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virology > exam 2 > Flashcards

exam 2 Flashcards

1
Q

polymerase chain reaction-PCR

A

amplification of viral genome/DNA

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2
Q

The steps of how PCR works

A
  1. denaturation
  2. annealing
  3. extension/elongation
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3
Q

Real Time/Quantitative PCR

A
  • 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
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4
Q

DNA sequencing

A

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

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5
Q

Next Generation Sequencing

A

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

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6
Q

Metagenomics

A
  • 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
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7
Q

Phylogenetic analysis

A

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

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8
Q

microarray

A
  • 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
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9
Q

Advantage of microarrays

A

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

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10
Q

Treatment of Viral Diseases

A
  • antiviral drugs
  • immune system stimulation
  • synthesize antibodies or administration of natural anti-serum (antibodies)
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11
Q

antiviral drugs

A
  • 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
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12
Q

immune system stimulation

A

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

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13
Q

Acyclovir

A
  • 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
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14
Q

What is acyclovir used to treat?

A
  • herpesvirus infections in humans
  • feline herpesvirus-1 induced corneal ulcers
  • equine herpesvirus-1 induced encephalomyelitis
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15
Q

What is acyclovir a synthetic nucleoside analog of?

A

-deoxyguanosine

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16
Q

mechanism of action of acyclovir

A
  • 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
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17
Q

Why is acyclovir non-toxic to uninfected host cell?

A
  • 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
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18
Q

Amantadine

A

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

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19
Q

mechanism of antiviral action of Amantadine

A
  • 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
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20
Q

Neuraminidase inhibitors

A
  • inhibitors of neuraminidase enzyme synthesized by influenza A and B
  • Oseltamivir (tamiflu)
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21
Q

Neuraminidase inhibitors: mechanism of action

A
  • 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
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22
Q

targets for anti-retroviral therapy

A
  • inhibit fusion
  • inhibit reverse transcriptase
  • inhibit protease
  • inhibit integrase
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23
Q

nucleoside analog reverse transcriptase inhibitors (NRTIs)

A
  • Zidovudine (ZDV) or AZT (azidothymadine)

- ddI (didanosine)

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24
Q

ZDV/AZT

A
  • 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
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25
Q

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

A

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

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26
Q

What is required to cleave HIV polyproteins into functional proteins?

A

-proteases

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27
Q

How do protease inhibitors work?

A
  • 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
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28
Q

Types of live attenuated virus vaccines

A
  • 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
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29
Q

replicating virus vaccines

A
  • produced from inactivated whole virions

- vaccines produced from purified native viral proteins

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30
Q

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

A

YASSS

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31
Q

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

A
  • 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
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32
Q

Prevention and control of virus- isolation

A
  • applies to animals known to be ill with contagious disease

- separate animals if showing clinical signs and/or test positive by diagnostic test

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33
Q

prevention and control- quarantine

A
  • 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
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34
Q

prevention and control-quarantine and culling

A
  • separate and restrict movement of animals
  • culling (killing) of animals
  • proper disposal of culled animals
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35
Q

prevention and control-decontamination

A

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

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36
Q

prevention and control-sterilization

A

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

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37
Q

prevention and control-disinfection

A
  • 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
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38
Q

prevention and control-antisepsis

A

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

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39
Q

prevention and control- sterilization methods

A
  • 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
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40
Q

Family of Pox virus

A

-Poxviridae

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41
Q

Subfamily of Pox virus

A
  • Chordopoxvirinae

- 8 genera–> diseases in humans, birds animals

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42
Q

relevant genuses of pox virus

A
  • orthopoxvirus
  • parapoxvirus
  • avipoxvirus
  • capripoxvirus
  • leporipoxvirus
  • suipoxvirus
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43
Q

shape of poxviruses

A
  • 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
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44
Q

What are the two infectious poxvirus particles?

A
  • intracellular mature virus (IMV)

- extracellular enveloped virus

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45
Q

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

A

-two membranes: envelope, inner membrane

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46
Q

What causes the EEV form to have two membranes?

A

-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

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47
Q

How do intracellular particles come out of the host cell?

