Viral infections in childhood Flashcards

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1
Q

List the 6 infections covered

A
  1. measles
  2. mumps
  3. rubella
  4. non-polio enteroviruses
  5. parvovirus B19
  6. HHV-6
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2
Q

Name common childhood rashes and their “numbers” and what agent causes them

A
  1. first disease; measles (rubeola); measles virus
  2. second disease; Scarlet fever; GAS
  3. third disease; rubella; rubella virus
  4. fifth disease; erythema infectiosum; parvovirus B19
  5. sixth disease; roseola infantum; HHV-6, HHV-7
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3
Q

Name the families of MMR

A
  1. Measles: paramyxoviridae
  2. Mumps: paramyxoviridae
  3. Rubella: togaviridae
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4
Q

Common properties of MMR viruses

A
  • ss RNA (MM are -, R is + sense)
  • lipid envelope
  • 1 antigenic type
  • humans are the only natural host
  • transmission via respiratory droplets
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5
Q

Important proteins of MMR

A
  • measles: hemagglutinin (H) binds to host cell receptors, fusion (F) surface protein mediated fusion, matrix M protein for virion assembly, 3 nonstructural (NP, P, L) associated with viral RNA and function in replication
  • mumps: surface hemagglutinin-neuraminidase (HN), F, M, NP, P and L
  • rubella: surface glycoprotein E1 (hemagglutinin) and E2, nucleocapsid protein (C), P150 and p90 nonstructural for replication
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6
Q

Pathogenesis of MMR

A
  • infect eyes, nose, mouth
  • replicate in nasopharynx and regional lymphnodes
  • viremia follows with infection of leukocytes
  • during viremia, viruses spread to many tissues
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7
Q

Prevaccine era: it was expected life event to get MMR; what age was the highest incidence and when during the year would it occur?

A
  • 5-9 years old

- winter and spring

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8
Q

Due to the MMR vaccine, what has been a dramatic shift in what and why is this significant?

A
  • age; teens and young adults

- they are much more likely to have severe symptoms and be sicker for a longer time

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9
Q

In countries where MMR viruses have been largely eliminated, _________ remain the most important source of infection and outbreaks.

A

-imported cases

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10
Q

Synonyms for Measles

A
  • rubeola
  • 5 day measles
  • hard measles
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11
Q

T/F: Measles has largely been eradicated world wide.

A
  • false; remains one of leading causes of death of children < 5 y.o.
  • significant localized epidemics and sustains transmission still occur today in developed countries
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12
Q

There was a measle resurgence in the US in 1989-1991. Why?

A
  • important cause was low vaccination coverage

- mainly unvaccinated or partially vaccinated children

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13
Q

Unvaccinated persons at risk for acquiring measles themselves and transmitting to others, includes what 2 populations?

A
  1. children too young to be vaccinated

2. population declining vaccination

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14
Q

Measles Illness: incubation period, prodrome, and rash(exanthem)

A

-Incubation period: 8-12 days; from exposure to prodrome
-Prodrome: lasts 3-5 days; 3 Cs of cough, coryza, conjunctivitis; ascending stepwise fever to 103. Koplik’s spots (enanthem - mouth) last from 1-2 days;** MOST INFECTIOUS PERIOD*
Rash: lasts 6-7 days; begins 12-24 hrs after koplik’s spots and on first day is when patient is most ill and fever is the highest; initially erythematous, discrete and maculopapular, progresses to confluence

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15
Q

Describe progression of rash in measles

A
  • first appears behind ears and on forehead at hairline
  • spread is centrifugal from head to feet including palms and soles last
  • initially discrete, erythematous and maculopapular but progresses to confluence in same centrifugal manner as its spread
  • follows centrifugal course of progression on its fading
  • areas may desquamate
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16
Q

When are measles patients most infectious?

A

-prodrome stage when cough and coryza is at peak

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17
Q

Describe Koplik’s spots and what illness they are pathognomonic for.

A
  • pinpoint gray-white spots on red base
  • appear on mucus membranes of cheek opposite molar teeth; resemble course grains of sand on inflamed surface
  • MEASLES!!!
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18
Q

When does exanthem period of measles begin?

A

-usually at 14th day after exposure (2-4 after prodrome) at peak of respiratory and fever

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19
Q

Describe the communicability, transmission, and risk factors of severe disease for measles

A
  • highly contagious with a 90% attach rate in susceptible population
  • spread by coughing and sneezing, close personal contact, or direct contact with respiratory secretion; AIRBORNE TRANSMISSION FOR UP TO 2 HOURS AFTER INFECTED PERSON WAS IN AREA
  • Risk factors: age (<2 or adults); unvaccinated children, nutritional status (malnourished, vit A deficiency); immunocompromised (HIV/AIDS)
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20
Q

Measles immunity and hypersensitivity

A
  • life long immunity after natural infection
  • cell mediated immunity needed to stop acute infection
  • rash may be due to hypersensitivity bc patients with cellular immunity deficiencies do not get rash and may have more severe disease
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21
Q

One or more in complications are seen in 30% of measles cases. Who gets them? give examples and which is most deadly?

