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About 25% of humans with chronic gastritis are negative for Helicobacter pylori, suggesting that other bacteria are capable of causing inflammation. Bacterial overgrowth may occur in the stomach under conditions of reduced acid secretion. In this review, we will explore what is generally known about non-H. pylori organisms and their ability to induce gastritis, with particular focus on Acinetobacter lwoffi.
The use of protein fingerprinting for the establishment of relatedness among isolates of Acinetobacter calcoaceticus subspecies anitratus, isolated from patients in a surgical intensive care unit was examined. Polyacrylamide gel electrophoresis was used to analyze the cellular proteins from whole cell lysates of 14 intensive care unit A calcoaceticus subspecies anitratus isolates and 11 control strains. Antimicrobial susceptibilities and plasmid profiles were also determined for all isolates. All intensive care unit A calcoaceticus subspecies anitratus isolates exhibited identical cellular protein fingerprints, no detectable plasmids, and minimum inhibitory concentrations within +/- 1 log2 dilution of the mode value for each of the antimicrobial agents tested. The other clinical isolates demonstrated a range of antimicrobial susceptibilities, various numbers and sizes of plasmids, and distinctly different protein fingerprints. These data indicate that protein fingerprinting may be useful as an epidemiologic tool in A calcoaceticus subspecies anitratus outbreaks and this method deserves further study.
Although Acinetobacter lwoffii is generally considered an ubiquitous and opportunistic bacterium, this germ has been isolated from the pulmonary and abdominal air sac swabs obtained from a Lovebird (Agapornis roseicollis), which died of a severe respiratory disease. Bacteriological tests (phenotypic and genotypic) led to the identification of A. lwoffii in pure culture. All the other parrots in the breeding centre were treated orally with oxytetracycline for 14 days and 3 months later no bird showed any signs of respiratory symptoms.
Epithelial cell death induced by Acinetobacter baumannii infection was investigated using in vitro assays. Eight hours after live A. baumannii infection, HeLa cells exhibited detachment from the dish, rounding morphologies, high proportions of trypan blue-positive cells and extensive DNA breakdown with faint apoptotic banding, which is indicative of cells undergoing apoptosis. The enzymatic activity of caspase-3 was increased in cells as early as 2 h after infection. In addition, apoptosis of HeLa cells was induced by treatment with bacterial culture filtrates but not with formalin-killed bacteria. These results indicate that A. baumannii infection triggers apoptosis in HeLa cells through caspase-3 activation.
Acinetobacter baumannii is a significant problem in critically ill patients. It is widespread, can colonise patients quickly and causes virulent infections. However, its overall impact on morbidity and mortality in the critically ill remains unmeasured. This study was designed to investigate A. baumannii colonisation and infection rates in a critically ill population over an 18-month period. Twenty-seven patients from a population of 347 were identified as having A. baumannii. Sixteen were colonised, whereas 11 were infected. Eleven of the 27 patients with A. baumannii died (41%). Of these, eight were colonised and three were infected. In the same period, 320 patients did not have A. baumannii and their mortality rate was 20% (n = 64). The mortality rate of patients with A. baumannii was significantly higher than that of patients without infection.
OBJECTIVE: To demonstrate the usefulness of REP-PCR and AP-PCR on molecular typing of A. baumannii isolates. METHOD: From February to November 1997, 29 inpatients at Ramón y Cajal Hospital, Madrid-23 in five intensive care units (ICUs) and six at two different medical departments-were either colonized or infected with imipenem- and meropenem-resistant Acinetobacter baumannii (IMRAB) strains (MICs of 64-256 mg/L). A wide antibiotic multiresistance profile was observed with IMRAB strains, and only tobramycin, sulbactam and colistin displayed valuable activity. For typing IMRAB isolates, repetitive extragenic palindromic sequence-based polymerase chain reaction (REP-PCR) and arbitrary primer sequence-based polymerase chain reaction (AP-PCR) methods were used and compared with pulsed-field gel electrophoresis (PFGE) as reference technique. For comparative purposes, 30 imipenem- and meropenem-susceptible A. baumannii (IMSAB) strains isolated before, during and after the outbreak were included in this study. RESULTS: The molecular typing results showed that the outbreak was caused by a single IMRAB strain (genotype 1). On the other hand, seven different genotypes were observed in the pre-, at- and post-outbreak strains tested by REP-PCR. Regarding AP-PCR, three of four at-outbreak IMSAB strains were indistinguishable from the IMRAB profile. Thus, with AP-PCR, only six genotypes were obtained, apart from the IMRAB genotype. CONCLUSION: Under our experimental conditions, REP-PCR had a higher discriminatory power than AP-PCR, with PFGE as reference technique. The REP-PCR technique is a useful and expeditious method for the epidemiologic characterization of A. baumannii nosocomial outbreaks, the results being comparable to those obtained with the PFGE technique.
