheep-associated MCF

Question 345

Wildebeest-associated MCF [Alcephaline herpesvirus-1

Answer 345

AHV-1 is trasmitted to cattle from wildebeests. Occurs in most African countries, where cattle commingle with infected normal wildebeest AHV-1 does not cause any disease in the wildebeest Epizootic and seasonal (during the wildebeest calving season)

Question 346

Sheep-associated MCF [ovine herpesvirus-2 (OvHV-2)]

Answer 346

Worldwide Transmitted from sheep to cattle Goats also can act as a source of infection to cattle Occurs year-round in cattle, with moderate increase during lambing season Usually sporadic, occasionally outbreaks

Question 347

T/F: In Africa, MCF is predominantly found where cattle are in close contact with blue-or black wildebeest, while outside Africa, it is usually associated with contact between sheep and susceptible species

Answer 347

True

Question 348

Transmission of wildebeest-associated MCF

Answer 348

Between wildebeest: horizontal and occasionally intrauterine transmission in wildebeest. Inapparent infection. From wildebeest to cattle: AHV-1 is present in nasal and ocular secretions of young wildebeest in a cell-free state. Ingestion of pasture contaminated with nasal or ocular secretions from young wildebeests. Direct or close contact, inhalation of aerosol with young wildebeest Direct or close contact with wildebeest during calving Virus in cell-associated form in adult wildebeest, so rarely transmitted from adults

Question 349

Transmission of sheep-associated MCF

Answer 349

Between sheep: Respiratory Transplacental rare Contact with nasal secretions Sheep to cattle: Not known Presumably by inhalation or ingestion

Question 350

Transmission of MCF between wildebeest and sheep

Answer 350

Inapparent infection in wildebeest and sheep. | Virus transmitted from wildebeest-to-wildebeest and sheep-to-sheep

Question 351

Cattle's role in MCF

Answer 351

Cattle are dead-end hosts. No evidence from transmission of virus from cattle-to-cattle. Cattle have cell-associated virus, but not cell-free virus, in secretions. This may explain the noncontagious nature of MCF when contact occurs with MCF affected cattle

Question 352

Pathogenesis of MCF

Answer 352

Infection followed by cell-associated viremia. Lymphoid proliferation and infiltration Necrotizing vasculitits Vascular lesions, gross lesions such as epithelial erosions and keratoconjunctivitis

Question 353

Clinical signs of MCF

Answer 353

Peracute form: sudden death Head and eye form: majority of cattle cases Alimentary/intestinal form: initially like head and eye form, but death occurs from severe diarrhea. Diarrhea is rarely observed in wildebeest derived MCF, but is more common in sheep associated MCF Mild form: inoculated animals; recovery expected

Question 354

Peracute form of MCF

Answer 354

Sudden Characteristic clinical signs of head and eye form may not appear High fever Acute gastroenteritis

Question 355

Head and eye form of MCF

Answer 355

``` Early stages Reddened eyelids Bilateral corneal opacity Crusty muzzle, nares Nasal discharge Salivation Erosions of the tongue, hard palate, and buccal papillae (along with necrosis) ```

Question 356

What is zebra striping?

Answer 356

Necropsy finding of MCF in the bovine colon. | Severe longitudinal linear congestion of the mucosa

Question 357

Control of MCF

Answer 357

Separation of cattle from wildebeest and sheep | Incidence too low to justify development of a vaccine

Question 358

Etiology of African Swine Fever (ASF)

Answer 358

Sole member of family Asfarviridae | Only known DNA arbovirus

Question 359

Hosts of ASF

Answer 359

All breeds and types of domestic pigs and European wild boar | Inapparent infection in warthogs, bush pigs and giant forest hogs, which act as reservoirs

Question 360

T/F: ASF is an OIE List A Disease

Answer 360

True

Question 361

Geographical distribution of ASF

Answer 361

Endemic: Most of sub-Saharan Africa Island of Sardinia (Italy) Recent outbreaks: Eastern Europe and Russia The virus has continued to spread within the Russian Federation

Question 362

ASF Virus Stability

Answer 362

