A. defectiva dialysis–related peritonitis requires more attention. A. defectiva, first isolated in 1961 by Frenkel & Hirsch, generally presents as Gram-positive cocci, but can also occur as coccobacilli or bacllli, and was previously classified as a nutritionally variant Streptococcus. The classification of A. defectiva was revised and it is now grouped into a separate genus based on chromosomal DNA-DNA hybridization and 16s rRNA gene sequencing data [4]. This species has also been reported as a causative agent of endocarditis, meningitis, otitis media, prosthetic joint infections, and osteomyelitis [5]. PD is an important therapy for patients with chronic kidney disease and is administered to more than 200,000 such patients globally. PD-related peritonitis leads to increased mortality and is a reason for dropout from the PD program. Organisms commonly viewed as causative of PD-related peritonitis include coagulase-negative Staphylococci, S. aureus, Streptococci, Pseudomonas sp, Klebsiella sp, E. coli, Enterococci, other gram-negative bacteria and fungi [6], but to date only two cases of A. defectiva have been reported [2,7].
Diagnosis of A. defectiva infections is challenging as laboratory personnel may be unfamiliar with A. defectiva due to its infrequent isolation. In addition, this species is often not included in the standard biochemical techniques and algorithms commonly used for bacterial identification. Reports of the detection of A. defectiva have been based on the use of newer diagnostics such as matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) and 16s rRNA sequencing [8]. Attention should be payed to the following features of A. defectiva: its pleomorphic appearance, slow growth rate and growth requirements. A. defectiva appears as Gram-variable cocci and has pleomorphic bacillary forms when cultured in blood culture broth. Prolonged culture for at least 72 h under 5–10% CO2 at atmospheric pressure is recommended. Furthermore, PD effluent culture requires the use of liquid concentration technology (such as centrifugation or microfiltration of the leachate), prior to culture [3].
The Clinical Laboratory Standards Institute (CLSI) recommends the broth microdilution (BMD) method for testing the antibiotic susceptibility of A. defectiva; however, A. defectiva does not grow in the antimicrobial susceptibility testing (AST) panels commonly used in clinical laboratories. Cation-adjusted Mueller-Hinton broth with 2.5–5% lysed horse blood supplemented with 0.001% pyridoxal must be added to the wells prior to culture [9]. In a study conducted on 25 A. defectiva isolates in the US (using CLSI breakpoints), 24% of the isolates were susceptible to penicillin, 92% to ceftriaxone, 48% to cefepime, 72% meropenem, 92% to cefotaxime, 100% to levofloxacin, 92% to clindamycin, 24% to erythromycin, and 100% to vancomycin [10]. Penicillin or ceftriaxone (if susceptible) is recommended as a treatment for Abiotrophia endocarditis and other serious infections caused by this organism [11]. However, in vitro susceptibility and the clinical response are inconsistent [12]. Such treatment failures may be due to the indolent nature of the infections as well as delays in the initiation of appropriate antimicrobial therapy on account of slow growth rate, pleomorphic appearance and growth requirement [13]. Furthermore, in one of the two previously reported cases of A. defectiva PD-related peritonitis, peritonitis led to peritoneal membrane failure and the patient was subsequently transferred to hemodialysis [7]. However, in our case, PD-related peritonitis due to A. defectiva occurred in a child and was effectively eradicated by administration of ceftazidime and vancomycin.
This case and other case reports [7,8] suggest that A. defectiva should be regarded as a possible cause of bacteraemia in PD-related peritonitis patients. Clinicians and microbiologists should pay greater attention to this organism in patients with peritoneal dialysis–related peritonitis, as its pathogenicity is often underestimated.