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Multisystems > Micro- Viral Exanthems > Flashcards

Micro- Viral Exanthems Flashcards

1
Q

What is an enanthem?

A

a sudden eruption appearing on the mucous membranes

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2
Q

What is an exanthem?

What are 4 common causes?

A

“breaking out” of a rash that appears on multiple areas of the body suddenly

  1. virus
  2. bacteria
  3. drugs
  4. immune dysregulation
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3
Q

What is a morbilliform exanthem?

What is a scarlatiniform exanthem?

A

Morbilliform - composed of macules/papules that resemble a measles rash

Scarlatiniform- composed of fine pinpoint, sandpaper papules resembling scarlet fever

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4
Q

What are the 4 immune dysregulation causes of exanthems?

A
  1. Kawasaki’s disease
  2. Still’s disease
  3. hemophagoctyic
  4. lymphohistiocytosis [HLH]
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5
Q

What are the 3 bacterial causes of exanthems?

A
  1. Group B Strep
  2. M. pneumonia
  3. H. flu
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6
Q

What are the 4 drug rxns responsible for exanthems?

A
  1. Sulfa/b-lactam antibiotics
  2. anti-epileptics
  3. serum-sickness rxn
  4. NSAIDS
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7
Q

What is the name/etiology for:

  1. first disease
  2. second
  3. third disease
  4. fourth disease
  5. fifth disease
  6. sixth disease
A
  1. measles- measles virus
  2. scarlet fever- Strep pyogenes
  3. rubella - rubella virus
  4. Duke’s disease - coxsackie and enterovirus
  5. erythema infectiosum - parvovirus B19
  6. Roseola infantum - HHV 6 and 7
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8
Q

Describe the genome of the measles virus.
What family does it belong to?
Where are the nucleocapsid and hemagluttinin formed?
Is it enveloped or non-enveloped?
How many serotypes are there?

A

Measles is SS-RNA with helical nucleocapsid
It belongs to the Paramyxoviridae family with parainfluenza, RSV, and mumps.

Nucleocapsid and hemagluttinin are formed in the cytoplasm.
The enveloped virus has only one serotype.

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9
Q

How is measles transmitted? What are the vectors?

What group is it most likely to be transmitted in?

A

The measles virus is restricted to humans and is transmitted via:

  1. respiratory droplets
  2. direct contact with nasal or throat secretions

It is transmitted in unvaccinated school populations and college students.

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10
Q

Describe the pathogenesis of measles including where the virus replicates and which cells specifically are infected.

A
  1. infects epithelial cells of the URT where they have primary multiplication
  2. viremia
  3. infect reticuloendothelial cells where they replicate again
  4. secondary viremia
  5. infect white blood cells [primarily monocytes]
  6. spread to skin and respiratory tract
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11
Q

What is the incubation period for measles?

When are they most contagious?

A

Incubation is 1week prior to the development of a rash.

They are most contagious from the first respiratory symptoms to 4 days after the onset of rash.

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12
Q

What are the early respiratory symptoms of measles?

A

Three C’s

  1. cough
  2. coryza [inflammation of mucous membrane in the nose]
  3. conjunctivitis
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13
Q

After febrile prodrome, what plays an important role in the skin manifestations of measles?

A

Virus specific T-cells attack viral infected endothelial cells of dermal capillaries causing:

  1. Koplik spots - blue/white spots on bright red background of the buccal mucousa [1-2 days before rash]
  2. morbilliform rash - macules/papules on the face [hairline/ears] that spreads to the trunk and extremities and lasts 4-7 days
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14
Q

After a few days of uncomplicated measles, the fever subsides and the rash fades, but what is left?

A
  1. transient petechiae/purpura which evidence the capillary leakage at the height of the illness
  2. desquamation
  3. post-inflammatory hyperpigmentation
  4. leukopenia
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15
Q

What age group has most severe measles?

A

Infants and adults have more severe measles than children

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16
Q

Acquired humoral and cell-mediated immunity after a naturally acquired measles infection is permanent. However, what will occur if the patient has defective cell-mediated immunity [like with HIV] ?

A

Measles can progress to:

  1. giant cell pneumonia
  2. subacute sclerosing panencephalitis [SSPE] which occurs several years after primary infection and is fatal
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17
Q

How is the diagnosis of measles usually made?

What are the 2 lab tests that can be used as confirmation?

A

Diagnosis is clinical and epidemiologic

Lab tests can confirm and are:

  1. isolation of measles virus from throat/nasopharyngeal swab or urine
  2. serological investigation where:
    - measles specific IgM = acute infection
    - >4 fold increase in IgG = recent infection
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18
Q

What is treatment for measles?

A

Supportive.