``` Virus survive at least 30 days in pens Very resistant to s wide range of pH Survive in chilled carcass Highly resistant to putrefaction Remains viable for long periods in blood, feces and tissues Can multiply in vectors ```

Question 363

Transmission of ASF

Answer 363

Vector: soft ticks (Ornithodorus sp, specifically O moubata in Africa) Ornithodorus sp are biological vectors of the virus Virus replicates in the tick, resulting in trans-stadial, transovarial, and sexual transmission (male-to-female) Infected ticks may live for several years and capable of transmitting virus to pigs during each blood meal

Question 364

ASF reservoirs (Sylvatic cycle)

Answer 364

Warthog Giant Forest Hog Bush Pig

Question 365

Cycles that exist in the transmission of ASF

Answer 365

Domestic cycle between pigs Enter ticks and begins the sylvatic cycle Adult warthogs: No viremia, virus in various lymphoid tissues Juvenile warthogs: Significant viremia

Question 366

Sylvatic cycle of ASF

Answer 366

Between warthogs and soft ticks ASF maintained because of soft ticks and asymptomatic infection in wild pigs After primary infection, young wild pigs develop a viremia with high enough virus titers to infect ticks feeding on them Older wild pigs are persistently infected, but rarely develop viremia

Question 367

Domestic cycle of ASF

Answer 367

Meat products -> waste food -> fomites -> direct contact via secretions and blood loss Primary outbreaks in domestic swine: Bite of infected tick Direct contact with infected animal Indirect contact on fomites Virus spreads to new areas when pigs are fed uncooked scraps that contain infected pork Aerosol spread Mechanical transmission through biting flies All body fluids and tissues contain large amounts of infectious virus Pigs that survive infection may become carriers and shed virus in secretions and excretions

Question 368

Pathogenesis of ASF

Answer 368

The effects of ASF virus are primarily hemorrhages and apoptosis There is leukopenia, thrombocytopenia

Question 369

Apoptosis of host cells with ASF

Answer 369

P54 protein (encoded by virus) directly induces apoptosis of host cells ASF infected macrophages release cytokines and apoptotic mediators Apoptosis of both lymphocytes and mononuclear phagocytic cells

Question 370

Mechanisms related to hemorrhages of ASF

Answer 370

Vascular damage from degeneration of vascular endothelium DIC Infection and necrosis of megakaryocytes Activation and extensive destruction of monocytes and macrophages Thrombocytopenia and coagulation defects lead to: Edema, infarction, exudation and hemorrhages in many organs and tissues

Question 371

Peracute clinical signs of ASF

Answer 371

Pigs may die suddenly

Question 372

Acute form clinical signs of ASF

Answer 372

High fever Cyanotic skin blotching on the ears, tail, lower legs or hams**** Respiratory distress Diarrhea: initially mucoid and later may become bloody Abortion: sometimes the first event seen in an outbreak Death

Question 373

T/F: In white-skinned pigs with suspected ASF, the ears, tail, legs and underside appear deeply flushed and may develop a bluish tinge or cyanosis

Answer 373

True

Question 374

Chronic form clinical signs of ASF

Answer 374

Emancipation and stunting Swollen joints Ulcers and reddened or raised necrotic skin foci Pneumonia Cutaneous lesions Fibrinous pericarditis and myocardial hemorrhage

Question 375

What happens to the spleen of pigs with ASF

Answer 375

Becomes large and friable or blackberry jam spleen

Question 376

Immunity to ASF

Answer 376

Although infected pigs produce virus-specific antibodies, sera from infected pigs do not neutralize the virus, hence humoral immune response does not seem to have substantial protective value Therefore, attempts to develop a vaccine have so far been unsuccessful

Question 377

To prevent ASF

Answer 377

Pig farmers and field personnel should be aware of ASF, able to recognize ASF and know what to do if they suspect ASF. Pigs should be kept in well-constructed pig sties under hygienic conditions with controlled entry to the piggery. Movement of pigs inside the country and especially across international borders should be controlled Pigs shouldn't be fed swill that might contain remains of pigs. To ensure safety, swill should be boiled for 30 minutes and cooled before feeding