A
  • through disruption

- only have inner membrane

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48
Q

structure of poxvirus

A
  • 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
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49
Q

poxvirus geneome

A
  • 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
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50
Q

replication and release of poxviruses

A
  • 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
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51
Q

stability of poxviruses

A
  • 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
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52
Q

transmission of poxviruses

A
  • skin: contact with broken or lacerated skin
  • respiratory route: aerosol (sheep-pox)
  • mechanically transmitted: biting arthopods (Myxoma virus and avipoxviruses)
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53
Q

Pathogenesis and immunity of poxviruses

A
  • highly epitheliotropic- causes cutaneous skin lesions
  • causes systemic diseases in birds and wild animals
  • most are host specific
  • orthopoxviruses- infect wide range of species
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54
Q

spread of poxvirus

A
  • following introduction into body, usually gains access to systemic circulation via lymph
  • secondary viremia disseminates virus back to skin and other target organs
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55
Q

skin lesions in poxvirus infection

A
  • 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
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56
Q

Cowpox

A
  • orthopoxvirus
  • distribution: endemic only in Europe and Asia
  • hosts: cattle, wild and domestic cats, humans, zoo animals, etc
  • reservoir host: rodents
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57
Q

transmission of cowpox-cattle

A
  • 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
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58
Q

economic importance of cowpox-cattle

A

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

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59
Q

clinical findings cowpox- cattle

A
  • 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
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60
Q

cowpox in cats- transmission

A
  • 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
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61
Q

cowpox in cats- clinical signs (primary lesions)

A
  • 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
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62
Q

cowpox in cats- secondary lesions

A
  • 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
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63
Q

cowpox in humans- transmission

A
  • 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
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64
Q

clinical signs of cowpox in humans

A
  • 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
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65
Q

monkeypox in humans

A

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

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66
Q

transmission of monkeypox in humans

A
  • 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
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67
Q

Psuedocowpox-definition

A
  • viral skin disease that causes mild sores on the teats and udders of cattle
  • can also infect humans- Milker’s nodule
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68
Q

Psuedocowpox-etiology

A

member of genus Parapoxvirus

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69
Q

Psuedocowpox- epidemiology

A

-reported from most countries

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70
Q

transmission of psuedocowpox

A
  • 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
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71
Q

pathogenesis of psuedocowpox

A

-characterized by hyperplasia of squamous epithelium

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72
Q

clinical signs-pseudocowpox

A
  • infections generally mild

- papule on teat

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73
Q

acute lesions- psuedocowpox

A
  • 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
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74
Q

chronic lesions– pseudocowpox

A
  • commences as erythema
  • yellow-gray, soft scruffy scabs which are rubbed off during milking
  • skin is corrugated
  • no pain
  • lesions may persist for months
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75
Q

diagnosis- psuedocowpox

A
  • 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
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76
Q

Ddx psuedocowpox

A
  • 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)
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77
Q

treatment psuedocowpox

A
  • removal of scabs
  • burn the scabs to prevent environmental contamination
  • application of an emollient ointment before milking
  • application of astringent preparation after milking
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78
Q

prevention of pseudocowpox

A
  • disinfection- iodophor teat dip
  • isolation and treatment of infected cows
  • reduce teat trauma, injuries to skin of teat predisposes to infection
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79
Q

Psuedocowpox in humans (Milker’s Nodule)

A
  • 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
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80
Q

Contagious Ecthyma- etiology

A

-Orf virus, genus parapoxvirus

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81
Q

Contagious Ecthyma- host

A

sheep and goats, primarily labs and goat kids

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82
Q

Distribution of contagious Ecthyma

A

-worldwide

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83
Q

Transmission Contagious Ecthyma

A
  • 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
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84
Q

Pathogenesis of Contagious Ecthyma

A
  • 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
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85
Q

clinical signs: contagious ecthyma

A
  • 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
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86
Q

vaccination- contagious echthyma

A
  • 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
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87
Q

ORF in humans

A
  • macro-papular lesions and large nodular lesions in finger, hand, arm, face and penis
  • secondary bacterial infections of lesions may cause complications
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88
Q

