On August 14, 1994, the Broward County Public Health Unit of the Florida Department of Health and Rehabilitative Services was notified of three children from Pompano Beach who were hospitalized with encephalitis attributed to cat scratch disease (CSD). All three children (aged 5, 6, and 11 years) were previously healthy and had no histories of seizure disorders or diagnoses of CSD. This report summarizes the investigation of these cases.

On August 12 and 13, during a 26-hour period, each child entered the emergency department of the same hospital with sudden onset of generalized seizures, coma, and respiratory depression requiring intubation and assisted ventilation. Two of the children had focal lymphadenopathy (axillary and epitrochlear) on admission; cervical lymphadenopathy developed in the third child during hospitalization. Clinical examinations and laboratory tests ruled out some causes of encephalopathy, including viral infections (e.g., herpes simplex and arboviruses), metabolic disorders, and toxic ingestions.

On September 5 and 27, additional cases of CSD encephalitis were confirmed in a 9-year-old boy and a 3-year-old girl from the same area (Fort Lauderdale and Boynton Beach). CSD lymphadenopathy had been diagnosed in both children approximately 3 weeks before the onsets of seizure and coma. Although the girl had been treated with successive courses of amoxicillin/clavulanate potassium and trimethoprim-sulfamethoxazole before the onset of CSD encephalitis, both of these cases were clinically similar to the first three cases.

Case and contact investigations identified exposure (e.g., handling and petting) to stray kittens as the only common link among the affected children; histories of overt scratches or bites were not elicited. Indirect fluorescent-antibody testing at CDC detected elevated antibody titers to Bartonella henselae, the etiologic agent for CSD, in all five patients (Table_1, page 915). Microscopic examination of lymph node biopsies was consistent with CSD for the two children with lymphadenopathy on presentation.

During hospitalization (range: 11-17 days), all children received supportive care and antibiotic and anticonvulsant therapy. All five children recovered without apparent sequelae. Reported by: JE Stone, MJ Gorensek, MD, J Del Toro, MD, J Wong, MD, CA Gadia, MD, Broward General Medical Center, JL Cresanta, MD, JP Griffiths, RG Self, MD, Broward County Public Health Unit, Fort Lauderdale; WG Hlady, MD, RS Hopkins, MD, State Epidemiologist, Florida Dept of Health and Rehabilitative Svcs. Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: CSD is caused by infection with Bartonella (formerly Rochalimaea) henselae, an organism that has been associated with bacillary angiomatosis in immunocompromised persons. CSD is associated with exposure to cats infected with B. henselae. An estimated 22,000 cases of CSD occur annually in the United States (1). CSD affects persons of all age groups and both sexes and generally is characterized by a self-limiting, regional lymphadenopathy. Uncommon manifestations of B. henselae infection include Parinaud oculoglandular syndrome, relapsing bacteremia, and endocarditis and bacillary peliosis (2). Affected lymph nodes usually are proximal to the site of a cat scratch or bite, frequently are tender, and may suppurate. Although antimicrobial agents such as trimethoprim-sulfamethoxazole, rifampin, amoxycillin, and tetracycline exhibit in vitro antimicrobial activity against B. henselae, antimicrobial therapy has not been consistently beneficial in reducing the duration or severity of CSD (3). Treatment of CSD is generally supportive, although excision of the affected lymph node(s) and the use of antimicrobials may be indicated for treatment of severe swelling, pain, or suppuration.

B. henselae infection in cats is asymptomatic. Cats can be asymptomatically bacteremic for several months and develop detectable antibodies concurrently with bacteremia (4). The seroprevalence of antibodies to B. henselae in cats is 14%-44% (5). Although B. henselae has been detected in fleas, the role of these and other ectoparasites in the transmission of B. henselae is unclear (2). Treatment with tetracycline has reduced bacteremia in cats; however, the effectiveness of treatment on preventing reinfection or recrudescence is unknown.

Encephalitis is a rare complication of CSD, occurring in 1%-7% of cases (3,5). Encephalitis typically develops 2-6 weeks after classic CSD -- a pattern illustrated by this report. Clusters of CSD-associated encephalitis are rare, although two cases occurred in Connecticut during a 2-month period (1). Possible explanations for the cluster of CSD encephalitis cases include a background epidemic of classic CSD; however, because initial epidemiologic surveys have found no evidence of this or the presence of a more virulent form of B. henselae, further laboratory and epidemiologic studies are being conducted.

Recommendations for the prevention of CSD are directed toward the need to minimize contact between infected cats and humans. Cat owners should be encouraged to ensure that their pets receive routine veterinary health care that includes periodic physical examinations to prevent or detect ectoparasite infestations and to maintain current vaccinations against other zoonotic diseases (i.e., rabies). The potential for the transmission of B. henselae also may be reduced by keeping kittens and other pets indoors and by not playing roughly with them. Finally, the public should be educated to avoid contact with stray animals, to wash and disinfect bite and scratch wounds, and to seek appropriate medical care for severe injuries.

References

1. Zangwill KM, Hamilton DH, Perkins BA, et al. Cat scratch disease in Connecticut: epidemiology, risk factors, and evaluation of a new diagnostic test. N Engl J Med 1993;329:8-13.

2. Koehler JE, Glaser CA, Tappero JW. Rochalimaea henselae infection -- a new zoonosis with the domestic cat as reservoir. JAMA 1994;271:531-5.

3. Carithers HA, Margileth AM. Cat-scratch disease. Am J Dis Child 1991;145:98-101.

4. Regnery R, Martin M, Olson J. Naturally occurring Rochalimaea henselae infections in domestic cats. Lancet 1992;340:557-8.

5. Childs JE, Rooney JA, Cooper JL, Olson JG, Regnery RL. Epidemiologic observations on infection with Rochalimaea species among cats living in Baltimore, Md. J Am Vet Med Assoc 1994;204:1775-8.

TABLE 1. Serologic results for cat-scratch disease encephalitis patients,
by age, date of onset, and date of serum specimen -- Broward and Palm
Beach counties, Florida, 1994
===========================================================================
Age (yrs)  Date of onset  Date of serum specimen   Antibody titer
---------------------------------------------------------------------------
    6          Aug 12             Aug 12               1:2048
   11          Aug 13             Aug 13               1:512
    5          Aug 14             Aug 14               1:8192
    9          Sep 5              Sep 5                1:>8192
    3          Sep 27             Sep 27               1:2048
===========================================================================

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