Pneumococcal Pneumonia

Infectious Disease MONDO:0005114 Pathograph 5 Show in embeddings browser Bacterial Respiratory Infection

Pneumococcal pneumonia is community-acquired pneumonia caused by Streptococcus pneumoniae, the most common bacterial cause of community-acquired pneumonia, particularly among hospitalized patients. After nasopharyngeal colonization, the encapsulated organism invades the lower respiratory tract and produces a typical lobar pneumonia. As a classic cell-walled (Gram-positive) bacterium, it is treated with beta-lactam antibiotics that target the penicillin-binding-protein transpeptidases — the diametric opposite of cell-wall-deficient atypical pathogens such as Mycoplasma. Acquired penicillin resistance via altered penicillin-binding proteins is widespread, and conjugate vaccines have reduced invasive pneumococcal disease.

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4
Pathophys.
4
Phenotypes
5
Pathograph
2
Medical Actions
3
Datasets

Pathophysiology

4
Pneumococcal Colonization and Lower Airway Invasion
Streptococcus pneumoniae colonizes the nasopharynx and, in susceptible hosts, invades the lower respiratory tract. It remains the most common bacterial cause of community-acquired pneumonia, especially among patients requiring hospitalization. This colonizing/invading organism is the proximal event from which the lobar pneumonia and the antibiotic-target biology follow.
respiratory epithelial cell CL:0002632 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves respiratory epithelial cell, annotated with epithelial cell of lower respiratory tract (CL:0002632). CL:0002632 is a cell type from the Cell Ontology.
adhesion of symbiont to host GO:0044406 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves adhesion of symbiont to host (GO:0044406). GO:0044406 is a biological process from the Gene Ontology.
Show evidence (1 reference)
PMID:42203421 SUPPORT Other
"Although Streptococcus pneumoniae remains the most common bacterial cause of CAP, particularly among patients requiring hospitalization, its frequency has declined."
Establishes S. pneumoniae as the most common bacterial cause of community-acquired pneumonia. Evidence source is OTHER as this is a review article.
Lobar Pneumonia
Invasion of the alveolar spaces produces a typical lobar pneumonia with consolidation, fever, productive cough, and dyspnea; bacteremia and parapneumonic effusion may complicate severe disease.
inflammatory response GO:0006954 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased inflammatory response (GO:0006954). GO:0006954 is a biological process from the Gene Ontology. ↑ INCREASED
lung UBERON:0002048 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in lung (UBERON:0002048). UBERON:0002048 is an anatomical location from the Uberon multi-species anatomy ontology.
Show evidence (1 reference)
PMID:42203421 SUPPORT Other
"Although Streptococcus pneumoniae remains the most common bacterial cause of CAP, particularly among patients requiring hospitalization, its frequency has declined."
Supports pneumococcal pneumonia as a leading form of community-acquired pneumonia, especially in hospitalized patients. Evidence source is OTHER as this is a review article.
Penicillin-Binding Protein Transpeptidase (Beta-Lactam Target)
As a cell-walled Gram-positive bacterium, S. pneumoniae depends on penicillin-binding-protein (PBP) transpeptidases to cross-link peptidoglycan. Beta-lactam antibiotics (penicillins, cephalosporins) acylate these PBPs and abolish transpeptidation, making them the mainstay of therapy — in direct contrast to cell-wall-deficient atypical pathogens that lack this target.
peptidoglycan-based cell wall biogenesis GO:0009273 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves peptidoglycan-based cell wall biogenesis (GO:0009273). GO:0009273 is a biological process from the Gene Ontology.
Show evidence (1 reference)
PMID:22203377 SUPPORT Other
"although glycan chain polymerization occurs in the absence of transpeptidation (for example, in the presence of penicillin), efficient transpeptidation requires ongoing GTase reactions"
States that penicillin abolishes transpeptidation (the PBP cross-linking reaction), confirming this node as the beta-lactam target. Evidence source is OTHER as this is a review article.
Acquired Penicillin Resistance via Altered PBPs
Penicillin resistance in pneumococci arises chiefly through mosaic penicillin-binding proteins with reduced beta-lactam affinity, and resistance to macrolides and other alternatives is widespread, complicating empirical therapy.
response to antibiotic GO:0046677 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves response to antibiotic (GO:0046677). GO:0046677 is a biological process from the Gene Ontology.
Show evidence (1 reference)
PMID:38667036 SUPPORT Other
"Resistance to major alternatives of penicillins, macrolides, and lincosamides has become widespread among pneumococci and streptococci, especially in Asia"
Documents widespread resistance among pneumococci to penicillins and major alternatives. Evidence source is OTHER as this is a review article.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Pneumococcal Pneumonia Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

