Scarlet fever
| Scarlet fever Classification and external resources | |
| ICD-10 | A38 |
|---|---|
| ICD-9 | 034 |
| DiseasesDB | 29032 |
| MedlinePlus | 000974 |
| eMedicine | derm/383 emerg/402, emerg/518 |
Scarlet fever or scarlatina is an acute, contagious infectious disease caused by an erythrogenic toxin producing strain of Streptococcus pyogenes (group A streptococci) and characterized by a sore throat, fever, a "strawberry" tongue (swollen, red, and bumpy), and a fine sandpaper rash over the upper body that may spread to cover almost the entire body. The name comes from the fact that the skin of the patient is flushed, particularly on the cheeks (Jacobs 2006).
Scarlet fever is primarily a childhood disease. If untreated, it can lead to such serious complications as rheumatic fever or glomerulonephritis (kidney inflammation.
Cause
A strain of Streptococcus pyogenes is responsible for scarlet fever. Streptococcus pyogenes is a spherical gram-positive bacteria that grows in long chains (Ryan and Ray 2004) and is the cause of Group A streptococcal infections (GAS). S. pyogenes displays group A antigen on its cell wall and beta-hemolysis when cultured on blood agar plate. S. pyogenes typically produces large zones of beta-hemolysis, the complete disruption of erythrocytes (red blood cells) and the release of hemoglobin, and it is therefore called Group A (beta-hemolytic) Streptococcus. Being classified as hemolytic bacteria means that they have the ability to destroy red blood cells. Streptococci are catalase-negative.
S. pyogenes is the cause of many important human diseases ranging from mild superficial skin infections to life-threatening systemic diseases. Infections typically begin in the throat or skin. Besides scarlet fever, other examples of S. pyogenes infections include such mild cases as pharyngitis ("strep throat") and localized skin infection ("impetigo"). Erysipelas and cellulitis are characterized by multiplication and lateral spread of S. pyogenes in deep layers of the skin. S. pyogenes invasion and multiplication in the fascia can lead to necrotizing fasciitis, a potentially life-threatening condition requiring surgical treatment.
Infections due to certain strains of S. pyogenes can be associated with the release of bacterial toxins. The strain of S. pyrogens that causes scarlet fever produces an erythrogenic toxin, which causes the skin to flush. Other toxigenic S. pyogenes infections may lead to streptococcal toxic shock syndrome, which can be life-threatening.
Description
Scarlet fever primarily impacts children between the ages of five and fifteen years of age (Jacobs and Carson-Dewitt 2005), and particularly those between four and eight years (Cooper 2005). About ten percent of the children who have strep throat, another childhood disease, develop the characteristic scarlet fever rash (Jacobs and Carson-Dewitt 2005).
Scarlet fever is highly contagious, and can be transmitted through the air by sneezing or coughing or by direct physical contact. Within two to five days of exposure to the infection, the symptoms usually begin (Cooper 2005). Within a few days the fever subsides and within two weeks recovery typically is complete.
Severe scarlet fever epidemics were common early in the twentieth century, but the disease has become rare as of the early 2000 (Cooper 2005). Antibiotics may be a partial reason for the decline in incidences, but the decline actually began before their widespread use, leading to speculation that the strain of bacteria causing the disease has actually become weaker over time (Cooper 2005; Jacobs and Carson-Dewitt 2005).
History
This disease was also once known as scarlatina (from the Italian scarlattina). Many novels depicting life before the nineteenth century describe scarlet fever as an acute disease being followed by many months spent in convalescence. The convalescence was probably due to complications with rheumatic fever. Prior to an understanding of how streptococcus was spread, it was also not uncommon to destroy or burn the personal effects of a person afflicted with scarlet fever to prevent transmission to other people.
Signs, symptoms, and diagnosis
Early symptoms indicating the onset of scarlet fever can include (Balentine and Kessler 2006; Dyne and McCartan 2005):
- Fever of 38 to 40 degrees C.(101-104 degrees F.)
- Fatigue
- Sore throat
- Headache
- Nausea or Vomiting
- Abdominal pain
- Flushed face with perioral pallor (circumoral pallor)
- Tachycardia (rapid pulse)
- Lymphadenopathy (enlarged lymph nodes)
- Punctate red macules on the hard and soft palate and uvula (ie, Forchheimer spots).
- Bright red tongue with a "strawberry" appearance (bumpy, swollen)
- Characteristic rash, which:
- is fine, red, and rough-textured; it blanches upon pressure
- appears 12–48 hours after the fever
- generally starts on the chest, axilla (armpits), and behind the ears
- is worse in the skin folds
- Pastia lines (where the rash becomes confluent in the arm pits and groins) appear and persist after the rash is gone
the fever usually fades in a few days and then rash begins to fade three to four days after onset and desquamation (peeling) begins. There is flaking on the face and body, while the skin on the palms of the hands and sole of the feet peel more dramatically (Jacobs 2006). The peeling typically begins with the face and then the peeling from the palsm and around the fingers about a week later can last up to a month (Dyne and McCartan 2005). Peeling also occurs in the groin, axilla, and the tips of the toes and fingers (Balentine and Kessler 2006).
Diagnosis of scarlet fever is clinical. The blood tests shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high ESR and CRP, and elevation of antistreptolysin O titer. Blood culture is rarely positive, but the streptococci can usually be demonstrated in throat culture.
Complications
The complications of scarlet fever include septic complications due to spread of streptococcus in blood and immune-mediated complications due to an aberrant immune response. Septic complications, today rare, include otitis, sinusitis, streptococcal pneumonia, empyema thoracis, meningitis and full-blown septicaemia (malignant scarlet fever).
Immune complications include acute glomerulonephritis, rheumatic fever, and erythema nodosum. The secondary scarlatinous disease (or secondary malignant syndrome of scarlet fever) included renewed fever, renewed angina, septic ORL complications and nephritis or rheumatic fever and is seen around the 18th day of untreated scarlet fever.
Treatment
Other than the occurrence of the diarrhea, the treatment and course of scarlet fever are no different from those of any strep throat. In case of penicillin allergy, clindamycin or erythromycin can be used with success.
Antibiotic treatment is usually given. It has however never been shown to reduce the chance that rheumatic fever develops.
ReferencesISBN links support NWE through referral fees
- Jacobs, S. J., and R. Carson-DeWitt. 2005. Scarlet fever. In K. M. Krapp and J. Wilson, eds., The Gale Encyclopedia of Children's Health: Infancy Through Adolescence. Detroit: Thomson Gale. ISBN 0787692417.
- Cooper, A. 2005. Scarlet fever. In J. L. Longe, The Gale Encyclopedia of Alternative Medicine. Farmington Hills, Mich: Thomson/Gale. ISBN 0787693960.
- Jacobs, S. 2006. Scarlet fever. In J. L. Longe, ed., The Gale Encyclopedia of Medicine. Detroit: Thomson Gale. ISBN 1414403682.
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