SCARLET FEVER

Scarlet fever is an acute infectious disease that is caused by group A streptococcus, is transmitted by an air-droplet way, and is characterized by intoxication, rashes on a skin {feels like sandpaper}, tonsillitis, regional lymphadenitis, and classic strawberry tongue.  The characteristic rash is due to the erythrogenic toxin, a substance produced by some types of the bacterium

The bacteria spreads by coughing and sneezing and usually affects people who have strep throat or strep skin infection. 

 

Pathogenesis

Specific strains of Group A Streptococcus produce a pyrogenic exotoxin which causes the specific rash in scarlet fever and this is used to differentiates it from isolated Group A Strep pharyngitis (or strep throat). The pyrogenic exotoxins are also called erythrogenic toxins and cause the erythematous rash of scarlet fever.

Pathogenesis has three lines:

  1. Toxic (toxical damage of cardiovascular, central nervous, endocrine systems).
  2. Septic – primary inflammation in the place of infection (tonsillitis, secondary bacterial complication).
  3. Allergic – sensibilization by GABHS proteins (depression of immunity leads to allergic complications – nephritis, arthritis, myocarditis, rheumatism.).

 

Clinical presentation: 

  • Onset is usually acute and is characterized by a sore throat (often with dysphagia), fever (often above 39°C), pharyngeal and purulent tonsilar exudates.
  • Anterior cervical lymph nodes, particularly the jugular-digastric nodes just beneath the angle of the mandible, are tender and enlarged. 
  • Erythema of the soft palate is common, and an enanthema of “doughnut” lesions on the soft palate.
  • Strawberry tongue.
  • Other features are nausea and vomiting, headache, abdominal discomfort. One to two days later the rashes like “sandpaper” appears, first on the neck and then on the trunk and extremities till the end of the day.

  The eruption is characterized by dusky red, blanching tiny papules that have a rough texture. Papules are usually absent from the face, palms, and soles, but the face characteristically shows flushing with circumoral pallor.

  • On the body, the rashes are intensified in skin folds and at sites of pressure. In the antecubital and axillary fosses, linear petechias are seen with accentuation of the erythema (Pastia’s lines).

The exanthema usually lasts 4 to 5 days and then begins to desquamate, first on the face last on the palms and soles.  Pharyngitis usually resolves in 5 to 7 days.

 

Characteristic skin rash that feels like “sandpaper” with strawberry tongue are classic for scarlet fever.

Complications

Suppurative complications: peritonsillar or retropharyngeal abscesses, cellulitis, mastoiditis or sinusitis. These rarely occur,but they arise from direct spread to structures which are close to the primary site of infection, which in most cases of Scarlet Fever is the pharynx.

  • Acute rheumatic fever This is a complication which results 2–6 weeks after a group A streptococcal infection of the upper respiratory tract
  • Poststreptococcal glomerulonephritis: This is inflammation of the kidney which presents 1–2 weeks after a group A streptococcal pharyngitis.
  • Poststreptococcal reactive arthritis: The presentation of arthritis after a recent episode of group A streptococcal pharyngitis raises suspicion for acute rheumatic fever since it is one of the Jones criteria for that separate complication.

 

Differential diagnosis.

  • Viral exanthem: Viral infections are often accompanied by a rash which can be described as morbilliform or maculopapular. This type of rash is accompanied by a prodromal period of cough and runny nose in addition to a fever, indicative of a viral process.
  • Allergic or contact dermatitis: The erythematous appearance of the skin will be in a more localized distribution rather than the diffuse and generalized rash seen in Scarlet Fever.
  • Drug eruption: These are potential side effects of taking certain drugs such as Penicillin. The reddened maculopapular rash which results can be itchy and be accompanied by a fever.
  • Kawasaki disease Children with this disease also present with a strawberry tongue and undergo a desquamative process on their palms and soles. However, these children tend to be younger than 5 years old, their fever lasts longer (at least five days) and they have additional clinical criteria (including signs such as conjunctival redness and cracked lips) which can help distinguish this from Scarlet Fever.
  • Toxic shock syndrome: Both Streptococcal and Staphylococcal bacteria can cause this syndrome. Clinical manifestations include diffuse rash and desquamation of the palms and soles. Can be distinguished from Scarlet Fever by low blood pressure, the rash will lack sandpaper texture, and multi-organ system involvement.
  • Staphylococcal scalded skin syndrome: This is a disease which occurs primarily in young children due to a toxin producing strain of the bacteria Staphylococcus Aureus. The abrupt start of the fever and diffused sunburned appearance of the rash can resemble Scarlet Fever. However, this rash is associated with tenderness and large blister formation. These blisters easily pop and then cause the skin to peel.
  • Staphylococcal Scarlet Fever: The rash is identical to the streptococcal scarlet fever in distribution and texture, but the skin affected by the rash will be tender.

 

Laboratory tests

  1. The diagnose is confirmed by throat culture with group A b-hemolytic streptococcus.
  2. Serology (antistreptolysin O, antidesoxyribonuclease B) with their grows in 2 weeks may be useful for documenting recent GABHS infection.
  3. The complete blood cell count is helpful: usually white blood cell count higher 12500 cells/mm3, neutrophyllosis, left shift, eosynophylia, elevated ESR.

 

Treatment  

  • Bed regime during an acute period. 
  • Etiological treatment for scarlet fever is:
  • In the mild case penicillin orally (penicillin V) for 10 days 50,000-100,000 EU/kg/day divided in 3-4 doses. Erythromycin (or another macrolides) is alternative antibiotic (30 –50mg/kg/day). The course of treatment is 10 days.
  • In the moderate case penicillin intramuscularly (penicillin G), the same dose as in the mild case. The course of treatment is 10-14 days.
  • In the severe case: cefalosporins of the 1st-2nd generation, klindamycin, vancomycin intravenously for 10-14 days.

Detoxication therapy:

  1. In the mild case large amount of oral fluids.
  2. In the moderate and severe cases – Glucose and saline solutions IV.
  3. Antihistamines (in average doses) – pipolphen, suprastin, claritin, cetirizin.
  4. Medicine which strengthens vascular wall (vit. C and PP: ascorutin, galascorbin)
  5. Control of fever (when the temperature is more than 38.5-39˚C); in children before 2 mo and in case of perinatal CNS damage, seizures in the history, severe heart diseases – when the temperature is up to 38˚C with acetaminophen (paracetamol 10-15 mg/kg not often than every 4 hours (not more than 5 times per day) or ibuprophen 10 mg/kg per dose, not often than every 6 hours.
  6. Local treatment with antiseptic fluids (gurgling), UV-insolation.

 

Patient may go home from infection department not earlier the 10th day of the illness, in 10 days blood analysis, urinalyses, ECG must be done.

 

Prevention: isolation of the patient on the 10 days, but he mustn’t visit school until 22 day of the disease. Contract persons (children before 8 years) must be isolated for 7 days (period of incubation).