Streptococcus, or rather the streptococcus family (the Streptococceae family) includes over 21 species of gram-positive, coagulase-negative, spherical or oval-shaped cocci, up to 2 microns long, which can form chains (6-12 cocci) or split (in the case of penumococci) ). The beginning of the rational classification of streptococci dates back to 1903, when Schotmüller and Brown distinguished forms haemolyzing red blood cells using the agar technique.
Streptococcus groups
In 1919, Brown introduced the term alpha, beta, and gamma hemolysis, and in 1933 Lancefield distinguished group of streptococci on the basis of the identification of the bicarbonate component (the so-called C antigen). The M protein characterizing the pathogenicity (virulence) of the microorganism was the basis for classifying the types within the groups. In group A of streptococci (Streptococcus pyogenes), more than 130 types have been diagnosed to date – since acquired immunity is type-specific. A large number of streptococcal types are responsible for a significant number of streptococcal infections.
Table 42.1 presents the division and basic characteristics of each group of streptococci (Streptococci) based on the method of haemolysis of sheep or sheep red blood cells enriched with agar culture medium. The factors that determine streptococcal infection in different groups of streptococci are presented below.
Grupa A (Group A Streptococci – GAS)
Streptococci from this group are sensitive to high temperature (sterilization conditions: temperature 60 ° C for 30 minutes). Increased haemolysis of red blood cells in the agar medium is observed in culture with the admission of atmospheric air, reduced by the addition of carbon dioxide (10%), pH 7,4-7,6 and 37 ° C.
The cell wall of group A streptococci includes:
• Hyaluronic acid shell, with the properties of inhibiting bacterial phagocytosis by multinucleated granulocytes and macrophages of the macroorganism. Hyaluronic acid has no antigenic features.
• Bicarbonate showing group specificity (in this case for group A), which means that the identification of appropriate carbohydrates correlates with belonging to the appropriate group of streptococci (in this case, group A).
• Fimbrie – fibrils protruding from the cell wall and “embedded” in the hyaluronic sheath, containing lipoteicholic acid. These structures determine the adhesion of bacteria to the mucosa epithelium. The fimbriae contain the M protein – a factor conditioning virulence with anti-phagocytic, anti-complementary features. The M protein is specific for a given type of streptococcus (within group A) and has antigenic features (it is highly immunogenic). The production of the M protein is a feature of GAS in the invasive phase, then they lose their ability to produce this protein (carrier of streptococci).
• Proteins T, R, SOF (opacity factor serum), identified in the cell wall of group A streptococci, have less clinical significance, although they can be used in epidemiological studies (especially SOF determination). The cell membrane of group A streptococci consists of a lipid-protein envelope conditioning, among others, penicillin resistance.
In group A streptococci, the following can be distinguished intracellular structures and enzymes:
• antibiotic resistance.
• Bacteriophages controlling antibiotic resistance and production of pyrogenic exotoxins.
• Bacteriocins – proteins with a bactericidal effect, directed against other gram-positive bacteria, which facilitates the colonization and development of an invasive disease.
• Streptolysin O, which is an antigenic haemolysin, has cytotoxic (especially cardiotoxic) properties. Streptolysin O activity is inhibited reversibly by oxygen-labile hemolysin, but irreversibly by phospholipids and lipoproteins, which are a component of the skin integuments. For this reason, ASO levels are not elevated in group A streptococcal infection.
• Streptolysin S, which is also haemolysin but has no antigenic properties. The action of this haemolysin damages cell membranes and organelles.
• Pyrogenic exotoxins (erythrogenic exotoxins), types A, B, C and streptococcal superantigen – are responsible for rash and toxic symptoms in scarlet fever, fever and leukocytosis. Exotoxins determine the severity of scarlet fever. The particularly severe course of this disease is associated with pyrogenic exotoxin A. The superantigen stimulates the activity of T lymphocytes and macrophages, which leads to the production of cytokines enhancing inflammatory-necrotic reactions in toxic shock syndrome.
• Immunity acquired after infection with a specific exotoxin can be confirmed by a negative result of the Dicków test (name of the researchers’ marriage), which consists in the subcutaneous administration of the erythrogenic venom type appropriate to the expected antibodies (neutralization reaction).
The incidence of scarlet fever is conditioned by the simultaneous sensitivity of a person to a specific type of streptococcus (within group A) and erythrogenic exotoxin. Most of the more than 130 known types of streptococci produce the same type of venom and therefore the incidence of scarlet fever is determined by the number of known types of erythrogenic exotoxins. Pharyngitis is the result of sensitivity to only a specific type of group A streptococcus and is therefore a very common disease in the population, especially in children 5-15 years of age.