A
  • more common in children 20
  • severe diarrhea, otitis media, pneumonia (viral and bacterial); acute encephalitis; subacute sclerosing panencephalitis (SSPE)
  • Pneumonia is most likely complication!!
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22
Q

SSPE

A

-rare but serious CHRONIC, degenerative CNS disease
-secondary to persistent replication of defective measles virus in brain
-occurs after natural infection;( inversely related to age and vaccine coverage)
-onset 6-9 years after measles infection
Symptoms: present with poor school performance, progressive personality changes and behavioral abnormalities, forgetfulness, physical and intellectual deterioration, poor comprehension, speech decline over 1-3 years
-develop periodic myoclonic jerks, motor dysfunction, loss of vitality, superinfection and metabolic imbalances that eventually lead to death
FATAL

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23
Q

3 forms of unusual measles presentation

A
  1. modified measles: mild form bc antibody is below level for protection for infection but sufficient to modify illness; usually in infants with residual maternal IgG
  2. atypical measles: people who received formalin-killed measles vaccine and then exposed to live virus; vaccine sensitizes recipient to measles antigens without providing immunity
  3. measles in immunocompromised (giant cell pneumonia):severe, protracted, and fatal; severe giant cell pneumonia without evidence of rash
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24
Q

Describe the atypical presentation of atypical measles

A
  • abrupt onset of fever, abdominal pain, pneumonia, and rash which begins on extremities and progressively moves to trunk and face
  • rash can be variety of presentations
25
Q

A strategy of the Measles Initiative is to have routine immunizations for children by what age?

A

-1st birthday

26
Q

Mumps illness: incubation period, prodrome, common feature…

A
  • 14-18 day incubation
  • nonspecific prodrome of low-grade fever, headache, malaise, myalgia
  • most common feature is painful swelling of salivary glands in 30-40%, particularly parotid glands
  • mainly bilateral swelling; can last a week!
  • way to remember this is that the verb mump means to mumble
27
Q

T/F: if you seen parotitis, it must be mumps.

A

-false; this can be caused by Influenza A, parainfluenza, CMV, etc…

28
Q

Mumps illness

A
  • most cases are mild and self-limited with only nonspecific or primarily respiratory symptoms
  • 30% subclinical
  • severe illness more likely in adults
  • greatest communicability is 1-2 days before to 5 days after onset of parotid swelling
29
Q

Common complications of mumps

A
  • orchitis is 20-30% of infected postpubescent males
  • oophoritis and mastitis in 5% of postpubertal females
  • sterility and impaired fertility common
  • MENINGITIS (15%) and much smaller risk of encephalitis
  • pancreatitis, myocarditis, arthritis less frequent
30
Q

Mumps orchitis

A
  • abrupt onset of testicular swelling
  • testicle becomes very painful and tender
  • fever, nausea, vomiting are common
  • involved testes is warm and scrotom is warm
  • pain/swelling for 1 way but tenderness can continue for many weeks
31
Q

Of the MMR vaccine, which is the least effective?

A
  • mumps

- still see breakouts in colleges

32
Q

Describe what other virus rubella resembles.

A

-mild case of measles in post natal infections

33
Q

Postnatally-acquired rubella: incubation period, symptoms

A
  • 14 day incubation
  • low-grade fever
  • generalized lymphadenopathy with most involving posterior auricular, posterior cervical, and suboccipital lymph nodes
  • discrete maculopapular, erythematous rash
34
Q

Complications of post-natal rubella

A
  • uncommon
  • transient arthritis and arthralgia frequent in adolescent and ADULT females
  • thrombocytopenic purpura
  • encephalitis
35
Q

Congenital Rubella Syndrome

A
  • result of utero fetal infection; usually in first 12 wks of pregnancy
  • can affect all organs and cause variety of malformations
  • congenital malformations: cardiac, ocular, hearing, CNS, bone, liver/spleen;
  • generalized growth retardation
36
Q

What is the most common malformation of congenital rubella syndrome?

A

-deafness

37
Q

Risk of rubella to unborn child is directly related to what?

A
  • gestational age at which mother contracts infections

- maximal damage occurs early in pregnancy

38
Q

Treatment and prevention of MMR

A
  • life-long immunity after natural infection
  • no specific therapy; supportive care
  • Vitamin A for measles in places with deficiency
  • ACTIVE immunization of live, attenuated vaccine (2 doses)
  • passive immune serum globulin to prevent or modify measles in susceptible host within 6 days of exposure
39
Q

What kind of vaccine is present for MMR? how many doses? what ages?