Treat secondary bacterial infections

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19
Q

Describe the measles vaccine.
Who is it contraindicated in?
When is it administered?

A

The vaccine is part of MMR [measles, mumps, rubella] and it consists of live attenuated viruses. For this reason it is contraindicated in:

  1. pregnant women
  2. immunosuppressed

It is required in the US for school-aged children and is given as 2 doses:
1 at 12-15 months and the 2nd at preschool

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20
Q

What can you do within 72 hours of exposure to measles that can provide post-exposure protection?

A

Give the live-attenuated vaccine

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21
Q

Describe the genome of rubella.
Describe the structure of the virus. Does it have an envelope?
How many serotypes exist?
What family does it belong to?

A

Rubella is SS-RNA.
It has a central icosahedral nucleocapsid core covered by a lipid-containing envelope.
The envelope has surface spikes with hemagglutinin.
Only one antigenic serotype exists.

It is in the Togavirus family

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22
Q

What is the transmission of Rubella?

What are the vectors?

A

Humans are the only natural host of rubella virus.
It is transmitted via:
1. respiratory droplets
2. direct contact
3. transplacentally [congenital rubella syndrome]

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23
Q

What prevents the spread of rubella to mothers [which reduces the spread of rubella to babies transplacentally]?

A

vaccinate children since they are the primary reservoirs

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24
Q

How does the distribution of rash and intensity compare between rubella and measles?

A

They have the same distribution, but measles is more intensely red

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25
Q

What is the pathogenesis of rubella?

A
  1. invades respiratory epithelium
  2. viremia
  3. regional/distant lymphatics and replicates in RES
  4. secondary viremia [6-20 days after infection]
  5. spread to other tissues and skin
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26
Q

How does the pathogenesis of rubella and measles compare in terms of skin manifestations ?

A

Both have:

  1. T-cell attack of virus-infected vascular endothelial cells–> skin rash
  2. Ag-Ab complex mediated vasculitis -> febrile exanthem illness
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27
Q

In a non-immune pregnant woman, when does fetal infection occur transplacentally?
What are the 2 mechanisms of fetal damage?

A

During the viremic phase.

  1. tissue necrosis without inflammation
  2. direct cytopathic effects
  3. apoptotic cell death
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28
Q

What is the most important factor for determining the outcome of congenital rubella?

A

The stage of pregnancy when the infection occurs
*first 2 months have a 75% probability of being affected with spontaneous abortion or multiple defects

Decreases to 30% in the 3rd month and 10% in the fourth month

Isolated deafness can occur as late as the end of the second trimester

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29
Q

What is the most prominent temporary defect that occurs as a result of rubella?
What are the most prominent permanent defects?

A

Temporary = low birth weight

Permanent:

  1. deafness
  2. cataracts or glaucoma
  3. congenital heart disease
  4. mental retardation
30
Q

How does the prodrome differ for adults and children with rubella infections?

A

Adults have:
anorexia, URT symptoms, malaise, conjunctivitis, headache, fever

Children have no constitutional signs

31
Q

Petechiae on the soft palate [Forchheimer’s sign] is part of the prodrome for what disease?

A

Rubella infection

32
Q

Why are lab tests more crucial for rubella than for measles?

What lab tests enable diagnosis?

A

Rubella has much more subtle clinical appearance than measles so you need to do lab tests.

  1. isolation of the virus from throat/nasopharyngeal swab or urine
  2. serology
    - IgM = acute
    - >4 fold increase in IgG= recent infection
33
Q

In pregnant women, acute rubella infections can be confirmed by what?

A

4-fold rise in Ab titer between acute and convalescent-phase serum specimen by ELISA.

Amnio and rubella culture can see if the infection is in the amniotic fluid

34
Q

What lab tests support the diagnosis of congenital rubella syndrome in the newborn?

A

specific IgM in a single specimen between 2 and 3 months after birth

35
Q

What does the live-attenuated rubella vaccine induce to disrupt the spread of virulent virus by nasal carriage?

A

It induces a respiratory mucousal IgA response

36
Q

To protect a fetus from exposure to rubella, how can maternal immunity be demonstrated prior to pregnancy?

A
  1. serologic testing
    - greater than 1:8 titer of IgG Ab indicates immunity
  2. proof of immunization
37
Q

Describe the genome and structure of Parvovirus B19.

Where does it replicate primarily?

A

SS-DNA [different from measles/rubella which are both SS-RNA]
no envelope [different from measles/rubella]
Icosahedral
Parvoviridae

It replicates primarily in erythroid progenitor cells

38
Q

What are the vectors for parvovirus B19?
What age group is most commonly affected?
What % of adults are seropositive to exposure to the virus?
How is it transmitted?