4
Immune 1
Pneumonia HP:0002090 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Pneumonia (HP:0002090). HP:0002090 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:42203421 SUPPORT Other
"Although Streptococcus pneumoniae remains the most common bacterial cause of CAP, particularly among patients requiring hospitalization, its frequency has declined."
Supports pneumococcal pneumonia (community-acquired pneumonia) as the defining manifestation. Evidence source is OTHER as this is a review article.
Metabolism 1
Fever HP:0001945 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Fever (HP:0001945). HP:0001945 is a phenotype from the Human Phenotype Ontology.
Respiratory 2
Cough HP:0012735 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Cough (HP:0012735). HP:0012735 is a phenotype from the Human Phenotype Ontology.
Dyspnea HP:0002094 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Dyspnea (HP:0002094). HP:0002094 is a phenotype from the Human Phenotype Ontology.
💊

Medical Actions

2
Beta-Lactam Antibiotic Therapy
Action: PharmacotherapyNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Pharmacotherapy (NCIT:C15986). NCIT:C15986 is a clinical intervention from the NCI Thesaurus. NCIT:C15986
Agent: benzylpenicillin (penicillin G) CHEBI:18208 Chemical Entities of Biological Interest (CHEBI) Relation: this treatment uses this therapeutic agent This treatment uses benzylpenicillin (penicillin G), annotated with benzylpenicillin (CHEBI:18208). CHEBI:18208 is a therapeutic agent from Chemical Entities of Biological Interest.
Penicillins (and cephalosporins such as ceftriaxone) acylate pneumococcal penicillin-binding-protein transpeptidases, blocking peptidoglycan cross-linking; they are the mainstay of therapy, with agent choice guided by local penicillin resistance.
Mechanism Target:
INHIBITS Penicillin-Binding Protein Transpeptidase (Beta-Lactam Target) — Beta-lactams acylate the PBP transpeptidases and abolish peptidoglycan cross-linking, killing the organism.
Pneumococcal Vaccination
Action: vaccinationNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is vaccination (NCIT:C15346). NCIT:C15346 is a clinical intervention from the NCI Thesaurus. Ontology label: Vaccination NCIT:C15346
Pneumococcal conjugate and polysaccharide vaccines reduce invasive pneumococcal disease and have contributed to the declining frequency of pneumococcal CAP.
Show evidence (1 reference)
PMID:42203421 SUPPORT Other
"Several factors likely contribute to the evolving etiology of CAP, including vaccination programs, pandemics, and changes in host immunity."
Supports vaccination programs as a driver of the declining frequency of pneumococcal CAP. Evidence source is OTHER as this is a review article.
📊

Related Datasets

3
RNA profiles in extracellular vesicles from severe sepsis patients reveal pathogen-specific immune signatures in meningococcal versus pneumococcal infections geo:GSE292448
This study is the first to investigate and compare RNA profiles in plasma extracellular vesicles (EVs) isolated from patients with severe sepsis caused by Neisseria meningitidis and patients with systemic infections due to Streptococcus pneumoniae. In some cases, invasive pneumococcal disease can resemble meningococcal infections at the time of hospital admission. Blood samples from a 1980s epidemic in Norway were used to isolate EVs and characterize their RNA content by microarray technology. The results revealed both shared and distinct RNA characteristics between the two patient groups, with 1,798 shared transcripts.
human MICROARRAY n=21
PMID:42112460
Identified by GEO DataSets index search for Pneumococcal Pneumonia (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
BIOLOGICAL EFFECTS OF CORTICOSTEROIDS ON PNEUMOCOCCAL PNEUMONIA IN MICE AND HUMANS geo:GSE246398
Rationale: Streptococcus pneumoniae is the most common bacterial cause of community acquired pneumonia. Some clinical trials have demonstrated a beneficial effect of corticosteroid therapy in community acquired pneumonia, but the mechanisms of this benefit remain unclear. Objectives: To investigate the biologic effects of corticosteroids in pneumococcal pneumonia in mice and in patients Methods: We studied lower respiratory tract transcriptomes from an observational cohort of mechanically ventilated patients and from a pneumonia model in mice. We also carried out comprehensive physiologic, biochemical, and histological analyses in mice to identify mechanisms of lung injury in S.
human BULK RNA SEQ n=15
PMID:38807178
Identified by GEO DataSets index search for Pneumococcal Pneumonia (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
TNF Superfamily Member 14 Drives Post-Influenza Depletion of Alveolar Macrophages Enabling Secondary Pneumococcal Pneumonia geo:GSE273805
Secondary bacterial infection, often caused by Streptococcus pneumoniae (Spn), is one of the most frequent and severe complications of influenza A virus (IAV)-induced pneumonia. Phenotyping of the pulmonary innate immune landscape after IAV infection revealed a significant depletion of the tissue-resident alveolar macrophage (TR-AM) population at day 7, which was associated with increased susceptibility to Spn outgrowth. To elucidate the molecular mechanisms underlying TR-AM depletion, and to define putative targets for treatment, we combined single-cell transcriptomics and cell-specific PCR profiling in an unbiased manner, using in vivo models of IAV infection and IAV/Spn co-infection.
mouse SINGLE CELL RNA SEQ n=7
PMID:41252214
Identified by GEO DataSets index search for Pneumococcal Pneumonia (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
{ }

