Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RUSVM Virology > Virology Test 2 > Flashcards

Virology Test 2 Flashcards

1
Q

What is the purpose of PCR?

A

Amplification of viral genome/DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 steps of PCR?

A

Denaturation
Annealing
Extension/elongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

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

Useful to study virus load in patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is DNA sequencing?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are advantages to using Next generation sequencing?

A 
Significantly cheaper
Quicker
Needs less DNA
High throughput
More accurate and reliable than Sanger sequencing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is metagenomics?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is phylogenetic analysis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in a microarray?

A

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Phylogenetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antiviral drugs

A

Class of medication used specifically for treating viral infections.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Immune system stimulation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Acyclovir antiviral activity is primarily restricted to________

A

Herpesviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Acyclovir as?

A

A prodrug, inactive form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Virus enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Acyclovir used to treat?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Acyclovir?

A

Synthetic nucleoside analog of deoxyguanosine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Two main steps of mechanism of antiviral effect of acyclovir

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Is acyclovir toxic to the uninfected host cell?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does amantadine do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the antiviral MOA of amantadine?

A

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Oseltamivir (Tamiflu) is what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

Neuroaminidase; NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Blocking the neuraminidase with NA inhibitors does what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

Virus spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are two nucleoside analog reverse transcriptase inhibitors (NRTIs)

A

Zidovudine (ZDV) or AZT (Azidothymidine)

ddI (Didanosine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are ZDV/AZT?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the MOA of ZDV/AZT?

A

Competitive inhibition of reverse transcriptase activity: AZT-triphosphate competes with the thymine deoxyribonucleotide triphosphate for the reverse transcriptase.

Insertion of AZT-monophosphate into cDNA blocks the growth of the cDNA being transcribed from the viral RNA by reverse transcriptase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A

FIV-positive cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

True/False: Acyclovir is a pro-drug?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

_____ are required to cleave the HIV polyproteins into functional proteins

A

Proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Easy question

What inhibits the proteases?

A

Protease inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A

Cannot.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do protease inhibitors work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are non-replicating viral vaccines made?

A

Inactive whole virions.

Purified native viral proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

A

Produced by recombinant DNA and related technologies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MOA of DIVA

A

Subunit ‘marker vaccine’ DIVA vaccines have only a portion (subunit) of the pathogen in the vaccine i.e. Has less antigens than natural strains.

If antibodies to other parts/antigens of the pathogen no included in the vaccine are detected the animal has been infected with the pathogen.

If only antibodies to the vaccine subunit/antigens are detected, the animal has not been infected.

An accompanying diagnostic test allows us to actually make the differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Isolation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Quarantine

A

Applies to those who have been exposed to a contagious disease.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Quarantine and Culling

A

To separate and restrict the movement of animals.

Culling of animals.

Proper disposition of culled animals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Decontamination

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Sterilization

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Disinfection

A

A process that eliminates many or all pathogenic microorganisms, except bacterial spores, on inanimate objects.

Less effective than sterilization, does not necessarily kill all microorganisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Antisepsis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the sterilization methods?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

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

A

Live-attenuated vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

True/False: Quarantine and isolation have the same meaning

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Autoclave is a method of _________

A

Sterilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the family of poxviruses?

A

Poxviridae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the subfamily of Poxviridae?

A

Chordopoxvirinae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How many genera are there for the pox virus?

A

8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

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

A 
Orthopoxvirus
Parapoxvirus
Avipoxvirus
Capripoxvirus
Leporipoxvirus
Suipoxvirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Properties of Poxviruses

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the two distinct infectious poxvirus particles that exist?

A

Intracellular mature virus (IMV)

Extracellular enveloped virus (EEV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

T/F: both IMV and EEV are infectious

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

EEV contains 2 membranes:

A

Envelope

Inner membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How do virions acquire the extra envelope?

A

Cells released by budding.

The envelope contains virus encoded-proteins from host cell membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

IMV have how many membranes?

A

1

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

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

A

False

Complex symmetry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

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

A

Dumbbell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is contained in the core of a poxvirus?

A

Viral DNA with several proteins

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

The genome of poxviruses consists of

A

Single molecule of linear ds DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A

Nucleic acid

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Where does replication of the poxvirus occur?

A

Predominantly in the cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How are poxviruses released after replication?

A

Budding
Exocytosis
Cell lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Most virions are not enveloped and are released by ____ _______

A

Cell lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Stability of poxviruses

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Poxvirus transmission

A

Skin: cannot infect intact skin. Contact of infectious material with broken or lacerated skin is a common route of poxvirus transmission.

Respiratory route: some by aerosol route (sheeppox)

Mechanically: arthropods (Myxoma virus and avipoxviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Pathogenesis and Immunity to poxvirus

A

Epitheliotropic causing cutaneous lesions

Sometimes cause systemic diseases in birds and wild animals

Many are host specific

Orthopoxviruses infect a wide range of species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Spread of poxvirus

A

Following introduction into the body, poxvirus usually gains access to the systemic circulation via the lymphatic system.

A secondary viremia disseminates the virus back to the skin and to other target organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the pathway of skin lesions in poxvirus infection?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is a macule

A

Flat and red. Local inflammation immune response infiltrating leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is a papule?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is a vesicle?

