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Molecular epidemiology of Acinetobacter baumannii in Central Intensive Care Unit in Kosova teaching hospital.

Acinetobacter spp. are opportunistic pathogens that have emerged to an infectious agent of importance to hospitals worldwide [1-3]. They can be found in the natural environment, hospital surroundings and on the skin of the human body. Some strains of Acinetobacter can survive environmental desiccation for weeks, promoting transmission through fomite contamination in hospitals [4].

Acinetobacter spp. cause a wide range of nosocomial infections, such as ventilator-associated pneumonia, bloodstream infections, urinary tract infections, surgical site infections and meningitis, especially in immunocompromised patients staying in ICU [5]. Other risk factors for colonization and infection are recent surgery, central vascular catheterization, tracheostomy, mechanical ventilation, enteral feeding and treatment with antibiotics (third-generation cephalosporins, fluoroquinolones or carbapenems)[6,7]. Extensive use of antimicrobials within hospitals has contributed to the emergence and increase of antimicrobial resistance among Acinetobacter strains [8].

Numerous reports implicates A. baumannii as a major pathogen involved in nosocomial infections causing epidemic outbreaks or endemic occurrence with a documented high mortality rates [9-12]. An increase in the number of A. baumannii isolates from clinical samples has been observed in microbiology laboratory over the past few years in ICU of university hospital in Kosova. But, this was not accompanied by detailed epidemiological and clinical investigation.

Knowledge regarding species, strains and clones of Acinetobacter circulating in Kosova hospitals is lacking. Published data concerning the clinical implications of Acinetobacter spp. infections in Kosova are scarce. A study regarding clinical samples of Acinetobacter spp. isolates and their susceptibility pattern undertaken during 2001-2004, showed a total of 242 Acinetobacter spp., of which A. baumannii predominate with 81.2% [13]. The majority of samples were revealed from patients staying in ICUs (62%). Based on laboratory report between March 2005 and August 2006, A. baumannii was responsible for 100 of the 719 infections, which occurred in the CICU (13.9%). Other most common isolated pathogens were P. aeruginosa (22.1%), S. aureus (15.39%), and Klebsiella pneumoniae (12.9%).

The present study was undertaken to elucidate the molecular epidemiology of Acinetobacter baumannii using pulse field gel electrophoresis (PFGE). Therefore, the objectives of the present study were (i) to assess the genetic relatedness of A. baumannii isolates in the ICU of our university hospital; and (ii) to study the clinical features of patients from whom A. baumannii had been isolated.

Material and Methods

Hospital Setting and Patients

The study was conducted at the University Clinical Centre of Kosova (UCCK), in Prishtina, the capital city of Kosova. The center has 2,100 beds with approximately 60,000 admissions per year and serves as the only referral tertiary care center for a population of around 2.1 million. The Central Intensive Care Unit is a mixed ICU with 12 beds. The bacterial isolates selected for the present study included 30 A. baumannii isolates from 30 patients from the ICU of UCCK, during the period from March 2006 to July 2006. Laboratory diagnosis of microbiological samples and susceptibility testing was done in the Department of Microbiology within the National Institute for Public Health of Kosova. The genotyping was performed in the Clinical Hospital Centre Zagreb, Department of Clinical and Molecular Microbiology in Zagreb, Croatia. Clinical specimens included cerebrospinal liquid, endotracheal aspirate, thoracal drain and tracheostoma. The following data were recorded from the medical charts of patients with A. baumannii infection or colonisation: age, gender, number of patient-days in hospital, underlying diseases or conditions, susceptibility pattern and clinical outcome. Nosocomial infections were classified according to standard CDC definitions, whilst A. baumannii was considered to be a colonising organism when it was isolated from clinical specimens, but the criteria for infection were not met [14]. Only one sample of A.baumanni per patient was enrolled in the study.

