Viral infection in a child (Mumps, Measles, Rubella, Erythema infectiosum, Parvovirus B19, Roseola infantum (HHV6), Chickenpox, Hand, foot and mouth disease) Flashcards

1
Q

What are the types of human herpes viruses?

A
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2
Q

Which infections are associated with these fetal complications?

  1. limb defects
  2. cerebral palsy
  3. cataracts
  4. hydrops fetalis
  5. choroidoretinitis
A
  1. limb defects - acute varicella in pregnancy
  2. cerebral palsy - acute CMV
  3. cataracts - rubella
  4. hydrops fetalis - parvovirus
  5. choroidoretinitis - toxoplasmosis
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3
Q

Which two infections shed antigens into urine?

A

Legionella penumophila

Streptococcus pneumoniae

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4
Q

What is the incubation period of measles? How long does the rash last?

A

Incubation 10-14 days

5 days

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5
Q

How is measles spread? What type of pathogen causes measles?

A

RNA paramyxovirus

Droplet spread

Highly infectious during viral shedding which starts just before symptoms and continues until ~day 5 of symptoms (when fever is worst)

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6
Q

What are the presenting features of measles?

A

Prodrome: irritability, conhynctivitis, fever.

  • Rash starts behind ears
  • Cough
  • Coryza
  • Rash 5 days
  • Fever
  • Koplik spots
  • Conjunctivitis
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7
Q

Which age groups have the most seveere disease with chickenpox, parvovirus b19 (HPV-B19) and measles?

A

Older children and adults

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8
Q

What is shown?

A

White spots on buccal mucosa, seen against a bright red background = Koplik spots

Pathognomonic of measles but difficult to see

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9
Q

Describe the appearance of this rash seen in measles.

A
  • Spreads downwards from behind the ears
  • Covers whole body
  • Discrete maculopapular rash initially then becomes blotchy and confluent
  • May desquamate in second week
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10
Q

What investigations are used to diagnose measles infection?

A

PCR

Serology - IgM antibodies can be detected within a few days of rash onset

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11
Q

What are the complications of measles?

A

NB: measles is a major cause of death in childhood in low-income countries

Respiratory:

  • Otitis media
  • Pneumonia
  • Secondary bacterial infection
  • Tracheitis

Neurological:

  • EEG abnormalitiies and febrile seizures
  • Encephalitis
  • SSPE (subacute sclerosing panencephalitis - in adolescence after measles in childhood)

Other:

  • Diarrhoea
  • Hepatitis
  • Appendicitis
  • Corneal ulceration
  • Myocarditis
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12
Q

What is the epidemiology of measles?

A

Incidence has declined dramatically since immunisation but a recent small increase has resulted from reduction in vaccine uptake (MMR)

MMR is the best at reducing morbidity and mortality from measles

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13
Q

What is the management of measles? What is the role of vitamins?

A

Supportive

Isolation

Inform public health - notifiable disease

Ribavarin if immunocompromised

Vitamin A may modulate the immune response and can be given in low-income countries - this is because vitamin A deficiency can lead to an impaired cell-mediated immune respoonse.

(Offer vaccine to any child who comes into contact with measles and is not immunised within 72 hours)

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14
Q

How can an impaired cellular response (e.g. in HIV) in measles lead to a difference in presentation?

A

Impaired cellular response may cause:

  • Absence of rash
  • Increased risk of dissemination e.g. giant-cell pneumonia or encephalitis
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15
Q

How common is encephalitis in measles? When does it occur? What are the symptoms and long-term complications?

A

1 in 5000 affected within a few days of illness

Symptoms of headache, lethargy, irritability and proceeding to seizures and ulimately coma.

Mortality is 15%

Morbidity - long-term seizures, deafness, hemiplegia, severe learning difficulties, affecting up to 40% of survivors.

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16
Q

What is the cause of SSPE in measles? When and how does it present? How common is it? How is it diagnosed?

A

Caused by a variant of the measles virus which persists in CNS

Presents ~7 years after measles illness with loss of neurological function which progresses to dementia and death over several years,

Affects 1 in 100,000 previously infected - most had measles at <2 years old. But rare overall since immunisation against measles.

