Definition/General
Introduction:
Cat scratch disease is a zoonotic infection caused by Bartonella henselae, a gram-negative bacterium
It typically presents as regional lymphadenopathy following cat scratch or bite
The condition is self-limiting in immunocompetent individuals
FNAC shows characteristic stellate microabscesses with surrounding granulomatous inflammation.
Origin:
Caused by Bartonella henselae, transmitted through cat scratches, bites, or flea bites
Cats serve as the primary reservoir, especially kittens
The organism invades endothelial cells and erythrocytes
Results in granulomatous inflammatory response in lymph nodes
Stellate abscesses are characteristic pathological feature.
Classification:
Clinical forms: Typical cat scratch disease (regional lymphadenopathy)
Parinaud oculoglandular syndrome (conjunctivitis + preauricular lymphadenopathy)
Encephalopathy (rare neurological complication)
Neuroretinitis (optic disc swelling)
Pathological patterns: Acute suppurative
Granulomatous
Mixed pattern.
Epidemiology:
Worldwide distribution with higher incidence in temperate climates
Seasonal variation (peak in fall and winter)
Bimodal age distribution: children and young adults
No gender predilection
Cat exposure history in 90% cases
Immunocompromised patients may develop severe disease.
Clinical Features
Presentation:
Regional lymphadenopathy (most common presentation, 85-90%)
Primary inoculation lesion at scratch site (papule or pustule)
Unilateral involvement typical
Axillary nodes most commonly affected (50%)
Cervical and inguinal nodes also frequent
Node tenderness in 60-70% cases.
Symptoms:
Low-grade fever in 30-40% patients
Malaise and fatigue
Headache
Anorexia
Conjunctivitis (in Parinaud syndrome)
Skin rash occasionally
Arthralgia
Sore throat
Most patients remain relatively well.
Risk Factors:
Cat exposure (major risk factor, especially kittens)
Cat scratch or bite history
Flea infestation of cats
Young age (children and adolescents)
Immunocompromised state
Warm, humid climate
Fall and winter seasons
Rural or suburban residence.
Screening:
Diagnosis primarily clinical with supportive tests
Bartonella henselae serology (IgM and IgG)
PCR testing of lymph node aspirate
Complete blood count (may show mild eosinophilia)
ESR may be elevated
Warthin-Starry silver stain for organisms
Culture (difficult, requires special media).
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Gross Description
Appearance:
Enlarged lymph nodes (typically 1-5 cm)
Nodes are tender and mobile
Unilateral regional distribution
Cut surface may show areas of suppuration
Stellate appearance of abscesses characteristic
Surrounding reactive tissue
Capsular thickening common.
Characteristics:
FNAC aspirate shows variable cellularity
Purulent material in suppurative cases
Mixed inflammatory infiltrate
Necrotic debris in background
Granulomatous inflammation
May be hemorrhagic
Proteinaceous background.
Size Location:
Axillary lymph nodes most common (50%)
Cervical nodes (25%)
Inguinal nodes (15%)
Preauricular nodes (in Parinaud syndrome)
Node size ranges from 1-8 cm
Regional distribution following lymphatic drainage
Unilateral involvement typical.
Multifocality:
Regional clustering of affected nodes
Single node group typically involved
Drainage area of inoculation site
Progression to adjacent node groups uncommon
Bilateral involvement rare
Generalized lymphadenopathy suggests other diagnosis.
Microscopic Description
Histological Features:
FNAC shows stellate microabscesses (pathognomonic feature)
Central necrosis with surrounding epithelioid cells
Neutrophilic infiltration
Granulomatous inflammation
Giant cells (Langhans and foreign body type)
Chronic inflammatory cells
Reactive lymphoid tissue in background.
Cellular Characteristics:
Stellate abscesses: Central area of neutrophils and necrotic debris with radiating arms
Epithelioid cells: Large cells with oval nuclei and abundant eosinophilic cytoplasm
Neutrophils: Abundant in acute phase
Lymphocytes: Small mature type with some activated forms
Plasma cells and eosinophils may be present
Giant cells: Multinucleated with Langhans or foreign body type.
Architectural Patterns:
Microabscesses with stellate configuration
Granulomatous reaction surrounding abscesses
Zonal architecture: central necrosis, epithelioid cells, chronic inflammation
Reactive follicular hyperplasia in background
Capsular and perinodal inflammation
Vascular proliferation may be present.
Grading Criteria:
No formal grading system for cat scratch disease
Assessment based on inflammatory phase: Acute (predominant neutrophils)
Subacute (mixed pattern)
Chronic (predominant granulomas)
Extent of necrosis
Presence of stellate abscesses
Granuloma maturity.