Microbiological Methods

A. baumannii strains were collected from clinical specimens by using standard methods, isolated in pure cultures on MacConkey agar plates. Organisms were identified by using the API system for the identification (bioMerieux, Marcy l'Etoile, France). From a fresh 18 hours plate culture of A. baumanii, a heavy, cloudy suspension of the organism was made in the CRYOBANK [TM] medium in the tube (COPAN Diagnostics Inc., CA, USA). Tube was mixed by shaking and inverting to allow the bacteria in the suspension to coat the beads. Using a sterile pipet the CRYOBANK [TM] medium was removed from the tube. Than, the tube was placed in a -70[degrees]C freezer to store the culture. Afterwards the samples were transported to Croatia where the bacteria were recovered removing the cap of the CRYOBANK [TM] tube. Using forceps one bead was rolled over the culture mediums (brain-heart infusion) and Kaufman-Muller broth. Isolates were verified in Croatia as A.baumannii using the Vitek 2 automatic system (bioMerieux, Marcy l'Etoile, France).

Antimicrobial Susceptibility

Antimicrobial resistance was determined by the disk diffusion method according to the Clinical and Laboratory Standards Institute criteria, former NCCLS [15]. The following antimicrobial drugs were tested: Ampicillin 10 [mu]g, Ceftriaxon 30 [mu]g, Gentamicin 10 [mu]g, Amikacin 30 [mu]g, Imipenem 10 [mu]g, Pipercilin + tazobactam 100 [mu]g, Cefoxitin 30 [mu]g, Ceftazidime 30 [mu]g, Tobramycin 10 [mu]g, Cotrimoxasole 1.25+23.75 [mu]g and Ciprofloxacin 5 [mu]g.

Molecular Typing by Pulsed-Field Gel Electrophoresis (PFGE) and Dendrogram Analysis

The preparation of genomic DNA of A. baumannii isolates was performed as described by Schwartz and Cantor with minor modifications. Macrorestriction analysis of chromosomal DNA with XbaI was carried out by PFGE following published procedures [16]. PFGE was run in a CHEF-DRIII apparatus (Bio-Rad Laboratories, CA, USA), with pulses ranging from 5 to 50 seconds at a voltage of 6 V/cm at 10-12[degrees]C for 20 h. Products were detected after staining with ethidium bromide (50 mg/mL) and photographed with Polaroid type 667 film. A ladder ofbacteriophage lambda concatemers (New England Biolabs) was used as molecular weight markers.

Clusters of possibly related isolates were identified by using the Dice coefficient of similarity and unweighted group method with arithmetic averages at 80%, which indicates fourto six fragment differences in gels. The relationships between all isolates were analysed using the GelComparII software package and presented as a dendrogram (Applied Maths NV, Belgium). DNA fingerprints were interpreted as recommended by Tenover et al. [17].

Results

From March 16th to July 27th 2006, a total of 30 Acinetobacter baumannii isolates were obtained from 30 patients (24 males, 6 females) admitted to the CICU. Their age range was from 2 to 82 years (mean age 47.5, median age 52.5 years). Based on evaluation of clinical charts, 22 patients were classified as infected and had nosocomial infections and eight of them were considered colonized with A. baumannii.

Isolates were most frequently recovered from endotracheal aspirate (n = 26); the other isolates were recovered from tracheostoma (n=2), thoracal drain (n=1) and cerebrospinal fluid (n = 1). Twenty patients developed nosocomial pneumoniae; one patient had a diagnosis of meningitis, and two had coinfection with bloodstream infection and surgical site infection. The most common diagnoses upon admission to the ICU were politrauma and cerebral hemorrhage. Other pathogens were co-isolated from nine patients: Staphylococcus aureus from two patients, P. aeruginosa from 4 patients, and Klebsiella pneumonaie from three patients.

The clinical characteristics of patients from whom A. baumannii was isolated are shown in Table 1.

The length of stay in ICU ranged from 1-59 days with median time of 17 days. The median time that had elapsed between admission and isolation of A. baumannii was 8 days. During the ICU stay, 16 patients died (crude mortality 53.3%) and the A. baumannii-attributable mortality was 62.5% (10 / 16). The time-frame of admission, discharge and isolation of A. baumanni from ICU patients is presented in Figure 1.

