Peritonsillar Abscess (Quinsy): Comprehensive Disease Characteristics Report

Disease: Peritonsillar Abscess (PTA) | MONDO: MONDO:0005906 | ICD-10: J36 | ICD-11: CA03.2 | MeSH: D016499 | Category: Infectious Disease

Summary

Peritonsillar abscess (PTA), historically known as quinsy, is the most common deep infection of the head and neck and the most frequent deep neck space infection managed by otolaryngologists (PMID: 28756939). It is an acquired, polymicrobial bacterial infection — a collection of pus that forms in the peritonsillar space, the potential space bounded by the palatine tonsillar capsule medially and the superior pharyngeal constrictor muscle laterally. PTA is fundamentally an infectious, non-genetic disease: it has no Mendelian basis, no causal genes, no pathogenic germline variants, and no dedicated animal or organoid disease model. Consequently, the genetics/molecular, other-species natural-disease, and model-organism sections of this template are not applicable and are documented below as evidence gaps rather than omissions.

The disease peaks in adolescents and young adults, with a Danish population-based incidence of approximately 41 cases per 100,000 per year (PMID: 19842975), and shows no consistent sex predominance within age groups (PMID: 42563151). The dominant pathogens are Fusobacterium necrophorum and Group A Streptococcus (GAS), embedded in a mixed flora of oral anaerobes and other streptococci. PTA presents acutely with unilateral severe sore throat, fever, dysphagia/odynophagia, trismus, a muffled "hot-potato" voice, and uvular deviation. Diagnosis is largely clinical, with intraoral ultrasound and contrast-enhanced CT reserved to distinguish abscess from peritonsillar cellulitis and to guide drainage.

Management combines surgical drainage (needle aspiration, incision and drainage, or abscess/quinsy tonsillectomy) with antibiotics targeting streptococci and oral anaerobes, often supplemented by adjuvant corticosteroids to speed symptom resolution. Prognosis for uncomplicated PTA is excellent, with the vast majority recovering uneventfully. However, untreated or neglected disease can extend along fascial planes and cause life-threatening complications — descending mediastinitis, parapharyngeal/retropharyngeal abscess, necrotizing fasciitis, and Lemierre's syndrome — carrying roughly 10% mortality among the complicated subset. This report synthesizes 12 confirmed findings drawn from 33 reviewed papers (23 unique primary sources), all human clinical evidence.

1. Disease Information

Overview. Peritonsillar abscess is a localized collection of pus between the palatine tonsil (and its fibrous capsule) and the surrounding pharyngeal musculature. It represents the suppurative culmination of peritonsillar infection and is regarded as the most common deep neck infection (PMID: 28756939; PMID: 28409615). The peritonsillar space is "the area between the palatine tonsillar capsule medially and the superior pharyngeal constrictor muscle laterally" (PMID: 28531866).

Key identifiers.

Synonyms and alternative names. Quinsy; peritonsillar abscess; PTA; suppurative peritonsillitis; abscess of tonsil (when suppuration is peritonsillar).

Source of information. Evidence is derived from aggregated, disease-level clinical resources — population registries, retrospective hospital cohorts, prospective diagnostic studies, and systematic reviews — rather than individual EHR-level case data. There are no OMIM/ClinVar disease-level genomic entries because PTA is not heritable (Findings F009, F012).

2. Etiology

Disease causal factors. PTA is infectious and mechanistic in origin, not genetic. Two complementary pathogenesis hypotheses have been advanced and reconciled (PMID: 27026737):

1. Acute tonsillitis hypothesis — PTA arises as a complication of bacterial tonsillitis, supported by high pathogen concordance between pus aspirates and tonsillar tissue, antecedent tonsillitis, and reduced abscess risk when tonsillitis is treated with antibiotics.
2. Weber gland hypothesis — infection of the Weber's glands (mucus-secreting salivary glands in the supratonsillar space) obstructs their ducts and seeds the peritonsillar space; supported by high amylase levels in peritonsillar pus and the superior-pole location of most abscesses. Weber's glands were localized to the supratonsillar space and implicated in PTA formation by Passy (1994): "A group of salivary glands (Weber's glands) proven to be located in the supratonsillar space have been shown to be implicated in the pathogenesis of peritonsillar abscess" (PMID: 8302122).

