Definition/General
Introduction:
Suppurative lymphadenitis is an acute bacterial infection of lymph nodes characterized by neutrophilic inflammation and pus formation
It represents the most severe form of acute bacterial lymphadenitis with tissue destruction and abscess formation
The condition typically results from pyogenic bacterial infections in the drainage area of affected lymph nodes.
Origin:
Caused by pyogenic bacteria reaching lymph nodes through lymphatic drainage
Staphylococcus aureus and Streptococcus pyogenes most common causes
Gram-negative bacteria (E
coli, Pseudomonas) in immunocompromised patients
Anaerobic bacteria from oral/dental infections
Polymicrobial infections possible
Hematogenous spread from distant infected sites
Direct extension from adjacent infected tissues.
Classification:
Classified by stage of infection: Early suppurative lymphadenitis (neutrophilic infiltration without abscess)
Abscess formation stage (central liquefactive necrosis)
Chronic suppurative lymphadenitis (persistent infection with fibrosis)
By causative organism: Staphylococcal
Streptococcal
Gram-negative bacterial
Anaerobic bacterial
Polymicrobial.
Epidemiology:
All age groups affected but more common in children and immunocompromised
Higher incidence in developing countries with poor hygiene
Seasonal variation with skin and soft tissue infections
Males slightly more affected due to higher trauma rates
Immunocompromised patients at higher risk
Healthcare-associated infections in hospitalized patients.
Clinical Features
Presentation:
Painful, rapidly enlarging lymph nodes (distinguishes from chronic conditions)
Erythema and warmth of overlying skin
Fluctuation when abscess forms
Regional lymphadenopathy following drainage patterns
Systemic signs of infection (fever, chills)
Primary infection site often identifiable
Tender, firm to fluctuant masses.
Symptoms:
High fever with chills and rigors
Severe pain at lymph node site
Malaise and weakness
Anorexia and nausea
Headache and myalgia
Skin breakdown over affected nodes
Purulent discharge if spontaneous drainage occurs
Sepsis in severe cases.
Risk Factors:
Immunocompromised state (HIV, chemotherapy, corticosteroids)
Diabetes mellitus
Chronic renal failure
Malnutrition
Skin and soft tissue infections in drainage area
Dental infections (cervical lymphadenitis)
Recent surgery or trauma
Intravenous drug use
Chronic skin conditions.
Screening:
Complete blood count (leukocytosis with left shift)
Blood cultures (bacteremia assessment)
Inflammatory markers (elevated ESR, CRP, procalcitonin)
Imaging studies (ultrasound, CT for abscess detection)
Fine needle aspiration for culture and cytology
Surgical drainage when indicated
Primary infection site evaluation.
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Gross Description
Appearance:
Markedly enlarged lymph nodes with tense, thickened capsule
Cut surface shows yellow-green purulent material (pus)
Central liquefactive necrosis with abscess cavity formation
Surrounding hemorrhagic tissue
Capsular rupture may be present with extranodal spread
Adherence to surrounding tissues.
Characteristics:
Fluctuant consistency due to pus formation
Multiloculated abscesses possible
Thick, purulent discharge on sectioning
Necrotic, friable tissue around abscess cavity
Hemorrhagic areas common
Capsular thickening and inflammatory changes
Extension into perinodal tissue.
Size Location:
Variable size from 2-10 cm
Cervical lymph nodes (head/neck infections, dental infections)
Axillary lymph nodes (upper extremity infections)
Inguinal lymph nodes (lower extremity, pelvic infections)
Mesenteric lymph nodes (intra-abdominal infections)
Mediastinal involvement rare.
Multifocality:
Usually single lymph node group initially affected
Progressive spread to adjacent nodes
Bilateral involvement in systemic infections
Multiple abscesses within same node
Extranodal extension common
Sinus tract formation to skin surface.
Microscopic Description
Histological Features:
Extensive neutrophilic infiltration throughout lymph node parenchyma
Central liquefactive necrosis with pus formation
Complete architectural effacement in affected areas
Bacterial colonies may be visible
Capsular involvement with inflammation and thickening
Surrounding granulation tissue
Microabscess formation in early stages.
Cellular Characteristics:
Abundant neutrophils (viable and degenerated)
Liquefactive necrosis with nuclear debris
Bacterial organisms visible on special stains
Histiocytes and macrophages at periphery
Granulation tissue with capillary proliferation
Fibroblasts in organizing areas
Chronic inflammatory cells at margins.
Architectural Patterns:
Complete architectural destruction in abscess areas
Central necrosis surrounded by inflammatory zone
Capsular involvement with extension beyond node
Microabscess formation pattern
Granulation tissue organization at periphery
Sinus tract formation toward skin
Fibrosis in healing areas.
Grading Criteria:
Extent of suppuration (focal, extensive, complete)
Degree of tissue destruction
Bacterial load (organism density)
Inflammatory response intensity
Capsular involvement extent
Extranodal extension presence
Organization and healing assessment.
