Streptococci & Enterococci
David A. Wininger, MDInternal Medicine Residency Program Director Associate Professor, Clinical Internal Medicine Division of Infectious DiseasesThe Ohio State University Wexner Medical Center614-293-3989 [email protected]
Learning Objectives
Recognize the structure and microbial physiology of Streptococci and Enterococci and integrate this information with the human pathophysiologic correlates Define the structure and composition of Streptcocci and Enterococci
Recognize the underlying genetic mechanisms of antibacterial resistance in Streptococci and Enterococci
Describe the nature and mechanisms of action of Streptococcal and Enterococcal virulence factors
Identify the normal human immune response to Streptococcal and Enterococcal infections
Learning Objectives
Recognize the epidemiology and ecology of Streptococcal and Enterococcal infections
Describe and differentiate the principles of laboratory diagnosis for Streptococcal and Enterococcal infections
Define the principles of infection prevention for Streptococcal and Enterococcal infections
Recognize treatment options and accurately evaluate their role in the therapy of infections due to Streptococci and Enterococci
Streptococci
Catalase negative
Gram Stain
Classification of Streptococci
Hemolytic pattern Alpha
Beta
Gamma
(On sheep blood agar)
Lancefield Groups: Cell wall carbohydrates by serologic tests Groups A-H, K-M, O-V
Biochemical properties – see discussion by species
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Group A Streptococci (S. pyogenes)
Sheep Blood Agar Plate
Beta hemolysis
Bacitracin inhibits growth
PYR positive
Group A Streptococci – Structure & Virulence Factors
• M-protein
• Lipoteichoic acid
• F-protein
• Capsule
Group A Streptococci – Virulence Factors
Toxins Pyrogenic exotoxins (SpeA, SpeB, SpeC, SpeF)
Super-antigens
Streptococcal Toxic Shock Syndrome, Scarlet Fever
Enzymes Streptolysin S Lyses red blood cells
Streptolysin O Basis of ASO test
Streptokinases Lyses clots
DNases Thins out pus
C5a peptidase Block chemotaxis
Group A Streptococci – Clinical Syndromes
Acute Streptococcal Pharyngitis (“Strep Throat”)
Group A Streptococci – Clinical Syndromes
Strawberry Tongue Desquamation(recovery phase)
Scarlet Fever(Group A Strep strains producing SPE)
Group A Streptococci – Clinical Syndromes
Impetigo Erysipelas Cellulitis
CDC/Dr. Thomas F. Sellers/Emory University
Group A Streptococci – Clinical Syndromes
Valvulitis (Mitral valve)
Erythema marginatum
Rheumatic Fever & Rheumatic Carditis(Non-suppurative, post-streptococcal)
Group A Streptococci – Clinical SyndromesAcute Post-Streptococcal
Glomerulonephritis (APSGN)
Post-Streptococcal Non-Suppurative Complications
Rheumatic Fever Mostly strep throat M-types
Acute Post-Streptococcal Glomerulonephritis (APSGN) Some after dermal infection
Rationale for finishing full antibiotic course Penicillin G works in preventing Rheumatic Fever, BUT NOT
APSGN
Group B Streptococci (S. agalactiae)
Laboratory Diagnosis: Culture shows a Beta-hemolytic Streptococci expressing “Group B” cell wall carbohydrate. Requires enriched media for optimal growth.
Main Virulence factor: Capsule that prevents phagocytosis
Epidemiology and Ecology: GI & GU tract colonization
Vulnerable populations: Neonates, colonized women post-partum, older patients with cancer or diabetes
Treatment: Easily treated with penicillins (i.e. Penicillin G, Ampicillin)
Cephalosporins or Vancomycin for penicillin-allergic patients
Group B Streptococci – Clinical Syndromes
Clinical Disease in Peri-partum Period Neonatal sepsis (early and late)
Neonatal meningitis
Post-partum sepsis
Prevention of Peri-partum Infections Pre-partum vaginal screening cultures
Carriers receive antibiotics in labor
Prophylaxis has reduced neonatal sepsis rates
No vaccine is available
Group B Streptococci – Clinical Syndromes
Non-pregnant Adults Urinary tract infections
Bacteremia and sepsis
Soft tissue infections
Musculoskeletal infections
Mainly in patients compromised by: Age
Diabetes mellitus
Cancer
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Streptococcus pneumoniae
Gram Stain Laboratory Diagnosis
Gram (+) diplococci “Lancet shaped” Alpha-hemolytic Fastidious nutritional req. Susceptible to optochin Bile soluble
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S. pneumoniae – Structure & Virulence Factors
Capsule Key virulence factor Anti-phagocytic For sero-typing Basis for vaccination Rough strains (avirulent)
Other Virulence Factors Surface adhesins Pneumolysin (cytotoxin) sIgA Protease Teichoic Acid H2O2
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S. pneumoniae – Clinical Syndromes
Pneumococcal Pneumonia
S. pneumoniae – Clinical SyndromesLung Tissue
Acute Left Maxillary Sinusitis
No Pneumonia Acute Pneumococcal Pneumonia
S. pneumoniae – Clinical Syndromes
Other associated infections Acute Otitis Media
Acute Bacterial Meningitis
Bacteremia (with pneumonia or meningitis)
Pneumococcal sepsis
CDC
S. pneumoniae – Treatment & Antibacterial Resistance Historically highly susceptible to penicillins
Increasing rates of penicillin resistance due to altered penicillin binding proteins (PBPs). Serious disease Need susceptibilities to rule out penicillin resistance
Primary empiric treatment usually consists of a 3rd Generation Cephalosporin (i.e. Ceftriaxone, Cefotaxime)
Alternative treatments include: Vancomycin
“Respiratory” (anti-pneumococcal) Fluroquinolones (i.e. Moxifloxacin, Levofloxacin)
S. Pneumoniae – Normal Human Immune Response & Prevention
Humoral immunity is key
Anticapsular antibodies are protective Basis for vaccination
Asplenics are at increased risk for serious sepsis!!!