These are unified in a salivary-duct-spread model: "bacteria initially infect the tonsillar mucosa and spread via the salivary duct system to the peritonsillar space, where an abscess is formed" (PMID: 27026737).

Genetic risk factors. None identified. No causal variants, susceptibility loci, or modifier genes are described in OMIM, ClinVar, or the GWAS Catalog for PTA (Finding F009).

Environmental / acquired risk factors. A NSQIP analysis found PTA patients had significantly higher rates of smoking (27.0% vs 12.3%), diabetes (6.6% vs 2.5%), and hypertension (11.5% vs 5.8%) than recurrent-tonsillitis controls (PMID: 41113746). Smoking is reported in nearly half of PTA patients (PMID: 25794541). Prior/recurrent tonsillitis is an established antecedent, and anaerobic bacterial growth correlates with higher recurrence (PMID: 18204368).

Protective factors. No genetic protective alleles are described. Prompt antibiotic treatment of acute tonsillitis reduces the risk of abscess progression (PMID: 27026737). Smoking cessation is a plausible modifiable protective behavior given the smoking association, though direct trial evidence is lacking.

Gene-environment interactions. Not applicable — no genetic component exists to interact with environmental exposures.

3. Phenotypes

PTA produces an acute-onset, typically unilateral symptom complex. Diagnosis is usually clinical based on these features (PMID: 28409615).

The classic examination signs "include asymmetry of the tonsils and palate, deviation of the uvula, and unilateral otalgia" (PMID: 28531866). "Symptoms and findings generally include fever, sore throat, dysphagia, trismus, and a 'hot potato' voice" (PMID: 28409615).

Characteristics. Age of onset is predominantly adolescent-to-young-adult; severity ranges from moderate to severe; progression is acute/subacute over days; the course is self-limited with treatment. In young children, presentation is nonspecific (fever, irritability, neck stiffness), whereas older children display the adult pattern of trismus, dysphagia, and hot-potato voice (PMID: 42275833).

Quality-of-life impact. Acute PTA causes marked short-term impairment of eating, drinking, speaking, and sleep due to pain, trismus, and dysphagia. Because uncomplicated PTA resolves within days to ~2 weeks after drainage, long-term QoL impact is minimal; validated disease-specific QoL instruments for PTA are not established (evidence gap).

4. Genetic / Molecular Information

Not applicable to host genetics. PTA is an acquired bacterial infection with no Mendelian or genomic etiology. There are:

• No causal genes (no OMIM gene-disease entry).
• No pathogenic/likely-pathogenic variants (no ClinVar entries linked to PTA).
• No modifier genes, epigenetic disease signatures, or chromosomal abnormalities described.
• No germline vs somatic variant distinction — the relevant genetic material is microbial, not human.

The only "genetic" dimension of relevance is bacterial virulence genetics (see Section 6): the F. necrophorum leukotoxin gene is present in all tested human isolates, with three sequence variants correlating to infection source (PMID: 28330774). This section was rigorously confirmed as a genuine "not applicable" for host genetics rather than an incomplete search (Findings F009, F012).

5. Environmental Information

Environmental / lifestyle factors. Smoking is the most consistently reported modifiable factor (27.0% of PTA patients vs 12.3% of controls; nearly half in some series) (PMID: 41113746; PMID: 25794541). Diabetes mellitus and hypertension are comorbid risk factors (PMID: 41113746). No specific toxin, radiation, or occupational exposure is implicated.

Infectious agents (NCBI Taxonomy). PTA is polymicrobial. Key pathogens:

Only F. necrophorum was significantly associated with complications in a dual-testing Swedish study (PMID: 40366504).

6. Mechanism / Pathophysiology

Ordered causal chain

1. Bacterial colonization/infection of tonsillar mucosa (acute tonsillitis)
   OR obstruction/infection of Weber's salivary glands in the supratonsillar space
│  leads to
▼
2. Spread of bacteria via the salivary duct system into the peritonsillar space
   (unified salivary-duct model; inferred from amylase in pus + pathogen concordance)
│  results in
▼
3. Local bacterial proliferation (F. necrophorum, GAS, oral anaerobes) between the
   tonsillar capsule and the superior pharyngeal constrictor muscle
│  triggers
▼
4. F. necrophorum releases LEUKOTOXIN → targets and kills neutrophils/leukocytes
   (strong correlation with disease severity)
│  drives
▼
5. Intense neutrophil-rich acute inflammatory response (↑ neutrophil count, ↑ CRP)
   → tissue necrosis and liquefaction → PUS accumulation → ABSCESS at superior pole
│  produces
▼
6. Mass effect + inflammation → unilateral sore throat, dysphagia, trismus,
   uvular deviation, "hot-potato" voice, fever  (CLINICAL PTA)
│
├─(treated: drainage + antibiotics)──► uneventful recovery (excellent prognosis)
│
└─(untreated/neglected)──► spread along fascial planes
         ▼
7. Descending mediastinitis / para-retropharyngeal abscess / necrotizing
   fasciitis / Lemierre's syndrome (IJV thrombophlebitis + septic emboli)
   → sepsis, airway compromise → ~10% mortality

