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Skin MS: Week 4 > Viral Skin Infections (Virus) > Flashcards

Viral Skin Infections (Virus) Flashcards

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1
Q

Vesicular or Pustural Rash Diseases - major viral causes

A 
HHV-1* (Neuro, HRM)
HHV-2* (Neuro, HRM)
HHV-3
Coxsackieviruses A and B
Smallpox
Orf virus* (in handout)
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2
Q

Maculopapular Rash Diseases - major viral causes

A 
Measles* (Neuro, IHO)
Rubella
Parvovirus B19
Roseoloviruses (HHV-6 and HHV-7)
HHV-4* (in IHO)
ECHO virus* (in handout)
West Nile Virus* (in handout)
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3
Q

Wartlike eruptions - major viral causes

A

HPV

Molluscum contagiosum

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4
Q

Steps of Viral Infection inside organism

A 
Replication at site of entry
Primary viremia 
Replication
Secondary viremia
Replication 
Transmission to other hosts 
*See picture*
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5
Q

Herpesvirus infections last a life time in a state called ____

A

latency

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6
Q

Herpesvirus do/do no integrate into host genome

A

Do not
They make proteins that mediate genome persistence in host cells by binding to the viral genome and ensuring that as the host cell divides that the viral genome is copied.

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7
Q

Herpesvirus can/cannot reactivate

A

Can - more infectious

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8
Q

virus - dsDNA (group I) - linear genome - icosahedral nucleocapsid - enveloped

A

herpesvirus family

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9
Q

herpesvirus subfamilies

A 
alpha:
simplexvirus (1 and 2)
Varicellovirus (VZV)
beta:
cytomegalovirus (HCMV, HHV-6/7)
gamma:
Lymphocryptovirus (EBV)
Kaposisarcoma-associated herpesvirus
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10
Q

herpesvirus tree

A

virus - dsDNA (group I) - linear genome - icosahedral nucleocapsid - enveloped

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11
Q

Herpes simplex 1

A

alpha - Human herpesvirus 1 (HHV-1)

Above waist - gingivostomatitis, herpes labialis, etc.

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12
Q

Herpes simplex 2

A

alpha - Human herpesvirus 2 (HHV2)

Below wait - genital herpes or neonatal herpes

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13
Q

Varicella-Zoster virus

A

alpha - HHV-3

Chickenpox or shingles

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14
Q

Human cytomegalovirus

A

beta - HHV 5

Congenital CMV infection, systemic, mono-like

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15
Q

Roseoloviruses

A

beta - HHV 6(a,b)/7 - exanthem subitum (6th disease), encephalitis in IC

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16
Q

Epstein-Barr Virus

A

gamma- HHV-4 - mononucleosis, lymphoid-organ related cancers

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17
Q

Kaposi Sarcoma-Associated Herpesvirus

A

gamma - HHV8 - Kaposi sarcoma

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18
Q

first disease

A

measles

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19
Q

second disease

A

strep pyogenes (scarlet fever)

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20
Q

third disease

A

rubella

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21
Q

fourth disease

A

staph aureus (SSSS)

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22
Q

fifth disease

A

parvovirus B19 (slapped cheek)

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23
Q

sixth disease

A

HH6/7 - roseola

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24
Q

Virus lifecycle

A

attachment - penetration/adsorption - synthesis - assembly - release

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25
Q

HHV1 and HHV2 cause

A

mucosal lesions, encephalitis

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26
Q

HHV1 and HHV2 transmission

A

saliva, vaginal secretions, lesion fluid
1 - mainly oral
2 - mainly sexual

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27
Q

HHV1 and HHV2 vaccines

A

no vaccine

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28
Q

HHV1 and HHV2 drugs

A

acyclovir etc.