A

B19 is specific to humans [other parvovirus can infect other hosts]
It most commonly affects children and by adulthood 50% of people are seropositive
It is transmitted via respiratory secretions of infected people BEFORE the onset of the rash. Winter/spring epidemics

39
Q

Describe the time frame and symptoms associated with Fifth Disease.

A
  1. Prodrome: fever, malaise, coryza 2 days before the rash
  2. Rash of confluent edematous plaques on malar cheeks [“slapped cheek”]
  3. macules and papules on the trunk in reticulated appearance
  4. Rash fades in 5-9 days
40
Q

In what persons is parvovirus B19 infection going to cause SERIOUS illness?
What illnesses are caused and why?

A
  1. sickle cell or similar types of chronic anemia the virus can cause transient aplastic crisis
    - virus makes hemolysis occur
    - virus arrests RBC maturation in pronormo or proerythro stage dropping Hct
  2. immunosuppressed - may develop chronic anemia or secondary pneumonia or infectious arthritis of large joints of the lower extremities
41
Q

Describe the results of parvovirus B19 intrauterine infections.
What % result in fetal death? When in the pregnancy do most of these deaths occur?

A

It results in fetal anemia with hydrops fetalis [accumulation of fluid in tissue].

<10% fetal deaths
When it occurs, it is in the first trimester

42
Q

A patient presents complaining of a progessive, symmetric swelling and erythema of the hands and feet. The exathem looks purpuric and has sharp demarcation at the wrists and ankles. He has also been experiencing respiratory symptoms, GI problems, fever, arthralgia and malaise.
What is the likely diagnosis?
What causes it?

A

Papular- Purpuric Gloves and Socks Syndrome [PPGSS]

caused by parvovirus B19

43
Q

How is parvovirus B19 infection diagnosed?

What additional test can be used for patients who developed aplastic anemia?

A

Epidemiological and clinical [early leukopenia followed by leukocytosis and lymphocytosis]
Confirm with:
1. detection of IgM [titer declines after 30-60 days]
2. 4-fold rise in IgG
3. PCR viral nucleic acid detection test

If a patient had aplastic anemia:
Bone marrow biopsy will show maturation arrest at pronormoblast [proerythroblast] stage of RBC development but no other lineages

44
Q

What is treatment for parvovirus B19 infection?

A

No treatment for acute

Chronic = IVIg in persistent infections of immunocomp.

45
Q

What is different between the erythema infectiosum rash and the PPGSS?

A

EI - if they have a rash, they are not infectious

PPGSS- if they have exanthem, they may still be viremic and infectious

46
Q

Describe the structure and genome of HHV6 and 7.
To what family do they belong?
Where does replication occur?

A

They are linear dsDNA viruses with envelopes [resistant to drying, solvent, heat]
Betaherpesviridae family.
Replication occurs in the nucleus, cytopathic for T cells

47
Q

What % of people are seropositive for HHV6 and HHV7?

A

By the age of 5 almost all children are seropositive for HHV6.
95% of all US adults are seropositive for HHV7.

48
Q

How is HHV6/7 transmitted?

Where does the virus achieve latency in the host?

A

It is transmitted by respiratory droplets.

Achieves latency in the lymphocytes and salivary glands of hosts.

49
Q

What disease is caused by HHV6/7?
What age group is primarily affected?
What is the presentation?

A

It causes Roseola Infantum in infants and children under 3.

  1. child gets high fever with possible
    - irritability, diarrhea, bulging fontanelle, cough, lymphadenopathy, edematous eyelids that last 3-5 days
  2. as the fever resolves they get pink erythematous macules and papules that start on the trunk and spread centrifugally.
  3. rash lasts 1-3 days
50
Q

What are the negative sequelae of roseola infantum?

A
  1. febrile seizures [unusual]
  2. latency of HHV6 in mononuclear cells and then if the patient becomes immunocompromised:
    - fever and rash reactivation
    - encephalitis, pneumonitis, hepatitis, colitis, gastroduodenitis
    - bone marrow suppression
    - mononucleosis
51
Q

What labs can be done to diagnose HHV6/7 infection?

Which is most useful for active infections?

A

clinically, leukopenia and leukocytopenia occur early

  1. serology
  2. culture
  3. immunohistochemistry
  4. antigenemia
  5. PCR ** most useful for active infections
52
Q

What is treatment for roseola infantum?

A

Majority are asymptomatic so treatment is supportive.

HHV6 encephalitis:
foscarnet, ganciclovir, cidofovir
*****resistant to acyclovir

53
Q

Describe the genome and structure of varicella-zoster. How does it differ from other viruses in its family?

A

It is dsDNA with an envelope.

It belongs to herpes family but differs in that it only has one serotype

54
Q

What is the characteristic appearance of VZV when it is cultivated in tissue culture?