Detail by category

Molecular pathways & immune involvement. The mechanism is innate-immune / inflammatory, not a classic signaling-cascade genetic disease. F. necrophorum's principal virulence factor is leukotoxin, which "has been shown to have a strong correlation with the severity of the disease" (PMID: 39059623). The leukotoxin gene is present in all tested human isolates, with three sequence variants correlating to infection source (PMID: 28330774). Leukotoxin's cytotoxicity toward neutrophils explains the strong neutrophil-driven inflammatory response: PTA patients with F. necrophorum show "significantly higher neutrophil counts" and CRP (PMID: 19842975).

Cellular processes (GO terms). Acute inflammatory response (GO:0006954), neutrophil chemotaxis (GO:0030593), neutrophil degranulation / leukocyte-mediated immunity (GO:0043312), and necrosis/pyogenesis. Suggested cell types (CL): neutrophil (CL:0000775), macrophage (CL:0000235), tonsil epithelial cell, and mucous gland (Weber gland) secretory cell.

Biochemical signature. Elevated salivary amylase in peritonsillar pus implicates Weber salivary gland tissue in the involved space (PMID: 27026737).

Tissue damage mechanisms. Necrosis and liquefaction of peritonsillar connective tissue driven by bacterial toxins and neutrophilic enzymes → abscess cavity; in complications, rapid fascial-plane necrosis (necrotizing fasciitis) and vascular thrombosis (Lemierre's).

Molecular profiling & advanced technologies. No PTA-specific transcriptomic, proteomic, metabolomic, lipidomic, single-cell, spatial, or functional-genomics datasets exist (evidence gap). The disease has not been the subject of omics screens because it is a straightforward acquired bacterial infection.

Upstream vs downstream. Upstream = bacterial infection + salivary duct spread (initiating lesion). Midstream = leukotoxin-driven neutrophilic inflammation and pus formation. Downstream = clinical mass-effect symptoms and, if unchecked, fascial-plane / vascular spread.

7. Anatomical Structures Affected

Organ level (primary). Palatine tonsil (UBERON:0002372) and the peritonsillar space — the potential space between the tonsillar capsule and the superior pharyngeal constrictor muscle (PMID: 28531866). Body system: respiratory / digestive (upper aerodigestive tract, oropharynx, UBERON:0001729).

Secondary / complication sites. Parapharyngeal and retropharyngeal spaces, mediastinum (UBERON:0003728) (descending mediastinitis), cervical soft tissue/fascia (necrotizing fasciitis), and the internal jugular vein (UBERON:0001586) (Lemierre's septic thrombophlebitis) (PMID: 32731900; PMID: 18435993).

Tissue and cell level. Oropharyngeal squamous epithelium, tonsillar lymphoid tissue, peritonsillar loose connective tissue, and Weber's mucous salivary glands in the supratonsillar space (PMID: 8302122). Infiltrating cells: neutrophils (CL:0000775), macrophages.

Subcellular level. Not a subcellular-organelle disease; the relevant compartment is the extracellular space (pus/abscess cavity).

Localization and lateralization. Abscesses are most often at the superior tonsillar pole near Weber's glands (PMID: 27026737). PTA is overwhelmingly unilateral; bilateral PTA is rare — only ~13 cases reported worldwide as of 2017 (PMID: 28531866).

8. Temporal Development

Onset. Acute to subacute, over days, typically following or concurrent with acute tonsillitis. Age of onset predominantly adolescent-to-young-adult (PMID: 42563151).

Progression. Untreated peritonsillar cellulitis progresses to organized abscess; the abscess exerts mass effect and, if neglected, spreads along fascial planes. There are no formal "stages" beyond cellulitis → abscess → complicated deep-neck spread.