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29
Q

HHV1 and HHV2 disease mechanism

A

virus spreads cell to cell, not neutralized by antibody
cell-mediated immunopathology –> damage and sxs
cell mediated immunity required for resolution of infection
virus establishes latency in neurons
reactivated by stress or immune suppression

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30
Q

VZV diseases

A

chickenpox, shingles

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31
Q

VZV transmission

A

respiratory droplets or contact

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32
Q

VZV risk factors

A

contact, IC

disease severity worsens as get older

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33
Q

VZV vaccines

A

Live vaccine for both (separate)

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34
Q

VZV drugs

A

antiviral drugs - acyclovir, foscarnet

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35
Q

VZV disease mechanisms

A

infects epithelial cells and fibroblasts, spread by viremia to skin, causes lesions (CP)
CM-immunopathology contributes to sxs
CM-immunity required for resolution of infection
Latent infection in neurons
Reactivation by immune suppression (from DRG) Reactivation leads to zoster or shingles, formation of lesions over entire dermatome

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36
Q

VZV incubation period

A

15 days, contagious period for 10, then latency in DRG

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37
Q

Poxvirus

A

virus - dsDNA (group 1) - linear genome - complex nucleocapsid - enveloped - poxviridae

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38
Q

Poxvirus subfamilies

A

Molluscipoxvirus (Molluscum contagiosum)
Orthpoxvirus (smallpox)
Parapoxvirus (Orf virus)

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39
Q

Poxvirus disease mechanisms

A

infects respiratory tract, spreads through lymphatics and blood
MC and zoonoses transmitted by contact
Sequential infection of multiple organs
cell-mediated and humoral immunity important to resolve

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40
Q

Picornavirus (enterovirus) disease mechanism

A 
Enter oropharyngeal or intestinal mucosa
secretory IgA can prevent infections
spread by viremia to target tissues
serum Ab blocks spread
virus shed in feces
high asymptomatic infection rate
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41
Q

virus - dsDNA (group 1) - linear genome - complex nucleocapsid - enveloped -

A

poxvirus

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42
Q

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucleocapsid - picornavirdidae

A

enterovirus

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43
Q

enterovirus

A

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucelocapsid - picornaviridae

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44
Q

enterovirus subfamilies

A 
poliovirus
coxsackievirus A & B --> HFM
Echovirus --> various rashes 
Rhinovirus
Enterovirus
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45
Q

Hand Foot Mouth caused by

A

Coxsackie A virus predominantly

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46
Q

Measles virus aka

A

Rubeola

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47
Q

virus - ssRNA (-) Group V - nonsegmented - helical nucleocapsid - enveloped - paramyxoviridae - morbillivirus

A

measles virus (rubeola)

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48
Q

Rubeola tree

A

virus - ssRNA (-) Group V - nonsegmented - helical nucleocapsid - enveloped - paramyxoviridae - morbillivirus - measles virus

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49
Q

measles disease mechanism

A

infects epithelial cells of respiratory tract, spreads to lymphocytes and by viremia
replicated in conjunctivae, respiratory tract, urinary tract, lymphatic system, blood vessels and CNS
T-cell response to virus-infected capillary endothelial cell –> rash
cell mediated immunity required to control infection
complications d/t immunopathogenesis or viral mutants

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50
Q

infects epithelial cells of respiratory tract, spreads to lymphocytes and by viremia
replicated in conjunctivae, respiratory tract, urinary tract, lymphatic system, blood vessels and CNS
T-cell response to virus-infected capillary endothelial cell –> rash
cell mediated immunity required to control infection
complications d/t immunopathogenesis or viral mutants

A

measles disease mechanisms

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51
Q

infects respiratory tract, spreads through lymphatics and blood
MC and zoonoses transmitted by contact
Sequential infection of multiple organs
cell-mediated and humoral immunity important to resolve

A

poxvirus disease mechanisms

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52
Q 
Enter oropharyngeal or intestinal mucosa
secretory IgA can prevent infections
spread by viremia to target tissues
serum Ab blocks spread
virus shed in feces
high asymptomatic infection rate
A

picornavirus disease mechanisms

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53
Q

virus spreads cell to cell, not neutralized by antibody
cell-mediated immunopathology –> damage and sxs
cell mediated immunity required for resolution of infection
virus establishes latency in neurons
reactivated by stress or immune suppression

A

HHV 1 and 2 disease mechanisms

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54
Q

infects epithelial cells and fibroblasts, spread by viremia to skin, causes lesions
CM-immunopathology contributes to sxs
CM-immunity required for resolution of infection
Latent infection in neurons
Reactivation by immune suppression (from DRG) Reactivation leads to zoster or shingles, formation of lesions over entire dermatome

A

VZV disease mechanisms

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55
Q

rubella virus aka

A

German measles

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56
Q

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucleocapsid - enveloped - togaviridae - rubivirus -

