AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Catscratch disease (CSD) is an infrequent self-limiting infectious disease classically characterized by painful regional lymphadenopathy following the scratch of a cat (typically a kitten). The first description is credited to Henri Parinaud, who referenced the condition in French medical literature in 1889. Dr. Robert Debré was the first to recognize the cat as a vector for this disorder and coined the term catscratch disease in 1931. After first being identified in 1985, Rochalimaea henselae, later reclassified as Bartonella henselae, was determined conclusively to be the primary organism causative of CSD.

For a related CME activity, see Companion Animals and Human Health: Part II -- Zoonotic Diseases. 

Pathophysiology

Bartonella henselae, a curved, pleomorphic, gram-negative bacillus, has been determined to be nearly exclusively responsible for CSD. Speculation exists that other pathogens, including Afipia felis and Bartonella clarridgeiae, produce a fraction of cases.

Studies have demonstrated seropositivity rates ranging from 3.1-61.6% in the general population depending on the country in which the study was performed. In all instances, few patients ever experienced symptoms, suggesting only a minority of exposures to B henselae result in CSD.

Frequency

United States

A limited survey performed in 1993 by the Centers for Disease Control and Prevention reported approximately 22,000 cases of CSD diagnosed annually, although many additional cases are likely unrecognized.¹ More than 2,000 hospital admissions are reported annually with a discharge diagnosis of CSD.¹ The estimated incidence among ambulatory patients is approximately 9.3 cases per 100,000 persons per year.¹ In 2000, approximately 437 pediatric hospitalizations associated with CSD were reported.²

Approximately 70-90% of CSD cases occur in the fall and early winter months. This seasonality is presumed to be due to a midsummer rise in kitten births accompanied by increased flea infestation.

Mortality/Morbidity

CSD is a self-limiting disorder with an excellent prognosis, even in patients with profound manifestations. Among healthy individuals, the condition usually resolves spontaneously over 2-5 months with rare permanent sequelae. However, immunocompromised patients may experience a dramatic and potentially life-threatening course of disease.

Sex

The male-to-female ratio is 3:2.

Age

Patients are younger than 21 years in approximately 80% of cases.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

• More than 90% of patients with the disease report recent contact with a cat, usually a kitten.
• In typical CSD, accounting for approximately 90% of cases, an incubation period of 3-12 days is followed by the development of one or more cutaneous papules or pustules at the inoculation site. The primary lesion lasts for 1-3 weeks then recedes as regional lymphadenopathy appears, generally immediately proximal to the inoculation site.
• Regional lymphadenopathy, which occurs in approximately 90% of patients, is characteristically the most remarkable manifestation and is usually the symptom that prompts medical evaluation. Lymphadenopathy primarily involves axillary nodes, followed in frequency by cervical and inguinal areas. Lymph nodes are often painful and spontaneously suppurate in 25-30% of cases.
• Constitutional symptoms are usually mild and may include malaise, low-grade fever, anorexia, nausea, fatigue, or headache.
• Atypical presentation (approximately 10% of cases) may include the following:
• • Altered mental status, confusion (encephalopathy)
  • Vision loss (neuroretinitis)
  • Prolonged fever
  • Joint pain (arthritis, synovitis)
  • Respiratory complaints (atypical pneumonitis)
  • Parinaud oculoglandular syndrome: An uncommon presentation of CSD (5-6% of cases), Parinaud oculoglandular syndrome caused by conjunctival inoculation. The syndrome is characterized by granulomatous conjunctivitis and ipsilateral preauricular lymphadenitis.
• Abdominal pain: The presence of abdominal pain with a history consistent with CSD suggests CSD hepatitis/splenitis, a self-limited granulomatous condition.

Physical

• Typical features
• • Erythematous, tender papules or pustules at inoculation site
  • Tender unilateral lymphadenopathy (>90%): Among patients with this disease, 50% have involvement of a single node, 30% have involvement of nodes in multiple sites, and 20% have involvement of several nodes in the same region.
• Low-grade fever (30-60%)
• Transient truncal maculopapular rash (5%)
• Atypical presentations
• • Seizures (often associated with encephalitis)
  • Transverse myelitis
  • Arthritis
  • Splenic abscess
  • Optic neuritis
  • Thrombocytopenic purpura
  • Encephalitis
  • • Occurring in approximately 2-4% of CSD cases, the condition is characterized by confusion, restlessness, combativeness, disorientation, and coma. Generalized headache and transient nuchal rigidity are often present.
    • Although encephalitis usually follows development of lymphadenopathy by 1-3 weeks, it may precede or occur without the presence of lymph node involvement.
    • CSD encephalitis is self-limited, does not mandate specific treatment, and rarely results in persistent impairment.
• Neuroretinitis
• • Neuroretinitis is characterized by a painless, unilateral, sudden loss of visual acuity; CSD neuroretinitis often follows lymphadenopathy or an influenzalike syndrome. Fundal examination reveals papilledema with macular exudates in a star pattern.
  • CSD neuroretinitis should be followed by an ophthalmologist but is predictably self-limited.
• Osteomyelitis

