Cat Scratch Disease
Roberto N. Miranda, MD
Key Facts
Terminology
Necrotizing inflammation caused by Bartonella henselae
Etiology/Pathogenesis
Bartonella henselae causes most cases of CSD
90% of patients report contact with cats
B. henselae causes CSD in mostly immunocompetent patients
B. henselae in immunocompromised patients can cause bacillary angiomatosis
Clinical Issues
Primary lesion in skin appears as 0.5-1 cm erythematous papule at site of cat scratch
Regional lymphadenopathy appears 1-3 weeks after inoculation
In immunocompetent patients, disease is self-limited and confined to lymph nodes
Microscopic Pathology
Follicular lymphoid hyperplasia with prominent germinal centers
Early lesions show eosinophilic necrosis admixed with neutrophils in subcapsular sinus
Advanced changes show stellate necrotizing microabscesses and granulomas
Ancillary Tests
Bacteria are more easily identified by immunohistochemistry than by Warthin-Starry stain
Serology is considered practical method for diagnosis, but it has shortcomings
TERMINOLOGY
Abbreviations
Cat scratch disease (CSD)
Synonyms
Parinaud oculoglandular syndrome
Definitions
Necrotizing inflammation caused by Bartonella henselae
ETIOLOGY/PATHOGENESIS
Infectious Agents
Bartonella henselae causes most cases of CSD
B. quintana causes a minority of CSD cases
Patients with CSD are usually immunocompetent
Bartonella henselae is name adopted since 1993
Earlier names were Afipia felis and Rochalimaea henselae
Bacteria are small, pleomorphic, curved, motile, Gram-negative bacilli, oxidase-negative
Culture is difficult; bacteria can take 2-6 weeks to grow
Better yield in systemic disease; poor yield from lymph node
Patients report contact with cats in 90% of cases
Approximately 60% of patients report antecedent cat scratch
Bacilli are transmitted to humans through bite or scratch of infested cat
Healthy cats with fleas are reservoir for B. henselae
B. henselae resides in erythrocytes of cats and does not cause illness
B. henselae has also been isolated from fleas of cats carrying bacilli
Granuloma formation results from activation and accumulation of histiocytes
Thought to be secondary to interferon-γ-mediated TH1 cell response
CLINICAL ISSUES
Epidemiology
Incidence
Bartonella henselae has worldwide distribution
Approximately 22,000 cases of CSD are diagnosed each year in United States
CSD is most frequent cause of benign lymphadenopathy in children and young adults
Seasonal distribution; most cases occur between July and January
Relative incidence of CSD in adults is increasing; currently approximately 40%
Presentation
Spectrum of disease ranges from localized to systemic
Most patients have mild disease with malaise, generalized aching; about 2/3 of patients have fever
Primary lesion in skin appears as 0.5-1 cm erythematous papule
At site of cat scratch
Skin lesion appears 3-10 days after inoculation
Initial papular lesion is followed by vesicle that oozes fluid and eventually dries
Upper extremities are more frequently affected, followed by cervical and facial regions
Regional lymphadenopathy appears 1-3 weeks after inoculation
Lymphadenopathy is tender with erythematous overlying skin
Suppuration occurs in approximately 10% of cases
Lymphadenopathy is localized or regional in 85% of patients, but it can affect multiple areas
Parinaud syndrome consists of conjunctivitis and preauricular lymphadenopathy
Conjunctiva shows ulceration, chronic inflammation, and necrotic granulomas
Laboratory Tests
Minimal leukocytosis with or without eosinophilia can occur
Bacteria can be isolated and cultured from clinical specimens
Intradermal skin test is obsolete because lack of standardization and risk of transmissible diseases
Test required use of aspirated suppurative material from clinical specimens
Natural History
In immunocompetent patients, CSD is self-limited and confined to lymph nodes
Usually lasts 2-4 months if no therapy is administered
1-2% of patients may have prolonged fever, suppurative lymphadenitis, or systemic symptoms
In immunocompromised patients, disease may become systemic, severe, and life-threatening
Multiorgan involvement in this subset of patients
Treatment
Varies depending upon clinical presentation and immune status of patient
CSD usually does not respond to therapy
Several studies could not demonstrate that antibiotic therapy changes course of disease
No decrease in duration of disease or probability of suppuration
Prognosis
CSD is self-limited disease with excellent prognosis
MACROSCOPIC FEATURES
General Features
Lymph nodes are enlarged, matted, and adherent to surrounding soft tissues or skin
Focal areas of necrosis or microabscesses are grossly visible
MICROSCOPIC PATHOLOGY
Histologic Features
Early lesions in lymph nodes
Follicular lymphoid hyperplasia with germinal centers showing abundant tingible body macrophages
Eosinophilic necrosis admixed with neutrophils or karyorrhexis in subcapsular sinus
Tends to extend into adjacent germinal centers
Patches of monocytoid cells within sinuses are also noted
Dilated sinuses contain lymphocytes, histiocytes, and immunoblasts
Progressive changes in lymph nodes
Small abscesses with necrosis and clusters of neutrophils
Initially in subcapsular sinus; subsequently in cortex and then medulla
Advanced changes in lymph nodes
Classic stellate necrotizing granulomas of CSD
Macrophages surround abscess-forming rim of epithelioid cells
Epithelioid cells include rare multinucleated, Langhans-type cells
Warthin-Starry silver impregnation stain is useful to visualize bacteria
Chances of visualizing bacteria in lymph nodes is highest in early lesions
Skin lesions
Rarely biopsied
Histologic features similar to those described in lymph nodes
ANCILLARY TESTS
Histochemistry
Warthin-Starry
Reactivity: Positive
Staining pattern
Not applicable
Small bacilli; L-shaped forms
Bacteria are present in patchy distribution
Affected areas can be devoid of bacteria; in other areas bacteria are present in clusters
Brown-Hopps Gram stain can confirm presence of bacteriaStay updated, free articles. Join our Telegram channel
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