First Documented Case of Percutaneous Endoscopic Gastrostomy (PEG) Tube-Associated Bacterial Peritonitis due to <i>Achromobacter</i> Species with Literature Review

Tripathi, Nishant; Koirala, Niki; Kato, Hirotaka; Singh, Tushi; Karri, Kishore; Thakur, Kshitij

doi:https://doi.org/10.1155/2020/4397930

Case Reports in Gastrointestinal Medicine

On this page

Abstract Introduction Discussion Conclusion Conflicts of Interest Authors’ Contributions References Copyright Related Articles

Case Report | Open Access

Volume 2020 | Article ID 4397930 | https://doi.org/10.1155/2020/4397930

First Documented Case of Percutaneous Endoscopic Gastrostomy (PEG) Tube-Associated Bacterial Peritonitis due to Achromobacter Species with Literature Review

Nishant Tripathi,¹Niki Koirala,²Hirotaka Kato,¹Tushi Singh,¹Kishore Karri,¹and Kshitij Thakur¹

Academic Editor: Engin Altintas

Received26 Aug 2019

Revised24 Oct 2019

Accepted11 Nov 2019

Published16 Jan 2020

Abstract

Introduction. Achromobacter species (spp.) peritonitis has seldom been identified in medical literature. Scarce cases of Achromobacter peritonitis described previously have been correlated with peritoneal dialysis and more sparingly with spontaneous bacterial peritonitis. Achromobacter exhibits intrinsic and acquired resistance, especially in chronic infections, to most antibiotics. This article conducts a literature review of all previously reported Achromobacter spp. peritonitis and describes the first reported case of Achromobacter peritonitis as a complication of percutaneous endoscopic gastrostomy (PEG) tube placement. Discussion. Achromobacter peritonitis as a complication of PEG-tube placement has not been previously reported. In our patients’ case, the recently placed PEG-tube with ascitic fluid leakage was identified as the most plausible infection source. Although a rare bacterial peritonitis pathogen, Achromobacter may be associated with wide antimicrobial resistance and unfavorable outcomes. Conclusion. No current guidelines provide significant guidance on treatment of PEG-tube peritonitis regardless of microbial etiology. Infectious Disease Society of America identifies various broad-spectrum antibiotics targeting nosocomial intra-abdominal coverage; some of these antimicrobial selections (such as cefepime and metronidazole combination) may yet be inadequate for widely resistant Achromobacter spp. Recognizably, the common antibiotics utilized for spontaneous bacterial peritonitis, i.e., third generation cephalosporins and fluoroquinolones, to which Achromobacter is resistant and variably susceptible, respectively, would be extensively insufficient. Piperacillin/tazobactam (P/T) and carbapenem were identified to provide the most reliable coverage in vitro; clinically, 5 out of the 8 patients who received either P/T or a carbapenem, or both, eventually experienced clinical improvement.

1. Introduction

Achromobacter species (spp.) are nonfermenting, oxidase positive, catalase positive, aerobic, and motile Gram-negative rods [1]. As environmental organisms, Achromobacter spp. are naturally distributed in aqueous surroundings including soil and water [2–4]. Similarly, they may contaminate fluids in the health care setting, and have been considered infectious etiologies in nosocomial infection outbreaks associated with contaminated fluids [5], pressure transducers [6], incubators [7], and disinfectants [7]. Although opportunistic organisms [8], Achromobacter spp. are deemed to be the etiology for a myriad of infectious diseases with significant morbidity and mortality such as biliary tract sepsis [9], meningitis [10], pneumonia [11], spontaneous bacterial peritonitis [12, 13], peritoneal dialysis associated peritonitis [5, 14], urinary tract infection [11], conjunctivitis [15], osteomyelitis [16], prosthetic knee infection [17], mesh infection [18], necrotizing pancreatitis [19], prosthetic valve endocarditis [20], bacteremia [6, 11, 21], and cystic fibrosis [4, 22], among others. While the majority of these diseases occur as a polymicrobial infection in immunocompromised states such as cancer [21], human immunodeficiency virus/acquired immunodeficiency syndrome [23], chronic renal failure or diabetes mellitus [20], a portion of them occur due to nosocomial outbreaks in immunocompetent hosts [11, 24].

The organism is highly resistant to commonly utilized antibiotics in intra-abdominal infections. Piperacillin/tazobactam (P/T) and carbapenems show activity in vitro and are considered the most active antimicrobials against Achromobacter spp. [2]. On the other hand, sulfamethoxazole/trimethoprim may be a reasonable non beta-lactam alternative [25]. Due to the extensive inherent and acquired resistance to significant number of antimicrobials, providing dual coverage for chronic infections may be prudent [25].

2. Case Summary

A 65-year-old Caucasian male with a history of chronic alcoholism (without cirrhosis or ascites), hypertension and prior tonsillar adenocarcinoma status post chemo-radiation presented to a regional hospital with progressive fatigue and jaundice, epigastric pain, and decreased appetite causing twenty-five-pound weight loss spanning over a month. Leukocytosis along with lactic acidosis was observed. Patient was treated empirically with P/T for biliary pancreatitis secondary to choledocolithiasis. Initial endoscopic retrograde cholangiopancreatography (ERCP) on day (D) 2 of hospitalization identified distal common bile duct stone; sphincterotomy was performed with 7- French 5 cm plastic common bile duct stent placement. Despite the interventions, liver enzymes continued to rise; antibiotic was altered to levofloxacin and metronidazole on D4 to cover intra-abdominal infections and a repeat ERCP was performed. Recently placed CBD stent, which appeared clogged with debris, was removed uneventfully with snare. Appropriate drainage from CBD and cystic duct was confirmed; however, gall bladder could not be visualized with contrast. Due to the development of pneumonia, antibiotics were switched to linezolid and doxycycline on D6 of hospitalization. On D11, due to poor nutritional status and emerging aspiration pneumonia, PEG-tube was inserted. Subsequently, developing and rapidly worsening ascites and ascitic fluid leakage around the PEG-tube insertion site was identified. Paracentesis was performed on D13 of hospitalization without evidence of peritonitis; however, antibiotics were escalated to meropenem and linezolid due to worsening clinical status. Due to thrombocytopenia, linezolid was discontinued, and antimicrobial therapy was narrowed to meropenem on D17. Due to worsening of ascitic fluid leakage around the PEG insertion site, and exacerbation of liver enzymes, the patient was transferred to our academic facility for further management, including possible cholecystectomy on D17.

