8 Gram-positive cocci.pdf

GRAM-POSITIVE COCCI Henson B. Turalde, RPh, LPT OUTLINE Staphylococci Streptococci Enterococci PROPERTY Staphylococcus Streptococcus Enterococcus Arrangement Clusters Chains Chains Catalase +...

GRAM-POSITIVE COCCI Henson B. Turalde, RPh, LPT OUTLINE Staphylococci Streptococci Enterococci PROPERTY Staphylococcus Streptococcus Enterococcus Arrangement Clusters Chains Chains Catalase + - - ARRANGEMENT CATALASE TEST  Gram-Positive Cocci Catalase test Catalase Positive Catalase Negative Staphylococcus Streptococcus STAPHYLOCOCCI STAPHYLOCOCCI gram-positive spherical cells arranged in grapelike irregular clusters aerobic or microaerophilic produce catalase, which converts H2O2 to H2O and O2 slowly ferment many carbohydrates, producing lactic acid but not gas relatively resistant to drying, heat (withstand 50°C for 30 minutes), and 10% NaCl STAPHYLOCOCCI Staphylococcus aureus Staphylococcus epidermidis Staphylococcus saprophyticus STAPHYLOCOCCI PROPERTY S. aureus S. epidermidis S. saprophyticus BAP hemolysis β γ γ Coagulase + - - MSA fermentation + - +/- Novobiocin S S R BLOOD AGAR PLATE COAGULASE TEST MANNITOL-SALT AGAR  Gram-Positive Cocci Catalase test Catalase Positive Catalase Negative Staphylococcus Streptococcus Coagulase Test Mannitol Salt Agar (MSA)  POSITIVE: Staphylococcus aureus MSA: golden yellow colonies S. aureus Enzymes Coagulase clots oxalated or citrated plasma binds to prothrombin to enzymatically activate and initiate fibrin polymerization alters ingestion by phagocytic cells or their destruction Clumping Factor adheres organism to fibrinogen and fibrin S. aureus Toxins Hemolysins lyse many cells e.g., RBCs and WBCs creates pores that cause release of inflammatory mediators e.g., IL-8, leukotriene, and histamine, which are responsible for necrosis and severe inflammation Exfoliative Toxins superantigens produce the generalized desquamation of staphylococcal scalded skin syndrome by dissolving the mucopolysaccharide matrix of the epidermis S. aureus Toxins Toxic Shock Syndrome Toxin-1 (TSST-1) a superantigen binds to MHCII molecules, resulting in T-cell stimulation, which promotes the manifestations of toxic shock syndrome (fever, shock, desquamative skin rash) Enterotoxins heat stable and resistant to gut enzymes causes food poisoning S. aureus Transmission members of the normal microbiota of skin and respiratory tract and GIT nasal carriage of S. aureus occurs in 20–50% of humans direct and indirect contact S. aureus Clinical Findings Furuncle/Carbuncle Impetigo/Pyoderma Bacteremia Food Poisoning Toxic Shock Syndrome Scalded Syndrome Furuncle/Carbuncle localized abscess Groups of S. aureus established in a hair follicle lead to tissue necrosis. Coagulase coagulates fibrin, resulting in wall formation. Within the center of the lesion, liquefaction occurs (enhanced by delayed hypersensitivity). Impetigo/Pyoderma local infection of superficial layers of skin, especially in children superficial vesicles → pustules → erosions covered with pus → yellow- brown honey-colored crust highly communicable, especially in hot, humid climates Bacteremia suppuration (abscess) occurs in other parts causing: Endocarditis Osteomyelitis – suppuration in blood vessels of the metaphysis of a long bone Meningitis Pneumonia Food Poisoning Inc. period: 1-8 hrs N/V, diarrhea, (-) fever Toxic Shock Syndrome abrubt onset of high fever, vomiting, diarrhea, myalgia, scarlatiniform rash, and hypotension with cardiac and renal failure in most severe cases often w/n 5 days after the onset of menses in young women who use high-absorbency tampons  Scalded Skin Syndrome redness and tenderness of the central face, neck, trunk, and intertriginous zones short-lived flaccid bullae and exfoliation of superficial epidermis (+) Nikolsky Sign crusted areas around mouth in a radial pattern S. aureus Treatment Furuncles/Carbuncles Antisepsis Drainage Bacteremia and Dissemination IV β-lactamase-resistant (antistaphylococcal) penicillins MRSA: vancomycin VRSA: linezolid, streptogramins  S. Aureus Antibiotic Resistance β-lactamase hydrolyzes β-lactam antibiotics give β-lactamase resistant penicillins (e.g. nafcillin, methicillin, oxacillin) mecA gene resistance to β-lactamase resistant penicillins due to low affinity PBPs: methicillin-resistant S. aureus (MRSA) give vancomycin  POSITIVE: Staphylococcus aureus MSA: golden yellow colonies  Coagulase Test Mannitol Salt Agar (MSA) NEGATIVE MSA: porcelain Novobiocin MSA: colorless white colonies colonies SENSITIVE: RESISTANT: Staphylococcus Staphylococcus epidermidis saprophyticus S. epidermidis causes 75% of coagulase-negative staphylococcal infections part of the normal flora of the skin, respiratory tract, and