Diagnosis is clinical supported by findings of high levels of measles antibody in blood and CSF and EEG abnormalities.

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17
Q

What kind of pathogen causes mumps? What time of year does it mostly occur?

A

RNA paramyxovirus

Tends to occur in winter and spring

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18
Q

How does mumps spread? What cells does it replicate in?

A

Spread by droplets

Replicates in epithelial cells

Repiratory tract epithelial cells -> parotid glands –> other tissues

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19
Q

What is the incubation period of mumps? When is a patient infectious during illness?

A

Infective 7 days before and 9 days after parotid swelling starts

Incubation period = 14-21 days

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20
Q

What are the clinical features of mumps?

A
  • Fever - disappears within 3-4 days
  • Malaise, muscular pain
  • Parotitis (‘earache’, ‘pain on eating/drinking’): unilateral initially then becomes bilateral in 70%

BUT subclinical in 30% of cases

May have pancreatic involvement –> raised plasma amylase

Generally mild and self limiting

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21
Q

What is the efficacy of the MMR for mumps?

A

80%

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22
Q

What is the management of mumps?

A
  • rest
  • paracetamol for high fever/discomfort
  • notifiable disease
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23
Q

What are the complications of mumps?

A
  • Orchitis - uncommon in pre-pubertal males but occurs in around 25-35% of post-pubertal males. Usually unilateral and although reduction in sperm count may occur infertility is uncommon. Typically occurs four or five days after the start of parotitis
  • Hearing loss - usually unilateral and transient
  • Meningoencephalitis
  • Pancreatitis –> raised amylase
  • Viral meningitis and encephalitis - lymphocytes raised in CSF in 50% but meningeal signs only seen in 10% and encephalitis in 1 in 5000

Rarely oophritis, mastitis and arthritis may occur.

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24
Q
A
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25
Q

What is the most common illness associated with parvovirus B19 infection?

A

Erythema infectiosum aka Fifth disease aka ‘Slapped-cheek’ syndrome

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26
Q

What is shown?

A

Slapped cheek disease caused by parvovirus B19

Howevver, in adults and women it can look like a lace-like rash as shown below.

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27
Q

Which two patient groups are at risk of parvovirus B19 infection? Is it common in the elderly?

A

Haemoglobinopathies - parvovirus replicates in red blood cell precursors expressing the P antigen. Can lead to aplastic crises.

Immunosuppressed patients - e.g. HIV, bone marrow transplant recipients.

Uncommon in elderly because seropositivity increases with age.

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28
Q

What is erythema infectiosum also known as? What is the cause?

A

Fifth disease - because it was the 5th of a group of illnesses with similar rashes to be named.

Parvovirus B19 - a DNA virus

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29
Q

What are the clinical features of erythema infectiosum? Which part of the body is rarely affected?

A

Viraemic phase of

  • mild fever - hardly noticeable
  • malaise
  • headache
  • myalgia

Followed by

  • characteritic rash on the face (‘slapped-cheek’) a week later - child starts to feel better when the rash appears
  • ‘lace’-like rash on trunk and limbs
  • arthralgia or arthritis are common in adults

Unlike other rashes it rarely affects the palms and soles.

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30
Q

What are the different types of disease/complications caused by parvovirus B19 infection?

A
  1. Asymptomatic infection - 5-10% of pre-schoolers and 65% of adults have antibodies
  2. Erythema infectiosum - most common
  3. Aplastic crisis - most serious consequence
  4. Fetal disease - mother-to-fetus trasmission may lead to featl hydrops and death from anaemia although most fetuses recover
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31
Q

Who is most effected by aplastic crises as a result of parvovirus B19?

A

Children with chronic haemolytic anaemia where there is an increased rate of cell turnover (e.g. sickle cell disease or thalassaemia) and in immunocompromised children (e.g. malignancy) who do not have an antibody response to neutralise the infectious agent.

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32
Q

What is the management of erythema infectiosum and what is the prognosis?

A

No specific treatment required

School exclusion not required - child not infectious once rash appears

Prognosis:

  • Child feels better as the rash appears
  • Rash peaks after a week then fades
  • For a few months afterwards, a warm bath, sunlight, heat or fever will trigger a recurrence of bright red cheeks and the rash itself.
  • Adults may get acute arthritis
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33
Q

What are the complications of parvovirus B29 in pregnancy?