The length of ICU stay for non-survivors and survivors was 14.5 and 18.5 days, respectively. The length of stay was significant in comparison between infected and colonised patients (19.5 vs. 9 days).

The length of ICU stay for epidemic strains and nonepidemic strains was 15.7 and 24.5 days, respectively.

Four patients yielded A. baumannii upon hospital admission and were transferred from other hospitals to ICU, while 22 patients yielded A. baumannii only following hospitalization. Twelve patients were transferred to ICU from other departments within the UCCK.

PFGE profiles of A. baumannii strains isolated from CICU is shown in the Figure 2.

[FIGURE 1 OMITTED]

[FIGURE 2 OMITTED]

Genotypic analysis of A. baumannii isolates from ICU patients identified nine major PFGE patterns, which we named from A to I, that differed in migration of at least four DNA fragments and showed a similarity of < 80% at dendrogram analysis. Of these, PFGE pattern E predominate with isolates from nine patients. Eight isolates were resistant to carbapenems.

Discussion

Although only 5-10% of all hospitalized patients are treated in ICUs, they account for approximately 25% of all nosocomial infections [18]. The incidence of nosocomial infections in ICUs is 5-10 times higher than that observed in general hospital wards [19,20]. In developing countries the occurrence of nosocomial infections is 12-20 fold higher [21].

A. baumannii outbreaks have been reported previously, particularly in ICU wards [22-26]. Severe underlying diseases, invasive diagnostic and therapeutic procedures used in ICUs have been demonstrated to predispose patients to severe infections with A. baumannii [27-29]. Our results show that nosocomial infections and colonizations by A. baumannii in the ICU were prolonged for several months. The impact of A. baumannii on ICU-acquired infections and colonization was substantial from clinical samples received in our laboratory from CICU. From March 2006 to August 2007 Acinetobacter spp. were the second most prevalent identified microorganism with 13.9% (100/719). Other most frequent isolates were P aeruginosa (22.1%), S. aureus (15.3%) and Klebsiella spp.(12.9%). Acinetobacter strains (n=100) showed globally high resistance pattern to cephalosporins (76.9%). Imipenem and amikacine were the most effective drugs against A. baumannii with sensitivity rate of 92.4% and 85.7% respectively (unpublished data).

Previous prevalence studies in Kosova showed hight rates of health care associated infections in UCCK (17.4%) and in CICU with 68.7% of patients having nosocomial infections, with a predominance of ventilator associated pneumonia (72.7% of infections) [30,31].

There are many causes for high rate of nosocomial infections in ICU and A. baumannii outbreaks. Main factor remains the lack of support and implementation of prevention and control policies. The proportion of health care workers working in CICU to patients staying in ICU is only 5 HCW per 12 patients per shift. CICU is referent center for intensive care for all 6 regional hospitals and other depratments within the UCCK.

Single use devices were reused due to limited budget. Suction catheters for aspiration of respiratory tract were amongst most used equipment in this group. Audit in the ward during the study period proved that these catheters were placed in a containers containing diluted chlorhexidine. The same catheters after "disinfection" were used for more than one patient carrying a significant risk for cross-infection. Some equipment used in ICU were outdated and their maintenance services were not regular.

A study of compliance with hand hygiene in CICU showed the alert rate of only 19% [32]. During the outbreak period alcoholic hand rubs were not in used in ICU. There are three washing sinks in the ward. Low number of wash sinks contributed to high rate of infection in ICU. Gloves were not changed after each contact with patients but they were used and maintained for successive patients intervention.

For many years in Kosova, the cephalosporins are the drugs of choice in empiric treatment in ICU and they have been used without any restrictions not only in ICUs but also in other hospital wards and ambulantory care. This could explain the high resistance rates of Acinetobacter baumannii to antimicrobials. For a decade in Kosova, all antimicrobials have been available in pharmacies without a physician's prescription.

CICU is reference center for patients from other hospital departments of CICU, from regional hospitals and also from the private hospitals. Delay of referral to this unit contributed to infections, severity of illness and poor outcome prognosis for the patients.

Delay is related to patients who are previously treated at the regional hospitals and they are not transferred on time to the CICU, which is the only ICU reference center for six regional hospitals and for 13 clinics within UCCK.

