exam 2

Question 1

polymerase chain reaction-PCR

Answer 1

amplification of viral genome/DNA

Question 2

The steps of how PCR works

Answer 2

1. denaturation
2. annealing
3. extension/elongation

Question 3

Real Time/Quantitative PCR

Answer 3

• advanced form of PCR which allows monitoring and quantification of increasing accumulation of PCR products/nucleic acid load as reaction progresses
• useful to study virus load in patient

Question 4

DNA sequencing

Answer 4

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

Question 5

Next Generation Sequencing

Answer 5

-significantly cheaper, quicker, needs significantly less DNA, has high throughput, and is more accurate and reliable than Sanger sequencing

Question 6

Metagenomics

Answer 6

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

Question 7

Phylogenetic analysis

Answer 7

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

Question 8

microarray

Answer 8

• several thousands of known DNAs (probes) amplified by PCRs/RT-PCRs, are spotted onto glass or silicon chip
• target/sample DNA are fluorescently labeled and then hybridized/added to chip containing DNA probes
• positive reactions between probe-DNA and sample DNA (hybridization) generate a fluorescent signal from the spot where the probe DNA is spotted in the chip

Question 9

Advantage of microarrays

Answer 9

-hundreds of pathogens can be screened for simultaneously using a single microarray chip

Question 10

Treatment of Viral Diseases

Answer 10

• antiviral drugs
• immune system stimulation
• synthesize antibodies or administration of natural anti-serum (antibodies)

Question 11

antiviral drugs

Answer 11

• 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
• used specifically for treating viral infections

Question 12

immune system stimulation

Answer 12

-interferons- have antiviral effects and modulate functions of immune system

Question 13

Acyclovir

Answer 13

• antiviral activity primarily restricted to herpesviruses
• administered as prodrug, inactive form
• requires virus enzymes in infected host cell to convert itself into active form, which then interferes with virus replication

Question 14

What is acyclovir used to treat?

Answer 14

• herpesvirus infections in humans
• feline herpesvirus-1 induced corneal ulcers
• equine herpesvirus-1 induced encephalomyelitis

Question 15

What is acyclovir a synthetic nucleoside analog of?

Answer 15

-deoxyguanosine

Question 16

mechanism of action of acyclovir

Answer 16

• competitive inhibition of viral DNA polymerase, as acyclovir-triphosphate competes with dGTP for viral DNA polymerase
• herpes simplex’s DNA polymerase enzyme incorporates acyclovir monophosphate into the growing DNA strand as if it were 2-deoxyguanosine monophosphate (G base), further elongation of the chain is impossible and viral DNA chain synthesis stops

Question 17

Why is acyclovir non-toxic to uninfected host cell?

Answer 17

• enzymes herpesvirus thymidine kinase and herpes virus DNA polymerase are viral enzyme, not found in uninfected host cells
• without these, acyclovir cannot be phosphorylated and incorporated into host DNA

Question 18

Amantadine

Answer 18

-inhibits replication of most strains of influenza A by blocking uncoating of virus

Question 19

mechanism of antiviral action of Amantadine

Answer 19

• M2 channel is target
• compounds clog channel and prevent it from pumping protons into virion
• in presence of amantadine, viral RNAs remain bound to M1 and cannot enter nucleus, virus replication inhibited

Question 20

Neuraminidase inhibitors

Answer 20

• inhibitors of neuraminidase enzyme synthesized by influenza A and B
• Oseltamivir (tamiflu)

Question 21

Neuraminidase inhibitors: mechanism of action

Answer 21

• blocking of neuraminidase with with NA inhibitors is effective way to treat influenza
• prevents release of virus and spread of infection, as HA of virus is still bound/attached to sialic acid containing receptors on surface of already infected host cell
• inhibition of neuraminidase, therefore slows virus spread, giving the immune system opportunity to catch up and mediate virus clearance

Question 22

targets for anti-retroviral therapy

Answer 22

• inhibit fusion
• inhibit reverse transcriptase
• inhibit protease
• inhibit integrase

Question 23

nucleoside analog reverse transcriptase inhibitors (NRTIs)

Answer 23

• Zidovudine (ZDV) or AZT (azidothymadine)

- ddI (didanosine)

Question 24

ZDV/AZT

Answer 24

• nucleoside analog reverse transcriptase inhibitors (NRTIs)
• nucleoside analog of thymine
• competitive inhibition of reverse transcriptase activity: AZT- triphosphate competes with thymine deoxyribonucleotide triphosphate for reverse transcriptase
• insertion of AZT- monophosphate into cDNA blocks the growth of cDNA being transcribed from viral RNA by reverse transcriptase

Question 25

T/F AZT has been shown to reduce clinical signs in FIV positive cats

Answer 25

-true, when administered at a dose of 10 mg/kg twice a day subq for 3 weeks

Question 26

What is required to cleave HIV polyproteins into functional proteins?

Answer 26

-proteases

Question 27

How do protease inhibitors work?

Answer 27

- inhibit proteases - HIV polyproteins cannot be cleaved into functional proteins - protease inhibitors bind to the active site of HIV protease, and prevent the enzyme from cleaving HIV polyproteins into functional proteins, as a result HIV cannot mature and non-infectious viruses are produced

Question 28

Types of live attenuated virus vaccines

Answer 28

- vaccines produced from naturally occurring attenuated viruses - vaccines produced by attenuation of viruses by serial passage in culture cells - vaccines produced by attenuation of viruses by serial passage in heterologous hosts - vaccines produced by attenuation of viruses by selection of cold-adapted mutants and reassortants

Question 29

replicating virus vaccines

Answer 29

- produced from inactivated whole virions | - vaccines produced from purified native viral proteins

Question 30

Can vaccines be produced by using recombinant DNA and related technologies?

Answer 30

YASSS

Question 31

DIVA (differentiating infected from vaccinated animals also the female version of a hustla)

Answer 31

- subunit "marker vaccines" have only a portion (subunit) of the vaccine (less antigens than natural strains) - if antibodies to other parts of the pathogen not included in vaccine then the animal has been infected - if only the antibodies to the vaccine are found, animal not infected

Question 32

Prevention and control of virus- isolation

Answer 32

- applies to animals known to be ill with contagious disease | - separate animals if showing clinical signs and/or test positive by diagnostic test

Question 33

prevention and control- quarantine

Answer 33

- applies to those exposed to contagious disease - not effective with diseases involving chronically infected healthy shedders - separate animal if exposed to a contagious disease, even if does not show clinical signs, and/or animal test negative by diagnostic test

Question 34

prevention and control-quarantine and culling

Answer 34

- separate and restrict movement of animals - culling (killing) of animals - proper disposal of culled animals

Question 35

prevention and control-decontamination

Answer 35

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

Question 36

prevention and control-sterilization

Answer 36

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

Question 37

prevention and control-disinfection

Answer 37

- describes a process that eliminates many or all pathogenic microorganisms, except bacterial spores, or inanimate objects - less effective than sterilization, does not necessarily kill all microorganisms

Question 38

prevention and control-antisepsis

Answer 38

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

Question 39

prevention and control- sterilization methods

Answer 39

- moist heat- autoclave - dry heat- hot air oven - chemical methods: gases like ethylene oxide, ozone - radiation: non-ionizing=ultraviolet radiation, ionizing= gamma rays, X-rays - sterile filtration: microfiltration using membrane filters

Question 40

Family of Pox virus

Answer 40

-Poxviridae

Question 41

Subfamily of Pox virus

Answer 41

- Chordopoxvirinae | - 8 genera--> diseases in humans, birds animals

Question 42

relevant genuses of pox virus

Answer 42

- orthopoxvirus - parapoxvirus - avipoxvirus - capripoxvirus - leporipoxvirus - suipoxvirus

Question 43

shape of poxviruses

Answer 43

- large, sometimes enveloped - most poxviruses are pleomorphic, typically brick shaped, possess an irregular surface of projecting tubular or globular structures - members of Parapoxvirus are ovoid, covered in thread-like surface tubules, which appear to be arranged in crisscross fashion resembling ball of yarn

Question 44

What are the two infectious poxvirus particles?

Answer 44

- intracellular mature virus (IMV) | - extracellular enveloped virus

Question 45

How many membranes does the extracellular form (EEV) have?

Answer 45

-two membranes: envelope, inner membrane

Question 46

What causes the EEV form to have two membranes?

Answer 46

-because it is released from cell by budding, rather than cellular disruption, they have an extra envelope that contains virus encoded-proteins from host cell membrane

Question 47

How do intracellular particles come out of the host cell?

Answer 47

- through disruption | - only have inner membrane

Question 48

structure of poxvirus

Answer 48

- do not confirm to icosahedral or helical symmetry, complex symmetry - virion outer layer encloses dumbbell shaped core and two lateral bodies - core contains viral DNA and several proteins - poxviruses have more than 200 genes in their genomes, as many of 100 of these encode proteins contained in virions

Question 49

poxvirus geneome

Answer 49

- single molecular of linear double-stranded DNA - many proteins encoded by the poxvirus genome are enzymes involved in nucleic acid synthesis and virion structural components - also encode proteins that specifically counteract host adaptive and innate immune responses

Question 50

replication and release of poxviruses

Answer 50

- occurs predominantly in cytoplasm - possible because poxviruses have evolved the enzymes required for transcription and replication of the viral genome - following replication, virions are released by budding (enveloped virions) by exocytosis, or by cell lysis- most(non-enveloped virions) - both enveloped and non-enveloped are infectious - enveloped virions are taken up by cells more readily and appear to be more important in spread of virions through body of animal

Question 51

stability of poxviruses

Answer 51

- virion of a poxvirus is an enveloped particle that differs significantly from enveloped viruses - show high environmental stability, remain infectious over a period of several months in an ambient environment - low lipid content, less sensitive to organic solvents/disinfectants compared to other enveloped viruses - extraordinarily high resistance to drying - can survive many years in dried scabs, or other virus laden material

Question 52

transmission of poxviruses

Answer 52

- skin: contact with broken or lacerated skin - respiratory route: aerosol (sheep-pox) - mechanically transmitted: biting arthopods (Myxoma virus and avipoxviruses)

