Lectures 13-16 Flashcards

1
Q

next generation sequencing

A

cheaper, quicker, needs less DNA, higher throughput, more accurate than Sanger sequencing

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2
Q

Metagenomics

A

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

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3
Q

Genome sequencing plays a role in surveillance studies as it allows:

A

pathogen detection, studies on genetic variation, IDing of novel and undiscovered strains, development of diagnostics, IDing of genes associated with drug resistance, development of therapeutics, judging the efficacy of current vaccines and formulating new vaccine strategies

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4
Q

Phylogenetic analysis

A

the use of viral genome sequence data to study evolution of viruses and genetic relationships among viruses

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5
Q

Microarray

A

checking to see if sample DNA binds to known DNA probes attached to glass. Fluorescent signal indicates sample hybridization.
Allows the screening of LOTS of pathogens simultaneously

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6
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

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7
Q

immune system stimulation

A

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

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8
Q

Acyclovir

A

administered as a prodrug. requires viral enzymes in infected host cell to convert into active form which interferes with viral replication
Synthetic nucleoside analog of deoxyguanosine

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9
Q

Acyclovir targets

A

herpes - humans
feline herpes-1 induced corneal ulcers
equine herpes-1 induced encephalomyelitis

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10
Q

acyclovir MOA

A

herpes DNA polymerase incorporates acyclovir monophosphate into the growing DNA strand as it was a G base. Further elongation not possible after this.
Acyclovir triphosphate competes with dGTP for viral DNA polymerase

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11
Q

Why doesn’t acyclovir target normal cells?

A

Acyclovir’s actions are through herpesvirus DNA polymerase - not found in normal cells

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12
Q

Amantadine

A

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

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13
Q

Amantadine MOA

A

M2 ion channel is the target. Amantadine particles block the channel to prevent it from pumping protons into the virion. In the presence of amantadine, viral RNAs remain bound to M2 and cannot enter the nucleus

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14
Q

Neuraminidase inhibitors

A

inhibitor of neuraminidase enzymes produced by influenza A and B viruses
Ex: oseltamivir (Tamiflu)

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15
Q

Neuraminidase inhibitors MOA

A

Blocking the function of neuraminidase with NA inhibitors is an effective way to treat influenza. This prevents release of virus and spread of infection as the hemagluttinin of virus is still bound/attached to the sialic acid containing receptors on the surface of the already infected host cell. Inhibition of neuraminidase therefore slows virus spread giving the immune system the opportunity to catch up

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16
Q

Nucleoside analog reverse transcriptase inhibitors (NRTIs) types

A

Zidovudine/Azidothymidine (ZDV/AZT)

Didanosine (ddI)

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17
Q

ZDV/AZT

A

Nucleoside analog of thymine. Causes competitive inhibition of reverse transcriptase activity - AZT-triphosphate competes with thymine deoxyribonucleotide tiphosphate for RT. Insertion of AZT-monophosphate into cDNA blocks the growth of the cDNA being transcribed from the viral RNA by RT.
AZT reduces CS in FIV-positive cats when administered at 10 mg/kg twice a day, subQ for 3 weeks

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18
Q

Protease inhibitors

A

drugs that inhibit proteases from cleaving viral polyproteins into functional proteins. Protease inhibitors bind to the active site of protease and thus the virus cannot mature and noninfectious viruses are produced

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19
Q

Live attenuated vaccine types

A

vaccines from naturally occurring attenuated viruses (cowpox for smallpox), vaccines produced by attenuation of viruses by serial passage in cultured 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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20
Q

non replicating virus vaccine types

A

vaccines produced from inactivated whole virions, vaccines produced from purified native viral proteins

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21
Q

Differentiating infected from vaccinated animals (DIVA)

A

subunit DIVA vaccines have only a portion of the pathogen in the vaccine (less antigens than normal). if antibodies are found to other parts of the pathogen –> animals has been infected with the pathogen
if only antibodies to the subunits are detected –> not infected

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22
Q

Isolation

A

applies to animals/persons who are known to be ill with a contagious disease

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23
Q

Quarantine

A

applies to those who have been exposed to a contagious disease (not effective with disease involving chronic shedders)

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24
Q

Decontamination

A

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

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25
Q

Sterilization

A

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

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26
Q

Disinfection

A

describes a process that eliminates many or all pathogenic microorganisms except bacterial spores on inanimate objects (less effective than sterilizing)

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27
Q

Antisepsis

A

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

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28
Q

Sterilization methods

A

Moist heat (autoclave), dry heat (hot air oven), chemical methods (gas - ethylene oxide, ozone), radiation (UV - non ionizing, Gamma and X - ionizing), sterile filtration (microfiltration)