A

Rubella virus

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57
Q

rubella virus tree

A

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucleocapsid - enveloped - togaviridae - rubivirus -

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58
Q

erythema infectiosum

A

fifth disease

mild by highly contagious disease - slapped-cheek appearance

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59
Q

fifth disease causative agent

A

parvovirus B19

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60
Q

Parvovirus B19

A

Virus - ssDNA group II - linear genome - icosahedral nucleocapsid - nonenveloped - parvoviridae - erythrovirus (parvovirus B19)

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61
Q

Virus - ssDNA group II - linear genome - icosahedral nucleocapsid - nonenveloped -

A

parvoviridae - erythrovirus (parvovirus B19)

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62
Q

Parvovirus complications

A

aplastic crisis, acute polyarthritis, abortion

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63
Q

Sixth disease “Roseola”

A

young children, babies
high fever up to 105 then maculopapular rash (or not)
First on chest and trunk
by time rash, disease almost over

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64
Q

Roseola causative agent

A

HHV6/7 - can remain latent

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65
Q

IF HHV6/7 reactivate from latency in adulthood

A

mono-like, hepatitis-like

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66
Q

vaccine or drugs for roseola?

A

None

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67
Q

Virus - dsDNA group 1 - circular genome - icosahedral nucleocapsid - nonenveloped - papoviridae

A

papillomavirus

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68
Q

infects epithelial cells of skin, mucous membranes
replication depends on stage of epithelial cell differentiation
cause benign outgrowth of cells into warts
some types are associated with dysplasia –> cancerous

A

HPV disease mechanisms

69
Q

HPV disease mechanisms

A

infects epithelial cells of skin, mucous membranes
replication depends on stage of epithelial cell differentiation
cause benign outgrowth of cells into warts
some types are associated with dysplasia –> cancerous

70
Q

HPV tree

A

Virus - dsDNA group 1 - circular genome - icosahedral nucleocapsid - nonenveloped - papoviridae

71
Q

Molluscum contagiosum type of virus and spread

A 
poxvirus
direct contact (STD) or indirect
72
Q

viral mechanisms of disease

A
  1. tumorigenesis
  2. host cell destruction (lysis, autophagy, apoptosis)
  3. host immune response leading to tissue damage
73
Q

Koplik spots

A

measles

lesions on buccal mucosa that precede the rash and are considered pathognomonic

74
Q

chickenpox vs. smallpos

A

vesicles –> pustules (often displayed at same time in chickenpox) whereas in smallpox are generally all at same stage

75
Q

Which strains of HPV –> cervical cancer?

A

16, 18 - cause genital warts –> cervical cancer

76
Q

HPV: : transmitted by _______, virus infects ________.

A

transmitted by close contact, virus infects squamous cells in the epidermis or mucous membranes.

77
Q

HPV: Lysogenic vs lytic

A

Lysogenic - basal cells, cannot replicate by transform using E6 and E7 - benign cell growth and vacuolization
Lytic - upper keratinized epithelium or basal cell and it rises and differentiates. Replication –> lysis –> further infection.

78
Q

HPV: Infection controlled through

A

cell mediated immunity

79
Q

dx of hpv

A

1% acetic acid turns lesions white
colposcopy + biopsy of white lesions
PCR

80
Q

Tx and vaccines for HPV

A

spontaneously regress in 1 to 2 years
Ablation
HPV vaccines - gardasis cervarix

81
Q

Molluscum Contagiosum (MCV): spread

A

autoinoculation, in which virus from one lesion spreads to other parts of the body via scratching, is common in children

82
Q

MCV: location

A

Unlike varicella or HSV infections, MCV infection is limited to the epidermis and does not establish a dormant state. The rash associated with this virus is most often seen on the trunk and anogenital regions.

83
Q

MCV in immunocompromised people

A

Immunosuppressed individuals may have multiple, large lesions that do not resolve spontaneously. MCV is most often seen in AIDS patients.

84
Q

MCV clinical presentation

A

pearly skin papules and nodules.

85
Q

HPV clinical presentation

A

Acute – warts (on penis, vulva, cervix, fingers, hands, soles, knees, elbows, oropharynx, larynx). Chronic – asymptomatic or carcinomas (cervical carcinoma, squamous cell carcinoma, laryngeal carcinoma).

