STREPTOCOCCI

1. STREPTOCOCCI

2. Streptococci are facultative anaerobic, • Gram-positive organisms that often occur as • chains or pairs and are catalase-negative • (staphylococci are catalase positive).

3. Streptococcus mutans.

4. Classification Streptococci can be classified by several schemes, for example, by the hemolytic properties of the organisms, and according to the presence of specific surface antigens determined by immunologic assays. A. Hemolytic properties on blood agar α-hemolysis: incomplete lysis of RBC with the formation of green pigment. β-hemolysis: complete hemolysis γ- No hemolysis B. Serologic (Lancefield) groupings Many species of streptococci have a polysaccharide in their cell walls known as C-substance, which is antigenic . The Lancefield scheme classifies primarily β-hemolytic streptococci into groups A through U on the basis of their C-substance. The clinically most important groups of β-hemolytic streptococci are Types A and B .

5. BAP: Hemolysis Gamma Alpha

6. BAP Hemolysis: Beta

7. GROUP A β-HEMOLYTIC STREPTOCOCCI (Streptococcus pyogenes) Capsule: antiphagocytosis.The capsule of group A streptococci is composed of hyaluronic acid. Group-specific cell wall antigen (Lancefield group A) Carbohydrate (A dimer of N-acetylglucosamine and rhamnose). Protein F: a major adhesin of S. pyogenes, binding with fibronectinin the pharyngeal epithelium. M protein: Forms hair-like projections (fimbriae) from the cell membrane. Major virulence factor of S. pyogenes. Enhances degradation of C3b via binding with factor H, and phagocytosis by PMNs is prevented. Promotes adherence to epithelial cells. Induces type-specific protective immunity (>100 serotypes).

8. M protein

9. Streptococcus pyogenes Pathogenesis(via invasiveness and production of toxins) Adherence to the epithelial cells; >10 adhesion molecules invasion into the epithelial cells; mediated by M protein and protein F important for persistent infections and invasion into deep tissues avoiding opsonization and phagocytosis; M protein, M-like proteins, and C5a peptidase producing enzymes and toxins

10. Streptococcus pyogenes Enzymes and toxins Streptokinase(fibrinolysin) Can lyse blood clots and may be responsible for the rapid spread of the organism. Used (IV injection) for treatment of pulmonary emboli, coronary artery thrombosis and venousthrombosis. Streptodornase(DNases A to D) DNAses that degrade the viscous DNA in necrotizing tissue or exudates, aiding the spread of infection. Hyaluronidase(spreading factor): Destroys connective tissue and aids in spreading infecting bacteria. C5a peptidase Prevents streptococci from C5a-mediated recruitment and activation of phagocytes, and is important for survival of S. pyogenes in tissue and blood.

11. Streptococcal pyrogenicexotoxins (Spe) Produced by both the scarlet fever strains and new invasive S.pyogenes strains. More than four serologically distinct toxins (SpeA, B, C and F). They are superantigens(except for Spe B, which is a cysteine protease)and may exhibit the followingbiological activities: Enhances release of proinflammatory cytokines (pyrogenicity) causes skin rash ,Immunosuppression ,Spe is associated with streptococcal toxic shock syndrome.

12. Hemolysins Streptolysin O: O2-labile; causes hemolysis deep in blood agar plates. ASO (antistreptolysin O) titer >160-200 units suggests recent infection or exaggerated immune response to an earlier respiratory infection. However, skin infection does not induce ASO. Streptolysin S: O2-stable. Causes b-hemolysis on the surface of blood agar plates.Cell-bound, not antigenic. Produced in the presence of serum. Kills phagocytes by releasing the lysosomal contents after engulfment.

13. Streptococcus pyogenes Clinical Diseases 1. Local infection with S. pyogenes Streptococcal sore throat (pharyngitis), and scarlet fever. Streptococcal pyoderma(impetigo, local infection of superficial layers of skin).Strains that cause skin infections are different from those that cause pharyngitis.

14. 2. Invasion by S. pyogenes Invasion from respiratory tract: otitis media, sinusitis, pneumonia, meningitis, osteomyelitis, and arthritis. Invasion from skin: erysipelas, cellulitis, and necrotizing fasciitis. Sepsis (streptococcal toxic shock syndrome, STSS): the organism is introduced into the subcutaneous tissue through a break in the skin cellulitis necrotizing fasciitis systemic toxicity, multiple organ failure, and death (mortality > 40%).

15. 3. Poststreptococcal diseases(occurs 1-4 weeks after acute S.pyogenes infection, hypersensitivity responses) Rheumatic fever: most commonly preceded by infection of the respiratory tract. Inflammation of heart (pancarditis), joints, blood vessels, and subcutaneous tissue. Results from cross reactivity of anti-M protein Ab and the human heart tissue. Acute glomerulonephritis: preceded by infection of the skin (more commonly) or the respiratory tract. Symptoms: edema, hypertension, hematuria, and proteinuria. Initiated by Ag-Ab complexes on the glomerular basement membrane. * Rheumatic fever can be reactivated by recurrent streptococcal infections, whereas nephritis does not.