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29
Q

Poxvirus family and subfamily

A

fam: poxviridae
sub: chordopoxvirinae

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30
Q

poxvirus properties

A

large, sometimes enveloped, DNA virus
mostly pleomorphic, typically brick shaped.
Irregular surface
Complex symmetry (not helical or icosahedral)
Core = dumbbell shaped
Genome = single molecule of linear dsDNA
many proteins encoded by the genome are for nuclei acid synthesis and virion structural components (also encodes things to evade immunity)

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31
Q

Parapoxvirus structure

A

ovoid, covered with surface tubules look like ball of yarn

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32
Q

Poxvirus replication

A

predominantly in cytoplasm. They have evolved to encode the enzymes required for transcription and replication.
Virions released via budding, exocytosis or cell lysis (most common). Enveloped virions taken up by cells more readily - more important in transmission

33
Q

Poxvirus stability

A

High environmental stability, remain infectious over a period of several months in the environment.
low lipid content = less sensitive to organic solvents/disinfectants
high resistance to drying

34
Q

Poxviruses transmission

A

3 main routes:
skin - infect broken skin
respiratory - transmitted via aerosol route
mechanical transmission - arthropod bite

35
Q

Poxvirus pathogenesis

A

cause cutaneous skin lesions. can cause systemic disease in birds and wild animals. Mainly host specific

36
Q

Spread of poxvirus

A

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

37
Q

Skin lesions in poxvirus

A

Macule –> papule –> vesicle –> pustule –> scab –> scar

Pustule rupture can lead to secondary bacT infection. Poxvirus can survive in dried scabs for years

38
Q

Cowpox scientific name

A

orthopoxvirus

39
Q

Cowpox distribution

A

endemic only in europe and asia

40
Q

cowpox hosts

A

cattle, wild and domestic cats, humans, zoo animals

41
Q

reservoir of cowpox

A

rodents

42
Q

Cowpox in cattle - transmission

A

usually though infected milkers hands or teat cups. infected farm cats may also transmit the disease. Rodents are reservoir and also source of transmission

43
Q

Cowpox in cattle - clinical findings

A

after incubating for 3-7 days, papules appear on the teats and udder. suckling calves may develop mouth lesions. Vesicles may not be evident or may rupture readily and leave raw & ulcerated areas that form scabs

44
Q

Cowpox in cats - transmission

A

usually via skin inoculation through a bite or skin wound. Commonly from rodents. Oro-nasal transmission possible.

45
Q

cowpox in cats - CS

A

primary lesions: single lesion, usually on head/neck/forelimb. may form a small scabbed wound or larger abscess
secondary lesions: 7-10 days after initial lesion, widespread secondary lesions will appear. Lesions initially are discrete, circular, ulcerated papules but soon become covered in scabs.
Many cats show no signs other than skin lesions, but some may have coryza and conjunctivitis. secondary bacT infections possible

46
Q

Cowpox in humans - tranmission

A

mainly caused by direct contact with cats. rarely from rodents/zoo animals. not commonly found in cattle so cows are low risk for transmission

47
Q

Cowpox in humans - CS

A

Macropapular lesions first observed on hands and face. Develops to vesicular then ulcerative lesion. Enlarged LNs, fever, vomiting, sore throat

48
Q

Monkeypox in humans

A

symptoms similar to smallpox.
Primary infection results from contact with blood/bodily fluids/rashes of infected animals.
Secondary transmission = human to human via infected resp. tract excretions/skin lesions/contaminated object

49
Q

Parapoxvirus diseases

A

pseudocowpox - cattle, humans
contagious ecthyma/orf virus - sheep, goats, humans
bovine papular stomatitis virus - cattle, humans

50
Q

Pseudocowpox transmission

A

source of infection is the infected cattle –> transmission via: contaminated milkers hands, teat cups, biting insects, suckling semen

51
Q

Pseudocowpox pathogenesis

A

lesions are characterized by hyperplasia of squamous epithelium
Mild CS

52
Q

Pseudocowpox acute lesions

A

erythema –> papules –> vesicle/pustule –> rupture –> scab
Scab = 0.5 to 25 cm in diameter, elevated due to accumulation of granular tissue. after 7-10 days, scab drops off and leaves a horseshoe ring of small scabs surrounding a wart-like granuloma

53
Q

Pseudocowpox chronic lesions

A

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

54
Q

Pseudocowpox diagnosis

A

horse-shoe shaped lesions are pathognomonic, isolation and detection of the virus by various diagnostic lab tests from vesicular fluid or teat skin

Differentials: cowpox, bovine herpesvirus ulcerative mastitis, vesicular stomatitis, udder impetigo, teat chaps, frost bite, black spot

55
Q

Pseudocowpox treatment

A

removal of scabs, burn the scabs to prevent environment contamination, application of an amollient ointment before milking, application of astringent preparation after milking

56
Q

Pseudocowpox prevention

A

disinfection, iodophor teat dip, isolation and treatment of infected cows, reduce teat trauma

57
Q

Pseudocowpox in humans

A

causes mild skin lesion called the milkers nodule. Lesions on the hands of dairy farmers/vets, lesions may vary from multiple vesicles to a single indurated nodule