Etiology- Sheeppox and goatpox

A

-members of genus Capripoxvirus

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89
Q

Distribution- sheeppox and goatpox

A

-endemic in Africa, Asia, and parts of Europe

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90
Q

Sheeppox and Goatpox

A
  • 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
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91
Q

transmission SPV, GPV

A
  • 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
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92
Q

pathogenesis of SPV

A
  • 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
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93
Q

Forms of Sheeppox

A
  • malignant

- benign

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94
Q

Malignant form of sheeppox

A
  • 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
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95
Q

benign form of sheppox

A
  • more common in adults and resistant breeds

- only skin lesions occur or a very mild systemic reaction

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96
Q

prevention and control of sheeppox

A

-notifiable/ reportable disease in most countries

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97
Q

vaccination of sheeppox

A
  • large variety of commercial vaccines, including subunit vax
  • killed vax elicit, at best temporary protection
  • live attenuated vaccines offer excellent protection, over a year
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98
Q

Goatpox

A
  • 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
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99
Q

Lumpy skin disease

A
  • 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
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100
Q

Swinepox

A
  • 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
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101
Q

Transmission swine pox

A
  • 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
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102
Q

Clinical signs of Swinepox

A
  • 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
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103
Q

control of swinepox

A
  • eradication of lice from piggery

- no commercially available vax

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104
Q

Fowlpox- etiology, hosts, distribution

A
  • member of genus Avipoxvirus- first virus to be grown in embryonated eggs
  • hosts- highly infectious disease of poultry and turkeys
  • distribution- worldwide
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105
Q

transmission of fowlpox virus

A
  • 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
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106
Q

clinical sings of fowlpox

A
  • cutaneous form (dry form)
  • diphtheritic form (wet form)
  • ocular form
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107
Q

cutaneous form of fowlpox (dry form)

A
  • 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
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108
Q

Diphtheritic (wet form) of Fowlpox

A
  • 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
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109
Q

ocular form of Fowlpox

A
  • conjunctivitis

- cheesy exudate accumulates under eyelids

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110
Q

Avipoxvirus- Bollinger bodies

A

-eosinophilic granular intracytoplasmic inclusion bodies

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111
Q

Avipoxvirus- Borrel bodies

A

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

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112
Q

Fowlpox Control

A
  • 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
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113
Q

Unclassified Poxviruses- Ulcerative dermatitis of sheep

A
  • 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
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114
Q

Diagnosis of poxviruses

A
  • 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
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115
Q

Histopathology of poxviruses

A
  • 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
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116
Q

Other diagnosis of Poxviruses

A
  • 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
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117
Q

Family Circoviridae: Genuses

A
  • Circovirus

- Gyrovirus

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118
Q

Genus: Circovirus- diseases

A
  • Porcine Circovirus type-1 (Non-pathogenic)

- Porcine circovirus type-2 (Post-Weaning multisystemic wasting syndrome) [PMWS]

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119
Q

Genus Gyrovirus: diseases

A

-chicken infectious anemia virus

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120
Q

Family Circoviridae

A
  • 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
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121
Q

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

A
  • etiology: caused by Porcine circovirus 2 (PCV2)
  • host: pigs. most common at 4-6 weeks of age or 2-3 post weaning
  • distribution: worldwide
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122
Q

PMWS transmission

A
  • wide-spread in most pig populations
  • fecal-oral transmission appears to be most common method of spread
  • vertical transmission (transplacental infection) occurs in swine
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123
Q

PMWS pathogenesis

A
  • 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
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124
Q

Transplacental infection PMWS

A
  • 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
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125
Q

PWMS clinical signs

A
  • 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
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126
Q

Diagnosis of PMWS

A

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

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127
Q

PMWS vax

A
  • 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
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128
Q

porcine dermatitis and nephropathy syndrome (PDNS)

A
  • associated with PCV2
  • sporadic
  • reported in older piglets
  • findings: necrotizing skin lesions, necrotizing vasculitis, necrotizing and fibrinous glomerulonephritis
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129
Q

Gyrovirus: Chicken infectious anemia

A
  • 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
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130
Q

Pathogenesis of Chicken infectious anemia

A
  • 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
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131
Q