A
  1. eosinophilic intranuclear inclusions

2. multinucleated giant cells [virally infected keratinocytes]

55
Q

What are the 2 distinct diseases caused by VZV?

A
  1. varicella [chicken pox]

2. herpes zoster [shingles]

56
Q

Describe the prodrome, rash and duration of varicella.

A

Prodrome: fever, chills, malaise, headache, myalgia, arthralgia then after 1-2 days:
Rash: erythematous macules or papules that progress to vesicles [dewdrops on rose petal] that lasts 6 days. Lesions occur in “crops” so several stages can be present at once

57
Q

How does the rash of chicken pox differ from smallpox?

A

Chicken pox occurs in successive crops so lesions will be present in several stages of development.
Smallpox has lesions all in the same stage of development

58
Q

Where does VZV establish latency? What percent of people will develop herpes zoster during their lifetimes? What 2 groups of people are most likely to be infected?

A

Latency is in the sensory ganglions and only 15% of people will develop shingles over their lifetime

  • immunocompromised
  • elderly
59
Q

A patient comes to see you and is presenting with zoster. This patient is young. What should you investigate for<

A

HIV or other things that could make them immunocompromised

60
Q

Describe the rash pattern for herpes zoster.

A

Erythematous base and restricted to skin areas supplied by the sensory nerves.
Lesions occur in crops and are irregular along the nerve path with blister like lesions in a strip-like pattern on ONE SIDE of the body

SEVERE PAIN is common [post-herpatic neuralgia, zoster-associated pain syndrome]

61
Q

What are the 2 major complications of herpes zoster?

Who is most likely to be affected?

A
  1. Pneumonia- adults or immunocompromised&raquo_space;>children
  2. encephalitis
  3. Reye’s syndrome
62
Q

What is the transmission of VZV?
What 3 groups of people are likely to have poor prognosis?
What group is at increased risk of disseminated disease?

A

It is transmitted by inhalation of respiratory aerosol from patients infected 1-2 days before the rash.
It is most prevalent in late winter/early spring.

Poor Prognosis:

  1. non-immune neonates
  2. immunodeficient
  3. oncology patients

Disseminated disease:
Children with acute leukemia

63
Q

How is VZV diagnosed?

A

Clinically- patient has vesicular lesions on erythematous base and no history of prior varicella infection [measure of immunity]

In complicated cases:

  1. cultivation of virus from skin lesions
  2. Tzanck smear- but can’t rule out HSV
  3. viral antigen in fluid by DFA
  4. serology to see if acute or chronic [IgM =acute]
  5. PCR- sensitive and specific
64
Q

What is treatment of varicella/herpes zoster?

A
  1. Acyclovir to shorten duration and pain severity [5/day]
    2, famciclovir and valacyclovir are more effective for decreasing duration, and decreasing duration of post-herpatic neuralgia [3/day but more expensive]
65
Q

Describe the vaccine for VZV.

Describe what can be done within 96 hours of infection in high risk individuals.

A

Vaccine is live-attenuated varicella virus for children over 1yr which increases IgG and T-cell immunity

VZIG [varicella zoster immune globulin] given w/in 96 hours if a susceptible person is infected

66
Q

What is the genome and family of enteroviruses?

A

ssRNA in the picornavirus family with:

-echo, coxisackie, entero, polio

67
Q

What is the most distinct feature of Hand-Foot-and-Mouth disease?
What age does it affect most?

A

Enteroviral exanthems - whitish vesicular lesion on palms and soles.
Enanthems - painful vesicles/erosion on uvula, gingiva, tonsils, buccal surface, palate, tongue

Affects children 1-4yrs old

68
Q

What 2 viruses have been linked to HFMD?
Which has worse sequelae?
What is treatment?

A

Coxsackie 16 and enterovirus 71

Entero71 has complications of pulmonary edema, hemorrhage, encephalitis, aseptic meningitis, flaccid paralysis, myocarditis.

Treatment is supportive.

69
Q

What is the presentation of herpangina?
What age does it affect?
What 2 viruses cause it?

A

Enanthems - painful vesicles and erythematous erosions on uvula, palate and tonsils.

Children 3-10

Coxsackie A and B

70
Q

Describe the structure and genome of polyomavirus.
What is an important factor that must be present for a human to be infected by this?
What exanthem appears?

A

It is a dsDNA virus with icosahedral shape and NO envelope.
Immunosuppresion appears to be an important factor [ex. PML caused by JC virus in HIV patients]

Exanthem is trichodysplasia spinulosa

71
Q

Describe the appearance of trichodysplasia spinulosa.

What virus causes it?

A

Caused by: polyomavirus

  1. folliculocentric erythematous papule
  2. follicular spicules of the face
  3. pruritic

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