Upon transfer, the patient was hemodynamically stable with a constellation of physical exam findings significant for leaking ascites, icterus, spider angioma, fine crackles throughout lung fields, and 3+ bilateral pitting edema; no evidence of encephalopathy was noted. The laboratory tests were remarkable for white blood cells 21,600/mcl, serum creatinine 0.55 mg/dl, aspartate aminotransferase 201 U/L, alanine transferase 74 U/L, alkaline phosphatase 458 U/L, total bilirubin 9.0 mg/dl, serum albumin 1.8 g/dl, and INR 1.5. Patient was further diagnosed with alcoholic cirrhosis decompensated by ascites with MELD-Na score of 23, and suspected alcoholic hepatitis with Maddrey’s discriminant function of 28. Antibiotic therapy was held until further work-up due to previously negative cultures and extended duration of therapy prior to transfer. Interventional radiology guided paracentesis was performed on D22 of hospitalization as bedside procedure was unsuccessful. Ascitic fluid analysis revealed albumin of 0.3 gm/dL and polymorphonuclear neutrophil count of 1950 cells/mcl. PEG-tube was retained to allow for maturation of PEG-tube tract; P/T and vancomycin were initiated and continued for two days (D22-D23); therapy was empirically altered to cefepime, metronidazole, and vancomycin to prevent acute kidney injury secondary to concomitant vancomycin and P/T use, which was continued for four days (D24-27). Ascitic fluid cultures revealed P/T susceptible and cefepime resistant Achromobacter xylosoxidans as the infectious etiology (Isolate was identified by MALDI TOF: MALDI Biotyper CA system. Please refer to Table 1 for minimal inhibitory concentration values). Empiric regimen of cefepime, metronidazole, and vancomycin was narrowed to P/T on D27. Bronchoalveolar Lavage on D27 due to worsening respiratory failure also identified A. xylosoxidans. Following five days of treatment with P/T, however, his abdomen demonstrated peritoneal signs with increasing ascites. Repeat paracentesis confirmed worsening bacterial peritonitis, with additional findings of vancomycin resistant Enterococcus and Candida glabrata. Despite broadened antimicrobial coverage with meropenem and vancomycin for four days (D28–D31), the patient deteriorated with acute kidney injury and hypotension, and was deceased within twenty-four hours of intensive care unit transfer.

3. Discussion

3.1. Nomenclature

The taxonomic designation for Achromobacter spp. has been inconsistent due to the limited differentiating capability of previous identification methods [26, 27]. Solely multilocus sequence typing (MLST) and species identification via nrdA sequence analysis for Achromobacter genus have been deemed to be effective in differentiating between various Achromobacter spp. [26, 27]. Prior to utilization of these methods, various alternate Achromobacter species might have been misidentified as Achromobacter xylosoxidans; currently, reclassification of Achromobacter species has resulted from utilization of these techniques [26–31]. The ascitic culture in our patient case was assessed by MALDI TOF MS (Matrix Assisted Laser Desorption/Ionization Time of Flight Mass Spectrometry); thus, exact species identification might not have been accurate. As such, our literature review attempts to include all previously documented Achromobacter species peritonitis cases to ensure an inclusive analysis.

3.2. Antimicrobial Susceptibility Patterns

Achromobacter susceptibility profile identifies the organism as being extensively resistant among various classes of antimicrobials, including fluoroquinolones, aminoglycosides, and the majority of broad-spectrum β-lactam antibiotics [32]. The resistance-nodulation-cell division (RND)-type multidrug efflux pumps, AxyABM [33, 34] and AxyXY-OprZ [35] have been associated with innate resistance. Essentially, resistant to all cephalosporins, except ceftazidime, due to the presence of AxyABM efflux system [29, 33], Achromobacter spp. may also contain AxyXY-OprZ efflux pump associated with aminoglycoside resistance [29, 35]. On the other hand, most isolates are typically susceptible to carbapenems, piperacillin, and P/T [29]. While a few acquired betalactamases have been described, overall acquired resistance mechanisms remain unknown [36–40].

3.3. PEG-Tube Associated Complications

This case report documents the first percutaneous endoscopic gastrostomy (PEG) tube-associated Achromobacter peritonitis. PEG-tube is a reliable source of enteral nutrition for patients with the inability to maintain oral nutrition on a long-term basis. Although minimally invasive, gastrostomy tubes have been associated with major complications such as peritonitis, major gastrointestinal bleeds, aspiration pneumonia, gastroenteric fistula, and gastrocolocutaneous fistula; minor complications include cellulitis, leakage around the tube, and granulation tissue at gastrostomy site [41–43]. In order to minimize these complications, the European Society for Clinical Nutrition and Metabolism guidelines on artificial enteral nutrition identifies a variety of contraindications to gastrostomy tubes including, serious coagulation disorders, INR greater than 1.5, platelets less than 50,000/mcl, marked peritoneal carcinomatosis, interposed organs (liver and colon), severe ascites, peritonitis, anorexia nervosa, severe psychosis, and discernibly limited life expectancy [44].

Specific risk factors for PEG-tube peritonitis include poor tissue healing, procedural, and technical issues, BMI over 30 kg/m2, albumin less than 2.5 g/dL, and dislodgement or reinsertion of tube [41, 42]. Pseudomonas aeruginosa, Methicillin resistant Staphylococcus aureus, and enteric Gram-negative rods are implicated as the most common infective etiologies of PEG site infections [45–47]. Abuksis et al. report 30-day mortality rate of 4.1–26% for stomal infections [48].

