Author: Brian Holtry

Early-onset group B streptococcal neonatal infection has three major clinical expressions: bacteremia with no identifiable focus of infection, pneumonia, and meningitis (Box 1). Signs and symptoms of early-onset group B streptococcal neonatal infection include lethargy, poor feeding, jaundice, abnormal temperature, grunting respirations, pallor, and hypotension.

Viridans streptococci are part of the normal microbial flora of humans and animals and are indigenous to the upper respiratory tract, the female genital tract, all regions of the gastrointestinal tract, and, most significantly, the oral cavity. Clinically significant species that are currently recognized as belonging to the viridans group of streptococci include Streptococcus anginosus S constellatus, S cristatus, S gordonii, S intermedius, S oralis, S mitis, S mutans, S cricettus, S rattis, S parasanguis, S salivarius, S thermophilus, S sanguinis, S sobrinus, and S vestibularis. Detailed studies of the ecology of strains in the oral cavity and oropharynx have been performed.

Viridans streptococci have a strong association with bacterial endocarditis (see site) (Box 1). A defectiva and A adjacens were once an important cause of culture-negative endocarditis. However, current laboratory media and techniques enable these “nutritionally variant streptococci” to be identified more readily.

Enterococci are able to grow and survive under harsh conditions and can be found in soil, food, water, and a wide variety of animals. The major habitat of these organisms is the gastrointestinal tract of humans and other animals, where they make up a significant portion of the normal gut flora. Most enterococci isolated from human stools are E faecalis, although E faecium are also commonly found in the human gastrointestinal tract. Small numbers of enterococci are occasionally found in oropharyngeal and vaginal secretions and on the skin, especially in the perineal area.

Urinary tract infections, including uncomplicated cystitis, pyelonephritis, prostatitis, and perinephric abscess, are the most common type of clinical infections produced by enterococci (Box 1). Most enterococcal urinary tract infections are nosocomial and are associated with urinary catheterization or instrumentation. Nosocomial enterococcal bacteremias are commonly polymicrobial. Portals of entry for enterococcal bacteremia include the urinary tract, intra-abdominal or pelvic sources, wounds (especially burns, decubitus ulcers, and diabetic foot infections), intravascular catheters, and the biliary tree.

Streptococcus pyogenes is a human pathogen without an animal reservoir. Group A streptococci (GAS) cause most streptococcal disease, but other groups are important pathogens in some settings (Box 1). Group A streptococcal infections have the highest incidence in children younger than age 10. The asymptomatic prevalence is also higher (15-20%) in children, compared with that in adults (<5%).

In the late 1980s, invasive GAS infections occurred in North America and Europe in previously healthy individuals of all ages. This illness is associated with bacteremia, deep soft-tissue infection, shock, multi-organ failure, and death in 30% of cases. StrepTSS occurs sporadically, although minor epidemics have been reported. Most patients present with a viral-like prodrome, history of minor trauma, recent surgery, or varicella infection.

S pneumoniae may exist in humans as either a nasopharyngeal colonist or as a pathogen in one of many clinical syndromes (Box 1). Although S pneumoniae has been found in other mammals, humans are thought to be the principal reservoir. As a colonist, S pneumoniae is found in up to 40% of children and 10% of adults.

This section focuses on the clinical findings, diagnosis, and treatment of pneumococcal meningitis. Please also see site for a general discussion of meningitis.

This section focuses on the clinical findings, diagnosis, and treatment of pneumococcal pneumonia. Bacteremia, progressive respiratory failure, and hemodynamic instability (ie, septic shock) are the most severe complications of pneumococcal pneumonia. As noted above, patients with either anatomic or functional asplenia are at particularly high risk for sepsis. Spread of infection via either contiguous extension or hematogenous routes constitutes the basis of extrapulmonary complications.