Question 53

Pathogenesis and immunity of poxviruses

Answer 53

- highly epitheliotropic- causes cutaneous skin lesions - causes systemic diseases in birds and wild animals - most are host specific - orthopoxviruses- infect wide range of species

Question 54

spread of poxvirus

Answer 54

- following introduction into body, usually gains access to systemic circulation via lymph - secondary viremia disseminates virus back to skin and other target organs

Question 55

skin lesions in poxvirus infection

Answer 55

- macule(flat, red, local inflammation immune response infiltrating leukocytes)-->papule(raised, red, more marked inflammation, invasion of neighboring tissue)-->vesicle(small blister when microbe invades epithelium)-->pustule-->scab - after scab can either go to scar once it heals or to ulcer as a complication - rupture of pustule can lead to secondary bacterial infection - poxvirus can survive in the dried scabs for months or years

Question 56

Cowpox

Answer 56

- orthopoxvirus - distribution: endemic only in Europe and Asia - hosts: cattle, wild and domestic cats, humans, zoo animals, etc - reservoir host: rodents

Question 57

transmission of cowpox-cattle

Answer 57

- transmission from cow to cow in a herd is through milker's hands or teat cups - infected farm cats can also transmit disease - rodents serve as reservoir and can transmit disease

Question 58

economic importance of cowpox-cattle

Answer 58

-losses to farmers due to inconvenience in milking because of sourness of teats and mastitis from secondary bacterial infections

Question 59

clinical findings cowpox- cattle

Answer 59

- during which cows may be mildly febrile, papules appear on teats and udder, sucking calves may develop lesions in mouth - vesicles may not be evident or may rupture readily, leaving raw, ulcerated areas that form scabs

Question 60

cowpox in cats- transmission

Answer 60

- usual route of infection in cats is skin inoculation, probably through bite or wound- rodents common source - can also be transmitted oro-nasal route - in exotic felids (cheetahs) viral pneumonia may be evident

Question 61

cowpox in cats- clinical signs (primary lesions)

Answer 61

- primary lesions: most affected cats have history of primary skin lesion, usually on head, neck, or forelimb - primary lesion can vary from small, scabbed wound to large abscess

Question 62

cowpox in cats- secondary lesions

Answer 62

- after primary lesion appears, widespread secondary lesions appear - throughout 2-4 days these develop into discrete, circular, ulcerated papules about .5-1cm in diameter - ulcers soon covered in scabs, healing usually complete by about 6 weeks - many cats show no signs other than skin lesions, but about 20% may develop mild coryza or conjunctivitis - complications can result from secondary bacterial infections

Question 63

cowpox in humans- transmission

Answer 63

- mainly caused by direct contact with cats - rarely from rodents and zoo animals - virus is not commonly found in cattle, chances of getting virus from cow is less

Question 64

clinical signs of cowpox in humans

Answer 64

- macropapular lesions first observed on hands and face, later develop into vesicular and then ulcerative lesions - enlarged, painful local lymph nodes - patients may report fever, vomiting, and sore throat

Question 65

monkeypox in humans

Answer 65

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

Question 66

transmission of monkeypox in humans

Answer 66

- primary infections of humans- results from direct contact with blood, body fluids, or rashes of infected animals. In Africa human infections have been documented through the handling of infected monkeys, Gambian rats, or squirrels - secondary transmission is human to human- resulting from close contact with infected respiratory tract excretions, with the skin lesions of an infected person, or with recently contaminated objects

Question 67

Psuedocowpox-definition

Answer 67

- viral skin disease that causes mild sores on the teats and udders of cattle - can also infect humans- Milker's nodule

Question 68

Psuedocowpox-etiology

Answer 68

member of genus Parapoxvirus

Question 69

Psuedocowpox- epidemiology

Answer 69

-reported from most countries

Question 70

transmission of psuedocowpox

Answer 70

- source of infection is infected cattle - contaminated milker's hands, teat cups - biting insects may transmit the virus - calves get infected during sucking infected teats - semen of bulls

Question 71

pathogenesis of psuedocowpox

Answer 71

-characterized by hyperplasia of squamous epithelium

Question 72

clinical signs-pseudocowpox

Answer 72

- infections generally mild | - papule on teat

Question 73

acute lesions- psuedocowpox

Answer 73

- erythema -->papules -->vesicle or pustule ---> rupture -->thick scab - thick scab .5-25 cm in diameter, becomes elevated due to accumulation of granulation tissue - after 7-10 days, the scab drops off, leaving horseshoe-shaped ring of small scabs surrounding small wart-like granuloma

Question 74

chronic lesions-- pseudocowpox

Answer 74

- commences as erythema - yellow-gray, soft scruffy scabs which are rubbed off during milking - skin is corrugated - no pain - lesions may persist for months

Question 75

diagnosis- psuedocowpox

Answer 75

- horseshoe-shaped ring like lesion, pathognomonic for disease - isolation and detection of the virus by various diagnostic lab methods from vesicular fluid or from teat skin

Question 76

Ddx psuedocowpox

Answer 76

- cowpox virus - bovine herpesvirus ulcerative mammilitis - vesicular stomatitis - udder impetigo (pustules on skin of udders and teats) - teat chaps and frostbite - black spot (formation of hyperkeratosis)

Question 77

treatment psuedocowpox

Answer 77

- removal of scabs - burn the scabs to prevent environmental contamination - application of an emollient ointment before milking - application of astringent preparation after milking

Question 78

prevention of pseudocowpox

Answer 78

- disinfection- iodophor teat dip - isolation and treatment of infected cows - reduce teat trauma, injuries to skin of teat predisposes to infection

Question 79

Psuedocowpox in humans (Milker's Nodule)

Answer 79

- mild skin lesion- Milker's nodule - lesions on hands of dairy farmers milking teats, or vets treating infected cows - lesions vary from multiple vesicles to single, indurated nodule

Question 80

Contagious Ecthyma- etiology

Answer 80

-Orf virus, genus parapoxvirus

Question 81

Contagious Ecthyma- host

Answer 81

sheep and goats, primarily labs and goat kids

Question 82

Distribution of contagious Ecthyma

Answer 82

-worldwide

Question 83

Transmission Contagious Ecthyma

Answer 83

- scabs that fall off from the healing lesions contain virus - virus are stable in environment, remain highly infectious for long periods under dry conditions - contaminated instruments - spread in flock is 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 84

Pathogenesis of Contagious Ecthyma

Answer 84

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

Question 85

clinical signs: contagious ecthyma

Answer 85

- first lesions develop in the mucocutaneous junction and are accompanied by swelling of the lips - from there, lesions spread to the muzzle and the nostrils, surrounding hairy skin and the buccal mucosa - animal may find it difficult to take food because of oral lesions - anorexia and weight loss - affected lambs/kids suckling ewes or goats may result in lesions on teats, may predispose to secondary bacterial infection, resulting in mastitis - severe cases may show lesions in genitals, coronets (feet) and ears--> lesions in feet may result in lameness, lesions in scrotum may cause infertility - scabs drop off and underlying tissues heal - complications can result from secondary bacterial infections, or from invasion of lesions by fly larvae - malignant form of disease also observed in sheep

Question 86

vaccination- contagious echthyma

Answer 86

- prepared from suspension of scabs in glycerol saline and painted into small area of sacrificed skin inside the thigh, where localized lesion develops - under no circumstances should the vax be used on farms without problem with orf - should inspect lamb 1 week after vaccination for local reactions which indicates viability of vaccines - vaccination does not offer long-lasting immunity, about 1-2 yrs - vaccinate lambs/kids in problem flocks/herds - vaccinate pregnant ewes before lambing

Question 87

ORF in humans

Answer 87

- macro-papular lesions and large nodular lesions in finger, hand, arm, face and penis - secondary bacterial infections of lesions may cause complications

Question 88

Etiology- Sheeppox and goatpox

Answer 88

-members of genus Capripoxvirus

Question 89

Distribution- sheeppox and goatpox

Answer 89

-endemic in Africa, Asia, and parts of Europe

Question 90

Sheeppox and Goatpox

Answer 90

- once believed to be strains of the same viruses, genetic sequencing has demonstrated to be separate viruses - most strains are host specific and cause severe clinical disease in either sheep or goats, some strains are equally virulent in both species - SPV and GPV cannot be distinguished from each other with serological techniques, including viral neutralization - SPV and GPV are also closely related to lumpy skin disease virus in cattle, but no evidence LSDV causes disease in sheep and goats

Question 91

transmission SPV, GPV

Answer 91

- highly contagious viruses - viruses enters by respiratory tract, transmission is commonly by aerosol route (most important/common route of transmission) - spread can also occur through mucous membrane or abraded skin, especially by direct contact with contaminated iatrogenic materials - virus present in nasal and oral secretions for several weeks after infection - virus can survive in dry scabs for months - evidence for mechanical transmission by biting arthopods

Question 92

pathogenesis of SPV

Answer 92

- sheeppox is systemic disease - incubation period is followed by leukocyte-associated viremia - virus localizes in skin and other internal organs - deposition of immune-complexes results in severe necrotizing vasculitis develop in arterioles and post-capillary venules of the skin (Type-III hypersensitivity reaction), results in ischemic necrosis of dermis and overlying epidermis

Question 93

Forms of Sheeppox

Answer 93

- malignant | - benign

Question 94

Malignant form of sheeppox

Answer 94

- seen in lambs and susceptible nonnative breeds (Merino) - later on: - -pox lesions develop on the skin and buccal, respiratory, and urinary tract mucosa - -in malignant form, pox lesions extend to pharynx, larynx, lungs, vagina, abomasum, and spleen, secondary pneumonia, abortion rare - -cutaneous nodules are distributed all over the body, nodules occasionally become vesicular, pustular, and finally scab - -lesions heal leaving a star shaped scar, free of hair or wool - high mortality and case fatality rate

Question 95

benign form of sheppox

Answer 95

- more common in adults and resistant breeds | - only skin lesions occur or a very mild systemic reaction

Question 96

prevention and control of sheeppox

Answer 96

-notifiable/ reportable disease in most countries

Question 97

vaccination of sheeppox

Answer 97

- large variety of commercial vaccines, including subunit vax - killed vax elicit, at best temporary protection - live attenuated vaccines offer excellent protection, over a year