Source YAML

click to show
name: Pneumococcal Pneumonia
creation_date: "2026-06-28T00:00:00Z"
description: >
  Pneumococcal pneumonia is community-acquired pneumonia caused by Streptococcus
  pneumoniae, the most common bacterial cause of community-acquired pneumonia,
  particularly among hospitalized patients. After nasopharyngeal colonization, the
  encapsulated organism invades the lower respiratory tract and produces a typical
  lobar pneumonia. As a classic cell-walled (Gram-positive) bacterium, it is
  treated with beta-lactam antibiotics that target the penicillin-binding-protein
  transpeptidases — the diametric opposite of cell-wall-deficient atypical
  pathogens such as Mycoplasma. Acquired penicillin resistance via altered
  penicillin-binding proteins is widespread, and conjugate vaccines have reduced
  invasive pneumococcal disease.
category: Infectious Disease
parents:
- Bacterial Respiratory Infection
synonyms:
- Streptococcus pneumoniae pneumonia
- Pneumococcal community-acquired pneumonia
disease_term:
  preferred_term: pneumococcal pneumonia
  term:
    id: MONDO:0005114
    label: pneumococcal infection
pathophysiology:
- name: Pneumococcal Colonization and Lower Airway Invasion
  role: trigger
  description: >
    Streptococcus pneumoniae colonizes the nasopharynx and, in susceptible hosts,
    invades the lower respiratory tract. It remains the most common bacterial cause
    of community-acquired pneumonia, especially among patients requiring
    hospitalization. This colonizing/invading organism is the proximal event from
    which the lobar pneumonia and the antibiotic-target biology follow.
  cell_types:
  - preferred_term: respiratory epithelial cell
    term:
      id: CL:0002632
      label: epithelial cell of lower respiratory tract
  biological_processes:
  - preferred_term: adhesion of symbiont to host
    term:
      id: GO:0044406
      label: adhesion of symbiont to host
  evidence:
  - reference: PMID:42203421
    reference_title: "Evolving Etiology of Community-Acquired Pneumonia."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Although Streptococcus pneumoniae remains the most common bacterial cause of
      CAP, particularly among patients requiring hospitalization, its frequency has
      declined.
    explanation: >-
      Establishes S. pneumoniae as the most common bacterial cause of
      community-acquired pneumonia. Evidence source is OTHER as this is a review
      article.
  downstream:
  - target: Lobar Pneumonia
    description: >-
      Lower-airway invasion produces a typical lobar pneumonia.
  - target: Penicillin-Binding Protein Transpeptidase (Beta-Lactam Target)
    description: >-
      The organism's cell-wall cross-linking enzymes are the target of beta-lactam
      therapy.

- name: Lobar Pneumonia
  role: consequence
  description: >
    Invasion of the alveolar spaces produces a typical lobar pneumonia with
    consolidation, fever, productive cough, and dyspnea; bacteremia and
    parapneumonic effusion may complicate severe disease.
  biological_processes:
  - preferred_term: inflammatory response
    term:
      id: GO:0006954
      label: inflammatory response
    modifier: INCREASED
  locations:
  - preferred_term: lung
    term:
      id: UBERON:0002048
      label: lung
  evidence:
  - reference: PMID:42203421
    reference_title: "Evolving Etiology of Community-Acquired Pneumonia."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Although Streptococcus pneumoniae remains the most common bacterial cause of
      CAP, particularly among patients requiring hospitalization, its frequency has
      declined.
    explanation: >-
      Supports pneumococcal pneumonia as a leading form of community-acquired
      pneumonia, especially in hospitalized patients. Evidence source is OTHER as
      this is a review article.
  downstream: []

