Candida parapsilosis is an important cause of bloodstream infections in the health care setting. We investigated a large C. parapsilosis outbreak occurring in a community hospital and conducted a case-control study to determine the risk factors for infection. We identified 22 cases of bloodstream infection with C. parapsilosis: 15 confirmed and 7 possible. The factors associated with an increased risk of infection included hospitalization in the intensive care unit (adjusted odds ratio, 16.4; 95% confidence interval, 1.8 to 148.1) and receipt of total parenteral nutrition (adjusted odds ratio, 9.2; 95% confidence interval, 0.9 to 98.1). Samples for surveillance cultures were obtained from health care worker hands, central venous catheter insertion sites, and medical devices. Twenty-six percent of the health care workers surveyed demonstrated hand colonization with C. parapsilosis, and one hand isolate was highly related to all case-patient isolates by tests with the DNA probe Cp3-13. Outbreak strain isolates also demonstrated reduced susceptibilities to fluconazole and voriconazole. This largest known reported outbreak of C. parapsilosis bloodstream infections in adults resulted from an interplay of host, environment, and pathogen factors. Recommendations for control measures focused on improving hand hygiene compliance.

We read with great interest the review by Grant L Campbell and colleagues 1 Campbell GL Marfin AA Lanciotti RS Gubler DJ West Nile virus. Lancet Infect Dis. 2002; 2: 519-529 Summary Full Text Full Text PDF PubMed Scopus (692) Google Scholar about West Nile virus (WNV). As stressed by the authors, muscle weakness is a prominent feature in many patients with WN encephalitis. It is also an apparent risk factor for death in patients with WN encephalitis. 2 Nash D Mostashari F Fine A et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. 2001; 344: 1807-1814 Crossref PubMed Scopus (1034) Google Scholar , 3 Petersen LR Marfin AA West Nile virus: a primer for the clinician. Ann Intern Med. 2002; 137: 173-179 Crossref PubMed Scopus (515) Google Scholar Several reports cited in the article 2 Nash D Mostashari F Fine A et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. 2001; 344: 1807-1814 Crossref PubMed Scopus (1034) Google Scholar , 4 Asnis DS Conetta R Teixeira AA Waldman G Sampson BA The West Nile virus outbreak of 1999 in New York City: the Flushing Hospital experience. Clin Infect Dis. 2000; 30: 413-418 Crossref PubMed Scopus (284) Google Scholar , 5 Sampson BA Ambrosi C Charlot A et al. The pathology of human West Nile virus infection. Hum Pathol. 2000; 31: 527-531 Summary Full Text PDF PubMed Scopus (180) Google Scholar attributed the weakness to Guillain-Barré syndrome, motor axonopathy, or severe axonal polyneuropathy. However, pathological confirmation is lacking and identification of the pathological basis for the muscle weakness remains an important public-health goal.

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV‐associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV‐associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment. Muscle Nerve 28: 302–308, 2003