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Path review > Mouse Pathology Review - DNA Viruses > Flashcards

Mouse Pathology Review - DNA Viruses Flashcards

1
Q

What kind of virus is Ectromelia virus

A

orthopoxvirus

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2
Q

What does ECTV stand for?

A

Ectromelia virus

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3
Q

Which mice are susceptible to ECTV?

What is a common presentation for these mice?

A
  • C3H
  • A
  • SWR
  • DBA
  • CBA
    BALB/c

They die acutely

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4
Q

Which mice are moderately resistant to ECTV?

A

SJL and AKR

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5
Q

Which mice are highly resistant to fatal infection of ECTV?

A

C57BL/6 mice

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6
Q

What is ECTV resistance based on?

A

Many genes, particularly variations in immune cells and cytokines?

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7
Q

Clinical signs of ECTV?

A
  • vary from ruffled fur to prostration to death in a matter of hours
  • Generalized rash that may last for weeks and leave scars
  • subclinical in resistant strains
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8
Q

Common gross lesions of Poxvirus

A
  • Alopecia, cutaneous erythema, erosions (rash), conjunctivitis, swelling, and Dry gangrene of extremities leading to amputation (ectromelia)
  • swollen, friable livers w/ pinpoint white/red foci
  • “Tiger stripe spleen” - splenic fibrosis -
  • intestinal hemorrhage of upper small intestine
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9
Q

Histo lesions of ECTV

A
  • *** Foci of coagulative necrosis in liver, spleen lymph nodes, Peyer’s patches, thymus
  • ***erosive enteritis
  • *** epidermal hyperplasia, hypertrophy and ballooning of epithelial cells
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10
Q

Strains resistant to ECTV will show more ____, while more susceptible strains will show more ___ of lympoid tissue

A
  • hyperplasia
  • necrosis
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11
Q

Types of Inclusion Bodies of ECTV

A

Type A: Eisinophilic, intracytoplasmic inclusion bodies in epithelial cells of the skin
— Marchal bodies
— epidermal skin cells, hepatocytes at periphery of necrosis

Type B: basophilic, intranuclear inclusion bodies potentially in any affected cell, but difficult to see

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12
Q

DNA viruses tend to make intranuclear inclusion bodies. What sets ECTV apart?

A

can be intracytoplasmic and intranuclear

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13
Q

Diagnosis of ECTV

A
  • ELISA
  • Histopathology
  • PCR, immunofluorescence
  • Hemagglutination assay (HAI)
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14
Q

Pathogenesis of ECTV

A

Skin invasion via trauma to skin -> local invasion and multiplication -> replication in regional LN -> hematogenous spread to major organs (primary viremia) -> replication in spleen and liver -> secondary viremia -> targets sites like skin, kidney, lung, intestine, and other organs and causing focal infections

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15
Q

Transmission of ECTV

A
  • Direct contact and cutaneous trauma (NOT contaminated animal products)
  • Not highly contagious
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16
Q

Repro concerns for ECTV

A
  • maternal antibodies protect against disease, but not infection
  • ECTV infects placenta and fetuses, leading to fecal death
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17
Q

Prevention and Control of ECTV

A
  • Decontamination: viral particles stable in environment
  • Quarantine and/or Depopulation
  • Vaccination w/ vaccina virus (will not always prevent infection but will lower it)
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18
Q

Research impacts of ECTV

A

Potential massive loss of life in susceptible strains

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19
Q

Types of Mouse Adenoviruses

A
  • Murine mastadenovirus-1 (MAdV-1)
  • Murine Mastadenovirus-2 (MAdV-2)
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20
Q

typical presentation in of MAdV-1 and MAdV-2 in immunocompetent mice

A

subclinical

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21
Q

Which cells does MAdV-1 target?

A
  • Monocyte-macrophage lineage
  • Renal distal tubular cells, respiratory epithelium, adrenal cortical cells, microvascular endothelium
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22
Q

Which cells are important for clearing MAdV-1 infection?

