Streptococcal Pharyngitis and Pneumonia

Overview

GAS (S. pyogenes) pharyngitis + Pneumococcal (S. pneumoniae) pneumonia. General S. pyogenes virulence/skin disease/sequelae = Streptococcal Infections topic. This topic = pharyngeal disease + full pneumococcal coverage.

GAS Pharyngitis

Clinical: fever, sore throat, tonsillar exudate, tender anterior cervical LAD. NO COUGH (distinguishes bacterial from far-more-common viral pharyngitis, which has cough/rhinorrhea/conjunctivitis).

Significance = SEQUELAE, not acute illness: ARF + PSGN (see Rheumatic Fever/Streptococcal Infections topics) — why accurate Dx + complete Rx matters disproportionately to acute severity.

Diagnosis: Centor criteria (fever, exudate, tender LAD, no cough) = pretest probability estimate before testing (most pharyngitis viral, testing all = false positives from carriage). RADT: minutes, high specificity, IMPERFECT sensitivity — negative + suspicious picture → THROAT CULTURE (reference standard, 24-48hr) to confirm. Carriage vs true infection: genuine challenge, but positive test + compatible picture generally treated regardless (low cost unnecessary Rx vs missing ARF-risk case).

Treatment: Penicillin (oral Pen V or IM benzathine penicillin G) 1st line — NEVER significant resistance (see Streptococcal Infections). FULL COURSE (10 days oral) needed to PREVENT ARF, not just resolve symptoms (which improve before course complete — key counseling point, premature stopping = common Rx failure for sequela prevention).

Pneumococcal Pneumonia

Organism: S. pneumoniae. Gram+ LANCET-SHAPED diplococcus, alpha-hemolytic. Distinguished from viridans strep (also alpha-hemolytic): OPTOCHIN SENSITIVE + BILE SOLUBLE (pneumococcus) vs resistant/insoluble (viridans) — see IE topic.

Virulence: POLYSACCHARIDE CAPSULE (>90 serotypes) — antiphagocytic, determines virulence + vaccine basis. SPLENECTOMIZED patients = dramatically elevated risk (spleen clears encapsulated organisms, see Components of Immune System topic) — pneumococcus = PARADIGM encapsulated pathogen example.

Clinical: CLASSIC community-acquired LOBAR PNEUMONIA — abrupt fever, rigors, pleuritic chest pain, RUST-COLORED SPUTUM. TEXTBOOK PROTOTYPE bacterial pneumonia (contrasted against “atypical” pneumonia presentations, see that topic). Also: bacterial meningitis (#1 cause, CNS topic), otitis media/sinusitis (Ocular/Ear topic), sepsis. OPSI (Overwhelming Post-Splenectomy Infection): fulminant rapidly fatal pneumococcal sepsis, asplenic patients — most feared manifestation of encapsulated biology.

Diagnosis: Gram stain sputum (Gram+ lancet diplococci + neutrophils). Culture (alpha-hemolytic, optochin+bile solubility confirm). Urinary pneumococcal antigen: rapid non-invasive, useful esp. if antibiotics already given before sputum obtained.

Treatment: Penicillin historically mainstay, but SIGNIFICANT RESISTANCE now global (altered PBP2b, same mechanism as MRSA PBP2a — see AMR topic). Current empirical: 3rd-gen cephalosporin or vancomycin (severe/resistant), per local patterns.

Vaccines — 2 TYPES (T-dependent/independent distinction, see Vaccines + Antigen/Antibody topics):

PPSV23: 23 serotypes, PURE polysaccharide (T-INDEPENDENT) — POOR immunogenicity <2yr age, no strong memory
PCV (conjugate, fewer serotypes + carrier protein): T-DEPENDENT response, durable memory, effective in infants → PCV used in ROUTINE INFANT schedule. PPSV23 = supplementary, specific older/high-risk populations.

Two Organisms, Two Respiratory Diseases

This topic covers group A streptococcal (S. pyogenes) pharyngitis and pneumococcal (Streptococcus pneumoniae) pneumonia — two genuinely distinct streptococcal respiratory diseases grouped together here as the classic streptococcal upper- and lower-respiratory-tract infections respectively. S. pyogenes’s general virulence factors, skin/soft-tissue disease spectrum, and immune-mediated sequelae (rheumatic fever, PSGN) are covered in full under Streptococcal Infections; this topic focuses on its pharyngeal disease specifically, alongside pneumococcal pneumonia in full.

Group A Streptococcal Pharyngitis

Why It Matters Beyond the Sore Throat

GAS pharyngitis itself is a self-limited illness — fever, sore throat, tonsillar exudate, tender anterior cervical lymphadenopathy, notably without cough (a genuinely useful clinical feature distinguishing bacterial from the far more common viral pharyngitis, where cough, rhinorrhoea, and conjunctivitis typically accompany the sore throat) — but its clinical importance rests almost entirely on what happens if it’s missed or inadequately treated: acute rheumatic fever and acute post-streptococcal glomerulonephritis (both covered in depth under Rheumatic Fever and Streptococcal Infections respectively) are immune-mediated sequelae that can follow untreated or inadequately treated pharyngitis, which is exactly why accurate diagnosis and prompt, complete treatment of GAS pharyngitis specifically (as opposed to the many other, non-consequential causes of sore throat) matters disproportionately to the apparent severity of the acute illness itself.