Despite the wide array of Achromobacter spp. infections previously reported, Achromobacter peritonitis is extremely rare and has been documented primarily in the setting of peritoneal dialysis. Despite the fact, Achromobacter infections in peritoneal dialysis are also exceptionally infrequent. Moreover, etiologies reported prior to nrdA sequencing might have been inaccurately identified as A. xylosoxidans and may rather represent Achromobacter spp. [11, 26–28]. In order to identify all reported and published cases of Achromobacter peritonitis, thorough PubMed (January 1^st, 1966–April 7^th, 2019) literature searches were conducted from March 20^th, 2019 through April 7^th, 2019, and October 10^th, 2019 through October 21^st, 2019 independently by both primary authors. Search terms that were used include “PEG or percutaneous endoscopic gastrostomy tube peritonitis” with no relevant results, “Achromobacter peritonitis” with four relevant results [49–52], and “Alcaligenes peritonitis” with additional 8 relevant results [12, 13, 53–58]. Five additional cases were identified through previously published case reports, and extensive search in PubMed with search terms “Achromobacter xylosoxidans”, “Achromobacter”, and “Alcaligenes” [5, 8, 14, 59, 60].

In totality, eighteen previous Achromobacter peritonitis cases were encountered; of which, two were diagnosed as spontaneous peritonitis [12, 13] while remaining sixteen cases of peritonitis were associated with peritoneal dialysis [5, 8, 14, 49–60]. No previous cases of PEG tube-associated Achromobacter peritonitis were discovered. Tables 1 and 2 summarize, in as much detail as could be obtained, the infectious diagnosis of each patient case, cultures, and sensitivities, antimicrobial therapies selected, and overall outcomes. Likewise, Figure 1 utilizes a bar graph to indicate the overall in vitro susceptibility profiles of the Achromobacter strains that were encountered in all nineteen cases of Achromobacter spp. peritonitis.

Figure 1

Susceptibility of Achromobacter spp. to various antimicrobials. Seven cases reported Achromobacter spp. sensitivity to piperacillin/tazobactam and all 7 isolates were susceptible to P/T. Similarly, 9 cases reported carbapenem sensitivity; 8 of 9 (88.89%) isolates were susceptible. SMZ/TMP and ceftazidime sensitivities were reported by 9 cases, of which 6 isolates (66.67%) were susceptible to each agent. On the other hand, 13 cases reported fluoroquinolones, of which, only 5 Achromobacter isolates (38.46%) were susceptible. Only 1 of 10 isolates (10%) were susceptible to aminoglycosides. None (0 out of 6) of the isolates were susceptible to first generation cephalosporins; and solely 1 out of 7 (14.29%) Achromobacter isolates were sensitive to third generation cephalosporins. Although Achromobacter susceptibility to other agents were also reported by most of the patient cases, sensitivity trends were not reported in this figure if data for at least five isolates could not be attained.

While 14 patients ultimately experienced clinical improvement, 4 patients were deceased. Patient responses to each antimicrobial group were assessed. P/T and carbapenem were identified to provide the most reliable coverage in vitro; clinically, 5 out of the 8 patients who received P/T or a carbapenem, or both, eventually experienced clinical improvement. Of the three patients who did not, patient in case nine was administered P/T but patient was deceased very shortly after presentation. Patient likely presented with high disease severity; thus, overall outcome may not reflect utility of the treatment. Likewise, patient in case thirteen was initiated on amikacin upon presentation, which was continued for seven days without confirmed susceptibility; the case report identified susceptible agents, which did not include any aminoglycosides. Following seven days of likely inadequate treatment, therapy was escalated to imipenem and P/T dual-therapy, which was narrowed to imipenem. Despite the eventual initiation of antimicrobials with verified susceptibility, patient failed to respond to therapy despite over 30 days of carbapenem therapy. Such response may have been due to delayed removal of peritoneal dialysis catheter as well as delayed initiation of adequate antimicrobial coverage. Finally, patient described in this case report was initiated on P/T and vancomycin; empirically, therapy was altered to cefepime, metronidazole and vancomycin for four days to prevent acute kidney injury. Unfortunately, the ascitic fluid culture resulted cefepime-resistant but P/T sensitive Achromobacter spp. Despite definitive treatment with P/T for five days and meropenem for four additional days, no recovery was observed. Such outcome may have resulted due to interruption of appropriate treatment as well as retention of PEG-tube despite multiple positive ascitic fluid cultures. No trend in antibiotic selection was observed among nine additional patients with clinical recovery who received agents other than carbapenems and P/T. While the International Society for Peritoneal Dialysis (ISPD) guideline suggests structurally similar Pseudomonas associated peritonitis treatment with dual antibiotic regimen, the guideline makes no specific recommendations for Achromobacter treatment [43]. Per in vitro and in vivo data collected in this article and through numerous studies, P/T and carbapenems yield the most preferable clinical outcomes in Achromobacter peritonitis [2, 24, 25, 34].