A

B-cells

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23
Q

Which cells are important for fighting disease and what else can they do?

A

T-cells; can also contribute to pathology (T-cells killing the virus may determine severity of clinical disease)

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24
Q

How is MAdV-1 shed?

A
  • in the urine
  • Direct contact and nasal secretions
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25
Q

Which strains develop hemorrhagic encephalitis with MAdV-1 infection?

A
  • C57BL/6
  • DBA/2
  • SJL
  • SWR
  • CD-1
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26
Q

Which strains develop disseminated disease with hemorrhagic encephalomyelitis?

A

B6-Rag1

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27
Q

Which strains develop a fatal disseminated disease with focal hemorrhagic enteritis and microvascular fatty change (Reye’s-like syndrome)?

A

BALB-scid and BALB-scid/beige

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28
Q

Which strains develop progressive wasting, disseminated infection, and duodenal hemorrhage?

A

Athymc C3HH3N-nude

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29
Q

Which type of brain matter is more affected by MAd-V1?

A

white matter – “a lot of it is being ‘unable to relax’”

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30
Q

Clinical signs of MAdV-1

A
  • runting
  • Dehydration
  • CNS signs from white matter injury
    — rigid tails, hypermetria, paraphimosis, ataxia, urinary bladder distention
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31
Q

Gross lesions of MAdV-1

A
  • thymic involution
  • necrosis in liver, spleen, and other organs
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32
Q

Histo lesions of MAdV-1

A
  • endothelial necrosis and hemorrhage
  • Intranuclear inclusions in foci of necrosis and hemorrhage in vary types of organs
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33
Q

T/F Rats will seroconvert and are susceptible to MAdV-2

A

False; they will not seroconvert

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34
Q

How is MAd-V2 shed?

A

in the feces

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35
Q

Tissue tropism of MAdV-1

A

multiple: intestine, salivary glands, spleen, brain, myocardium, brown fat

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36
Q

Tissue tropism of MAdV-2

A

enterotropic

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37
Q

Prevalence of MAdV-1 in vivaria

A

historic only

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38
Q

Prevalence of MAd-V2 in vivaria

A

natural infection in modern vivaria, low

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39
Q

Clinical signs in natural infection of MAd-V1

A

none described

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40
Q

Clinical signs in natural infection of MAdV-2

A

runting of suckling mice

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41
Q

Clinical signs in experimental infection of MAdV-1

A

severe with pup infection: runting, lethargy, scruffy, death in 10 days, wasting disease in nude mice

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42
Q

Clinical signs of experimental infection of MAdV-2

A

Absent except for runting of suckling mice

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43
Q

Clinical signs of MAdV-2

A

Rare, aside from runting of suckling pups

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44
Q

Histopathological findings of MAdV-2

A

intranuclear inclusions in intestinal epithelium of infant mice > adult mice (apical location, rather than basal)

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45
Q

Transmission of MAdV-2

A

shed in feces

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46
Q

Diagnosis of MAdV

A
  • Serology
  • Intranuclear inclusions in intestine are pathognomonic for MAdV-2
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47
Q

Prevention and Control of murine adenoviruses

A
  • Serologic monitoring
  • Segregate infected colonies until infection is over (MAdV-2 only)
  • Rederivation

“MAV1 - either suck it up and accept its presence or cull”
“MAV-2 - self-limiting, so can segregate colonies”

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48
Q

Research concerns of MAdV

A

primarily pathogenicity impact on immunodeficient mice

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49
Q

DDx for ECTV

A

causes of hepatitis, such as
- MHV vs Tyzzer’s dz vs salmonellosis vs other

Skin lesions
- bite wounds vs. trichotillomania vs. hypersensitivity vs. other forms of dermatitis

gangrene or digit / tail amputation
- trauma vs. ringtail

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50
Q

Which subcategory of herpesvirus is the worst?

A

alpha-herpesviruses

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51
Q

What are the three subcategories of herpseviruses

A
  • alpha-herpesviruses
  • beta-herpesviruses
  • gamma-herpesviruses
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52
Q

What is the other name for Murine herpesvirus 1?

