Streptococcus. Pyogenes and Streptococcus pneumoniae PDF

Streptococcus. Pyogenes and Steptococcus pneumoniae Prepared by Dr. Abdulla Kamil Abdulla Shwani/Ph.D. Medical Microbiology/Virology  Classification of Streptococci Two major methods used for classification of Streptococci : A-. Hemolytic properties on blood agar B. Serolog...

Streptococcus. Pyogenes and Steptococcus pneumoniae Prepared by Dr. Abdulla Kamil Abdulla Shwani/Ph.D. Medical Microbiology/Virology  Classification of Streptococci Two major methods used for classification of Streptococci : A-. Hemolytic properties on blood agar B. Serologic (Lancefield) groupings Classification of Streptococci cont. A-. Hemolytic properties on blood agar: α-Hemolytic Streptococci cause a chemical change in the hemoglobin of red cells in blood agar, resulting in the appearance of a green pigment that forms a ring around the colony. β- Hemolytic Streptococci cause gross lysis of red blood cells, resulting in a clear ring around the colony. γ-Hemolytic is a term applied to Streptococci that cause no color change or lysis of red blood cells such as Enterococci. Classification of Streptococci cont. 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. Classification schemes for Streptococci.  S. pyogenes General prosperities: – Gram positive cocci – Chains or pairs – Non-motile – Non-spore forming – Facultative anaerobes – Fastidious – Catalase negative (Staphylococci are catalase positive) microorganisms that will grow only if special nutrients are present in their culture medium  B. Culture: Most Streptococci grow in solid media, usually 1–2 mm in diameter. S. pyogenes is β- hemolytic; other species have variable hemolytic characteristics  A. Structure and physiology ‫ ﺋﻪﻣﺎﻧﻪی‬A ‫ﺗﺎﯾﺒﻪﺗﻤﻪﻧﺪﯾﯿﻪ ﭘ ﮑﻬﺎﺗﻪﯾﯿﻪﮐﺎﻧﯽ ﺑﻪﺷﺪار ﻟﻪ ﻧﻪﺧﯚﺷﯿﻨﺎﺳﯽ ﯾﺎن ﻧﺎﺳﯿﻨﻪوەی ﺳﺘﺮ ﭙﺘﯚﮐﯚﮐﯽ ﮔﺮوﭘﯽ‬ ‫ﺧﻮارەوە ﻟﻪﺧﯚدەﮔﺮن‬ Structural features involved in the pathology or identification of group A Streptococci include the following: 1. Capsule: Hyaluronic acid, identical to that found in human connective tissue, it is also anti-phagocytic.  A. Structure and physiology cont. 2. Cell wall: these components include the following: a. M protein: S. pyogenes is not infectious in the absence of M protein. M proteins interferes with complement binding. b. Group A-specific C-substance: This component is composed of rhamnose and N-acetylglucosamine. c. Protein F (fibronectin-binding protein): Protein F mediates bacterial attachment to fibronectin in the pharyngeal epithelium. Cytolytic toxins and other exoenzymes produced by Streptococcus pyogenes. Cytolytic toxins and other exoenzymes produced by Streptococcus pyogenes. Cont. Epidemiology The only known reservoir for S. pyogenes in nature is the skin and mucous membranes of the human host. Respiratory droplets or skin contact spreads group A streptococcal (GAS) infection from person to person, especially in crowded environments such as classrooms and children's play areas may be happened. Pathogenesis S. pyogenes cells, in an inhaled droplet for example, attach to the pharyngeal mucosa via actions of protein F, lipoteichoic acid, and M protein. The bacteria may simply replicate sufficiently to maintain themselves without causing injury, in which case the patient is then considered colonized. Alternatively, bacteria may grow and secrete toxins, causing damage to surrounding cells, invading the mucosa. The patient then has streptococcal pharyngitis. Occasionally, causing cellulitis (acute inflammation of subcutaneous tissue). Clinical significance S. pyogenes is a major cause of cellulitis. Other more specific syndromes include the following: 1. Acute pharyngitis or pharyngo-tonsillitis. 2. Impetigo 3. Erysipelas ‫ ﺗ ﻜﭽﻮوﻧﻲ ﻟﻪش‬،‫ﻫﻪوﻛﺮدﻧ ﻜﻲ ﺟﯚري ﺗﻴﭙﺮي ﺷﺎﻧﻪﻛﺎﻧﻲ ﭘ ﺴﺘﻪ ﻟﻪﮔﻪ ﺗﺎو‬ 4. Puerperal sepsis  Clinical significance 5. Streptococcal toxic shock syndrome. 6. Poststreptococcal sequelae including the followings: a. Acute rheumatic fever: This autoimmune disease occurs 2-3 weeks after the initiation of streptococcal pharyngitis. It is caused by cross- reactions between antigens of the heart and joint tissues and streptococcal antigen. It is characterized by fever, rash, carditis, and arthritis.  Clinical significance b. Acute glomerulonephritis: This rare, post-infectious sequelae occurs as soon as 1 week after impetigo or pharyngitis ensues, because of a few nephritogenic strains of group A streptococci. Antigen- antibody complexes on the basement membrane of the glomerulus initiate the disease. Acute pharyngitis or pharyngo- tonsillitis. Erysipelas Cellulitis Laboratory identification Rapid latex antigen kits for direct detection of group A streptococci in patient samples are widely used. In a positive test, the latex particles clump together, whereas in a negative test, they stay separate, giving the suspension a milky appearance. Depending on the form of the disease, specimens for laboratory analysis can be obtained from throat swabs, pus and lesion samples, sputum, blood, or spinal fluid.  