Question 98

Goatpox

Answer 98

- occurs in Africa, Asia, and parts of Europe - reportable disease - clinically similar to sheeppox - young kids suffer systemic disease- mucosae - milder form of disease seen in adults

Question 99

Lumpy skin disease

Answer 99

- member of genus Capripoxvirus - Distribution: Enzootic in sub-Saharan Africa and Middle east with recent incursion in Iraq - arthropod vector and direct contact - host- cattle, all ages and types susceptible - clinical findings: fever, multiple nodular lesions on skin and mucous membrane, lymphadenopathy

Question 100

Swinepox

Answer 100

- member of genus suipoxvirus - worldwide, widespread sporadic disease - host- pigs- generally benign with low mortality and low morbidity in older pigs, high case fatality in congenitally infected and very young suckling piglets

Question 101

Transmission swine pox

Answer 101

- direct contact associated with skin injury, virus can survive in scab for years - mechanical transmission by pig louse, Hematopinus suis, lice can carry virus for weeks or months - also mechanical transmission by flies and insects - evidence of transplacental infection of neonatal pigs

Question 102

Clinical signs of Swinepox

Answer 102

- typical pox lesions - lesions may occur anywhere, most obvious on skin of abdomen and inner aspects of thighs - exudative epidermitis (greasy pig disease) and secondary bacterial dermatitis occasionally occur as a sequel to swine pox - in severe infections, especially in congenitally-acquired pox infections (where piglets are born with or develop lesions over the entire body shortly after birth) lesions may occur in upper respiratory and digestive tracts

Question 103

control of swinepox

Answer 103

- eradication of lice from piggery | - no commercially available vax

Question 104

Fowlpox- etiology, hosts, distribution

Answer 104

- member of genus Avipoxvirus- first virus to be grown in embryonated eggs - hosts- highly infectious disease of poultry and turkeys - distribution- worldwide

Question 105

transmission of fowlpox virus

Answer 105

- virus is extremely resistant to desiccation, can survive in exfoliated scabs for long periods - routes of transmission: within a flock through minor wounds and abrasions in mouth, comb, wattles or skin as a result of fighting, pecking, or other injuries - -mechanically by mosquitoes, lice and ticks - -possibly by aerosol route

Question 106

clinical sings of fowlpox

Answer 106

- cutaneous form (dry form) - diphtheritic form (wet form) - ocular form

Question 107

cutaneous form of fowlpox (dry form)

Answer 107

- most common form - low mortality - probably results from injecting by biting arthopods, or mechanical transmission to injured or lacerated skin - small papules on comb, wattles or around beak - lesions occasionally develop on legs, feet, and around cloaca - nodules become yellowish and progress to a thick scab - sharp fall in egg production - in uncomplicated cases, affected birds recover in about 4 weeks

Question 108

Diphtheritic (wet form) of Fowlpox

Answer 108

- probably caused by droplet infection - involves infection of mucous membranes of mouth, pharynx, larynx, and sometimes trachea - necrotic psuedomembrane may cause death by asphyxiation - prognosis=poor

Question 109

ocular form of Fowlpox

Answer 109

- conjunctivitis | - cheesy exudate accumulates under eyelids

Question 110

Avipoxvirus- Bollinger bodies

Answer 110

-eosinophilic granular intracytoplasmic inclusion bodies

Question 111

Avipoxvirus- Borrel bodies

Answer 111

-occur inside Bollinger bodies, minute spherical bodies obtained by tryptic digestion of Bollinger bodies

Question 112

Fowlpox Control

Answer 112

- Vaccination- modified live fowlpox or pigeon pox virus vaccines of chicken embryo or avian cell culture origin commercially available, recombinant fowlpox vectored vax developed - control mosquitoes and other biting insects

Question 113

Unclassified Poxviruses- Ulcerative dermatitis of sheep

Answer 113

- transmitted through damaged skin or by coitus - lesions are usually ulcers with raw crater that bleeds easily, manifests in two clinical forms: lip and leg ulceration, venereal form - venereal form is transmitted ulceration of prepuce and penis or vulva, ram becomes unfit for natural breeding

Question 114

Diagnosis of poxviruses

Answer 114

- clinical signs - sampling material: scrapings from skin lesions, vesicular fluid, crusts, scabs - electron microscopy: characteristic morphology and size of poxviruses, orthopoxviruses are brick shaped, parapoxviruses are ovoid

Question 115

Histopathology of poxviruses

Answer 115

- presence of characteristic intracytoplasmic inclusion bodies - type B or Guarnieri inclusion bodies- most pox viruses, slightly basophilic and composed of viral particles and proteins aggregates - type A or ATI inclusion bodies- cowpox and ectromelia virus, strongly eosinophilic - Bollinger and Borrel bodies in avipoxvirus infection

Question 116

Other diagnosis of Poxviruses

Answer 116

- inoculation in embryonated egg - chorioallantoic membrane- pox lesions - parapoxviruses do not multiply in chicken embryo - serological assays such as ELISA - detection of poxvirus nucleic acid by PCR

Question 117

Family Circoviridae: Genuses

Answer 117

- Circovirus | - Gyrovirus

Question 118

Genus: Circovirus- diseases

Answer 118

- Porcine Circovirus type-1 (Non-pathogenic) | - Porcine circovirus type-2 (Post-Weaning multisystemic wasting syndrome) [PMWS]

Question 119

Genus Gyrovirus: diseases

Answer 119

-chicken infectious anemia virus

Question 120

Family Circoviridae

Answer 120

- viruses with circular single-stranded DNA genomes - genus Circovirus has circular, single-stranded ambisense DNA - genus gyrovirus has circular, single-stranded negative sense DNA - chicken infectious anemia virus has 12 trumpet-like structures that are less obvious in other circoviruses - virus replication occurs in actively dividing cell- viral DNA replication occurs in the nucleus - virions are very stable

Question 121

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

Answer 121

- etiology: caused by Porcine circovirus 2 (PCV2) - host: pigs. most common at 4-6 weeks of age or 2-3 post weaning - distribution: worldwide

Question 122

PMWS transmission

Answer 122

- wide-spread in most pig populations - fecal-oral transmission appears to be most common method of spread - vertical transmission (transplacental infection) occurs in swine

Question 123

PMWS pathogenesis

Answer 123

- individual to coalescing foci of granulomatous inflammation in lymphoid tissues, lungs, liver, kidney, heart, and intestines, sometimes with prominent "botryoid" (grape-like) intracytoplasmic inclusion bodies in virus infected macrophages - lymphoid depletion: loss of B and T cells

Question 124

Transplacental infection PMWS

Answer 124

- infection during first and second trimesters results in fetal death and resorption of aborted fetuses with severe cardiac congestion - infection during last trimester has minimal effect on fetuses

Question 125

PWMS clinical signs

Answer 125

- subclinical infection most common - common clinical signs= lethargy, progressive weight loss, cough, dyspnoea, slow growth, lymphadenopathy (swollen inguinal lymph nodes), diarrhea, skin discoloration, congenital tremors, less commonly icterus - co infection with porcine parvovirus, porcine reproductive, and respiratory virus (PRRSV), SIV, mycoplasma hyopneumoniae, and/or a variety of opportunistic bacteria may cause severe disease and more pronounced lesions

Question 126

Diagnosis of PMWS

Answer 126

-serological assays: most pigs are seropositive, therefore antigen detection is not of much value

Question 127

PMWS vax

Answer 127

- chimeric vaccines: use non-pathogenic porcine circovirus 1 (PCV-1) as a genetic backbone for expression of immunogenic capsid protein of PCV-2 - inactivated or baculovirus-expressed vax: virus-like particles that include capsid protein of PCV-2 are also available as vaccines - Sow vaccination antepartum

Question 128

porcine dermatitis and nephropathy syndrome (PDNS)

Answer 128

- associated with PCV2 - sporadic - reported in older piglets - findings: necrotizing skin lesions, necrotizing vasculitis, necrotizing and fibrinous glomerulonephritis

Question 129

Gyrovirus: Chicken infectious anemia

Answer 129

- host: highly contagious disease of young chickens (2-4 weeks of age), older chickens more resistant to clinical disease - transmission: virus shed in feces and feather dander, horizontal transmission through inhalation or oral exposure,virus also transmitted vertically through egg

Question 130

Pathogenesis of Chicken infectious anemia

Answer 130

- principal sites of replication: hemocytoblasts in bone marrow, precursor T cells in cortex of the thymus, dividing CD4 and CD8 cells in spleen , repllication in hemocytoblasts lead to anemia, replication in T cells cause immunosuppression - apoptin protein of CAV virus induces apoptosis and causes destruction of infected lymphocytes - immunosuppression and aplastic anemia: blood may be watery and clot slowly, result of thrombocytopenia - birds more vulnerable to secondary bacterial and fungal infections - virus replication in oviduct of chicken may be regulated by estrogen, allowing more efficient vertical transmission

Question 131

Chicken Infectious Anemia: Clinical signs and lesions

Answer 131

- chickens are anorectic, lethargic, depressed, reduced body weight gain, and pale - blood may be watery and clot slowly as a result of thrombocytopenia - PCV is low (in chicks, anemia is defined as PCV <27) - subcutaneous hemorrghages and skeletal hemorrhages, pale muscles - thymic atrophy - aplastic bone marrow - pale carcass, atrophied bursa

Question 132

Diagnosis: Chicken infectious Anemia

Answer 132

-examination of the blood: Low PCV, examination of blood for total erythrocytic count will reveal anemia, thrombocytopenia, blood watery and will clot slowly

Question 133

Vaccination- chicken infectious Anemia

Answer 133

- presence of antibodies in breeders greatly reduces vertical and horizontal transmission - protect progeny from vaccinated breeders from early infections by means of maternally derived antibodies - live vax are available for vax of anti-body negative breeder flocks before start of egg production

Question 134

Family Herpesviridae- morphology

Answer 134

-enveloped, spherical to pleomorphic

Question 135

Family Herpesviridae-genome

Answer 135

-double-stranded DNA genome

Question 136

Viral replication of Family Herpesviridae

Answer 136

- DNA replication and encapsidation- nucleus - viral envelope acquired by budding through inner layer of nuclear envelope - mature virions accumulate within vacuoles in cytoplasm and are released by exocytosis or cytolysis