Chicken Infectious Anemia: Clinical signs and lesions

A
  • 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
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132
Q

Diagnosis: Chicken infectious Anemia

A

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

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133
Q

Vaccination- chicken infectious Anemia

A
  • 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
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134
Q

Family Herpesviridae- morphology

A

-enveloped, spherical to pleomorphic

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135
Q

Family Herpesviridae-genome

A

-double-stranded DNA genome

136
Q

Viral replication of Family Herpesviridae

A
  • 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
137
Q

General Characteristics of Herpesviridae family

A
  • 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
138
Q

Cellular characteristics of Herpesviridae

A
  • eosinophilic intranuclear inclusion bodies
  • type A Cowdry bodies
  • formation of Syncytium
139
Q

Subfamily Alphaherpesvirinae

A
  • Subfamily: Gammaherpesvirinae

- Subfamily: Betaherpesvirinae

140
Q

Properties of alpha-herpesviruses

A
  • 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
141
Q

Subtypes of Bovine herpesvirus-1 (alphaherpesvirinae)

A
  • there are three, we only care about 2
  • BHV-1.1 (respiratory subtype)
  • BHV 1.2 (genital subtype)
142
Q

Transmission of Bovine herpesvirus-1 (alphaherpesvirinae)

A
  • respiratory disease and conjunctivitis result from droplet transmission
  • genital disease may result from coitus or artificial insemination with infective semen
143
Q

Pathogenesis of Bovine herpesvirus-1 (alphaherpesvirinae)

A
  • 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
144
Q

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

A
  • trigeminal nerve: respiratory disease with BHV-1

- sciatic nerve- genital disease with BHV-1

145
Q

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

A
  • 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
146
Q

Bovine Herpesvirus-1- abortion

A

-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

147
Q

Systemic disease in newborn calves- bovine herpesvirus-1

A
  • severe in calves less than 10 days of age, often fatal

- infected in utero or right after birth

148
Q

Bovine herpesvirus 1-genital disease- female

A
  • 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
149
Q

Bovien herpesvirus 1- genital disease- male

A

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

150
Q

Control of Bovine Herpesvirus 1

A
  • 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
151
Q

Types of Bovine Herpesvirus-2

A
  • bovine ulcerative mammillitis

- psuedo-lumpy skin disease

152
Q

Bovine Ulcerative Mammillitis

A
  • 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
153
Q

Pseudo-lumpy skin Disease

A
  • 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
154
Q

Types of Porcine herpesvirus 1/suid herpesvirus 1

A

-Pseudorabies (Aujesky disease, Mad itch)

155
Q

Pseudorabies

A
  • 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
156
Q

Psuedorabies- transmission

A
  • 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
157
Q

Pathogenesis of Pseudorabies

A
  • 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
158
Q

Clinical signs of Pseudorabies in pigs

A
  • 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
159
Q

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

A

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

160
Q

Clinical signs of Pseudorabies in weaned pigs and growing pigs

A

-CNS signs reduced, increase in respiratory signs

161
Q

Clinical signs of Pseudorabies in nonimmune pregnant sows

A
  • 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
162
Q

Necropsy findings of Pseudorabies in pigs

A
  • gross lesions often absent or minimal

- serous to fibrinous rhinitis is common and necrotic tonsillitis

163
Q

Secondary hosts of Pseudorabies

A
  • ruminants
  • dogs
  • cats
  • goats, sheep, horses
  • intense pruritus
  • hyperacute, rapid progress, high mortality
164
Q

Pseudorabies- cattle

A
  • mad itch
  • intense pruritis (itching)
  • cattle may become frenzied
  • progressive involvement of CNS, stage of paralysis, ataxia
  • death from respiratory failure
165
Q

Pseudorabies- dogs and cats

A
  • 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
166
Q

Vaccination- Pseudorabies in pigs

A
  • 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
167
Q

Equine herpesvirus-1

A
  • 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
168
Q

Pathogenesis of equine herpesvirus-1

A
  • 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
169
Q

What is the principal route of EHV-1 infection?

