Scarlet fever is an acute respiratory infection caused by group A streptococci. It is characterized clinically by fever, pharyngitis, a diffuse red rash over the body and marked post-rash desquamation, with a few patients developing heart, kidney and joint damage and disease in the recovery period due to metaplasia.
I. Pathogenesis.
Group A streptococcus is hemolytic type B, so it is also called group A hemolytic streptococcus type B. There are 80 protein serotypes, the cell wall of the cell wall acid and M protein, can make the bacteria attached to the host mucosa and can resist the phagocytosis of the host leukocytes, constituting its important pathogenic force. In addition its pathogenic power also comes from.
1, fever-causing exotoxin: that is, erythrotoxin, A, B, C 3 antigenic types, whose antibodies have no cross-protective effect. Erythrotoxins can be delivered by phagosomes, turning bacteria originally free of erythrotoxins into virus-producing strains.
2, hemolysin can lyse red blood cells, kill white blood cells and platelets, and have the effect of damaging the heart.
3, hyaluronidase can dissolve hyaluronic acid between tissues.
4. streptokinase can prevent blood clotting.
5.Streptokinase can dissolve DNA.
6.Nicotinamide adenine dinucleotidase can destroy the corresponding tissue components.
7.Serum turbidity factor can inhibit the body from producing immune response.
II. Epidemiology
1, the epidemiological situation: the past for the world’s infectious diseases, mostly occur in temperate, cold and tropical, since the application of antibiotics, foreign developed countries and regions have rarely reported, China is now disseminated cases.
2, changes in the disease: there is a clear trend of milder, which is related to the body’s immunity and social factors, and at the same time with the strains of bacteria and virulence changes may also be related.
3.Epidemic process three links.
(1) Source of infection: mainly scarlet fever and pharyngitis patients and carriers. Scarlet fever is most contagious from 24h before the onset to the peak of the disease.
The nasopharynx of health care workers or carriers elsewhere can cause scarlet fever in postoperative patients or maternal units within the disease area.
(2) Transmission routes: respiratory tract, mouth, wound or birth canal
(3) Immunity of the organism: Antibacterial immunity: specific antibodies to M protein, no protection against different types of bacteria.
Anti-virulence immunity: mainly specific antibodies to fever-causing exotoxin (erythrotoxin), no cross-immune reaction because of the different antigenicity of types A, B and C.
III. Pathogenesis and pathology
The plasmatic acid of group A streptococci makes the bacteria easy to attach to the mucosa; M protein can resist phagocytosis of the body cells; the bacteria can multiply at the invasion site to produce fever-causing exotoxin, causing fever, rash, and systemic toxic reaction; hyaluronidase can dissolve tissue interstitium; streptokinase can prevent blood clotting and can dissolve the clotted blood clot. Streptokinase can lyse viscous DNA, etc., so that the host’s tissue barrier is broken and bacteria can expand into nearby tissues and even into the bloodstream.
The body generates non-specific and specific immune responses that interact to form 3 types of scarlet fever lesions.
1. Infectious lesions: local reaction to septic lesions caused by bacterial invasion sites – → bacteriology – → sepsis – → migratory septic infection
2, toxic lesions: mainly caused by exotoxins. Patients find fever, dizziness, headache, general malaise and other toxicological manifestations. Erythrotoxins can cause skin congestion, edema, epithelial cell proliferation, and leukocyte infiltration, most obviously around the hair follicles, forming a typical scarlet fever-like rash, and finally the epidermis dies and falls off to form a desquamated skin, and the mucous membranes can bleed in a punctate pattern to form an “internal rash”. The liver, spleen, lymph nodes and other interstitial vessels are surrounded by mononuclear cell infiltration. The myocardium may have cell swelling and degeneration. The kidney may show interstitial inflammation, and the central nervous system may have dystrophic changes in toxic patients.
3. Metaplastic lesions: caused by CIC, rheumatoid arthritis, endocarditis, acute glomerulonephritis
IV. Clinical manifestations.
The incubation period is 1-7 days, with an average of 2-4 days. The main symptoms are acute onset of fever, marked sore throat, diffuse red rash all over the body and peeling skin after the rash recedes. Patients can have mild or severe manifestations of systemic toxicity, and there are several different clinical types with different severity of the disease as follows.