Acinetobacter baumannii is an important cause of nosocomial infections in many hospitals. It is difficult to control and infection caused is difficult to treat due to its high resistance in the environment and its ability to develop resistance to antimicrobials. Bacteremia, followed by respiratory tract and surgical wound infections, is the most significant infection caused by A. baumannii. The known risk factors for A. baumannii bacteremia are invasive procedures and the use of broad-spectrum antimicrobials. Consequently, episodes of bacteremia due to A. baumannii occur most frequently in critically-ill patients admitted to an intensive care unit. The clinical manifestations of bacteremia by A. baumannii are not specific. The most common sources of bacteremia are intravascular catheters and the respiratory tract. A. baumannii bacteremia is associated with a high crude mortality rate, but it is difficult to distinguish morbidity and mortality attributable to A. baumannii from that attributable to the common and severe co-morbidity in these patients. A. baumannii is a bacterium that appears to have a propensity for developing multiple antimicrobial resistance extremely rapidly. These data are disturbing because the therapeutic possibilities decrease while inappropriate antimicrobial treatment contributes to patient mortality. Generally, imipenem is the most active agent against A. baumannii. However, the description of imipenem-resistant A. baumannii strains is becoming increasingly common. The usual treatment for A. baumannii bacteremia is an active beta-lactam alone, preferably one with a limited spectrum. Before beginning treatment of a bacteremia by A. baumannii, it is very important to carry out a clinical evaluation of the patient to eliminate the possibility of a pseudobacteremia, and thereby avoid unnecessary treatment.
OBJECTIVE: To determine whether non-epidemiologically related, antibiotic-resistant isolates of Acinetobacter baumannii from different geographical origins possess common type 1 integrons. METHODS: The epidemiologic relationships between seven A. baumannii strains recovered from different Spanish hospitals were established by pulsed-field gel electrophoresis, the presence of integrons being determined by PCR and DNA sequencing. RESULTS: Integron analysis showed the presence of four different integrons, containing six different known genes (aacC1, aacA4, aadA1, aadB, oxa21 and oxa37) plus an ORF. It was found that the same integron was present in different unrelated strains and that related strains could have different integrons. CONCLUSION: These results show the potential risk of integron dissemination among different strains of A. baumannii.
Thrombotic thrombocytopenic purpura (TTP)/Hemolytic-uremic syndrome (HUS) is a syndrome characterized by thrombocytopenia, microangiopathic hemolytic anemia, fever, renal failure and neurologic manifestation. Almost all cases are idiopathic. However, secondary TTP/HUS associated with viral, bacterial and mycobacterial infections, drugs, connective tissue disease, solid tumors, bone marrow transplantation and pregnancy have been described. Early relapse associated with infection is a rare occurrence. The patient we report had a classic case of postdiarrheal TTP/HUS that responded to plasmapheresis but relapsed during treatment as reflected by the increased schistocytosis, decreased hematocrit, increased lactate dehydrogenase, and decreased platelet counts. This relapse may be attributed to Acinetobacter anitratus bacteremia, secondary to central line infection. Administration of antimicrobial treatment resulted initially in a mild improvement. However, this was followed by a fatal relapse. The importance of monitoring the possible bacterial colonization of an indwelling catheter is thus emphasized.
BACKGROUND: Acinetobacter baumannii has become an increasingly important nosocomial pathogen, particularly in intensive care units (ICUs). The aim of this investigation was to study the molecular epidemiology of A baumanii in a university hospital in Italy. METHODS: All A baumanii isolates were collected and typed with phenotypic and genotypic methods during a 7-month period. A 1-year prospective surveillance of ICU-acquired infections was performed by using the National Nosocomial Infections Surveillance methodology. RESULTS: A baumanni accounted for 28.4% of all infections and 46.7% of all pneumonia acquired in the ICU, with a nosocomial infection rate of 12.4% or 8 infections per 1000 patient-days. Risk factors for A baumannii acquisition in the ICU were mechanical ventilation and previous use of broad-spectrum antibiotics, whereas administration of carbapenems showed a significant protective effect. Pulsed-field gel electrophoresis of genomic Apa I digests identified at least 5 outbreaks in the ICU caused by 5 different clones, one replacing the other in a well-defined temporal order. CONCLUSIONS: Whereas the sequential temporal cluster of epidemic clones in the ICU is intriguing and requires further research, the clear evidence of cross-contamination of A baumannii isolates involved with infections in the ICU demands extensive preventive efforts.
