Acinetobacter co-infection and coagulase-negative Staphylococcus: case report and literature review

Abstract

Continuous ambulatory peritoneal dialysis (CAPD) is a safe, convenient, and cost-effective therapy in end-stage renal disease. The major complication of peritoneal dialysis (PD) is peritonitis. Gram-positive cocci are isolated in majority of the episodes. Among gram-negative bacteria, Acinetobacter species have been reported in peritonitis, sometimes as a concomitant that may be asymptomatic and require no treatment. Little has been written about the clinical features and outcome of PD-related peritonitis caused by co-infection of Acinetobacter species with other pathogens. We herein present a case of peritonitis caused by co-infection with Acinetobacter species and coagulase-negative staphylococci, which resulted in patient dropout and mortality. We review the literature about Acinetobacter peritonitis and current treatment protocols.

Keywords:

• Acinetobacter
• peritoneal dialysis
• peritonitis
• coagulase-negative Staphylococcus

INTRODUCTION

Continuous ambulatory peritoneal dialysis (CAPD) is a safe, convenient, and cost-effective alternative to hemodialysis. The major complication of CAPD is infection with an average incidence of 1.4 infectious episodes per person each year.¹ Gram-positive cocci are isolated in the majority of peritonitis episodes² and coagulase-negative staphylococci (70%) are the most common etiologic organisms.¹ Gram-negative bacteria are isolated in at least 15–25% of cases of peritonitis episodes during chronic peritoneal dialysis (PD). Among the gram-negative bacteria, Acinetobacter species have been reported in several series of PD-related peritonitis, sometimes as a concomitant that may be asymptomatic and require no treatment.² Little has been written about the clinical features and outcome of PD-related peritonitis caused by co-infection of Acinetobacter species with other pathogens. We herein present a case of peritonitis caused by co-infection with Acinetobacter species and coagulase-negative staphylococci, which resulted in PD dropout and mortality. We also review the literature about Acinetobacter peritonitis and current treatment protocols.

CASE REPORT

The patient was a 71-year-old male who had end-stage renal disease due to hypertension and was on CAPD therapy for the last 7 years. He had admitted to hospital with the complaints of abdominal pain and a cloudy peritoneal dialysate present for the last 5 days. On physical examination, the blood pressure was 90/50 mmHg and other systemic physical examination findings were within normal range, with no signs of exit-site or tunnel infection. The patient's high sensitive C-reactive protein level was 12.5 mg/dL (the upper normal limit of the test was 0.8 mg/dL), blood urea nitrogen was 10.6 mmol/L, and creatinine was 477.4 μmol/L. The initial laboratory parameters are summarized in Table 1. The patient was hospitalized for PD-related peritonitis, and initial empirical antibiotic therapy including ampicillin-sulbactam and ciprofloxacin was began after the cultures were obtained. The peritoneal culture revealed coagulase-negative Staphylococcus; therefore the therapy was switched to teicoplanin. The sensitivity pattern of the isolated microorganism is shown in Table 2. Ultrasound revealed no intra-abdominal pathology except for bilaterally atrophic kidneys compatible with end-stage renal disease. The control dialysate culture was sterile. The patient was discharged with an ambulatory parenteral antibiotic scheme (the total duration of antibiotic therapy being 3 weeks), after the dialysate was clear on examination, and the dialysate leukocyte count and serum high sensitive C-reactive protein returned to normal ranges.

TABLE 1.  The laboratory parameters of the patient at the time of hospital admission during the first and the recurrent peritonitis attacks

Parameter	First attack	Recurrent attack
Hemoglobin (g/L)	122.0	107.1
WBC (10^3/mm^3)	14.38	8.66
Aspartate aminotransferase (IU/L)	10	23
Alanine aminotransferase (IU/L)	5	8
Albumin (g/L)	21.3	22.0
High sensitive C-reactive protein (mg/dL)	12.5	27.2
Gram stain of PDE	Gram (+) cocci	Gram (+) cocci
Dialysate WBC count (/mm^3)	150	1500
Dialysate neutrophil %	80	95

Notes: WBC, white blood cell; PDE, peritoneal dialysis effluent.

TABLE 2.  The antimicrobial sensitivity patterns of the isolated microorganisms in the first and the recurrent attacks

	Coagulase-negative staphylococci		Acinetobacter species
Ticarcilllin/clavulanic acid	R	Amikacin	R
Amoxicillin/clavulanic acid	R	Ampicillin/sulbactam	PS
Cephazolin	R	Cefotaxime	R
Gentamycin	S	Ceftazidime	R
Trimethoprim/ sulphamethoxazole	S	Ceftriaxone	S
Vancomycin	S	Ciprofloxacin	R
Ofloxacin	S	Gentamycin	S
Ampicillin	R	Imipenem	S
Cefotaxime	R	Levofloxacin	S
Chloramphenicol	S	Meropenem	S
Ciprofloxacin	S	Tetracycline	PS
Penicillin G	R	Ticarcilllin/clavulanic acid	S
Teichoplanin	S	Tobramycin	S
Imipenem	R	Trimethoprim/ sulphamethoxazole	S

Notes: R, resistant; S, sensitive; PS, poorly sensitive.

