70 Marienfeld: Expressive aphasia presentation of B. henselae encephalitis febrile patient with an elevated WBC count, and the recent exposure history. CSD en- cephalopathy was considered more likely. Focal neurologic presentations in a popula- tion this age often prompt concern for stroke. When this has been thoroughly eval- uated, it is important to consider that sys- temic infections such as CSD in the proper clinical setting also can present with focal neurologic symptoms. Most commonly, CSD is diagnosed in patients younger than 21 [10]; in one study, 79.2 percent were younger than 18 [2]. The majority of reports involving neurologic pre- sentations of CSD are from the pediatric lit- erature. In one report, roughly 12 percent had neurologic complications [4], and other reports include severe encephalopathy [11], status epilepticus [12], anti-epileptic drug re- sistant seizures [11,13], recurrent status epilepticus and prolonged encephalopathy with hemiparesis and chorea [13], pleural ef- fusions and encephalopathy [14], fatal meningitis and encephalitis [15], fatal dis- seminated systemic disease and encephalitis [16], and acute hemiplegia [17]. There has been one report of an adolescent boy whose CSD encephalopathy presented with acute- onset, self-resolving, recurrent expressive aphasia [18]. A comprehensive look at the neurologic complications of B. henselae since 1995 re- ported that encephalopathy, in particular, was noted, though there have been associations with aseptic meningitis and dementia in pa- tients co-infected with human immunodefi- ciency virus [19]. More recent reports describe MRI changes associated with CSD neurologic manifestations [17,20,21,22]. Larger studies estimate between 0.17 percent to 2 percent of patients develop encephalopa- thy [3,23]. Over the past two decades, there have been several case reports of CSD with encephalopathy or meningoencephalitis and status epilepticus [13,24-29]. Such reports have prompted recommendations for the consideration of CSD in the differential di- agnosis of any previously healthy adult pre- senting with neurologic complications who has a history of lymphadenopathy, especially if he owns a cat [1]. One study showed en- cephalopathy in 61 of 76 patients with neu- rologic complications of CSD, with 15 showing cranial or peripheral nerve involve- ment. Of these patients, 78 percent recovered within one to 12 weeks, and 100 percent re- covered within one year, with roughly 50 percent receiving antibiotics. None had any neurologic sequelae [30]. Our patient responded to antibiotics rapidly. The self-limited form of CSD is often unaffected by antibiotic treatment [3]. With severe or persistent CSD infection, several antibiotics are effective, including erythromycin and doxycycline [1]. While there is little evidence based treatment for neurologic disease of CSD, expert opinion recommends a combination of doxycycline plus rifampin for 10 to 14 days. Most serious and potentially life-threatening infections re- spond well to antibiotic therapy [1]. REFERENCES 1. Smith DL. Cat-scratch disease and related clinical syndromes. Am Fam Physician. 1997;55(5):1783-9,1793-4. 2. Bass JW, Vincent JM, Person DA. The ex- panding spectrum of Bartonella infections: II. Cat-scrach disease. Pediatr Infect Dis J. 1997;16(2):163-79. 3. Murakami K, Tsukahara M, Tsuneoka H, Lino H, Ishida C, Tsujino K, et al. Cat Scratch Disease: analysis of 130 seropositive cases. J Infect Chemother. 2002;8(4):349-52. 4. Reynolds MG, Holman RC, Curns AT, O’Reilly M, McQuiston JH, Steiner CA. Epi- demiology of cat-scratch disease hospitaliza- tions among children in the United States. Pediatr Infect Dis J. 2005;24(8):700-4. 5. Rolain JM, Brouqui P, Koehler JE, et al. Rec- ommendations for treatment of human infec- tions caused by Bartonella species. Antimicrob Agents Chemother. 2004;48:1921. 6. Regnery RL, Olson JG, Perkins BA, Bibb W. Serological response to “Rochalimaea hense- lae” antigen in suspected cat scratch disease. Lancet. 1992;339:1443. 7. Jensen WA, Fall MZ, Rooney J, et al. Rapid identification and differentiation of Bar- tonella species using a single-step PCR assay. J Clin Microbiol. 2000;38:1717. 8. Topakian R, Barrick TR, Howe FA, et al. Blood-brain barrier permeability is increased in normal-appearing white matter in patients with lacunar stroke and leucoaraiosis. J Neu- rol Neurosurg Psychiatry. 2010;81:192-7. 9. Wardlaw J, Farrall A, Armitage PA, Carpen- ter T, Chappell F, Doubal F, et al. Changes in Background Blood–Brain Barrier Integrity