86
Q

MCV pathology (spread, cause of nodules)

A

Virus transmitted by casual contact and infects epidermal cells creating large eosinophilic inclusion bodies that contain virus particles (molluscum bodies) within them. The molluscum bodies enlarge the infected cells to form dome-like structures that leads to the eventual rupture of the infected cells forming a central crater.

87
Q

MCV dx

A

clinical presentation (non-painful domes with dimpled center). Skin biopsy (molluscum bodies and in epidermal layer, limited inflammation)

88
Q

MCV tx

A

self resolves in 6 to 12 months or surgically remove lesions (cryotherapy, laser treatment)

89
Q

Smallpox eradication

A

The last case of smallpox was reported in Somalia in 1977. Now only a few vials of the virus exist including a couple here in the United States. The eradication effort against smallpox worked because only one smallpox stereotype existed, there is no smallpox carrier state, and there are no animal reservoirs of the virus.

90
Q

Smallpox causative agent

A

Variola virus

91
Q

Smallpox clinical presentation

A

rash (macules –> vesicles)

92
Q

Smallpox: pathology when inhaled in aerosols

A

virus infects upper respiratory epithelium and from here it penetrates the mucosa and enters the bloodstream establishing primary viremia. At this point the virus infects and multiplies within the internal organs and a large number of virions are released into the bloodstream establishing secondary viremia. From here the virus spreads throughout the body, giving focal infections in the skin, lungs, intestines, kidneys, and brain.

93
Q

Smallpox: pathology when skin is infected

A

virus particles collect and replicate in the epidermis. These collections form macules first in the head and then later in the extremities. The virus replicates and generates a host immune response and the macules become puss-filled vesicles. Crusts form in 2 to 3 weeks and infectious particles are released.

94
Q

Smallpox dx

A

detection in vesicular fluid, serology

95
Q

Smallpox tx

A

vaccination (now only to those in military)

96
Q

Orf virus clinical presentation

A

Exanthemous disease causing denuded lesions.

Ecthyma contagiosum

97
Q

Orf virus pathology

A

Zoonotic disease where humans contract infections by coming in direct contact with infected sheep and goats or fomites carrying the virus. This virus causes a local, purulent-appearing papule. Generally there are no systemic infections with an immunocompetent host. Serious damage may be inflicted on the eye if the eye becomes infected by this virus, even with healthy individuals.

98
Q

Orf virus dx

A

case hx and clinical presentation

99
Q

orf virus tx

A

1% topical cidofovir

100
Q

Varicella-Zoster Virus (HHV-3) clinical presentation

A

Varicella (chickenpox) or zoster (shingles)

101
Q

VZV spread

A

high contagious

respiratory secretions or contact w/ ruptured vesicles

102
Q

VZV pathology

A

The virus infects the respiratory tract and following a two-week incubation period the virus establishes viremia in the host. This is accompanied by flulike symptoms and widespread vesicles with a red base appearing as “dew on a rose petal” (varicella). The rash continues to spread centrifugally and is typically mild in children but may be severe in adults where it can progress to pneumonia or encephalitis. The varicella resolves within two weeks and the virus enters local sensory nerve endings where it is axonally transported proximally to sensory ganglion cell bodies establishing latent infection of the dorsal root ganglion.

103
Q

VZV reactivation

A

Stress or some other form of immunocompromise can lead to viral reactivation. This results in axonal transport of virus from the ganglia to the nerve endings where a recurrent painful vesicular rash appears over the sensory dermatome (zoster).

104
Q

VZV dx

A

detection of virus. Clinical inspection of the rash. Multinucleate giant cells on Tzanck smear of skin lesions. Eosinophilic Cowdry intranuclear inclusion bodies on skin biopsy.

105
Q

VZV tx

A

Supportive. For severe infections acyclovir or famciclovir can be used. Anti-VZV immunoglobulin can be effective in immunocompromized individuals. There is a vaccine available (live-attenuated VZV).

106
Q

_______ can be associated with aspirin treatment for chickenpox in children.

A

Reye’s syndrome (liver damage and encephalomyelitis)

107
Q

HSV-1 epidemiology

A

most common cause of sporadic encephalitis in the United States (HSV-1 in adults and HSV-2 in neonates). Most adults have been infected by HSV-1 or -2, but very few infections are symptomatic and only 25% of latent infections exhibit recurrent infections.