Tap water can play a role as a source of nosocomial pathogens, and faucet aerators have occasionally been mentioned in the literature associated with colonization or infection in hospitalized patients. In this study, we report on outbreak of bacteraemia in paediatric oncology patients caused by Acinetobacter junii. Environmental sampling showed the water system to be contaminated with A. junii. Molecular typing using automatic laser fluorescence analysis of randomly amplified polymorphic DNA (RAPD-ALFA) revealed two distinct strains. The outbreak strain, isolated from blood cultures of the affected children, was only found in the water taps of staff rooms. Aerators were commonly found to be contaminated, and more so than water obtained after removal of these devices. We believe that conventional aerators consisting of several wire meshes can serve as a reservoir for low levels of bacteria present in the water system. We recommend, especially for high-risk areas, either that aerators should not be used, or the use of aerators consisting of radially and vertically arranged lamellae, which do not lead to the collection of sediment or water stagnation, and to clean them regularly.
In an attempt to define the epidemiology of Acinetobacter baumannii infection, 27 isolates, obtained from hospital-acquired respiratory infections, were typed using random amplified polymorphic DNA (RAPD) profile and antimicrobial susceptibility patterns. Ten different patterns were obtained with ERIC2 primer: 14 isolates had a similar profile representing a single strain. Within RAPD types, isolates could be further classified based on their antibiogram; however, strains of different types had similar antibiograms. This study showed that many different genetic types of A. baumannii are prevalent in our hospital. While antibiograms alone are not sufficiently discriminatory, RAPD typing helps in identifying outbreaks and in assessing infection control procedures within a hospital.
Over a three month period there was an outbreak of infection, due to a multi-drug resistant Acinetobacter baumannii in the intensive care burns unit with spread of infection to other patients, both within the unit and elsewhere in the hospital. Microbiological sampling of the environment and of the healthcare workers' (HCWs) hands were carried out. Strain relatedness of the isolates was confirmed by pulsed field gel electrophoresis. Fifteen patients were involved in the outbreak, whose infections were all hospital-acquired. The burns room environment was contaminated with the A. baumannii, as was the door handle of the door leading from the ante-chamber between both rooms. This allowed the hands of HCWs to be contaminated by A. baumannii despite appropriate handwashing procedures prior to leaving the rooms. Two staff members were colonized with A. baumannii. One HCW who was directly involved in patient care was found to be "heavily" colonized, the other, with less patient contact, was only "lightly" colonized. Review of handwashing practices revealed that chlorhexidine/alcohol hand wash solution was not used by the HCW whose hands were heavily colonized.A combination of a review of handwashing practice, education about the spread of bacteria via hands and contaminated environment, and the revision of infection control procedures in the unit contributed to a prompt termination of the outbreak.
Acinetobacter baumannii was considered endemic in a university-affiliated tertiary hospital. A significant increase was noted in the proportion of nosocomial infections associated with this micro-organism from 1996 to 1999, although no apparent clusters could be found. Between July 1998 and February 2000, 58 nosocomial isolates of A. baumannii were collected and characterized by antibiotyping and a genotyping method, infrequent-restriction-site PCR (IRS-PCR). High resistance to the 14 antimicrobial agents examined was observed among the isolates. Of the 13 antibiograms detected, eight were multi-resistant to gentamicin and almost all of the traditional and extended-spectrum beta-lactams. These multi-resistant strains consisted of 41 isolates (71%), distributed amongst different wards and intensive care units (ICUs). By IRS-PCR, 23 types were obtained, with one major type found among 28 (48%) isolates. All of these 28 isolates were collected from surgical ICUs. It appears that a single strain of multi-resistant A. baumannii was responsible for the prevalence of nosocomial infection amongst surgical patients, clearly differentiating this outbreak from the previous endemic situation. An efficient molecular typing method played a vital role in making this discrimination.
