Asok Kurup

Nebulized Colistin in the Treatment of Pneumonia Due to Multidrug-Resistant Acinetobacter baumannii and Pseudomonas aeruginosa

Twenty-one patients with multidrug-resistant (MDR) Acinetobacter baumannii and Pseudomonas aeruginosa pneumonia were treated with nebulized polymyxin E (colistin). Overall clinical and microbiological response rates were 57.1% and 85.7%, respectively. Nebulized colistin may be reasonably efficacious and safe for treatment of MDR pneumonia. Its role in therapy warrants further investigation in comparative studies.

Clinical features and treatment outcomes of vancomycin-intermediate Staphylococcus aureus (VISA) and heteroresistant vancomycin-intermediate Staphylococcus aureus (hVISA) in a tertiary care institution in Singapore

This retrospective case–control study was undertaken to review the clinical features associated with heteroresistant vancomycin-intermediate Staphylococcus aureus (hVISA) and vancomycin-intermediate S. aureus (VISA) infections and the local impact they have on clinical outcome. Compared with vancomycin-susceptible S. aureus (n = 30), hVISA and VISA infections (n = 10) are found to be associated with a longer period of prior glycopeptide use (P = 0.01), bone/joint (P < 0.01) and prosthetic infections (P = 0.04), as well as treatment failure, as evidenced by longer bacteremic (P < 0.01) and culture positivity (P < 0.01) periods. This was observed to have resulted in longer hospital length of stay (P < 0.01) and total antibiotic therapy duration (P = 0.01). There was, however, no significant difference in the overall patient mortality or the hospitalization cost (P = 0.12) in both groups. Clinicians should be cognizant of the association between hVISA/VISA with high bacterial load deep-seated infections. We recommend targeted and even universal screening for hVISA/VISA in methicillin-resistant S. aureus (MRSA) infections.

Dissemination of Multisusceptible Methicillin-Resistant Staphylococcus aureus in Singapore

ABSTRACT Analysis of hospital-acquired methicillin-resistant Staphylococcus aureus strains isolated from a tertiary public hospital in Singapore revealed that multisusceptible strains had gradually started to replace the endemic multiresistant strain (ST239-MRSA-III) since 2002. Molecular typing showed that this was a predominantly clonal outbreak of a UK-EMRSA-15 strain (ST22-MRSA-IV).

Consensus statement on the management of invasive candidiasis in Intensive Care Units in the Asia-Pacific Region.

Invasive candidiasis has emerged as an important nosocomial infection, especially in critically ill patients. The incidence of candidaemia in Intensive Care Units (ICUs) is 5- to 10-fold higher than in the entire hospital and the crude mortality rate of patients with candidaemia is between 35% and 60%. Candida albicans remains the predominant cause of invasive candidiasis in ICUs, followed by Candida tropicalis, Candida glabrata and Candida parapsilosis. Invasive isolates of Candida spp. remain highly susceptible to fluconazole (>90% susceptible), although among Asia-Pacific countries the susceptibility rate of C. glabrata to fluconazole varies widely from 22% to 72%. Early diagnosis and prompt initiation of antifungal therapy are crucial for the effective treatment of invasive candidiasis. However, invasive candidiasis is difficult to diagnose owing to its non-specific clinical features, and delayed therapy is a major contributor to poor outcomes. Combining clinical risk factors with Candida colonisation parameters appears promising for guiding early interventions. Because of considerable regional variability, local epidemiological knowledge is critical in the effective management of invasive candidiasis among ICU patients in Asia-Pacific.

Four cases of necrotizing fasciitis caused by Klebsiella species.

Presented here are four cases of necrotizing fasciitis caused by Klebsiella spp. that were treated at one hospital over a 2-year period. Klebsiella necrotizing fasciitis can occur via direct inoculation, local trauma or, more commonly, hematogenous spread from other septic foci. Early, aggressive, surgical debridement and appropriate antimicrobial treatment are the cornerstones of treatment for this condition. Necrotizing fasciitis due to Klebsiella spp. is unique in that it is commonly associated with multiple septic foci. While liver abscesses and endogenous endophthalmitis are better-known associations of disseminated Klebsiella infection, necrotizing fasciitis is increasingly recognized as one of the manifestations of this syndrome. When treating Klebsiella necrotizing fasciitis, awareness of the potential for multiorgan involvement should prompt a thorough search for associated foci of infection.