PD catheter was removed in 9 out of 14 non-SBP patients with clinical cure. All patients with resolved infection received at least seven days of antimicrobial treatment. Five patients received seven to ten days; four patients received fourteen days; two patients received twenty-one days, and one patient received over 30 days of antibiotics. Glucose containing peritoneal dialysate and aqueous environment foster Achromobacter proliferation and associated infection. Moreover, Achromobacter colonies may have the ability to surround the PD catheter with biofilm [14, 52, 61, 62]. Bacteria in biofilms in vivo are significantly less susceptible to antimicrobials identified to have adequate coverage through laboratory testing in vitro [43]. This fact may further clarify the treatment failures, relapses, and patient deaths resulting in patients who received P/T or carbapenems in these case reports. In addition to appropriate antimicrobial therapy, case seventeen also highlights the importance of timely removal of peritoneal dialysis catheter. Donderski et al. [52] report multiple peritonitis relapse associated readmissions; fortunately, no further episodes were reported following PD catheter removal and a course of adequate antimicrobial regimen. Thus, multiple case studies highlight the importance of timely removal of Achromobacter infected PD catheters; Donderski et al. [52] identify catheter removal as the most preferred treatment method. ISPD Peritonitis Recommendations: 2016 Update on Prevention and Treatment identifies peritonitis as a common and serious complication of PD [43]. Severe or prolonged peritonitis can induce functional and structural deformations resulting in membrane failure. Gram-negative peritonitis presents higher risks of catheter loss and death compared to Gram-positive infections [63–67]. ISPD guideline recommends removal of PD catheter in cases of recurrent, relapsed, and refractory (lack of clearance of ascitic fluid despite 5 days of appropriate antimicrobial treatment) peritonitis in order to protect the peritoneal membrane [43]. Timely catheter removal is essential in recurrent episodes. Nonetheless, PD catheter or PEG-tube removal within ten days to four weeks of insertion may not allow respective insertion tracts to mature causing further leakage and complications [44, 68–70].

Additionally, ISPD suggests at least 3 weeks of treatment in nonpseudomonas Gram-negative, and polymicrobial PD peritonitis [43]. No current guidelines provide significant direction on treatment of PEG tube peritonitis regardless of microbial etiology. Nevertheless, clinical practice guidelines for antimicrobial prophylaxis in surgery strongly recommends prophylactic antibiotic use to significantly reduce the risk of peristomal wound infection associated with PEG-tube insertion [71]. ASPEN guidelines recommend gastropexy using temporary sutures or T-fasteners to secure the stomach to the abdominal wall [72]. These techniques allow for appropriate attachment of tube, minimizing potential for peritoneal leakage, and reducing difficulty and challenges associated with tube replacement, if indicated [72]. Upon development of peritonitis, tube feeds should be held with initiation of broad-spectrum antibiotics. Evidence of perforation should be assessed via abdominal imaging; potential for wound should be evaluated. Surgical consult to perform laparotomy should be obtained. As misplaced tube may cause peritonitis and death, test must be performed to detect misplacement of tube at exchange. In instances of early inadvertent gastrostomy tube removal, parenteral broad-spectrum antibiotics and monitoring for peritonitis signs are indicated [72]. Although recommendations for total duration of antibiotics for treatment of PEG-tube peritonitis could not be encountered in current literature, in case of suspected peritonitis, clinical knowledge extrapolated from similar gastrointestinal perforations suggests that antibiotics may be discontinued after seven days if peritonitis is not observed [70]. Longer duration of treatment may be required in cases of confirmed PEG-tube peritonitis, particularly in cases without adequate source control [70]. Due to the lack of data to guide treatment of PEG tube-associated Achromobacter peritonitis, we attempted to draw similarities between Achromobacter peritonitis due to PEG-tube and PD. Nonetheless, the authors acknowledge that one of the major differences between the two insertions is the accessibility of the peritoneal cavity; while PD catheter readily allows for diagnosis as well as intraperitoneal treatment of peritonitis, PEG tubes should ideally not provide direct access to the peritoneal cavity.

Multiple risk factors for PEG-tube related complications could be identified in the patient presented in our case study. Undiagnosed advanced liver disease, severe ascites, hypoalbuminemia, prolonged hospitalization, and immunocompromise secondary to liver cirrhosis, all place the patient is at high risk for PEG-tube related complications. Polymicrobial nature of the patient’s peritonitis also portends adverse outcomes; likewise, patient’s ultimate demise indicates the severity of the disease.

4. Conclusion

Achromobacter spp. peritonitis as a complication of PEG-tube placement has not been previously reported. In our patients’ case, the recently placed PEG-tube with ascitic fluid leakage was identified as the most plausible infection source. Although a rare bacterial peritonitis pathogen, Achromobacter spp. may be associated with wide antimicrobial resistance and unfavorable outcomes. Thus, clinicians should consider broad empirical antimicrobial regimen, with Achromobacter coverage, such as P/T or a carbapenem, if any concern for Achromobacter spp. secondary peritonitis associated with PEG placement exists, as they may not always represent clinical sample contamination. While the management of secondary peritonitis involving biliary stent and PEG-tube would generally include surgical intervention for infection source control with broad spectrum antibiotics targeting nosocomial coverage per Infectious Disease Society of America, some of antimicrobial selections (such as cefepime and metronidazole combination) may yet be inadequate for widely resistant Achromobacter species. Recognizably, the common antibiotics for spontaneous bacterial peritonitis, i.e., third generation cephalosporins and fluoroquinolones, to which Achromobacter is resistant and variably susceptible, respectively, would be extensively insufficient. Moreover, repeat ascitic fluid culture may be beneficial in verifying continued susceptibility of selected definitive antibiotics. In addition, as these pathogens are generally identified in polymicrobial infections, their presence may serve as a surrogate marker of unfavorable outcomes. Due to the high disease severity, delay or interruption in efficacious therapy may lead to increased mortality rates.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Authors’ Contributions

Nishant Tripathi and Niki Koirala developed the concept and design of the literature review; Hirotaka Kato and Nishant Tripathi developed the concept of case report; Nishant Tripathi, Niki Koirala, Hirotaka Kato, Tushi Singh, Kishore Karri, and Kshitij Thakur performed acquisition of clinical information regarding the patient case. Nishant Tripathi and Niki Koirala each independently conducted PubMed searches to gather relevant articles for the literature review. Nishant Tripathi and Niki Koirala acquired relevant data from the gathered articles, analyzed, and interpreted the data. Nishant Tripathi, Niki Koirala, and Hirotaka Kato drafted the manuscript. All authors revised the manuscript critically, approved the final draft of the manuscript to be published, and agree to be accountable for all aspects of the work.