A

Mouse Cytomegalovirus (MCMV)

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53
Q

Clinical signs of natural infection of MCMV?

A

subclinical in lab animals

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54
Q

Clinical signs of Experimental infection of MCMV?

A

multisystemic necrosis, inflammation, and death of neonatal mice

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55
Q

Histopath lesions of MCMV?

A
  • enlarged cells with intranuclear and intrcytoplasmic inclusions (nucleus is easily 10x normal size), particularly in the salivary glands, esp. the submandibular gl.
  • Lymphoplasmacytic infiltrates
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56
Q

Strains resistant to MCMV

A
  • C57BL/6
  • B10
  • CBA
  • C3H

Resistance is associated with the H-2k haplotype

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57
Q

Strains susceptible to MCMV

A
  • BALB/c
  • A

Will see worse necrosis and inflammation in organs of T-cell-deficient mice

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58
Q

Pathogenesis of MCMV

A

experimental inoculation -> viremia and multisystemic dissemination to lung, heart, liver, spleen, gonads, and salivary glands ->rapid clearance from every but PERSISTENT in salivary glands. Intranuclear inclusions can be seen in acinar epithelial cells

59
Q

Diagnosis of MCMV

A
  • Histopathology

—in situ hybridization to assist

Serology and PCR not reliable bc subclinical in most situations

60
Q

what is the major target of MCMV

A

macrophages; blood monocytes are important for viremic phase of infection

61
Q

Which cell type helps to clear MCMV

62
Q

T/F MCMV is a latent infection, which means that stress or immunosuppression can result in reactivation of the virus

63
Q

T/F MCMV readily crosses the placenta

64
Q

What can MCMV infection cause in pregnant mice?

A

Fetal death and resorption, delayed birth, experimentally infected mice.

65
Q

Transmission of MCMV

A
  • direct contact with infected mouse or bodily fluids (saliva, urine, tears)
  • contaminated animal products
  • sexual and in utero transmission due to infection of gonads
66
Q

Prevention of MCMV

A

KEEP WILD RODENTS OUT

67
Q

Research concerns of MCMV

A
  • immune suppression by virus
  • reactivation of latent persistent infection by either lymphoproliferative stimuli or immunosuppression
  • potential for immune-complex glomerulonephritis in persistent infections
  • synergistic effect with Pseudomonas aeruginosa
68
Q

What is another name for murine herpesvirus 3?

A

Mouse Thymic Virus (MTV)

69
Q

Prevalence of MTV

A

wild mice: common
Lab mice: rare

70
Q

Tropism of MTV

A

lymphocytotrophic - selectively targetrs CD4+ cells

but some infection/replication in thymic epithelial cells and macrophages

71
Q

Where is MTV virus shed

72
Q

Why are serology and PCR-based diagnosis not used for MCMV

A

they are not used because it is assumed that the virus has a very low prevalence

73
Q

Clinical signs of MTV

A

it is subclincal, no CS

74
Q

Gross findings of MTV

A

Acute thymic necrosis in neonatal mice (most susceptible in first 6 days of age)

  • infection is persistent, but thymus will eventually return to normal size
75
Q

Histopath lesions of MTV

A
  • necrosis of thymic lymphocytes, and lesser necrosis of lymphocytes in LNs and spleen
  • intranuclear inclusion bodies
  • granuloma formation in recovery
76
Q

Strains susceptible to MTV

A
  • BALB/c and A strains can get gastritis if infected as neonates
  • Autoimmune oophoritis and anti-thyroglobulin development in other mice strains
77
Q

Research implication of MTV

A

immunosuppression

78
Q

What effect will MTV have on athymic nude mice?

