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Dermatological Block > Viruses > Flashcards

Viruses Flashcards

1
Q

Measles and Mumps structure

A

enveloped negative strand RNA viruses

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2
Q

Rubella structure

A

Enveloped positive strand RNA virus

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3
Q

Erythema infectiosum infectious agent

A

Caused by Parvovirus B19; also called fifth disease

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4
Q

Erythema infectiosum modes of transmission

A

respiratory tract secretions, percutaneous exposure to blood or blood products, vertical transmission from mother to fetus

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5
Q

Erythema Infectiosum incubation period and infectious time

A

1-2weeks from exposure to onset of rash; most infectious before onset of rash

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6
Q

Parvovirus B19 infectious cycles

A

bi-phasic: lytic, infectious phase; then non-infectious, immunologic phase where IgG neutralizes circulating virus

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7
Q

Parvovirus B19 symptoms

A

symptoms are immune mediated; cytokines produce prodromal flu-like symptoms followed by cell-mediated response causing a rash

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8
Q

Measles type

A

Morbillivirus of Paramyxoviridae family; differentiated from other paramyx viruses receptor usage (primary MV receptor are CD46, SLAM, Nectin 4; has H Protein) and forms intracellular inclusion bodies (distinctive feature of cytopathology)

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9
Q

Measles healthcare policy and vaccination

A

report to health department cases of measles; vaccine can be given within 72 hours of exposure

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10
Q

Measles Clinical Defniition

A

Generalized rash lating more than 3 days and temperature greater than 101 and cough, coryza, conjunctivitis.

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11
Q

Basis of Measles rash

A

Morbiliform rash due to cytotoxic T cells attacking measles virus infected vascular endothelial cells in the skin

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12
Q

Measles mode of transmission

A

highly contagious and spread via respiratory droplets

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13
Q

Primary cause of death in Measles

A

bacterial pneumonia due to measles induced immunosuppression

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14
Q

Symptoms of Measles

A

start 10-14 days post exposure; prodrome of fever, cough, conjunctivitis, coryza, with high fever, photophobia, followed by appearance of maculopapular rash

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15
Q

Rash coincides with what in Measles

A

coincides with a strong cell-mediated immune response and virus clearance

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16
Q

Koplik spots

A

bluish-white abruptions found in the mouth, often preceding rash; pathognomonic for measles

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17
Q

Measles complications

A

immune suppression probably due to infection of monocytes and other immune effector cell; acute disseminated encephalomyelitis, post infectious encephalomyelitis, measles inclusion body encephalitis, subacute sclerosing panencephalitis

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18
Q

Measles vaccine

A

antigenic ally stable monotypic virus, so works every year; live attenuated measles virus provides life long immunity

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19
Q

Viruses that cause harm to fetus if infection during pregnancy

A

Parvo-B19 and Rubella

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20
Q

Rubella symptoms

A

mild disease characterized by a low-grade fever, occasional conjunctivitis and sore throat, LAD, and a morbilliform rash that starts on the face and spreads to the rest of the body

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21
Q

Rubella transmission and replication

A

Transmitted via aerosols; repicaltion occurs in URT mucosa and the nasopharyngeal lymph nodes; viremia develops, rash develops after 16-21 days; virus shedding continues after the rash disappears

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22
Q

Rubella birth defects

A

cause mental retardation, motor disabilities, hearing loss, congenital heart disease, and cataracts; more serious the during 1st and 2nd trimester

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23
Q

Parvovirus B19 affects on pregnancy

A

hydrops fetalis, intrauterine growth retardation, pleural and pericardial effusions, and death

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24
Q

Parvovirus B19 complications

A

immunodeficiency (chronic erythroid hypoplasa with severe anemia) and chronic hemolytic anemia (esp in sickle cell)

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25
Q

Four major Enteroviruses

A

Coxsackievirus, Echovirus, Enterovirus, Poliovirus

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26
Q

Enterovirus differentiation from Rhinovirus

A

acid stabile, less stringent growth requirements, and humans are only known reservoir