Course and duration. Self-limited with treatment — the vast majority recover uneventfully within days after drainage and antibiotics (PMID: 32731900). Not chronic or lifelong.

Remission and recurrence. Treatment-induced resolution is the norm. Recurrence occurs in roughly 10–22%; anaerobic bacterial growth correlates with higher recurrence and serves as a relative indication for interval tonsillectomy (PMID: 18204368).

Critical intervention window. Early drainage before fascial-plane spread is the key window; delay is repeatedly implicated in fatal necrotizing/mediastinal complications.

9. Inheritance and Population

Epidemiology.

Inheritance. Not applicable — no inheritance pattern, penetrance, expressivity, anticipation, mosaicism, founder effect, consanguinity role, or carrier frequency, because PTA is a non-genetic acquired infection (Finding F009).

Population demographics. No ethnic predilection is established. Microbiology varies geographically/temporally — e.g., a Taiwanese series found Klebsiella pneumoniae prominent (23.2%) and increasing in the elderly (OR 2.76), unlike Scandinavian series dominated by F. necrophorum (PMID: 28756939). Complicated cases skew male (70%) and older (49% >40 years) (PMID: 32731900).

10. Diagnostics

Clinical diagnosis predominates. Prospective data show clinical impression alone is unreliable (sensitivity 78%, specificity 50%), whereas CT (sensitivity 100%, specificity 75%) and intraoral ultrasound (sensitivity 89%, specificity 100%) reliably distinguish abscess from peritonsillar cellulitis (PMID: 10435129).

"Contrast-enhanced CT remains the gold standard for stable patients, but point-of-care ultrasound has high accuracy for peritonsillar abscesses" (PMID: 42275833). A prospective clinical-vs-CT study in 133 consecutive patients further addresses diagnostic accuracy (PMID: 39857112).

Microbiology. Culture and, increasingly, molecular testing of aspirated pus identify pathogens; dual (culture + PCR) testing raises F. necrophorum detection (PMID: 40366504).

Genetic / omics testing. Not applicable — no genetic testing, karyotyping, microarray, or omics diagnostics are relevant to this acquired infection.

Differential diagnosis. Peritonsillar cellulitis (no drainable collection), retropharyngeal/parapharyngeal abscess, infectious mononucleosis, epiglottitis, dental/odontogenic abscess, and tonsillar/oropharyngeal neoplasm. Distinguishing features are best resolved by imaging and aspiration; clinicians face challenges recognizing evolving odontogenic vs peritonsillar abscesses in repeat presenters (PMID: 39953620).

Screening. No population screening is applicable for an acute sporadic infection.

11. Outcome / Prognosis

Prognosis is excellent for uncomplicated PTA. "The vast majority of patients with peritonsillar abscess (PTA) recover uneventfully on abscess drainage and antibiotic therapy" (PMID: 32731900). Most patients are managed as outpatients (PMID: 28409615).

Complications and mortality. A narrative review identified 17 distinct complications; the most frequent were descending mediastinitis (n=113), para-/retropharyngeal abscess (n=96), necrotizing fasciitis (n=38), and Lemierre's syndrome (n=35), with an overall mortality of 10% among complicated cases; 70% were male and 49% were >40 years (PMID: 32731900). Predominant bacteria in complications: viridans streptococci (25%), beta-hemolytic strep (20%), F. necrophorum (13%), S. aureus (11%). Deep neck infection reviews list "airway obstruction, jugular vein thrombosis, descending mediastinitis, sepsis, acute respiratory distress syndrome, and disseminated intravascular coagulation" as life-threatening (PMID: 18435993).

Prognostic factors. Older age (>40), male sex, delayed drainage, immunocompromise/comorbidity (diabetes), and F. necrophorum infection (the only pathogen associated with complications) portend worse outcomes (PMID: 32731900; PMID: 40366504).

12. Treatment

Core strategy. "Drainage of the abscess, antibiotic therapy, and supportive therapy for maintaining hydration and pain control are the cornerstones of treatment" (PMID: 28409615).

Surgical drainage (three options; NCIT: Incision and Drainage, Tonsillectomy). "There are three surgical treatment options for patients with peritonsillar abscess (PTA): needle aspiration, incision and drainage (ID), and abscess tonsillectomy (ATE)" (PMID: 34111309).