A

Small blister: microbe invades epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

T/F: Ulceration will never develop with poxvirus lesions

A

False

They are possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

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

A

Pustules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Distribution of cowpox

A

Endemic only in Europe and Asia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Hosts of cowpox

A

Cattle
Wild and domestic cats
Humans
Zoo animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Reservoir host of cowpox

A

Rodents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Transmission of cowpox in cattle

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Economic importance of cowpox in cattle

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Clinical findings with cowpox in cattle

A

Mildly febrile, papule appear on teats and udders

Sucking calves may develop lesions in mouth

Vesicles may not be evident or may rupture readily leaving ulcerated areas that form scabs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Transmission of cowpox in cats

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Primary lesions of cowpox in cats

A

Primary skin lesion - head, neck or forelimb

May form small, stabbed wound to large abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Secondary lesions of cowpox in cats

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Transmission of cowpox in humans

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Clinical signs of cowpox in humans

A 
Macropapular lesions on hands and face -> vesicular and ulcerative lesions.
Enlarged painful local lymph nodes
Fever
Vomiting 
Sore throat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Monkeypox in humans

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Transmission of monkeypox in humans

A

Primary - direct contact with blood, bodily fluids, or rashes of infected animals. In Africa, human infections have been documented through the handling of infected monkeys, Gambian rats or squirrels.

Secondary- human to human. Close contact with infected respiratory tract excretions, with the skin lesions of an infected person or with recently contaminated objects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Pseudocowpox: que es?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Etiology of pseudocowpox

A

Member of the genus parapoxvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Epidemiology of pseudocowpox

A

Reported from most countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Transmission of pseudocowpox

A 
Infected cattle
Contaminated milker's hands, teat cups
Biting insects
Calves get during suckling
Semen of bulls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Pathogenesis of pseudocowpox

A

Hyperplasia of squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Clinical signs of pseudocowpox

A

General mild

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Acute lesions of pseudocowpox

A

Erythema -> papules -> vesicle or pustule -> rupture -> thick scab

Thick scab (.5 to 25 cm) becomes elevated due to accumulation of granulation tissue.
7-10, scab falls off leaving horseshoe-shaped ring of small scabs surrounding a small wart-like granuloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Chronic lesions of pseudocowpox

A 
Starts as erythema
Yellow-gray, soft scurfy scabs which are rubbed off during milking
Skin is corrugated
No pain
Lesions may persist for months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Diagnosis of pseudocowpox

A

Horseshoe-shaped ring like lesions are pathognomonic.

Isolation and detection of the virus by various diagnostic lab methods from vesicular fluid or from teat skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Differential diagnosis of pseudocowpox

A 
Cowpox virus
Bovine herpesvirus ulcerative mammalitis
Vesicular stomatitis
Udder impetigo (bacterial dermatitis characterized by the development of small pustules on the skin of the udder and teats)
Teat chaps and frostbite
Black spot (a form of hyperkeratosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Treatment of pseudocowpox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Prevention of pseudocowpox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Pseudocowpox in humans or Milker’s nodules

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is the etiology of Contagious ecthyma, ORF?

A

Orf virus, Genus Parapoxvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Who is the host of ORF?

A

Sheep and goat. Primarily in lambs and goat kids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the distribution of ORF?

A

Worldwide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Transmission of ORF?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Pathogenesis of contagious ecthyma (ORF)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Clinical signs of orf

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Severe cases show what clinical signs of ORF?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Vaccination of ORF

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Pregnant ewes should be vaccinated before/after lambing

A

Before

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

ORF in humans

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Etiology and distribution of sheeppox and goatpox

A

E: members of the Genus Capripoxvirus

D: Endemic in Africa, Asia and parts of Europe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

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

A

Genetic sequencing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

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

A

No sir they cannot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

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

A

Lumpy skin disease virus (LSDV)

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Transmission of sheeppox and goatpox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Pathogenesis of sheeppox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

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

A

Severe necrotizing vasculitis develops in arterioles and postcapillary venules of skin.

Results in ischemic necrosis of dermis and overlying epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are the two forms of sheeppox

A

Malignant

Benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Malignant form from sheeppox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

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

A 
Pharynx
Larynx
Lungs
Vagina
Abomasum
Spleen

Secondary pneumonia common
Abortion rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

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

A

High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Benign form of sheeppox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Prevention and control of sheeppox

A

Notifiable disease in most countries of the world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Are vaccines available for sheeppox?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Where is Goatpox found?

A

Africa
Asia
parts of Europe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Is goatpox reportable?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Goatpox disease is clinically similar to?

A

Sheeppox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Age group affected by goatpox systemic disease

A

Young kids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Age group affected by mild forms of goatpox

A

Adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Etiology of lumpy skin disease

A

Members of genus Capripoxvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Distribution of lumpy skin disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Transmission of lumpy skin disease

A

Arthropod vector

Direct contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Host of lumpy skin disease

A

Cattle

All ages and types susceptible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Clinical findings of lumpy skin disease

A

Fever
Multiple nodular lesions on skin and mucus membranes
Lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Etiology of swinepox

A

Members of genus Suipoxvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Distribution of swinepox

A

Worldwide

Widespread, sporadic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Hosts of swinepox

A

Cattle

JK, making sure you’re paying attention.

Pigs
Benign with low mortality and morbidity in older.
High case fatality in congenitally infected and very young sucking piglets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Transmission of swinepox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

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

A

Transplacental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What are the typical pox lesions of swinepox?

A 
Skin lesions occur anywhere, most obvious on abdomen and inner thighs.
Exudative epidermitis (greasy pig disease) and secondary bacterial dermatitis occasionally follow swine pox.
Severe infections, especially in congenitally-acquired pox infections can have lesions occur in upper respiratory and digestive tracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Control of swinepox

A

Eradication of lice from piggery

No commercially available vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Etiology of fowlpox

A

Genus Avipoxvirus

*first virus grown in embryonated eggs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Hosts of fowlpox

A

Poultry and turkeys

Are turkeys not poultry?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Distribution of fowlpox

A

Worldwide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Transmission of fowlpox

A

Extremely resistant to desiccation
Can survive in exfoliated scabs for long time.