References

E. Yabuuchi and A. Oyama, “Achromobacter xylosoxidans n. sp. from human ear discharge,” Japanese Journal of Microbiology, vol. 15, no. 5, pp. 477–481, 1971.
View at: Publisher Site | Google Scholar
V. Waters, “New treatments for emerging cystic fibrosis pathogens other than Pseudomonas,” Current Pharmaceutical Design, vol. 18, no. 5, pp. 696–725, 2012.
View at: Publisher Site | Google Scholar
L. Amoureux, J. Bador, S. Fardeheb et al., “Detection of Achromobacter xylosoxidans in hospital, domestic, and outdoor environmental samples and comparison with human clinical isolates,” Applied Environmental Microbiology, vol. 79, no. 23, pp. 7142–7149, 2013.
View at: Publisher Site | Google Scholar
A. Lambiase, M. R. Catania, M. Del Pezzo et al., “Achromobacter xylosoxidans respiratory tract infection in cystic fibrosis patients,” European Journal of Clinical Microbiology & Infectious Diseases, vol. 30, no. 8, pp. 973–980, 2011.
View at: Publisher Site | Google Scholar
M. E. Reverdy, J. Freney, J. Fleurette et al., “Nosocomial colonization and infection by Achromobacter xylosoxidans,” Journal of Clinical Microbiology, vol. 19, no. 2, pp. 140–143, 1984.
View at: Google Scholar
J. Gómez-Cerezo, I. Suárez, J. J. Ríos et al., “Achromobacter xylosoxidans bacteremia: a 10-year analysis of 54 cases,” European Journal of Clinical Microbiology and Infectious Diseases, vol. 22, no. 6, pp. 360–363, 2003.
View at: Google Scholar
J. Molina-Cabrillana, C. Santana-Reyes, A. González-García, A. Bordes-Benítez, and I. Horcajada, “Outbreak of Achromobacter xylosoxidans pseudobacteremia in a neonatal care unit related to contaminated chlorhexidine solution,” European Journal of Clinical Microbiology & Infectious Diseases, vol. 26, no. 6, pp. 435–437, 2007.
View at: Publisher Site | Google Scholar
Y. Igra-Siegman, H. Chmel, and C. Cobbs, “Clinical and laboratory characteristics of Achromobacter xylosoxidans infection,” Journal of Clinical Microbiology, vol. 11, no. 2, pp. 141–145, 1980.
View at: Google Scholar
S. O. Teng, T. Y. Ou, Y. C. Hsieh, W. C. Lee, Y. C. Lin, and W. S. Lee, “Complicated intra-abdominal infection caused by extended drug-resistant Achromobacter xylosoxidans,” Journal of Microbiology, Immunology and Infection, vol. 42, no. 2, pp. 176–180, 2009.
View at: Google Scholar
F. Bellissimo, M. R. Pinzone, S. Tosto, G. Nunnari, and B. Cacopardo, “Achromobacter xylosoxidans meningitis in an immunosuppressed patient,” An International Journal of Medicine, vol. 107, no. 1, pp. 65-66, 2014.
View at: Publisher Site | Google Scholar
K. Marion-Sanchez, K. Pailla, C. Olive, X. Le Coutour, and C. Derancourt, “Achromobacter spp. healthcare associated infections in the French West Indies: a longitudinal study from 2006 to 2016,” BMC Infectious Diseases, vol. 19, no. 1, p. 795, 2019.
View at: Publisher Site | Google Scholar
C. Palmero Palmero, A. Giráldez Gallego, S. García Morillo, and M. L. Miranda Guisado, “Spontaneous bacterial peritonitis caused by Alcaligenes xylosoxidans,” Medicina Clinica, vol. 115, no. 1, pp. 36-37, 2000.
View at: Google Scholar
J. Castellote, G. Tremosa, S. L. Ben, and S. Vazguez, “Spontaneous bacterial peritonitis due to Alcaligenes xylosoxidans,” The American Journal of Gastroenterology, vol. 96, no. 5, pp. 1650–651, 2001.
View at: Publisher Site | Google Scholar
J. L. Tsai and S. F. Tsai, “Case report: the first case of Achromobacter xylosoxidans-related tunnel infection in a patient receiving peritoneal dialysis,” Medicine (Baltimore), vol. 96, no. 16, p. e6654, 2017.
View at: Publisher Site | Google Scholar
J. I. Arshad, A. Saud, D. E. White, N. A. Afshari, and R. R. Sayegh, “Chronic conjunctivitis from a retained contact lens,” Eye Contact Lens, 2019.
View at: Publisher Site | Google Scholar
T. Shinha and I. C. Oguagha, “Osteomyelitis caused by Achromobacter xylosoxidans,” IDCases, vol. 2, no. 1, pp. 11-12, 2015.
View at: Publisher Site | Google Scholar
P. Taylor and L. Fischbein, “Prosthetic knee infection due to Achromobacter xylosoxidans,” The Journal of Rheumatology, vol. 19, no. 6, pp. 992-993, 1992.
View at: Google Scholar
V. Gupta, S. Nirkhiwale, P. Gupta, and S. Phatak, “Achromobacter xylosoxidans mesh related infection: a case of delayed diagnosis and management,” Journal of Infection, vol. 64, no. 3, pp. 1–5, 2012.
View at: Publisher Site | Google Scholar
V. K. Eshwara, C. Mukhopadhyay, S. Mohan, R. Prakash, and G. Pai, “Two unique presentations of Achromobacter xylosoxidans infections in clinical settings,” The Journal of Infection in Developing Countries, vol. 5, no. 2, pp. 138–141, 2011.
View at: Publisher Site | Google Scholar
M. S. Ahmed, C. Nistal, R. Jayan, M. Kuduvalli, and H. K. Anijeet, “Achromobacter xylosoxidans, an emerging pathogen in catheter-related infection in dialysis population causing prosthetic valve endocarditis: a case report and review of literature,” Clinical Nephrology, vol. 71, no. 3, pp. 350–354, 2009.
