Scarlet fever

Overview scarlet fever (fever and rash) to beta haemolytic streptococcus group A caused by acute respiratory infections. Clinical characteristics of a sudden high fever, angina, diffuse systemic congestive point retreat rash and skin rashes after apparent scaling. A few patients who can cause kidney, bone damage. Etiology of beta-hemolytic streptococcus diameter of 0.6-1.0μm, the chain was arranged. Tip blood on the hemolytic reaction was, this is known as hemolytic streptococcus. Pathogen gram-positive, spherical or oval, no spores, no flagellum, the blood or serum good growth medium. Beta-hemolytic streptococcus according to the cell wall polysaccharide antigen contained in the different, divided into 18 groups, Group A streptococcus about 80 multiple serogroups. Any serotypes of group A bacteria, as long as it can generate sufficient rash toxin, can cause scarlet fever. Streptococcal M protein is a pathogen of the important factors, it can resist its body leukocyte phagocytosis. Available to the body after infection of the M protein-specific immunity, which can be maintained for several years, but only on the same strain of immunization. Most Group A Streptococcus few can produce toxins and enzymes, bacteria constitute the pathogenicity. If rash toxin (Erythrogenic toxin), the toxin at least three different antigens, enable patients susceptible to a number of scarlet fever. Hemolytic-O and S can damage red blood cells, leukocytes, and platelets can cause tissue necrosis. Hyaluronidase, streptokinase (fiber - Rong) soluble interstitial hyaluronic acid, easy to make bacteria in tissue proliferation. Streptokinase, blood plasminogen into plasmin. thereby preventing blood coagulation or soluble have solidified the clot. Road chain enzyme called DNA enzyme can be highly viscous solution of DNA. Nicotinamide adenine dinucleotide enzyme can analyze the corresponding composition, thereby undermining some of the body's defense capability. Strong resistance strain in vitro, heating 60 ℃ 30 minutes shall be killed. in the 0.2 - 0.5% 0.5% mercuric chloride or carbolic acid solution 15 minutes of death. Epidemiology (1) the source of infection patients and carriers. Normal nasopharynx, skin can be infected. Scarlet fever patients 24 hours before the onset of disease to the peak period of the most infectious and peeling period free of infectious dandruff. (2) The main mode of transmission is air transmitted through respiratory droplets. Even through contaminated milk or other food-borne. Individual circumstances, the bacteria through the skin wound or invasive maternal birth canal, which leads to a "surgical scarlet fever" or "obstetric scarlet fever." (3) the susceptibility of scarlet fever were generally susceptible, human infection can produce two types of immunity. 1. Antibacterial immunity Group A streptococcus infection mainly produces body resistance M protein antibodies, it could eliminate M protein antigen on human phagocytic function of the resistance, but only with type-specific. 2. Drug body immunity infection can produce scarlet fever rash anti-toxin antibodies, But different antigen rash of toxins without cross-immunity. Thus with a scarlet fever, if infected with the toxin another rash of group A streptococci can be further incidence. 3. Scarlet fever epidemic of the disease is temperate, tropical and boreal rare. In China throughout the year may incidence. But in winter and spring styles. Pathogenesis and pathological changes in group A streptococcal pharyngeal isthmus by the intrusion, pharyngeal mucosa and the local proliferation of lymphoid tissue continuously produce toxins and extracellular enzymes, the body of the cause of infection, Toxic and allergic diseases. (1) infectious disease pathogens through M antigen in pharyngeal mucosa adhesion so that local produce inflammatory changes, so inflamed tonsils and pharynx, and the surface was covered inflammatory exudation and will have ulcers. Bacteria can be localized by the space into a nearby lymph node, caused tonsillectomy, sinusitis, otitis media, mastoiditis, neck lymphadenitis, cellulitis, a small number of patients with severe bacteria can invade the bloodstream. there sepsis and septic migratory lesions. (2) Streptococcal toxic lesions of the skin rash toxins from the blood circulation into the local, caused fever, headache, skin rash and other symptoms of systemic poisoning. Congestive skin, edema of leukocyte infiltration, the typical scarlet fever rash. Finally shedding dead skin. Congestive mucosa, sometimes point was bleeding, formation mucosa measles. Liver, spleen, lymph nodes, such as different levels of monocyte infiltration, decongestants and fatty degeneration. Turbidity swelling and myocardial degeneration and necrosis were serious. Renal interstitial inflammation was. See the central nervous system changes malnutrition. (3) allergic disease in some patients in the first stage of two-three weeks there heart, kidney, synovial tissue and other places of non-suppurative inflammation. Cardiac involvement there will be myocarditis, pericarditis and endocarditis, the mechanism of occurrence may be Streptococcus cardiac enzyme release so that their own antigen, leading to autoimmunity. Polyarthritis possible by the streptococcus specific antigen and antibody formation of complexes aroused. Glomerulonephritis likely to antigen-antibody complex deposition in the glomerular cause.