GIT causes disease in immunocompromised patients infects orthopedic and cardiovascular prosthetic devices S. saprophyticus part of the normal flora of the skin, respiratory tract, and GIT relatively common cause of UTIs in young women  Gram-Positive Cocci Catalase test Catalase Positive Catalase Negative Staphylococcus Streptococcus STREPTOCOCCI STREPTOCOCCI gram-positive spherical cells arranged in pairs or chains mostly facultative anaerobes do not produce catalase  STREPTOCOCCI Viridans Enterococcus PROPERTY S. pyogenes S. agalactiae S. pneumoniae streptococci sp. Lancefield Group A B Non-groupable Heterogenous D BAP Hemolysis β β ɑ ɑ γ LANCEFIELD GROUPING based on Lancefield antigens (carbohydrates) present in the cell wall groups A-H and K-U Determined by an amino sugar: Group A - N-acetylglucosamine Group B - rhamnose-glucosamine Group C - rhamnose-N-acetylgalactosamine Group D - glycerol teichoic acid containing D-alanine and glucose Group F - glucopyranosyl-N-acetylgalactosamine  Gram-Positive Cocci Catalase test Catalase Positive Catalase Negative Staphylococcus Streptococcus Blood Agar Plate  α-hemolytic Quellung Reaction German word for “swelling” Optochin sensitivity Antibodies bind to bacterial capsule to make it more opaque Quellung reaction SENSITIVE: RESISTANT: Streptococcus Viridans pneumoniae Streptococci  S. pneumoniae a.k.a. pneumococci diplococci or streptococci, lancet shaped has polysaccharide capsule normal flora of the upper respiratory tract of 5–40% of humans can cause pneumonia, sinusitis, otitis, bronchitis, bacteremia, meningitis, & peritonitis S. pneumoniae Capsule 91 types major virulence factor Diagnosis: Quellung Reaction (VR: capsular swelling) S. pneumoniae Epidemiology most common cause of: Community-Acquired Pneumonia Otitis Media Acute Sinusitis Bacterial Meningitis S. pneumoniae Clinical Findings Community-acquired pneumonia sudden onset fever, chills, and sharp pleural pain, bloody or rusty colored sputum Bacteremia from pneumonia → triad of: Meningitis Endocarditis Septic arthritis S. pneumoniae Treatment parenteral β-lactams Ampicillin Cefotaxime Ceftriaxone Cefuroxime S. pneumoniae Prevention Pneumococcal polysaccharide vaccine containing 23 types (PPSV23) Pneumococcal conjugated vaccine containing 13 types (PCV13)  Viridans Streptococci the most prevalent members of the normal microbiota of the upper respiratory tract important for the healthy state of the mucous membranes optochin-resistant not soluble in bile (deoxycholate) may reach the bloodstream as a result of trauma principal cause of endocarditis on abnormal heart valves S. mitis S. anginosus S. mutans S. salivarius S. bovis group group group group group Viridans Streptococci Dental Caries due to large polysaccharides (e.g., dextrans or levans, from sucrose) synthesized by S. mutans Acute Endocarditis rapid destruction of the valves leads to fatal cardiac failure in days-weeks unless surgery is performed to place a prosthetic valve during antimicrobial treatment or following therapy Subacute Endocarditis slowly progressive often involves abnormal valves (congenital deformities and rheumatic or atherosclerotic lesions) most frequently caused by Viridans streptococci vegetations consist of fibrin, platelets, blood cells, and bacteria fever, anemia, weakness, heart murmur, embolic phenomena, enlarged spleen, and renal lesions occurs in ≥30% dental extraction patients invariably fatal in untreated cases  α-hemolytic Optochin sensitivity Quellung reaction SENSITIVE: RESISTANT: Streptococcus Viridans pneumoniae Streptococci  Blood Agar Plate β-hemolytic Bacitracin Sensitivity GABHS GBS SENSITIVE: 12 RESISTANT: Streptococcus Streptococcus pyogenes agalactiae S. pyogenes Antigenic Structure M Protein major virulence factor filamentous structure anchored to the cell membrane that penetrates and projects from the cell wall resist phagocytosis by PMNs by inhibiting the alternative complement pathway basis of immunity to GABHS (due to antibodies to M protein) >150 types (can have repetitive infection) induce antibodies that react with human cardiac sarcolemma S. pyogenes Enzymes Streptokinase (Fibrinolysin) transforms plasminogen into plasmin, which digests fibrin, allowing bacteria to escape from blood clots given IV for treatment of pulmonary emboli, coronary artery thrombosis, and venous thrombosis Deoxyribonuclease (DNAse) degrades DNA liquefies pus, allowing the bacteria to spread used in enzymatic debridement Hyaluronidase hydrolyzes hyaluronic acid, a component of ground substance in ECM of CT aids in spreading S. pyogenes Toxins Pyrogenic Exotoxins (Erythrogenic Toxins) superantigens associated with streptococcal toxic shock syndrome and scarlet