Gram-negative rod infections; II. Acinetobacter infections in general hospital.
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Acinetobacter↗
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An unusual presentation of epidural Acinetobacter infection.
OBJECTIVE: We report a case of spinal-cord compression caused by epidural fat infection with Acinetobacter. The initial magnetic resonance imaging (MRI) scan suggested epidural hematoma or abscess, although both were absent at surgery. CASE REPORT: A 60-year-old man had a thoracic epidural sited at the level of T8/9 for postoperative analgesia after major abdominal surgery. A mixture of bupivacaine 0.1% and fentanyl 2 microg/mL was infused at a rate of 10 mL/h for 48 hours postoperatively. The epidural catheter was then removed, but 24 hours later, the patient still had weakness and numbness in his lower limbs. An MRI scan showed cord compression secondary to a hematoma or abscess from the level of T6 to T11. At laminectomy, no hematoma or abscess was found, but edematous epidural fat was excised. This fat was sent for culture and Acinetobacter was grown. Appropriate antibiotic therapy was given. Over a period of 12 months, the patient has regained near-normal power and sensation. CONCLUSION: Epidural Acinetobacter infection may present atypically without signs of meningism. MRI imaging may be confusing in these infections and lead to incorrect radiological diagnoses. Spinal-cord compression, as a complication of epidural catheter placement, does not have to be caused by hematoma or abscess.
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Acinetobacter infection in neurosurgical intensive care patients.
BACKGROUND: This study was performed to analyse the incidence of Acinetobacter infections in neurosurgical patients in the postoperative period. METHODS: Two thousand three hundred and twenty postoperative cranial neurosurgical intensive care unit (ICU) patients were studied from March 1995 to August 1996; 419 patients had a variety of infections and 42 patients had multiple infections. Acinetobacter was isolated in 103 patients (24.6% of total patients infected and 4.4% of total patients analysed). Statistical analyses were performed to identify the risk factors, antibiotic sensitivity and outcome of therapy of Acinetobacter infection. RESULTS: Acinetobacter infection was not significantly related to the length of hospital stay prior to surgery but was related significantly to the length of stay in the ICU after surgery. Acinetobacter was isolated from sputum/tracheal secretions in 47/103 (45.6%), followed by cerebrospinal fluid [24/103 (23.3%)], urine [15/103 (14.56%)] and blood [15/103 (11.65%)]. Acinetobacter infection was present in 54 (3.21%) of 1680 patients who had undergone routine/elective surgery and in 49 (7.66%) of 640 patients following emergency surgery. Elective/supportive ventilation for > 5 days, external ventricular cerebrospinal fluid drainage for > 5 days, intracranial pressure monitoring and prolonged indwelling Foley's urinary catheter during the perioperative period were independent risk factors (p < 0.005). Acinetobacter isolated from sputum/tracheal secretions were mostly sensitive to amikacin, cefotaxime and ceftriaxone; while those grown from the cerebrospinal fluid were more often sensitive to ciprofloxacin, amikacin and netilmycin. Twenty-four patients succumbed to Acinetobacter infection; in 11 of these patients the organism was resistant to all antibiotics. CONCLUSION: Acinetobacter is an important nosocomial infection in neurosurgical intensive care patients.
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Multiresistant Acinetobacter infections: a role for sulbactam combinations in overcoming an emerging worldwide problem.
Recent studies have highlighted the emergence of infections involving multiresistant Acinetobacter clinical isolates. Sulbactam offers direct antimicrobial activity against Acinetobacter species. Accordingly, co-administration of sulbactam with ampicillin or cefoperazone offers the potential of effective empirical therapy against Acinetobacter and other bacteria such as Enterobacteriaceae in institutions in which they are susceptible. Many in vitro studies have indicated that Acinetobacter remains fully susceptible to ampicillin-sulbactam or cefoperazone-sulbactam. Furthermore, ampicillin-sulbactam has proven clinically effective and well tolerated in the treatment of severe acinetobacter infections, including bacteremia. Therefore, ampicillin-sulbactam is a sensible option for the treatment of life-threatening acinetobacter infections.
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Seasonal variation of Acinetobacter infections: 1987-1996. Nosocomial Infections Surveillance System.
To determine whether nosocomial infections due to Acinetobacter species have increased over the past 10 years and whether infections continue to have a pronounced seasonal variation, we analyzed infections reported by hospitals in the National Nosocomial Infections Surveillance System that performed adult and pediatric intensive care unit surveillance from 1987 through 1996. Overall, 3447 nosocomial acinetobacter infections were reported during 5,596, 156 patient-days. There was a yearly median of 7.2 infections (range, 5.0-10.5) per 10,000 patient-days and a downward trend in the rate of acinetobacter infections overall (P<.05) and of 2 major types of infection (P<.05): bloodstream infections (yearly median, 1.6 per 10, 000 central venous catheter-days; range, 1.3-2.9) and pneumonia (yearly median, 7.6 per 10,000 ventilator-days; range, 6.5-12.0). Throughout this period, average rates were significantly higher during July-October than during November-June for acinetobacter infections overall (8.0 vs. 5.2; P<.01) and for bloodstream infections (2.0 vs. 1.2; P<.01) and pneumonia (9.7 vs. 6.6; P<.01).