Transmitted within flocks through minor wounds and abrasions of mouth, comb, wattles, or skin from fighting or pecking each other.
Mechanically by mosquitoes, lice and ticks.
Possibly aerosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are the 3 forms of fowlpox disease

A

Cutaneous (dry)
Diphtheritic (wet)
Ocular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

The cutaneous or dry form of fowlpox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Diphtheritic (wet) form of fowlpox

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Ocular form of fowlpox

A

Conjuntivitis

Cheesy exudate accumulates under eyelids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What are Bollinger bodies of avipoxvirus?

A

Eosinophilic granular intracytoplasmic inclusion bodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What are Borrel bodies of avipoxvirus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Vaccination for fowlpox control

A

Modified live fowlpox or pigeon pox virus vaccines of chicken embryo or avian cell culture origin are available commercially.

Recombinant fowlpox vectored vaccines have been developed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

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

A

Control mosquito population and other biting insects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Transmission of ulcerative dermatosis of sheep (unclassified poxvirus)

A

Infection through damaged skin or by coitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Clinical forms of ulcerative dermatosis of sheep

A

Usually ulcers with raw crater that bleeds easily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Ulcerative dermatosis of sheep manifests in what two clinical forms?

A

Lip and les ulceration

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

How do we diagnose poxviruses?

A

Clinical signs

Sample material: scrapings from skin lesions, vesicular fluid, crusts, scabs

Electron microscopy: characteristic morphology and size of poxviruses. Orthopoxviruses are brick shaped. Parapoxviruses are ovoid.

Serological assays (ELISA)
Detection of poxvirus nucleic acid by PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

How do we use histopathology to diagnose poxvirus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are Type-B (Guanrnierei) inclusion bodies?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What are Type-A (ATI) inclusion bodies

A

Induced by some poxviruses - cowpox and ectromelia virus.

Strongly eosinophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Can we inoculate embryonated eggs to diagnose poxviruses?

A

Yes
Chorioallantoic membrane -> pock lesions.

*Parapoxviruses do NOT multiply in chicken embryo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

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

A

Porcine circovirus type-1 (non-pathogenic)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What virus is under the family Circoviridae, genus Gyrovirus?

A

Chicken infectious anemia virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

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

A

Circovirus: ambisense DNA

Gyrovirus: negative sense DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

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

A

Chicken infectious anemia virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Virus replication occurs in what type of cells for Circoviridae?

A

Actively dividing cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Where does DNA replication occur?

A

Nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

T/F: Circoviridae virions are not very stable

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Etiology of post-weaning multisystemic wasting syndrome (PMWS)

A

Porcine circovirus 2 (PCV2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Hosts of PMWS

A

Pigs

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Transmission of PMWS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Pathogenesis of PMWS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What is lymphoid depletion?

A

Loss of B-cells and T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Transplacental infection of PMWS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Clinical signs of PMWS

A 
Subclinical infection most common.
Lethargy
Progressive weight loss
Cough
Dyspnea
Slow growth
Lymphadenopathy
Diarrhea
Skin discoloration 
Congenital tremors
Icterus (less common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

PMWS commonly gets a co-infection with which viruses?

A

Porcine parvovirus (PPV)
Porcine reproductive and respiratory virus (PRRSV)
SIV
Mycoplasma hyopneumonea

Other opportunistic bacteria that may cause severe disease and more pronounced lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Diagnosis of PMWS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Vaccines for PMWS

A

Chimeric vaccines: use non-pathogenic porcine circovirus 1 (PCV-1) as a genetic backbone for expression of the immunogenicity capsid protein of PCV-2.

Inactivated or baculovirus-expressed vaccines: virus-like particles include the capsid protein of PCV-2

Sow vaccination antepartum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

What is Gyrovirus cause?

A

Chicken infectious anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

Host of chicken infectious anemia

A

Highly contagious disease of young chickens (2-4 wo)

Older chickens more resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Transmission of chicken infectious anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Pathogenesis of chicken infectious anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Clinical signs and lesions of chicken infectious anemia

A 
Anorectic
Lethargic
Depressed
Reduced body weight gain
Pale 
Thrombocytopenia: watery blood with slow clot
PCV low
SQ hemorrhages and skeletal hemorrhages
Pale muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Differences in anatomy with chicken infectious anemia

A

CAV-induced thymic atrophy

Pale, aplastic bone marrow

Pale carcass

Atrophied bursa

198
Q

Diagnosis of chicken infectious anemia

A

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

199
Q

Vaccination for chicken infectious anemia

A

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

200
Q

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

A

True

201
Q

Do Herpesviridae have ss or ds DNA?

A

ds

202
Q

Viral replication of Herpesviridae

A

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

203
Q

Do Herpesviruses survive well outside of the host cell?

A

Nope to the nope nope

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

204
Q

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

A

False, all of them

205
Q

T/F: herpesviruses are oncogenic

A

True

206
Q

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

A

Stress; glucocorticoid

207
Q

What type of inclusion bodies belong to Herpesviruses?

A

Eosinophilic intranuclear

Known as type A Cowdry bodies

208
Q

T/F: Herpesviruses can cause syncytium

A

True

209
Q

What are the properties of Alphaherpesvirinae?

A

Generally highly cytopathic in cell culture

Relatively short replication cycle

210
Q

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

A

False, broad host range

211
Q

Where do most localized lesions occur from alphaherpesviruses?

A

Skin

Mucosa of the respiratory and genital tracts

212
Q

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

A

Very young; immunocompromised

213
Q

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

A

Abortion

214
Q

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

A

BHV-1.1 (respiratory subtype)

BHV-1.2 (genital subtype)

215
Q

Transmission of BHV

A

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

216
Q

Pathogenesis of BHV

A

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

217
Q

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

A

True

218
Q

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

A

True

219
Q

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

A

False, they can be

220
Q

Where are the sites of latency for BHV?