Question 137

General Characteristics of Herpesviridae family

Answer 137

- do not survive well outside of the host - moist, cool environmental conditions promote extended survival of herpesviruses - latently infected animals= reservoir for transmission - persistent infection with periodic or continuous shedding occurs in all herpesvirus infections - some herpesviruses are oncogenic - reactivation of latent herpesvirus infection usually associated with stress caused by intercurrent infections, shipping, cold, crowding, or by administration of glucocorticoids

Question 138

Cellular characteristics of Herpesviridae

Answer 138

- eosinophilic intranuclear inclusion bodies - type A Cowdry bodies - formation of Syncytium

Question 139

Subfamily Alphaherpesvirinae

Answer 139

- Subfamily: Gammaherpesvirinae | - Subfamily: Betaherpesvirinae

Question 140

Properties of alpha-herpesviruses

Answer 140

- generally high cytopathic in cell culture - relatively short replication cycle - some, such as pseudorabies virus (suid herpesvirus1) have a broad host range, whereas most are highly restricted in their natural host range - many produce localized lesions, particularly in the skin or on the mucosae of the respiratory or genital tracts - generalized infections characterized by foci of necrosis in almost any organ or tissue are typical of infection of very young or immunocompromised animals - in pregnant animals, virus can cross placenta, leads to abortion, characterized by multifocal areas of necrosis in several fetal organs

Question 141

Subtypes of Bovine herpesvirus-1 (alphaherpesvirinae)

Answer 141

- there are three, we only care about 2 - BHV-1.1 (respiratory subtype) - BHV 1.2 (genital subtype)

Question 142

Transmission of Bovine herpesvirus-1 (alphaherpesvirinae)

Answer 142

- respiratory disease and conjunctivitis result from droplet transmission - genital disease may result from coitus or artificial insemination with infective semen

Question 143

Pathogenesis of Bovine herpesvirus-1 (alphaherpesvirinae)

Answer 143

- in 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 nuclei at the periphery of necrotic foci - intense inflammatory response within the necrotic mucosa, frequently with formation of overlying accumulation of fibrin and cellular debris (psuedomembrane) - life-long latent infection with periodic shedding occurs after BHV-1 infection - all seropositive animals considered potential carriers - virus can be reactivated from latency by corticosteroids or stress

Question 144

pathogenesis-signs of latency of Bovine herpesvirus-1 (alphaherpesvirinae)

Answer 144

- trigeminal nerve: respiratory disease with BHV-1 | - sciatic nerve- genital disease with BHV-1

Question 145

clinical signs of respiratory form of Bovine herpesvirus-1 (alphaherpesvirinae)

Answer 145

- red nose, necrotic rhinitis, dust pneumonia - inflamed nares give appearance of "red nose" due to hyperemia - grayish necrotic foci on mucous membrane - nasal discharge becomes more profuse and mucoprurulent - fibrinonecrotic rhinitis - uncomplicaated cases recover in 10-14 days - complications may result from secondary bacterial infection such as Mannheimia hemolytica and Pasteurella multocida (shipping fever) - death usually result of secondary bronchopneumonia - ocular form- conjunctivitis is common finding in typical "red nose", confined to conjunctiva, no lesions on cornea except diffuse edema

Question 146

Bovine Herpesvirus-1- abortion

Answer 146

-occurs as common sequel to natural infection (can occur 100 days after infection) -result of some modified-live virus vaccines given to pregnant animals -animals in contact with IBR susceptible pregnant animals -fetuses in second half of gestation have higher incidence of abortion, early embryonic death also possible often preceded by pustular vulvovaginitis

Question 147

Systemic disease in newborn calves- bovine herpesvirus-1

Answer 147

- severe in calves less than 10 days of age, often fatal | - infected in utero or right after birth

Question 148

Bovine herpesvirus 1-genital disease- female

Answer 148

- infectious pustular vaginitis - after coitus - frequent urination - tail usually held at elevated position, excessive tail switching - vaginal mucosa red and swollen - mild vaginal discharge - vulva swollen, red spots and discrete pustules may be noted

Question 149

Bovien herpesvirus 1- genital disease- male

Answer 149

-Balanoposthitis- inflammation and pustules in the mucosa of penis and prepuce

Question 150

Control of Bovine Herpesvirus 1

Answer 150

- vaccine - modified live vaccines, subunit, and inactivated vaccines available - parenteral and intranasal vax also available - both stimulate production of humoral antibodies - parenteral vaccine may cause abortion in pregnant cows - intranasal safe for pregnant cows

Question 151

Types of Bovine Herpesvirus-2

Answer 151

- bovine ulcerative mammillitis | - psuedo-lumpy skin disease

Question 152

Bovine Ulcerative Mammillitis

Answer 152

- cattle, heifers, usually within 2 weeks after calving - through direct contact and fomite-mediated, through trauma to skin - mechanical transmission by stable flies and other arthopods - in severe cases, teat is swollen and painful, skin is bluish, exudes serum, formation of raw ulcers - high incidence of mastitis

Question 153

Pseudo-lumpy skin Disease

Answer 153

- cattle infected - most commonly in southern Africa - mechanical transmission of virus occurs by arthropods - mild fever, followed by sudden appearance of skin nodules: a few, or many on the face, neck, back, and perineum

Question 154

Types of Porcine herpesvirus 1/suid herpesvirus 1

Answer 154

-Pseudorabies (Aujesky disease, Mad itch)

Question 155

Pseudorabies

Answer 155

- primarily disease of swine - diverse range of secondary hosts, including horses, cattle, sheep, goats, dogs, cats, feral species, can become infected and develop disease - humans refractor to infection

Question 156

Psuedorabies- transmission

Answer 156

- in primary host: recovered pigs act as primary reservoirs and are latent carrier of virus for life, rats can also act as reservoirs and transmit disease farm-to-farm - transmission routes of primary host- shed in saliva, nasal discharge, milk of infected pigs, licking, biting, aerosol, ingestion of contaminated caracass, water and feed - not shed by urine or feces, - secondary host transmission dogs and cats- ingestion of infected pig carcass/meat or rodents, cattle- direct contact with infected pigs: oral and nasal routes

Question 157

Pathogenesis of Pseudorabies

Answer 157

- primary site of viral replication is upper respiratory tract - virus replicates in tonsils and nasopharynx - virus spreads via lymphatics to regional lymph nodes, where replication continues - brief viremia associated with virulent strains, with localization of virus in different organs - virus spread in CNS: via axons of cranial nerves, continues to spread in CNS, preference for neurons of pons and medulla - CNS lesions: ganglioneuritis, nonsuppurative meningoencephalitis, perivascular cuffing

Question 158

Clinical signs of Pseudorabies in pigs

Answer 158

- non-immune piglets: ~100% mortality rate - nonimmune pregnant sows: ~50% abortion rate - older pigs, growers, and adult pigs: mild disease, mortality rate <2% - pruritis (itching) dominant feature in secondary hosts, rare in pigs

Question 159

Clinical signs of pseudorabies in piglets born to non-immune sows

Answer 159

most susceptible, signs of CNS disease (incoordination of hindlimbs, fitting, tremors and paddling) more commonly seen

Question 160

Clinical signs of Pseudorabies in weaned pigs and growing pigs

Answer 160

-CNS signs reduced, increase in respiratory signs

Question 161

Clinical signs of Pseudorabies in nonimmune pregnant sows

Answer 161

- infection before 30th day of gestation results 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 162

Necropsy findings of Pseudorabies in pigs

Answer 162

- gross lesions often absent or minimal | - serous to fibrinous rhinitis is common and necrotic tonsillitis

Question 163

Secondary hosts of Pseudorabies

Answer 163

- ruminants - dogs - cats - goats, sheep, horses - intense pruritus - hyperacute, rapid progress, high mortality

Question 164

Pseudorabies- cattle

Answer 164

- mad itch - intense pruritis (itching) - cattle may become frenzied - progressive involvement of CNS, stage of paralysis, ataxia - death from respiratory failure

Question 165

Pseudorabies- dogs and cats

Answer 165

- dogs: frenzy associated with pruritis, self mutilation, paralysis of jaws and pharynx with drooling of saliva, plaintive howling, unlike rabies dogs do not tend to attack - cats: disease progress so rapidly that pruritis may not be observed

Question 166

Vaccination- Pseudorabies in pigs

Answer 166

- vaccination of swine in enzootic areas reduce losses - vaccination does 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-mutant, live-attenuated, and inactivated vaccines are available

Question 167

Equine herpesvirus-1

Answer 167

- endemic in horse populations around the world - transmission: inhalation of infected aerosols, direct or indirect contact with nasal discharges, aborted fetuses, placenta, or placental fluids - latency: latent form can reside in host tissues of CNS (neuron cell bodies (specifically trigeminal ganglia) and lymph system (leukocytes, more specifically lymphocytes) without causing any clinical symptoms of disease - when host is immunosuppressed; the virus is then reactivated, causing disease, or shedding of virus once again

Question 168

Pathogenesis of equine herpesvirus-1

Answer 168

- EHV-1 infects epithelial cell - in respiratory epithelial goes into latent phase in neurons in the trigeminal ganglia where it can be reactivated - if virus spreads to lymph nodes, it can be reactivated in latently infected circulating T-lymphocytes - virus can infect leukocytes and can cause a cell-associated viremia, can spread to and infect endothelial cells lining blood vessels leading to vasculitis, thrombosis, and ischemia - in uterus= abortion - in CNS=encephalomyelitis

Question 169

What is the principal route of EHV-1 infection?

