Title : Acinetobacter junii bacteremia associated with cellulitis in a patient receiving chronic hemodialysis: A rare opportunistic bloodstream infection
Abstract:
Summary: Acinetobacter junii is a rarely reported cause of human infection. We report a case of A.junii bacteremia in a 79-year-old man with end-stage renal disease on hemodialysis who presented with lower extremity cellulitis and sepsis. Blood cultures obtained prior to antibiotic administration confirmed A. junii bacteremia. The patient was treated with ceftazidime and vancomycin based on susceptibility testing, administered after hemodialysis sessions to maintain adequate pharmacokinetic exposure. Repeat blood cultures demonstrated microbiological clearance and the patient achieved clinical recovery. A.junii is a rare but clinically significant opportunistic pathogen. This case demonstrates the importance of dialysis-adjusted antimicrobial therapy in managing rare bloodstream infections for ESRD patients.
Background: Acinetobacter junii is an uncommon human pathogen. Current genomic epidemiological analyses suggest that A. junii is globally distributed, across human, animal, and environmental reservoirs. Genetic differentiation between isolates from different ecological sources raises the possibility of cross-sector transmission. Consequently, there is growing recognition of A. junii as an emerging opportunistic pathogen. Despite this expanding ecological presence, A. junii remains a rarely reported cause of human infection, and its clinical presentation is still incompletely characterized.
Patients with end-stage renal disease receiving hemodialysis are vulnerable to infection. Hemodialysis is associated with persistent systemic inflammation, dysfunction of both innate and adaptive immune responses, which impair host defense against infection. These immunologic alterations create a permissive environment for infections caused byuncommon or opportunistic pathogens. In this context, the identification of Acinetobacter junii in a patient with ESRD warrants careful consideration of its pathogenic significance.
Case Presentation: A 79-year-old man with end-stage renal disease (ESRD) requiring chronic hemodialysis and a history of hypertension presented to the emergency department with one week of progressive erythema and pain of the left lower extremity. The erythema initially began at the left ankle and gradually extended proximally to below the knee. The pain progressively worsened and was described as burning and pulsatile, with a severity of 8/10. He denied purulent drainage, bullae, necrosis, or rapidly spreading skin discoloration.
The night prior to admission, he developed acute dyspnea accompanied by fever and chills, with worsening shortness of breath. He denied cough, chest pain, nausea, vomiting, or diarrhea. The patient also reported missing his two most recent hemodialysis sessions because of transportation difficulties.
He lives on a farm and has frequent exposure to soil and animals, including six horses and two dogs. He occasionally walks barefoot and reported possible minor skin breaks but denied any significant trauma.
On presentation to the emergency department, he was febrile (39.3 °C), tachycardic (106 beats/min), tachypneic (24 breaths/min), and hypoxic (SpO? 89% on room air), requiring supplemental oxygen at 2 L via nasal cannula. Physical examination revealed circumferential erythema of the left lower extremity extending from the ankle to below the knee, with warmth, tenderness, and pitting edema.
Investigation: Initial laboratory evaluation demonstrated leukocytosis with neutrophilic predominance (white blood cell count 13.62 ×10?/L) and marked thrombocytosis (platelet count 614 ×10?/L), findings consistent with an acute inflammatory response. Hemoglobin was mildly decreased at 12.4 g/dL. Serum chemistry revealed renal dysfunction consistent with the patient’s known end-stage renal disease, with creatinine 8.77 mg/dL and blood urea nitrogen 70 mg/dL. Mild hyperkalemia was present (potassium 5.4 mmol/L). C- reactive protein was markedly elevated at 9.72 mg/dL, supporting a significant systemic inflammatory process. Serum lactate remained within normal limits.
Examination of the left lower extremity revealed diffuse erythema and swelling extending from the ankle to below the knee, with associated warmth and tenderness. The involved skin appeared poorly demarcated with pitting edema but without bullae, necrosis, fluctuance, or crepitus. These findings raised concern for cellulitis.