Infection of central nervous system by motile Enterococcus: first case report.

ABSTRACT A 66-year-old man with four indwelling ventriculoperitoneal shunts for multiloculated hydrocephalus from a complicated case of meningitis a year before developed shunt infection based on a syndrome of fever, drowsiness, and cerebrospinal fluid neutrophil pleocytosis in the background of repeated surgical manipulation to relieve successive shunt blockages. The cerebrospinal fluid culture, which yielded a motile Enterococcus species, was believed to originate from the gut. This isolate was lost in storage and could not be characterized further. The patient improved with vancomycin and high-dose ampicillin therapy. He relapsed a month later withEnterococcus gallinarum shunt infection, which responded to high-dose ampicillin and gentamicin therapy. This is probably the first case report of motile Enterococcus infection of the central nervous system.

Control of a hospital-wide vancomycin-resistant Enterococci outbreak

Background To analyze control measures used to eradicate a large vancomycin-resistant Enterococci (VRE) outbreak in a nonendemic 1600-bed tertiary care institution. Methods In mid-March 2005, VRE Van B was isolated from 2 clinical samples from different wards. Despite such measures as screening patients sharing rooms with index cases and isolating VRE patients, 43 isolates from different wards were detected by the end of March 2005. To eradicate a hospital-wide outbreak, a coordinated strategy between March and June 2005 comprised (1) formation of a VRE task force, (2) hospital-wide screening, (3) isolation of carriers, (4) physical segregation of contacts, (5) surveillance of high-risk groups, (6) increased cleaning, (7) electronic tagging of VRE status, and (8) education and audits. This is a retrospective study of this multipronged approach to containing VRE. The adequacy of rectal swab sampling for VRE was assessed in a substudy of 111 patients. The prevalence of methicillin-resistant Staphylococcus aureus (MRSA)/VRE co-colonization or co-infection also was determined. Results A total of 19,574 contacts were identified. Between April and June 2005, 5095 patients were screened, yielding 104 VRE carriers, 54 of whom (52%) were detected in the first 2 weeks of hospital-wide screening. The initial positive yield of 11.4% of persons actively screened declined to 4.2% by the end of June 2005. Pulsed-field typing revealed 1 major clone and several minor clones among the 151 total VRE cases, including 4 clinical cases. Hospital-wide physical segregation of contacts from other patients was difficult to achieve in communal wards. Co-colonization or co-infection with MRSA, which was present in 52 of 151 cases (34%) and the indefinite electronic tagging of positive VRE status strained limited isolation beds. Analysis of 2 fecal or rectal specimens collected 1 day apart may detect at least 83% of VRE carriers. Conclusion A multipronged strategy orchestrated by a central task force curbed but could not eradicate VRE. Control measures were confounded by hospital infrastructure and high MRSA endemicity.

Recurrent necrotizing fasciitis caused by methicillin-resistant Staphylococcus aureus

Reported here is a rare case of recurrent necrotizing fasciitis due to methicillin-resistant Staphylococcus aureus (MRSA). A 46-year-old female with poorly controlled diabetes and chronic ingestion of steroid-containing medications was admitted for treatment of necrotizing fasciitis of the right thigh. Three months following hospital discharge she was readmitted with necrotizing fasciitis of the left hand. On both occasions, MRSA was isolated from tissue cultures obtained during surgical debridement. Patients who develop necrotizing fasciitis are predisposed to severe soft tissue infections due to associated comorbid conditions such as diabetes mellitus. Recurrent soft tissue infection in a patient with previous MRSA-related necrotizing fasciitis should therefore be treated with a high index of suspicion.

Clinical Characteristics and Outcome of Severe Melioidosis Requiring Intensive Care

