Bacteremia due to Acinetobacter ursingii in infants: reports of two cases

Bacteremia due to Acinetobacter ursingii in infants: reports of two cases

Nurhayat Yakut¹, Eda Kadayifci Kepenekli¹, Ayse Karaaslan¹, Serkan Atici¹, Gulsen Akkoc¹, Sevliya Ocal Demir¹, Ahmet Soysal^1,&, Mustafa Bakir¹

 

¹Division of Pediatric Infectious Diseases, Department of Pediatrics, Marmara University School of Medicine, Istanbul, Turkey

 

 

^&Corresponding author
Ahmet Soysal, Division of Pediatric Infectious Diseases, Department of Pediatrics, Marmara University School of Medicine, Istanbul, Turkey

 

 

 

 

Acinetobacter species are the most common causative agents of health care associated infections such as meningitis, ventilator-associated pneumonia, endocarditis and catheter-related bacteremia [1, 2]. Despite their low virulence, they have increasingly been recognized as opportunistic microorganisms particularly in hospitalized and immunocompromised patients. Acinetobacterspecies can be found widely in nature. The organism can be a part of the flora of the skin, the oral cavity and the upper respiratory, genital and gastrointestinal tracts. The skin may become a reservoir for Acinetobacter in hospitalized patients and health care provider [3]. Patients who have undergone a tracheostomy are at particularly high risk for colonization by Acinetobacter. Because they survive on inanimate surfaces for a long-term, these microorganismscan be commonly found in the hospital environment, particularly in moist areas such as in humidifiers and ventilators. Colonized medical equipment such as respiratory equipment and intravenous catheters may be responsible from nosocomial outbreaks [4]. Although A. ursingii, has recently been isolated from a clinical specimen, reports of infection with A. ursingii in children are rare [5]. Herein we report two cases with bacteremia due to A.ursingii in immuno-competent infants who were successfully treated.

 

 

Patient 1

 

A two-month-old boy had been hospitalized in pediatric surgery unit for suspected tracheo-osefageal fistula. He was referred from another hospital with the diagnosis of recurrent aspiration pneumonia unresponsive to antibiotic therapy.On the admission, he had tachypnea and subfebrile fever on physical examination.Laboratory tests showed a white blood cell (WBC) of 10900/µl, C-reactive protein (CRP) of 11.8 mg/L and normal biochemistry values. Peripheral blood culture wasobtained.Twelve hours later, the BacT/Alert device (bioMerièux, Marseille, France) gave a signal indicating a growth of microorganism. Gram staining was positive forgram-negative coccobacilli. The microorganism was nonmotile, strictly aerobic, catalase-positive and oxidase-negative. Empirical antibiotic treatment with meropenem and amikacin was started. The next day, Vitek MS (bioMerièux, Marseille, France) identified the microorganism as Acinetobacterursingii and reliability was 99.9%. The E-test used to describe antimicrobiological susceptibility showed that the microorganism was susceptible to ampicillin-sulbactam, gentamicin,ciprofloxacin and imipenem. The antibiotic therapy was de-escalated to ampicillin-sulbactam. On the third day of the treatment, control peripheral blood culture was taken and remainedsterile.He was successfully treated with ampicillin-sulbactam.

 

Patient 2

 

A fourteen-month-old boy with the diagnosis of gastroesophageal reflux disease was admitted to our hospital with complaints of vomiting and diarrhea for amonth.On admission, his physical examination revealed fever (38.4^°C). Because of the prolonged diarrhea and vomiting, patient was hospitalized and further investigated. Laboratory tests showed a WBC of 5800/µl, CRP of 3.2 mg/L and normal biochemistry values.Peripheral blood culture was obtainedand signaled growth for gram-negative bacilli. Empirical antibiotic treatment with meropenem and amikacin was started. Microorganism was identified as Acinetobacterursingii by Vitek MS (bioMerièux) with a reliability of 99.9%. The e-test showed that A. ursingii was susceptible to ampicilin-sulbactam, gentamicin, ciprofloxacin and imipenem. The antibiotic therapy was deescalated to ampicin-sulbactam. On the third day of the treatment, control peripheral blood culture remained sterile. He was successfully treated with ampicillin-sulbactam.

 

 

Acinetobacterursingii can cause life-threatening bloodstream infection especially in immunocompromised patients, but their correct identification is problematic. Currently, more than 32 genomic species have been identified by molecular methods [6,7]. Virulence, epidemiology, antimicrobial susceptibility, clinical significance of Acinetobacter speciesmay vary. Therefore, determining the prevalence of the Acinetobacter species causing invasive infection may be helpful in the management of infection [8,9]. Risk factors for infection with A.ursingii emerged as noso-comial pathogens during the last 3 decades including underlying serious disease such as cancer, intravascular catheterization, treatment with broad spectrum antibiotics, prolonged hospitalization. Due to their ability for long-term survival in the environment, A.ursingii may spread among patients and cause nosocomial infections and outbreaks. Although A.ursingii have low pathogenic potential, it has increasingly been described as opportunistic pathogen particularly in immuno-supressed and patients in intensive care units [10]. Acinetobacter may cause suppurative infection such as peritonitis, endocarditis, osteomyelitis, arthritis, pancreatic and liver abcesses. Clinical manifestations are similar to other bacterial infections and may vary depending on the serious underlying disease and immune status. A.ursingii related bloodstream infection may occur as primary or secondary to respiratory or urinary tract and wound infection. Immuno-supressed neonates are at particularly high risk for primary bacteremia, and clinical signs may vary ranging from an asymptomatic to septic shock and disseminated intravascular coagulation. Because of increasing antibiotic resistance, treatment of infections due to Acinetobacter spp. has become difficult. Antibiotic treatment should be determined by in vitro susceptibility testing. A. ursingii seems to be more susceptible to antimicrobial agents compared to A.baumannii Infections due to A.ursingii are rare in healthy children. There are a few reports of infection with A.ursingii in the literature; most of the cases are immunocompromised with underlying serious disease. Report of a bacteremia caused by A.ursingii in an adult patient with oro-pharyngeal cancer was reported [11].

 

 

Although A. ursingii, has recently been isolated from a clinical specimen, reports of infection with A. ursingii in children are rare. Our patients had neither of central venous catheter, immunocompromised status, severe underlying co-morbidities and prolonged hospitalization. Source of A.ursingii may either be the hospital or colonization prior to admission. As a conclusion, although rare, A.ursingii should be kept in mind as an opportunistic microorganism in children.

 

 

The authors declare no competing interests.

 

 

All authors interested in management, treatment and outcome the patient. All authors have been involved in drafting the manuscript or revising critically for important intellectual content. All authors read and approved the final manuscript.

 

 

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