Laboratory identification cont. S. pyogenes forms characteristic small, opalescent colonies surrounded by a large zone of B-hemolysis on sheep blood agar. [Note: Hemolysis of the blood cells is caused by streptolysin S, which damages mammalian cells resulting in cell lysis. This organism is highly sensitive to bacitracin. S. pyogenes is also catalase-negative and optochin resistant. Serologic tests detect a patient's antibody titer to Streptolysin O (ASO titer test) after GAS infection. Latex agglutination for identification of group A β- hemolytic streptococci. ASO titer test Treatment Antibiotics are used for all GAS infections. S. pyogenes has not acquired resistance to penicillin G, which remains the antibiotic of choice for acute streptococcal disease. In a patient allergic to penicillin, a macrolide such as clarithromycin or azithromycin is the preferred drug. Penicillin G plus clindamycin are used in treating necrotizing fasciitis and in streptococcal toxic shock syndrome. Clindamycin is added to penicillin to inhibit protein (ie, toxin) synthesis so that a huge amount of toxin is not released abruptly from rapidly dying bacteria.  Prevention Rheumatic fever is prevented by rapid eradication of the infecting organism. Prolonged prophylactic antibiotic therapy is indicated after an episode of rheumatic fever, because having had one episode of this autoimmune disease in the past is a major risk factor for subsequent episodes if the patient is again infected with S. pyogenes.  Steptococcus pneumoniae (PNEUMOCOCCUS) S. pneumoniae are gram-positive, non-motile, encapsulated cocci. They are lancet shaped, and their tendency to occur in pairs accounts for their earlier designation as Diplococcus pneumoniae. S. pneumoniae is the most common cause of community-acquired pneumonia and adult bacterial meningitis and is an important cause of otitis media, and sinusitis,. The risk of disease is highest among young children , older adults, smokers, and persons with certain chronic illnesses. Like other streptococci, S. pneumoniae is fastidious (has complex nutritional requirements) and routinely cultured on blood agar. It releases an α-hemolysin that damages red cell membranes, causing colonies to be α-hemolytic and give green color. Virulence factors of S. pneumoniae 1. Capsule: The S. pneumoniae polysaccharide capsule is both antiphagocytic and antigenic. 2. Pili: Pili enable the attachment of encapsulated pneumococci to the epithelial cells of the upper respiratory tract 3. Choline-binding protein A: Choline-binding protein A is a major adhesin allowing the pneumococcus to attach to carbohydrates on epithelial cells of the human nasopharynx.  Virulence factors of S. Pneumoniae cont. 4.Autolysins: Autolysins are enzymes that hydrolyze the components of a biological cell in which it is produced. 5. Pneumolysin: It causes lysis once it is released by autolysin from the interior of the bacterium. This toxin stimulates production of proinflammatory cytokines, inhibits the activity of polymorphonuclear leukocytes, and activates complement. Clinical significance The diseases caused by this bacteria are: 1. Acute bacterial pneumonia. 2. Otitis media: The most common bacterial infection of children. 3. Bacteremia/sepsis 4. Meningitis: S. pneumoniae became the most common cause of adult bacterial meningitis Lab. Diagnosis Specimens for laboratory evaluation can be obtained from a nasopharyngeal swab, blood, pus, sputum, or spinal fluid. a-Hemolytic colonies appear when S. pneumoniae is grown on blood agar overnight under aerobic conditions at 37°C. Lancet-shaped, gram- positive diplococci are observed on a Gram stain of the sample. Growth of these bacteria is inhibited by low concentrations of Optochin, and the cells are lysed by bile acids. The appearance of capsular swelling (the Quellung reaction) is observed when the pneumococci are treated with type-specific antisera. Optochin test for S. pneumoniae Quellung reaction Lysis by bile acids Treatment S. pneumoniae isolates were highly sensitive to penicillin G, the initial agent of choice, until the late 1980s. Since then, the incidence of penicillin resistance has been increasing worldwide. The mechanism of this resistance is an alteration of one or more bacterial penicillin-binding proteins, rather than production of β-lactamase. Most resistant strains remain sensitive to third-generation cephalosporins (such as cefotaxime or ceftriaxone), and all strains isolated in the United States are still sensitive to Vancomycin. Tolerance to Vancomycin has been observed, but the clinical significance of this phenomenon is unclear. Third-generation cephalosporins and vancomycin are therefore the agents of choice for invasive infections by penicillin-resistant strains of S. pneumoniae.