Asymmetric type F botulism with cranial nerve demyelination.

We report a case of type F botulism in a patient with bilateral but asymmetric neurologic deficits. Cranial nerve demyelination was found during autopsy. Bilateral, asymmetric clinical signs, although rare, do not rule out botulism. Demyelination of cranial nerves might be underrecognized during autopsy of botulism patients.

Epidemiology of an outbreak of antibiotic-resistant Klebsiella pneumoniae at a tertiary care medical center.

BACKGROUND: In 2004, a 650-bed, tertiary care medical center experienced an outbreak of multiple antibiotic-resistant Klebsiella pneumoniae (MR-KP) that included extended-spectrum beta-lactamase (ESBL)-producing and non-ESBL-producing strains. METHODS: Characteristics associated with MR-KP were evaluated by case-control study with variables tested by conditional regression analyses. Pulsed-field gel electrophoresis (PFGE) was used to compare the molecular relatedness of isolates. RESULTS: In 2004, the incidence rate of MR-KP increased significantly compared with 2003 (relative risk [RR], 5.1; 95% confidence interval [CI]: 3.10-8.37) when only ESBL-producing K pneumoniae were present. The increase involved both ESBL-producing MR-KP and MR-KP in which ESBL production was not detected by the testing in use. Nineteen isolates were identical or closely related by PFGE. Characteristics associated with MR-KP were longer length of hospital stay (odds ratio [OR], 2.92; 95% CI: 1.17-7.30; P = .022), greater total antibiotic-days (OR, 2.81; 95% CI: 1.19-6.65; P = .018], and higher Acute Physiology and Chronic Health Evaluation (APACHE) II score (OR, 1.15; 95% CI: 1.06-1.25; P = .001). When the MR-KP cases were subdivided into ESBL-producing K pneumoniae and ESBL-negative K pneumoniae, while controlling for length of stay, total antibiotic-days was significantly associated with ESBL-producing K pneumoniae (OR, 3.8; 95% CI: 1.2-12.1; P = .02). CONCLUSION: Compared with patients housed on the same unit at the same time, patients with MR-KP had a longer length of stay and greater antibiotic exposure. Patients with longer length of stay and greater total antibiotic exposure should be potential targets for stringent infection control measures.

Dissociation between inhibition and killing by levofloxacin in human granulocytic anaplasmosis.

Human granulocytic anaplasmosis (HGA) is a potentially fatal tick-borne infection caused by Anaplasma phagocytophilum. Treatment options are limited for this entity, with doxycycline being the drug of choice. Certain fluoroquinolones such as levofloxacin are active against A. phagocytophilum in vitro. We report a hospitalized patient with HGA who improved coincident with a 13-day course of levofloxacin therapy, but clinically and microbiologically relapsed 15 days after completion of treatment. Relapse of infection after levofloxacin therapy was reproduced in a severe combined immune-deficient (SCID) mouse infection model. Quinolone therapy should not be considered curative of HGA.

Listeria monocytogenes encephalitis mimicking West Nile encephalitis.

We present a case of a 50-year-old man who presented to Winthrop-University Hospital in the midst of the 2002 West Nile encephalitis (WNE) outbreak with the cardinal clinical findings of WNE, ie, fever, encephalopathy, weakness, and muscle tremors. During the summer of 2002, several cases of aseptic meningitis/viral encephalitis were admitted to our emergency room weekly. In addition, cases of WNE were being admitted at the same time. During this period we had 3 cases of WNE. Our patient presented with the clinical findings of WNE. However, laboratory and radiologic findings suggested the possibility of Listeria monocytogenes encephalitis. The cerebrospinal fluid findings included red blood cells, which, in the absence of a traumatic tap or HSV encephalitis, argue against the diagnosis of WNE but are consistent with L. monocytogenes encephalitis. Computed tomography scan showed communicating hydrocephalus, which also suggests the possibility of L. monocytogenes and argued against the diagnosis of WNE. Clinicians should be vigilant for the mimics of WNE in geographical areas where WNE outbreaks are occurring.