Grupa B (Group B Streptococci . GBS)
Initially, Streptococcus agalactiae was known to be a causative agent of mastitis in cows from the end of the 1887th century (Nocard. 1935). In 70, a case of sepsis and pneumonia in a woman giving birth was described, related to infection with this pathogen, which was classified as group B streptococcus (GBS). In the 0,2s, GBS was the dominant causative agent of sepsis and meningitis in newborns (5,4-1000 per 90 live births). At the end of the 9s, the prophylaxis of streptococcal infections (chemoprophylaxis during childbirth) was introduced. The identification of the TYPES of streptococci in this group is based on the differences in the structure of capsular polysaccharides, of which 5 types have been identified (I a, I b, II? ¨ VIII). GROUP B streptococcal cell membrane contains capsular (polysaccharide) antigens constituting a virulence factor that is specific for a particular type of streptococcus within group B. Moreover, GBS cell membrane contains esterases that inactivate the C XNUMXa complement component, which has an anti-chemotactic effect for peripheral blood neutrophils and beta-hemolysin that increases tissue destruction.
Groups C and G
There is a high antigenic similarity in both groups of streptococci and therefore additional biochemical and genetic tests were necessary in order to distinguish individual groups. Most pathogenic types for humans contain an M protein with characteristics similar to the M protein in group A of streptococci. Streptococci of these groups secrete streptolysin O and streptokinase. There are reports of the similarity of streptococcus types within groups C and G.
Rump D (enterokoki)
Group D streptococci are part of the normal environment of the digestive tract. In 50% of newborns, the digestive system becomes colonized by them during the first week of life. Other possible sites of colonization with group D streptococci are skin, mouth, gallbladder and vagina. Enterococci are less virulent than streptococci of groups A, C and B and are more resistant to environmental factors. They are heavily involved in nosocomial infections. Invasive infections most often affect people with reduced immunity (congenital or acquired), newborns and the elderly.
Streptococcus pneumoniae (pneumokoki)
They are streptococci with a polysaccharide shell, which has the characteristics of specificity for a given type of pneumococcus. On this basis, more than 80 types of pneumococci have been identified. The cell wall contains the C antigen (phosphocholine + galactosamine 6-phosphate) that inhibits phagocytosis, which facilitates the invasion of bacteria. The cell membrane is a polysaccharide structure with antigenic features. The M protein, isolated in the cell membrane with features responsible for pneumococcal virulence, does not have such pronounced antiphagocytic features as in other streptococci.
The most important diseases associated with streptococcal infection (Streptococceae): Streptococcal pharyngitis (streptococcal pharyngitis)
Beady pharyngitis
Streptococcal pharyngitis and / or tonsillitis is an acute disease of the upper respiratory tract, characterized by swelling, redness and soreness due to congestion in the pharynx and / or tonsils and the soft palate. It is the dominant cause of bacterial acute pharyngitis in the population. Tonsillitis may be characterized by purulent or fibrinous exudate (60-90% of cases), but its absence does not rule out the diagnosis.
1. Epidemiology (occurrence of strep throat)
Children 5-15 years of age are more likely to suffer from bead pharyngitis than adults, who have a milder streptococcal pharyngitis and may therefore be undiagnosed. Children under 2 years of age are rarely ill, possibly due to maternal antibodies that can be transmitted through the placenta and are specific for a given type of GAS. Children under 13 years of age develop streptococcal pharyngitis 3 times (1-8 cases). The disease occurs more often in cooler seasons and in zones 7 of the temperate climate than in the tropical (unlike in streptococcal skin infections).
Some types of group A streptococci causing pharyngitis have been shown to be closely related to glomerulonephritis (the so-called nephritogenic serotypes, e.g. M-12). A distinction is made between the droplet path of infection or by direct contact, especially in large groups of people. The risk of infection in home contact is approximately 25%, assuming that the infectivity in a successfully treated person is 24 hours from the start of therapy, in untreated or ineffective patients up to 7 days. After an acute infection, the possibility of asymptomatic carriage was shown, which is estimated at 5-20% in children, while in adults it does not exceed 5%.
2. The etiology of strep throat
Streptococci from group A dominate, but also from groups C and G (the latter more often in tropical zones). With endemic pharyngitis, the infection with group C streptococci as a result of consumption of unpasteurized cow’s milk (epidemics in Romania, Great Britain, USA, Israel) should be taken into account.