Immunohistochemistry
Positive Markers:
CD68 positive in epithelioid cells and macrophages
Lysozyme positive in epithelioid cells
CD3 positive in T-lymphocytes
CD20 positive in B-lymphocytes (background)
Neutrophil markers (CD15, MPO) in acute areas
CD34 highlights increased vascularity.
Negative Markers:
Cytokeratin negative (excludes carcinoma)
CD30 and CD15 negative in epithelioid cells (excludes Hodgkin lymphoma)
S-100 negative in epithelioid cells
Langerin negative (excludes LCH)
ALK negative (excludes ALCL)
Melanoma markers negative.
Diagnostic Utility:
IHC has limited diagnostic utility for cat scratch disease
Mainly used to exclude other conditions
CD68 positivity confirms histiocytic nature of epithelioid cells
Useful in differential diagnosis with lymphoma
Special stains more useful than IHC for organism detection.
Molecular Subtypes:
Cat scratch disease shows granulomatous inflammatory response
Th1-mediated immunity
Interferon-gamma production
TNF-alpha elevation
IL-12 and IL-18 upregulation
Nitric oxide production by macrophages
Complement activation.
Molecular/Genetic
Genetic Mutations:
No specific genetic mutations in host for cat scratch disease
Host immune response determines disease severity
HLA associations may influence susceptibility
Cytokine gene polymorphisms affect immune response
Complement deficiencies may predispose to severe disease
Bacterial virulence factors important.
Molecular Markers:
Bartonella henselae DNA detection by PCR
16S rRNA amplification
Specific gene targets (groEL, rpoB)
Real-time PCR for quantification
Serology for antibody detection
Culture-independent methods preferred
Immunofluorescence for organism visualization.
Prognostic Significance:
Excellent prognosis in immunocompetent patients
Self-limiting disease resolving in 2-6 months
Complete recovery expected
Complications rare in healthy individuals
Immunocompromised patients may develop severe disease
Parinaud syndrome has good prognosis
Neurological complications usually resolve completely.
Therapeutic Targets:
Supportive care usually sufficient
Antibiotics for severe cases (azithromycin, doxycycline, ciprofloxacin)
Analgesics for pain relief
Anti-inflammatory drugs
Needle aspiration for large suppurative nodes
Surgical drainage rarely needed
Prevention: avoid cat scratches, flea control.
Differential Diagnosis
Similar Entities:
Tuberculosis
Atypical mycobacterial infection
Tularemia
Lymphogranuloma venereum
Hodgkin lymphoma
Kikuchi disease
Toxoplasmosis
Suppurative bacterial lymphadenitis
Sarcoidosis.
Distinguishing Features:
Tuberculosis: Caseating granulomas, AFB positive
Atypical mycobacteria: Different organisms on special stains
Tularemia: Different exposure history, serology
Lymphogranuloma venereum: Sexual transmission, different organisms
Hodgkin lymphoma: Reed-Sternberg cells, CD15/CD30 positive
Kikuchi disease: Crescentic histiocytes, no neutrophils.
Diagnostic Challenges:
Distinguishing from other granulomatous lymphadenitis
Stellate abscesses may be missed on limited sampling
Organism detection requires special stains
Serology may be negative early in disease
PCR not universally available
Clinical correlation essential.
Rare Variants:
Parinaud oculoglandular syndrome
Neuroretinitis
Encephalopathy
Osteomyelitis
Endocarditis
Bacillary angiomatosis (in immunocompromised)
Peliosis hepatis
Fournier gangrene (extremely rare).
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
Fine needle aspiration cytology of [site] lymph node
Clinical History
Cat exposure history: [present/absent]. Duration of lymphadenopathy: [duration]. Associated symptoms: [fever, malaise]. Inoculation lesion: [present/absent]
Adequacy
Adequate for evaluation - cellular smears with adequate inflammatory tissue
Morphological Features
Cellular smears showing stellate microabscesses with central necrosis and neutrophils. Surrounding granulomatous inflammation with epithelioid cells and giant cells. Background reactive lymphoid tissue
Stellate Abscesses
Present - characteristic finding with central neutrophilic necrosis and radiating arms (pathognomonic for cat scratch disease)
Special Stains
Warthin-Starry silver stain: [positive/negative for organisms]. GMS stain: [if performed]. PAS stain: [if performed]
Molecular Studies
PCR for Bartonella henselae: [positive/negative if performed]. Bartonella serology: [if available]
Cytological Diagnosis
Granulomatous lymphadenitis with stellate microabscesses, consistent with cat scratch disease
Recommendations
Clinical correlation with cat exposure history. Bartonella serology if not done. Conservative management - self-limiting disease. Antibiotics if severe or immunocompromised
Comments
The presence of stellate microabscesses in the appropriate clinical setting (cat exposure) is highly suggestive of cat scratch disease. This is typically a self-limiting condition in immunocompetent individuals