Gram Positive Cocci-Streptococcus

Streptococcus pathogenicity

1. GRAM POSITIVE COCCI (Streptococcus) SAMIRA FATTAH HAMID Ph.D. Medical Bacteriology College of Health Sciences Hawler Medical University

2. GENUS: STREPTOCOCCI Characteristics: Gram- positive, facultative anaerobes. Non-motile, non - sporulating. Spherical or oval cells, form pairs or chains during growth. catalase negative (unlike Staphylococcus)

3. Classification The streptococci are a large and heterogeneous group of bacteria, and no one system suffices to classify them. classification of streptococci based on a series of observations: Hemolysis Many streptococci are able to hemolyze red blood cells in vitro in varying degree. Clinically important streptococci are traditionally differentiated based on their hemolysis pattern.

4. Hemolysis Types Hemolysis Appearance Designation Example - Complete colorless, clear Sharply Beta(β) S. pyogenes defined zone -Partial Greenish discoloration Alpha(α) Viridans streptococci -None No change Gamma(δ) Enterococci

5. Classification B. Group-Specific Substance (Lancefield Classification) based on the carbohydrate composition of bacterial antigens found on their cell walls, identified using group specific antiserum.

6. Classification C. Capsular Polysaccharides The antigenic specificity of the capsular polysaccharides is used to classify S. pneumoniae into more than 90 types. D. Biochemical Reactions Biochemical tests include sugar fermentation reactions, tests for the presence of enzymes, and tests for susceptibility or resistance to certain chemical agents.

7. Streptococcus pyogenes (Group A β- hemolytic streptococci) individual cocci are spherical or ovoid and are arranged in chains. The lengths of the chains vary widely and are conditioned by environmental factors. produce capsules composed of hyaluronic acid. β- hemolytic on blood agar

8. Streptococcus pyogenes (Group A β- hemolytic streptococci) Antigenic Structure M Protein is a filamentous rodlike coiled structure anchored to the cell membrane that penetrates and projects from the streptococcal cell wall. When M protein is present, the streptococci are virulent, and in the absence of M type-specific antibodies, they are able to resist phagocytosis by polymorphonuclear leukocytes. S. pyogenes that lack M protein are not virulent. Because there are more than one types of M protein, a person can have repeated infections with S. pyogenes of different M types.

9. Streptococcus pyogenes (Group A β- hemolytic streptococci) Antigenic Structure Toxins and Enzymes Streptokinase (Fibrinolysin) produced by many strains of group A β-hemolytic streptococci. It transforms the plasminogen of human plasma into plasmin, an active proteolytic enzyme that digests fibrin clot and other proteins, allowing the bacteria to escape from blood clots. Streptokinase has been given intravenously for treatment of pulmonary emboli, coronary artery, and venous thromboses. Deoxyribonucleases Streptococcal deoxyribonucleases A, B, C, and D degrade DNA (DNases) and similar to streptokinase facilitate the spread of streptococci in tissue by liquefying pus. Mixtures of streptokinase and DNases are used in “enzymatic debridement.” They help to liquefy exudates and facilitate removal of pus and necrotic tissue.

10. Streptococcus pyogenes (Group A β- hemolytic streptococci) Antigenic Structure Hyaluronidase Hyaluronidase splits hyaluronic acid . are antigenic and specific for each bacterial or tissue source. After infection with hyaluronidase-producing organisms, specific antibodies are found in the serum. Pyrogenic Exotoxins There are three antigenically distinct streptococcal pyrogenic exotoxins ( Spe ): A, B, and C. it has been associated with streptococcal toxic shock syndrome and scarlet fever . acts as superantigens, stimulate T cells by binding to the class II major histocompatibility complex . The activated T cells release cytokines that mediate shock and tissue injury.

11. Streptococcus pyogenes (Group A β- hemolytic streptococci) Antigenic Structure Hemolysins The β-hemolytic group A S. pyogenes elaborates two hemolysins ( streptolysins ) that not only lyse the membranes of erythrocytes but also damage a variety of other cell types: Streptolysin O Streptolysin S Streptolysin O combines quantitatively with Antistreptolysin O (ASO), an antibody that appears in humans after infection with any streptococci that produce streptolysin O. This antibody blocks hemolysis by streptolysin O. This phenomenon forms the basis of a quantitative test for the antibody. Streptolysin S is responsible for the hemolytic zones around streptococcal colonies growing on the surface of blood agar plates. It is not antigenic.

12. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Diseases Attributable to Invasion by S. pyogenes, β-Hemolytic Group A Streptococci Erysipelas Lesions are raised and characteristically red and extends along lymphatic pathways with only minimal local suppuration. From the lymphatics, the infection can extend to the bloodstream. Cellulitis Rapidly spreading infection of the skin and subcutaneous tissues. It follows infection associated with mild trauma, burns, wounds, or surgical incisions. Pain, tenderness, swelling, and erythema occur.

13. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Diseases Attributable to Invasion by S. pyogenes, β-Hemolytic Group A Streptococci Necrotizing fasciitis ( streptococcal gangrene) There is extensive and very rapidly spreading necrosis of the skin, tissues, and fascia. sometimes termed flesh-eating bacteria . Puerperal fever If the streptococci enter the uterus after delivery, puerperal fever develops, which is essentially a septicemia originating in the infected wound (endometritis). Bacteremia or sepsis Infection of traumatic or surgical wounds with streptococci results in bacteremia, which can rapidly be fatal.

14. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Diseases Attributable to Invasion by S. pyogenes, β-Hemolytic Group A Streptococci Streptococcal Toxic Shock Syndrome Characterized by bacteremia, respiratory failure, multiorgan failure and shock Erythema and desquamation may occur. The infections tend to occur after soft tissue infection like in necrotizing fasciitis and myositis, Death occurs in about 30% of patients. Scarlet fever Association with S. pyogenes pharyngitis or with skin or soft tissue infection. Caused by pyrogenic exotoxin. The rash appears on the trunk after 24 hours of illness and spreads to involve the extremities. Streptococcal toxic shock syndrome and scarlet fever are clinically overlapping diseases.

15. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Diseases Attributable to Local Infection with S. pyogenes and Their By-products Streptococcal sore throat S. pyogenes adheres to the pharyngeal epithelium by means of lipoteichoic acid and by means of hyaluronic acid in encapsulated strains. In children and adults, the disease is characterized by intense nasopharyngitis, tonsillitis, and intense redness and edema of the mucous membranes, with purulent exudate; enlarged, tender cervical lymph nodes; and (usually) a high fever. In infants and small children infection extend to the middle ear.

16. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Diseases Attributable to Local Infection with S. pyogenes Streptococcal pyoderma Local infection of superficial layers of skin, especially in children, is called impetigo (sometimes both S. pyogenes and S. aureus are present.). It is covered with pus and later is encrusted. More widespread infection occurs in eczematous or wounded skin or in burns and may progress to cellulitis. Group A streptococcal skin infections are often attributable to M types 49, 57, and 59–61

17. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Poststreptococcal Diseases Acute glomerulonephritis Develops 1–5 weeks after S. pyogenes skin infection (pyoderma, impetigo) or pharyngitis. Glomerulonephritis may be initiated by antigen antibody complexes on the glomerular basement membrane. The most important antigens are thought to be SpeB . A few patients die, some develop chronic glomerulonephritis with ultimate kidney failure, and the majority recovers completely.

18. Streptococcus pyogenes (Group A β- hemolytic streptococci) Pathogenesis and Clinical Findings Poststreptococcal Diseases Rheumatic fever Certain strains of group A streptococci contain cell membrane antigens that cross-react with human heart tissue antigens. Sera from patients with rheumatic fever contain antibodies to these antigens. patients with more severe streptococcal sore throats have a greater chance of developing rheumatic fever. symptoms and signs of rheumatic fever include: fever, malaise and evidence of inflammation of all parts of the heart (endocardium, myocardium, and pericardium). Patients may develop severe and progressive congestive heart failure.

19. Antibody cross-reaction with heart

20. Streptococcus pyogenes (Group A β- hemolytic streptococci) Treatment penicillin G. Macrolides (such as Erythromycin) and Clindamycin recommended for penicillin-allergic patients and for patients with necrotizing fasciitis.