A

Can affect unborn baby in first 20 weeks and if exposed should seek advice as maternal IgM and IgG will need to be checked.

34
Q

What are the consequences of parvovirus infection in pregnancy?

A

Fetal bone marrow aplasia, especially anaemia causing hydrops fetalis.

35
Q

When is a person with erythema infectiosum/parvovirus B19 infectious?

A

3-5 days before the appearance of the rash

No specific treatment

36
Q

What is roseola infantum aka? What is it caused by?

A

Exanthema subitum (bc rash apears so suddenly after fever) or sixth disease (lasts ~6 days) = roseola infantum

HHV6 (and sometimes HHV7)

37
Q

What is the incubation period of roseola infantum? What age group is most commonly affected?

A

5-15 days

Most affected are children aged 6months-2 years

38
Q

What are the clinical features of roseola infantum? Is school exclusion necessary?

A
  • High fever with malaise lasting a few days
  • Followed by generalised maculopapular rash which appears after fever wanes
  • Nagayama spots which are papular exanthen on the uvula and soft palate
  • Febrile convulsions in 10-15%
  • Diarrhoea and cough are common
  • Many have a subclinical infection

No school exclusion

39
Q

How is roseola infantum diagnosed?

A

Usually by the rash and symptoms

Sometimes by antibodies to HHV-6/7

40
Q

What is roseola infantum frequently misdiagnosed as? What is a complication of this?

A

Measles or rubella

Doctors frequently prescribe antibiotics to a febrile child with HHV-6 and then when the rash appears, it is attributed to an allergic reaction.

41
Q

What is shown?

How does the measles rash differ from roseola rash?

A

Roseola infanum shown

Roseola starts on the torso and spreads outwards

42
Q

Is the roseola rash itchy? Is it infectious?

A

Rash is not itchy nor infectious

Spread by oral secretions

43
Q

What is another complication of HHV6/7? What is the prognosis?

A

Aseptic meningitis

Encephalitis

Hepatitis

Mononucleosis like syndrome

But usually good prognosis and no long-term side effects. Usually lifelong immunity to HHV6 develops.

44
Q

What is this called? (accompanies a maculopapular rash)

A

Nagayama spots on the uvula and soft palate

Occurs in roseola infantum

45
Q

What are the effects of chickenpox on the immune system?

A

Chickenpox increases risk of bacterial superinfections with staphylococci and streptococci in the short term –>sepsis, toxic shock syndrome, or necrotising fasciitis

46
Q

What is chickenpox? What is the reactivation of the latent form called?

A

Chickenpox is caused by primary infection with varicella zoster virus.

Shingles is a reactivation of the dormant virus in dorsal root ganglion

47
Q

How does chickenpox spread? What is the incubation period?

A

spread via the respiratory route (can be caught from someone with shingles)

incubation period = 10-21 days

48
Q

How long is a person with chickenpox infectious? Is schol exclusion necessary?

A

Infectivity = 4 days before rash, until 5 days after the rash first appeared*

School exclusion: NICE advise that the most infectious period is 1–2 days before the rash appears, but infectivity continues until all the lesions are dry and have crusted over (usually about 5 days after the onset of the rash).

49
Q

What are the clinical features of chickenpox?

A

Fever initially

Itchy rash starting on the head/trunk before spreading - macular then papular then vesicular.

Mild systemic upset

50
Q

Describe the rash in chickenpox. What does it mean if new lesions keep appearing beyond day 10?

A

Macular –> papular –> vesicular –> pustular –> crusting

50–500 lesions start on head and trunk, progress to peripheries but may be just a few lesions

Appear as crops of papules, vesicles with surrounding erythema and pustules at different times for up to one week.

Lesions may occur on the palate.

Itchy and scratching; may result in permanent, depigmented scar formation or secondary infection.

New lesions appearing beyond 10 days suggest defective cellular immunity

51
Q

What is the management of chickenpox?

A

Keep cool, trim nails

Calamine lotion

School exclusion

Immunocompromised patients and newborns with peripartum exposure should receive varicella zoster Ig (VZIG) - give IV acyclovir if chickenpox develops

52
Q

What are the complications of chickenpox? What is the most common complication?