View at: Publisher Site | Google Scholar
G. Aisenberg, K. V. Rolston, and A. Safdar, “Bacteremia caused by Achromobacter and Alcaligenes species in 46 patients with cancer (1989–2003),” Cancer, vol. 101, no. 9, pp. 2134–2140, 2004.
View at: Publisher Site | Google Scholar
L. Amoureux, J. Bador, E. Siebor, N. Taillefumier, A. Fanton, and C. Neuwirth, “Epidemiology and resistance of Achromobacter xylosoxidans from cystic fibrosis patients in Dijon, Burgundy: first French data,” Journal of Cystic Fibrosis, vol. 12, no. 2, pp. 170–176, 2013.
View at: Publisher Site | Google Scholar
R. Manfredi, A. Nanetti, M. Ferri, and F. Chiodo, “Bacteremia and respiratory involvement by Alcaligenes xylosoxidans in patients infected with the human immunodeficiency virus,” European Journal of Clinical Microbiology and Infectious Diseases, vol. 16, no. 12, pp. 933–938, 1997.
View at: Publisher Site | Google Scholar
S. L. Claassen, J. M. Reese, V. Mysliwiec, and S. D. Mahlen, “Achromobacter xylosoxidans infection presenting as a pulmonary nodule mimicking cancer,” Journal of Clinical Microbiology, vol. 49, no. 7, pp. 2751–2754, 2011.
View at: Publisher Site | Google Scholar
I. J. Abbott and A. Y. Peleg, “Stenotrophomonas Achromobacter, and nonmelioid Burkholderia species: antimicrobial resistance and therapeutic strategies,” Seminars in Respiratory and Critical Care Medicine, vol. 36, no. 1, pp. 99–110, 2015.
View at: Publisher Site | Google Scholar
T. Spilker, P. Vandamme, and J. J. Lipuma, “Identification and distribution of Achromobacter species in cystic fibrosis,” Journal of Cystic Fibrosis, vol. 12, no. 3, pp. 298–301, 2013.
View at: Publisher Site | Google Scholar
T. Spilker, P. Vandamme, and J. J. LiPuma, “A multilocus sequence typing scheme impliespopulation structure and reveals several putative novel Achromobacter species,” Journal of Clinical Microbiology, vol. 50, pp. 3010–3015, 2012.
View at: Publisher Site | Google Scholar
P. A. Vandamme, C. Peeters, E. Inganäs et al., “Taxonomic dissection of Achromobacter denitrificans Coenye et al. 2003 and proposal of Achromobacter agilis sp. nov., nom. rev., Achromobacter pestifer sp. nov., nom. rev., Achromobacter kerstersii sp. nov. and Achromobacter deleyi sp. nov,” International Journal of Systematic and Evolutionary Microbiology, vol. 66, no. 9, pp. 3708–3717, 2016.
View at: Publisher Site | Google Scholar
L. Amoureux, J. Bador, T. Verrier, H. Mjahed, C. De Curraize, and C. Neuwirth, “Achromobacter xylosoxidans is the predominant Achromobacter species isolated from diverse non-respiratory samples,” Epidemiology Infection, vol. 144, no. 16, pp. 3527–3530, 2016.
View at: Publisher Site | Google Scholar
P. Vandamme, E. R. B. Moore, M. Cnockaert et al., “Achromobacter animicus sp. nov., Achromobacter mucicolens sp. nov., Achromobacter pulmonis sp. nov. and Achromobacter spiritinus sp. nov., from human clinical samples,” Systematic and Applied Microbiology, vol. 36, pp. 1–10, 2013.
View at: Publisher Site | Google Scholar
P. Vandamme, E. R. B. Moore, M. Cnockaert et al., “Classification of Achromobacter genogroups 2, 5, 7 and 14 as Achromobacter insuavis sp.nov., Achromobacter aegrifaciens sp. nov., Achromobacter anxifer sp. nov. and Achromobacter dolens sp. nov., respectively,” Systematic and Applied Microbiology, vol. 36, pp. 474–482, 2013.
View at: Publisher Site | Google Scholar
M. Almuzara, A. Limansky, V. Ballerini, L. Galanternik, A. Famiglietti, and C. Vay, “In vitro susceptibility of Achromobacter spp. isolates: comparison of disk diffusion, Etest and agar dilution methods,” International Journal of Antimicrobial Agents, vol. 35, no. 1, pp. 68–71, 2010.
View at: Publisher Site | Google Scholar
J. Bador, L. Amoureux, J. M. Duez et al., “First description of an RND-type multidrug efflux pump in Achromobacter xylosoxidans, AxyABM,” Antimicrobial Agents and Chemotherapy, vol. 55, no. 10, pp. 4912–4914, 2011.
View at: Publisher Site | Google Scholar
J. Bador, L. Amoureux, E. Blanc, and C. Neuwirth, “Innate aminoglycoside resistance of Achromobacter xylosoxidans is due to AxyXY-OprZ, an RND-type multidrug efflux pump,” Antimicrobial Agents and Chemotherapy, vol. 57, no. 1, pp. 603–605, 2013.
View at: Publisher Site | Google Scholar
J. Bador, C. Neuwirth, P. Liszczynski et al., “Distribution of innate efflux-mediated aminoglycoside resistance among different Achromobacter species,” New Microbes New Infections, vol. 12, no. 10, pp. 1–5, 2015.
View at: Publisher Site | Google Scholar
S. Iyobe, H. Kusadokoro, A. Takahashi et al., “Detection of a variant metallo-beta-lactamase, IMP-10, from two unrelated strains of Pseudomonas aeruginosa and an Alcaligenes xylosoxidans strain,” Antimicrobial Agents and Chemotherapy, vol. 46, no. 6, pp. 2014–2016, 2002.
