Scarlet Fever

Scarlet fever also known as scarlatina is a syndrome characterized by:

1. Exudative tonsillitis

2. Exudative pharyngitis

3. Fever

4. Bright red exanthematous skin rashes.

This syndrome is caused by exotoxins produced by group A beta hemolytic streptococci. These organims can be found in abudance in discharge from nose, throat and skin. Food borne out breaks are also known.

Scarlet fever is known to evolve from tonsillar / pharyngeal focal infections. Skin rashes are known to develop in about 10% of these patients. The site of bacterial replication is usually inconspicuous when compared with the dramatic effects of released toxin. It can be lethal if streptococcal toxic syndrome develops.

Scarlet fever can also occur following streptococcal infection of skin, soft tissue and even surgical wounds.

Pathophysiology:

Group A streptococci are normal inhabitants of throat and nasophaynx Group A streptococci can cause pharyngitis, and skin infections, pneumonia, bacteremia and lymphadenitis also. Majority of streptoccoi are known to produce toxins and the erythrogenic toxin produced by them have been implicated in scarlet fever. This toxin was first discovered by Dick in 1924.

It is known to affect school going children because of crowded class rooms and lack of hygiene.

The incubation period for scarlet fever is about 12 hours to 7 days. These patients are usually contageous during acute phase as well as during subclinical phase also.

It is known to affect children between ages 1 -10. It can rarely occur in older children and adults also. Children on reaching the age of 10 would have developed life long protective antibodies against streptococcal pyrogenic exotoxins. This condition is rare in children under 1 year because of the presence of maternal anti exotoxin antibodies.

This disease was dreadful during preantibiotic era. With the advent of antibiotics and improved immune status scarlet fever are not so disastrous these days.

Complications:

1. Septicemia

2. Vasculitis

3. Hepatitis

4. Rheumatic fever

Whenever scarlet fever has been determined to be due to soft tissue infection or near the bone, evaluation for bony involvement should be considered.

Clinical findings:

Fever

Tachycardia

Cervical adenopathy

Mucous membrane lesions (bright red petechiae could be seen over tonsils, posterior pharyngeal wall and soft palate.

Heavily coated tongue

Oedematous red papilla seen in the tongue (strawberry tongue). This occurs between days 4 and 5 after the whitish membrane sloughs off. Skin exanthem usually develop within 48 hours after the onset of fever. It usually begins as erythematous patches below the ears, on the neck, chest and axilla. The skin after these eruptions feels rough like coarse sand paper. These erythematous lesions are known to blanch on pressure. The skin usually feel itchy but these rashes are not painful. Spread to the trunk and extremities takes about one more day to occur.

Capillary fragility is found to be increased and frequent capillar ruptures are also common. Transverse areas of hyperpigmentation with linear petechial lesions in the axillary, antecubital and inguinal areas are also seen. These arrays can also be present even 48 hours after the rashes vanish.

The cutaneous rashes lasts for 4-5 days and is usually followed by desquamation. This desquamation is one of the features of scarlet fever rashes. This peeling phase occur in about a week and begins from the face. Peeling from the palms and fingers occur one more week later (during the second week).

Complications:

1. Cervical lymphadenitis

2. Otitis media / acute mastoiditis

3. Ethmoiditis

4. Peritonsillar abscess

5. Sinusitis

6. Bronchopneumonia

7. Meningitis

8. Brain abscess

9. Intracranial venous thrombosis

10. Septicemia, meningitis, osteomyelitis and septic arthritis

11. Hepatitis

12. Vasculitis

13. Uveitis

14. Myocarditis

15. Streptococcal toxic syndrome

Common among these are otitis media, pneumonia, septicemia, osteomyelitis, rheumatic fever and acute glomerulo nephritis.

This condition should be differentiated from other viral exanthematous fevers like:

Rubella

Infectious mononucleosis

Enteroviral infections

HIV infections

Streptobacillus moniliformis (rat bite fever)

Diagnosis:

Based mostly on clinical presentation.

Investigations:

Throat / nasal culture

Rapid streptococcal test

Anti deoxyribonuclease B, ASO titres

Antibodies to streptococcal extracellular products

Antihyaluronidase

Antifibrinolysin

Complete blood count: Leukocytosis Eosinophilia up to 20% can occur during the second week.

Urine analysis and liver function tests should be performed

Direct antigen detection kits (rapid antigen tests) - These tests allow immediate diagnosis and prompt administration of antibiotics.

Antideoxyribonuclease B and ASO titres:

These tests are used to confirm previous group A streptococcal infections. An increase in ASO titres may be observed but could be a late finding.

Streptococcal antibody tests provide confirmatory evidence of recent infection. This of course is of no value in acute infection and is not indicated in acute infections. This test could be of value in patients with suspected acute renal failure / acute glomerulonephritis.

Goals of treatment:

1. To prevent acute rheumatic fever

2. To reduce spread of infection

3. To prevent post streptococcal sequel like AGN

4. To prevent other suppurative sequel like adenitis, mastoiditis, ethmoiditis, abscess and cellulitis

5. To shorten the course of illness

Antibiotic therapy should be initiated without delay. Penicillin / amoxicillin are the drug of choice. In the presence of odynophagia the patient should be admitted for administration of parental antibiotics.