Gram Positive Cocci: Streptococci

Streptococci are Gram positive cocci arranged in chains or pairs, catalase negative, the key test distinguishing streptococci from staphylococci.

They are facultative anaerobes, nonmotile, and non-spore-forming, and are classified by two complementary systems: haemolysis pattern on blood agar, and Lancefield grouping, a carbohydrate cell wall antigen classification applicable to the beta-haemolytic group and a small number of others.

Alpha-haemolytic organisms include Streptococcus pneumoniae and the viridans group streptococci. Beta-haemolytic organisms include Streptococcus pyogenes, Lancefield group A, and Streptococcus agalactiae, Lancefield group B. Gamma-haemolytic, non-haemolytic, organisms include enterococci and some other streptococci.

Lancefield grouping is a serological classification based on a specific carbohydrate antigen in the cell wall, applicable primarily to beta-haemolytic streptococci. Group A is Streptococcus pyogenes. Group B is Streptococcus agalactiae. Alpha-haemolytic organisms, S. pneumoniae and the viridans group, are not meaningfully Lancefield-grouped and are instead differentiated by other tests, optochin susceptibility and bile solubility for S. pneumoniae.

Morphology. Gram positive cocci in chains.

Important laboratory features. Catalase negative, beta-haemolytic, Lancefield group A, bacitracin susceptible, the classic bedside and laboratory test distinguishing it from other beta-haemolytic streptococci.

Reservoir. Human throat and skin. Humans are the only significant reservoir.

Transmission. Respiratory droplets for pharyngitis, and direct contact for skin infection.

Virulence factors. M protein is the principal virulence factor, an antiphagocytic surface protein that also shows molecular mimicry with human cardiac and joint tissue, the basis of the autoimmune complications below. Streptolysin O and streptolysin S are membrane-damaging haemolysins; streptolysin O is immunogenic and is the basis of the ASOT, anti-streptolysin O titre, test used to support a diagnosis of recent infection or its complications.

Streptococcal pyrogenic exotoxins are superantigens, responsible for scarlet fever and streptococcal toxic shock syndrome. Hyaluronidase and streptokinase are spreading factors, facilitating tissue invasion. DNase degrades host DNA within pus, contributing to spread.

Major diseases. Suppurative disease: pharyngitis, strep throat, impetigo, cellulitis, erysipelas, necrotising fasciitis, streptococcal toxic shock syndrome, scarlet fever.

Nonsuppurative, post-infectious, immune-mediated disease: acute rheumatic fever, which follows pharyngitis specifically, not skin infection, mediated by M protein molecular mimicry with cardiac tissue, and post-streptococcal glomerulonephritis, which can follow either pharyngitis or skin infection, immune complex-mediated.

Diagnosis. Throat swab culture or rapid antigen detection test for pharyngitis. ASOT supports a diagnosis of recent infection when investigating suspected rheumatic fever or glomerulonephritis, but is not useful for diagnosing the acute infection itself, since the titre rises over one to three weeks.

Resistance patterns. Remains universally susceptible to penicillin, which remains first-line therapy, a notable exception to the general trend of increasing streptococcal and staphylococcal resistance elsewhere.

Prevention. Prompt antibiotic treatment of pharyngitis reduces the risk of acute rheumatic fever, the principal public health rationale for treating streptococcal sore throat.

Morphology. Gram positive cocci in chains.

Important laboratory features. Catalase negative, beta-haemolytic, Lancefield group B, bacitracin resistant, distinguishing it from group A, CAMP test positive.

Reservoir. Vaginal and gastrointestinal flora, present in a substantial minority of healthy women, approximately 10 to 30 percent colonisation rate.

Transmission. Vertical transmission from a colonised mother to the neonate during labour and delivery.

Virulence factors. Polysaccharide capsule, antiphagocytic, the basis of serotype classification, and the CAMP factor, which enhances staphylococcal beta-haemolysin activity, the basis of the CAMP test.