Answer 169

-respiratory tract

Question 170

More pathogenesis of equine herpesvirus-`

Answer 170

- respiratory tract is principal route of infection - following infection of epithelial cells, EHV-1 infects endothelial cells in lamina propria - virus infected mononuclear cells and T lymphocytes subsequently appear in drainage lymph nodes, released into circulation producing viremia - following infection of respiratory epithelium, latent infections are established in circulating T lymphocytes and tigeminal ganglionic neurons - reactivation results in shedding of virus from nasal epithelium and probably uterine infection - central lesion responsible for respiratory, reproductive and CNS effects is infection of endothelial cells, leads to vascular necrosis, thrombus formation, and subsequent death to tissues serviced by these blood vessels (ischemia) - 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 CNS signs or abortion

Question 171

effects of pathogenesis of EHV-1

Answer 171

- immunosuppression - respiratory disease- younger horses, rhinopneumonitis - encephalomyelopathy (EHM, equine herpesvirus myeloencephalopathy), may affect horses of any age or breed - reproductive form- majority of abortions occur between 8-10 months of gestation - reproductive efficiency not compromised - cases of abortion usually sporadic - if large numbers of susceptible mares are exposed to the aborted conceptus, extensive outbreaks of abortion occur - natural immunity to EHV-1 may last 2-3 years, thus explaining why "abortion storms" tend to display three year cycles

Question 172

Equine Herpes virus 4

Answer 172

- Equine Viral Rhinopneumonitis - antigenically related to EHV-1 - transmission: most infections are sporadic, mostly observed in horses under two years of age - -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 173

Pathogenesis and clinical signs of equine herpesvirus-4

Answer 173

- causes less severe tissue destruction than EHV-1 - rarely causes abortion when it infects pregnant mares - rarely results in viremia - death is rare - clinical signs: infection results primarily in upper respiratory tract disease (rhinopharyngitis and tracheobronchitis)

Question 174

vaccine for EHV-1 and EHV-4

Answer 174

- ideal vaccine should prevent early infection of suckling foals as well as latency of infection in pregnant mares - live attenuated and inactivated commercial EHV-1 vaccines are available, including combined products that include both EHV-1 and EHV-4 - immunity is short-lived

Question 175

General properties: Family Parvoviridae

Answer 175

- viruses are very stable | - disinfection of contaminated premises is difficult

Question 176

Replication of Parvoviridae

Answer 176

- replication occurs in nucleus of dividing cells | - infection leads to large intranuclear inclusion bodies

Question 177

Genus Parvovirus

Answer 177

- virus replication occurs only in cells that pass through mitotic S phase (actively dividing cells) - cannot replicate in stationary cells, reply on enzymes of actively dividing cells (mitosis)

Question 178

Human Parvovirus

Answer 178

- human parvovirus B19 - different from parvovirus in dogs and cats, no evidence of transmission of B19 to humans from dogs or cats or vice versa

Question 179

Feline Panleukopenia

Answer 179

- feline distemper, feline infectious enteritis - etiology: feline parvovirus - host: highly contagious, often fatal disease of cats, severe in kittens

Question 180

epidemiology of feline panleukopenia

Answer 180

- virus is ubiquitous because of its contagious nature and capacity for persistence in environment - virtually all cats are exposed and infected within first year of life - unvaccinated kittens that acquire maternal antibodies are protected up to three months of age - most infections are subclinical, as much as 75% of unvaccinated healthy cats have demonstrable antibody titers by 1 year of age - cats can shed the virus in their urine or feces for a maximum of 6 weeks after recovery - FPV is maintained in population by environmental persistence rather than prolonged viral shedding - owners losing kitten to feline panleukopenia should not introduce new kitten into household without having it vaccinated - most common in kittens

Question 181

Transmission of feline panleukopenia

Answer 181

- 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 182

Hallmark of Panleukopenia

Answer 182

- more severe the leukopenia, poorer the prognosis - profound leukopenia involves destruction of all WBC elements, including lymphocytes, neutrophils, monocytes, and platelets - thrombocytopenia (due to damage of bone marrow) may accompany leukopenia

Question 183

Feline Panleukemia- pathogenesis

Answer 183

- enteritis: virus selectively damages replicating cells deep in the crypts of the intestinal mucosa - loss of cells from tip of villus continues as normal process, however since virus replicates and destroys cells of crypts, there is no replacement of the lost absorptive cells at the tips of the villi with cells from the crypts - results in: shortening of intestinal villi, marked villus blunting and fusion, malabsorption, and diarrhea

Question 184

In utero infection- feline panleukopenia

Answer 184

- early in utero infection in pregnant queen can result in: early fetal death and resorption with infertility, 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 of the same litter

Question 185

CNS infection- feline panleukopenia

Answer 185

- optic nerve and retina are susceptible to damage by FPV during prenatal or early neonatal development - cerebellar damage most commonly reported - cerebella hypoplasia is usually observed in fetus during the last 2 weeks of pregnancy and first 2 weeks of life - lysis of mitotic cells of the external germinal layer - impaired cerebellar development - ataxia

Question 186

Disseminated Intravascular Coagulation- Feline panleukopenia

Answer 186

- kittens with FPV infection also susceptible to secondary bacterial infection - Gram-negative endotoxemia, with or without bacteremia is common sequalae of system 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 187

Clinical signs of feline panleukopenia- intestinal crypt epithelium

Answer 187

- villous collapse, enteritis | - diarrhea

Question 188

clinical signs of feline panleukopenia- lymph node, thymus

Answer 188

- germinal center depletion, apoptosis of lymphocytes, thymic atrophy - lymphopenia

Question 189

clinical signs of feline panleukopenia- bone marrow

Answer 189

- stem stell depletion | - neutropenia (later thrombocytopenia and anemia)

Question 190

clinical signs of feline panleukopenia- all cells in fetus

Answer 190

- fetal death | - loss of pregnancy

Question 191

clinical signs of feline panleukopenia- developing cerebellum

Answer 191

- cerebellar hypoplasia | - cerebellar ataxia

Question 192

clinical signs- general feline panleukopenia

Answer 192

- fever, depression, anorexia, rough coat, repeated vomiting, profuse, persistent and frequently bloody diarrhea - severe dehydration, hypothermia, sudden death from complications with secondary bacterial infections, dehydration, DIC - queens infected or vaccinated during pregnancy may show infertility or abortion of dead or mummified fetuses - cerebellar hyperplasia, kittens ataxic, usually not apparent until kitten begins to walk at 3-4 weeks - retinal degeneration in infected kittens

Question 193

diagnosis- feline panleukopenia

Answer 193

- hematology: leukopenia, neutropenia more consistent than lymphopenia, total WBC counts <2000 cells/uL associated with poorer prognosis - fecal viral antigen testing using immunochromatography test kit or ELISA- results may remain positive up to two weeks following MLV vax

Question 194

serological testing- feline panleukopenia

Answer 194

- single sample antibody titers do not distinguish between active infection or past exposure - paired serum samples, first one as soon as possible during illness, second one 2 weeks after - fourfold rise in titer= indicative of acute infection - virus neutralization test commonly used

Question 195

Treatment FPV

Answer 195

- good nursing care, fluid therapy, withholding in early stages to lessen vomition and slow down mitotic activity of cells - broad spectrum antibiotics to prevent secondary infection

Question 196

control of FPV

Answer 196

- large catteries: strict hygiene and quarantine of incoming cats - disinfection: inactivated by bleach, 4% formaldehyde, and 1% glutaraldehyde in 10 mins at room temp

Question 197

vaccination FPV

Answer 197

- attenuated (modified) live vaccines (MLV) - inactivated vaccines - MLV should not be administered to pregnant, sick, immunosupressed cats or kittens less than 4 weeks old

Question 198

Canine parvovirus-1

Answer 198

- mild to inapparent illness (diarrhea) in dogs, especially in young pups less than 8 weeks old - not important

Question 199

canine parvovirus 2

Answer 199

- one of the most common infectious diseases of dogs - three antigenic variants: CPV-2a, CPV-2b, CPV-2c - CPV-2b and CPV-2c more common in north America

Question 200

epidemiology of canine parvovirus 2

Answer 200

- virus is highly contagious, very stable in environment - resistant to many common detergents and disinfectants - infectious CPV can persist indoors at room temp for at least 2 months

Question 201

transmission of Canine Parvovirus-2

Answer 201

- oro-nasal exposure to contaminated feces - in utero infection - contact with virus- contaminated fomites (environment, personnel, equipment)

Question 202

Canine parvovirus-2 clinical findings

Answer 202

- enteritis - myocarditis - panleukopenia

Question 203

Enteritis CPV-2

Answer 203

- infects germinal epithelium of intestinal crypts, causing destruction and collapse of epithelium - hemorrhagic diarrhea- severe - no replacement of cells lost from tip of villus- collapse and necrosis of intestinal villi - villi shortened - ballooned small intestine - ingesta visible through small intestine wall

Question 204

myocarditis-canine parvovirus 2

Answer 204

- develops from infection in utero or from pups <6 wks of age - myocardial necrosis with acute cardiopulmonary failure - sudden death, or die after a short period of clinical signs (dyspnea, crying, retching)

Question 205

diagnosis- canine parvovirus

Answer 205

- serology (antibody detection) is not best method, most dogs vaccinated or previously exposed - SNAP parvo test

Question 206

vaccination- canine parvovirus

Answer 206

-because of potential damage by CPV to myocardial or cerebellar cells, inactivated are used rather than modified live- vaccines in pregnant dogs or colstrum-deprived puppies vaccinated before 6-8 wks of age

Question 207

Canine parvovirus- tamiflu

Answer 207

- MOA not clear - speculation is that neuraminidase is an important enzyme used by pathogenic bacteria invading through the protective mucous barrier of GI tract, by this process indirectly facilitate CPV infection - tamiflu may act on bacterial neuraminidase

Question 208

Porcine parvovirus

Answer 208

- infectious cause of reproductive failure throughout the world - SMEDI- stillbirth, mummification, embryonic death, infertility - most herds, large portion of gilts are naturally infected before they conceive, and hence are immune

Question 209

transmission of porcine parvovirus

Answer 209

- oronasal in non-immune pregnant sow followed by transplacental transmittion - death at different stages of pregnancy is typical of PPV infection

Question 210

pathogenesis of PPV

Answer 210

- oronasal infection of non-immune pregnant dam followed by viremia - after maternal infection for the virus to reach the fetus

