Infectious Disease and Microbiology – Streptococcus agalactiae (Group B Streptococcus)

Overview

Streptococcus agalactiae, commonly called Group B Streptococcus (GBS), is a Gram-positive coccus and an important cause of neonatal sepsis and meningitis. It commonly colonizes the gastrointestinal and female genital tracts, allowing maternal transmission to the newborn around the time of delivery.

GBS is also an important cause of urinary tract infection, bacteriuria, chorioamnionitis, and postpartum endometritis in pregnant patients. In addition, invasive GBS disease is increasingly recognized in nonpregnant adults, particularly older adults and those with significant underlying illnesses.

Classification

Genus: Streptococcus

Species: Streptococcus agalactiae

Lancefield group: Group B

Common abbreviation:

GBS

Microbiologic Characteristics

S. agalactiae is a:

• Gram-positive coccus

• Facultatively anaerobic organism

• Catalase-negative bacterium

• Usually β-hemolytic

• Organism arranged in chains or pairs

• Encapsulated bacterium

The polysaccharide capsule is an important:

Virulence factor

because it helps the organism resist:

Phagocytosis and host immune clearance

High-Yield Microbiology Pattern

Gram-positive cocci in chains

• ●

Catalase negative

• ●

β-hemolytic

• ●

Group B

→ Think Streptococcus agalactiae

Laboratory Identification

Classic laboratory characteristics include:

CAMP positive

and:

Hippurate positive

S. agalactiae is also classically resistant to:

Bacitracin

which helps distinguish it from Group A Streptococcus in traditional laboratory identification.

CAMP Test

The:

CAMP TEST

is a classic microbiology examination clue for GBS.

S. agalactiae produces CAMP factor, which enhances the hemolysis produced by Staphylococcus aureus.

Therefore:

CAMP-positive β-hemolytic Streptococcus

→ S. agalactiae

Epidemiology

S. agalactiae has a:

Worldwide distribution

The organism commonly colonizes the:

• Gastrointestinal tract

• Rectum

• Vagina

• Genitourinary tract

Colonization is frequently:

Asymptomatic

Maternal Colonization

Maternal rectovaginal colonization is particularly important because the organism can be transmitted to the infant:

During labor and delivery

This provides the major pathway leading to:

Early-onset neonatal GBS disease

Neonatal Group B Streptococcal Disease

GBS is a major cause of serious bacterial infection in:

NEWBORNS

Neonatal disease is traditionally divided into:

Early-onset disease

and

Late-onset disease

Early-Onset Neonatal Disease

Early-onset disease develops during approximately the:

First 6 days of life

and often begins within the:

First 24 hours after birth

The major mechanism is:

Maternal colonization

↓

Exposure during labor/delivery

↓

Neonatal colonization

↓

Invasive infection

Early-Onset Clinical Manifestations

The major manifestations include:

• Sepsis

• Pneumonia

• Respiratory distress

• Bacteremia

• Meningitis

Sepsis and pneumonia are particularly characteristic of:

Early-onset disease

High-Yield Early-Onset Pattern

Newborn

• ●

First hours/days of life

• ●

Respiratory distress

• ●

Sepsis ± pneumonia

• ●

Maternal GBS colonization

→ Think S. agalactiae

Risk Factors for Early-Onset Disease

Important risk factors include:

• Maternal GBS colonization

• Previous infant with invasive GBS disease

• GBS bacteriuria during pregnancy

• Preterm delivery

• Prolonged rupture of membranes

• Maternal intrapartum fever

These factors increase the probability of:

Vertical transmission and neonatal invasive disease

Late-Onset Neonatal Disease

Late-onset GBS disease generally occurs after the first several days of life and during the:

First few months of infancy

Unlike early disease, transmission may be:

Maternal or environmental

Late-Onset Clinical Manifestations

An especially important manifestation is:

MENINGITIS

Late-onset disease may also cause:

• Bacteremia

• Sepsis

• Bone and joint infection

• Other focal infections

High-Yield Neonatal Distinction

Early-onset GBS

Birth–6 days

→ Maternal vertical transmission

→ Sepsis + pneumonia

Late-onset GBS

After the first week into early infancy

→ Meningitis particularly important

Meningitis

S. agalactiae is an important cause of:

Neonatal bacterial meningitis

Possible manifestations include:

• Fever or temperature instability

• Poor feeding

• Lethargy

• Irritability

• Apnea

• Seizures

• Bulging fontanelle

Neonatal meningitis may lack the classic findings seen in older children and adults.

Infection During Pregnancy

GBS can cause infections involving the:

Urinary and genital tracts

during pregnancy.

Important manifestations include:

• Asymptomatic bacteriuria

• Cystitis

• Pyelonephritis

• Chorioamnionitis

• Endometritis

GBS Bacteriuria During Pregnancy

Detection of:

GBS in the urine during pregnancy

is clinically important because it suggests substantial maternal colonization and is associated with increased neonatal transmission risk.

Postpartum Endometritis

GBS may contribute to:

Postpartum uterine infection

Clinical manifestations can include:

• Fever

• Lower abdominal or uterine tenderness

• Abnormal postpartum discharge

• Systemic illness

Adult Group B Streptococcal Disease

GBS is not exclusively a neonatal pathogen.

The source emphasizes increasing recognition of infection in:

Men and nonpregnant women

Invasive Disease in Nonpregnant Adults

GBS can cause:

• Bacteremia

• Sepsis

• Skin and soft-tissue infection

• Pneumonia

• Urinary tract infection

• Osteomyelitis

• Septic arthritis

• Endocarditis

Invasive disease is particularly important among:

Older adults and medically vulnerable patients

High-Yield Adult Pattern

Older or medically complex adult

• ●

Bacteremia, cellulitis, UTI, or osteoarticular infection

• ●

Group B Streptococcus

→ S. agalactiae can be a true invasive pathogen

Diagnosis

The primary diagnostic method is:

CULTURE

Appropriate specimens depend on the clinical syndrome and include:

• Blood

• CSF

• Urine

• Genital specimens

• Other normally sterile fluids

Antigen Detection

The source also describes:

Antigen detection techniques

in body fluids, including:

CSF

as potential diagnostic methods.

