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Dr.T.V.Rao MD 3 Streptococcus Classification • Lancefield classification system based on cell wall Antigens – 20 groups (A,B,C,….) • Another classification system is based on hemolysis reactions • b-hemolysis – A,B,C,G & some D strains • a-hemolysis – S. pneumoniae & others collectively called viridans a specific immuneAntigen- any cell particle or chemical that inducesresponse by B cells or T cells
Identification Scheme Schema to differentiate Group A and B from other b-hemolytic streptococci
Dr.T.V.Rao MD 5 Streptococcus• Gram-positive spherical/ovoid cocci arranged in long chains; commonly in pairs• Non-spore-forming, nonmotile• Can form capsules and slime layers• Facultative anaerobes,Capnophilic• Catalase Negative• Most parasitic forms are fastidious and require enriched media• Small, non pigmented colonies• Sensitive to drying, heat, and disinfectants
Dr.T.V.Rao MD 9 b-hemolytic S. pyogenes• Main representative of group A• Most serious streptococcal pathogen• Strict parasite• Inhabits throat, nasopharynx, occasionally skin• Produces cell surface antigens and virulence factors C-carbohydrates, M-protein (fimbrae), streptokinase, Hyaluronidase, DNase, hemolysins (SLO, SLS), pyogenic toxin
Dr.T.V.Rao MD 10 b-hemolytic S. pyogenesAntigens:• C-carbohydrates- specialized polysaccharides or teichoic acids found on cell wall surface, protect bacterium from being dissolved by the lysozyme defense of host• M-protein (fimbrae)-spiky surface projection, resist phagocytosis and improves adherenceEnzymes and extracellular toxins:• Streptokinase-digests clots• Hyaluronidase- digests binding substance in connective tissue• DNase- digists DNA• hemolysins (SLO, SLS)- streptolysins that cause b-hemolysis and damage cells and tissues• pyogenic toxin-key toxin in development of scarlet fever, causes bright red rash and fever by effecting temperature regulating center
Dr.T.V.Rao MD 11Pathogenesis of Streptococcus• Streptococcuspyogenesproduce infectionwith a tendencyto spread locally,along thelymphatics andthrough the bloodstream
Dr.T.V.Rao MD 12 Virulence Factors of b-Hemolytic S. PyogenesProduces surface antigens: • C-carbohydrates – protect against lysozyme • Fimbriae – adherence • M-protein – contributes to resistance to phagocytosis • Hyaluronic acid capsule – provokes no immune response • C5a protease hinders complement and neutrophil response
Dr.T.V.Rao MD 14 Virulence Factors• Streptolysin O: thiol-activated toxin (Groups A,C,G) • damages membranes: RBCs, myocardial cells, PMNs • role in intracellular survival• Erythrogenic toxins: rash of scarlet fever • pyrogenicity, lethal shock • 105-fold increased sensitivity to endotoxin• Pyrogenic exotoxin A • contributes to streptococcal TSLS • stimulates cytokine production by T cells • endothelial cell damage, hypotensive shock, ischemia-based necrosis
Dr.T.V.Rao MD 15 Complications of Streptococcal group A Infection• Otitis media• Sinusitis• Peritonsillar abscess (quinsy)• Suppurative cervical adenopathy• Rheumatic fever• Post streptococcal glomerulonephritis
Dr.T.V.Rao MD 16 CLINICAL SYNDROMES. Scarlet fever – a complication of pharyngitis if the causative agent is capable of producing erythrogenic toxin initial symptoms of pharyngitis, diffuse erythematous rash with sparing of the palms & soles Circumoral pallor “strawberry tongue”
Dr.T.V.Rao MD 17Group A Streptococcus infection manifest with Throat Pain
Dr.T.V.Rao MD 18 Diagnosis and Treatment of Strep Throat• Tell tale symptoms are slight fever associated with sore throat and visual of pus in back of throat• Quick diagnostic tests (Molecular) available but must be confirmed by throat swab and growth on blood agar (beta hemolysis)
Dr.T.V.Rao MD 19Collecting a appropriate specimen is highly essential
Dr.T.V.Rao MD 20 Respiratory Infections• The primary site of invasion of the human body by Streptococcus pyogenes is throat• Sore throat Tonsillitis• Pharyngitis• Lipoteichoic acid covering the Pili of Streptococcus attach to epithelium of Pharynx• The Glycoprotein fibronectin on the surface of the epithelial cells probably serves as the lipteichoic acid ligand
Dr.T.V.Rao MD 21 Tonsillitis• Tonsillitis is more common in the older children and adults than the younger children• Hypersensitivity ???• Can lead to suppurative complications such as otitis media, mastoiditis, Quinsy• Ludwig’s angina and suppurative adenitis• Pneumonia as complication in Influenza or other respiratory viral diseases
