Scarlet fever is a notifiable disease that presents with a characteristic rash covering the body in children infected with group A beta-haemolytic streptococcus (GABHS).
It was once a serious illness but with antibiotic development and immunity its incidence, morbidity and mortality have reduced substantially. However, the Health Protection Agency (HPA) documented a rise in unconfirmed notifications of scarlet fever in England and Wales between 2008 and 2009.1
Pathophysiology and epidemiology
GABHS is carried asymptomatically in the nasopharynx in 10 to 15% of children. It is also found on the skin and in the throat, where it causes impetigo or bacterial sore throat. Scarlet fever can develop from any GABHS infection but most commonly evolves from a tonsillar or pharyngeal focus.
GABHS secretes a variety of haemolysing enzymes and toxins including an erythrogenic toxin that in susceptible individuals results in the pathognomonic rash of scarlet fever.
Due to the need for susceptibility, only 10% of those with a streptococcal infection develop scarlet fever.
Scarlet fever has a peak incidence in two to eight-year-olds and affects males and females equally. It is rare in the under-twos due to maternal antibodies. By the age of 10 years, 80% of the population will have developed lifelong immunity induced by either overt infection or carrier state.
Scarlet fever is highly contagious, especially during acute and subclinical stages. Transmission occurs via airborne respiratory particles dispersed by coughing, sneezing or direct contact.
The disease usually follows a benign course; morbidity and mortality can arise from complications. These include peritonsillar abscess, sinusitis and meningitis. There is a 0.3 to 3% risk of rheumatic fever and a 10 to 15% risk of glomerulonephritis with a nephrogenic strain of GABHS.
An incubation period of two to four days is followed by a sudden onset fever (>38 degsC) with signs and symptoms of an exudative tonsillitis (sore throat, headache, abdominal pain, myalgia, malaise and vomiting). Note that the focus of infection may be at another site, for example a surgical wound.
An erythematous pharynx and Forchheimer spots are often present - erythematous oral mucous membranes with petechiae and red macules on the hard and soft palate and uvula. On day one or two, a white 'strawberry' tongue develops (white fur coats the tongue with red papillae projecting through).
By day four or five, a red strawberry tongue develops as the fur coating disappears leaving a red raw tongue with prominent papillae. The characteristic rash develops 24 to 48 hours after the fever starts.
The characteristics of the rash are:
- It begins on the neck and chest.
- It disseminates to the trunk and extremities over 24 hours.
- Initially there is generalised erythema with scarlet macules (boiled lobster appearance).
- It progresses to look like sunburn with goose pimples.
- The spots give the skin a sandpaper-like texture.
- Circumoral pallor is present.
- Fragile capillaries in the armpits and elbows rupture causing red streaks known as Pastia's lines; these last one to two days after the rash has gone.
- By day six the rash fades and desquamation occurs for up to six weeks (especially on the fingers, toes and armpits).
Diagnosis is clinical, however confirmation of GABHS is important to confirm the infection. The criterion standard for diagnosis of GABHS infection is a throat culture, which has 90% sensitivity.
However, a positive test is not always proof due to carrier states.
To carry out a throat swab, vigorously swab the posterior pharynx, tonsils and exudate avoiding the lips, tongue and buccal mucosa.
Antigen detection kits have been developed for near patient testing, allowing quick diagnosis and appropriate antibiotic use. However they are limited due to cost and variable specificity and sensitivity.
Antistreptolysin O titres detect the presence of streptococcal antibodies; this test confirms recent but not active infection. Antibody levels increase one week post-infection with peak levels at three to four weeks, followed by rapid decline.
Antibody levels only rise in 70 to 80% of patients and false positives are seen in TB or liver disease. It can be helpful if a recent infection of group A streptococcus is required to aid diagnosis, for example post-streptococcus glomerulonephritis or rheumatic fever.
FBC will show a rise in white cells in scarlet fever, with a 5% lymphocytosis. By the second week there is an eosinophilia of up to 20%.
The aim of treatment is fourfold:
- Prevent rheumatic fever.
- Prevent other complications.
- Reduce the spread of infection.
- Shorten the course of the illness.
Antibiotics are necessary for eradication. They also speed recovery and prevent complications. If untreated, patients can be infectious for two to three weeks after signs and symptoms have resolved.
First-line treatment is a 10-day course of penicillin; there should be rapid resolution of symptoms within 24 hours. Erythromycin can be used if there is penicillin allergy. Early use of antibiotics can reduce the incidence of rheumatic fever but does not prevent glomerulonephritis.
Symptomatic relief should be given via paracetamol and ibuprofen along with rest and hydration. To prevent spread, emphasise the need for hand washing and to avoid sharing towels, clothing, bedding and utensils.
Admit to hospital if the patient requires IV hydration, is having difficulty swallowing or if there are severe complications. The HPA advises that children can return to school 24 hours after starting antibiotics.
- Dr Taylor-Walker is a locum GP in Leicestershire
1. HPA. Group A streptococcal infections: fourth update on seasonal activity, 2008/09. Health Protection Report 2009; 3(29). www.hpa.org.uk/hpr/archives/2009/news2909.htm#gas0809
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