Twenty-seven days after the first episode of peritonitis, the patient re-admitted to the hospital with abdominal pain and a cloudy peritoneal dialysate. The laboratory parameters during the recurrent peritonitis episode are also summarized in Table 1. The peritoneal culture revealed coagulase-negative staphylococci with the same sensitivity pattern observed in the previous attack with concomitant Acinetobacter species. The sensitivity pattern of the Acinetobacter species is also shown in Table 2. The patient was hospitalized and an antibiotic regimen including teicoplanin and gentamicin was initiated. The patient's peritoneal dialysate remained cloudy for the first 5 days of the initiation of the antibiotic therapy; therefore the peritoneal catheter was removed and daily intermittent hemodialysis therapy was prescribed. The patient's clinical status progressively deteriorated and the recurrent coagulase-negative staphylococcal peritonitis episode with Acinetobacter co-infection resulted in mortality.

DISCUSSION

The outcome of PD-related peritonitis much depends on the infecting microorganism. The clinical severity of gram-positive peritonitis is generally mild; most patients can be managed as outpatients and will respond to either intraperitoneal or systemic antimicrobial therapy. Infections due to gram-negative rods, on the other hand, are typically more serious, especially those due to Pseudomonas aeruginosa. Acinetobacter species account for 1.1–10.7% of the cases of PD-related peritonitis, yet little is written about the role and the natural history of Acinetobacter species as an agent of PD-related infection.¹ We herein report a case of peritonitis caused by Acinetobacter species and coagulase-negative staphylococci, which had an unexpectedly grave prognosis as far as the mild course of Acinetobacter co-infection was concerned.

Acinetobacter species are pleomorphic nonfermenting aerobic bacilli, originally felt to be low virulence colonizers rather than significant pathogens. In recent years, reports of Acinetobacter species as a serious pathogen have become more frequent. Although the majority of clinical reports describe hospital-acquired infection in the intensive care setting (associated with instrumentation, debilitating illnesses, decreased host resistance and prior antibiotic treatment),² up to 79.3% of PD-related Acinetobacter peritonitis may be community-acquired.³ Peritonitis due to Acinetobacter species may occur during a vulnerable period when host defenses are compromised, particularly following another episode of peritonitis or in the early period following catheter placement and initiation of PD.²

Galvao et al. surveyed 23 episodes of Acinetobacter peritonitis. In their study, Acinetobacter accounted for the first peritonitis episode (no prior episode) in five cases and the second peritonitis episode (one prior episode) in another six cases, no co-infection was reported.² Interestingly in our case, a coagulase-negative staphylococcal peritonitis episode preceded the Acinetobacter co-infection with the same microorganism. In their study, the duration of prior PD experience varied between <1 month and >56 months, more than half cases occurring in the first year.² In our case, the PD experience was 84 months. The cumulative incidence of Acinetobacter peritonitis increased significantly during the first 2 or 3 months following any prior episode of peritonitis,² which was 27 days in our case. They found no predominating age group (the oldest patient was 66 years old) or underlying diagnosis, and PD dropout to hemodialysis or mortality was uncommon.² However, in our patient Acinetobacter peritonitis episode resulted in PD dropout and mortality. The unexpectedly grave prognosis observed in our case may be due to the relatively older age of our patient or due to the coagulase-negative staphylococcal co-infection.

Valdez et al. retrospectively analyzed 18 cases of Acinetobacter peritonitis and reported that all cases were community-acquired.¹ Similarly, Lye et al. reported that in their series, 79.3% of Acinetobacter peritonitis was community-acquired.³ In our case, the Acinetobacter infection was also community-acquired. It has been declared that 6.3% of Acinetobacter peritonitis episodes followed a previous episode of peritonitis by coagulase-negative Staphylococcus infection.³ Valdez et al. reported that the response to antibiotic therapy was good in Acinetobacter peritonitis and most patients retained their peritoneal catheter, removal of the catheter being necessary in only one out of 18 cases.¹ On the other hand, Lye et al. reported that patient dropout rate per infection was significantly higher for Acinetobacter peritonitis than coagulase-negative Staphylococcus peritonitis.³ In our case, preceding coagulase-negative Staphylococcus peritonitis resolved with no patient dropout, whereas subsequent Acinetobacter co-infection resulted in patients dropout and mortality.

Much institutional variation in drug susceptibility of Acinetobacter may exist. In vitro susceptibility testing generally reveals that there are no antimicrobial agents to which Acinetobacter species are uniformly sensitive.¹ Aminoglycoside antibiotics appear to be the mainstay and often sufficient treatment of Acinetobacter peritonitis.² Apart from aminoglycosides, trimethoprim–sulfamethoxazole, carboxypenicillins, ticarcillin, and piperacillin, the long-acting tetracyclines have been the most consistently active agents. Recent in vitro susceptibility studies of various newer antimicrobial agents, including both gentamicin-susceptible and gentamicin-resistant strains, show imipenem, ciprofloxacin, and ceftazidime to be most active against Acinetobacter species.¹

In conclusion, PD-related Acinetobacter peritonitis is generally known to have a benign course with resolution. However, Acinetobacter co-infection with coagulase-negative Staphylococcus in PD-related peritonitis may have an unexpectedly grave prognosis and result in mortality.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.