16. S. agalactiae(group B, β--hemolytic, contains type-specific capsular polysaccharides which is the most important virulence factor and can induce protective antibodies; may colonize at lower gastrointestinal tract and genitourinary tract) Neonatal sepsis or meningitis Early-onset (during the first week of life): infection acquired in utero or at birth. Pneumonia is common in addition to meningitis. Late-onset (older infants): infection acquired from an exogenous source. (Premature infants are at greater risk.) Infection of pregnant women Urinary tract infections, amnionitis, endometritis, and wound infections Infection in men and nonpregnant women Patients are generally older and have underlying conditions. Bacteremia, pneumonia, bone and joint infections, skin and soft tissue infections. Mortality is higher.

17. Viridans streptococci(a-hemolytic or nonhemolytic, most are nongroupable; they, except for S. suis, are divided into 5 subgroups based on the specific diseases they cause) These streptococci colonize the oropharynx, GI tract, and GU tract; rarely on the skin surface. Diseases: Subacuteendocarditis(group: Mitis) Intra-abdominal infections(group: Anginosus) Dental caries (group: Mutans) Cariogenicity of S. mutans is related to its ability to synthesize glucan from fermentable carbohydrates (e.g. sucrose) as well as to modify glucan in promoting and increased adhesiveness.

18. Treatment All S. pyogenes are sensitive to penicillin G. Effective doses of penicillin or erythromycin for 10 days can prevent poststreptococcal diseases. Drainage and aggressive surgical debridement must be promptly initiated in patients with serious soft tissue infections. Group B streptococci are also susceptible to penicillin G. Antibiotic sensitivity test is helpful for treatment of bacterial endocarditis.

19. S. pneumoniae Morphology and Physiology Gram-positive lancet-shaped diplococci for typical organisms. a-hemolytic (pneumolysin is similar to streptolysin O). Growth is enhanced by 5-10% CO2. Capsular polysaccharide: type-specific, 90 types. Smooth (capsular polysaccharide-producing) vs. rough colonies *Quellung reaction (for rapid identification or typing of the bacteria)

20. S. pneumoniae Pathogenesis and Immunity Pneumococci produce disease through their ability to multiply in the tissues (invasiveness). Virulence factors: capsule, cell wall polysaccharide, phosphocholine, pneumolysin, IgA protease, etc.40-70% of humans are at sometimes carrier of virulent pneumococci. Normal respiratory tract has natural resistance to the pneumococcus.Major host defense mechanisms: ciliated cells of respiratory tract and spleen. Loss of natural resistance may be due to: 1. Abnormalities of the respiratory tract (e.g. viral RT infections). 2. Alcohol or drug intoxication; abnormal circulatory dynamics. 3. Patients undergone renal transplant; chronic renal diseases. 4. Malnutrition, general debility, sickle cell anemia, hyposplenism or splenectomy, nephrosis or complement deficiency. 5. Young children and the elderly.

21. S. pneumoniae Clinical diseases Pneumococcal pneumonia develops when the bacteria multiply rapidly in the alveolar space after aspiration. The affected area is generally localized in the lower lobes of the lungs (lobar pneumonia). Children and the elderly can have a more generalized bronchopneumonia. Resolution occurs when specific anticapsular antibodies develop. Sudden onset with fever, chills and sharp chest pain. Bloody, rusty sputum. Empyema (mostly caused by type 3) is a rare but significant complication. Complications caused by spreading of pneumococci to other organs: sinusitis, middle ear infection,meningitis, endocarditis, septic arthritis.

22. S. pneumoniae Treatment, Prevention, and Control Penicillins are the drugs of choice. However, strains resistant to penicillin and other antibiotics are common nowadays.

23. Enterococci (E. faecalis, E. faecium) Physiological properties are similar to the streptococci. Form large colonies on blood plate; most are nonhemolytic. Microscopic morphology is similar to S. pneumoniae. Resistant to 6.5% NaCl, 0.1% methyl blue and grow in bile-esculin agar. More resistant to antibiotics than the streptococci. Colonize the large intestine of humans and animals. An opportunist.

24. Enterococci Clinical Diseases One of the leading causes of nosocomial infections. Urinary tract (UTI), peritoneum (peritonitis) and heart tissue (endocarditis- a severe complication) are involved most often. Particularly common in patients with intravascular or urinary catheters, and in hospitalized patients with prolonged broad-spectrum antibiotic treatment. Intra-abdominal abscess and wound infections: generally polymicrobial. Many strains are completely resistant to all conventional antibiotics. Vancomycin-resistant strains have been isolated.

25. Enterococci Treatment, Prevention, and Control Resistance in enterococci to aminoglycosides and vancomycin is mediated by plasmids and can be transferred to other bacteria. Combined antibiotic therapy: an aminoglycoside and a cell-wall-active antibiotic. New antibiotics have been developed for treatment of enterococci resistant to both ampicillin and vancomycin.