fever Hemolysins streptolysin O – induces antistreptolysin O (ASO) production streptolysin S – responsible for β-hemolysis on BAP; not antigenic  S. pyogenes Clinical Findings Poststreptococcal Invasion Local Infection Systemic Infection Diseases Erysipelas Streptococcal Streptococcal Toxic Rheumatic Fever Cellulitis Pharyngitis Shock Syndrome Acute Necrotizing Fasciitis Impetigo/ Scarlet Fever Glomerulonephritis (Streptococcal Streptococcal Gangrene) Pyoderma Puerperal Fever Bacteremia/Sepsis Erysipelas portal of entry: skin raised, red lesions brawny edema and a rapidly advancing, sharply demarcated margin Cellulitis portal of entry: parenteral (mild trauma, burns, wounds, or surgical incisions) acute, rapidly spreading infection of the skin and subcutaneous tissues pain, tenderness, swelling, and erythema Necrotizing Fasciitis (Streptococcal Gangrene) portal of entry: parenteral “flesh eating disease” extensive and very rapidly spreading necrosis of the skin, tissues, and fascia Puerperal Fever portal of entry: uterus After delivery, puerperal fever develops, which is a septicemia originating in the infected wound (endometritis). Bacteremia/Sepsis portal of entry: parenteral (traumatic or surgical wounds) can be rapidly fatal Streptococcal Pharyngitis most common infection caused S. pyogenes adherence to pharyngeal epithelium via lipoteichoic acid (on pili) binding to fibronectin (on epithelial cells) Streptococcal Pharyngitis Infants and Small Children: subacute nasopharyngitis (weeks) thin serous discharge, little fever, tendency to extend to the middle ear and the mastoid enlarged cervical lymph nodes Older Children and Adults: acute, intense nasopharyngitis, tonsillitis, intense redness and edema purulent exudate, high fever enlarged, tender cervical lymph nodes Streptococcal TSS shock, bacteremia, respiratory failure, and multiorgan failure death in ≈30% tend to occur after minor trauma in otherwise healthy persons with several presentations of soft tissue infection Scarlet Fever associated with pharyngitis or with skin or soft tissue infection strawberry tongue and bright red, sandpaper rash clinically overlapping w/ streptococcal TSS Poststreptococcal Diseases autoimmune disorders After an acute S. pyogenes infection, there is a latent period of 1–4 weeks (mean 7 days), after which poststreptococcal glomerulonephritis (PSGN) or rheumatic fever (RF) occasionally develops. Glomerulonephritis is more commonly preceded by skin infection. Rheumatic fever is more commonly preceded by pharyngitis. Rheumatic Fever most serious sequela of S. pyogenes mainly a disease of children 5–14 years often preceded by S. pyogenes pharyngitis 1–5 weeks (mean 19 days) M types 1, 3, 5, 6, and 18 – more frequently involved higher chance with more severe streptococcal sore throats marked tendency to be reactivated by recurrent streptococcal infections S. pyogenes Treatment Penicillin G Poststreptococcal Glomerulonephritis develops 1–5 weeks (mean 7 days) after S. pyogenes skin infection (pyoderma, impetigo) or pharyngitis initiated by antigen—antibody complexes on the glomerular basement membrane hematuria, proteinuria, edema, high blood pressure, and urea nitrogen retention, low serum complement majority recovers few patients die some develop chronic glomerulonephritis with kidney failure S. agalactiae part of the normal vaginal flora and lower GIT in 5–30% of women Neonatal Sepsis: infection during the 1st month; may present as fulminant sepsis, meningitis, or respiratory distress syndrome increasing infections in elderly adults and immunocompromised hosts Prevention: screening pregnant women at 35–37 weeks of pregnancy (rectal and vaginal swabs) IV ampicillin  Blood Agar Plate β-hemolytic Bacitracin Sensitivity GABHS GBS SENSITIVE: RESISTANT: Streptococcus Streptococcus pyogenes agalactiae  γ-hemolytic 6.5% NaCl POSITIVE: NEGATIVE: Enterococcus sp. Streptococcus bovis ENTEROCOCCI Enterococci previously classified as group D streptococci commensal bacteria of the normal enteric microbiota infections arise via translocation from the GIT most common causes of infection: Enterococcus faecalis (85-90%) Enterococcus faecium (5-10%) among the most frequent causes of health care–associated infections: urinary tract wounds biliary tract blood Treatment frequently resistant to various antibiotics (E. faecium > E. faecalis) first-line: cell-wall active antibiotic (eg, ampicillin or vancomycin) + aminoglycoside for VREF: linezolid, quinupristin–dalfopristin, daptomycin  critical multidrug-resistant bacteria ESKAPE Pathogens leading cause of HAIs Enterococcus faecium Staphylococcus aureus Klebsiella pneumoniae Acinetobacter baumannii Pseudomonas aeruginosa Enterobacter sp