A
  • Secondary bacterial infection of lesions-
    • most common complication - staphylococcal, streptococcal
    • may lead to TSS or NF
  • Central nervous system
    • Encephalitis/cerebellitis (cerebellar involvement is characteristic of VZV) - generalised but not as severe as HSV and has a good prognosis; occurs around a week after onset of rash; child is ataxic
    • Aseptic meningitis
  • In the immunocompromised -
    • Pneumonia / pneumonitis
    • Disseminated haemorrhagic lesions
    • DIC
    • Arthritis, nephritis, pancreatitis are rarely seen
53
Q

How do secondary bacterial infections of lesions commonly present? What are the complications? What increases the risk?

A

Suspect if high fever persists after first few days - usually indicated when fever initially settles then recurs

NSAIDs increase risk

May present as one infected lsion/small area of cellulitis but in some invasive GAS soft tissue infection may occur and cause necrotising fasciitis and toxic shock syndrome

54
Q

What is seen on this post-varicella pneumonia CXR?

A

Chest x-ray showing miliary opacities secondary to healed varicella pneumonia.

Multiple tiny calcific miliary opacities noted throughout both lungs - these are of uniform size and dense suggesting calcification.

There is no focal lung parenchymal mass or cavitating lesion seen. The appearances are characteristic for healed varicella pneumonia.

55
Q

What are the complications of varicella zoster in pregnancy? What is the management?

A

15% of pregnancies are susceptible to VZV

  • <20 weeks gestation there is <2% risk of skin scarring, ocular/neurological damage and digital dysplasia to fetus
  • 5days before or after delivery there is 25% risk of vesicular rash and 30% risk of mortality

Exposed mothers can be protected with VZIG and treated with aciclovir. High risk infants should receive VZIG early and aciclovir if any signs of infection.

56
Q

How does VZV encephalitis present?

A

Cerebellar involvement is characteristic of VZV

Generalised but not as severe as HSV and has a good prognosis

Occurs around a week after onset of rash

Child is ataxic

Resolves within a month

57
Q

What is the pathophysiology of purpura fulminans caused by VZV?

A

Consequence of vasculitis in the skin and subcutaneous tissues. It is best known in relation to meningococcal disease and can lead to loss of large areas of skin by necrosis.

May rarely occur after VZV infection due to production of antiviral antibodies, which cross-react and inactivate the inhibitory coagulation factors protein C or protein S. This results in an increased risk of clotting, which most often manifests as purpuric skin rash.

58
Q

How does VZV present in the immunocompromised?

A

Severe disseminated disease with mortality up to 20%

Vesicular eruptions persist and may become haeomorrhagic

59
Q

Along which types of nerves does shingles present?

A

Sensory nerves - most commonly in the thoracic area

60
Q

What does the distribution of this rash suggest?

A

Herpes zoster (shingles) in a child.

Distribution is along the S1 dermatome.

If recurrent or multidermatomal then suggests primary or secondary T cell immune defect

61
Q

How does shingles present in children?

A

Vesicular rash along dermatomal distribution

Rare to have neuralgic pain (unlike in adults)

Shingles in childhood is more common in those who had chickenpox in the first year of life

62
Q

What pathogen causes hand, foot and mouth disease? How is it transmitted?

A

Most commonly coxsackie A16 (CA16) and enterovirus 71 (E71) (members of the Picornaviridae family, Enterovirus genus).

Faeco-oral and respiratory droplet route - infected individual can shed the virus for some weeks.

63
Q

How does hand, foot and mouth disease present?

A

Mild systemic upset (sore throat, fever, myalgia)

Oral ulcers initially which are yellow surrounded by red haloes

Painful vesicles on hands, feet, mouth, tongue, buttock then appear and last 7-10 days (start as 2-5 mm erythematous macules but rapidly progress to grey vesicles with an erythematous base)

It is very contagious and typically occurs in outbreaks at nursery

E71 sometimes causes vomiting

64
Q

What investigations are done for HFMD?

A

Usually clinical diagnosis but swabs can be taken from throat, vesicle or rectum. PCR is then used but only in specialist centres.