Diagnosis

Clinical scoring systems (such as the Centor criteria — fever, tonsillar exudate, tender anterior cervical adenopathy, absence of cough) help estimate the pre-test probability of GAS as the cause before ordering any test, since most pharyngitis is viral and testing everyone with a sore throat would generate far more false positives (from asymptomatic GAS carriage) than true clinically significant cases. Rapid antigen detection test (RADT) on a throat swab gives a result within minutes, with high specificity but imperfect sensitivity — a negative RADT in a clinically suspicious case is generally followed by throat culture (the traditional reference standard, though slower, taking 24–48 hours) to confirm before ruling out GAS. Distinguishing true infection from asymptomatic carriage is a genuine, specific diagnostic challenge worth naming — a positive test in a patient with a viral pharyngitis and incidental GAS carriage doesn’t mean GAS is actually causing the current illness, though in practice a positive test in a clinically compatible picture is generally treated regardless, given the relatively low cost of unnecessary treatment against the real cost of missing a case that could progress to rheumatic fever.

Treatment

Penicillin (oral penicillin V, or a single IM dose of benzathine penicillin G for adherence-uncertain patients) remains first-line, for the same reasons covered under Streptococcal Infections — S. pyogenes has never developed clinically significant penicillin resistance. A full course (typically 10 days for oral therapy) is needed specifically to prevent rheumatic fever, not merely to resolve symptoms, which themselves often improve well before the full course is complete — a genuinely important patient-counselling point, since premature discontinuation once symptoms improve is a real, common cause of treatment failure to prevent the sequelae that actually matter.

Pneumococcal Pneumonia

The Organism

Streptococcus pneumoniae is a Gram-positive, lancet-shaped diplococcus, alpha-haemolytic on blood agar (distinguished from the other major alpha-haemolytic group, viridans streptococci, by optochin sensitivity and bile solubility — pneumococcus is sensitive/soluble, viridans streptococci are resistant/insoluble, a distinction covered under Infective Endocarditis’s viridans streptococci discussion and directly relevant here as the practical laboratory discriminator between the two). Its major virulence factor is a polysaccharide capsule — over 90 distinct serotypes exist, and capsular type both determines virulence/invasiveness and forms the basis of the pneumococcal vaccines (below) — the capsule’s antiphagocytic function is the central reason splenectomized patients face dramatically elevated risk from this organism specifically (see Components of Immune System and MHC for the spleen’s role in clearing encapsulated organisms), making pneumococcus the paradigm example of an encapsulated pathogen throughout this curriculum.

Clinical Manifestations

Pneumococcus is the classic cause of community-acquired lobar pneumonia — abrupt-onset high fever, rigors, pleuritic chest pain, and a productive cough with characteristically rust-coloured sputum (from blood pigment mixed with purulent exudate) — a presentation genuinely distinctive enough, in a previously healthy adult, to be considered the textbook prototype of bacterial pneumonia against which other, “atypical” pneumonia presentations (covered under their own topic) are explicitly contrasted. Beyond pneumonia, pneumococcus is also a leading cause of bacterial meningitis (see Central Nervous System Infections), otitis media and sinusitis (see Ocular and Ear Infections for the otitis component), and, in the context of bloodstream invasion, sepsis — with overwhelming post-splenectomy infection (OPSI), a fulminant, rapidly fatal pneumococcal sepsis syndrome specific to asplenic patients, representing the most feared single manifestation of this organism’s encapsulated-pathogen biology.

Laboratory Diagnosis

Gram stain of sputum showing Gram-positive, lancet-shaped diplococci alongside neutrophils supports the diagnosis; culture on blood agar shows alpha-haemolytic colonies, confirmed by optochin sensitivity/bile solubility as above. Urinary pneumococcal antigen testing offers a genuinely useful rapid, non-invasive diagnostic option in adults with suspected pneumococcal pneumonia, complementing (though not replacing) culture-based diagnosis, particularly useful when the patient has already received antibiotics before a sputum specimen could be obtained.

Treatment and Prevention

Penicillin was historically the mainstay, but penicillin resistance has become genuinely significant globally (via altered penicillin-binding proteins, PBP2b, mirroring the same PBP-alteration resistance mechanism covered under MRSA — see Antimicrobial Agents and Antimicrobial Resistance), meaning current empirical treatment often uses a third-generation cephalosporin or, for severe/resistant disease, vancomycin, guided by local resistance patterns and susceptibility testing. Two vaccine types exist, reflecting the same T-dependent/T-independent antigen distinction covered under Vaccines and Immunoprophylaxis and Antigen and Antibody: the pneumococcal polysaccharide vaccine (PPSV23), covering 23 serotypes but, being a pure polysaccharide (T-independent) antigen, poorly immunogenic in children under 2 and generating no strong memory response; and the pneumococcal conjugate vaccine (PCV, covering a smaller number of serotypes but conjugated to a carrier protein), converting the response to T-dependent, generating durable memory and effective immunogenicity even in young infants — which is exactly why PCV, not PPSV23, is the vaccine used in routine infant immunization schedules, with PPSV23 reserved for supplementary use in specific older/high-risk populations.