Genotypic analysis of A. baumannii isolates from ICU patients identified nine major PFGE patterns. The most predominant clones of A. baumannii (E and F) were related with more than one outbreak during the study period occurring sequentially. Case-control study was not performed in epidemiological investigation. The data were recorded from the medical charts of patients with A. baumannii infection or colonization. Some genetically indistinguishable A. baumannii isolates (931, 933 and 934) were isolated on the same day (May 2, 2006) and had similar antimicrobial susceptibility pattern, suggesting common source of infection. The median time from admission to isolation of this bacteria revealed that it's shorter than in other publications [23-27].

In cases where the genetically same strains were not related in timely manner, the only explanation would be poor hand hygiene of health care workers (HCW). Another argument is high endemic rate of MRSA, which is 61.3% of all S. aureus isolates [13]. These facts suggests the horizontal transmission of the epidemic strains from one patient to another through the hospital staff.

As in other publications endotracheal aspirates were predominant clinical samples received from ICU [33,34].

The length of stay was significant in comparison between infected and colonised patients. This finding is consistent with reports of other outbreaks [6,29,33,34]. But there was no significant diference between non survivors and survivors. This can be explained with a fact that some patients spent some hospital days in regional hospitals before referral to CICU and also six patients were sent for treatment in other ICUs in neighbouring countries. As in previous studies, the respiratory tract was the most frequent site of isolation of A. baumannii in ICU patients [35,36]. Colonization with A. baumannii in not performed routinely at admission to ICU.

In conclusion, we show here that A. baumannii strains cause large and sustained hospital outbreak due to insufficient preventive measures. These results emphasize the need for preventive interventions in ICU.

Received on 6 May 2009; revised 20 November 2009.

References

[1.] Schreckenberger PC, Daneshvar MI, Weyant RS, Hollis DG. Acinetobacter, Achromobacter, Chryseobacterium, Moraxella, and other nonfermentative Gram-negative rods. In: Murray PR, Baron EJ, Jorgensen JH, Landry ML, Pfaller MA, eds. Manual of clinical microbiology. 9th ed. Washington, DC: ASM Press, 2007:770-802.

[2.] Fournier PE, Richet H. The epidemiology and control of Acinetobacter baumannii in health care facilities. Clin Infect Dis 2006;42:692-699.

[3.] Munoz-Price LS, Weinstein RA. Acinetobacter infection. N Engl J Med. 2008 Mar 20;358(12):1271-81.

[4.] Getchell-White SI, Donowitz LG, Groschel DH. The inanimate environment of an intensive care unit as a potential source of nosocomial bacteria: evidence for long survival of Acinetobacter calcoaceticus. Infect Control Hosp Epidemiol 1989;10:402-407.

[5.] Garnacho-Montero J, Ortiz-Leyba C, Fernandez-Hinojosa E, et al. Acinetobacter baumannii ventilator-associated pneumonia: epidemiological and clinical findings. Intensive Care Med 2005;31:649-655

[6.] Baran G, Erbay A, Bodur H, Onguru P, Akinci E, Balaban N, Cevik MA. Risk factors for nosocomial imipenem-resistant Acinetobacter baumannii infections. Int J Infect Dis. 2008 Jan; 12(1):16-21.

[7.] Playford EG, Craig JC, Iredell JR. Carbapenem-resistant Acinetobacter baumannii in intensive care unit patients: risk factors for acquisition, infection and their consequences. J Hosp Infect. 2007 Mar;65(3):204-11

[8.] Murray CK, Hospenthal DR. Acinetobacter infection in the ICU. Crit Care Clin. 2008 Apr;24(2):237-48.

[9.] Villegas MV, Hartstein AI. Acinetobacter outbreaks, 1977-2000. Infect Control Hosp Epidemiol 2003;24:284-295

[10.] Meric M, Kasap M, Gacar G, Budak F, Dundar D, Kolayli F, Eroglu C, Vahaboglu H. Emergence and spread of carbapenem-resistant Acinetobacter baumannii in a tertiary care hospital in Turkey. FEMS Microbiol Lett. 2008 May;282(2):214-8.

