Scarlet fever

Scarlet fever or scarlet fever is an acute, febrile infectious disease caused by serogroup A Streptococcus pyogenes. Its incubation period is from 2 to 4 days.

Epidemiology

It is a disease transmitted by contagion, generally through the respiratory route, which occurs most frequently in school-age children from 2 to 10 years of age (even up to 12), but rarely in adults.

Sometimes it can occur after strep throat, and it can also occur after other strep conditions such as a wound infection or postpartum sepsis. In certain rare cases, scarlet fever can arise from a skin infection called 'impetigo', which is also caused by Streptococcus bacteria. In these cases, the child may not have a sore throat.

An individual can have scarlet fever several times due to the formation of specific antibodies against pyrogenic exotoxins. Patients with specific antibacterial immunity against one type of strep (with or without antitoxic immunity) may not contract the disease from exposure to that type. Patients without specific bacterial immunity (but with antitoxic immunity) may develop pharyngitis, and patients without either type of immunity may develop pharyngitis and scarlet fever.

Clinical picture: symptoms and signs

The picture begins with a high fever of abrupt onset, above 38°C, inflammation of the tonsils or pharynx, cervical adenopathies (inflammation of the neck glands) and other symptoms such as chills, joint pain throughout the body, nausea, vomiting, loss of appetite, very bad stomach pains and sore and sore throat.

The most obvious symptom of scarlet fever, the rash appears one to five days after the onset of fever. At first, it often looks like a sunburn with small raised dots that can be itchy. The rash first begins on the neck and face; it usually does not affect the area around the mouth (Filatov's triangle). It spreads to the chest and back and then spreads to the rest of the body. In the skin folds, especially in the armpits and elbows, the rash is a more intense red that is arranged in a linear fashion (Pastia lines). The areas of the skin that show the rash turn white when pressed and are rough to the touch, being described as 'sandpaper skin'. or "goosebumps". On the sixth day of infection, the rash begins its involution, but the affected skin may begin to desquamate, which may last up to 3 weeks. Vesicular pinhead lesions (miliary sudamine) may appear on the abdomen and chest. At its best, the rash has a diffuse, bright scarlet appearance. The lesions usually appear spontaneously at the scratching sites, or when taking the pressure measurement with the baumanometer, the lesions will appear at the site where the cuff was placed (Rumpell-Leede sign).

It is also accompanied by enanthema (an eruption of the mucous membranes), with reddening of the pharynx and tonsils, or yellowish-white spots of pus, and the tongue is covered in a whitish coating, with red papillae ("tongue in white strawberry") that then disappears on the fifth day, remaining red ("strawberry or raspberry tongue"). .

Treatment

Since this disease is caused by a streptococcus, it is treated with antibiotics. The antibiotic of first choice is penicillin, which can be oral such as penicillin V or amoxicillin, or intramuscular such as benzathine penicillin. An alternative for patients allergic to penicillin is erythromycin or azithromycin. Treatment should last at least 10 days, as improper treatment can lead to complications.

Pathophysiology

The scarlet fever rash, which is what differentiates scarlet fever from isolated group A strep throat (or strep throat), is caused by specific strains of group A streptococci that produce a pyrogenic strep exotoxin, which it is primarily responsible for the cutaneous manifestation of the infection. These toxin-producing strains cause scarlet fever in people who do not yet have antitoxin antibodies. Pyrogenic streptococcal exotoxins - SPE A, B, C. and F have been identified. Pyrogenic exotoxins, also called erythrogenic toxins, cause the erythematous rash of scarlet fever. The strains of group A streptococci that cause scarlet fever require bacteriophages. specific for the production of pyrogenic exotoxins. Specifically, the T12 bacteriophage is responsible for the production of speA. The streptococcal pyrogenic exotoxin A, speA, is the one most frequently associated with cases of scarlet fever that are complicated by the immune-mediated sequelae of acute rheumatic fever and poststreptococcal glomerulonephritis.

These toxins are also known as "superantigens" because they can elicit a broad immune response by activating some of the cells that are primarily responsible for a person's immune system. Although the body responds to toxins it encounters by making antibodies, those antibodies will only protect against that particular subset of toxins. They will not necessarily completely protect a person from future group A streptococcal infections, as the disease can produce 12 different pyrogenic exotoxins, and future infections can produce a different subset of those toxins.

Microbiology

The disease is caused by the secretion of pyrogenic exotoxins by the infecting Streptococcus bacterium. Streptococcal pyrogenic exotoxin A (speA) is probably the best studied of these toxins. It is carried by the T12 bacteriophage which integrates into the streptococcal genome from where the toxin is transcribed. The phage itself integrates into a chromosome serine tRNA gene.

The International Committee on Taxonomy of Viruses has not classified the T12 virus into any taxa. It has a double-stranded DNA genome and, for morphological reasons, appears to belong to the family Siphoviridae.

The speA gene was cloned and sequenced in 1986. It is 753 base pairs long and encodes a 29.244 kiloDalton (kDa) protein. The protein contains a putative signal peptide of 30 amino acids; removal of the signal sequence gives a predicted molecular weight of 25.787 kDa for the secreted protein. Both a promoter and a ribosome binding site (Shine-Dalgarno sequence) are present upstream of the gene. There is a transcriptional terminator located 69 bases downstream of the translation stop codon.

Strep phages other than T12 can also carry the speA gene.

Complications

May have infectious complications, such as pharyngeal abscesses or otitis, and late non-infectious complications, such as poststreptococcal glomerulonephritis, rheumatic fever, or uremia; although today almost exclusively mild forms are observed.

Differentials

• Kawasaki disease
• Infectious mononucleosis
• Other causes of exantema