Question 378

During ASF outbreaks

Answer 378

IMMEDIATELY NOTIFY AUTHORITIES Infected and suspected infected farms must be placed in quarantine No movement of pigs or any products of pig origin should be allowed All infected an in-contact pigs must be slaughtered Carcasses must be burnt or buried deeply on site Vehicles should be disinfected on entering and leaving farms Personnel should ensure that shoes, clothes and equipment are disinfected between farms

Question 379

Family Parvoviridae general properties

Answer 379

Viruses are very stable | Disinfection of contaminated premises is difficult

Question 380

Replication of Parvoviridae

Answer 380

Occurs in the nucleus of dividing cells | Infection leads to large intranuclear inclusion bodies

Question 381

Genus parvovirus

Answer 381

Virus replication occurs only in cells that pass through mitotic S phase (actively dividing cells) Cannot replicate in stationary cells, as rely on enzymes of actively dividing cells (mitosis)

Question 382

Human parvovirus B19

Answer 382

Different from parvovirus seen in dogs and cats. No evidence of transmission of B19 to humans from dogs or cats, or vice versa

Question 383

Feline panleukopenia is aka what?

Answer 383

Feline distemper | Feline infectious enteritis

Question 384

Etiology of feline panleukopenia

Answer 384

Feline parvovirus

Question 385

Hosts of feline panleukopenia

Answer 385

Highly contagious, often fatal disease of cats | Severe in mittens

Question 386

Epidemiology of FPV

Answer 386

The virus is ubiquitous because of its contagious nature and capacity for persistence in the environment Virtually all cats are exposed and infected within first year of life Unvaccinated kittens that acquire maternal antibodies are protected up to 3 months of age Most infections are subclinical, as much as 75% of unvaccinated healthy cats have demonstrable antibody titers by 1 year of age

Question 387

Can cats shed FPV in their urine or feces? If so,for how long?

Answer 387

Yes, 6 weeks after recovery

Question 388

T/F: FPV is maintained in population by prolonged viral shedding rather than by environmental persistence

Answer 388

False, other way around

Question 389

Owners losing a kitten to FPV should/should not introduce a new kitten into the household without having it vaccinated

Answer 389

Should NOT

Question 390

Transmission of FPV

Answer 390

Cats are infected oro-nasally by exposure to infected animals, their feces, secretions or contaminated fomites In-utero transmission occurs Mechanical transmission by flies

Question 391

What are the hallmarks of Panleukopenia

Answer 391

The more severe the leukopenia, the poorer the prognosis The characteristic profound leukopenia involves destruction of all WBC elements, including lymphocytes, neutrophils, monocytes and platelets Thrombocytopenia may accompany leukopenia

Question 392

FPV enteritis

Answer 392

Virus selectively damages replicating cells deep in the crypts of the intestinal mucosa. Loss of cells from tip of villus continues as a normal process. Since virus replicates and destroys cells of crypts, there is no replacement of the lost absorptive cells at tips of the villi with cells of the crypts Resulting in shortening of intestinal villi, marked villus blunting and fusion, malabsorption and diarrhea

Question 393

FPV in-utero infections

Answer 393

Early in-utero in pregnant queens can result in: Early fetal death and resorption with fertility Abortions Birth of mummified fetuses Infection closer to end of gestation: Birth of live kittens with varying degree of damage to the late-developing neural tissues Variable effects on kittens from the same litter

Question 394

FPV CNS infections

Answer 394

CNS, optic nerve and retina are susceptible to damage by FPV during prenatal or early neonatal development Of neurological lesions, cerebellum damage has been most commonly reported Cerebellar hypoplasia is usually observed in fetuses infected during the last 2 weeks of pregnancy and the first two weeks of life

Question 395

FPV cerebellar hypoplasia

Answer 395

Lysis of mitotic cells of the external germinal layer | Impaired cerebellar development

Question 396

T/F: Ataxia is common in kittens with FPV

Answer 396

True

Question 397

FPV and DIC

Answer 397

Kittens with FPV infection are susceptible to secondary infections Gram- endotoxemia, with or without bacteremia is common sequelae of systemic FPV infection Endotoxin (LPS) induces expression of tissue factor [factor III] on endothelial cells Tissue factor is a potent activator of coagulation, resulting in DIC, followed by hemorrhages