A

none really, since it has a destructive effect on T lymphocytes, which they lack

79
Q

Tissue tropism of MCMV

A

multiple tissues, but histopath in salivary glands

80
Q

Tissue tropism of MTV

A

infects salivary glands; lesion only in thymus, LN, spleen

81
Q

MCMV Prevalence in vivaria/reservoir

A

rare / wild mice

82
Q

MTV prevalence in vivaria / reservoir

A

rare / wild mice

83
Q

Is latent infection of feature of MCMV

84
Q

is latent infection of feature of MTV

85
Q

Limitations to detection of MCMV

A

salivary gland lesions not always present; mice may not seroconvert

86
Q

limitations to detection of MTV

A

mice infected as neonates may not seroconvert

87
Q

Name two mouse parvoviruses

A

Minute Virus of Mice

Mouse Parvovirus

88
Q

Which mouse parvovirus is more prevlant?

A

MPV > MVM (75% of parvoviral infections)

89
Q

T/F immunity to one parvovirus confers immunity of the other

A

false; it does not

90
Q

Which structural capsid protein contributes the most antigenic and biologic differences between MVM and MPV

91
Q

Pathogenesis of MVM and MPV

A
  • S-phase-dependent (so young animals are more affected (rapidly dividing cells present))
  • oral inoculation -> replicate in intraepithelial lymphocytes, lamina propria, and endothelium of SI -> disseminate to multiple organs (kidney, intestines, lymphoid tissue, liver, lung (lesser extent)
92
Q

T/F rodent parvoviruses cause intestinal disease

A

false; the intestinal crypts lack proteins for viral binding and infection

93
Q

Site of initial replication of mouse parvoviruses

A

In lymphocytes

94
Q

T/F clinical signs are seldom present in mouse parvovirus infections

A

technically true, as MVM and MPV do not carry clinical signs

95
Q

transmission of murine parvoviruses

A

feces and urine via oronasal inoculation

96
Q

What cells have the highest tropism for murine parvoviruses

A
  • endothelial cells
  • hematopoietic cells
  • lymphoreticular cells

– MVM also targets erythrocytes and can replicate in renal tubular epithelium

97
Q

Clinical signs of MVM and MPV

A

none, infections are typically subclinical

Experimental infections can cause disease in neonates and some strains

98
Q

Gros lesions of MVM and MPV

A
  • MVM: possible cerebellar hypoplasia (targeting granular layers) in neonates
  • MPV: usually none.
99
Q

Histopath lesions for MPV and MVM

A

generally none, aside from inclusion bodies

100
Q

What clinical signs can be seen with MVMi variant of MVM? what is the other name?

A

mortality in neonates due to hemorrhage, hematopoietic involution, and renal papillary infarction

immunosuppressive strain of MVM

101
Q

Which strains are susceptible to infection with MVM/MVMi?

A
  • DBA/2 neonates susceptible to severe disease
  • SCID adults can die and/or develop severe leukemia
  • C57BL/6 neonates are resistant
102
Q

MVM has is more ______ in duration, which MPV causes _______ infections with ____ shedding and possible immunologic changes

A
  • limited
  • persistent
  • prolonged
103
Q

Diagnosis of MPV and MVM

A
  • serology (primary method) - tests for VP2 (specific for each parovirus)

PCR, ISH, IHC also possible but more reliable during active infections

104
Q

Which tissue is the most reliable source for PCR detection of MVM and MPV

A

mesenteric lymph nodes

105
Q

Transmission of MVM and MPV

A
  • feces and urine (soiled bedding) by oronasal exposure
  • direct contact
  • contaminated animal products
106
Q

Prevention and Control of MPV / MVM

A
  • Decontamination since virus persists in environment
  • Quarantine since immunocompetent mice can clear infection (MVM)
  • cage-by-cage Test-and-cull (MPV)
  • Rederivation and embryo transfer also paossible
107
Q

Research concerns for MPV and MVM

A
  • studies of immune response or mitotically active cells
  • infection of animal cells or products can affect experiments
108
Q

How long is MVM thought to last in immunocompetent hosts?