3. Pathophysiology of the disease
The condition for the occurrence of streptopharyngitis is the adhesion of the appropriate type of GAS to the cells of the epithelium lining the tonsils and pharynx and effective “competition” with the natural flora of the environment, especially with gram-positive bacteria, hemolytic green streptococci (Streptococcus viridans), through the participation of fimbriae and bacteriocins. Damage to tissues and cells, including macrophages and neutrophils, “facilitates” the hyaluronic acid of the bacterial cell wall. The anti-phagocytic and anti-complementary features of M proteins are decisive in the spread of streptococcal infection, as they not only reduce phagocytosis, but also inhibit chemotaxis and impede the inflow of cells from the granulocytic system. The ability to cause necrosis and the haemolytic properties of pyrogenic exotoxins, and possibly also the cell wall peptidoglycans and the haemolysins O and S streptolysins (especially for myocardial cells) intensify the invasiveness of streptococci. Streptococci can travel to nearby lymph nodes and cause transient bacteremia, especially in younger children (including immunocompetent individuals). During the recovery period (also spontaneous), the virulence of bacteria disappears (the production of M protein is lost). Type-specific antibodies are found in the serum 6-8 weeks after the onset of infection. They provide protection against reinfection with the same type of streptococcus.
4. Symptoms and course of strep throat
The hatching period for streptococcus is on average 2-5 days (1-7 days). The mouth and throat are the gateways of infection. There are different clinical forms of streptococcal angina:
- catarrhal angina,
- follicular angina,
- pseudo-diphtheria angina.
The most typical, although less common, is the image of follicular angina (a. Lacunaris), with visible purulent plugs on the tonsils. Symptoms appear suddenly, they are: headache and throat pain as well as increasing fever, most often preceded by abdominal pain and vomiting in younger children. Then redness and swelling of the pharyngeal mucosa appear. There is hyperemia and swelling of the mucosa of the pharynx, tonsils and soft palate, with clearly visible swelling of the uvula – an image of a vivid red throat (“scarlet”).
From the second day onwards, there is exudate on the tonsils, initially mucous, coalescing. Tonsil exudate may be purulent, mucous or fibrinous, and may involve limited or entire surfaces of the tonsils. It is also possible only hyperemia without visible exudate. At this time, a fairly distinct white coating with swelling of the taste buds is present on the tongue mucosa, which is a very important clinical feature of streptococcal infection. In 30-60% of patients, lymph nodes, to a different degree, are enlarged, especially the anterior cervical, usually symmetrically, without edema of the peri-ligament tissue, moderately cohesive, tender on palpation, without a tendency to soften and without lesions of the skin. Moreover, slight enlargement of the spleen and liver as well as other groups of peripheral lymph nodes can be found.
Symptoms of strep pharyngitis begin to subside after about 3-5 days, unless early complications occur, affecting up to 1% of patients, including:
• purulent inflammation of the cervical lymph nodes;
• otitis media;
• inflammation of the paranasal sinuses;
• peritonsillar abscess (pay attention to the symmetry of the pharynx image);
• in extreme cases – Ludwig’s angina (necrotizing fasciitis of neck).
The latency period for late complications is:
• for glomerulonephritis – up to 10 days;
• for rheumatic fever – up to 18 days.
Rheumatic fever it occurs in about 50% of people who have already suffered this complication and in 0,1-0,3% of those untreated during a streptococcal infection. There are no specific clinical features of acute bacterial pharyngitis or tonsillitis, especially in the initial stage of the disease. Observations on more than 4000 patients (cross-section of the entire population) made the bacterial (over viral) etiology more probable in cases where: there was environmental contact with a patient (or treated) due to streptococcal pharyngitis, high fever with nausea and / or vomiting, painful enlargement lymph nodes, the onset of the disease was sudden and concerned a person aged 5-15 years. Centor and McIsaac developed a point scale for the probability of S. pyogenes infection in bacterial pharyngitis or tonsillitis (Table 42.2).
In children up to 3 years of age, streptococcal infection of the upper respiratory tract does not have the appearance of pharyngitis, but is only characterized by a prolonged period of increased body temperature (moderate), the presence of serous, catarrhal secretions and generalized lymphadenopathy. This syndrome is called “streptococosis”.
Source: J. Cianciara, J. Juszczyk, Infectious and parasitic diseases; Czelej Publishing House