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Acinetobacter
Introduction
Acinetobacter is a gram-negative, aerobic, non-fermentative, oxidase-negative, and nonmotile organism.[1] Acinetobacter has several species, but A. baumannii has the greatest clinical significance.[2] Acinetobacter can be found in soil and water. Patients are frequently cultured from urine, saliva, respiratory secretions, and open wounds. The organism is also known to colonize intravenous fluids and other irrigation solutions.[3][4]
In general, Acinetobacter has low virulence but is capable of causing infection in immunocompromised and neutropenic patients. Most of the infections are a result of nosocomial spread and colonization rather than de novo infections. Thus, great care is required when Acinetobacter is isolated - whether it is an actual infection or colonization. Risk factors for Acinetobacter infection include:
- Prolonged stay in the intensive care unit
- Prolonged antibiotic exposure
- Mechanical ventilation
- Use of a central venous catheter
- Hemodialysis[5][6][7]
Most Acinetobacter infections are group outbreaks, and isolated cases are rare. Infections may complicate intravenous (IV) catheter treatment, mechanical ventilation, and even peritoneal dialysis. In most cases, the presence of Acinetobacter in the respiratory secretions of ventilated patients represents colonization.
Etiology
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Etiology
Even though Acinetobacter is mostly a nosocomial pathogen and is isolated from hospitalized patients, care should be exercised in determining if the isolate is a cause or simply a result of colonization. Acinetobacter is a water-loving organism and has the propensity to colonize body organs that contain fluid. Thus, in hospitalized patients, Acinetobacter is often found in the peritoneal fluid, cerebrospinal fluid (CSF), saliva, respiratory secretions and urinary tract.[8][9]
Epidemiology
Acinetobacter gained clinical significance in the 1960s with the increasing growth of Intensive care units at hospitals.[10] Though Acinetobacter is an organism of low virulence, its ability to survive desiccation and persist in the environment for an extended duration of time makes it easily transmissible in the healthcare setting. Nosocomial spread by healthcare personnel, respiratory equipment like ventilators, and other devices has been reported frequently. It can be found in all types of secretions, such as wounds, saliva, urine, and blood. The organism has low virulence but is still capable of causing infections in patients with febrile neutropenia and those who have received organ transplants.[11]
Acinetobacter has also been recognized in wounds sustained by combat injuries in returning soldiers from Iraq and Afghanistan.
Mortality/Morbidity
The morbidity of this organism is related to the patient's underlying medical condition and immune status. The organism is not very virulent, but due to various innate mechanisms, it has the capacity to acquire resistance. Multidrug-resistant, extensively drug-resistant, and pan-drug-resistant isolates of Acinetobacter have been described as non-susceptible to at least one agent in three or more antibiotic classes, non-susceptible to at least one agent in all but two or fewer antibiotic classes and non-susceptible to all antibiotic classes. Multi-drug resistant Acinetobacter was designated a threat category of ‘Serious’ in the Centers for Disease Control antimicrobial resistance report published in 2013. Though not virulent by itself, the morbidity and mortality of Acinetobacter are high in sick patients with multiorgan disease. In the case of infections being caused by resistant strains of A.baumanii, mortality rates of up to 70% have been reported. [10]
Pathophysiology
Various mechanisms contribute to the pathogenesis and virulence of Acinetobacter. Acinetobacter elaborate on lipopolysaccharide (LPS) or lipooligosaccharide (LOS) in their outer membranes.[12] Modification in the synthesis of these structures imparts antibiotic resistance and increased resistance desiccation.[13] Acinetobacter species also have Capsules that protect them from complement-mediated killing.[14] Pili on the surface of Acinetobacter contribute to its twitching motility, biofilm formation, and adherence to environmental surfaces.[13] Acinetobacter also secretes various proteins that lead to antibiotic resistance by efflux or degradation.[15]
Histopathology
The infection caused by Acinetobacter is similar in histopathology to any other gram-negative bacilli. Gross or microscopic observation does not provide any clue to the organism, and culture is required to confirm the diagnosis.[16]
History and Physical
Prolonged hospitalization or antibiotic therapy predisposes to Acinetobacter colonization, and because colonization is the rule and infection is the exception, colonized patients have no physical findings.
Most patients are in the hospital when infected with Acinetobacter. The one organ most commonly involved is the lung, primarily because of the colonization of the airways and respiratory equipment used for mechanical ventilation.
Pneumonia, wound infection, catheter-associated bacteremia, or nosocomial meningitis have all been described by Acinetobacter.[17]
There are no pathognomic findings in Acinetobacter infections, and they need to be differentiated from other gram-negative infections like Enterobacter, Burkholderia, Pseudomonas, and Serratia. Since Acinetobacter is chiefly a colonizing organism, the physician has the onus to prove that it is causing the pathology in any given clinical scenario.