Causes

As indicated by its name, the preponderance of cases can be traced back to the scratch of a cat. Other suspected sources include dog and monkey bites, pins, thorns, and splinters. Cat fleas have been shown to be responsible for transmission of B henselae between cats; however, no evidence exists to suggest transmission from cat fleas to humans. Human-to-human transmission has not been verified.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Atypical mycobacterium infection
Chronic granulomatous disease
Collagen vascular disease
Lymphoma
Pyogenic lymphadenitis
Histoplasmosis
Sporotrichosis
Malignancy/lymphoma

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• Routine laboratory tests in patients with suspected catscratch disease (CSD) are usually unremarkable and are very unlikely to aid in diagnosis. Findings such as mild leukocytosis and elevated erythrocyte sedimentation rate are common but are also nonspecific and of little value.
• Until recently, diagnosis was based on the fulfillment of specific clinical criteria. The recent development of serologic testing has effectively provided laboratory confirmation of the diagnosis. The addition of PCR from lymph node biopsy provides an even more sensitive detection of disease. When such testing is performed, it is usually performed on an outpatient basis.
• • Indirect fluorescent antibody (IFA) for Bartonella has poor sensitivity (as low as 53%) but has a relatively good specificity of 93-96%. Most populations have low (2-6%) background seropositivity rates, limiting false positive tests. The IFA shows cross-reactivity between Bartonella species.
  • Infection is best demonstrated by rising immunoglobulin G (IgG) titers; however, patients may already have high levels at presentation. Titers above 1:64 are supportive of the diagnosis in the appropriate clinical setting.
• Histopathological features of lymph nodes are consistent but not pathognomonic for CSD. Features include granuloma formation, stellate abscesses, and lymphocytic infiltrates.
• Brown-Hopp tissue Gram stain and Warthin-Starry silver staining show small, curved, gram-negative bacilli.

Other Tests

• Cerebrospinal fluid (CSF): Findings are usually normal, but they may show mild pleocytosis or elevated protein. Laboratory results are unable to confirm or exclude CSD encephalitis, but they are vital in excluding other potentially life-threatening conditions.
• Electroencephalogram (EEG): Findings may demonstrate diffuse slowing in patients with encephalopathy, which like other ancillary tests, is nonspecific and resolves with clinical recovery.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Emergency Department Care

ED management of CSD is primarily symptomatic, as the disease spontaneously resolves in 2-4 months.

• Administer antipyretics and analgesics as needed.
• Local heat may be applied to the involved lymph nodes.
• Avoid incision and drainage because this may leave scars and draining fistulae without hastening recovery.
• Aspiration of tender, fluctuant nodes may relieve pain.
• Antibiotics are not indicated in most cases, but they may be considered for severe or systemic disease. Reduction of lymph node size has been demonstrated with a 5-day course of azithromycin and may be considered in patients with severe, painful lymphadenopathy; however, no advantage is shown in the duration of symptoms.
• • Immunocompromised patients should be treated with antibiotics because they are particularly susceptible to systemic disease and bacteremia. Drugs of particular effectiveness include the following:
  • • Trimethoprim-sulfamethoxazole
    • Gentamicin
    • Ciprofloxacin
    • Rifampin
  • B henselae is generally resistant to penicillin, amoxicillin, and nafcillin.

Consultations

Emergent consultation is not usually required. Consider emergent or outpatient consultation in cases of diagnostic uncertainty or with specific organ system involvement as indicated.

• Infectious disease specialist
• Ophthalmologist (in neuroretinitis)
• Neurologist (in encephalitis or seizures)

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

In general, treatment beyond administration of analgesia and recommendation for warm compresses is unnecessary because the condition spontaneously resolves without sequelae in most cases. Response to antibiotics in patients with systemic manifestations has been shown only anecdotally.

Drug Category: Antibiotics

Although not indicated in all patients, those with painful lymph node enlargement refractory to needle aspiration may benefit from a short course of antibiotics. As discussed, antibiotics are generally recommended for a patient with underlying immune compromise with CSD.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Immunocompetent patients and immunocompromised patients without evidence of systemic disease may be followed on an outpatient basis.

Further Outpatient Care

• Patients should follow up in 2-6 months for confirmation of symptom resolution.
• Disposal of the cat is not necessary, since its ability to transmit the organism is transient.

Prognosis

• The prognosis for immunocompetent patients with CSD is excellent. Complete recovery without sequelae occurs in nearly all patients. Even in patients with CNS involvement, recovery without neurologic sequelae within weeks to months can be expected.
• Patients who are immunocompromised are in jeopardy of systemic disease and resultant complications. However, with appropriate antibiotic use and management of complications, these patients also typically experience full resolution of disease.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Failure to consider CSD as a possible diagnosis is a pitfall.
• Although CSD neuroretinitis and encephalitis are self-limited and not life-threatening, other potentially serious etiologies must be ruled out.
• Current recommendations generally favor treatment with antibiotics for CSD in an immunocompromised patient.

Special Concerns

• Immunocompromised patients: Persons with AIDS or other immunocompromising conditions, such as alcoholism or use of immunosuppressive therapy, may experience more dramatic and often more atypical manifestations of CSD. Patients are at increased risk of systemic disease including encephalitis and fever with bacteremia. Treatment with antibiotics and close observation are indicated in this group of patients.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Rick Kulkarni, MD, to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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Article Last Updated: Mar 6, 2008