Invasive Group A Strep (GAS) and chicken pox

With thanks to Dr Kat Smith, education fellow and paediatric registrar at King’s College Hospital who answered my call last month for more writers to help me put together the monthly Paediatric Pearls newsletters.

 

Group A Streptococcal Infection in Chickenpox

 

Chickenpox in children is common and usually follows a mild and self-limiting (if somewhat itchy) course. After an incubation period of 10-21 days the first signs of illness are viral prodrome, mild pyrexia, and the classic cropping vesicular rash; the pyrexia is typically mild (38-39oC) and lasts 3-4 days.

 

In otherwise healthy children the most common complication of chickenpox is secondary bacterial skin infection, typically caused by scratching lesions. Whilst most of these are mild impetigo or localised cellulitis, the increased incidence of group A streptococcal (GAS) colonisation in children (around 10% are asymptomatic carriers in the throat or on skin) makes invasive GAS infection a real concern.

 

Secondary bacterial skin infection

This is characterised by erythema +/- tenderness around lesions. Children may be well in themselves if the infection is superficial; if they become more unwell this raises the suspicion of a more serious or invasive bacterial infection.

 

Serious bacterial superinfection / Invasive GAS infection

Around a third of children admitted to hospital with chickenpox have secondary skin infection, some of whom develop invasive infections such as pneumonia, osteomyelitis and septicaemia. GAS in particular can be associated with more fulminant infectious processes such as necrotising fasciitis and toxic shock syndrome (TSS); both are associated with high mortality and morbidity in children.

Features that should prompt consideration of a serious bacterial superinfection are:

  • A lethargic or unwell-looking child; remember, children with chickenpox are typically uncomfortable but well.
  • Spiking, high-grade pyrexia
  • Pyrexia for longer than 4 days, particularly after initial improvement
  • Diarrhoea or vomiting
  • Soft tissue pain which seems disproportionate to other examination findings (an early sign of necrotising fasciitis)

 

How to prevent bacterial superinfection

Because scratching lesions is the most likely way to allow bacteria to breach the body’s normal defences, the primary aim of prevention is to limit scratching:

  • Keep skin moisturised. Many parents still use calamine lotion but it is worth noting that it becomes ineffective once dry, and traditional emollients (e.g. 50:50) may be more effective.
  • There is evidence that sedating antihistamines offer some benefit; chlorphenamine is licensed for this use.
  • Dress children in smooth, loose, cotton clothing.
  • Keep fingernails trimmed short.
  • There are rare reports of NSAIDs potentially worsening skin infections in chickenpox, so ibuprofen should be used with caution. In practice, it would be unusual for a child to need ibuprofen if receiving regular paracetamol; pain or pyrexia necessitating its use in addition to paracetamol should prompt consideration of serious bacterial superinfection.
  • There is no evidence to support the use of acyclovir in young, immunocompetent children with self-limiting, uncomplicated chickenpox; it does not decrease the incidence of complications.

 

What to do if you suspect bacterial superinfection

  • Otherwise well children with evidence of few, small areas of bacterial superinfection can be managed in the community with oral antibiotics and safety-netting advice.
  • Children with evidence of collection, extensive areas of bacterial superinfection, who are unwell, or have other features consistent with possible serious bacterial superinfection, need urgent referral to secondary care.
  • In secondary care, unwell children with evidence of shock / sepsis need urgent resuscitation and intravenous antibiotic administration; if possible this should include clindamycin, due to its vital role in inhibiting toxin production by GAS.
  • Invasive GAS infection has high mortality, and if suspected there should be a low threshold to involve senior staff, regional PICU services, and in the case of necrotising fasciitis, surgical teams (for early debridement); early use of inotropes and IVIG may also be required.

 

Bibliography

Chickenpox NICE Clinical Knowledge Summary (which I found to be the best resource by far): http://cks.nice.org.uk/chickenpox

Cohen J, Breuer J. Chickenpox treatment. Systematic review 912. BMJ Clinical Evidence.

Papadopoulos, AJ. Chickenpox. emedicineWebMD. www.emedicine.com

 

 References

 Re: “the increased incidence of group A streptococcal (GAS) colonisation in children (around 10% are asymptomatic carriers in the throat or on skin)”

Shaikh N, Leonard E, Martin JM. Prevalence of streptococcal pharyngitis and streptococcal carriage in children: a meta-analysis. Pediatrics. 2010 Sep;126(3):e557-64

 

Re. “Around a third of children admitted to hospital with chickenpox have secondary skin infection”:

Bovill B, Bannister B. Review of 26 years/ hospital admission for chickenpox in North London. Journal of Infection. 1998;36(suppl1);17-23.

 

Re: “necrotising fasciitis and toxic shock syndrome (TSS); both are associated with high mortality and morbidity in children.” AND “IVIG may also be required.”

Chuang YY, Huang YC, Lin TY. Toxic shock syndrome in children: epidemiology, pathogenesis, and management. Paediatr Drugs. 2005;7(1):11-25.

Re. “There is evidence that sedating antihistamines offer some benefit”

Tebruegge M, Kuruvilla M, Margarson I. Does the use of calamine or antihistamine provide symptomatic relief from pruritus in children with varicella zoster infection? Archives of Disease in Childhood. 2006:91(12);1035-1036.

 

Re: (continued from above) “chlorphenamine is licensed for this use.”

BNFC, available at: https://www.medicinescomplete.com/mc/bnfc/current/PHP1934-chlorphenamine-maleate.htm?q=chlorphenamine&t=search&ss=text&tot=40&p=1#_hit

 

Re: “if possible this should include clindamycin, due to its vital role in inhibiting toxin production by GAS.” (as well as having it drilled in to us by the microbiologists at St Thomas’):

http://emedicine.medscape.com/article/228936-medication#2

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