A

-respiratory tract

170
Q

More pathogenesis of equine herpesvirus-`

A
  • 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
171
Q

effects of pathogenesis of EHV-1

A
  • 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
172
Q

Equine Herpes virus 4

A
  • 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
173
Q

Pathogenesis and clinical signs of equine herpesvirus-4

A
  • 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)
174
Q

vaccine for EHV-1 and EHV-4

A
  • 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
175
Q

General properties: Family Parvoviridae

A
  • viruses are very stable

- disinfection of contaminated premises is difficult

176
Q

Replication of Parvoviridae

A
  • replication occurs in nucleus of dividing cells

- infection leads to large intranuclear inclusion bodies

177
Q

Genus Parvovirus

A
  • 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)
178
Q

Human Parvovirus

A
  • 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
179
Q

Feline Panleukopenia

A
  • feline distemper, feline infectious enteritis
  • etiology: feline parvovirus
  • host: highly contagious, often fatal disease of cats, severe in kittens
180
Q

epidemiology of feline panleukopenia

A
  • 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
181
Q

Transmission of feline panleukopenia

A
  • cats are infected oro-nasally by exposure to infected animals, their feces, secretions, or contaminated fomites
  • in utero-transmission occurs
  • mechanical transmission by flies
182
Q

Hallmark of Panleukopenia

A
  • 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
183
Q

Feline Panleukemia- pathogenesis

A
  • 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
184
Q

In utero infection- feline panleukopenia

A
  • 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
185
Q

CNS infection- feline panleukopenia

A
  • 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
186
Q

Disseminated Intravascular Coagulation- Feline panleukopenia

A
  • 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
187
Q

Clinical signs of feline panleukopenia- intestinal crypt epithelium

A
  • villous collapse, enteritis

- diarrhea

188
Q

clinical signs of feline panleukopenia- lymph node, thymus

A
  • germinal center depletion, apoptosis of lymphocytes, thymic atrophy
  • lymphopenia
189
Q

clinical signs of feline panleukopenia- bone marrow

A
  • stem stell depletion

- neutropenia (later thrombocytopenia and anemia)

190
Q

clinical signs of feline panleukopenia- all cells in fetus

A
  • fetal death

- loss of pregnancy

191
Q

clinical signs of feline panleukopenia- developing cerebellum

A
  • cerebellar hypoplasia

- cerebellar ataxia

192
Q

clinical signs- general feline panleukopenia

A
  • 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
193
Q

diagnosis- feline panleukopenia

A
  • 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
194
Q

serological testing- feline panleukopenia

A
  • 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
195
Q

Treatment FPV

A
  • 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
196
Q

control of FPV

A
  • large catteries: strict hygiene and quarantine of incoming cats
  • disinfection: inactivated by bleach, 4% formaldehyde, and 1% glutaraldehyde in 10 mins at room temp
197
Q

vaccination FPV

A
  • attenuated (modified) live vaccines (MLV)
  • inactivated vaccines
  • MLV should not be administered to pregnant, sick, immunosupressed cats or kittens less than 4 weeks old
198
Q

Canine parvovirus-1

A
  • mild to inapparent illness (diarrhea) in dogs, especially in young pups less than 8 weeks old
  • not important
199
Q

canine parvovirus 2

A
  • 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
200
Q

epidemiology of canine parvovirus 2

A
  • 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
201
Q

transmission of Canine Parvovirus-2

A
  • oro-nasal exposure to contaminated feces
  • in utero infection
  • contact with virus- contaminated fomites (environment, personnel, equipment)
202
Q

Canine parvovirus-2 clinical findings

A
  • enteritis
  • myocarditis
  • panleukopenia
203
Q

Enteritis CPV-2

A
  • 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
204
Q

myocarditis-canine parvovirus 2

A
  • 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)
205
Q

diagnosis- canine parvovirus

A
  • serology (antibody detection) is not best method, most dogs vaccinated or previously exposed
  • SNAP parvo test
206
Q

vaccination- canine parvovirus

A

-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

207
Q

Canine parvovirus- tamiflu

A
  • 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
208
Q

Porcine parvovirus

A
  • 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
209
Q

transmission of porcine parvovirus

A
  • oronasal in non-immune pregnant sow followed by transplacental transmittion
  • death at different stages of pregnancy is typical of PPV infection
210
Q