109
Q

Name the two polyomaviruses of mice

A
  • Polyoma virus (PyV)
  • K virus
110
Q

What is the major viral oncogene of PyV

A

Middle T antigen (MT antigen)

111
Q

T/F natural infection with polyomavirus is rare, but experimental infection has been used to induce tumors

112
Q

Clinical Signs of PyV

A
  • subclinical in natural infections of immunocompetent mice
  • tumors, neuro dz, and wasting in immunodeficient mice
113
Q

C57BL/6 are ____ to PyV, while AKR and CBA mice are ________

A
  • resistant
  • highly susceptible
114
Q

Gross lesions of PyV

A
  • neonatal mice and immunodeficient mice: multifocal necrosis and inflammation followed by tumor formation in numerous tissues
  • immunocompetent mice: won’t see much
115
Q

Transmission of PyV

A
  • IN (virus shed in urine, feces, and saliva); direct contact?
  • Contamination of cell lines and transplantable tumors
116
Q

prevention and control of PyV

A

elimination of infected mice and materials

117
Q

Research concerns of PyV

A

infection of research cell lines, contamination, and spread to susceptible mice

118
Q

tissue tropism of PyV

A

Polytropic - will infect many cells

  • intranuclear inclusions most obvious in renal tubules and in cytolytic lesions
119
Q

In which tissue does PyV persist for months

A

lung and kidneys, other sites can clear the virus

120
Q

Types of tumors from PyV in susceptible strains

A
  • Epithelial tumors (hair follicle origin): mammary gland, salivary gland, and thymis
  • mesenchymal tumors: renal carcinomas, osteosarcomas, hemangiosarcomas, and fibrosarcomas
122
Q

T/F: neonatal mice are susceptible to infection via oronasal inoculation, and you may see low mortality in initial stages

A

false; will see high mortality

123
Q

Clinical disease of PyV in neonates

A
  • runting syndrome
  • polyarteritis
  • enhanced autoimmune disease
124
Q

Clinical disease of PyV in nude mice

A
  • multisystemic wasting disease
  • paralysis (infection of oligodendroglia and demyelination, or tumors of vertebrae)
125
Q

K virus is also referred to as _____ and _____

A
  • Kilham’s virus
  • Murine Pneumotropic Virus (MptV)
126
Q

T/F K virus is oncogenic

A

False; it is not oncogenic

127
Q

transmission of K virus

A
  • oronasal
  • fecal-oral
128
Q

Which mice develop disease with K virus

A
  • Neonatal mice (usually resistant by 12-18d of age)
  • immunodeficient mice
129
Q

What is the main viral target of K virus

A
  • vascular endothelium
    – replicates in the intestinal capillary endothelium
    – high tissue tropism for pulmonary endothlium
130
Q

Gross findings of K virus

A
  • restricted to lungs
    — congestion, edema, hemorrhage, and atelectasis
131
Q

Histopath findings of K virus

A
  • lymphocytic interstitial pneumonia during recovery
  • Can have leukocytic infiltrates in liver sinusoids and nuclear ballooning of cells lining sinusoids
  • viral persistence in renal tubular epithelium
132
Q

PyV prevalence in vivaria

A

rare, but commonly used in research

133
Q

K virus prevalence in vivaria

A

essentially eliminated

134
Q

PyV tissue tropism

A

Polytropic

lung and kidney; multi-organ tumor function

135
Q

K virus tissue tropism

A

vascular endothelium

136
Q

PyV CS in natural infection

A

immunodeficient mice: wasting, tumor induction, neuro signs

137
Q

K virus CS in natural infection

138
Q

PyV virus CS in experimental infection

A

acute dz in neonates with tumor formation in survivors

139
Q

K virus CS in experimental infection

A

Dyspnea, pulmonary hemorrhage, and edema in neonates and nudes

140
Q

Does PyV have Intranuclear inclusions?

141
Q

Does K virus have intranuclear inclusions?

142
Q

What does papillomavirus (MusPV) cause in T-cell-deficient mice

A
  • papillomas
143
Q

T/F murine papillomavirus is oncogenic

A

false, it is not

Path review (9 decks)

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