108
Q

HSV-1 clinical presentation

A

Gingivostomatitis, keratoconjunctivitis, herpes labialis (cold sores), temporal lobe encephalitis

109
Q

HSV-1 pathology: (reservoir, transmission, infection)

A

humans are only reservoir
transmitted by saliva
invades mucous membranes –> primary local infection-typically asymptomatic but can cause vesicular lesions that ulcerate in the mouth (gingivostomatis) and eye keratoconjuctivitis (on cornea, typically presents as branching “dencritic ulcer”). The primary infection resolves after 2 to 3 weeks.
virus enters local sensory nerve endings and is transported along the axon proximally to the sensory ganglion cell bodies to establish latent infection in the trigeminal ganglion or other sensory ganglia.

110
Q

HSV-1 reactivation

A

Stress (fever, menstruation, sunlight) can lead to virus reactivation.
axonal transport of the virus from the ganglia to the nerve endings where it establishes a local recurrent infection which may result in herpetic labialis (cold sores around the mouth), gingvostomatitis or keratoconjunctivitis.
Rarely - via cranial nerves to brain –> focal necrotic lesions in the temporal lobe leading to inflammation, encephalitis and permanent neurological abnormalities or death.

111
Q

HSV-1 dx

A

detection of virus (PCR, good for early detection in encephalitis), multinucleate giant cells on Tzanck smear of skin lesions, eosinophilic Cowdry intranuclear inclusion bodies on skin biopsy. Fluorescent antibody test available.

112
Q

HSV-1 tx

A

acyclovir, trifluridine (topical, for eye infections)

113
Q

HSV-2 clinical presentation

A

genital herpes or neonatal herpes

114
Q

HSV-2 reservoir and spread

A

humans are the only reservoir for this virus and infection transmission is by sexual contact.

115
Q

HSV-2 infection

A

virus invades mucous membranes and sets up a local primary infection that is typically asymptomatic but can cause vesicular lesions in the genital and perianal area.
The primary infection resolves after 2 to 3 weeks when the virus enters the local sensory nerve endings and is transported via the axon proximally to sensory ganglion cell bodies and establishes latent infection of the lumbosacral ganglia.

116
Q

HSV-2 reactivation

A

Stress (fever, menstruation, sunlight) can initiate viral reactivation leading to axonal transport of the virus from the ganglia to the nerve endings resulting in a milder, recurrent vesicular infection at the primary site.

117
Q

HSV-2 to fetus

A

If a pregnant mother is infected the virus may transfer to the fetus through the placenta or during delivery. The infected child typically will have congenital defects or the infection may result in abortion or neonatal encephalitis.

118
Q

HSV-2 dx

A

detection of virus (PCR, good for early detection in encephalitis), multinucleate giant cells on Tzanck smear of skin lesions, eosinophilic Cowdry intranuclear inclusion bodies on skin biopsy.

119
Q

HSV-2 tx

A

Prevention – cesarean section in infected mothers.

120
Q

Roseoloviruses HHV6/7 Clinical presentation

A 
Exanthem subitum (sixth disease)
Reactivation can occur in organ transplant patients leading to enchepalitis, bone marrow suppression and pneumonitis.
121
Q

HHV6/7 spread

A

Virus is transmitted through aerosols.

122
Q

HHV6/7 epidemiology

A

Infection is typically seen in children ages 3 months to 3 years. This infection can occur year-round but has a higher incidence in the spring.

123
Q

HHV6/7 pathology

A

Primarily an infection in children that typically results in either a subclinical infection or an acute febrile illness. A fine maculopapular rash on the neck and trunk can be seen in some cases.

124
Q

HHV6/7 dx

A

clinical presentation. In severe cases definitive diagnosis by ELISA or indirect immunofluorescence is possible.

125
Q

HHV6/7 tx

A

Ganciclovir, supportive

126
Q

EBV (HHV-4) risks

A

patients with infectious mononucleosis are at risk for splenic rupture due to splenomegaly and should avoid contact sports.
A rash occurs in a few cases of mononucleosis however if ampicillin is given to treat tonsillitis (before EBV is diagnosed) then a rash occurs in most cases.

127
Q

EBV clinical presentation

A

infectious mononucleosis (“kissing disease”), lymphoid organ-related cancers: Burkitt’s lymphoma, nasopharyngeal cancer (East Asia).