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Epidemiological investigation of nosocomial Acinetobacter infections using arbitrarily primed PCR & pulse field gel electrophoresis.
BACKGROUND & OBJECTIVE: Nosocomial infections caused by Acinetobacter spp. are a significant problem worldwide. Information on epidemiological investigation of outbreaks caused by Acinetobacter species in India is lacking. The present investigation was carried out to elucidate molecular epidemiology of Acinetobacter species isolated from nosocomial infections in a tertiary care hospital in south India using two DNA-based typing methods. METHODS: The medical records of 43 patients with Acinetobacter infection during a period of 24 months were reviewed and Acinetobacter isolates obtained from these patients were characterized phenotypically by assimilation tests and genotypically by arbitrarily primed PCR (AP-PCR) and pulse field gel electrophoresis (PFGE). Susceptibility testing results of the Acinetobacter isolates were also analysed. RESULTS: Most of the infections were nosocomial, and the majority of these were acquired in intensive care units (ICUs). A. baumannii accounted for 41.8 per cent (n=18) of all pneumonia acquired in the ICU. AP-PCR with M13 primer distinguished 8 different PCR patterns comprising of 2 to 6 DNA fragments of 0.1 to 1.0 kb. PFGE identified 9 distinct profiles with five subvarients. By APPCR, epidemiologically unrelated strains could not be differentiated and often differences within biotypes of A. baumannii were not detectable. ApaI macrorestriction (PFGE) identified at least 4 outbreaks caused by 3 clones of A. baumannii and one clone of DNA group 13TU, one replacing the other in a well-defined temporal order. INTERPRETATION & CONCLUSION: Most of A. baumannii isolates were multidrug resistant. PFGE was more discriminatory [Discriminatory Index (DI)=0.96 than AP-PCR fingerprinting (DI=0.88)] in the present study. However, AP-PCR fingerprinting is more useful as a simple and rapid identification technique for epidemiological investigation of nosocomial Acinetobacter infections.
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Room humidifiers as the source of Acinetobacter infections.
Twenty-four patients contracted systemic infections with Acinetobacter calcoaceticus during a four-month period. Unheated room humidifiers at the patients' bedsides were implicated as the source of infection in six. The outbreak was terminated with the removal of the humidifers.
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Implications for Burns Unit design following outbreak of multi-resistant Acinetobacter infection in ICU and Burns Unit.
We reviewed the emergence of 13 cases of multi-resistant Acinetobacter infection in burns patients over a 12-month period. The outbreak was started in a non-burn patient in the intensive care unit (ICU) that spread to burns patients in ICU and then the Burns Unit. The importance of opportunistic infection, potential risk factors, treatment and clinical outcome of Acinetobacter infection in burns patients from this cluster of cases is described. This paper implicates the movement of burns patients and medical equipment between ICU and the Burns Unit in the spread of this infection. Future design of Burn Units should aim to incorporate features to allow the management of all burns cases in one location with all intensive care, burns and theatre facilities built in close proximity.
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Acinetobacter infection is associated with acquired glucose intolerance in burn patients.
Infection with antibiotic-resistant Acinetobacter spp. is an increasing problem in critical care environments worldwide. Acinetobacter spp. are known to produce an insulin-cleaving protease. We hypothesized that infection with Acinetobacter spp. was associated with the acquisition of glucose intolerance in burn patients. Data were collected prospectively on all 473 patients admitted to the Burns Centre between January 2002 and March 2003. A total of 3.4% of patients acquired glucose intolerance during admission. Patients with Acinetobacter spp. infection were 9.8 times more likely to develop glucose intolerance than those without the infection (P < .0001). The association persisted after controlling for TBSA (P < .001). In patients with deep Acinetobacter spp. infection, 47% had glucose intolerance, compared with 12% in those with infection of the burn only (P = .03). In patients with pre-existing diabetes mellitus, 27% developed Acinetobacter spp. infection compared with only 8.5% of patients without diabetes (P = .04). This study demonstrates a clear association between Acinetobacter spp. infection and glucose intolerance in burns patients.
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Multidrug-resistant Acinetobacter infections: an emerging challenge to clinicians.