A

Trigeminal nerve: respiratory disease with BHV-1.

Sciatic nerve: genital disease with BHV-1

221
Q

Clinical signs of BHV

A

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

222
Q

Clinical signs for the respiratory BHV form

A

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

223
Q

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

A

Mannheimia hemolytica and Pasteurella multocida (shipping fever)

Secondary bronchopneumonia

224
Q

Ocular form of IBR

A

Conjunctivits is a common finding in typical “red nose”

225
Q

Do not misdiagnose BHV as what?

A

Pink-eye or infectious bovine keratoconjunctivitis.

IBR lesions are confined to the conjunctiva and no lesions on cornea except diffuse edema.

226
Q

Abortion caused by BHV-1

A

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

227
Q

BHV-1 causing systemic disease of newborn calves

A

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

228
Q

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

A

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

229
Q

BHV-1 genital disease: balanoposthitis

A

Inflammation and pustules in the mucosa of the penis and prepuce

230
Q

Control (vaccination) of BHV

A

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

231
Q

What two diseases are caused by BHV-2

A

Bovine ulcerative mammalitits

Pseudo-lumpy skin disease

232
Q

Host of bovine ulcerative mammalitis

A

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

233
Q

Transmission of Bovine ulcerative mammilitis

A

Direct contact and fomite-mediated, through skin trauma

Mechanical transmission by stable flies and other arthropods

234
Q

Clinical signs of bovine ulcerative mammilitis

A 
Severe cases: teats swollen and painful
Skin is bluish
Exudes serum
Formation of raw ulcers
High incidence of mastitis
235
Q

Pseudo-lumpy skin disease

A

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

236
Q

Clinical signs of pseudo-lumpy skin disease

A

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

237
Q

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

A

Pseudorabies (Aujeszky disease, Mad itch)

238
Q

Etiology of Pseudorabies

A

Porcine herpesvirus 1/Suid herpesvirus 1

239
Q

Hosts of pseudorabies

A

Primarily swine

Secondary:
Horse
Cattle
Sheep
Goats
Dogs
Cats
Many feral species

Humans are refractory to infection

240
Q

Transmission of pseudorabies in primary hosts

A

Recovered pigs act as primary reservoirs, and are latent carriers for life.
Rodents can be reservoirs and transmit disease from farm to farm.

Routes:
She’d in saliva, nasal discharges and milk of infected pigs
Not shed in urine or feces
Licking, biting, aerosol, ingestion of contaminated carcass, water and feed.

241
Q

Transmission of pseaudorabies in secondary hosts

A

Dogs and cats: ingestion of infected pig carcass/meat, or rodents

Cattle: direct contact with infected pigs, oral and nasal routes

242
Q

Pathogenesis of pseudorabies

A

Primary site of viral replication is upper respiratory tract

243
Q

Spread of pseudorabies

A

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

244
Q

Pseudorabies virus spread in CNS

A

Via axons of cranial nerves

Preference for neurons and the pons and medulla

245
Q

CNS lesions due to pseudorabies

A

Ganglioneuritis
Nonsuppurative meningoencephalitis
Perivascular cuffing

246
Q

Clinical signs of pseudorabies

A

Nonimmune piglets: 100% mortality rates
Nonimmune pregnant sows: ~50% abortion rate
Older piglets, growers, and adult pigs: mild disease, mortality <2%

Pruritus (itching), a dominant feature in secondary hosts, is rare in pigs

247
Q

Piglets born to nonimmune sows with pseudorabies

A

Most susceptible

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

248
Q

Weaned pigs and growing pigs with pseudorabies

A

CNS signs may be reduced and an increase in respiratory signs

249
Q

Nonimmune pregnant sows with pseudorabies

A

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

250
Q

Necropsy findings of swine with pseudorabies

A

Gross lesions are often absent or minimal

Serous to fibrinous rhinitis is common and a necrotic tonsillitis

251
Q

Clinical signs of pseudorabies in secondary hosts

A

(Ruminants, dogs, cats, horses)

Intense pruritus
Hyperacute
Rapid progress
High mortality

252
Q

Cattle with pseudorabies

A 
Aka Mad itch
Intense pruritus 
Cattle may become frenzied
Progressive involvement of CNS, stage of paralysis, ataxia
Death from respiratory failure
253
Q

Dogs and cats with pseudorabies

A

Dogs:
Frenzy associated with pruritus, self-mutilation
Paralysis of jaws and pharynx with drooling
Plaintive howling
Dogs do not tend to attack

Cats:
Progress is so rapid that pruritus may not be observed

254
Q

Vaccination of pseudorabies

A

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

255
Q

What are the two important Equine herpesviruses?

A

Equine herpes virus 1 (EHV-1)

Equine herpes virus 4 (EHV-4)

256
Q

Distribution of EHV-1

A

Endemic in horse populations around the world

257
Q

Transmission of EHV-1

A

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

258
Q

Latency of EHV-1

A

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

259
Q

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

A

True

260
Q

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

A

Respiratory

261
Q

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

A

True

262
Q

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

A

Mononuclear; T lymphocytes

263
Q

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

A

True

264
Q

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

A

Nasal; uterine

265
Q

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

A

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

266
Q

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

A

CNS; abortion

267
Q

Pathogenesis of EHV-1

A

Immunosuppression

268
Q

EHV-1 Respiratory disease

A

Affects mostly younger horses

Rhinopneumonitis

269
Q

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

A

May affect horses of any age or breed

270
Q

EHV-1 Reproductive form

A

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

271
Q

Equine viral Rhinophneumonitis

A

EHV-4 antigenically related to EHV-1

272
Q

Transmission of Equine viral rhinopneumonitis

A

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

273
Q

Pathogenesis of EHV-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

274
Q

Clinical signs for EHV-4

A

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

275
Q

Vaccination of EHV-1 and EHV-4

A

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

276
Q

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

A

Hemorrhagic disease of puppies (fading puppy syndrome)