Vaccinate patients prior to elective splenectomy
23-valent vs. 13-valent conjugate vaccine
Acute inflammatory response during disease Neutrophils
Viridans Streptococci
A heterogeneous group (not a single species) Often alpha hemolytic (“Viridis” – Green)
S. mitior, S. mutans, and numerous others
S. bovis bloodstream infections occult colon cancer!!
Laboratory Diagnosis Culture “Viridans”- grouping is often enough
Speciation Biochemicals and Mass Spectroscopy
Epidemiology/Ecology Normal flora or colonizers of oral, GI and GU tracts
Viridans streptococci
Clinical Syndromes Endocarditis, bacteremia, dental abscess and intra-abdominal abscess.
(No noteworthy virulence factors)
Normal Human Immune Response/Prevention Ubiquitous organisms that take advantage of breaks in normal mucosal
surfaces, triumphing due to sheer numbers and structural defects of the host (bad teeth, abnormal heart valves, prosthetic materials) but can be cleared with acute inflammation (neutrophils)
Treatment Often penicillin susceptible, but resistance happens; can add
aminoglycoside (for synergy) or use vancomycin while awaiting MIC’s.
Enterococci E. faecalis and E. faecium
Most common pathogenic species
Laboratory Diagnosis Group D “strep”
Usually alpha hemolytic (can vary!)
Hardy: grows in wide temp range, pH range, salt concentrations, bile salts, aerobic and anaerobic conditions
PYR positive
Catalase negative
Gram Stain
Enterococci
Ecology and Epidemiology Fecal flora (GI tract) and can colonize GU tract Overgrow when antibiotics eliminate other endogenous flora Spreads patient to patient
Virulence Factors Adherence and biofilm formation (pili, surface proteins, etc.)
Clinical Syndromes Urinary Tract Infections Bacterial endocarditis and other bacteremias Abdominal wounds and intra-abdominal infections
Enterococci – Antibacterial Resistance & Treatment
Inherent resistance to some classes (i.e. cephalosporins)
Intrinsic decreased susceptibility to others (i.e. penicillins)
Multidrug resistance, including to Vancomycin (VRE)
Most commonly seen in E. faecium strains
Treatment depends on susceptibility
Penicillin G or Ampicillin
Vancomycin
Synergy with aminoglycosides (i.e. Gentamicin, Streptomycin)
VRE – Mechanism of Resistance
Vancomycin Resistant Enterococci (VRE)
Antimicrobial Treatment Options Linezolid Daptomycin Tigecycline Quinupristin/Dalfopristin
Infection Control Precautions Minimize antibiotic “pressure” Contact isolation precautions
Summary – Streptococci & Enterococci
Gram positive cocci in pairs or chains
Targeted sites of infection depending on the species
Pathogenesis merger of the sites of initial contact or colonization and the virulence features of the species
Diagnosis based on Gram stain morphology, hemolysis pattern on Sheep Blood Agar and presence or absence of characteristic cell wall carbohydrates
Penicillin optimal treatment for a subset of the strep species
Enterococci Restricted antimicrobial treatment options
Streptococci and Enterococci Quiz
Thank you for completing this module
• If you have any questions, write to me at [email protected]
• Phone messages can be left at 614-293-3989.
David Wininger, MD
References
Medical Microbiology, 7th Ed. Murray, Rosenthal & Pfaller; Chapter 19, pages 188-204; Chapter 20, pages 205-208.
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