58
Q

Contagious ecythema/ORF transmission

A

scabs fall off (contain virus) –> virus is stable in environment under dry conditions, contaminated instruments transmit as well –> rapid spread in a flock
Virus infects healthy animals through damaged skin, oral lesions in lambs or kids result from nursing

59
Q

ORF pathogenesis

A

damage to the skin is essential –> skin response is necrosis and sloughing of the affected area and underlying regions of the dermis. Also includes delayed-type hypersensitivity reaction and an influx of inflammatory cells
Macule –> papule –> vesicle –> pustule –> ulcer –> scab

60
Q

ORF clinical signs

A

swollen lips, lesions spread around the muzzle, nostrils, buccal mucosa, anorexia and weight loss, lesions on teats, possible secondary bacterial infection, genital lesions, feet lesions, ear lesions, lameness, infertility
1-4 weeks = scab falls off

61
Q

Contagious ecthyma/ORF vaccination

A

vaccine is prepared from suspension of scabs in glycerol saline and is painted onto a small area of scarified skin inside the thigh where a localized lesion develops.
dont use on farms where ORF is not a problem
Inspect 1 week post vaccine for the lesion – indicates viability of the vaccine
not long lasting immunity - 1-2 years
kids/lambs at 6-8 weeks in problem herds
Pregnant ewes only 7-8 weeks before lambing (earliest)

62
Q

ORF in humans

A

macro-papular lesions in the finger, hand, arm, face, penis.
Secondary bacterial infection possible

63
Q

Capripoxvirus diseases

A

sheeppox, goatpox, lumpy skin disease

64
Q

Sheeppox (SPV) and Goatpox (GPV) transmission

A

most important route = aerosols in resp tract.
highly contagious virus
spread may also occur through: mucus membranes, abraded skin, direct contact with iatrogenic materials, mechanical arthropod trasmission.
Viruses can survive in oral/nasal secretions and scabs for a while

65
Q

SPV pathogenesis

A

SPV is systemic. Incubation is followed by leukocyte-associated viremia. After, the virus localizes in the skin and other internal organs. Deposits immune complexes –> severe necrotizing vasculitis –> ischemic necrosis of dermis and epidermis

66
Q

SPV malignant form

A

pox lesions develop on skin and buccal/resp/GI/UG tract mucosae. lesions extend to pharynx/larynx/lungs/vagina/abomasum/spleen. Secondary pneumonia is common.
Nodules occasionally become vesicular, pustular and then scab.
Lesions heal leaving a star-shaped scar, free of hair

67
Q

SPV benign form

A

more common in adults and resistant breeds. Only skin lesions occur. No or very mild systemic reaction

68
Q

SPV prevention and control

A

notifiable disease!!
control with vaccine - killed vaccines only offer temp. protection. Live attenuated offer very good protection (over a year)

69
Q

GPV

A

reportable disease!

young kids suffer similar systemic disease to SPV. Milder form seen in adults

70
Q

Lumpy skin disease

A

transmission: via arthropod vector or direct contact
host: cattle, all ages and all types
clinical findings: fever, multiple nodular lesions on skin and mucous membranes, lymphadenopathy

71
Q

Swinepox

A

transmission: mechanical via haematopinus suis, transplacental
CS: typical pox lesions, occurring anywhere on the body, exudative epidermitis and bacterial dermatitis are “sequel” to swinepox.
Severe infections = lesions may appear in resp and GIT
Control = eradication of lice from piggery, no vaccine

72
Q

Fowlpox transmission

A

transmitted through minor wounds and abrasions of the mouth/comb/wattles/skin, mechanically via lice/mosquitoes/ticks, possibly via aerosols

73
Q

fowlpox forms

A

cutaneous form, diphtheritic form, ocular form

74
Q

Cutaneous form of fowlpox

A

dry form. Most common form. low mortality. results from injecting by arthropods or mechanical transmission to injured skin. small papules on comb/wattles/beak. Lesions occur on legs/feet/cloaca. nodules become yellowish and progress to a thick scab, sharp fall in egg production, recovery in 4 weeks

75
Q

Diphtheritic form of fowlpox

A

wet form. probably transmitted via droplets. infection of mucous membranes of mouth/pharynx/larynx/trachea. lesions result in necrotic pseudomembrane which may cause death by asphyxiation. prognosis is poor

76
Q

Bollinger bodies

A

eosinophilic granular intracytoplasmic inclusion bodies seen in avipoxvirus

77
Q

Borrel bodies

A

occur inside bollinger bodies. minute spherical bodies obtained by tryptic digestion of Bollinger bodies

78
Q

Fowlpox control

A

vaccination - modified live fowlpox virus vaccines of chicken embryo or avian cell culture origin available. Recombinant fowlpox vectored vaccines have been developed. Control mosquito/biting insect populations