pathogenesis of PPV

A
  • oronasal infection of non-immune pregnant dam followed by viremia
  • after maternal infection for the virus to reach the fetus
211
Q

clinical signs of PPV

A
  • increase in mummified fetuses after normal gestation

- abortions are common

212
Q

time of infection is critical for PPV

A
  • 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
213
Q

PPV in boars, sows, and gilts

A

-mostly inapparent or subclinical infection

214
Q

diagnosis- porcine parvovirus

A

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

215
Q

porcine parvovirus- vaccination/immunity

A
  • 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
216
Q

Subfamily: Alphaherpesvirinae

A
  • Canine herpesvirus-1

- hemorrhagic disease of puppies (fading puppy syndrome)

217
Q

Hemorrhagic disease of puppies

A
  • canine herpesvirus 1, subfamily: Alphaherpesvirinae
  • in dogs, wild canids
  • highly fatal, generalized hemorrhagic disease of puppies
218
Q

transmission of canine herpesvirus-1 in neonates

A
  • 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)
219
Q

transmission of canine herpesvirus 1 in older dogs

A
  • venereal transmission

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

220
Q

Pathogenesis of canine herpesvirus in puppies-in utero

A

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

221
Q

Pathogenesis of herpesvirus in puppies- systemic

A
  • 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)
222
Q

pathogenesis of herpesvirus in puppies- CNS infection

A
  • 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
223
Q

Factors governing systemic neonatal infections- herpesvirus- in puppies

A
  • 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
224
Q

Maternal immunity- canine herpesvirus

A
  • maternal antibodies provide protection

- pups born from seronegative bitches are highly vulnerable to severe form of disease

225
Q

Clinical signs of herpesvirus in puppies

A
  • 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
226
Q

Adult genital herpesvirus infection

A
  • 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
227
Q

adult respiratory herpesvirus infection

A

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

228
Q

adult ocular herpesvirus infection

A

-conjunctivitis

229
Q

control of herpesvirus in puppies

A
  • 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
230
Q

Feline herpesvirus-1

A
  • feline rhinotracheitis
  • one of the most common causes of infectious respiratory disease in cats
  • other major cause is feline calicivirus
231
Q

transmisison of feline herpesvirus

A
  • 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
232
Q

Pathogenesis of feline rhinotracheitis

A
  • 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
233
Q

clinical signs of feline rhinotracheitis

A
  • 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
234
Q

Clinical signs of feline rhinotracheitis in pregnant queen

A
  • 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
235
Q

feline rhinotracheitis- other signs

A
  • 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
236
Q

vaccination- feline herpesvirus 1

A
  • three types of FHV-1 and FCV vaccines available
  • modified live virus- parenterally
  • MLV intranasally
  • inactivated vaccine parenterally
237
Q

Avian alphaherpesvirinae

A
  • infectious laryngotracheitis (Gallid herpesvirus 1)

- Marek’s disease (Gallid herpesvirus 2)

238
Q

Etiology- Gallid herpesvirus 1

A

-highly contagious infection of chickens

239
Q

Transmission of Infectious laryngotracheitis

A
  • 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
240
Q

Pathogenesis of infectious laryngotracheitis

A
  • 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
241
Q

Clinical signs- severe form of infectious laryngotracheitis

A
  • 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
242
Q

Clinical signs- low virulence strains of infectious laryngotracheitis

A
  • 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
243
Q

diagnosis of infectious laryngotracheitis

A
  • 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
244
Q

Control of infectious laryngotracheitis

A

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

245
Q

vaccination- infectious laryngotracheitis

A
  • 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
246
Q

farm biosecurity for ILT

A

-implementation of farm biosecurity measures

247
Q

Marek’s disease (Gallid herpesvirus 2)

A
  • 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
248
Q

pathotypes of gallid herpesvirus 2

A
  • 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
249
Q

Pathogenesis of Marek’s disease

A
  • 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
250
Q

Fully productive Marek’s disease infection

A
  • 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
251
Q

Productive- restrictive infection Marek’s disease

A
  • 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
252
Q

non-productive infection-Marek’s disease

A
  • viral genome persists in T cells (primarily CD4+)