Question 398

Clinical signs of FPV

Answer 398

``` Most common in kittens Fever Depression Anorexia Rough coat Repeated vomiting Profuse, persistent and frequently bloody diarrhea Severe dehydration Hypothermia Sudden death from complications of secondary infection, dehydration and DIC ```

Question 399

What are the consequences and clinical manifestations of FPV affected intestinal crypt epithelium?

Answer 399

Villous collapse, enteritis Diarrhea

Question 400

What are the consequences and clinical manifestations of FPV infected lymph nodes, thymus?

Answer 400

Germinal center depletion, apoptosis of lymphocytes, thymic atrophy Lymphopenia

Question 401

What are the consequences and clinical manifestations of FPV infected bone marrow?

Answer 401

Stem cell depletion Neutropenia -> thrombocytopenia and anemia

Question 402

What are the consequences and clinical manifestations of all fetus FPV infected cells

Answer 402

Fetal death Loss of pregnancy

Question 403

What are the consequences and clinical manifestations of FPV infected developing cerebellum cells?

Answer 403

Cerebellar hypoplasia Cerebellar ataxia

Question 404

T/F: Queens infected or vaccinated during pregnancy may show infertility or abortion of dead or mummified fetuses.

Answer 404

True

Question 405

How old are kittens when cerebellar hypoplasia and ataxic signs appear?

Answer 405

3-4 weeks

Question 406

_____ degeneration is seen in kittens infected with FPV

Answer 406

Retinal

Question 407

Diagnosis of FPV

Answer 407

Hematology: leukopenia, neutropenia more consistent than lymphopenia - total WBC counts <2000 cells/uL are associated with a poorer prognosis Fecal viral antigen testing using immunochromatographic test kit or ELISA: results may remain positive up to 2 weeks following MLV vaccination

Question 408

Serological testing for diagnosis of FPV

Answer 408

Single sample antibody titers do not distinguish between active or past infections/exposure to virulent or vaccine strains Paired serum samples, the 1st ASAP during illness, and second 2 weeks after. A fourfold rise in titer is considered indicative of acute infection Virus neutralization test is commonly used

Question 409

Treatment of FPV

Answer 409

Good nursing care, fluid therapy, withholding in early stages to lessen volition and slow down mitotic activity of cells Broad spectrum antibiotics to prevent secondary bacterial infection

Question 410

Control of FPV

Answer 410

Large catteries: strict hygiene and quarantine of incoming cats Disinfection: inactivated by bleach [6% sodium hypochlorite], 4% formaldehyde and 1% glutaraldehyde in 10 minutes at room temp

Question 411

Vaccination of FPV

Answer 411

Attenuated (modified) live vaccines (MLV) ``` MLV should not be administered to: Pregnant cats Immunosuppressed cats Sick cats Kittens less than 4 weeks old ```

Question 412

Is canine parvovirus 1 an important virus in dogs?

Answer 412

Nope. Mild to inapparent illness (diarrhea) in dogs, especially in young pups less than 8 weeks old.

Question 413

Name that virus: one of the most common infectious diseases of dogs. Has three antigenic variants: CPV-2a, CPV-2b, CPV-2c

Answer 413

Canine parvovirus 2 (CPV-2)

Question 414

Distribution of CPV-2

Answer 414

North America, CPV-2b and CPV-2c are more common

Question 415

Epidemiology of CPV-2

Answer 415

Virus is highly contagious and very stable in the environment Resistant to many common detergents and disinfectants Infectious CPV can persist indoors at room temp for at least 2 months

Question 416

Transmission of CPV-2

Answer 416

Oro-nasal exposure to contaminated feces In-utero infection Contact with virus-contaminated fomites (environment, personnel, equipment)

Question 417

Pathogenesis and clinical findings of CPV-2

Answer 417

Enteritis Myocarditis Panleukopenia Similar to FPV

Question 418

Enteritis with CPV-2

Answer 418

CPV-2 infects the germinal epithelium of the intestinal crypts, causing destruction and collapse (and necrosis) of the epithelium. No replacement of cells lost from tip of villus. Villi shortened and hemorrhagic diarrhea Hemorrhagic enteritis Ballooned small intestine Ingesta visible through small intestine wall

Question 419

Myocarditis with CPV-2

Answer 419

Develops from infection in-utero or from pups <6 wo Myocardial necrosis with acute cardiopulmonary failure Sudden death, or die after short period of clinical signs

Question 420

Diagnosis of CPV-2

Answer 420

Serology (antibody detection) is not best method to test CPV, because most dogs are vaccinated, or have been previously exposed

Question 421

What test is done in clinic that can test for parvo?

Answer 421

SNAP Parvo Test

Question 422

Vax for CPV

Answer 422

Because of potential damage by CPV to myocardial or cerebellar cells, inactivated rather than modified-live vaccines are indicated in pregnant dogs or colostrum-deprived puppies vaccinated before 6-7 wo

Question 423

Use of oseltamivir (tamiflu) in the treatment of canine parvoviral enteritis

Answer 423

MOA no clear, as parvovirus does not use neuraminidase in its replication Speculation is that neuraminidase is an important enzyme used by pathogenic bacteria invading through the protective mucous barrier of the GI tract, and by this process indirectly facilitate CPV infection. Tamiflu may act on these bacterial neuraminidase

Question 424

Porcine parvovirus

Answer 424

Is an infectious cause of reproductive failure in swine throughout the world Some manifestations of the disease are described by the acronym SMEDI (stillbirth, mummification, embryonic death, infertility) In most herds, a large proportion of gilts are infected naturally before they conceive, and hence are immune

Question 425

Transmission of porcine parvovirus

Answer 425

Oronasal in the non-immune pregnant sow followed by transplacental transmission. Venereal transmission is possible

Question 426

Pathogenesis of porcine parvovirus

Answer 426

Organs also infection of the nonimmune pregnant dam followed by viremia After maternal infection of the virus to reach the fetus

Question 427

Transplacental infection of porcine parvovirus

Answer 427

Death at different stages of pregnancy is typical of PPV infections

Question 428

What is the hallmark of PPV?

Answer 428

Increase in mummified fetuses after a normal gestation period

Question 429

Are abortions common in PPV

Answer 429

Uncommon

Question 430

What Times of infection is critical for PPV

Answer 430