277
Q

Etiology of Hemorrhagic disease of puppies

A

Canine herpes virus 1, subfamily: Alphaherpesvirinae

278
Q

Hosts of CHV-1

A

Dogs
Wild canids

Highly fatal
Generalized hemorrhagic disease of puppies

279
Q

Transmission of CHV-1 in neonates

A 
Contact with infected oral, nasal or vaginal secretions of dam
Contact with secretions of litter mates
In-utero transmission
From passage through birth canal
Contact with infected fomites (rare)
280
Q

Transmission of CHV-1 in older dogs

A

Venereal transmission

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

281
Q

Pathogenesis of In utero CHV-1 infection in puppies

A

Abortion
Still birth
Infertility

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

282
Q

Pathogenesis of systemic neonatal infection

A

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

283
Q

Pathogenesis of CNS infection of CHV-1

A

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

284
Q

What are the two main factors governing systemic neonatal infection?

A

Body temperature of puppies is critical

Maternal immunity

285
Q

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

A

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

286
Q

Why is maternal immunity important?

A

Maternal antibodies provide protection.

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

287
Q

Clinical signs of CHV-1 in puppies

A 
Painful crying
Abdominal pain
Anorexia
Dyspnea
Passing soft, odorless greenish stool
No elevation in body temp

Survivors develop persistent neurolgical signs, such as ataxia, blindness

288
Q

CHV-1 Adult genital infection

A

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

Male:
Balanoposthitis

289
Q

CHV-1 Adult respiratory infection

A

Older dogs:

Mild respiratory infection (rhinitis and pharyngitis)

290
Q

Ocular infection from CHV-1

A

Conjunctivitis

291
Q

CHV-1 Control

A

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

292
Q

Feline herpesvirus 1 causes what?

A

Feline Rhinotracheitis

293
Q

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

A 
Feline herpes virus 1
Feline calicivirus (FCV) (family Caliciviridae)
294
Q

Transmission of Feline herpesvirus 1

A

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

295
Q

Pathogenesis of FHV-1

A

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

296
Q

Clinical signs of FHV-1

A 
Kittens (up to 4 weeks):
Severe upper respiratory disease
Extensive rhinotracheitis
Fatal bronchopneumonia may develop
Conjunctivitis and ulcerative keratitis

Cats (6 months or older):
Mild or subclinical disease in older kittens

297
Q

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

A

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

298
Q

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

A

Conjunctivitis with hyperemia and serous ocular discharge

Ulcerative keratitis

299
Q

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

A

Yes

300
Q

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

A

No, rare

301
Q

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

A

True

302
Q

Vax of FHV-1

A

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

303
Q

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

A 
Infectious laryngotracheitis (Gallid herpesvirus 1)
Marek's disease (Gallid herpesvirus 2)
304
Q

Etiology of infectious laryngotracheitis (ILT)

A

Gallid herpesvirus 1

305
Q

Hosts of ILT

A

Highly contagious infection of chickens

306
Q

Transmission of ILT

A

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

307
Q

Pathogenesis of ILT

A

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

308
Q

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

A

True

309
Q

Severe form of ILT

A

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

310
Q

Clinical signs of ILT

A

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

311
Q

Diagnosis of ILT

A

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

312
Q

Control of ILT

A

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

313
Q

3 types of vaccines for ILT

A
  1. Chick embryo origin (CEO) - have the capability of reverting to virulence and causing full-blow ILT signs, induces better immunity.
  2. Tissue culture origin (TCO) - only given by eye drop and does not spread significantly or revert to virulence. Level of induced immunity is limited
  3. Pox-vectored recombinant vax
    * These are applied via eye drop, or through mass vax by water or spray
314
Q

Farm biosecturity of ILT

A

Implementation of farm biosecurity measures

315
Q

What is Marek’s Disease?

A

Caused by Gallid herpesvirus 2

Important disease of poultry

316
Q

Hosts of Marek’s disease

A

Chickens are the most important natural host

Turkeys, quails, pheasants are susceptible

317
Q

Transmission of Marek’s disease

A

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

318
Q

What are the 4 pathotypes of Gallid herpes virus 2?

A

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

319
Q

Mild [mMdv]

A

Mostly associated with neural MD.

Disease is preventable with HVT (turkey herpesvirus vaccine)

320
Q

Virulent [vMDV]

A

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

321
Q

Very virulent [vvMDV]

A

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

322
Q

Very virulent plus [vv+MDV]

A

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

323
Q

Marek’s disease pathogenesis

A

Fully productive infection: occurs in feather follicle epithelium. Infected T cells appear to be the ‘Trojan horse’ by which MDV enters the feather follicle epithelium

Inhalation of virus -> initial round of replication in epithelial cells -> macrophage associated viremia -> virus is detectable in the spleen, thymus and the bursa of Fabricius -> productive restrictive infection: cytolytic replication primarily in B cells and later activated CD4+ T cells -> non-productive latent infection in CD4+ T cells -> non-productive neoplastic transformation: some latently infected CD4+ T cells

324
Q

For MD, what is a fully productive 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

325
Q

Productive-restrictive infection for MD

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 immunosuppression

326
Q

Non-productive infection of MD

A

Viral genome persists in T cells (primary CD4+)

No antigens expressed

327
Q

Non-productive neoplastic transformation of MD

A

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

328
Q

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

A

Cytopathic; feather follicles

329
Q

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

A

T lymphocytes

330
Q

Clinical features of MD

A

Neurolymphomatosis
Visceral lymphomatosis
Ocular lymphomatosis
Cutaneous lymphomatosis

331
Q

Neurolymphomatosis

A

Enlargement of nerve trunks.
Nerves lose their striations
Edematous, grey, or yellowish in appearance.