Evaluation
Acinetobacter is a common colonizer of patients in the intensive care unit and those who have multiple comorbid disorders. It is most likely to cause infections in patients who are immunocompromised and those with a compromise of their cardiopulmonary system. The organism can readily be cultured, but the findings need to be correlated to the clinical picture.
Laboratory Studies
There may be leukocytosis with a left shift.[18] However, the findings are nonspecific and do not always indicate the presence of a bacterial infection. When there is an outbreak of Acinetobacter, the organism is usually readily isolated and cultured from body fluids. More importantly, the outbreak usually involves multiple patients.
Imaging Studies
A chest x-ray is required if pneumonia is suspected. Other imaging tests depend on signs and symptoms.
Procedures
If meningitis is suspected, then CSF needs to be analyzed and cultured.
Histologic Findings
There are no specific histopathological features of an Acinetobacter infection that can differentiate it from any other gram-negative bacilli.
Treatment / Management
Acinetobacter is multidrug resistant. Cephalosporins, macrolides, and penicillins have little or no anti-Acinetobacter activity. Use of these drugs may predispose the Acinobacter infection. When an infection is suspected in the presence of a long-term catheter or a pacemaker, it should be removed.[19]
Any external device, infected line, shunt, or drain must be removed to obtain a cure.[19] If the patient has a collection of an abscess or necrotic tissue, it needs to be debrided thoroughly.
One should avoid treating colonization as it only leads to more antibiotic resistance.
Over the last few years, drug resistance has become a common problem in the United States. Medications that may be effective include meropenem, sulbactam/durlobactam, colistin, polymyxin B, and amikacin. Alternatives include minocycline, rifampin, and tigecycline. Monotherapy is standard, as combination therapy has not been shown to be more effective. The duration of therapy is from 7 to 10 days, depending on the patient's illness.
Differential Diagnosis
- Burkholderia cepacia infection
- Catheter-associated bacteremia
- Enterobacter species
- Flavobacterium meningosepticum
- Nosocomial meningitis
- Pneumonia
- Pseudomonas aeruginosa infection
- Serratia marcescensn infection
- Stenotrophomonas maltophilia infection
- Wound infection
Pearls and Other Issues
Patients in the intensive care unit are the most difficult to treat as colonization is common, and it is difficult to distinguish this from an infection. All patients noted to have colonization with Acinetobacter should be isolated from other patients to prevent further colonization. Once an infection is treated, the patient's clinical course must be followed rather than cultures because colonization may offer a falsely positive diagnosis.
The prognosis of an isolated Acinetobacter infection is excellent in patients who are otherwise healthy. Immunosuppressed patients tend to have poor outcomes.
Enhancing Healthcare Team Outcomes
Over the past decade, Acinetobacter infections have become common in hospitalized patients. Since this organism can infect almost any organ system, an interprofessional approach to diagnosis and management is essential. The organism is often difficult to isolate because of colonization, so an infectious disease consult should be obtained. Infection control teams should be involved earlier on to prevent outbreaks and utilize ways to prevent nosocomial transmission by eradication of bacteria and strict isolation techniques. The outcomes for most patients with Acinetobacter infection are excellent as long as there is no other comorbidity. However, those with immunosuppression may have a guarded prognosis.
Management should involve a coordinated effort of nurses, pharmacists, and clinicians.
References
Wang T, Costa V, Jenkins SG, Hartman BJ, Westblade LF. Acinetobacter radioresistens infection with bacteremia and pneumonia. IDCases. 2019:15():e00495. doi: 10.1016/j.idcr.2019.e00495. Epub 2019 Jan 28 [PubMed PMID: 30906692]
Level 3 (low-level) evidenceAntunes LC, Visca P, Towner KJ. Acinetobacter baumannii: evolution of a global pathogen. Pathogens and disease. 2014 Aug:71(3):292-301. doi: 10.1111/2049-632X.12125. Epub 2014 Jan 27 [PubMed PMID: 24376225]
Eze EC, Chenia HY, El Zowalaty ME. Acinetobacter baumannii biofilms: effects of physicochemical factors, virulence, antibiotic resistance determinants, gene regulation, and future antimicrobial treatments. Infection and drug resistance. 2018:11():2277-2299. doi: 10.2147/IDR.S169894. Epub 2018 Nov 15 [PubMed PMID: 30532562]