- no antigens expressed

253
Q

non-productive neoplastic transformation- Marek’s disease

A
  • some latently infected T cells undergo neoplastic transformation
  • new agent, MATSA (Marek’s disease associated tumor specific antigen) appears in transformed T cells
254
Q

Marek’s disease- pathogenesis

A
  • 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
255
Q

Clinical features of Marek’s disease

A
  • neurolymphomatosis
  • visceral lymphomatosis
  • ocular lymphomatosis
  • cutaneous lymphomatosis
256
Q

neurolymphomatosis

A
  • enlargement of nerve trunks
  • lose striations
  • edematous, grey, or yellowish in appearance
  • lameness, droopy wings, paresis of legs, limberneck, torticollis, incoordination
257
Q

Visceral lymphomatosis

A
  • 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
258
Q

Ocular lymphomatosis- Marek’s disease

A
  • 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
259
Q

Cutaneous lymphomatosis- Marek’s disease

A
  • plucking of feathers reveal nodular lesions on skin

- enlarged feather follicles (commonly termed leukosis)

260
Q

Vaccination of Marek’s disease

A
  • 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
261
Q

Subfamily: Betaherpesvirinae

A
  • 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
262
Q

Inclusion body rhinitis

A
  • porcine herpesvirus 2, porcine cytomegalovirus (PCMV), subfamily Betaherpesvirinae
  • pigs, severe in piglets
  • primarily spread through inhalation, transplacental transmission
263
Q

Pathogenesis- inclusion body rhinitis

A
  • 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
264
Q

Clinical signs- inclusion body rhinitis

A
  • 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
265
Q

Subfamily: Gammaherpesvirinae

A
  • 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
266
Q

Malignant Catarrhal fever

A
  • 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
267
Q

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

A
  • 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
268
Q

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

A
  • 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
269
Q

Where MCF is found

A

-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

270
Q

Transmission of MCF between Wildebeest

A

-horizontal and occasional intrauterine transmission in Wildebeest, inapparent infection

271
Q

Transmission of MCF from Wildebeest to cattle

A
  • 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
272
Q

Transmission of MCF between sheep

A
  • respiratory (aerosol)
  • transplacental= rare
  • contact with nasal secretons
273
Q

transmission from sheep to cattle

A
  • not known

- presumably inhalation or ingestion

274
Q

MCF infection in Wildebeest and Sheep

A
  • inapparent infection

- virus transmitted Wildebeest to Wildebeest, sheep to sheep

275
Q

MCF cattle

A
  • 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
276
Q

Pathogenesis MCF

A
  • infection followed by cell associated viremia
  • lymphoid proliferation and infiltration
  • necrotizing vasculitis
  • vascular lesions- gross lesions, such as epithelial erosions and conjunctivitis
277
Q

Clinical signs of MCF

A
  • 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
278
Q

Head and Eye form of MCF

A
  • 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
279
Q

Necropsy finding MCF

A
  • zebra striping: bovine, colon severe longitudinal linear congestion of mucosa
  • erosions in hard palate
280
Q

Control of Malignant Catarrhal fever

A
  • seperation of cattle from wildebeest and sheep

- incidence to low to justify development of vaccine

281
Q

African swine fever- etiology and hosts

A
  • 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
282
Q

Geographical distribution of African Swine fever

A
  • endemic in most of sub-Saharan Africa, and island of Sardinia (Italy)
  • recent outbreaks in Eastern Europe and Russia
283
Q