Dr.T.V.Rao MD 22 Skin Infections• Str pyogenes causes a variety of suppurative skin conditions of the skin – burn wounds with progress to produce lymphangitis and cellulites• Infection of minor abrasions can be fatal septicaemia
Dr.T.V.Rao MD 23 Erysipelas• Diffuse infection involving the superficial lymphatics• The skin is red swollen and indurated• Seen in older patients
Dr.T.V.Rao MD 24 ErysipelasErysipelas –pathogen entersthrough a break inthe skin andeventually spreadsto the dermis andsubcutaneoustissues cause acuteinflammation, canremain superficial orbecome systemic
Dr.T.V.Rao MD 25 Impetigo• Caused by limited number of serotypes• Impetigo and streptococcal infection of the scabies lesions are main cause of Glomerulonephritis in children in the tropics
Dr.T.V.Rao MD 26 Pyoderma• In pyoderma antibody response to streptolysin O is not high and ASO estimations does not have as much clinical significance as in Pharyngeal infections• Antibody to DNAase and B and Hyaluronidase are more useful in diagnosis of pyoderma with glomerulonephritis
Dr.T.V.Rao MD 27 Invasive Group A Streptococcal Infections• Streptococcal toxic shock syndrome • Multi-organ system failure similar to staphylococcal toxic shock • Initial infection may have been pharyngitis, cellulitis, peritonitis, or other wound infections
Dr.T.V.Rao MD 28 Flesh Eating Bacteria• Cellulitis- leading to Necrotising Fasciitis• Leads to necrosis of subcutaneous issues and muscular tissues and adjutant fascia• Other complications Toxic shock syndrome
Dr.T.V.Rao MD 29Invasive Group A Streptococci and “flesh- eating” syndrome or necrotizing fasciitis Caused by virulent strains of Streptococcus pyogenes
Dr.T.V.Rao MD 30 Genital Infection and Streptococcus• Land mark history Semmelweis in 1847 on Puerperal Sepsis• A simple hand washing reduced infections
Dr.T.V.Rao MD 31Group A streptococcal infection and health care Ignaz Philipp Semmelweis (1818-1865) All students or doctors who enter the wards for the purpose of making an examination must wash their hands thoroughly in a solution of chlorinated lime which will be placed in convenient basins near the entrance of the wards. This disinfection will be considered sufficient for this visit. Between examinations the hands must be washed in soap and water. 1847
Dr.T.V.Rao MD 32 Suppurative Conditions• Abscess in the abdomen, Brain Lungs, Liver• Other organs
Dr.T.V.Rao MD 33 Non Suppurative Conditions• Acute Rheumatic Fever• Acute glomerulonephritis• Carditis.• Involvement of Connective tissues of the heart
Dr.T.V.Rao MD 34 Rheumatic Fever• Delayed consequence of an untreated upper respiratory infection with group A streptococci• Causes serious, debilitating damage to the heart.• Associated with large amount of M protein and a capsule• Due to immune response against Strep antigens similar to heart antigens.
Dr.T.V.Rao MD 35Group A Streptococcus infection can lead to Rheumatic Heart Disease
Dr.T.V.Rao MD 36Heart disease due to Rheumatic Fever-group Astreptococcal infection can extend to the heart
Dr.T.V.Rao MD 38 Streptococcus pyogenes Sequellae to strep throat• Heart valve damage (rheumatic heart disease) • < 3% of people with strep throat, weeks after sore throat • migrating arthritis; heart valve damage (50%), some fatal • recurrences common, lifelong penicillin therapy • shared antigen: M protein, cardiac myosin • attack by T cells, Ab: inflammation, valve damage
Dr.T.V.Rao MD 39 Post streptococcal diseases• Rheumatic Fever- autoimmune disease involving heart valves, joints, nervous system. Follows a strep throat• Acute glomerulonephritis or Bright’s Disease- inflammatory disease of renal glomeruli and structures involved in blood filter of kidney. Due to deposition of Ag/Ab complexes
Dr.T.V.Rao MD 40 Rheumatic Fever• Diagnosis is based on symptoms and is difficult• Occurs most frequently between ages of 6 and 15• US it is about 0.05% of pop having strep infections• 100x more frequent in tropical countries
Dr.T.V.Rao MD 41 Is it rheumatic feverSore knees ankles wrists elbowsHeart murmurHard to breathJerking twitching movements ofthe bodyHot personRecent sore throat or skin sores
Dr.T.V.Rao MD 42 Rheumatic Fever• Most common cause of permanent heart valve damage in children• Exact cause not yet known but there appears to be some antibody cross reactivity between the cell wall of S. pyogenes and heart muscle
Dr.T.V.Rao MD 43Post Streptococcal Glomerulonephritis• Follows strep infection of skin or pharynx• Characterized by damage to glomeruli of kidneys• Deposition of Ag-Ab complexes, activation of complement.• Inflammatory response causes damage.