21. Streptococcus agalactiae Group B streptococci β- hemolytic Are part of the normal vaginal flora and lower gastrointestinal tract in 5–30% of women. Group B streptococcal infection during the first month of life may present as sepsis, meningitis, or respiratory distress syndrome. elderly adults and immunocompromised hosts, are most at risk for invasive disease. Clinical manifestation : Bacteremia, skin and soft tissue infections, respiratory infections, and genitourinary infections.

22. Streptococcus pneumoniae Gram-positive diplococci , often lancet shaped or arranged in chains Possessing a capsule of polysaccharide that permits typing with specific antisera. Normal inhabitants of the upper respiratory tract of 5–40% of humans and can cause: pneumonia, sinusitis, otitis, bronchitis, bacteremia, meningitis and peritonitis. Antigenic Structure pneumococcal cell wall has peptidoglycan and teichoic acid, similar to other streptococci. capsular polysaccharide

23. Streptococcus pneumoniae Pathogenesis In adults, types 1–8 are responsible for about 75% of cases of pneumococcal pneumonia and for more than half of all fatalities in pneumococcal bacteremia. in children, types 6,14, 19, and 23 are frequent causes. The virulence of the organism is a function of its capsule, which prevents or delays ingestion by phagocytes. Clinical Findings The onset of pneumococcal pneumonia is usually sudden, with fever, chills, and sharp pleural pain. The sputum is bloody or rusty colored. Early in the disease, when the fever is high, bacteremia is present in 10–20% of cases.

24. Streptococcus pneumoniae Loss of Natural Resistance Because 40–70% of humans are at some time carriers of virulent pneumococci, the normal respiratory mucosa must possess great natural resistance to the pneumococcus. Among the factors that probably lower this resistance and thus predispose to pneumococcal infection are the following: Viral and other respiratory tract infections that damage surface cells. Abnormal accumulations of mucus ( eg. allergy), which protect pneumococci from phagocytosis. Alcohol or drug intoxication, which depresses phagocytic activity, depresses the cough reflex. Other mechanisms, such as malnutrition, sickle cell anemia, nephrosis, or complement deficiency.

25. Streptococcus pneumoniae Treatment Penicillin G Vancomycin. Because resistance profiles are not predictable, routine susceptibility testing should be performed for all pneumococcal infections.

26. Enterococci Gram-positive Catalase-negative Facultatively anaerobic. Oval-shaped, arranged in pairs or short chains. There are at least 47 species of enterococci. Enterococcus faecalis and Enterococcus faecium are the two species most commonly isolated from clinical specimens. Enterococci are part of the normal enteric microbiota. Usually nonhemolytic, but are occasionally α-hemolytic grow well in 6.5% NaCl. grow well at a wide temperature range between 10°C and 45°C,

27. Enterococci Pathogenesis Most enterococcal infections appear to arise from the endogenous flora via translocation from their major colonization site (GI tract). Virulence is mediated by two major properties: intrinsic antimicrobial resistance of enterococci ability to adhere to cells and tissues and form biofilms.

28. Enterococci Clinical Findings In hospitalized patients, the most common sites of infection are the urinary tract, burn and surgical wounds, biliary tract, and blood. Urinary tract infections are associated with indwelling catheters, instrumentation, or structural abnormalities of the genitourinary tract. Intra-abdominal and pelvic infections. Bacteremia and endocarditis. Infections of the respiratory tract have been described, but occur rarely. Enterococci are part of the normal adult vaginal microbiota, and can therefore be acquired by neonates during vaginal delivery.

29. Enterococci Treatment Treatment of enterococcal infection can be challenging to clinicians due to the fact that enterococci are frequently resistant to various antibiotics. Are intrinsically resistant to cephalosporins, penicillinase-resistant penicillins , and monobactams. Traditionally, therapy for systemic enterococcal infections consists of the combination of a cell-wall active antibiotic ( eg , ampicillin or vancomycin) with an aminoglycoside.

30. Peptostreptococcus These streptococci grow only under anaerobic or microaerophilic conditions and variably produce hemolysins. They are part of the normal microbiota of the mouth, upper respiratory tract, bowel, and female genital tract. They often participate with many other bacterial species in mixed anaerobic infections, such infections may occur in wounds, in the breast, in postpartum endometritis, after rupture of an abdominal viscus, in the brain, or in chronic suppuration of the lung. The pus usually has a foul odor.