During a three-month period in 1999, 25 strains of carbapenem resistant Acinetobacter baumannii were isolated from 12 of 170 hospitalized intensive care unit (ICU) patients, of which 16 were considered to be clinically significant. These strains were indistinguishable by biotyping and antibiograms, but genotyping was not performed. Appropriate antibiotic treatment, isolation precautions, and infection control education of the staff failed to halt the outbreak. Environmental contamination was therefore investigated, and A. baumannii was found out in 22 (39.3%) of 56 environmental samples obtained by swabbing. Different antibiotic sensitivity patterns were obtained in the majority of these isolates, but four (7.1%) of the strains were found to have the same sensitivity pattern as the strain causing the outbreak. As a result the ICU was closed, equipment and the environment cleaned, with hypochlorite and terminal disinfection carried out. No bacteria were grown on repeat environmental cultures. Environmental contamination has an important reservoir role in outbreaks of A. baumannii in ICUs and must be eradicated in order to overcome such outbreaks.
We describe an outbreak of Acinetobacter baumannii in a neonatal intensive care unit (NICU), and our investigation to determine the source and mode of transmission and identify the population at risk. A case (infected infant) was defined as a patient hospitalized in the NICU during the outbreak period, with clinical signs of sepsis and isolation of A. baumannii. In colonized infants, A. baumannii was isolated from body surfaces without signs of infection. Infected infants were separated and treated by a different medical team. Cultures were taken from working surfaces and along the infant's admission passage from the delivery room to the NICU. The outbreak strain was identified by pulsed-field gel electrophoresis (PFGE). Nine cases and eight colonized infants met the definition criteria. Cases were younger than colonized infants with regard to gestational age and age of diagnosis and had lower birthweights (P<0.01). The outbreak strain was only isolated from hygroscopic bandages used on skin under the ventilation tube and umbilical catheters. Discontinuing the use of the bandages put an end to the outbreak. We conclude that a rapid and thorough investigation of the environment during an outbreak of A. baumannii is essential to finding the source of the infection, and that hygroscopic bandages may be a source of such outbreaks.
The effect of three aminoglycoside antibiotics--netilmicin (CAS 56391-57-2), gentamicin (CAS 1403-66-3) and amikacin (CAS 37517-28-5)--at subinhibitory concentrations (sub-MICs; 1/4 or 1/16 of the MICs) on the cytotoxic activity of Acinetobacter baumannii was studied. The cytotoxic factor was manifested by reduction of the number of isolated rat lung type II cells evaluated by alkaline phosphatase determination. All aminoglycosides at both concentrations studied (with the exception of 1/4 of the MIC of amikacin) did not modify cytotoxic activity of A. baumannii. This activity was partially inhibited only after treatment with amikacin at 1/4 of the MIC. In this case the number of type II cells after incubation with antibiotic treated A. baumannii was higher (71%) as compared to the number of type II cells cultured with untreated A. baumannii (47%).
BACKGROUND: Highly resistant (HR) Acinetobacter baumannii (AB) are frequently hospital-acquired and may be important causes of severe nosocomial infections. OBJECTIVE: Determine risk factors associated with such colonization/infection. METHOD: Retrospective review in 2000 of all AB isolates from sterile (blood, cerebrospinal fluid [CSF]) and nonsterile (respiratory, urine, and miscellaneous) sites. HR was defined as resistance to amikacin and/or imipenem and/or ampicillin-sulbactam. Isolates were analyzed as representing infection or colonization. A database including prior hospitalization, prior antibiotic use, nursing home residency, and procedures undergone was compiled. RESULTS: One hundred twenty-two cases of AB were identified. Eighty-four met the definition of HR; 6 (4.9%) were completely resistant to all antibiotics. Four (4.7%) isolates were from sterile body sites (3 blood, 1 CSF); 43 (51.2%) were from respiratory sites; 20 (23.8%) were from urinary sites; and 17 (20.2%) were from "other" sites. Only 4 (20%) of the urinary, 6 (35.2%) of the miscellaneous, and 23 (53.4%) of the respiratory isolates were deemed true pathogens; all blood/CSF isolates were considered pathogens. Associated risk factors included prior antibiotic usage (71%); prior hospitalization (24%); prior nursing home residency (34%); ventilator use (77%); tracheostomy placement (56%); and Foley catheterization (85%). Twenty-seven (63%) of 43 respiratory, 8 (40%) of 20 urinary, and 6 (35%) of 17 "other" body isolates were treated. Outcome was not statistically significant in treated versus untreated patients. All patients with CSF/blood isolates underwent successful microbiologic eradication with 50% survival. The overall mortality rate was 10%. CONCLUSION: Antibiotics, Foley catheters, and tracheostomy/ventilator usage were strongly associated with AB isolation. Prior hospitalization and nursing home residency were less common risk factors. Outcome was not different in treated versus untreated patients, indicating colonization is a marker of severe illness but is not necessarily causal.