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27
Q

Enterovirus spread and replication

A

spread by oral-fecal route or by aerosol contamination of fomites; repicale in lymphoid tissue of URT and the gut, followed by viremia; usually asymptomatic

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28
Q

Coxsackie A16 causes what

A

Hand, Foot, and Mouth Disease

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29
Q

Hand foot and mouth symptoms

A

ulcerative lesions on the tonsils and uvula (herpangina), fever, sore throat, HA, ab pain, vesicular lesions on hands and feet

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30
Q

Hand foot and mouth treatment

A

Disease is self limiting and requires only symptomatic management but it is highly contagious

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31
Q

Hand foot and mouth virus isolation

A

can be caused by Coxsackievirus A16, A6 and eneterovirus 71; can be isolated from lesions and from feces

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32
Q

Enterovirus control

A

no vaccines available for any other enterovirus than polio; most infections and self limiting and are often asymptomatic

33
Q

Roseola infantum symptoms

A

young child, high fever, nasal congestion and loose stools for under one week, followed by a rosy-pink rash on torso, arms, and neck that is not pruitus and goes away after a few days

34
Q

Age range for Rosela infections

A

6mo-4years; most common exanthem before age 2; nearly everyone has been exposed by age 3-4

35
Q

Complications of HHV-6/7 infection

A

reactivation in brain, lungs, heart, kidney, and GI tract; associated with immunosuppression (stem cell transplant); reactivation in brain can cause cognitive dysfunction, permanent disability and death

36
Q

Mumps pathogenesis

A

infection in mucosal epithelium of nasopharynx and URT; incubation of ~18 days; virus si shed in saliva 6 days before onset of clinical disease

37
Q

Mumps symptoms

A

swelling and inflammation of parotid gland; no rash

38
Q

Mumps complication

A

virus replication in CNS causing aseptic meningitis or infection of cochlea leading to deafness; symptomatic gonadal involvement causing enlargement of the testes which can cause tissue damage and sterility

39
Q

Viral cause of Roseola

A

HHV-6/7

40
Q

HPV structure

A

circular ds-DNA, non-enveloped icosahedral capsid virus

41
Q

HPV pathogenesis

A

many strains; infect epithelia of skin and mucous membranes, causing warts in different locations and of different morphology depending on strain of virus; warts are benign neoplasms that can progress to malignancy

42
Q

Permissive cells

A

infectious virus progeny are produced (lytic replication)

43
Q

Non-permissive cells

A

genome is replicated, but no virus particles are produced; late (structural) proteins are not expressed, no capsize proteins are made; this leads to cell transformation

44
Q

Morphogenesis of a wart

A

HPV latently infects basal epithelial cell; as the cell replicates and proliferates, there is high level episomal replication of the virus as well; once a terminally differentiated keratinocyte, virus assembly and release occurs with HPV shedding

45
Q

Benign tumors of HPV

A

non-permissive, persistently infected cells that have a genome that is circular, full-length and extra-chromosomal

46
Q

Malignant tumors of HPV

A

a partial genome that has lost the E2 gene is integrated into the host DNA, resulting in retention of E6 and E7 and disregulation of E2 mediated transcriptional control

47
Q

E6 function

A

degradation of p53

48
Q

E7 function

A

inactivates Rb protein

49
Q

HPV diagnosis

A

clinical appearance, genotyping is possible; HPV cannot be routinely grown in the lab

50
Q

HPV treatment

A

most warts spontaneously regress; can be removed surgically, cryosurgical, or through corrosives; drug treatment is also available; recurrences are common due to survival of infected cells in basal layer

51
Q

HPV Vaccine

A

virus like particles from HPV 6, 11, 16, 18 made in yeast that consist of the L1 capsid protein from each that self assembles into pseudocapsids