Replacing routine tonsillectomy with I&D as first-line reduced inpatient days (4 vs 7) and hemorrhage (0.3% vs 5.1%) (PMID: 25794541). In children, immediate tonsillectomy is low-risk but often unnecessary given >90% success of needle aspiration/I&D (PMID: 15448926).

Pharmacotherapy (NCIT: Antibiotic Therapy). "Peritonsillar abscesses are polymicrobial infections, and antibiotics effective against group A streptococcus and oral anaerobes should be first-line therapy" (PMID: 28409615). Empiric regimens include ampicillin-sulbactam (adding vancomycin if MRSA risk) (PMID: 42275833); penicillin plus metronidazole and clindamycin are alternatives. Relevant CHEBI: ampicillin (CHEBI:28971), metronidazole (CHEBI:6909), clindamycin (CHEBI:3745), dexamethasone (CHEBI:41879).

Adjuvant corticosteroids (NCIT: Corticosteroid Therapy). A systematic review of 3 RCTs (n=153) found adjuvant dexamethasone/methylprednisolone after drainage produced statistically significant improvement in body temperature in all trials, with pain/mouth-opening/hospital-stay benefits in some, and no adverse effects: "All three RCTs reported statistically significant improvement in body temperature from adjuvant steroid administration compared to placebo" (PMID: 28561258). "Corticosteroids may be helpful in reducing symptoms and speeding recovery" (PMID: 28409615). (Note: a Cochrane sore-throat steroid review explicitly excluded PTA, PMID: 32356360.)

Supportive care. Hydration, analgesia, and antipyretics.

Advanced / experimental / personalized therapeutics. Not applicable — no gene, cell, RNA, targeted, or immunotherapy is relevant; pharmacogenomics does not guide PTA treatment.

13. Prevention

Primary prevention. Prompt and adequate antibiotic treatment of acute bacterial tonsillitis may reduce progression to abscess (PMID: 27026737). Smoking cessation is a plausible modifiable measure given the strong smoking association (PMID: 41113746). No vaccine exists against the polymicrobial etiologic agents.

Secondary prevention. Early recognition and drainage prevent deep-neck spread; timely imaging/aspiration in atypical or repeat presenters is emphasized, as clinicians face challenges recognizing evolving abscesses in patients with repeated healthcare visits (PMID: 39953620).

Tertiary prevention. Interval/elective tonsillectomy is offered to patients with recurrent PTA or with anaerobic growth (a relative indication) to prevent recurrence: "Anaerobic bacterial growth correlates with a higher rate of recurrence, and may serve as an additional relative indicator for tonsillectomy" (PMID: 18204368).

Immunization, genetic screening, counseling. Not applicable.

14. Other Species / Natural Disease

Not applicable. PTA as defined (abscess of the human peritonsillar space near Weber's glands) is a human-specific clinical entity. There is no OMIA entry, no naturally occurring animal counterpart, no breed predisposition, and no orthologous-gene framework — because the disease is anatomical/infectious rather than genetic. Zoonotic transmission is not a feature; the causative bacteria are members of the normal human oral flora. Documented as an evidence-based "not applicable" (Finding F012).

15. Model Organisms

Not applicable. No dedicated animal, cellular, organoid, or iPSC disease model of peritonsillar abscess exists (Finding F012). The only laboratory tool identified is a low-cost, high-fidelity physical PTA drainage simulator for training emergency-medicine and otolaryngology residents — a procedural mannequin, not a biological disease model (PMID: 37465440). Bacterial virulence (e.g., F. necrophorum leukotoxin) has been studied in vitro and in animal isolates, but not as a host disease model of PTA.

Mechanistic Model / Interpretation

PTA is best understood as a two-hit acquired infection: (1) bacterial infection of the tonsillar mucosa and/or Weber's salivary glands, followed by (2) spread through the salivary duct system into the peritonsillar potential space, where F. necrophorum leukotoxin and streptococcal virulence drive a neutrophil-rich necrotizing inflammation that liquefies into pus. The superior-pole predilection, the elevated pus amylase, and the pathogen concordance with tonsillar tissue together reconcile the historical "tonsillitis vs Weber gland" debate into a single salivary-duct-spread model (PMID: 27026737; PMID: 8302122).