[11.] Kraniotaki E, Manganelli R, Platsouka E, Grossato A, Paniara O, Palu G. Molecular investigation of an outbreak of multidrug-resistant Acinetobacter baumannii, with characterisation of class 1 integrons. Int J Antimicrob Agents. 2006 Sep;28(3):193-9.

[12.] Zarrilli R, Crispino M, Bagattini M, Barretta E, Di Popolo A, Triassi M, Villari P. Molecular epidemiology of sequential outbreaks of Acinetobacter baumannii in an intensive care unit shows the emergence of carbapenem resistance. J Clin Microbiol. 2004 Mar; 42(3):946-53.

[13.] A. Kurti, L. Raka, Gj. Mulliqi: Acinetobacter species-clinical sample isolates and antibiotic susceptibility in Kosova, 8th European Congress of Chemotherapy and Infection, Budapest, Hungary, 25-28 October 2006.

[14.] Garner JS et al. CDC definitions for nosocomial infections. Am J Infect Contr 1988;16:128-40.

[15.] Clinical and Laboratory Standards Institute. Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically, 6th edn. Approved standard M7-A6. Wayne, PA: CSLI, 2005.

[16.] Seifert H, Dolzani L, Bressan R et al. Standardization and interlaboratory reproducibility assessment of pulsed-field gel electrophoresis-generated fingerprints of Acinetobacter baumannii. J Clin Microbiol 2005; 43: 4328-4335.

[17.] Tenover F, Arbeit R, Goering R. How to select and interpret molecular strain typing methods for epidemiological studies of bacterial infections: a review for healthcare epidemiologists. Infect Control Hosp Epidemiol 1997; 18: 426-439.

[18.] Eggimann P., Pittet D. Infection Control in the ICU. Chest 2001;120:2059-2093.

[19.] Pittet D, Sax H. Health-care associated infections. In: Cohen J, Powderly W, editors. Infectious diseases. 2nd ed. Mosby; 2003. p. 881-92.

[20.] Ponce-de-Leon-Rosales S, Macias A. Global perspectives of infection control. In: Wenzel: Prevention and control of nosocomial infections. 4th ed. Philadelphia LWW, 2003:14-33.

[21.] Patricia Lynch P, Victor D. Rosenthal V, Michael A. Borg M, and Eremin S. Infection Control in Developing Countries. In Jarvis: Bennett and Brachman's Hospital Infections. 4th ed. 2007:255-270.

[22.] Corbella X, Montero A, Pujol M et al. Emergence and rapid spread of carbapenem resistance during a large and sustained hospital outbreak of multiresistant Acinetobacter baumannii. J Clin Microbiol 2000; 38: 4086-4095.

[23.] Rodriguez-Bano J, Cisneros JM, Fernandez-Cuenca F et al. Clinical features and epidemiology of Acinetobacter baumannii colonization and infection in Spanish hospitals. Infect Control Hosp Epidemiol 2004; 25: 819-824.

[24.] Turton JF, Kaufmann ME, Warner M et al. A prevalent, multiresistant clone of Acinetobacter baumannii in Southeast England. J Hosp Infect 2004; 58: 170-179.

[25.] Marque' S, Poirel L, He'ritier C et al. Regional occurrence of plasmid-mediated carbapenem-hydrolyzing oxacillinase OXA-58 in Acinetobacter spp. in Europe. J Clin Microbiol 2005; 43: 4885-4888.

[26.] Pournaras S, Markogiannakis A, Ikonomidis A et al. Outbreak of multiple clones of imipenem-resistant Acinetobacter baumannii isolates expressing OXA-58 carbapenemase in an intensive care unit. J Antimicrob Chemother 2006; 57: 557-561.

[27.] Husni RN, Goldstein LS, Arroliga AC, Hall GS, Fatica C, Stoller JK, Gordon SM. Risk factors for an outbreak of multi-drug-resistant Acinetobacter nosocomial pneumonia among intubated patients. Chest. 1999 May;115(5):1378-82.