View at: Publisher Site | Google Scholar
M. L. Riccio, L. Pallecchi, R. Fontana, and G. M. Rossolini, “In70 of plasmid pAX22, a bla(VIM-1)-containing integron carrying a new aminoglycoside phosphotransferase gene cassette,” Antimicrobial Agents and Chemotherapy, vol. 45, no. 4, pp. 1249–1253, 2001.
View at: Publisher Site | Google Scholar
K. S. Shin, K. Han, J. Lee et al., “Imipenem-resistant Achromobacter xylosoxidans carrying blaVIM-2-containing class 1 integron,” Diagnostic Microbiology and Infectious Disease, vol. 53, no. 3, pp. 215–220, 2005.
View at: Publisher Site | Google Scholar
C. Neuwirth, C. Freby, A. Ogier-Desserrey et al., “VEB-1 in Achromobacter xylosoxidans from cystic fibrosis patient France,” Emerging Infectious Diseases, vol. 12, no. 11, pp. 1737–1739, 2006.
View at: Publisher Site | Google Scholar
A. El Salabi, P. S. Borra, M. A. Toleman, Ø. Samuelsen, and T. R. Walsh, “Genetic and biochemical characterization of a novel metallo-β-lactamase, TMB-1, from an Achromobacter xylosoxidans strain isolated in Tripoli, Libya,” Antimicrobial Agents and Chemotherapy, vol. 56, no. 5, pp. 2241–2245, 2012.
View at: Publisher Site | Google Scholar
R. D. Shah, N. Tariq, C. Shanley, J. Robbins, and R. Janczyk, “Peritonitis from peg tube insertion in surgical intensive care unit patients: identification of risk factors and clinical outcomes,” Surgical Endoscopy, vol. 23, no. 11, pp. 2580–2586, 2009.
View at: Publisher Site | Google Scholar
W. Luman, K. R. Kwek, K. L. Loi, M. A. Chiam, W. K. Cheung, and H. S. Ng, “Percutaneous endoscopic gastrostomy–indications and outcome of our experience at the Singapore general hospital,” Singapore Medical Journal, vol. 42, no. 10, pp. 460–465, 2001.
View at: Google Scholar
P. K. Li, C. C. Szeto, B. Piraino et al., “ISPD peritonitis recommendations: 2016 update on prevention and treatment,” Peritoneal Dialysis International, vol. 36, no. 5, pp. 481–508, 2016.
View at: Publisher Site | Google Scholar
C. Löser, G. Aschl, X. Hébuterne et al., “ESPEN guidelines on artificial enteral nutrition–percutaneous endoscopic gastrostomy (PEG),” Clinical Nutrition, vol. 24, no. 5, pp. 848–861, 2005.
View at: Publisher Site | Google Scholar
S. Krishna, S. Singh, K. R. Dinesh, R. Kp, I. Siyad, and S. Karim, “Percutaneous endoscopic gastrostomy (PEG) site infections: a clinical and microbiological study from university teaching hospital, India,” Journal of Infection Prevention, vol. 16, no. 3, pp. 113–116, 2015.
View at: Publisher Site | Google Scholar
K. A. Chaudhary, O. J. Smith, P. G. Cuddy, and W. K. Clarkston, “PEG site infections: the emergence of methicillin resistant Staphylococcus aureus as a major pathogen,” The American Journal of Gastroenterology, vol. 97, no. 7, pp. 1713–1716, 2002.
View at: Publisher Site | Google Scholar
G. G. Rao, M. Osman, L. Johnson, D. Ramsey, S. Jones, and H. Fidler, “Prevention of percutaneous endoscopic gastrostomy site infections caused by methicillin-resistant Staphylococcus aureus,” Journal of Hospital Infection, vol. 58, no. 1, pp. 81–83, 2004.
View at: Publisher Site | Google Scholar
G. Abuksis, M. Mor, N. Segal et al., “Percutaneous endoscopic gastrostomy: high mortality rates in hospitalized patients,” The American Journal of Gastroenterology, vol. 95, no. 1, pp. 128–132, 2000.
View at: Publisher Site | Google Scholar
M. Melgosa, O. Espinazo, A. Alonso, Perea A. García, and M. Navarro, “Dialysis-associated Alcaligenes xylosoxidans peritonitis: a pediatric case,” Peritoneal Dialysis International, vol. 24, no. 1, pp. 72–75, 2004.
View at: Google Scholar
G. Koçak, A. Azak, B. Huddam, S. Yanik, and M. Duranay, “Continuous ambulatory peritoneal dialysis-related peritonitis in an uremic outpatient: Achromobacter xylosoxidans,” Blood Purification, vol. 34, no. 1, pp. 1-2, 2012.
View at: Publisher Site | Google Scholar
E. Cankaya, M. Keles, E. Gulcan, A. Uyanik, and H. Uyanik, “A rare cause of peritoneal dialysis-related peritonitis: Achromobacter denitrificans,” Peritoneal Dialysis International, vol. 34, no. 1, pp. 135–137, 2014.
View at: Publisher Site | Google Scholar
R. Donderski, M. Grajewska, A. Mikucka, B. Sulikowska, E. Gospodarek-Komkowska, and J. Manitius, “Achromobacter xylosoxidans relapsing peritonitis and Streptococcus suis peritonitis in peritoneal dialysis patients: a report of two cases,” Case Reports in Nephrology, vol. 2018, Article ID 9454520, 5 pages, 2018.
View at: Publisher Site | Google Scholar
A. J. Morrison Jr and K. Boyce, “4th Peritonitis caused by Alcaligenes denitrificans subsp. xylosoxydans: case report and review of the literature,” Journal of Clinical Microbiology, vol. 24, no. 5, pp. 879–881, 1986.
View at: Google Scholar
S. S. Haqqie, M. Roth, and G. R. Bailie, “Unsuccessful treatment of CAPD peritonitis caused by Alcaligenes xylosoxidans subsp. denitrificans,” Renal Failure, vol. 17, no. 5, pp. 611–614, 1995.