Question 211

clinical signs of PPV

Answer 211

- increase in mummified fetuses after normal gestation | - abortions are common

Question 212

time of infection is critical for PPV

Answer 212

- embryo/fetus (<30 days): dies and reabsorbed, 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, also mount an immune response and survival in-utero

Question 213

PPV in boars, sows, and gilts

Answer 213

-mostly inapparent or subclinical infection

Question 214

diagnosis- porcine parvovirus

Answer 214

-serological tests are of limited value, virus is so widespread in swine, vaccination may interfere

Question 215

porcine parvovirus- vaccination/immunity

Answer 215

- PPV can cause persistent infection with periodic shedding of virus - vaccinate all susceptible breeding stock twice, 2 weeks apart, several weeks before breeding - gilts may be naturally infected several weeks before breeding, by mingling with older breeding stock that may be shedding virus

Question 216

Subfamily: Alphaherpesvirinae

Answer 216

- Canine herpesvirus-1 | - hemorrhagic disease of puppies (fading puppy syndrome)

Question 217

Hemorrhagic disease of puppies

Answer 217

- canine herpesvirus 1, subfamily: Alphaherpesvirinae - in dogs, wild canids - highly fatal, generalized hemorrhagic disease of puppies

Question 218

transmission of canine herpesvirus-1 in neonates

Answer 218

- contact with infected oral, nasal, or vaginal secretions of dams - contact with secretions of littermates - in utero transmission - from passage through birth canal - contact with infected fomites (rare)

Question 219

transmission of canine herpesvirus 1 in older dogs

Answer 219

- venereal transmission | - contact with saliva, nasal discharge, or urine of infected dogs or puppies

Question 220

Pathogenesis of canine herpesvirus in puppies-in utero

Answer 220

-in utero: abortion, stillbirth, infertility, if puppy survives most develop systemic CHV-1 infections within 9 days of birth

Question 221

Pathogenesis of herpesvirus in puppies- systemic

Answer 221

- systemic neonatal infection: pups less than 1 week are most susceptible to fatal generalized infection - initial replication occurs in nasal epithelium, tonsils, and pharynx - mucosal invasion followed by leukocyte (macrophage) associated viremia - virus replication in endothelial cells - diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in several organs - thrombocytopenia, DIC (disseminated intravascular coagulation)

Question 222

pathogenesis of herpesvirus in puppies- CNS infection

Answer 222

- menigoencephalitis commonly occurs in oro-nasally infected neonates - virus may travel up nerve axons to CNS - puppies die from systemic illness before neurologic signs evident

Question 223

Factors governing systemic neonatal infections- herpesvirus- in puppies

Answer 223

- body temperature is critical - CHV-1 replicates optimally at 33C, the temp of the outer genital and respiratory tract - hypothalamic thermoregulatory centers of the pup are not fully operative until 2-3 weeks of age - pup critically dependent on ambient temp and maternal contact for maintenance of normal body temp - more severe the hypothermia, more severe and rapid the course of the disease

Question 224

Maternal immunity- canine herpesvirus

Answer 224

- maternal antibodies provide protection | - pups born from seronegative bitches are highly vulnerable to severe form of disease

Question 225

Clinical signs of herpesvirus in puppies

Answer 225

- painful crying, abdominal pain, anorexia, dyspnea, passing soft, odorless greenish stool, no elevation in body temp - animals that survive systemic disease develop persistent neurological signs, such as ataxia and blindness

Question 226

Adult genital herpesvirus infection

Answer 226

- bitches: usually 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 dogs: balanoposthitis

Question 227

adult respiratory herpesvirus infection

Answer 227

-older dogs: mild respiratory infection (rhinitis and pharyngitis)

Question 228

adult ocular herpesvirus infection

Answer 228

-conjunctivitis

Question 229

control of herpesvirus in puppies

Answer 229

- reduce hypothermia by providing heated whelping boxes, or placing puppies under infrared lamps - low prevalence of severe illness in pups (<20%) and paucity of clinical signs in adult animals has resulted in lack of availability of vaccines

Question 230

Feline herpesvirus-1

Answer 230

- feline rhinotracheitis - one of the most common causes of infectious respiratory disease in cats - other major cause is feline calicivirus

Question 231

transmisison of feline herpesvirus

Answer 231

- FHV-1 shed primarily in ocular, nasal, and oral secretions - spread is largely by direct contact with infected cat - aerosol route= not important - natural routes of infection are nasal, oral, and conjunctiva - virtually all recovered cats become latently infected carriers - reactivation (from stress, steroids) may cause viral shedding in oronasal and conjunctival secretions

Question 232

Pathogenesis of feline rhinotracheitis

Answer 232

- virus replication takes place predominantly in the mucosa of 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 233

clinical signs of feline rhinotracheitis

Answer 233

- kittens (up to 4 weeks) - severe upper respiratory disease - extensive rhinotracheitis - fatal bronchopneumonia (from secondary bacterial infection) may develop - conjunctivitis, ulcerative keratitis - cats more than 6 months: mild or subclinical disease in older kittens

Question 234

Clinical signs of feline rhinotracheitis in pregnant queen

Answer 234

- abortion, around 6th week of pregnancy - no evidence that virus crosses the placenta - may be due to severe systemic effects of illness, and not direct effect of virus

Question 235

feline rhinotracheitis- other signs

Answer 235

- conjunctivitis, hyperemia, serous ocular discharge - ulcerative keratitis - ulcers on tongue of cat common in feline calicivirus infection, rare in cats with FHV-1 infection - severe necrohemorrhagic rhinitis - multifocal necrohemorrhagic palatitis

Question 236

vaccination- feline herpesvirus 1

Answer 236

- three types of FHV-1 and FCV vaccines available - modified live virus- parenterally - MLV intranasally - inactivated vaccine parenterally

Question 237

Avian alphaherpesvirinae

Answer 237

- infectious laryngotracheitis (Gallid herpesvirus 1) | - Marek's disease (Gallid herpesvirus 2)

Question 238

Etiology- Gallid herpesvirus 1

Answer 238

-highly contagious infection of chickens

Question 239

Transmission of Infectious laryngotracheitis

Answer 239

- mostly by inhalation - droplets to conjunctiva - occasionally by ingestion - recovered and vaccinated chickens can also serve as carriers of ILT and can shed the virus when 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, domesticated dogs and wild animals that feed on improperly disposed dead birds

Question 240

Pathogenesis of infectious laryngotracheitis

Answer 240

- severe laryngotracheitis in affected birds - extensive diptheritic membrane formation can form a second tube for the length of the trachea, blocks air passage, death from asphyxia - ILT virus can persist in infected birds, trigeminal ganglion is the target for ILT virus latency - hemmorhagic or necrotizing hemorrhagic tracheitis

Question 241

Clinical signs- severe form of infectious laryngotracheitis

Answer 241

- severe respiratory distress, head shaking with coughing is characteristic - neck is raised and the head extended during inspiration- pump handle respiration - couch may result in expulsion of bloody mucous, blood may stain beak and neck feathers

Question 242

Clinical signs- low virulence strains of infectious laryngotracheitis

Answer 242

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

Question 243

diagnosis of infectious laryngotracheitis

Answer 243

- necropsy finding: tracheal plug (diphtheritic membrane) - detection of typical intranuclear inclusions in respiratory tissues - virus isolation in nasal mucosa - virus grows well in CAM of embryonated eggs

Question 244

Control of infectious laryngotracheitis

Answer 244

-in event of outbreak, slaughter infected birds, disinfect premises

Question 245

vaccination- infectious laryngotracheitis

Answer 245

- types of vaccine available 1. chick embryo origin, 2. tissue culture origin, 3. pox-vectored recombinant vaccine - CEO vaccines have capability of reverting to virulence and causing full-blown ILT signs, induce better immunity - TCO vaccine only given by eye drop, does not spread significantly or revert to virulence, level of immunity limited - these are applied via eye drop or mass vaccination by water spray

Question 246

farm biosecurity for ILT

Answer 246

-implementation of farm biosecurity measures

Question 247

Marek's disease (Gallid herpesvirus 2)

Answer 247

- very important disease of poultry - etiology: gallid herpesvirus 2 - hosts: chickens are most important natural host, turkeys, quails, pheasants susceptible - transmission: highly contagious, inhalation of infectious feather debris, chicken dander or dust, cell free viruses release from 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 248

pathotypes of gallid herpesvirus 2

Answer 248

- mild: mMDV: mostly associated with neural MD, disease is preventable with HVT (turkey herpesvirus vaccine) - virulent [vMDV] associated with high incidence of neural and visceral lymphomas, viruses are oncogenic in HVT vaccinated chickens, disease preventable with bivalent vaccines - very virulent plus [vv+MDV]: associated with high incidence of neural and visceral lymphomas, viruses are oncogenic in chickens vaccinated with bivalent vaccines

Question 249

Pathogenesis of Marek's disease

Answer 249

- fully productive infection occurs in feather follicle epithelium, infected T cells appear to be "Trojan horse" by which MDV enters the feather- follicle epithelium - inhalation of virus--> initial round of replication in epithelial cells--> macrophage associated viremia --> virus detectable in spleen, thymus, and bursa of Fabricius--> productive restrictive infection: Cytolytic replication primarily in B cells and later in activated CD4+ T cells-->non-productive latent infection in CD4+ T cells--> nonproductive neoplastic transformation: some latently infected CD4+ T cells

Question 250

Fully productive Marek's disease infection

Answer 250

- 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 251

Productive- restrictive infection Marek's disease

Answer 251

- 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 immunosupression

Question 252

non-productive infection-Marek's disease

Answer 252

- viral genome persists in T cells (primarily CD4+) | - no antigens expressed

Question 253

non-productive neoplastic transformation- Marek's disease

Answer 253

- some latently infected T cells undergo neoplastic transformation - new agent, MATSA (Marek's disease associated tumor specific antigen) appears in transformed T cells

Question 254

Marek's disease- pathogenesis

Answer 254

- virus is slowly cytopathic and remain associated with cells - cell free infectious viruses are almost impossible to obtain, except in dander from feather follicles - Lesions in Marek's disease result from infiltration and in situ proliferation of transformed T lymphocytes - cell lysis also results in marked inflammatory response