- name: Penicillin-Binding Protein Transpeptidase (Beta-Lactam Target)
  role: therapeutic_vulnerability
  conforms_to: "bacterial_cell_wall_synthesis_inhibition#Peptidoglycan Cross-Linking by Penicillin-Binding Proteins"
  description: >
    As a cell-walled Gram-positive bacterium, S. pneumoniae depends on
    penicillin-binding-protein (PBP) transpeptidases to cross-link peptidoglycan.
    Beta-lactam antibiotics (penicillins, cephalosporins) acylate these PBPs and
    abolish transpeptidation, making them the mainstay of therapy — in direct
    contrast to cell-wall-deficient atypical pathogens that lack this target.
  biological_processes:
  - preferred_term: peptidoglycan-based cell wall biogenesis
    term:
      id: GO:0009273
      label: peptidoglycan-based cell wall biogenesis
  evidence:
  - reference: PMID:22203377
    reference_title: "From the regulation of peptidoglycan synthesis to bacterial growth and morphology."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      although glycan chain polymerization occurs in the absence of
      transpeptidation (for example, in the presence of penicillin), efficient
      transpeptidation requires ongoing GTase reactions
    explanation: >-
      States that penicillin abolishes transpeptidation (the PBP cross-linking
      reaction), confirming this node as the beta-lactam target. Evidence source is
      OTHER as this is a review article.
  downstream:
  - target: Acquired Penicillin Resistance via Altered PBPs
    description: >-
      Pneumococci escape beta-lactams by remodeling the PBP target.