A
  • live, attenuated vaccine
  • 2 doses
  • 12-15 months, 4-6 years
40
Q

Human Enteroviruses: what family do they belong to? describe their structure, where they replicate.

A
  • Picornavirus
  • small SS + sense RNA
  • replicate in GI tract
  • 102 serotypes in 4 groups!!
  • NO envelope (fecal oral!) icosahedral symmetry
41
Q

What are the 4 groups that make up enterovirus?

A

-Human enterovirus A, B, C, and D

42
Q

Enterovirus epidemiology

A
  • worldwide
  • humans only natural host
  • spread by fecal-oral route
  • temperate climates get epidemics in summer and fall (tropical all year round)
  • no heterotypic immunity bc many serotypes circulate at a time
  • spread greatest within families from young children, closed institutions, summer camps!!
43
Q

When do we see enterovirus breakouts/epidemics??

A

-summer and fall!!!!!

44
Q

Enterovirus pathogenesis

A
  • initially replicate in oropharynx and intestinal tract
  • then infect and replicate within lymphoid cells underlying intestinal mucosa, enter blood stream, and primary viremia spreads to different target tissues
45
Q

What immune response is involved in protect and resolution of enterovirus disease?

A

-humoral (antibody)

46
Q

List mild and potentially serious infections that can occur due to nonpolio enterovirus

A
  • mild: fever, rash, hand-foot-mouth- syndrome, pharyngitis, conjunctivitis, croup
  • serious: meningitis, encephalitis, acute paralysis, neonatal sepsis…
47
Q

Hand-foot-mouth disease: what does it present with and what causes it?

A
  • vesicular lesions on hand, feet, and tonsils and palate

- coxsackie A16

48
Q

Major EV syndromes (3)

A
  1. nonfocal, acute, febrile illness (fever, poor feeding, abdominal distention, lethargy, hypotonia); common cause in infants, oftens leads to evaluation for bacterial sepsis and neonatal HSV, aspeptic meningitis in 50%!!
  2. Aseptic meningitis (headache, fever, achiness, still neck, vomiting, photophobia, 2-6 days); most community acquired aseptic meningitis due to EV
  3. Encephalitis: accounts for about 10-20% of acute encephalitis; can get brainstem encephalitis
49
Q

What is the most common manifestation of nonpolio EV in infants?

A
  • acute, nonfocal febrile illness

* * IN SUMMER**

50
Q

Compare CSF glucose levels, protein levels, cell # and cell type between viral and bacterial meningitis.

A
  • viral: normal glucose, mild increase in protein, moderate increase in cells, lymphocytes
  • bacterial: low glucose, high protein, high cells, PMNs
51
Q

Parvovirus B19: family, structure, hosts, tropism

A
  • parvoviridae
  • ssDNA virus; no envelope
  • 3 proteins in genome
  • humans are only natural host
  • Extreme cell tropism: replicates in RBC precursors in BM and causes temporary cessation of RBC production
52
Q

5 parts of Parvovirus B19 clinical disease

A
  • erythemia infectiosum (fifths disease)
  • polyarthragia, polyarthritis
  • aplastic crisis (severe anemia) in sick cell disease and other hemaglobinopathies
  • chronic anemia in AIDS
  • abortion, still birth, fetal hydrops
53
Q

Erythema infectiosum is associated with what virus and what is the funny description of this rash?

A
  • Parvovirus B19

- “slapped cheek” rash

54
Q

Fifth Disease clinical presentation

A
  • distinct clinical feature: intensely red rash on cheeks
  • area around mouth often remains pale
  • lace-like rash may erupt on arms, legs, stomach
  • rash may itch, tends to come and go, and sometimes brought on by heat
  • 5-10 years old likely to catch disease, most often recognized in school outbreaks
  • benign disease; rarely cause for concern
55
Q

HHV-6: what is its family, what does it infect, who is mostly affected?

A
  • herpesviridae
  • lymphotrophic virus (infect CD4 and CD8, NK cells, macrophages)
  • infants 0-3 years
56
Q

Clinical manifestations of HHV-6 primary infection

A
  1. roseola infantum-rose rash of infants; also called exanthum subitum or 6th disease; in 20% of infected children
  2. undifferentiated febrile illness without rase
  3. febrile seizures/convulsions
    * *can cause primary or reactivated disease in bone marrow and solid organ transplant recipients
57
Q

HHV-7 causes ______ % of roseola.

A

-10%

58
Q

HHV-6 Exanthem Subitum (roseola)

A
  • sometimes called baby measles
  • illness commonly in children 6months-2 years
  • rared in children before or after this age
  • Key clinical features: appears as fever subsides, macular or maculopapular, seen on neck, face, or trunk; spreads to extremities, persists for hours to 2 days