ASF stability

A
  • 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
284
Q

transmission of ASF

A
  • 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
285
Q

Sylvatic cycle transmission of ASF

A
  • 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
286
Q

domestic cycle of African Swine Fever

A
  • 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
287
Q

Pathogenesis of African swine fever

A
  • 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
288
Q

Peracute ASF

A

-pigs may die suddenly

289
Q

Clinical signs of Acute form of ASF

A
  • 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
290
Q

Chronic form of ASF

A
  • 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
291
Q

Immunity to African Swine fever

A
  • 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
292
Q

ASF prevention

A
  • 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
293
Q

during an ASF outbreak

A
  • 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
294
Q

General characteristics of family: Papillomaviridae

A
  • 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
295
Q

Replication of papillomaviruses

A

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

296
Q

Oncogenic Papillomaviruses

A
  • 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
297
Q

Bovine Papillomatosis- host and transmission

A
  • 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
298
Q

Fibropapilloma

A
  • 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
299
Q

Cutaneous papillomas

A
  • bovine papillomaviruses type 3
  • lack fibrous core
  • usually flat with broad base, unlike more usual fibropapillomas that protrude and are often pedunculated
300
Q

Bracken fern and bovine papillomaviruses

A
  • 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
301
Q

Treatment of bovine papillomatosis

A
  • surgical excision, or cryosurgery with liquid nitrogen
  • topical agents- Podophyllin and undiluted medical grade DMSO
  • bovine interferon-alpha
  • wart vaccine
302
Q

Canine Oral Papillomatosis

A
  • 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
303
Q

Clinical signs of Canine Oral Papillomatosis

A
  • 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
304
Q

Treatment of Canine Oral Papillomatosis

A
  • surgical excision, cryosurgery, electrosurgery

- autogenous vaccines

305
Q

Equine Sarcoids

A
  • 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
306
Q

Transmission of equine sarcoids

A
  • mode of transmission not confirmed
  • flies as vectors?
  • fomites, transmitted via stable management practices
307
Q

Equine sarcoids- lesions

A
  • commonly occur in traumatized areas
  • single or multiple
  • growths may reach size of man’s fist, bulge under skin
  • may become ulcerated
308
Q

Treatment of equine sarcoids

A

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

309
Q

Adenoviridae- morphology

A
  • 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
310
Q

Properties of Adenoviridae

A
  • 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
311
Q

Pathogenesis of adenovirus

A
  • 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
312
Q

Adenovirus, Genus: Mastadenovirus

A
  • mammalian adenoviruses

- single penton fiber projects from each vertex

313
Q

Adenovirus, Genus: Aviadenovirus

A
  • avian adenoviruses

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

314
Q

Infectious Canine Hepatitis (ICH, Rubarth’s disease)

A
  • 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
315
Q

Sites of virus replication- Infectious Canine Hepatitis

A
  • 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
316
Q

Pathogenesis of Infectious Canine Hepatitis

A
  • 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
317
Q

Pathogenic changes in infectious canine hepatitis

A
  • 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
318
Q

Ocular lesions in Infectious Canine Hepatitis

A
  • 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
319
Q

How corneal edema develops

A
  • 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
320
Q

Complications from infectious canine hepatitis

A
  • disseminated intravascular coagulation, from damage to endothelium and inability of disease liver to remove clotting factors
  • bacterial pyelonephritis resulting from renal damage
321
Q

Clinical signs of infectious canine hepatitis

A
  • 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
322
Q

Peracute cases of infectious canine hepatitis

A

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

323
Q

acute cases of infectious canine hepatitis

A
  • 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
324
Q

Diagnosis of infectious canine hepatitis

A
  • 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
325
Q

Treatment of infectious canine hepatitis

A
  • treatment symptomatic and supportive

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

326
Q

immunity

A
  • 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
327
Q

Canine Infectious Tracheobronchitis (kennel cough)

A
  • 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
328
Q

Uncomplicated ITB

A
  • 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
329
Q

Complicated ITB

A
  • severe pneumonia or bronchopneumonia

- life threatening

330
Q

Treatment of Canine Infectious Tracheobronchitis

A
  • 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
331
Q

Equine Adenovirus

A
  • 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
332
Q

Chicken Adenovirus

A
  • inclusion body hepatitis

- egg drop syndrome ‘76

333
Q

duck adenovirus

A

-hepatitis (rare)

334
Q

quail adenovirus

A

-bronchitis

335
Q

turkey adenovirus

A
  • hemorrhagic enteritis

- egg drop syndrome

336
Q

pheasant adenovirus

A

-marble spleen disease

virology (12 decks)

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