[28.] Cardenosa Cendrero JA, Sole-Violan J, Bordes Benitez A, Noguera Catalan J, Arroyo Fernandez J, Saavedra Santana P, Rodriguez de Castro F. Role of different routes of tracheal colonization in the development of pneumonia in patients receiving mechanical ventilation. Chest. 1999 Aug; 116(2):462-70.

[29.] Tejada Artigas A, Bello Dronda S, Chacon Valles E, Munoz Marco J, Villuendas Uson MC, Figueras P, Suarez FJ, Hernandez A. Risk factors for nosocomial pneumonia in critically ill trauma patients. Crit Care Med. 2001 Feb;29(2):304-9.

[30.] Raka L, Zoutman D, Mulliqi G, Krasniqi S, Dedushaj I, Raka N, Ahmeti S, Shala M, Vishaj A, Elezi Y. Prevalence of nosocomial infections in high-risk units in the university clinical center of Kosova. Infect Control Hosp Epidemiol. 2006 Apr;27(4):421-3.

[31.] Spahija G, Raka L, Mulliqi G, Spahija N, Bukoshi Z, Hoxha F, Krasniqi A. Prevalence of Nosocomial Infections in Adult Intensive Care Units at a Kosova Teaching Hospital. Infect Control Hosp Epidemiol. 2008 May; 29(5):475.

[32.] Rosenthal VD, Ajita Mehta, Luis Cuellar, Carlos Alvarez Moreno, Hakan Leblebicioglu, Naoufel Madani, Lourdes Duenas, Regina Berba, Mitrev Z, Raka L, Souha Kanj-Sharara, Fernandez-Hidalgo, Salisu Abubakar, Altaf Ahmed, Sanjeev Singh, Subhash Kumar Todi, Nagamani Sen, Monica Viegas, Nayide Barahona Guzman, A. Nevzat Yalcin, Teodora Atencio Espinoza, Alberto Armas Ruiz, Gorki Grinberg. Hand Hygiene Compliance in 84 ICUs of 16 countries.Findings of the International Nosocomial Infection Control Consortium (INICC). SHEA Annual Conference, Orlando, Florida, 5-8 April, 2008.

[33.] Bergogne-Berezin E, Towner KJ. Acinetobacter spp. as nosocomial pathogens: microbiological, clinical, and epidemiological features. Clin Microbiol Rev 1996; 9: 148-165.

[34.] Webster CA, Crowe M, Humphreys H, Towner KJ. Surveillance of an adult intensive care unit for long-term persistence of a multi-resistant strain of Acinetobacter baumannii. Eur J Clin Microbiol Infect Dis 1998; 17: 171-176.

[35.] Bergogne-Berezin E, Towner KJ. Acinetobacter spp. as nosocomial pathogens: microbiological, clinical, and epidemiological features. Clin Microbiol Rev 1996; 9: 148-165.

[36.] Corbella X, Montero A, Pujol M et al. Emergence and rapid spread of carbapenem resistance during a large and sustained hospital outbreak of multiresistant Acinetobacter baumannii. J Clin Microbiol 2000; 38: 4086-4095.

Lul Raka (1,2), Smilja Kalenc (3), Zrinka Bosnjak (3), Ana Budimir (3), Stjepan Katic (3), Dubravko Sijak (3), Gjyle Mulliqi-Osmani (1,2), Dick Zoutman (4) and Arberesha Jaka (1)

(1) Medical School, Prishtina University, Prishtina, Kosova; (2) National Institute for Public Health of Kosova, Prishtina, Kosova (3) Department of Clinical and Molecular Microbiology, Clinical Hospital Centre Zagreb, Zagreb, Croatia; (4) Queen's University and Kingston General Hospital, Kingston, Ontario, Canada

Address for correspondence: Dr. Lul Raka. "Emin Duraku", N=166, 71000 Kacanik, Kosova; Phone: +3813829080666 and +37744368289. Email: lulraka@hotmail.com.
Table 1. Clinical and PFGE data of the patients with
Acinetobacter baumannii isolates.