52
Q

Pox viral structure

A

large complex structure that is enveloped; ds linear DNA genome

53
Q

Pox virus replication

A

all replication takes place within cytoplasm; virus penetrates the cells and loses its outer membrane, then as it releases viral DNA makes its own enzymes needed for replication, replicates within the cytoplasm and the virus is released from the cell by cell disruption or exocytosis

54
Q

Small pox symtoms

A

systemic disease with generalized rash that had high fatality; fever and rash precede the pustules that are created by small vessel cutaneous hemorrhage

55
Q

Small pox virus infective mechanism

A

inhalation or transmission by scabs, replication in URT, lymphatics (macrophages) transmit virus to lymph nodes where a viremia occurs that is associated with hemorrhage of small vessels in dermis and infection of other organs; viremia is associated with the appearance of pustules

56
Q

Mortality in small pox

A

death is due to toxic effects on vascular endothelium

57
Q

Childhood molluscum contagiosum

A

lesions on the face, trunk, and limbs that spread from skin to skin

58
Q

Young adult molluscum contagiosum

A

mostly lower abdomen lesions, sexually-transmitted

59
Q

Molluscum contagious disease course and diagnosis

A

lesions disappear in 2-12 months; diagnosis by appearance, confirmed by presence of cytoplasmic inclusions in keratinocytes of the affected area

60
Q

Small pox vaccine

A

live vaccine, localized lesion that heals in two weeks, wanes after 3 years, gone after 20 years

61
Q

Keys to small pox eradication

A

humans are only reservoir; no healthy carriers existed; no sub-clinical infections; effective vaccine was available

62
Q

Adverse small pox vaccine reactions

A

Could not be given to: pregnant or breast feeding women, immunodeficient, atopic dermatitis pts, under 18yo in non-emergency situation, people with heart disease; generalized vaccinia, inadvertent inoculation, erythema multiforme; adverse reactions are common

63
Q

Life-threatening small pox vaccine complications

A

progressive vaccinia and eczema vaccinatum

64
Q

Herpes Viral Structure

A

linear, dsDNA genome, icosahedral capsid, enveloped, dozen glycoproteins; DNA is replicated and viruses are assembled in the nucleus

65
Q

Lytic Cycle of Herpes Virus

A

Immediately upon entry into the cell the virus makes transcription factors, then it replicates, then makes structural proteins and is exocytosed from the host cell to infect other cells

66
Q

Herpes Neuronal Replication

A

peripheral sensory neurons directly take up the progeny of epithelial replication, these progeny viruses as they replicate are trans synaptically transported in the retrograde direction

67
Q

Herpes Latency

A

nor virus particles are produced, entire genome is maintained extrachromosomally, and few viral genes are expressed

68
Q

Location of HSV-1 latency

A

Trigeminal Nerve

69
Q

Location of HSV-2 latency

A

sacral and lumbar nerves

70
Q

Location of VZV latency

A

Dorsal Root

71
Q

Herpes LAT

A

Latency associated transcript; it prevents lytic replication, prevents apoptosis of infected neuron and evades immune surveillance (CD8), allowing the virus to enter latency

72
Q

HSV-1 Disease locations

A

skin (especially around mouth), eyes, encephalitis

73
Q

HSV-2 Disease locations

A

Urogenital and Meningitis

74
Q

HSV pathogenesis

A

spread via secretions through breaks in skin or mucosa; replicates in epithelial cells at site of infection then spread to lymph nodes; primary infection is often unapparent

75
Q

HSV Diagnosis

A

clinical features, serology for primary infections; PCR, Tzanck smear

76
Q

VZV Pathogenesis

A

primary infection causes chickenpox; spread by aerosol, causing itchy rash starting on scalp and trunk

77
Q

VZV Reactivation

A

reactivation causes shingles, sudden onset of pain and rash along thoracic dermatome or forehead with a rash lasting 2-4 weeks, thought the pain lasts much longer

78
Q

VZV diagnosis

A

clinical appearance; Tzanck smear

Dermatological Block (6 decks)

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