Lameness
Droopy wings
Paresis of legs
Limberneck
Torticollis
Incoordination
332
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.
The bursa is only rarely tumorous and more frequently is atrophic. The absence of burial tumors helps distinguish this disease from lymphoid leukosis

333
Q

Ocular lymphomatosis

A

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

334
Q

Cutaneous lymphomatosis

A

Plucking of feathers reveal nodular lesions on skin

Enlarged feather follicles (commonly termed skin leukosis)

335
Q

Vaccination for MD

A

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

336
Q

General properties of the subfamily Betaherpesvirinae

A

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

337
Q

Etiology of Inclusion Body Rhinitis

A

Porcine herpesvirus 2 aka Porcine cytomegalovirus (PCVM) subfamily Betaherpesvirinae

338
Q

Hosts of Inclusion Body Rhinitis

A

Pigs

Severe disease in piglets

339
Q

Transmission of Inclusion Body Rhinitis

A

Primarily inhalation

Transplacental transmission

340
Q

Pathogenesis of Inclusion Body Rhinitis

A

Widespread petechiae and edema
Most common in thoracic cavity and SQ tissues

Primary site of viral replication: nasal mucus glands, epithelial cells of upper respiratory tract

In some neonates, bone marrow damage and anemia

Still birth, mummification, neonatal death

Endothelial cell damage and necrosis: petechial hemorrhages and edema

341
Q

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

A

Intranuclear; nasal

342
Q

Clinical signs of Inclusion Body Rhinitis

A

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

343
Q

Subfamily Gammaherpesvirinae general properties

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 occurs in lymphoid tissues
Some members cause lymphoid tumors

344
Q

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

A

Viruses in subfamily Gammaherpesvirinae
At least 10 viruses have been recognized

Two most important MCF viruses are:
Alcephaline herpesvirus-1 (AHV-1) aka Wildebeest-associated MCF
Ovine herpesvirus-2 (OvHV-2) aka Sheep-associated MCF

345
Q

Wildebeest-associated MCF [Alcephaline herpesvirus-1

A

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

346
Q

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

A

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

347
Q

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

A

True

348
Q

Transmission of wildebeest-associated MCF

A

Between wildebeest: horizontal and occasionally intrauterine transmission in wildebeest. Inapparent infection.

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

349
Q

Transmission of sheep-associated MCF

A

Between sheep:
Respiratory
Transplacental rare
Contact with nasal secretions

Sheep to cattle:
Not known
Presumably by inhalation or ingestion

350
Q

Transmission of MCF between wildebeest and sheep

A

Inapparent infection in wildebeest and sheep.

Virus transmitted from wildebeest-to-wildebeest and sheep-to-sheep

351
Q

Cattle’s role in MCF

A

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

352
Q

Pathogenesis of MCF

A

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

353
Q

Clinical signs of MCF

A

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

354
Q

Peracute form of MCF

A

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

355
Q

Head and eye form of MCF

A 
Early stages
Reddened eyelids
Bilateral corneal opacity
Crusty muzzle, nares
Nasal discharge
Salivation
Erosions of the tongue, hard palate, and buccal papillae (along with necrosis)
356
Q

What is zebra striping?

A

Necropsy finding of MCF in the bovine colon.

Severe longitudinal linear congestion of the mucosa

357
Q

Control of MCF

A

Separation of cattle from wildebeest and sheep

Incidence too low to justify development of a vaccine

358
Q

Etiology of African Swine Fever (ASF)

A

Sole member of family Asfarviridae

Only known DNA arbovirus

359
Q

Hosts of ASF

A

All breeds and types of domestic pigs and European wild boar

Inapparent infection in warthogs, bush pigs and giant forest hogs, which act as reservoirs

360
Q

T/F: ASF is an OIE List A Disease

A

True

361
Q

Geographical distribution of ASF

A

Endemic:
Most of sub-Saharan Africa
Island of Sardinia (Italy)

Recent outbreaks:
Eastern Europe and Russia
The virus has continued to spread within the Russian Federation

362
Q

ASF Virus Stability

A 
Virus survive at least 30 days in pens
Very resistant to s wide range of pH
Survive in chilled carcass 
Highly resistant to putrefaction
Remains viable for long periods in blood, feces and tissues
Can multiply in vectors
363
Q

Transmission of ASF

A

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

364
Q

ASF reservoirs (Sylvatic cycle)

A

Warthog
Giant Forest Hog
Bush Pig

365
Q

Cycles that exist in the transmission of ASF

A

Domestic cycle between pigs
Enter ticks and begins the sylvatic cycle

Adult warthogs:
No viremia, virus in various lymphoid tissues

Juvenile warthogs:
Significant viremia

366
Q

Sylvatic cycle of ASF

A

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

367
Q

Domestic cycle of ASF

A

Meat products -> waste food -> fomites -> direct contact via secretions and blood loss

Primary outbreaks in domestic swine:
Bite of infected tick
Direct contact with infected animal
Indirect contact on fomites
Virus spreads to new areas when pigs are fed uncooked scraps that contain infected pork
Aerosol spread
Mechanical transmission through biting flies

All body fluids and tissues contain large amounts of infectious virus
Pigs that survive infection may become carriers and shed virus in secretions and excretions

368
Q

Pathogenesis of ASF

A

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

369
Q

Apoptosis of host cells with ASF

A

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

370
Q

Mechanisms related to hemorrhages of ASF

A

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

371
Q

Peracute clinical signs of ASF

A

Pigs may die suddenly

372
Q

Acute form clinical signs of ASF

A

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

373
Q

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

A

True

374
Q

Chronic form clinical signs of ASF

A

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

375
Q

What happens to the spleen of pigs with ASF

A

Becomes large and friable or blackberry jam spleen

376
Q

Immunity to ASF

A

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

377
Q

To prevent ASF

A

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

378
Q

During ASF outbreaks

A

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

379
Q

Family Parvoviridae general properties

A

Viruses are very stable

Disinfection of contaminated premises is difficult

380
Q

Replication of Parvoviridae

A

Occurs in the nucleus of dividing cells

Infection leads to large intranuclear inclusion bodies

381
Q

Genus parvovirus

A

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

382
Q

Human parvovirus B19

A

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

383
Q

Feline panleukopenia is aka what?

