Outbreaks due to Clostridium difficile polymerase chain reaction (PCR) ribotype 027, toxinotype III, were detected in 7 hospitals in the Netherlands from April 2005 to February 2006. One hospital experienced at the same time a second outbreak due to a toxin A–negative C. difficile PCR ribotype 017 toxinotype VIII strain. The outbreaks are difficult to control.

To elucidate the prevalence, characteristics and risk factors of community-onset Clostridium difficile infection (CO-CDI), an uncontrolled prospective study was performed. For 3 months in 2007-2008, three laboratories in The Netherlands tested all unformed stool samples submitted by general practitioners (GPs) for C. difficile by enzyme immunoassay for toxins A and B, irrespective of whether GPs specifically requested this. Patients with positive results were asked to complete a questionnaire. Positive stool samples were cultured for C. difficile, and isolates were characterized. In all, 2443 stool samples from 2423 patients were tested, and 37 patients (1.5%) with positive toxin test results were identified. Mixed infections were not found. Age varied from 1 to 92 years, and 18% were under the age of 20 years. Diarrhoea was typically frequent and watery, sometimes with admixture of blood or fever. Eight of 28 patients (29%) suffered recurrences. Among 31 patients with toxin-positive stool samples for whom information was available, 20 (65%) had not been admitted to a healthcare institution in the year before, 13 (42%) had not used antibiotics during the 6 months before, and eight (26%) had neither risk factor. A separate analysis for patients whose samples were both toxin-positive and culture-positive produced similar results. Cultured C. difficile isolates belonged to 13 different PCR ribotypes, and 24% of the isolates were non-typeable (rare or new) PCR ribotypes. In conclusion, CO-CDI can affect all age groups, and many patients do not have known risk factors. Several PCR ribotypes not encountered in hospital-associated outbreaks were found, suggesting the absence of a direct link between outbreaks and community-onset cases.

Aerococcus urinae is a pathogen that rarely causes severe or fatal infections. We describe four cases of severe A. urinae bloodstream infections. All patients had underlying urologic conditions. Urine cultures, however, were negative. CASE REPORTSPatient A, an 81-year-old man with a history of benign prostatic hyperplasia, was admitted to our department because of fever. He had been home for 4 days after a 2-week admission for Aerococcus urinae bacteremia for which no source could be identified. Transesophageal echocardiography (TEE) showed no vegetations. The fever responded well to a 10-day course of high-dose intravenous penicillin, and blood cultures were negative on the last day of admission. At readmission, the patient showed no clinical signs of heart failure and no heart murmurs were heard on auscultation. Electrocardiography (ECG) was normal. Laboratory findings showed an erythrocyte sedimentation rate of 54 mm/h, a white blood cell count of 15.4 ϫ 10 9 /liter, and a C-reactive protein (CRP) level of 138 mg/liter. Urinalysis did not show white blood cells or nitrite, and urine cultures performed before the initiation of antibiotic treatment were negative. The chest radiograph and ultrasound examination of the abdomen were normal. The blood cultures drawn on the day of admission showed growth with Gram-positive cocci resembling staphylococci, and intravenous flucloxacillin was subsequently started. However, subinoculation onto blood agar showed alpha-hemolytic colonies resembling viridans streptococci which were identified as A. urinae using the Vitek system (99% reliability; bioMérieux, France) and 16S rRNA PCR (97 to 99% reliability). The antibiotic treatment was switched to penicillin after sensitivity testing showed a MIC of 0.023 mg/liter. Repeated TEE demonstrated a vegetation on the mitral valve with regurgitation and prolapse. The patient was treated with 12 million IU/day intravenous penicillin for 6 weeks and 3 mg/kg of body weight gentamicin once a day for 2 weeks. He declined mitral valve surgery.Patient B, a 78-year-old man with a history of ischemic heart disease and polymyalgia rheumatica, was recently diagnosed with stage IV non-small cell lung carcinoma. After two courses of chemotherapy (carboplatin/gemcitabine), he refrained from further treatment. One day after suprapubic catheterization of the bladder, the patient became septicemic. His temperature was 39.6°C, and he was hypotensive, with a blood pressure of 65/40 mm Hg and a heart rate of 92 beats per minute (b/min). After performing blood and urine cultures, fluid resuscitation was immediately started, as well as intravenous cefuroxime administration on the presumptive diagnosis of a urinary tract infection. An ECG was normal. The laboratory findings showed a CRP level of 46 mg/liter, sodium 140 mmol/liter, potassium 3.5 mmol/liter, urea 9.0 mmol/liter, and creatinine 107 mol/liter. Cefuroxime was replaced with flucloxacillin when Gram-positive organisms, thought to be staphylococci, were identified in the blood cultures. However, ...

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log 10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence.

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