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 David.wininger@osumc.edu

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

Downloaded from: Principles and Practice of Infectious Diseases (on 17 January 2005 06:10 PM)

Downloaded from: Principles and Practice of Infectious Diseases (on 17 January 2005 06:10 PM) © 2004 Elsevier

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

Downloaded from: Principles and Practice of Infectious Diseases (on 17 January 2005 06:09 PM) © 2004 Elsevier

Streptococcus pneumoniae

Gram Stain Laboratory Diagnosis

Gram (+) diplococci “Lancet shaped” Alpha-hemolytic Fastidious nutritional req. Susceptible to optochin Bile soluble

Downloaded from: Principles and Practice of Infectious Diseases (on 17 January 2005 06:11 PM) © 2004 Elsevier

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

Downloaded from: Principles and Practice of Infectious Diseases (on 17 January 2005 06:09 PM) © 2004 Elsevier

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 david.wininger@osumc.edu

• 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.

Survey

We would appreciate your feedback on this module. Click on the button below to complete a brief survey. Your responses and comments will be shared with the module’s author, the LSI EdTech team, and LSI curriculum leaders. We will use your feedback to improve future versions of the module.

The survey is both optional and anonymous and should take less than 5 minutes to complete.

Survey