``` Embryo/fetus (<30 days): dies and resorbed. Dams may return to estrus Early fetus (30-70 days): fetuses die and become relatively dehydrated (mummified) Late fetus (>70 days to term): frequently develop lesions, but also mount an immune response and usually survival in-utero ```

Question 431

T/F: with PPV, boars, sows and gilts have mostly inapparent or subclinical infections

Answer 431

True

Question 432

Diagnosis for PPV

Answer 432

Serologic tests are of limited value, because the virus is so widespread in swine, and vaccination may interfere

Question 433

Immunity to PPV

Answer 433

Unlike most parvoviruses, PPV can cause persistent infection with periodical shedding of virus

Question 434

Vaccination/immunization to PPV

Answer 434

Many inactivated and live vaccines available to prevent PPV Best way: vax all susceptible breeding stock twice, 2 weeks apart, several weeks before breeding Alternatively, gilts can be naturally infected several weeks before breeding, by mingling with older breeding stock that may be shedding the virus

Question 435

Can papillomaviruses transform cultured cells?

Answer 435

Yes

Question 436

What do papillomaviruses produce on the skin and mucous membranes of most animal species?

Answer 436

Warts or papilloma I hope you got that one!

Question 437

The warts from papillomavirus are ______ ______ are hyperplastic epithelial outgrowths that generally regress ________

Answer 437

Benign neoplasms; spontaneously

Question 438

T/F: Papillomaviruses are not species and site specific

Answer 438

False, they are specific

Question 439

T/F: serologic cross-reactivity has not been detected among papillomaviruses of different species

Answer 439

True

Question 440

Can the warts of papillomavirus progress to malignancy?