A

Feline distemper

Feline infectious enteritis

384
Q

Etiology of feline panleukopenia

A

Feline parvovirus

385
Q

Hosts of feline panleukopenia

A

Highly contagious, often fatal disease of cats

Severe in mittens

386
Q

Epidemiology of FPV

A

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

387
Q

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

A

Yes, 6 weeks after recovery

388
Q

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

A

False, other way around

389
Q

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

A

Should NOT

390
Q

Transmission of FPV

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

391
Q

What are the hallmarks of Panleukopenia

A

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

392
Q

FPV enteritis

A

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

393
Q

FPV in-utero infections

A

Early in-utero in pregnant queens can result in:
Early fetal death and resorption with fertility
Abortions
Birth of mummified fetuses

Infection closer to end of gestation:
Birth of live kittens with varying degree of damage to the late-developing neural tissues
Variable effects on kittens from the same litter

394
Q

FPV CNS infections

A

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

395
Q

FPV cerebellar hypoplasia

A

Lysis of mitotic cells of the external germinal layer

Impaired cerebellar development

396
Q

T/F: Ataxia is common in kittens with FPV

A

True

397
Q

FPV and DIC

A

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

398
Q

Clinical signs of FPV

A 
Most common in kittens
Fever
Depression
Anorexia
Rough coat
Repeated vomiting
Profuse, persistent and frequently bloody diarrhea
Severe dehydration
Hypothermia
Sudden death from complications of secondary infection, dehydration and DIC
399
Q

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

A

Villous collapse, enteritis

Diarrhea

400
Q

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

A

Germinal center depletion, apoptosis of lymphocytes, thymic atrophy

Lymphopenia

401
Q

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

A

Stem cell depletion

Neutropenia -> thrombocytopenia and anemia

402
Q

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

A

Fetal death

Loss of pregnancy

403
Q

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

A

Cerebellar hypoplasia

Cerebellar ataxia

404
Q

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

A

True

405
Q

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

A

3-4 weeks

406
Q

_____ degeneration is seen in kittens infected with FPV

A

Retinal

407
Q

Diagnosis of FPV

A

Hematology: leukopenia, neutropenia more consistent than lymphopenia - total WBC counts <2000 cells/uL are associated with a poorer prognosis

Fecal viral antigen testing using immunochromatographic test kit or ELISA: results may remain positive up to 2 weeks following MLV vaccination

408
Q

Serological testing for diagnosis of FPV

A

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

409
Q

Treatment of FPV

A

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

410
Q

Control of FPV

A

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

411
Q

Vaccination of FPV

A

Attenuated (modified) live vaccines (MLV)

MLV should not be administered to:
Pregnant cats
Immunosuppressed cats
Sick cats
Kittens less than 4 weeks old
412
Q

Is canine parvovirus 1 an important virus in dogs?

A

Nope.

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

413
Q

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

A

Canine parvovirus 2 (CPV-2)

414
Q

Distribution of CPV-2

A

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

415
Q

Epidemiology of CPV-2

A

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

416
Q

Transmission of CPV-2

A

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

417
Q

Pathogenesis and clinical findings of CPV-2

A

Enteritis
Myocarditis
Panleukopenia

Similar to FPV

418
Q

Enteritis with CPV-2

A

CPV-2 infects the germinal epithelium of the intestinal crypts, causing destruction and collapse (and necrosis) of the epithelium. No replacement of cells lost from tip of villus. Villi shortened and hemorrhagic diarrhea

Hemorrhagic enteritis
Ballooned small intestine
Ingesta visible through small intestine wall

419
Q

Myocarditis with CPV-2

A

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

420
Q

Diagnosis of CPV-2

A

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

421
Q

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

A

SNAP Parvo Test

422
Q

Vax for CPV

A

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

423
Q

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

A

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

424
Q

Porcine parvovirus

A

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

425
Q

Transmission of porcine parvovirus

A

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

426
Q

Pathogenesis of porcine parvovirus

A

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

427
Q

Transplacental infection of porcine parvovirus

A

Death at different stages of pregnancy is typical of PPV infections

428
Q

What is the hallmark of PPV?

A

Increase in mummified fetuses after a normal gestation period

429
Q

Are abortions common in PPV

A

Uncommon

430
Q

What Times of infection is critical for PPV

A 
Embryo/fetus (<30 days): dies and resorbed. Dams may return to estrus
Early fetus (30-70 days): fetuses die and become relatively dehydrated (mummified)
Late fetus (>70 days to term): frequently develop lesions, but also mount an immune response and usually survival in-utero
431
Q

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

A

True

432
Q

Diagnosis for PPV

A

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

433
Q

Immunity to PPV

A

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

434
Q

Vaccination/immunization to PPV

A

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

435
Q

Can papillomaviruses transform cultured cells?

A

Yes

436
Q

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

A

Warts or papilloma

I hope you got that one!