128
Q

EBV spread

A

transmitted by saliva and respiratory secretions.

129
Q

EBV infection

A

Infects the oropharynx epithelium, which leads to viremia. Here the virus binds to and infects B cells. The virus remains latent in B cells as episomal DNA. The infected and B cells are transformed and multiply. This creates an immune response to the infected B cells and the lymph nodes and spleen both enlarge and the host experiences flulike symptoms and a painful, red sore throat (mononucleosis). The immune response eventually controls the B cell expansion and the infection resolves.

130
Q

EBV in immunocompromised people

A

If the immune system is compromised you get uncontrolled B-cell proliferation and unrepaired mutations accumulate which may increase chances for neoplasms like Burkitt’s lymphoma.

131
Q

EBV dx

A

monospot test – detects heterophil antibody (nonspecific antibody that agglutinates sheep RBCs.)
Blood smear – atypical lymphocytes (cytotoxic T lymphocytes that react against infected B cells)
Serology – anti-EBV IgM (acute infection), IgG (past infection).

132
Q

EBV tx

A

acyclovir in severe cases

133
Q

Parvovirus B19 in IC, fetuses

A

in immunodeficiency patients parvovirus infection can lead to chronic severe anemia. Fetuses who require higher red blood cell production and are immunodeficient are especially vulnerable to parvovirus infections. Infected fetuses may develop severe anemia and hydrops fetalis.

134
Q

Parvovirus B19 clinical presentation

A

erythema infectiosum (“fifth disease” - slapped cheeks), transient aplastic anemia crisis

135
Q

Parvovirus B19 pathology

A

virus establishes infection in nasal cavity followed by a six day incubation which leads to viremia and fever.
virus infects and lyses erythoid precursor cells in the bone marrow. This leads to mildly reduced reticulocytes, lymphocytes, neutrophils, and platelets. Normal hosts can tolerate a lack of erythropoiesis for 1 week.
Immune complexes form which leads to erythema infectiosum which is a rash with a “slapped cheek” appearance. This is accompanied by muscle aches for several days.

In patients requiring increased erythropoiesis (sickle cell anemia, thalassemias) there is a transient aplastic crisis and severe reticulocytopenia with normal myeloid lineage.

136
Q

Parvovirus B19 dx

A

detect viral DNA, serology

137
Q

Parvovirus B19 tx

A

Supportive. RBC transfusion. In immunocompromised individuals – Ig transfer.

138
Q

Coxsackievirus A & B clinical presentation

A

Coxsackie A – herpangia, hand-foot-and-mouth disease.
Coxsackie B – pleurodynia, myocarditis, pericarditis.
A and B – aseptic meningitis, paralysis, upper respiratory tract infection.

139
Q

Coxsackievirus epidemiology

A

infections are typical in summer and fall and the virus is transmitted via aerosols or fecal to oral route.

140
Q

Coxsackievirus pathology

A

The virus travels in the G.I. tract and infects mucosal epithelial cells. Local replication ensues and virus spreads in the bloodstream. From here the virus infects and can lyse skin and mucosal epithelium (Group A) to form vesicles leading to herpangina (red oropharynx vesicles, fever, sore throat), hand-foot-and-mouth disease.

141
Q

Coxsackievirus complications

A

In Group B infections the virus travels to the heart and pleural surfaces to cause pleurodynia, myocarditis, and pericarditis.

In Group A and B infections the virus can travel to the meninges and anterior horn motor neurons to cause meningitis and paralysis.

142
Q

Coxsackievirus dx

A

isolate virus, serology

143
Q

Coxsackievirus tx

A

Symptomatic infections – anti-inflammatory agents. No antivirals or vaccines available.

144
Q

ECHO virus clinical presentation

A

Acute febrile illness often in male children. Non-specific exanthem.

145
Q

ECHO virus spread

A

Fecal to oral route of transmission, sometimes salivary aerosols.

146
Q

ECHO virus pathology

A

Infection in neonates can be fatal. Myocarditis is a frequent complication in adult infections. Infection typically causes a non-specific illness with fever. Sometimes a rash can be produced that spreads from the face down to the neck and upper extremities and chest.

147
Q

ECHO virus dx

A

serology

148
Q

ECHO virus tx

A

Supportive. New antiviral called pleconaril interferes with viral attachment and penetration.