Nr    Gender/   Day of      Length of   Diagnosis
      age       isolation   ICU stay

1     M/ 66     17          18          Tumor cerebri
2     M/ 33     4           28          Tumor cerebri
3     M/ 62     3           8           Tumor cerebri
4     M/ 17     1           14          Diabetes mellitus
5     M/ 11     12          37          Politrauma
6     M/ 62     4           6           Politrauma
7     M/41      4           28          Politrauma
8     F/33      10          14          Politrauma
9     M/ 51     14          59          Cerebral infarct
10    M/ 2      1           10          Politrauma
11    M/ 21     8           10          Politrauma
12    M/ 72     3           5           Cerebral infarct
13    M/ 43     1           13          cardiac arrest
14    M/ 55     4           8           Politrauma
15    M/ 74     18          23          Politrauma
16    M/ 71     9           34          Politrauma
17    M/ 57     2           8           Politrauma
18    M/ 46     14          20          Tumor cerebri
19    F/ 20     2           15          Pulmonal infiltrat
20    M/ 22     1           1           Politrauma
21    M/ 50     5           11          Tumor cerebri
22    F/ 24     15          30          Myocardiopathia
23    M/ 82     8           32          Peritonitis
24    F/ 54     26          44          Peritonitis
25    F/ 72     12          34          cardiac arrest
26    M/ 60     10          14          Cerebral infarct
27    M/ 74     8           17          Politrauma
28    F/ 71     10          19          Tumor cerebri
29    M/ 61     16          19          Cerebral infarct
30    M/ 20     8           11          Politrauma

Nr    Sensitive            Outcome        Sample

1     AMI                  Died           EA
2     TOB, AMI, DM         Died           CLS
3     AMI, IMI, TOB, GEN   Died           EA
4     AMI, CIP             Recovered      EA
5     TOB, AMI, IMI        Transferred    EA
6     AMI, IMI             Died           EA
7     IMI                  Recovered      EA
8     AMI, IMI             Transferred    EA
9     TOB, AMI, CAZ        Died           TRA
10    IMI                  Died           EA
11    IMI, AMI             Died           EA
12    AMI, IMI             Died           EA
13    GEN, AMI, CAZ        Recovered      EA
14    AMI, IMI             Recovered      EA
15    TOB, AMI             Recovered      EA
16    AMI, CIP, IMI        Recovered      EA
17    GEN, TOB, AMI, IMI   Transfer       EA
18    AMI, IMI             Recovered      EA
19    AMI, IMI             Died           TC
20    IMI, CAZ, AMI        Transferred    EA
21    IMI                  Died           EA
22    AMI                  Died           EA
23    AMI, IMI             Died           EA
24    TOB, AMI,            Transferred    TRA
25    AMI, IMI             Died           EA
26    AMI                  Died           EA
27    IMI,CAZ.AMI          Recovered      EA
28    AMI,IMI              Transferred    EA
29    AMI                  Died           EA
30    AMI, IMI             Died           EA

Nr    Isolate    PFGE type

1     1277       F4
2     1592       G1
3     1007       A3
4     930        E5
5     1570       C1
6     838        E2
7     972        B2
8     868        E3
9     1622       A2
10    1461       C2
11    1517       F6
12    768        E3
13    1191       B1
14    869        E1
15    933        D1
16    907        E5
17    1574       F5
18    943        D1
19    929        E5
20    1003       A1
21    575        E4
22    1438       F3
23    931        D1
24    1605       H1
25    1188       I1
26    815        F1
27    1009       A1
28    933        D1
29    907        E5
30    948        F2

EA=endotracheal aspirate; AMI=amikacin, IMI=imipenem, TOB=tobramycin,
CIP=ciprofloxacine, CAZ=cephtazidime, GEN=gentamycine;
TRA=tracheostoma; TC=Thoracal drain.
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Author:Raka, Lul; Kalenc, Smilja; Bosnjak, Zrinka; Budimir, Ana; Katic, Stjepan; Sijak, Dubravko; Mulliqi-O
Publication:The Brazilian Journal of Infectious Diseases
Date:Nov 1, 2009
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