The clinical phenotype (trismus, uvular deviation, hot-potato voice) is a mechanical/inflammatory consequence of the expanding collection compressing and irritating the pterygoid muscles, palate, and uvula. The therapeutic logic follows directly: evacuate the pus (drainage) and kill the flora (anti-strep + anti-anaerobe antibiotics), with corticosteroids dampening the inflammatory sequelae. The prognosis dichotomy — excellent if drained, ~10% mortality if allowed to spread — reflects whether the infection is contained or breaches fascial planes into the mediastinum, neck fascia, or jugular vein.

HOST FACTORS            PATHOGEN FACTORS          OUTCOME MODIFIERS
smoking, diabetes  ─┐   F. necrophorum leukotoxin ┐  early drainage → recovery
prior tonsillitis  ─┼─► + GAS + oral anaerobes ───┼► delay/age>40/male → complications
Weber gland anatomy┘   polymicrobial synergy      ┘  anaerobes → recurrence

Evidence Base

All evidence is human clinical — consistent with PTA being an acquired infectious disease with no genetic or model-organism dimension.

Limitations and Knowledge Gaps

1. No host-genetic, omics, or model-organism data. Sections 4, 14, and 15 are genuine "not applicable" determinations, not incomplete searches. No transcriptomic/proteomic/metabolomic/single-cell/spatial datasets specific to PTA exist.
2. Diagnostic-accuracy studies are small. The pivotal imaging comparison had only n=14 (PMID: 10435129); confidence intervals are wide.
3. Surgical evidence is largely retrospective. No high-quality RCT establishes superiority of needle aspiration vs I&D vs tonsillectomy; the debate remains open (PMID: 31863198).
4. Steroid RCTs are few and small (3 trials, n=153) (PMID: 28561258).
5. Geographic microbiology variability (Scandinavian F. necrophorum dominance vs Taiwanese K. pneumoniae) limits generalization of empiric antibiotic choices.
6. No validated PTA-specific quality-of-life instrument.
7. Recurrence-rate estimates (~10–22%) derive from heterogeneous series without standardized follow-up.

Proposed Follow-up Experiments / Actions

1. Multicenter RCT of needle aspiration vs incision & drainage (with standardized antibiotics) powered for recurrence and length-of-stay, to resolve the open surgical debate.
2. Prospective molecular-microbiology cohort (PCR + culture) across geographies to define pathogen-specific complication risk and refine empiric antibiotic guidelines, extending the F. necrophorum–complication link (PMID: 40366504).
3. Adequately powered corticosteroid RCT with patient-reported outcomes and adverse-event capture, including children.
4. Point-of-care ultrasound validation in emergency settings versus CT, in a large prospective sample, to reduce radiation and cost.
5. Prospective recurrence registry stratified by microbiology (anaerobe status) and smoking, to define who benefits from interval tonsillectomy.
6. Leukotoxin biomarker study — test whether F. necrophorum leukotoxin variant/level in aspirated pus predicts severity and complications, translating the mechanistic finding (PMID: 39059623; PMID: 28330774) into a prognostic tool.

Report compiled from 12 confirmed findings across 33 reviewed papers (23 unique primary sources). Evidence type: exclusively human clinical (population registries, retrospective cohorts, small prospective diagnostic studies, and systematic reviews).

Artifacts

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• OpenScientist final report

Reference Validation

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Term Validation

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Terms the report names something else

These identifiers resolve, so nothing about them looks wrong, and the ontology calls them something unrelated to what the report calls them. That usually means the identifier is not the one the sentence needs:

• MONDO:0005906 (2 mentions) - the report calls it "MONDO"; MONDO calls it peritonsillar abscess
• HP:0001609 (1 mention) - the report calls it "nearest, dysphonia"; HP calls it Hoarse voice
• HP:0010282 (1 mention) - the report calls it "Abnormality of the uvula"; HP calls it Thin lower lip vermilion
• HP:0031936 (1 mention) - the report calls it "nearest, otalgia"; HP calls it Delayed ability to walk

Terms whose name is worth a second look

The report's name for these is recognisably related to the term's own name without being one of them. A loose paraphrase reads the same way as a citation of the wrong sibling term - and so does a related synonym, which the ontology records precisely because it names something adjacent rather than the same thing - so these are listed rather than judged:

• HP:0033050 (1 mention) - the report calls it "Pharyngitis"; HP calls it Pharyngalgia
• HP:0001974 (1 mention) - the report calls it "Leukocytosis"; HP calls it Increased total leukocyte count, and lists "Leukocytosis" among its other names