Infection - Varicella Zoster, HUS, MMR Flashcards

1
Q

Presentation of chickenpox

A

Chickenpox is characterised by widespread, erythematous, raised, vesicular, blistering lesions. The rash usually starts on the trunk or face and spreads outwards affecting the whole body over 2 – 5 days. Eventually the lesions scab over, at which point they stop being contagious.

Other symptoms:

  • Fever is often the first symptom
  • Itch
  • General fatigue and malaise
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2
Q

Describe the infectivity of chickenpox

A
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3
Q

Complications of acute chickenpox infection

A
  • Bacterial superinfection
  • Dehydration
  • Conjunctival lesions
  • Pneumonia
  • Encephalitis (presenting as ataxia)
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4
Q

Long term complications of chickenpox

A

After the infection the virus can lie dormant in the sensory dorsal root ganglion cells and cranial nerves and reactivate later in life as shingles or Ramsay Hunt syndrome.

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5
Q

Complications of chickenpox in pregnancy

A

Chickenpox in pregnancy, before 28 weeks gestation, can cause developmental problems in the fetus in a small portion of patients. This is known as congenital varicella syndrome.

Chickenpox in the mother around the time of delivery can lead to life threatening neonatal infection and is treated with varicella zoster immunoglobulins and aciclovir.

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6
Q

Chickenpox is usually a mild self limiting condition that does not require treatment in otherwise healthy children.

Who may require treatment and what does this involve?

A

Aciclovir may be considered in immunocompromised patients, adults and adolescents over 14 years presenting within 24 hours, neonates or those at risk of complications.

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7
Q

Pathophysiology of haemolytic uraemia syndrome

A
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8
Q

Classic triad of haemolytic uraemic syndrome:

A
  • Haemolytic anaemia: anaemia caused by red blood cells being destroyed
  • Acute kidney injury: failure of the kidneys to excrete waste products such as urea
  • Thrombocytopenia: low platelet count
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9
Q

What is the most common cause of haemolytic uraemic syndrome?

A

The most common cause is a toxin produced by the e. coli 0157 bacteria, called the shiga toxin. Shigella also produces this toxin.

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10
Q

When infected with E.coli O157 or Shigella what increases the risk of getting haemolytic uraemia syndrome?

A

The use of antibiotics and anti-motility medications such as loperamide to treat gastroenteritis caused by these pathogens increases the risk of developing HUS.

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11
Q

Presentation of haemolytic uraemic syndrome

A

E. coli 0157 causes a brief gastroenteritis, often with bloody diarrhoea. The symptoms of haemolytic uraemic syndrome typically start around 5 days after the onset of the diarrhoea.

Signs and symptoms of HUS may include:

  • Reduced urine output
  • Haematuria or dark brown urine
  • Abdominal pain
  • Lethargy and irritability
  • Confusion
  • Oedema
  • Hypertension

Bruising

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12
Q

Management of haemolytic uraemic syndrome

A

HUS is a medical emergency and has a 10% mortality. It needs to be managed by experienced paediatricians under the guidance of a renal specialist. The condition is self limiting and supportive management is the mainstay of treatment.

Patient may require dialysis, blood transfusion or anti hypertensives.

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13
Q

What is Kawasaki disease?

A

It is a systemic, medium-sized vessel vasculitis.

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14
Q

Who dose Kawasaki disease typically effect?

A

It affects young children, typically under 5 years. There is no clear cause or trigger. It is more common in Asian children, particularly Japanese and Korean children. It is also more common in boys

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15
Q

A key complication of Kawasaki disease is:

A

Coronary artery aneurysm

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16
Q

Clinical features of Kawasaki disease

A

A key feature that should make you consider Kawasaki disease is a persistent high fever (above 39ºC) for more than 5 days. Children will be unhappy and unwell. The key skin findings are a widespread erythematous maculopapular rash and desquamation (skin peeling) on the palms and soles.

Other features include:

  • Strawberry tongue (red tongue with large papillae)
  • Cracked lips
  • Cervical lymphadenopathy
  • Bilateral conjunctivitis
17
Q

Investigations for Kawasaki disease

A
  • Full blood count can show anaemia, leukocytosis and thrombocytosis
  • Liver function tests can show hypoalbuminemia and elevated liver enzymes
  • Inflammatory markers (particularly ESR) are raised
  • Urinalysis can show raised white blood cells without infection
  • Echocardiogram can demonstrate coronary artery pathology
18
Q

What are the three phases of Kawasaki disease?

A

Acute phase: The child is most unwell with the fever, rash and lymphadenopathy. This lasts 1 – 2 weeks.

Subacute phase: The acute symptoms settle, the desquamation and arthralgia occur and there is a risk of coronary artery aneurysms forming. This lasts 2 – 4 weeks.

Convalescent stage: The remaining symptoms settle, the blood tests slowly return to normal and the coronary aneurysms may regress. This last 2 – 4 weeks.

19
Q

Management of Kawasaki disease

A
  • High dose aspirin to reduce the risk of thrombosis
  • IV immunoglobulins to reduce the risk of coronary artery aneurysms

Patients will need close follow up with echocardiograms to monitor for evidence of coronary artery aneurysms.

20
Q

Kawasaki disease is one of the few scenarios where aspirin is used in children. Why is aspirin usually avoided in children?

A

Risk of Reye’s syndrome

21
Q

How are measles, mumps and rubella spread?

A

Respiratory droplets

22
Q

How long is the incubation period for mumps and how long does the condition normally last?

A

The incubation period is 14 – 25 days. Mumps is usually a self limiting condition that lasts around 1 week.

23
Q

Presentation of mumps

A

Patients experience an initial period of flu-like symptoms known as the prodrome. These occur a few days before the parotid swelling:

  • Fever
  • Muscle aches
  • Lethargy
  • Reduced appetite
  • Headache
  • Dry mouth

Parotid gland swelling, either unilateral or bilateral, with associated pain is the key feature that should make you consider mumps.

24
Q

Complications of mumps

A
  • Pancreatitis
  • Orchitis
  • Meningitis
  • Sensorineural hearing loss
25
Q

How is mumps diagnosed?

A

Clinical diagnosis

The diagnosis can be confirmed using PCR testing on a saliva swab. The blood or saliva can also be tested for antibodies to the mumps virus.

26
Q

Management of mumps

A

Supportive

Inform public health of suspected and confirmed cases

27
Q

Presentation of measles

A

Prodrome (2–4d): fever, conjunctivitis, coryza, diarrhoea, Koplik spots (white spots on red buccal mucosa).

Then generalized, maculopapular rash, classically face/necktrunklimbs

28
Q

Management of measles

A

Supportive

Prevent with vaccination

Human immunoglobulin within 3d of exposure in non- immune

29
Q

Presentation of rubella

A

Usually mild/subclinical.

Prodrome: fever, conjunctivitis, rhinorrhoea

Rash: generalized, pink, maculopapular. Lymphadenopathy

30
Q

Effects of rubella infection during pregnancy

A

Up to 90% risk of fetal malformation in 1st trimester, sensorineural hearing loss/retinopathy in 2nd trimester

31
Q

How to prevent rubella infection during pregnancy?

A

Vaccinate pre-pregnancy. Live vaccines contraindicated in pregnancy.