OBJECTIVE: To review and evaluate clinically relevant epidemiology, microbiology, and clinical studies regarding the treatment of multidrug-resistant Acinetobacter infections. DATA SOURCES: Pertinent literature was identified by a MEDLINE search (1966-September 2003) and through secondary bibliographies of pertinent articles. STUDY SELECTION AND DATA EXTRACTION: All English-language articles identified from data sources were evaluated for clinical relevance. DATA SYNTHESIS: Acinetobacter baumannii has emerged as a worldwide problem as a nosocomial pathogen in hospitalized patients. Acinetobacter spp. can cause a multitude of infections including pneumonia, bacteremia, meningitis, urinary tract infections, and skin and soft tissue infections, and the mortality associated with these infections is high. Isolates resistant to almost all commercially available antimicrobials have been identified, thus limiting treatment options. The development of new agents and reappraisal of older compounds (ie, polymyxins, ampicillin/sulbactam) are necessary as we consider the optimal treatment of these multidrug-resistant organisms. CONCLUSIONS: There is no simple answer to the treatment of Acinetobacter infections. Eradication of Acinetobacter spp. requires adherence to good infection control practices and prudent antibiotic use, as well as effective antimicrobial therapy. Alternative therapies such as colistin, ampicillin/sulbactam, and tetracycline are potential options, but prospective, randomized, controlled trials are still lacking.
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Alert surveillance of intensive care unit-acquired Acinetobacter infections in a Sicilian hospital.
The epidemiological impact of Acinetobacter baumannii nosocomial infections in a Sicilian intensive care unit (ICU) was investigated to determine the Acinetobacter-specific infection rates, to estimate the preventable proportion of Acinetobacter infections, i.e., those resulting from cross-transmission, and to investigate the molecular epidemiology of antimicrobial resistance in Acinetobacter. The impact of Acinetobacter nosocomial infection in the ICU was determined to be 3.0 new cases per 100 admissions. Site-specific rates confirmed that ICU-acquired pneumonia was the most important infection type. The incidence rate, adjusted by the number of patient-days, was 3.3 infections/1000 patient-days. The estimated preventable proportion of A. baumannii nosocomial infections in the ICU was 66.7%. A class 1 integron, characterised by its gene cassette content, was present in all A. baumannii isolates of four different pulsed-field gel electrophoresis types, and was associated significantly with clones implicated in cross-transmission episodes. Furthermore, the same integron was detected in two genetically distinct isolates responsible for recurrent infection in the same patient, suggesting the occurrence of horizontal gene transfer in vivo. Even in an endemic setting with low infection rates, spread of A. baumannii was caused mainly by infection control shortcomings that require appropriate surveillance and control policies.
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The epidemiology of acinetobacter infections in Hong Kong.
A retrospective survey was conducted of the characteristics of acinetobacter infections in Hong Kong--seasonal and geographic distributions, frequency of isolation from various body sites, antimicrobial susceptibility and molecular epidemiology. Most (80%) isolates of Acinetobacter spp. belonged to DNA groups 2 (A. baumannii) or 13, as defined by growth at 44 degrees C. An increased isolation rate in summer was related to higher ambient temperatures. The notion that acinetobacters are opportunist nosocomial pathogens was supported by the body site- and ward-specific distributions, which were similar to those of Pseudomonas aeruginosa and in marked contrast to those of coagulase-negative staphylococci and Escherichia coli. Typing of Acinetobacter isolates by arbitrary-primed polymerase chain reaction revealed extensive genotypic polymorphism, suggesting that numerous unrelated strains were circulating between patients. In view of the association with a high incidence of polymicrobial bacteraemia and multiresistance to antibiotics, a careful selection of appropriate antibiotics in combination is necessary for empirical therapy of infections caused by Acinetobacter spp.
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Cefuroxime for Acinetobacter infection.
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Acinetobacter Infections↗
Treatment of Acinetobacter infections.
Gram-negative non-fermentative aerobic bacilli are becoming increasingly more involved in nosocomial infections. It has generally been recognised that the members of the Acinetobacter genus are among the most common agents responsible for severe hospital infections; their clinical importance has increased due to the development of antibacterial resistance mechanisms by these organisms. Over the last two decades the antibacterial armamentarium has progressed significantly and newer broad spectrum antibiotics have been used during therapy of hospital infections due to drug-resistant Acinetobacter spp. Despite various mechanisms of resistance to beta-lactams, aminoglycosides, fluoroquinolones developed by these organisms, the control of Acinetobacter infections can be effected by the use of several antibiotic combinations in 'conventional' antibiotic therapy. Recent surveys have pointed out the importance of using combinations of 2-amino-5-thiazolyl cephalosporins, or imipenem with aminoglycosides, or alpha-carboxy- penicillins (ticarcillin) combined with beta-lactamase inhibitors. Amongst the latter drugs, the place of sulbactam should be redefined thanks to its intrinsic activity against the Acinetobacter species, associated with its inhibitory power against beta-lactamases. The fluoroquinolones were initially very active against Acinetobacter infections, but resistance to this major class of drugs has occurred very rapidly. However, newer compounds of this class with increased anti-Acinetobacter activities can be used in combinations with beta-lactams or aminoglycosides. The potential role of rifampicin is still underestimated for the treatment of Acinetobacter infections despite promising in vitro activity. Novel derivatives of cephalosporins, carbapenems, fluoroquinolones, or completely new antibiotic classes, of which several investigational drugs seem promising, may constitute the future of antibiotic therapy and hence the treatment of Acinetobacter infections.