Answer 440

Yes. This is a property of specific virus strains i.e. HPV causing cervical carcinoma in women

Question 441

Replication of papillomaviridae

Answer 441

Replication of papillomaviruses is linked intimately to the growth and differentiation of cells in stratified epithelium of the skin and some mucous membranes

Question 442

The story of oncogenic papillomaviruses

Answer 442

In benign warts, the papillomavirus DNA is episomal, meaning it isn't out integrated into the host-cell DNA and persists as an autonomously replicating episome. In papillomavirus-induced malignant cancers the viral DNA integrated into that of the host. Thus, integration probably is necessary for Malignant transformation

Question 443

Host of Bovine papillomatosis

Answer 443

Cattle Warts are more commonly seen in cattle than in any other domestic animals Natural bovine papillomavirus infection of horses (WHAT????) may occur after exposure of the horses to cattle

Question 444

Transmission of bovine papillomavirous

Answer 444

Between animals by contaminated fomites, such as milking equipment, halters, nose leads, grooming and earmarking equipment Sexual transmission of venereal warts in cattle

Question 445

Fibropapilloma is mostly caused by what? What is it?

Answer 445

Bovine papillomavirus types 1, 2, and 5 Papilloma have a fibrous core covered to a variable depth with stratified squamous epithelium, the outer layers of which are hyperkeratinized Lesions vary from small firm nodules to large cauliflower-like growths Grayish to black in color and rough and spiny to the touch

Question 446

Where are fibropapillomas common?

Answer 446

Udder and teats Head Neck Shoulders May also occur in the omasum, vagina, penis and anus

Question 447

Cutaneous papillomas are caused by what and what are they?

Answer 447

Bovine papillomavirus type 3 Lesions lack a fibrous core Are usually flat with a broad base, unlike the more usual fibropapillomas that protrude and are often pedunculated

Question 448

What is the relationship between Bracken Fern and Bovine Papillomavirus?

Answer 448

Bovine papillomavirus 4 can cause transient papilloma in the alimentary tract. Ingestion of the bracken fern can result in transition to invasive carcinoma of the alimentary tract In cattle that eat broken fern, papillomavirus types 1 and 2 may also contribute to the syndrome of "enzootic hematuria" that is characterized by hematuria and/or urinary bladder cancer

Question 449

Treatment of bovine papillomatosis

Answer 449

Surgical excision, or cryosurgery with liquid nitrogen Topical agents, podophyllin and undiluted medical grade DMSO (dimethylsulfoxide) Bovine interferon-alpha Wart vaccine (yes, it's a thing apparently)

Question 450

Canine oral papillomatosis

Answer 450

Contagious, self-limiting disease affecting oral cavity of dogs The warts usually begin on the lips, and can spread to the buccal mucosa, tongue, palate and pharynx. Later may become roughened and cauliflower-like. Do not extend below epiglottis or into esophagus Lesions typically regress spontaneously Progression to squamous cell carcinoma occurs very rarely

Question 451

Clinical signs of canine oral papillomatosis

Answer 451

Halitosis (bad breath), hemorrhage, ptyalism (hypersalivation), discomfort Numerous warts may interfere with mastication and deglutition Warts may regress, or secondary bacterial infection and ulceration may occur Ocular warts: conjunctiva, cornea, eyelid margins Recovered dogs are refractory to reinfection

Question 452

Treatment of canine oral papillomatosis

Answer 452

Surgical excision, cryosurgery, electrosurgery | Auto genius vaccines

Question 453

Equine sarcoids

Answer 453

Commonly occur in horses, donkeys and mules between 1-6 yo. Most common neoplasm of horses**** They are locally invasive benign fibroblastic skin tumors Associated with bovine papillomaviruses 1 and 2 Do not metastasize. They may persist for life. Are locally invasive. Recur after surgical removal

Question 454

Equine sarcoids transmission

Answer 454

Mode of transmission has not been confirmed Flies act as vectors maybe? Fomites, transmitted via stable management practices

Question 455

What do equine sarcoids look like?