To further evaluate for deep soft-tissue infection or abscess formation, contrast- enhanced CT imaging of the left lower extremity was obtained. Imaging demonstrated diffuse subcutaneous soft-tissue edema consistent with cellulitis without evidence of abscess or deep soft-tissue collection. No imaging features suggestive of necrotizing infection were identified. These findings supported left lower extremity cellulitis as the most likely source of infection.
Because the patient presented with acute dyspnea and hypoxia on admission, chest radiography was obtained and demonstrated mild bilateral interstitial pulmonary edema without focal consolidation. CT pulmonary angiography was subsequently performed to exclude pulmonary embolism and demonstrated no evidence of thromboembolic disease. Duplex ultrasonography of the bilateral lower extremities was also obtained to evaluate for deep venous thrombosis and demonstrated diffuse subcutaneous edema of the left lower extremity without evidence of thrombosis.
Given the patient’s fever and systemic symptoms concerning for sepsis, two sets of peripheral blood cultures were obtained prior to antibiotic administration. Both culture sets subsequently grew Acinetobacter junii, supporting the diagnosis of A.junii bacteremia in the setting of cellulitis.
Differential Diagnosis: The primary diagnostic consideration was severe left lower extremity cellulitis complicated by bacteremia in a high-risk host with end-stage renal disease receiving maintenance hemodialysis. The patient presented with fever, leukocytosis, and progressive unilateral erythema and swelling of the affected extremity. Clinical examination demonstrated diffuse erythema with poorly demarcated borders and pitting edema without bullae, necrosis, fluctuance, or crepitus, findings most consistent with cellulitis.
Deep venous thrombosis (DVT) was considered given the presence of unilateral leg swelling and pain. However, venous duplex ultrasonography demonstrated no evidence of thrombosis, making this diagnosis unlikely.
Necrotizing soft tissue infection was also considered because of the patient’s systemic inflammatory response and severe localized pain. However, the absence of rapidly progressive skin changes, bullae formation, skin necrosis, crepitus, or hemodynamic instability argued against necrotizing infection. Imaging further supported a superficial soft tissue process without deep fascial involvement.
Because the patient also presented with dyspnea and hypoxia, cardiopulmonary causes including pulmonary embolism and pneumonia were evaluated. These diagnoses were excluded based on imaging studies demonstrating no evidence of pulmonary embolism or focal pulmonary infection. The patient’s respiratory symptoms were therefore attributed to volume overload in the setting of missed hemodialysis sessions.
The identification of Acinetobacter junii in two separate peripheral blood culture sets obtained prior to antibiotic administration established true bacteremia rather than contamination. In the context of the patient’s clinical findings and imaging results, the most likely source of bacteremia was soft tissue infection of the left lower extremity.
Treatment: The patient was admitted with sepsis secondary to left lower extremity cellulitis in the setting of end-stage renal disease on maintenance hemodialysis. Given leukocytosis, elevated inflammatory markers, fever, and concern for severe soft tissue infection with possible bacteremia. Initial Management includes empiric broad-spectrum intravenous antibiotics were initiated with ceftriaxone and vancomycin. Blood cultures obtained on admission subsequently grew Acinetobacter junii in two out of two sets. After susceptibility data review, antibiotics were tailored to Ceftazidime 2 g IV and vancomycin 1g IV after each hemodialysis session. The decision to add vancomycin was to ensure adequate Gram-positive coverage while awaiting clinical response. A total 6-week course of intravenous antibiotics was planned, administered at the patient’s outpatient hemodialysis center.
Outcome and Follow up: After initiation of targeted antimicrobial therapy, the patient demonstrated gradual clinical improvement. Laboratory evaluations indicated stabilization of hemodynamic status and decreasing inflammatory markers. Repeat blood cultures obtained 48 hours after initiation of antibiotic therapy showed no microbial growth. These cultures remained negative after five days of incubation, confirming microbiological clearance of bacteremia. The patient subsequently completed a full course of intravenous antimicrobial therapy while continuing scheduled hemodialysis sessions.