Immunohistochemistry
Positive Markers:
CD15 highlights neutrophils prominently
CD68 positive in histiocytes and macrophages
Myeloperoxidase (MPO) positive in neutrophils
Lysozyme positive in neutrophils and macrophages
CD3 shows T-cells in preserved areas
CD20 shows B-cells if any preserved follicular areas
Ki-67 high in inflammatory areas.
Negative Markers:
Lymphoid markers (CD45RA, CD45RO) in necrotic areas
CD1a and Langerin negative
CD30 negative (excludes lymphoma)
Cytokeratin negative (excludes carcinoma)
S-100 negative
Melanoma markers negative
Specific lymphoma markers negative.
Diagnostic Utility:
Limited utility given obvious inflammatory nature
CD15 and MPO confirm neutrophilic infiltration
Gram stain and special stains for organism identification more important
Culture and antibiotic sensitivity essential
Molecular methods for organism identification when culture negative
Exclusion of malignancy when indicated.
Molecular Subtypes:
Bacterial species identification by PCR and sequencing
Antibiotic resistance genes detection
Virulence factor identification
Methicillin resistance (MRSA detection)
Extended-spectrum beta-lactamase (ESBL) detection
Vancomycin resistance genes
Biofilm formation genes.
Molecular/Genetic
Genetic Mutations:
Host genetic susceptibility factors
Complement deficiencies
Neutrophil dysfunction syndromes
Primary immunodeficiency genes
Bacterial resistance mutations
Virulence gene variations
No specific host mutations for suppurative lymphadenitis.
Molecular Markers:
Pro-inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-8)
Neutrophil activation markers
Complement activation products
Acute phase reactants (C-reactive protein, procalcitonin)
Bacterial toxins and endotoxins
Neutrophil extracellular traps (NETs)
Antimicrobial peptides.
Prognostic Significance:
Good prognosis with appropriate antibiotic therapy and drainage
Delayed treatment may lead to complications
Immunocompromised patients have worse outcomes
Sepsis indicates serious prognosis
Complete resolution expected with adequate treatment
Chronic infections possible with inadequate therapy
Scarring may result from extensive tissue destruction.
Therapeutic Targets:
Broad-spectrum antibiotics initially, then organism-specific
Surgical drainage for large abscesses
Source control (treatment of primary infection)
Supportive care (fluid resuscitation, pain management)
Anti-staphylococcal agents (vancomycin, linezolid for MRSA)
Anti-streptococcal agents (penicillin, clindamycin)
Anaerobic coverage when indicated.
Differential Diagnosis
Similar Entities:
Necrotizing lymphadenitis (Kikuchi disease)
Tuberculosis with liquefactive necrosis
Fungal lymphadenitis
Malignant lymphoma with necrosis
Metastatic carcinoma with necrosis
Cat scratch disease with suppuration
Actinomycosis
Nocardiosis.
Distinguishing Features:
Suppurative lymphadenitis: abundant neutrophils, bacterial organisms, acute presentation, positive cultures
Kikuchi: absence of neutrophils, crescentic histiocytes, young Asian females
Tuberculosis: caseous necrosis, epithelioid granulomas, AFB positive
Lymphoma: malignant cells, specific immunophenotype, progressive course
Cat scratch: stellate abscesses, Warthin-Starry positive, cat exposure.
Diagnostic Challenges:
Extensive necrosis may obscure bacterial organisms
Culture-negative cases require molecular methods
Mixed infections complicate organism identification
Underlying malignancy may predispose to secondary infection
Atypical organisms in immunocompromised patients
Antibiotic pre-treatment may affect culture results.
Rare Variants:
Necrotizing fasciitis with lymph node involvement
Gas gangrene with lymphadenitis
Melioidosis (Burkholderia pseudomallei)
Glanders (Burkholderia mallei)
Tularemia with suppuration
Plague (Yersinia pestis)
Anthrax lymphadenitis
Polymicrobial necrotizing infections.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
[Lymph node excision/drainage] from [anatomical location], measuring [X.X] cm, with purulent material
Diagnosis
Suppurative lymphadenitis with abscess formation
Stage Classification
Stage: [early suppurative/abscess formation/chronic], extent: [focal/extensive/complete]
Histological Features
Shows [extensive neutrophilic infiltration] with [central liquefactive necrosis] and [bacterial organisms]
Size and Extent
Size: [X.X] cm, suppuration: [extensive/focal], capsular involvement: [present/absent]
Organism Detection
Organisms: [visible on Gram stain/culture results], morphology: [description]
Special Studies
Gram stain: [positive/negative for bacteria], morphology: [cocci/rods/mixed]
Culture: [organism identification], sensitivity: [antibiotic pattern]
Molecular: [if performed] PCR for [specific organisms/resistance genes]
Final Diagnosis
Suppurative lymphadenitis, [specific organism when identified], requiring antibiotic therapy and drainage