Munier AL, Biard L, Legrand M, Rousseau C, Lafaurie M, Donay JL, Flicoteaux R, Mebazaa A, Mimoun M, Molina JM. Incidence, risk factors and outcome of multi-drug resistant Acinetobacter baumannii nosocomial infections during an outbreak in a burn unit. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases. 2019 Feb:79():179-184. doi: 10.1016/j.ijid.2018.11.371. Epub 2018 Dec 6 [PubMed PMID: 30529108]
Maragakis LL, Perl TM. Acinetobacter baumannii: epidemiology, antimicrobial resistance, and treatment options. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2008 Apr 15:46(8):1254-63. doi: 10.1086/529198. Epub [PubMed PMID: 18444865]
Playford EG, Craig JC, Iredell JR. Carbapenem-resistant Acinetobacter baumannii in intensive care unit patients: risk factors for acquisition, infection and their consequences. The Journal of hospital infection. 2007 Mar:65(3):204-11 [PubMed PMID: 17254667]
Level 2 (mid-level) evidenceZhou HY, Yuan Z, Du YP. Prior use of four invasive procedures increases the risk of Acinetobacter baumannii nosocomial bacteremia among patients in intensive care units: a systematic review and meta-analysis. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases. 2014 May:22():25-30. doi: 10.1016/j.ijid.2014.01.018. Epub 2014 Mar 4 [PubMed PMID: 24607429]
Level 1 (high-level) evidenceGarnacho-Montero J, Timsit JF. Managing Acinetobacter baumannii infections. Current opinion in infectious diseases. 2019 Feb:32(1):69-76. doi: 10.1097/QCO.0000000000000518. Epub [PubMed PMID: 30520737]
Level 3 (low-level) evidenceGiacobbe DR, Mikulska M, Viscoli C. Recent advances in the pharmacological management of infections due to multidrug-resistant Gram-negative bacteria. Expert review of clinical pharmacology. 2018 Dec:11(12):1219-1236. doi: 10.1080/17512433.2018.1549487. Epub 2018 Dec 6 [PubMed PMID: 30444147]
Level 3 (low-level) evidenceWong D, Nielsen TB, Bonomo RA, Pantapalangkoor P, Luna B, Spellberg B. Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges. Clinical microbiology reviews. 2017 Jan:30(1):409-447 [PubMed PMID: 27974412]
Level 3 (low-level) evidencede Azevedo FKSF, Dutra V, Nakazato L, Mello CM, Pepato MA, de Sousa ATHI, Takahara DT, Hahn RC, Souto FJD. Molecular epidemiology of multidrug-resistant Acinetobacter baumannii infection in two hospitals in Central Brazil: the role of ST730 and ST162 in clinical outcomes. Journal of medical microbiology. 2019 Jan:68(1):31-40. doi: 10.1099/jmm.0.000853. Epub 2018 Dec 5 [PubMed PMID: 30516469]
Level 2 (mid-level) evidenceLee CR, Lee JH, Park M, Park KS, Bae IK, Kim YB, Cha CJ, Jeong BC, Lee SH. Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options. Frontiers in cellular and infection microbiology. 2017:7():55. doi: 10.3389/fcimb.2017.00055. Epub 2017 Mar 13 [PubMed PMID: 28348979]
Level 1 (high-level) evidenceHarding CM, Hennon SW, Feldman MF. Uncovering the mechanisms of Acinetobacter baumannii virulence. Nature reviews. Microbiology. 2018 Feb:16(2):91-102. doi: 10.1038/nrmicro.2017.148. Epub 2017 Dec 18 [PubMed PMID: 29249812]
Lees-Miller RG, Iwashkiw JA, Scott NE, Seper A, Vinogradov E, Schild S, Feldman MF. A common pathway for O-linked protein-glycosylation and synthesis of capsule in Acinetobacter baumannii. Molecular microbiology. 2013 Sep:89(5):816-30. doi: 10.1111/mmi.12300. Epub 2013 Jul 12 [PubMed PMID: 23782391]
Level 3 (low-level) evidenceWeber BS, Harding CM, Feldman MF. Pathogenic Acinetobacter: from the Cell Surface to Infinity and Beyond. Journal of bacteriology. 2015 Dec 28:198(6):880-7. doi: 10.1128/JB.00906-15. Epub 2015 Dec 28 [PubMed PMID: 26712938]
Lal B, Vijayakumar S, Anandan S, Veeraraghavan B. Specimen Collection, Processing, Culture, and Biochemical Identification of Acinetobacter spp. Methods in molecular biology (Clifton, N.J.). 2019:1946():1-15. doi: 10.1007/978-1-4939-9118-1_1. Epub [PubMed PMID: 30798539]
Sievert DM, Ricks P, Edwards JR, Schneider A, Patel J, Srinivasan A, Kallen A, Limbago B, Fridkin S, National Healthcare Safety Network (NHSN) Team and Participating NHSN Facilities. Antimicrobial-resistant pathogens associated with healthcare-associated infections: summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2009-2010. Infection control and hospital epidemiology. 2013 Jan:34(1):1-14. doi: 10.1086/668770. Epub 2012 Nov 27 [PubMed PMID: 23221186]
Bozorgmehr R, Bahrani V, Fatemi A. Ventilator-Associated Pneumonia and Its Responsible Germs; an Epidemiological Study. Emergency (Tehran, Iran). 2017:5(1):e26 [PubMed PMID: 28286833]
Burnham JP, Rojek RP, Kollef MH. Catheter removal and outcomes of multidrug-resistant central-line-associated bloodstream infection. Medicine. 2018 Oct:97(42):e12782. doi: 10.1097/MD.0000000000012782. Epub [PubMed PMID: 30334966]