- name: Acquired Penicillin Resistance via Altered PBPs
  role: adaptive_escape
  conforms_to: "bacterial_cell_wall_synthesis_inhibition#Acquired Resistance and Drug Inactivation"
  description: >
    Penicillin resistance in pneumococci arises chiefly through mosaic
    penicillin-binding proteins with reduced beta-lactam affinity, and resistance to
    macrolides and other alternatives is widespread, complicating empirical therapy.
  biological_processes:
  - preferred_term: response to antibiotic
    term:
      id: GO:0046677
      label: response to antibiotic
  evidence:
  - reference: PMID:38667036
    reference_title: "A Review of the Impact of Streptococcal Infections and Antimicrobial Resistance on Human Health."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Resistance to major alternatives of penicillins, macrolides, and lincosamides
      has become widespread among pneumococci and streptococci, especially in Asia
    explanation: >-
      Documents widespread resistance among pneumococci to penicillins and major
      alternatives. Evidence source is OTHER as this is a review article.
  downstream: []
phenotypes:
- category: Respiratory
  name: Pneumonia
  description: >
    Typical lobar community-acquired pneumonia is the defining manifestation.
  phenotype_term:
    preferred_term: Pneumonia
    term:
      id: HP:0002090
      label: Pneumonia
  evidence:
  - reference: PMID:42203421
    reference_title: "Evolving Etiology of Community-Acquired Pneumonia."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Although Streptococcus pneumoniae remains the most common bacterial cause of
      CAP, particularly among patients requiring hospitalization, its frequency has
      declined.
    explanation: >-
      Supports pneumococcal pneumonia (community-acquired pneumonia) as the defining
      manifestation. Evidence source is OTHER as this is a review article.
- category: Constitutional
  name: Fever
  description: >
    High fever is typical of acute pneumococcal pneumonia.
  phenotype_term:
    preferred_term: Fever
    term:
      id: HP:0001945
      label: Fever
- category: Respiratory
  name: Cough
  description: >
    Productive cough is a cardinal symptom.
  phenotype_term:
    preferred_term: Cough
    term:
      id: HP:0012735
      label: Cough
- category: Respiratory
  name: Dyspnea
  description: >
    Shortness of breath reflects alveolar consolidation.
  phenotype_term:
    preferred_term: Dyspnea
    term:
      id: HP:0002094
      label: Dyspnea
treatments:
- name: Beta-Lactam Antibiotic Therapy
  description: >
    Penicillins (and cephalosporins such as ceftriaxone) acylate pneumococcal
    penicillin-binding-protein transpeptidases, blocking peptidoglycan cross-linking;
    they are the mainstay of therapy, with agent choice guided by local penicillin
    resistance.
  therapeutic_modality: SMALL_MOLECULE
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: benzylpenicillin (penicillin G)
      term:
        id: CHEBI:18208
        label: benzylpenicillin
  target_mechanisms:
  - target: Penicillin-Binding Protein Transpeptidase (Beta-Lactam Target)
    treatment_effect: INHIBITS
    description: >-
      Beta-lactams acylate the PBP transpeptidases and abolish peptidoglycan
      cross-linking, killing the organism.
- name: Pneumococcal Vaccination
  description: >
    Pneumococcal conjugate and polysaccharide vaccines reduce invasive pneumococcal
    disease and have contributed to the declining frequency of pneumococcal CAP.
  therapeutic_modality: VACCINE
  treatment_term:
    preferred_term: vaccination
    term:
      id: NCIT:C15346
      label: Vaccination
  evidence:
  - reference: PMID:42203421
    reference_title: "Evolving Etiology of Community-Acquired Pneumonia."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      Several factors likely contribute to the evolving etiology of CAP, including
      vaccination programs, pandemics, and changes in host immunity.
    explanation: >-
      Supports vaccination programs as a driver of the declining frequency of
      pneumococcal CAP. Evidence source is OTHER as this is a review article.
notes: >
  Created as part of the Respiratory Infections project. The deliberate
  cell-walled (typical-pneumonia) counterpart to Mycoplasma_Pneumoniae_Pneumonia:
  conforms to the bacterial_cell_wall_synthesis_inhibition module's PBP
  cross-linking (beta-lactam target) and acquired-resistance nodes. disease_term
  uses MONDO:0005114 (pneumococcal infection) with a more specific preferred_term
  because MONDO lacks a dedicated "pneumococcal pneumonia" term. The
  infectious_agent (NCBITaxon) block was omitted at creation and S. pneumoniae is
  described in the text.
datasets:
- accession: geo:GSE292448
  title: RNA profiles in extracellular vesicles from severe sepsis patients reveal pathogen-specific immune signatures in meningococcal versus pneumococcal infections
  description: This study is the first to investigate and compare RNA profiles in plasma extracellular vesicles (EVs) isolated from patients with severe sepsis caused by Neisseria meningitidis and patients with systemic infections due to Streptococcus pneumoniae. In some cases, invasive pneumococcal disease can resemble meningococcal infections at the time of hospital admission. Blood samples from a 1980s epidemic in Norway were used to isolate EVs and characterize their RNA content by microarray technology. The results revealed both shared and distinct RNA characteristics between the two patient groups, with 1,798 shared transcripts.
  organism:
    preferred_term: human
    term:
      id: NCBITaxon:9606
      label: Homo sapiens
  data_type: MICROARRAY
  sample_count: 21
  publication: PMID:42112460
  notes: Identified by GEO DataSets index search for Pneumococcal Pneumonia (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
- accession: geo:GSE246398
  title: BIOLOGICAL EFFECTS OF CORTICOSTEROIDS ON PNEUMOCOCCAL PNEUMONIA IN MICE AND HUMANS
  description: 'Rationale: Streptococcus pneumoniae is the most common bacterial cause of community acquired pneumonia. Some clinical trials have demonstrated a beneficial effect of corticosteroid therapy in community acquired pneumonia, but the mechanisms of this benefit remain unclear. Objectives: To investigate the biologic effects of corticosteroids in pneumococcal pneumonia in mice and in patients Methods: We studied lower respiratory tract transcriptomes from an observational cohort of mechanically ventilated patients and from a pneumonia model in mice. We also carried out comprehensive physiologic, biochemical, and histological analyses in mice to identify mechanisms of lung injury in S.'
  organism:
    preferred_term: human
    term:
      id: NCBITaxon:9606
      label: Homo sapiens
  data_type: BULK_RNA_SEQ
  sample_count: 15
  publication: PMID:38807178
  notes: Identified by GEO DataSets index search for Pneumococcal Pneumonia (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
- accession: geo:GSE273805
  title: TNF Superfamily Member 14 Drives Post-Influenza Depletion of Alveolar  Macrophages Enabling Secondary Pneumococcal Pneumonia
  description: Secondary bacterial infection, often caused by Streptococcus pneumoniae (Spn), is one of the most frequent and severe complications of influenza A virus (IAV)-induced pneumonia. Phenotyping of the pulmonary innate immune landscape after IAV infection revealed a significant depletion of the tissue-resident alveolar macrophage (TR-AM) population at day 7, which was associated with increased susceptibility to Spn outgrowth. To elucidate the molecular mechanisms underlying TR-AM depletion, and to define putative targets for treatment, we combined single-cell transcriptomics and cell-specific PCR profiling in an unbiased manner, using in vivo models of IAV infection and IAV/Spn co-infection.
  organism:
    preferred_term: mouse
    term:
      id: NCBITaxon:10090
      label: Mus musculus
  data_type: SINGLE_CELL_RNA_SEQ
  sample_count: 7
  publication: PMID:41252214
  notes: Identified by GEO DataSets index search for Pneumococcal Pneumonia (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.