65
Q

How long is a person with HFMD infectious? What is the incubation period?

A

Incubation 3-7 days

Infected person can shed the virus for some weeks

66
Q

What other conditions can be caused by enteroviruses?

A
  • Hand foot and mouth disease
  • Herpangina - vesicular and ulcerated lesions on the soft palate and uvula (posterior oral cavity) causing anorexia, pain on swallowing, and fever. Severe cases may require intravenous fluids and appropriate analgesia.
  • Meningitis/encephalitis - most make a full recovery
  • Pleurodynia (Bornholm disease)
  • Myocarditis/pericarditis
  • Enteroviral neonatal sepsis syndrome - first weeks of life from transplacental or intrapartum infection of the infant, mimics sepsis symptoms, no drugs are effective
67
Q

When is HFMD most common?

A

In children younger than 10yrs and especially <4yrs

Most adults are immune following previous exposure

68
Q

Is school exclusion necessary in HFMD?

A

No but children who are unwell should be kept off school until they feel better

Should contact HPA if you suspect that there may be a large outbreak.

69
Q

What is the management of HFMD? What reassurance should you provide?

A

Self-limiting within a few days

Symptomatic treatment only - anagesia, hydration as dehydration is common due to poor fluid intake, suggest soup diet. If the mouth is very painful then topical lidocaine oral gel, benzydamine spray or mouth wash can be used. Mouth rinses with warm salty solution if relied upon not to swallow it.

Reassure that no link to disease in cattle or animals

70
Q

If you suspect HFMD but lesions are only on the posterior oral cavity, what is the cause?

A

Herpangina - also caused by coxsackievirus and echoviruses

Also consider gingivitis, HSV, viral pharyngitis, Kawasaki disease.

71
Q

Does HFMD have complications?

A
  • Secondary infection of scratched lesions
  • Dehydration

Less common:

  • Although mild can cause fatalaties e.g. epidemic occurred in China in 2009 and caused >200 fatalities.
  • Usually this is due to enterovirus 71 which more commonly causes neurological complications (e.g. aseptic meningitis) and fatalities but CA16 can also cause deaths.
72
Q

How do you prevent HFMD?

A

Good hand hygiene, covering nose and mouth when coughing or sneezing

73
Q

What pathogen causes rubella? What is rubella aka?

A

Togavirus

Rubella is also called German measles

74
Q

How common is rubella? When are outbreaks most common?

A

Very rare with MMR vaccine (<5 cases in UK per year)

Outbreaks more common around winter and spring

75
Q

What is the incibation period of rubella? How long are individuals infectious? How is it spread?

A
  • the incubation period is 14-21 days
  • individuals are infectious for ~11 days (7 days before symptoms appear to 4 days after the onset of the rash)
  • respiratory route spread
76
Q

How do you diagnose rubella infection?

A

Clinical differentiation from other viral infections is unreliable

Diagnosis needs to be confirmed serologically if there is any risk of exposure of a non-immune pregnancy woman

77
Q

What are the clinical features of rubella?

A

Prodrome, e.g. low-grade fever or none

Rash: maculopapular, initially on the face/behind ears before spreading to the whole body, usually fades by the 3-5 day

Lymphadenopathy: suboccipital and postauricular

78
Q

Does school exclusion/notification apply for rubella?

A

Yes - 5 days from onset of rash

79
Q

What is the management of rubella?

A
  • Ask about contact with pregant women
  • School exclusion for 5 days after rash onset
  • Antipyretics for fever
  • No effective antiviral treatment

Prevention lies in immunisation

80
Q

What are the complications of rubella? What partcular group are complications most severe for?

A
  • arthritis
  • thrombocytopaenia
  • encephalitis - usually ~6 days after rash
  • myocarditis

Pregnant women - if contracted during weeks 8-10 of pregnancy there is a 90% risk of congenital rubella syndrome

81
Q

What are the features of congenital rubella syndrome?

A
  • sensorineural deafness
  • congenital cataracts
  • congenital heart disease (e.g. patent ductus arteriosus)
  • growth retardation
  • hepatosplenomegaly
  • purpuric skin lesions
  • ‘salt and pepper’ chorioretinitis
  • microphthalmia
  • cerebral palsy