Question 255

Clinical features of Marek's disease

Answer 255

- neurolymphomatosis - visceral lymphomatosis - ocular lymphomatosis - cutaneous lymphomatosis

Question 256

neurolymphomatosis

Answer 256

- enlargement of nerve trunks - lose striations - edematous, grey, or yellowish in appearance - lameness, droopy wings, paresis of legs, limberneck, torticollis, incoordination

Question 257

Visceral lymphomatosis

Answer 257

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

Question 258

Ocular lymphomatosis- Marek's disease

Answer 258

- greying of iris (grey eye, cat's eye, pearl eye) of one or both eyes - interference with normal pupilar constriction and dilation - partial or total blindness

Question 259

Cutaneous lymphomatosis- Marek's disease

Answer 259

- plucking of feathers reveal nodular lesions on skin | - enlarged feather follicles (commonly termed leukosis)

Question 260

Vaccination of Marek's disease

Answer 260

- most widely used vaccine consists of turkey herpesvirus (HVT) - bivalent vaccines consisting of HVT and either the SB-1 or 301B/1 strains of Gallid herpesvirus 3 (Serotype 2, avirulent strain) - most protective commercial vaccine currently available appears to be CV1988/Rispens an attenuated Marek's disease virus strain that is also commonly mixed with HVT at vaccination

Question 261

Subfamily: Betaherpesvirinae

Answer 261

- slow replicating viruses - chronic infections - infected cells often enlarged (cytomegaly) - maintained in latent form in secretory glands (salivary glands) and lymphoreticular cells (macrophages, lymphocytes) - often associated with continuous viral excretion

Question 262

Inclusion body rhinitis

Answer 262

- porcine herpesvirus 2, porcine cytomegalovirus (PCMV), subfamily Betaherpesvirinae - pigs, severe in piglets - primarily spread through inhalation, transplacental transmission

Question 263

Pathogenesis- inclusion body rhinitis

Answer 263

- widespread petechiae and edema - most common in thoracic cavity and subcutaneous tissues - primary site of viral replication: nasal mucous glands, epithelial cells of upper respiratory tract - in some neonates, bone marrow damage, anemia - endothelial cell damage and necrosis: petechial hemorrhages and edema - still birth, mummification, neonatal death - infected cells are enlarged and posses intranuclear inclusion bodies, especially in nasal glands

Question 264

Clinical signs- inclusion body rhinitis

Answer 264

- in suckling pigs <3 weeks old, mucopurulent rhinitis - infected neonatal piglets appear weak, anemic or stunted, edema around throat and tarsal joints - fetal mummification, stillbirths, neonatal deaths, failure of piglets to thrive have been associated with infection of naive, pregnant sows - subclinical disease in older animals

Question 265

Subfamily: Gammaherpesvirinae

Answer 265

- 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 in lymphoid tissue - some members can cause lymphoid tumors

Question 266

Malignant Catarrhal fever

Answer 266

- bovine malignant catarrh - etiology: malignant catarrhal fever is caused by viruses in subfamily Gammaherpesvirinae - at least 10 MCF viruses have been recognized - two most important MCF viruses are: Alcephaline herpesvirus-1 (Wildebeest- associated MCF), ovine herpesvirus 2- known as sheep associated MCF

Question 267

Wildebeest associated MCF [Alcephaline herpesvirus-1 (AHV-1)]

Answer 267

- transmitted to cattle from wildebeest - Wildebeest associated MCF occurs in most African countries, where cattle and wildebeest comingle - AHV-1 does not cause any disease in principal host,, Wildebeest - Wildebeest-associated MCF is Epizootic and seasonal

Question 268

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

Answer 268

- worldwide - transmitted from sheep to cattle - goats can also act as source of infection to cattle - occurs yearround in cattle, moderate increase during lambing season - usually sporadic, occasional outbreaks

Question 269

Where MCF is found

Answer 269

-in Africa, predominantly where cattle are in close contact with blue or black Wildebeest, outside Africa, usually associated with contact between sheep and susceptible species

Question 270

Transmission of MCF between Wildebeest

Answer 270

-horizontal and occasional intrauterine transmission in Wildebeest, inapparent infection

Question 271

Transmission of MCF from Wildebeest to cattle

Answer 271

- AHV-1 present in nasal and ocular secretions of young wildebeest in cell-free state - direct or close contact, inhalation of aerosol with young wildebeest - direct or close contact with wildebeest during calving (virus in cell-free state in young) - virus in cell-associated form in adult wildebeest, rarely transmitted from adults

Question 272

Transmission of MCF between sheep

Answer 272

- respiratory (aerosol) - transplacental= rare - contact with nasal secretons

Question 273

transmission from sheep to cattle

Answer 273

- not known | - presumably inhalation or ingestion

Question 274

MCF infection in Wildebeest and Sheep

Answer 274

- inapparent infection | - virus transmitted Wildebeest to Wildebeest, sheep to sheep

Question 275

MCF cattle

Answer 275

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

Question 276

Pathogenesis MCF

Answer 276

- infection followed by cell associated viremia - lymphoid proliferation and infiltration - necrotizing vasculitis - vascular lesions- gross lesions, such as epithelial erosions and conjunctivitis

Question 277

Clinical signs of MCF

Answer 277

- peracute form: sudden death, characteristic signs of head and eye form may not occur, high fever, acute gastroenteritis - 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 278

Head and Eye form of MCF

Answer 278

- early stages: reddened eyelids, bilateral corneal opacity, crusty muzzle/nares, nasal discharge, salivation - later stages: erosions on the tongue, hard palate, necrosis and erosion of the buccal papillae

Question 279

Necropsy finding MCF

Answer 279

- zebra striping: bovine, colon severe longitudinal linear congestion of mucosa - erosions in hard palate

Question 280

Control of Malignant Catarrhal fever

Answer 280

- seperation of cattle from wildebeest and sheep | - incidence to low to justify development of vaccine

Question 281

African swine fever- etiology and hosts

Answer 281

- sole member of family Asfarviridae - only known DNA arbovirus - host: all breeds and types of domestic pigs and European wild boar - inapparent infection in warthogs, bush pigs, and giant forest hots, which act as reservoirs - OIE list A disease

Question 282

Geographical distribution of African Swine fever

Answer 282

- endemic in most of sub-Saharan Africa, and island of Sardinia (Italy) - recent outbreaks in Eastern Europe and Russia

Question 283

ASF stability

Answer 283

- can survive at least 30 days in pens - very resistant to wide range of pH - survive in chilled carcass - highly resistant to putrefaction - remains viable for long periods in blood, feces and tissues, uncooked or undercooked pork products - can multiply in vectors

Question 284

transmission of ASF

Answer 284

- vector: soft ticks (Ornithodorous spp, specifically O moubata in Africa) - Ornithodorus are biological vectors of the virus - virus replicates in the tick, resulting in trans-stadial, transovarial, and sexual tick to tick transmission (male-to-female) - infected ticks may live for several years and be capable of transmitting virus to pigs during each blood meal - reservoir hosts: warthog, giant forest hog, bush pig - significant viremia in juvenile warthogs - adult warthogs have no viremia, but virus is in various lymphoid tissues

Question 285

Sylvatic cycle transmission of ASF

Answer 285

- transmission of ASF virus between warthogs and soft ticks= sylvatic cycle - ASF virus is maintained in a sylvatic cycle involving 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 286

domestic cycle of African Swine Fever

Answer 286

- bite of infected tick - direct contact with infected animal (oronasal spread) - indirect contact with 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 287

Pathogenesis of African swine fever

Answer 287

- primarily hemorrhages and apoptosis - Leukopenia, lymphopenia, thrombocytopenia - apoptosis of host cells by p54 protein encoded by virus, ASF infected macrophages release cytokines and apoptotic mediators, apoptosis of both lymphocytes and mononuclear phagocytic cells - related to hemorrhages: vascular damage, 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 288

Peracute ASF

Answer 288

-pigs may die suddenly

Question 289

Clinical signs of Acute form of ASF

Answer 289

- high fever - cyanotic skin blotching on ears, tail, lower legs, or hams - respiratory distress - diarrhea: initially mucoid, later may become bloody - abortion: sometimes first event seen in outbreak - death

Question 290

Chronic form of ASF

Answer 290

- emaciation and stunting - swollen joints - ulcers and reddened or raised necrotic skin foci - pneumonia - enlarged friable spleen (blackberry jam spleen) - cutaneous lesions - fibrinous pericarditis and myocardial hemorrhage

Question 291

Immunity to African Swine fever

Answer 291

- although infected pigs produce virus-specific antibodies, sera from infected pigs do not neutralize the virus, humoral immune response does not seem to have substantial protective value - vaccine development= unsuccessful

Question 292

ASF prevention

Answer 292

- awareness of pig farmers and field personnel - pigs should be kept in well-constructed pig sties under hygienic conditions with controlled entry to piggery - movement of pigs inside the country and especially across international borders should be controlled - pigs should not be fed swill that might contain remains of pigs, to ensure safety, swill should be boiled for 30 mins and cooled before feeding

Question 293

during an ASF outbreak

Answer 293

- immediately notify authorities (Animal health department) - infected and suspected infected farms must be placed in quarantine - no movements of pigs or any products of pig origin should be allowed - all infected and 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 294

General characteristics of family: Papillomaviridae

Answer 294

- can transform cultured cells - produce papillomas (warts) on skin and mucous membranes of most animal species - warts are benign neoplasms hyperplastic epithelial outgrowths that generally regress spontaneously - are usually species and site specific - serologic cross-reactivity has not been detected among papillomaviruses of different species - papillomas may progress to malignancy, which in part is a property of specific virus strains ex: HPV causing cervical carcinoma in women

Question 295

Replication of papillomaviruses

Answer 295

-linked to the growth and differentiation of cells in stratified squamous epithelium of the skin and some mucous membranes

Question 296

Oncogenic Papillomaviruses

Answer 296

- in benign warts, papillomavirus DNA is episomal, not integrated into host cell DNA and persists as autonomously replicating episome - in papillomavirus-induced malignant cancers, the viral DNA is integrated into that of the host, probably necessary for malignant transformation