Answer 455

Lesions commonly occur in traumatized areas Single or multiple Growths may reach size of man's fist, bulge under skin May become ulcerated

Question 456

Treatment of equine sarcoids

Answer 456

Cryotherapy Surgical or laser excision Local immune modulation Local radiotherapy

Question 457

Morphology of Adenoviridae

Answer 457

Non-enveloped, precisely hexagonal in outline | 12 vertex penton capsomers each with a fiber protrude from the surface of capsid

Question 458

Genome and replication of Adenoviridae

Answer 458

Intranuclear inclusion bodies are formed, containing large numbers of virions, often in para-crystalline arrays

Question 459

Adenoviridae general properties

Answer 459

Agglutinate RBCs. Hemagglutination occurring when the tips of penton fibers bind to surface of receptors on RBCs. Some viruses are oncogenic in lab animals Relatively stable in the environment, but are inactivated easily by common disinfectants Most have narrow host ranges

Question 460

Pathogenesis of adenoviruses

Answer 460

Cause acute respiratory or gastroenteric disease of varying severity Mostly subclincal infections Cause immunosuppression

Question 461

Long periods of latency of adenoviruses

Answer 461

Viruses persist in lymphoid and other tissues, such as tonsil, adenoids, and Peyer's patches Reactivated in immunocompromised animals Can be highly pathogenic in immunodeficient animals

Question 462

Oncogenesis of adenoviruses

Answer 462

Under specialized conditions, some have been shown to be oncogenic

Question 463

What are the two most important genera of adenoviruses?

Answer 463

Mastadenovirus: mammalian adenoviruses. A single penton fiber projects from each vertex Aviadenovius: Avian adenoviruses. Each penton fiber is bifurcated, appear as two fibers extending from each penton base

Question 464

Etiology of infectious canine hepatitis (ICH, Rubarth's Disease)

Answer 464

Canine adenovirus-1 (CAV-1)

Question 465

Transmission of CAV-1

Answer 465

Acute infection: found in all secretions and excretions Afterwards, virus shed in urine for at least 6-9 months ``` Route: oronasal transmission Contact with: Secretions/excretions of infected dog Contaminated fomites Ectoparasites can harbor CAV-1 ```

Question 466

Sites of ICH virus replication

Answer 466

``` Macrophages Kupffer cells Hepatocytes Vascular endothelium of different organs including CNS Parenchyma cells of organs and tissues ``` Liver, kidneys, spleen and lungs are the main target organs!

Question 467

Pathogenesis of ICH

Answer 467

``` At time of infection, dogs already with sufficient antibody titers (>500) show little clinical evidence of disease In acute cases, sufficient antibody response by day 7 post-infection [>500 antibody response by day 7 PI] clears virus from blood and liver and restricts hepatic damage Persistently low antibody titer (>4) will lead to widespread centrilobular to panlobular hepatic necrosis Partial immunity (antibody titer >16, but <500) may result in chronic active hepatitis and hepatic fibrosis ```

Question 468

What happens in chronic cases of ICH?

Answer 468

Cirrhosis

Question 469

What happens to the kidneys during ICH?

Answer 469

Acute infection - glomerulonephritis | Chronic kidney lesions may result from immune-complex reactions after recovery from acute or subclinical disease

Question 470

Corneal edema with ICH

Answer 470

Blue eye Occurs in about 20% of natural infections Less than1% of dogs after S/C MLV-CAV-1 vax Seen in dogs during recovery or chronic cases

Question 471

How does corneal edema develop?

Answer 471

CAV-1 antibody production increases, and formation of viral-antibody immune complexes This results in complement activation, neutrophil chemotaxis Cause extensive damage to corneal endothelium Disruption of intact corneal endothelium allows aqueous to enter the cornea Accumulation of edematous fluid within corneal stroma results in corneal edema

Question 472

Complications from ICH

Answer 472

DIC: Results from: Damage to endothelium Inability of diseased liver to remove activated clotting factors Bacterial pyelonephritis resulting from renal damage

Question 473

ICH clinical signs

Answer 473

Most frequent in dogs less than 1 yo Concurrent parvovirus or distemper infection worsens the prognosis Unvaccinated dogs of all ages are susceptible Most infections are asymptomatic Signs vary from a slight fever to death

Question 474

Peracute cases of ICH

Answer 474

Severely infected dogs become moribund and die within few hours after onset of clinical signs