View at: Publisher Site | Google Scholar
M. A. El-Shahawy, D. Kim, and M. F. Gadallah, “Peritoneal dialysis-associated peritonitis caused by Alcaligenes xylosoxidans,” American Journal of Nephrology, vol. 18, no. 5, pp. 452–455, 1998.
View at: Publisher Site | Google Scholar
S. Tang, C. C. Cheng, K. C. Tse et al., “CAPD-associated peritonitis caused by Alcaligenes xylosoxidans sp. xylosoxidans,” American Journal of Nephrology, vol. 21, no. 6, pp. 502–506, 2001.
View at: Publisher Site | Google Scholar
S. G. Ledger and P. Cordy, “Successful treatment of Alcaligenes xylosoxidans in automated peritoneal dialysis-related peritonitis,” Peritoneal Dialysis International, vol. 27, no. 5, pp. 596–598, 2007.
View at: Google Scholar
S. F. Tsai and K. H. Shu, “CAPD peritonitis caused by Alcaligenes xylosoxidans in a diabetic cirrhosis patient,” Renal Failure, vol. 32, no. 7, pp. 899–901, 2010.
View at: Publisher Site | Google Scholar
T. G. Oh, J. H. Baek, S. J. Jeong et al., “Continuous ambulatory peritoneal dialysis-associated peritonitis caused by Achromobacter xylosoxidans: a case report and comprehensive literature review,” Infection Chemotherapy, vol. 43, no. 3, pp. 275–278, 2011.
View at: Publisher Site | Google Scholar
M. T. Tsai, W. C. Yang, and C. C. Lin, “Continuous ambulatory peritoneal dialysis-related exit-site infections caused by Achromobacter denitrificans and A. xylosoxidans,” Peritoneal Dialysis International, vol. 32, no. 3, pp. 362-363, 2012.
View at: Publisher Site | Google Scholar
R. H. Pereira, R. S. Leão, A. P. Carvalho-Assef et al., “Patterns of virulence factor expression and antimicrobial resistance in Achromobacter xylosoxidans and Achromobacter ruhlandii isolates from patients with cystic fibrosis,” Epidemiology Infection, vol. 145, no. 3, pp. 600–606, 2017.
View at: Publisher Site | Google Scholar
S. K. Tom, Y. C. Yau, T. Beaudoin, J. J. LiPuma, and V. Waters, “Effect of high-dose antimicrobials on biofilm growth of Achromobacter species isolated from cystic fibrosis patients,” Antimicrobial Agents and Chemotherapy, vol. 60, no. 1, pp. 650–652, 2015.
View at: Publisher Site | Google Scholar
E. M. Jarvis, C. M. Hawley, S. P. McDonald et al., “Predictors, treatment, and outcomes of nonPseudomonas Gram-negative peritonitis,” Kidney International, vol. 78, no. 4, pp. 408–414.
View at: Publisher Site | Google Scholar
J. Valdés-Sotomayor, A. Cirugeda, M. A. Bajo et al., “Increased severity of Escherichia coli peritonitis in peritoneal dialysis patients independent of changes in in vitro antimicrobial susceptibility testing,” Peritoneal Dialysis International, vol. 23, no. 5, pp. 450–455, 2003.
View at: Google Scholar
N. Prasad, A. Gupta, R. K. Sharma, K. N. Prasad, S. Gulati, and A. P. Sharma, “Outcome of Gram-positive and Gram-negative peritonitis in patients on continuous ambulatory peritoneal dialysis: a single-center experience,” Peritoneal Dialysis International, vol. 23, no. 2, pp. 144–147, 2003.
View at: Google Scholar
C. C. Szeto, V. C. Chow, K. M. Chow et al., “Enterobacteriaceae peritonitis complicating peritoneal dialysis: a review of 210 consecutive cases,” Kidney International, vol. 69, no. 7, pp. 1245–1252, 2006.
View at: Publisher Site | Google Scholar
A. Zurowska, R. Feneberg, B. A. Warady et al., “Gram-negative peritonitis in children undergoing long-term peritoneal dialysis,” American Journal of Kidney Diseases, vol. 51, no. 3, pp. 455–462, 2008.
View at: Publisher Site | Google Scholar
S. A. Galat, K. D. Gerig, J. A. Porter, and F. A. Slezak, “Management of premature removal of the percutaneous gastrostomy,” The American Surgeon, vol. 56, no. 11, pp. 733–736, 1990.
View at: Google Scholar
Y. Al-Abboodi, A. Ridha, M. Fasullo, and T. H. Naguib, “Risks of PEG tube placement in patients with cirrhosis-associated ascites,” Clinical and Experimental Gastroenterology, vol. 10, pp. 211–214, 2017.
View at: Publisher Site | Google Scholar
M. R. Taheri, H. Singh, and D. R. Duerksen, “Peritonitis after gastrostomy tube replacement: a case series and review of literature,” Journal of Parenteral and Enteral Nutrition, vol. 35, no. 1, pp. 56–60, 2011.
View at: Publisher Site | Google Scholar
M. C. Allison, J. A. Sandoe, R. Tighe, I. A. Simpson, R. J. Hall, and T. S. Elliott, “Antibiotic prophylaxis in gastrointestinal endoscopy,” Gut, vol. 58, no. 6, pp. 869–880, 2009.
View at: Publisher Site | Google Scholar
J. I. Boullata, A. L. Carrera, L. Harvey et al., “ASPEN Safe practices for enteral nutrition therapy,” Journal of Parenteral and Enteral Nutrition, vol. 41, no. 1, pp. 15–103, 2017.
View at: Publisher Site | Google Scholar

Copyright

Copyright © 2020 Nishant Tripathi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PDF Download Citation

Download other formats

Order printed copies

Views

791

Downloads

1420

Citations