Major diseases. The leading cause of early-onset neonatal sepsis and meningitis, within the first week of life, acquired during delivery, and a cause of late-onset neonatal disease, up to three months, mechanism less clearly linked to delivery. Also causes infection in pregnant women, chorioamnionitis, postpartum endometritis, and, less commonly, in nonpregnant adults with underlying illness, elderly, diabetic, immunosuppressed patients, causing bacteraemia and skin or soft tissue infection.

Diagnosis. Antenatal screening by vaginal and rectal swab culture at 35 to 37 weeks gestation is standard practice in many settings, with positive results guiding intrapartum antibiotic prophylaxis.

Resistance patterns. Remains penicillin susceptible. Penicillin, or ampicillin, is standard intrapartum prophylaxis and treatment.

Prevention. Intrapartum antibiotic prophylaxis for colonised mothers, or those with other risk factors, is the principal strategy for preventing early-onset neonatal disease.

Morphology. Gram positive diplococci, lancet-shaped, flattened at the adjacent poles.

Important laboratory features. Catalase negative, alpha-haemolytic, optochin susceptible, distinguishing it from viridans streptococci, which are optochin resistant, and bile soluble, a second confirmatory test.

Reservoir. Human nasopharynx. Asymptomatic colonisation is common, particularly in children.

Transmission. Respiratory droplets. Disease typically arises from an endogenously colonising strain rather than fresh acquisition, often following a preceding viral respiratory infection that disrupts normal mucosal defences.

Virulence factors. Polysaccharide capsule is the dominant virulence factor and the basis of both serotype classification, over 90 serotypes, and the conjugate and polysaccharide vaccines. Pneumolysin is a pore-forming toxin. IgA protease cleaves secretory IgA at the mucosal surface.

Major diseases. The leading bacterial cause of community-acquired pneumonia, and a leading cause of bacterial meningitis, particularly in adults and in unvaccinated children, otitis media, sinusitis, and bacteraemia. Patients without a functioning spleen, splenectomy, sickle cell disease with autosplenism, are at markedly increased risk of fulminant pneumococcal sepsis, since the spleen is central to clearing encapsulated organisms.

Diagnosis. Sputum or CSF Gram stain and culture, urinary pneumococcal antigen test, rapid, useful in pneumonia, blood culture in invasive disease.

Resistance patterns. Penicillin resistance, via altered penicillin-binding proteins, not beta-lactamase production, is well established and geographically variable in prevalence, relevant to empirical antibiotic selection, particularly for meningitis, where achieving adequate CSF drug levels is more challenging.

Prevention. Conjugate pneumococcal vaccines, covering the most invasive and common serotypes, used in the routine childhood schedule, and polysaccharide vaccine, broader serotype coverage, used in older adults and specific high-risk groups including asplenic patients.

Morphology. Gram positive cocci in chains.

Important laboratory features. Catalase negative, alpha-haemolytic, optochin resistant, the key distinguishing feature from S. pneumoniae, not meaningfully Lancefield-grouped, a heterogeneous group of multiple species rather than a single organism.

Reservoir. Normal flora of the oral cavity, upper respiratory tract, and gastrointestinal tract.

Transmission. Endogenous. Disease arises from the patient's own flora entering the bloodstream, classically via a breach in the oral mucosa, dental procedures, poor dentition.

Virulence factors. Relatively low intrinsic virulence. The key property is the ability of certain species to adhere avidly to damaged or abnormal heart valve surfaces via dextran production.

Major diseases. The classic cause of subacute bacterial endocarditis, typically affecting a previously abnormal or damaged native heart valve, following transient bacteraemia from a dental or oral procedure.

Diagnosis. Blood culture, multiple sets, given the subacute, often low-grade bacteraemia. Identification to species level supports but is not solely diagnostic of endocarditis, which relies on the combined clinical, microbiological, and echocardiographic Duke criteria.

Prevention. Antibiotic prophylaxis before dental procedures is now restricted to specific high-risk cardiac conditions in most current guidelines, reflecting a shift away from broad prophylactic use.