Journal Article↗
Clinical and epidemiological features of an outbreak of acinetobacter infection in an intensive therapy unit.
Sporadic examples of infection with multi-resistant Acinetobacter spp. have occurred in Nottingham hospitals since at least 1977, punctuated by more prolonged outbreaks involving larger numbers of patients, particularly those confined to the intensive therapy unit (ITU) with severe underlying disease. In the most recent outbreak, 11 patients were infected with multi-resistant Acinetobacter strains and 26 patients were colonised. Four of the infected patients died directly or indirectly from infection with multi-resistant Acinetobacter spp., either while in the ITU or after discharge to a general ward. The mean interval from admission to the first isolation of a multi-resistant Acinetobacter strain was 6.7 and 12.1 days in the infected and colonised groups, respectively. Multi-resistant Acinetobacter strains were isolated most frequently from the respiratory tract, and eight patients had probable or suspected pneumonia caused by a multi-resistant Acinetobacter sp. All infected patients were treated with imipenem, with or without an aminoglycoside, except one patient who died before a diagnosis of acinetobacter infection was confirmed. Multi-resistant Acinetobacter spp. were isolated from various environmental sites in the ITU, and patient and environmental isolates were found to be related closely by biotyping, antibiograms, pulsed-field gel electrophoresis of chromosomal fingerprints and ribotyping. The outbreak was controlled ultimately by transfer of infected or colonised patients to an isolation cubicle, cohort nursing, emphasis on the importance of hand washing before and after patient contact and when handling case notes, and the use of disposable aprons and gowns during patient contact.(ABSTRACT TRUNCATED AT 250 WORDS)
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Use of cefotaxime for treatment of Acinetobacter infections.
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Acinetobacter Infections↗
Seasonal incidence of Acinetobacter infection.
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Acinetobacter Infections↗
Acinetobacter infections in patients with human immunodeficiency virus infection: microbiological and clinical epidemiology.
BACKGROUND: We evaluated the role of complications caused by Acinetobacter spp. in the setting of HIV infection. METHODS: Clinical records of 1,923 consecutive HIV-infected patients hospitalized in a 9-year period were retrospectively reviewed, in order to identify all cases of Acinetobacter spp. complications, and to assess their occurrence and outcome according to several epidemiological, clinical and laboratory parameters. RESULTS: Ten patients out of 1,923 (0.52%) developed Acinetobacter spp. infections: sepsis in four cases, urinary tract infection in three, pneumonia in two and septicaemic pneumonia in the remaining patient. All patients were severely immunocompromised, as shown by a mean CD4+ lymphocyte count of 122 cells/microl and a frequent prior diagnosis of AIDS. As opposed to other infections, septicaemia was associated with a significantly lower CD4+ cell count and a more frequent occurrence of neutropenia. Hospital-acquired Acinetobacter spp. infections were significantly more frequent than community-acquired ones, and prevailingly involved patients with AIDS and leucopenia, being responsible for frequent blood dissemination. Antimicrobial, corticosteroid and cotrimoxazole treatment were frequently carried out during the month preceding disease onset. Antibiotic susceptibility studies proved the complete resistance of microbial isolates to ampicillin and cephalothin and poor sensitivity to second-generation cephalosporins and gentamicin, while greater susceptibility was shown to ceftazidime, netilmicin and amikacin, followed by piperacillin, cotrimoxazole and quinolones. Appropriate antimicrobial treatment led to clinical and microbiological cure in all cases, with no related mortality or relapses. CONCLUSIONS: Since only 23 episodes of HIV-associated Acinetobacter spp. infections have been described to date in 11 different reports (nine cases of bacteraemia, eight of pneumonia, two of urinary tract involvement, one of intravenous access device infection, one of meningitis and two with unspecified localization), our series represents the largest one dealing with HIV-associated Acinetobacter spp. infections. According to our experience, Acinetobacter spp. may be responsible for appreciable morbidity among patients with HIV infection, above all when a low CD4+ cell count, neutropenia and hospitalization are present. Clinicians and microbiologists who work in the field of HIV infection should consider the potential pathogenic role of Acinetobacter spp. organisms even in the absence of some presumed risk factors, because of the relationship between these infections and immunodeficiency, hospitalization, other infectious complications, prior antibiotic and steroid treatment and extended antimicrobial resistance patterns.
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