STUDY OBJECTIVE To describe the clinical characteristics and outcome of patients with severe melioidosis requiring intensive care. DESIGN Retrospective chart review. SETTING Two ICUs from a tertiary-care teaching hospital. PATIENTS Twenty-seven adult ICU patients with microbiologically documented melioidosis. INTERVENTIONS None. MEASUREMENTS AND RESULTS The median age was 59 years with a male preponderance (26:1). Twenty patients (74%) had medical comorbidities, with diabetes mellitus being the most common (59.3%). Almost all patients (96.3%) were bacteremic. Twenty patients (74.1%) presented with pneumonia. Twenty patients (74.1%) were in septic shock, and 16 patients (59.3%) had ARDS. Twelve patients (44.4%) required hemodialysis. The patients had a median of three organ dysfunctions, and the median APACHE (acute physiology and chronic health evaluation) II score was 27. The overall mortality was 48.1%. Mortality among patients with septic shock was 60%. The median ICU length of stay for survivors and nonsurvivors was 11 days and 2 days, respectively. Multivariate analysis revealed that the number of organ dysfunctions is an independent predictor of mortality (odds ratio, 8.2; 95% confidence interval, 1.3 to 51.4). CONCLUSIONS The outcome of severe melioidosis requiring intensive care is poor, with death being predicted by the number of organ dysfunctions.

Group B Streptococcus necrotizing fasciitis: an emerging disease?

Necrotizing fasciitis is perhaps the most severe form of soft tissue infection primarily involving the superficial fascia and subcutaneous tissue. This condition is associated with severe sepsis, a fulminant course and high mortality. While group A Streptococcus (GAS) remains the most common etiologic agent in necrotizing fasciitis due to a single organism [1], we have recently noted an emergence of group B Streptococcus (GBS) or Streptococcus agalactiae as a causative agent. This report describes our recent experience with GBS necrotizing fasciitis seen in Singapore between the years 2000 and 2002. Five patients with monomicrobial necrotizing fasciitis caused by GBS were identified during this time period. All patients were female, with ages ranging from 38 to 66 years. Diabetes mellitus was a frequent association and was noted in four of the patients. Early aggressive surgical debridement is the cornerstone management of necrotizing fasciitis and was performed in all cases. The procedure was repeated until all necrotic and non-viable tissues were excised. Two to three debridements were necessary to achieve this. The group B streptococci isolated from all five patients were susceptible to penicillin, ampicillin and erythromycin. Table 1 summarizes the clinical presentation, antimicrobial therapy and outcome of the five cases. At our hospital, we generally treat patients with severe GBS soft tissue infections with high-dose parenteral penicillin once the organism has been isolated. Highdose intravenous penicillin is the drug of choice since resistance to penicillin is not an issue with GBS. Once the infection has been controlled, the parenteral regimen is replaced by an oral β-lactam agent such as penicillin or amoxicillin. Antimicrobial therapy is continued for 4–6 weeks, until all wounds are covered with split thickness skin grafts. However, in the five cases reported here there were some variations in the antimicrobial therapy administered because of the preferences of individual treating physicians. Some authors have advocated the use of clindamycin in combination with penicillin in cases of GBS necrotizing fasciitis [2, 3], and there is now growing in vitro and in vivo evidence that clindamycin may be the preferred agent for treating streptococcal necrotizing fasciitis. While not used to treat our patients, the combination of clindamycin and penicillin may be superior to penicillin alone and should be considered in the treatment of future cases of invasive GBS infections [2, 3]. Skin and soft tissue infections are the most common manifestations of invasive GBS infection [4, 5]. However, monomicrobial necrotizing fasciitis caused by GBS in non-pregnant adults is extremely rare, with just over ten cases being reported in the English-language medical literature to date [2, 3, 6–9]. The addition of the five cases we observed make clear that GBS is capable of causing necrotizing fasciitis. While the virulence factors that enable GBS to cause necrotizing fasciitis have not yet been established, this emerging clinical entity has been reported increasingly in recent years [2, 3, 6–9]. All five of our cases occurred during a relatively short period of time, between 2000 and 2002. Horizontal transfer of DNA encoding virulence factors (such as M1 or M3 surface proteins) among different strains of GAS have been demonstrated previously [10, 11]. Gardam et al. [2] postulated that a similar process may have occurred between group A and B streptococci, conferring the mutant strain of GBS with increased ability to spread through tissue planes, resulting in rapid tissue necrosis. This theory is supported by a report of the isolation of a 12,000-kD pyrogenic toxin similar to that found in GAS from a GBS strain in a case of toxic shock syndrome caused by this organism [12]. This sharing of C.-H. Wong (*) . K.-C. Tan Department of Plastic Surgery, Singapore General Hospital, Outram Road, Singapore, Singapore, 169608 e-mail: wchinho@hotmail.com Tel.: +65-63214686 Fax: +65-62209340