Dr.T.V.Rao MD 44 PSGN: Pathogenesis• The precise nature of the antigensinvolved in the formation of thenephritogenic immune complexes isunknown • Streptococcal antigenic substances have been inconsistently detected in glomeruli and circulating immune complexes have been detected in some patients
Dr.T.V.Rao MD 45 PSGN: Pathogenesis (Contd)• Since streptococcal antigens do not always cause disease, other mechanisms may be involved, including • Alterations in IgG or glomerular components making them immunogenic• Antigens derived from infectious agents may bind to glomerular structures and induce development of in situ immune complexes
Dr.T.V.Rao MD 46 Glomerulonephritis• Diagnosis based on history of Strep throat and clinical findings.• Symptoms include fever, malaise, edema, hypertension and blood or protein in urine• Occurs in 0.5% of those having strep throat.
Dr.T.V.Rao MD 47 Glomerulonephritis. Acute Glomerulonephritis – associated with M types producing URI & skin infections particularly associated with types 12, 4, 2 & 49 which are nephritogenic initiated by ag-ab complexes on the glomerular basement membrane hematuria, proteinuria, edema & hypertension
Dr.T.V.Rao MD 48Streptococcal tests Bacitracin disc test- only Streptococcus pyogenes is sensitive to minute bacitracin conc. Group A streptococci are negative for SXT sensitivity and the CAMP test Rapid, direct test kit for diagnosis of group A infections, throat swab introduced to latex beads and monoclonal antibodies Positive-the C-carbohydrate on group A streptococci causes clumping Negative-milky smooth reaction
Dr.T.V.Rao MD 49 TREATMENT1. Penicillin G – drug of choice2. Erythromycin Antistreptococcal chemoprophylaxis in persons who have suffered an acute attack of rheumatic fever Penicillin G 1.2 M units IM every 3-4 weeks or daily oral penicillin or oral sulfonamide
Dr.T.V.Rao MD 50 Staphylococcus agalactiae: Invasive Infections• Early-onset infection • Occurs in neonates who are less than 7 days old neonates • Vertical transmission of the organism from the mother • Manifests in the form of pneumonia or meningitis with bacteremia • Associated with a high mortality rate
Dr.T.V.Rao MD 51 Staphylococcus agalactiae: Invasive Infections• Late-onset infection • Occurs between 1 week and 3 months after birth • Usually occurs in the meningitis form • Mortality rate is not as high as early-onset• In adults • Occurs in immunosuppressed patients or those with underlying diseases • Often found in a previously healthy adult who just experienced childbirth
Dr.T.V.Rao MD 52 Streptococcus Group D and Enterococcus Species• Members of the gut flora• Associated infections • Bacteremia • Urinary tract infections • Wound infections • Endocarditis
Streptococcus Group D and Enterococcus Species• Microscopic morphology • Cells tend to elongate• Colony morphology • Most are non-hemolytic, although some may show a- or, rarely, b- hemolysis • Possess Group D antigen
Laboratory Diagnosis: Streptococcus Group D and Enterococcus Species• Identification tests • Catalase: may produce a weak catalase reaction • Hydrolyze bile esculin • Differentiate Group D from Enterococcus sp. with 6.5% NaCl or PYR test
Dr.T.V.Rao MD 55 Streptococos mutans• Streptococos mutans was first described by JK Clark in 1924 after he isolated it from a carious lesion but it wasnt until the 1960s that real interest in this microbe was generated when researchers began studying dental caries in ernest. Many strains were isolated which were biochemically very similar but carried different antigenic markers. Altogether, 7 serotypes designated a, b, c, d, e, f and g were described.
Dr.T.V.Rao MD 56 Streptococcus mutans• Streptococcus mutans, inhabits the mouth of all humans. The mouth is populated by great numbers of Streptococci plaques developing on the surfaces of teeth. Teeth contain approximately 10 streptococci per gram wet weight (John, Lewis). This species, Streptococcus mutans, make up thirty to sixty percent of the total bacteria inhabiting the surfaces of human teeth, tongue, cheeks, and in saliva (John, Lewis).
Dr.T.V.Rao MD 57• Programme created by Dr.T.V.Rao MDfor Medical and Paramedical Students in the Developing World • Email • email@example.com