Question 475

Acute cases of ICH

Answer 475

Fever of >104F (40C), depression, and anorexia Vomiting Occasionally abdominal pain, tenderness and hepatomegaly Intense hyperemia or petechiae hemorrhages of the oral mucosa Pale mucous membrane, jaundice Enlarged tonsils, swollen lymph nodes Subcutaneous edema of the head, neck and trunk CNV involvement is unusual and is typically the result of vascular injury Icterus is uncommon in early acute phase of ICH Corneal edema and anterior uveitis occur when clinical recovery begins

Question 476

Necropsy and histopathology findings of ICH

Answer 476

Paint-brush hemorrhages on the gastric serosa, lymph nodes, thymus, pancreas and subcutaneous tissues Centrilobular necrosis in liver, with neutrophilic and monocytic infiltration, and hepatocellular intranuclear inclusions Grayish white foci may be seen in the kidney cortex of recovered dogs or dogs with chronic disease

Question 477

Diagnosis of ICH

Answer 477

Biochemistry and hematology: Leukopenia persists throughout febrile period Increased ALT and AST due to hepatic injury Proteinuria Prolonged prothrombin time, thrombocytopenia Virus isolation: URINE, blood, tissue homogenates, etc

Question 478

Treatment of ICH

Answer 478

Symptomatic and supportive. The goals of therapy are to limit secondary bacterial invasion, support fluid balance, and control hemorrhagic tendencies.

Question 479

Immunity to ICH

Answer 479

Recovered animals are immune to systemic form of disease Maternal antibodies interferes with active immunization until puppies are 9-12 wo Attenuated CAV-1 live vaccines have produced transient unilateral or bilateral opacities of the cornea. Vaccine virus can cause mild subclinical interstitial nephritis, and may be shed in urine. Discounted in many countries. CAV-2 attenuated live virus strains provide cross-protection against CAV-1. CAV-2 attenuated vaccines are preferentially used because they have very little tendency to produce corneal opacities or uveitis, and the virus is not shed in urine

Question 480

Canine infectious tracheobronchitis (ITB, kennel cough) is what and what is the etiology?

Answer 480

Self-limiting upper respiratory disease of dogs Multiple things can cause kennel cough. CAV-2 and Bordetella bronchiseptica (primary pathogen) are most prevalent

Question 481

Transmission of ITB

Answer 481

Highly contagious via aerosolized droplets | Stress, unfavorable conditions increases severity of disease

Question 482

Signs of uncomplicated ITB

Answer 482

Prominent sign is paroxysms of harsh, dry coughing, followed by etching and gagging. Coughing causes a high pitched "honking" sound Rhinitis, serous nasal discharges, sometimes conjunctivits

Question 483

Signs of "complicated" ITB

Answer 483

Severe pneumonia or bronchopneumonia | Life threatening

Question 484

Treatment of ITB

Answer 484

Antitussives when used in conjunction with broncodilators

Question 485

Immunity to ITB

Answer 485

Modified-live virus vaccines against distemper, parainfluenza, and CAV-2, which also provides protection against CAV-1

Question 486

Equine adenovirus

Answer 486

EAV-1 and EAV-2 Most are asymptomatic or present as mild upper or lower respiratory tract diseases EAV-1 is associated with severe respiratory disease in Severe Combined Immunodeficiency (SCID) foals As maternal antibody wanes, these foals become susceptible to adenovirus infection Infection is progressive, and these foals invariably die with 3 months

Question 487

Clinical signs of SCID in foals

Answer 487

Severe bronchiolitis and pneumonia. Respiratory distress and related signs

Question 488

Avian adenoviruses in chickens

Answer 488

Inclusion body hepatitis | Egg drop syndrome '76

Question 489

Avian adenovirus of ducks

Answer 489

Hepatitis (rare)

Question 490

Avian adenoviruses of quail

Answer 490

Bronchitis

Question 491

Avian adenovirus of turkeys

Answer 491

Hemorrhagic enteritis | Egg drop syndrome

Question 492

Avian adenovirus of pheasants

Answer 492

Marble spleen disease