1.General type: prodromal phase
(1) Fever: acute onset of fever, body temperature around 39℃, accompanied by sore throat, vomiting, headache, general discomfort, abdominal pain
(2) pharyngitis: pharyngeal isthmus and tonsils are obviously red and swollen, tonsillar glandular fossa at the point of purulent discharge, or even a large pseudomembrane, but is relatively soft and easy to erase
(3) strawberry tongue: white strawberry tongue: tongue is white moss, papillae red and swollen and out of the background outside.
Red strawberry tongue (Yang berry tongue): 2-3 days later, the white moss falls off, the tongue is flesh red, the papillae are still raised.
Rash phase: The rash appears on the 2nd day of fever, starting from behind the ears and neck, quickly expanding to the chest, back, abdomen and upper extremities, and extending to the lower extremities around 24h, developing from proximal to distal.
The typical rash is.
① diffuse flushing of the skin all over the body based on the scattering of dense and uniform chicken skin ulcer-like congested rash consistent with the hair follicles, about 1 mm in diameter, fading when pressed, and the rash and diffuse flushing reappearing after removal of pressure, the rash is mostly patchy, or may be slightly elevated into a papule.
② no healthy skin between rashes.
(iii) Papanicolaou lines.
④ ring mouth pale circle, rash distribution of the trunk and the proximal extremities, four distal less, the rash peaks within 4h.
Recovery period: 3 to 4 days according to the order of the rash recede after a week began to peel, the order is the same as the rash, the degree of peeling and rash lightness consistent with the rash, rash less and light peeling bran-like, rash heavy can be flaky. The skin of the hands and feet at the cuticle is also obvious, some people can be gloves sock-like, peeling skin can last 1 to 2 weeks.
2. Light scarlet fever: the fever is not high, the pharyngitis is not heavy, the skin is not obviously flushed, and the rash is mostly seen on the neck and chest.
The rash is usually seen on the cervical thorax and fades quickly, but metaplasia can still occur after the disease.
3.Septic scarlet fever: above 40℃, headache, sore throat, vomiting and other symptoms are obvious, the pharynx, i.e. tonsils, are obviously edematous, congested and ulcerated, purulent secretions are often in large pseudomembranes, often causing purulent otitis media, sinusitis, mastoiditis, cervical lymphadenitis and cellulitis, and can develop into septicemia and shock, the rash can be a corn rash with small pus heads. The rash may be a small pustular corn rash. The body temperature is chills fever, and the skin peels off significantly during the recovery period, lasting up to 3-5 weeks.
4. Toxic scarlet fever: Toxicemic symptoms are obvious. Body temperature up to 40℃
The rash is numerous and heavy, and the hemorrhagic rash increases, and the patient may soon develop hypotension and shock. The rash becomes vague and visible after shock.
5. Surgical type of scarlet fever (obstetric type): the rash first appears near the wound and then develops outward, without pharyngitis, and the disease is mostly mild.
V. Diagnosis and differential diagnosis.
1. Diagnosis: Clinical manifestations
Epidemiological data
Laboratory: elevated WBC; Sg 80% or more; pharynx is positive bacteria in swab culture
2, differential diagnosis.
(1) Differentiate from other causes of pharyngitis
(1) diphtheria: diphtheria pharyngitis is lighter than scarlet fever, and the pseudomembrane is tough and not easily obliterated.
(ii) Infectious mononucleosis: pharyngitis or even ulceration, elevated WBC, and elevated mononuclear cells.
(2) Differentiation from other eruptive diseases
(1) Scarlet fever-like manifestations caused by other streptococci: group C streptococci.
(ii) Scarlet fever-like rash of Staphylococcus aureus.
(③) drug rash.
VI. Complications.
(a) Early septic damage: seen in the young and frail, otitis media, lymphadenitis, pneumonia, septicemia, meningitis, arthritis.
Late metabolic damage: after 2-3 weeks of disease, nephritis, rheumatic fever, arthritis.
VII. Treatment
1, general treatment: respiratory isolation for 6 days, patients should be bedridden.
2, pathogenic treatment: penicillin as the drug of choice, 20-40,000 u/Kg.d , >= 10 days course of drug resistance with erythromycin, 20-40 mg/Kg , divided into 3 doses.
3, complication treatment: antiviral ball corresponding treatment: abscess incision; anti-shock.
VIII. Prevention
1.Control the source of infection.
2.Cut off the transmission route.
3.Protect the susceptible: avoid public places during the epidemic.