Question 297

Bovine Papillomatosis- host and transmission

Answer 297

- host: cattle - warts more commonly seen in cattle than in any other domestic animal - natural bovine papillomavirus infection of horses may occur after exposure of horses to cattle - transmission: between animals by contaminated fomites, sexual transmission of venereal warts in cattle

Question 298

Fibropapilloma

Answer 298

- mostly caused by Bovine papillomavirus types 1,2, and 5 - papillomas have a fibrous core covered to a variable depth with stratified squamous epithelium, outer layers hyperkeratinized - lesions vary from small, firm nodules to large cauliflower-like growths - grayish to black in color and rough and spiny to the touch - common on udder and teats, and on head, neck and shoulders - may also occur in omasum, vagina, vulva, penis, and anus

Question 299

Cutaneous papillomas

Answer 299

- bovine papillomaviruses type 3 - lack fibrous core - usually flat with broad base, unlike more usual fibropapillomas that protrude and are often pedunculated

Question 300

Bracken fern and bovine papillomaviruses

Answer 300

- bovine papillomavirus 4 can cause transient papillomas in the alimentary tract - ingestion of bracken fern can result in transition to invasive carcinoma of the alimentary tract - in cattle that eat bracken fern, papillomavirus types 1 and 2 may also contribute to the syndrome- "enzootic hematuria"- characterized by hematuria and/or urinary bladder cancer

Question 301

Treatment of bovine papillomatosis

Answer 301

- surgical excision, or cryosurgery with liquid nitrogen - topical agents- Podophyllin and undiluted medical grade DMSO - bovine interferon-alpha - wart vaccine

Question 302

Canine Oral Papillomatosis

Answer 302

- contagious, self-limiting disease affecting the oral cavity of dogs - warts usually begin on lips, can spread to buccal mucosa, tongue, palate, and pharynx, may become cauliflower-like - do not extend below epiglottis or into esophagus - lesions typically regress spontaneously - very rarely progress to squamous cell carcinoma

Question 303

Clinical signs of Canine Oral Papillomatosis

Answer 303

- 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 304

Treatment of Canine Oral Papillomatosis

Answer 304

- surgical excision, cryosurgery, electrosurgery | - autogenous vaccines

Question 305

Equine Sarcoids

Answer 305

- Sarcoids commonly occur in horses, donkeys, and mules between 1 to 6 years of age - most common neoplasm in horses - locally invasive benign fibroblastic skin tumors - associated with bovine papillomaviruses 1 or 2 - sarcoids do not metastasize, they may persist for life, locally invasive, recur after surgical removal

Question 306

Transmission of equine sarcoids

Answer 306

- mode of transmission not confirmed - flies as vectors? - fomites, transmitted via stable management practices

Question 307

Equine sarcoids- lesions

Answer 307

- commonly occur in traumatized areas - single or multiple - growths may reach size of man's fist, bulge under skin - may become ulcerated

Question 308

Treatment of equine sarcoids

Answer 308

-cryotherapy, surgical or laser excision, local immune modulation, local radiotherapy

Question 309

Adenoviridae- morphology

Answer 309

- non-enveloped, hexagonal in outline - 12 vertex penton capsomers each with fiber protrude from surface of capsid - intranuclear inclusion bodies formed, contain large numbers of virons, often in para-crystalline arrays

Question 310

Properties of Adenoviridae

Answer 310

- many adenoviruses aggutinate red blood cells - hemagglutination occurs when tips of penton fibers bind to surface receptors on red blood cells - some viruses oncogenic in lab animals - relatively stable in environment, inactivated easily by common disinfectants - most of adenoviruses have narrow host ranges

Question 311

Pathogenesis of adenovirus

Answer 311

- many cause acute respiratory or gastroenteric disease of varying severity - mostly subclinical infections - immunosuppression - long periods of latency- virus persists in lymphoid and other tissues, reactivated in immunocompromised animals, can be highly pathogenic in immunodeficient animals - oncogenesis: under specialized conditions, some adenoviruses have been shown to be oncogenic

Question 312

Adenovirus, Genus: Mastadenovirus

Answer 312

- mammalian adenoviruses | - single penton fiber projects from each vertex

Question 313

Adenovirus, Genus: Aviadenovirus

Answer 313

- avian adenoviruses | - each penton fiber is bifurcated, appears as two fibers extending from each penton base

Question 314

Infectious Canine Hepatitis (ICH, Rubarth's disease)

Answer 314

- Canine adenovirus-1 (CAV-1) - acute infection: CAV-1 is found on all secretions and excretions - afterwards, virus shed in urine for at least 6-9 months - oronasal transmission - spread through contact with: secretions/excretions of infected dog, contaminated fomites, ectoparasites

Question 315

Sites of virus replication- Infectious Canine Hepatitis

Answer 315

- marcrophages - Kupffer cells - Hepatocytes - Vascular endothelium of different organs, including CNS - parenchymal cells of organs and tissues - liver, kidneys, spleen, and lungs, are main target organs

Question 316

Pathogenesis of Infectious Canine Hepatitis

Answer 316

- 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 317

Pathogenic changes in infectious canine hepatitis

Answer 317

- Cirrhosis in chronic cases - kidney: acute infection, glomerulonephritis - chronic kidney lesions may result from immune-complex reactions after recovery from acute or subclinical disease - chronic glomerulonephritis

Question 318

Ocular lesions in Infectious Canine Hepatitis

Answer 318

- Corneal edema (blue eye) - occurs in about 20% of natural infections - less than 1% of dogs after S/C MLV-CAV-1 vaccination - seen in dogs during recovery or chronic cases

Question 319

How corneal edema develops

Answer 319

- CAV-1 antibody production increases, formation of viral- antibody immune complexes - results in complement activation, neutrophil chemotaxis - causes extensive damage to corneal endothelium - disruption of intact corneal endothelium allows aqueous to enter cornea - accumulation of edematous fluid within corneal stroma results in corneal edema

Question 320

Complications from infectious canine hepatitis

Answer 320

- disseminated intravascular coagulation, from damage to endothelium and inability of disease liver to remove clotting factors - bacterial pyelonephritis resulting from renal damage

Question 321

Clinical signs of infectious canine hepatitis

Answer 321

- most frequent in dogs less than 1 year of age - concurrent parvoviral or distemper infection worsens the prognosis - unvaccinated dogs of all ages are susceptible - most infections asymptomatic - signs vary from slight fever to death

Question 322

Peracute cases of infectious canine hepatitis

Answer 322

-severely infected dogs become moribund and die within a few hours after onset of clinical signs

Question 323

acute cases of infectious canine hepatitis

Answer 323

- clinical signs that survive acute viremic phase - fever of 104 F, depression, anorexia - vomiting - occasionally abdominal pain, abdominal tenderness and hepatomegaly - intense hyperemia or petechiae hemorrhages of the oral mucosa - pale mucous membrane, jaundice - enlarged tonsils, swollen lymph nodes - subcutaneous edema of head, neck, and trunk - CNS involvement unusual, typically result of vascular injury, convulsions may appear from forebrain damage - icterus uncommon in early acute phase of ICH - corneal edema and anterior uveitis occur when clinical recovery begins - blue eye - fine spots of bleeding iin mucous surface of dog

Question 324

Diagnosis of infectious canine hepatitis

Answer 324

- clinical signs - necropsy and histopathology: paint-brush hemorrhages on gastric serosa, lymph nodes, thymus, pancreas, and sub-q tissues, centrilobular necrosis in liver with neutrophilic and monocytic infiltration, and hepatocellular intranuclear inclusions, greyish white foci may be seen in kidney cortex of recovered dogs with chronic disease - biochemistry and hematology: leukopenia persists through febrile period, increased ALT and AST due to hepatic injury, proteinuria, prolonged prothrombin time, thrombocytopenia - virus isolation in urine, blood, tissue homogenates, etc

Question 325

Treatment of infectious canine hepatitis

Answer 325

- treatment symptomatic and supportive | - goals of therapy are to limit secondary bacterial invasion, support fluid balance,and control hemorrhagic tendencies

Question 326

immunity

Answer 326

- recovered animals immune to systemic form of disease - maternal antibodies interfere with active immunization until puppies are 9-12 weeks of age - attenuated CAV-1 live vaccines have produced transient unilateral or bilateral opacities of the cornea, vaccine virus can cause mild subclinical interstitial nephritis, may be shed in urine, discontinued in many countries - CAV-2 attenuated virus strains provide cross protection against CAV-1, CAV-2 attenuated vaccines are preferentially used because they have little tendency to produce corneal opacities or uveitis, virus not shed in urine

Question 327

Canine Infectious Tracheobronchitis (kennel cough)

Answer 327

- self-limiting upper respiratory disease of dogs - caused by CAV-2 and Bordetella bronchiseptica (primary pathogen) - highly contagious, via aerosolized droplets - stress, unfavorable conditions increases severity of disease

Question 328

Uncomplicated ITB

Answer 328

- prominent clinical sign is paroxysms of harsh, dry coughing, followed by etching and gagging - cough sounds like a "honk" - rhinitis, serous nasal discharges, sometimes conjunctivitis

Question 329

Complicated ITB

Answer 329

- severe pneumonia or bronchopneumonia | - life threatening

Question 330

Treatment of Canine Infectious Tracheobronchitis

Answer 330

- antitussives (cough supressant) when used in conjunction with bronchodilators - immunity- modified-live virus vaccines against distemper, parainfluenza and CAV-2, which also provides protection against CAV-1

Question 331

Equine Adenovirus

Answer 331

- Equine Adenovirus-1, Equine Adenovirus-2 - most equine adenovirus infections are asymptomatic or present as mild upper or lower respiratory tract disease - 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, foals invariably die within 3 months of age - Clinical signs in SCID foals: severe bronchiolitis and pneumonia, respiratory distress and related signs

Question 332

Chicken Adenovirus

Answer 332

- inclusion body hepatitis | - egg drop syndrome '76

Question 333

duck adenovirus

Answer 333

-hepatitis (rare)

Question 334

quail adenovirus

Answer 334

-bronchitis

Question 335

turkey adenovirus

Answer 335

- hemorrhagic enteritis | - egg drop syndrome

Question 336

pheasant adenovirus

Answer 336

-marble spleen disease