In contemporary practice, culture and molecular methods are generally more important for establishing invasive infection.

Maternal Screening

An important preventive strategy is:

Screening pregnant patients for GBS colonization late in pregnancy

using appropriate vaginal and rectal specimens.

The purpose is to identify patients who should receive:

Intrapartum antibiotic prophylaxis

to prevent early-onset neonatal disease.

Treatment

The source identifies:

PENICILLIN G

or:

AMPICILLIN

as primary treatment options.

GBS has traditionally remained highly susceptible to:

β-lactam antibiotics

making penicillin the classic drug of choice.

Neonatal Empiric Therapy

When serious neonatal infection is suspected before the organism is known, empiric treatment commonly needs to cover several neonatal pathogens.

A classic empiric combination is:

Ampicillin + an aminoglycoside such as gentamicin

with the final regimen adjusted once culture results identify the pathogen and infection site.

Additional Treatment

The source lists:

Macrolide antibiotics

as additional therapy.

However, macrolide resistance can occur in GBS.

Therefore, macrolides should not automatically be assumed to be active without:

Susceptibility information

when they are being considered for treatment.

Prevention of Neonatal Disease

One of the most important aspects of GBS management is:

INTRAPARTUM ANTIBIOTIC PROPHYLAXIS

Eligible colonized pregnant patients receive antibiotics:

During labor

to reduce neonatal exposure to the organism.

Why Intrapartum Prophylaxis Works

Maternal GBS colonization

↓

Antibiotic administered during labor

↓

Reduced maternal genital bacterial burden

↓

Reduced neonatal exposure

↓

Reduced:

EARLY-ONSET GBS DISEASE

Important Prevention Pearl

Intrapartum prophylaxis is particularly effective against:

Early-onset neonatal GBS disease

It does not provide equivalent prevention of:

Late-onset disease

Streptococcus agalactiae vs. Streptococcus pyogenes

Both are:

β-hemolytic streptococci

but they belong to different Lancefield groups.

S. agalactiae

→ Group B

→ CAMP positive

→ Bacitracin resistant

→ Neonatal sepsis/meningitis

→ Maternal genital colonization

S. pyogenes

→ Group A

→ CAMP negative

→ Classically bacitracin susceptible

→ Pharyngitis, impetigo, cellulitis, scarlet fever, rheumatic fever

High-Yield Comparison

Group A

→ S. pyogenes

Group B

→ S. agalactiae

Streptococcus agalactiae vs. Listeria monocytogenes

Both are important causes of:

Neonatal sepsis and meningitis

However:

S. agalactiae

→ Gram-positive coccus

→ Group B Streptococcus

→ CAMP positive

→ Maternal genital colonization

Listeria monocytogenes

→ Gram-positive bacillus

→ Intracellular organism

→ Tumbling motility

→ Associated with pregnancy, neonates, older adults, and impaired cellular immunity

Prevention

Important preventive measures include:

• Maternal GBS screening

• Appropriate intrapartum antibiotic prophylaxis

• Recognition of GBS bacteriuria during pregnancy

• Recognition of previous neonatal invasive GBS disease

• Prompt evaluation of symptomatic newborns

High-Yield Clinical Pattern

Pregnant patient

• ●

Rectovaginal GBS colonization

↓

Transmission during delivery

↓

Newborn develops sepsis/pneumonia during first days of life

→ Think STREPTOCOCCUS AGALACTIAE

High-Yield Microbiology Pattern

β-hemolytic GPC

• ●

Catalase negative

• ●

CAMP positive

• ●

Group B

• ●

Neonatal sepsis/meningitis

→ S. AGALACTIAE

Exam Essentials

Genus: Streptococcus

Species: S. agalactiae

Lancefield group: B

Common name: Group B Streptococcus (GBS)

Organism: Gram-positive coccus

Arrangement: Chains or pairs

Catalase: Negative

Hemolysis: Usually β-hemolytic

CAMP test: Positive

Hippurate: Positive

Classic bacitracin pattern: Resistant

Distribution: Worldwide

Reservoir: Gastrointestinal and female genital tracts

Early-onset disease: First 0–6 days of life

Major early-onset manifestations: Sepsis and pneumonia, with meningitis possible

Important late-onset manifestation: Meningitis

Maternal disease: UTI/bacteriuria, chorioamnionitis, and endometritis

Adult disease: Increasingly important cause of invasive infection in nonpregnant adults

Diagnosis: Culture

Classic treatment: Penicillin G or ampicillin

Prevention: Maternal screening + intrapartum antibiotic prophylaxis

Memory Aid

GROUP B = BABY

B = Baby

B = Birth transmission

B = Bacteremia

B = Brain infection (meningitis)

And:

CAMP = Group B

CAMP-positive β-hemolytic Streptococcus

→ Think S. agalactiae

Key clinical pearl: Streptococcus agalactiae is Group B Streptococcus, a CAMP-positive, usually β-hemolytic Gram-positive coccus that colonizes the maternal gastrointestinal and genital tracts. Its classic clinical importance is vertical transmission during delivery, producing early-onset neonatal sepsis and pneumonia and potentially meningitis. Maternal screening and appropriate intrapartum antibiotic prophylaxis are central to preventing early-onset neonatal GBS disease, while penicillin or ampicillin remains the classic definitive therapy for susceptible invasive infection.