437
Q

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

A

Benign neoplasms; spontaneously

438
Q

T/F: Papillomaviruses are not species and site specific

A

False, they are specific

439
Q

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

A

True

440
Q

Can the warts of papillomavirus progress to malignancy?

A

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

441
Q

Replication of papillomaviridae

A

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

442
Q

The story of oncogenic papillomaviruses

A

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

443
Q

Host of Bovine papillomatosis

A

Cattle

Warts are more commonly seen in cattle than in any other domestic animals

Natural bovine papillomavirus infection of horses (WHAT????) may occur after exposure of the horses to cattle

444
Q

Transmission of bovine papillomavirous

A

Between animals by contaminated fomites, such as milking equipment, halters, nose leads, grooming and earmarking equipment

Sexual transmission of venereal warts in cattle

445
Q

Fibropapilloma is mostly caused by what? What is it?

A

Bovine papillomavirus types 1, 2, and 5

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

446
Q

Where are fibropapillomas common?

A

Udder and teats
Head
Neck
Shoulders

May also occur in the omasum, vagina, penis and anus

447
Q

Cutaneous papillomas are caused by what and what are they?

A

Bovine papillomavirus type 3

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

448
Q

What is the relationship between Bracken Fern and Bovine Papillomavirus?

A

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

449
Q

Treatment of bovine papillomatosis

A

Surgical excision, or cryosurgery with liquid nitrogen
Topical agents, podophyllin and undiluted medical grade DMSO (dimethylsulfoxide)
Bovine interferon-alpha

Wart vaccine (yes, it’s a thing apparently)

450
Q

Canine oral papillomatosis

A

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

451
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

452
Q

Treatment of canine oral papillomatosis

A

Surgical excision, cryosurgery, electrosurgery

Auto genius vaccines

453
Q

Equine sarcoids

A

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

454
Q

Equine sarcoids transmission

A

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

455
Q

What do equine sarcoids look like?

A

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

456
Q

Treatment of equine sarcoids

A

Cryotherapy
Surgical or laser excision
Local immune modulation
Local radiotherapy

457
Q

Morphology of Adenoviridae

A

Non-enveloped, precisely hexagonal in outline

12 vertex penton capsomers each with a fiber protrude from the surface of capsid

458
Q

Genome and replication of Adenoviridae

A

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

459
Q

Adenoviridae general properties

A

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

460
Q

Pathogenesis of adenoviruses

A

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

Cause immunosuppression

461
Q

Long periods of latency of adenoviruses

A

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

462
Q

Oncogenesis of adenoviruses

A

Under specialized conditions, some have been shown to be oncogenic

463
Q

What are the two most important genera of adenoviruses?

A

Mastadenovirus: mammalian adenoviruses. A single penton fiber projects from each vertex

Aviadenovius: Avian adenoviruses. Each penton fiber is bifurcated, appear as two fibers extending from each penton base

464
Q

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

A

Canine adenovirus-1 (CAV-1)

465
Q

Transmission of CAV-1

A

Acute infection: found in all secretions and excretions
Afterwards, virus shed in urine for at least 6-9 months

Route: oronasal transmission
Contact with: 
Secretions/excretions of infected dog
Contaminated fomites
Ectoparasites can harbor CAV-1
466
Q

Sites of ICH virus replication

A 
Macrophages
Kupffer cells
Hepatocytes
Vascular endothelium of different organs including CNS
Parenchyma cells of organs and tissues

Liver, kidneys, spleen and lungs are the main target organs!

467
Q

Pathogenesis of ICH

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
468
Q

What happens in chronic cases of ICH?

A

Cirrhosis

469
Q

What happens to the kidneys during ICH?

A

Acute infection - glomerulonephritis

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

470
Q

Corneal edema with ICH

A

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

471
Q

How does corneal edema develop?

A

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

472
Q

Complications from ICH

A

DIC: Results from:
Damage to endothelium
Inability of diseased liver to remove activated clotting factors

Bacterial pyelonephritis resulting from renal damage

473
Q

ICH clinical signs

A

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

474
Q

Peracute cases of ICH

A

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

475
Q

Acute cases of ICH

A

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

476
Q

Necropsy and histopathology findings of ICH

A

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

477
Q

Diagnosis of ICH

A

Biochemistry and hematology:
Leukopenia persists throughout febrile period
Increased ALT and AST due to hepatic injury
Proteinuria
Prolonged prothrombin time, thrombocytopenia

Virus isolation: URINE, blood, tissue homogenates, etc

478
Q

Treatment of ICH

A

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

479
Q

Immunity to ICH

A

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

480
Q

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

A

Self-limiting upper respiratory disease of dogs

Multiple things can cause kennel cough. CAV-2 and Bordetella bronchiseptica (primary pathogen) are most prevalent

481
Q

Transmission of ITB

A

Highly contagious via aerosolized droplets

Stress, unfavorable conditions increases severity of disease

482
Q

Signs of uncomplicated ITB

A

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

483
Q

Signs of “complicated” ITB

A

Severe pneumonia or bronchopneumonia

Life threatening

484
Q

Treatment of ITB

A

Antitussives when used in conjunction with broncodilators

485
Q

Immunity to ITB

A

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

486
Q

Equine adenovirus

A

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

487
Q

Clinical signs of SCID in foals

A

Severe bronchiolitis and pneumonia. Respiratory distress and related signs

488
Q

Avian adenoviruses in chickens

A

Inclusion body hepatitis

Egg drop syndrome ‘76

489
Q

Avian adenovirus of ducks

A

Hepatitis (rare)

490
Q

Avian adenoviruses of quail

A

Bronchitis

491
Q

Avian adenovirus of turkeys

A

Hemorrhagic enteritis

Egg drop syndrome

492
Q

Avian adenovirus of pheasants

A

Marble spleen disease

RUSVM Virology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions