Streptococci & Enterococci
David A. Wininger, MD
Internal Medicine Residency Program Director
Associate Professor, Clinical Internal Medicine
Division of Infectious Diseases
The Ohio State University Wexner Medical Center
614-293-3989
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
Gram Stain
 Catalase negative
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
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© 2004 Elsevier
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
Scarlet Fever
(Group A Strep strains producing SPE)
Strawberry Tongue
Desquamation
(recovery phase)
Group A Streptococci – Clinical Syndromes
Impetigo
Erysipelas
CDC/Dr. Thomas F. Sellers/Emory
University
Cellulitis
Group A Streptococci – Clinical Syndromes
Rheumatic Fever & Rheumatic Carditis
(Non-suppurative, post-streptococcal)
Valvulitis (Mitral valve)
Erythema marginatum
Group A Streptococci – Clinical Syndromes
Acute 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
Streptococcus pneumoniae
Gram Stain
 Laboratory Diagnosis






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Gram (+) diplococci
“Lancet shaped”
Alpha-hemolytic
Fastidious nutritional req.
Susceptible to optochin
Bile soluble
© 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





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Surface adhesins
Pneumolysin (cytotoxin)
sIgA Protease
Teichoic Acid
H2O2
© 2004 Elsevier
S. pneumoniae – Clinical Syndromes
Pneumococcal Pneumonia
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© 2004 Elsevier
S. pneumoniae – Clinical Syndromes
Lung Tissue
No Pneumonia
Acute Pneumococcal
Pneumonia
Acute Left
Maxillary Sinusitis
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
Gram Stain
 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
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
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.
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