149
Q

Measles virus clinical presentation

A

Rubeola. Flu-like symptoms, Koplik’s spots followed by rash, and sometimes encephalitis. Subacute sclerosing panaencephalitis (SSPE) can occur in infections with complications.

150
Q

Measles virus epidemiology

A

this virus spreads human to human by respiratory aerosol droplets.

151
Q

Measles virus spread throughout body

A

The virus infects, replicates within, and eventually destroys epithelial cells. This leads to the first (primary) viremia. From here the virus infects and replicates in reticuloendothelial cells leading to secondary viremia which allows the virus to spread to several other areas in the body.

152
Q

Measles virus pathogenesis: mucosa, koplik’s, rash

A

At the mucosa, infection promotes inflammation around capillaries.
In the mouth you see Koplik’s spots (red lesions with a blue-white center).
At the dermis, infection also promotes inflammation around capillaries that forms a rash starting at the head and progressing to the feet, disappearing in the order that it appears.

153
Q

Measles virus in the CNS

A

In the brain, infection can lead to meningitis and encephalitis.
Infections with measles virus variants can lead to a chronic low-level infection of the central nervous system. This creates inflammatory lesions in the brain that gradually present as personality and cognitive changes (subacute sclerosing panenchalitis or SSPE) this eventually leads to death.

154
Q

Measles virus pathogenesis in GI and lungs

A

In the respiratory tract and lung, giant cells form with inclusion bodies (Warthin-Finkeldey cells) this cell damage leads to a cough.

155
Q

Measles dx

A

isolate the virus from nasopharyngeal secretions, blood, and urine. Warthin-Finkeldey cells (multinucleated giant cells with inclusion bodies in the nucleus and cytoplasm) in respiratory secretions. Serology.

156
Q

Measles tx

A

Vaccine of a live-attenuated virus in the MMR vaccine. In severe cases in infants administer high doses of vitamin A.

157
Q

Rubella Virus clinical presenation

A

German measles
rubella – fever followed by descending rash.
Congenital rubella – congenital malformations (deafness, patent ductus arteriosus, pulmonary artery stenosis, cataracts, microcephaly)

158
Q

Rubella virus spread

A

this virus is transmitted by aerosol and infects nasopharynx

159
Q

Rubella virus pathology

A

replicates in the local lymph node. Systemic spread is through the bloodstream. An antibody mediated reaction leads to maculopapular rash beginning in the face and spreading to the extremities. Antibody complexes many result in arthritis in women.

160
Q

Rubella in a pregnant woman

A

If the virus infects pregnant women in their first trimester then the virus may cross the placenta and reach the fetus. Here the virus infects fetal cells and promotes mitotic arrest, necrosis, or chromosomal damage. This leads to congenital defects in the brain, heart, and eyes.

161
Q

Rubella dx

A

Detection of anti-rubella antibodies. IgM if recent infection – IgG if immune. Virus in aminocentesis indicates congenital rubella.

162
Q

Rubella tx

A

self-limiting – no antiviral. Vaccine – live-attenuated rubella virus in MMR vaccine.

163
Q

clusters of dead crows usually herald human cases of ______

A

West Nile Virus

164
Q

West Nile Virus clinical presentation

A

most infections are asymptomatic. West Nile Fever – fever, fatigue, headache, myalgia, anorexia, eye pain, nausea, vomiting, diarrhea, rash. West Nile encephalitis – neuroinvasive disease causing encephalitis (more typical in the elderly) or meningitis (more typical in children). Symptoms range from mild confusion to tremor, extrapyramidal symptoms, flaccid paralysis, or severe encephalopathy that may progress to coma or death, particularly in the elderly or immunocompromised.

165
Q

West Nile virus epidemiology

A

Virus is maintained in a cycle of infection that includes mosquitos, birds and humans. Spreads to incidental human host by a mosquito bite

166
Q

West Nile Virus pathology

A

replicates in the skin Langerhans cells which migrate into the regional lymph nodes followed by viremia and infection of multiple organs including the CNS.

167
Q

West Nile Virus dx

A

IgM Ab in serum or CSF. PCR of the CSF.

168
Q

West Nile Virus tx

A

Supportive. Prevention against mosquito bites.

Skin MS: Week 4 (10 decks)

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