Discussion: Acinetobacter junii is an uncommon cause of human infection and accounts for less than 1% of clinical Acinetobacter isolates. Most clinically significant infections are caused by A. baumannii, whereas infections due to A. junii are rarely reported in the literature.8 The largest clinical series to date described 43 cases of A. junii bacteremia over a ten-year period at a tertiary medical center, highlighting the rarity of this organism even in large healthcare systems. 5 These observations underscore the importance of reporting additional cases to better define its clinical spectrum.
Several predisposing risk factors have been consistently reported in cases of A. junii infection. These include prior exposure to broad-spectrum antibiotics, malignancy, immunosuppressive therapy, invasive medical procedures and the presence of indwelling medical devices such as central venous catheters or nephrostomy tubes.7,9 Although most reported cases of Acinetobacter junii infection occur in hospitalized or immunocompromised patients, emerging genomic epidemiological studies suggest that this organism is widely distributed across environmental and animal reservoirs. Environmental sources such as soil, water, and livestock environments have been identified as potential ecological reservoirs for A. junii, raising the possibility of cross- sector transmission. In this case, the patient’s frequent exposure to farm animals and soil may represent a potential environmental interface for infection.
The clinical manifestations of A. junii infection appear to be diverse. Reported infections include bacteremia, pneumonia, peritonitis, meningitis, corneal infections, and skin and soft-tissue infections. These reports suggest that A. junii can cause infections involving multiple organ systems, particularly in patients with significant comorbidities or immunosuppressive conditions. In the largest clinical study of A. junii bacteremia, most isolates demonstrated high susceptibility to carbapenems, fluoroquinolones, and aminoglycosides. Henao-Martínez et al. described a case of community-acquired cellulitis with bacteremia caused by A. junii-johnsonii that initially received broad- spectrum empiric therapy and was subsequently narrowed to levofloxacin monotherapy with complete clinical resolution.² These findings support the effectiveness of targeted antimicrobial therapy once susceptibility results are available.
Although many Acinetobacter junii isolates remain susceptible to commonly used antimicrobial agents, emerging resistance mechanisms have increasingly been reported. Genomic epidemiological studies have identified clinically significant resistance determinants in A. junii, including carbapenemase genes such as NDM-1 and OXA-58, as well as other β-lactamase–encoding genes. Some of these resistance determinants appear to be plasmid-associated, suggesting the potential for horizontal gene transfer and dissemination across clinical and environmental reservoirs. The presence of these resistance elements illustrates the organism’s capacity to acquire antimicrobial resistance and the importance of susceptibility-guided therapy when managing A. junii infections.
In this case, ceftazidime was administered following hemodialysis sessions based on antimicrobial susceptibility results. In anuric hemodialysis patients, post-dialysis dosing maintained therapeutic serum concentrations for both 48-hour and 72-hour interdialytic intervals, supporting its effectiveness for treating Gram-negative bacteremia in this population.? This dosing strategy offers a practical advantage in patients receiving maintenance hemodialysis by allowing antimicrobial administration immediately after dialysis sessions while minimizing the risk of drug accumulation and toxicity. The favorable clinical response and microbiological clearance observed in our patient further support the effectiveness of dialysis-adjusted antimicrobial therapy. It also demonstrates the importance of individualized antibiotic dosing in patients with end-stage renal disease.
Previous studies suggest that A. junii bacteremia have relatively low virulence compared with other Acinetobacter species. In the 43-patient cohort reported by Tsai et al., most patients had low Pitt bacteremia scores and only a small proportion developed septic shock. Despite a high rate of inappropriate empirical antibiotic therapy, the overall in-hospital mortality rate was approximately 7%, suggesting that A. junii infections may be associated with relatively favorable outcomes compared with infections caused by A. baumannii.
A. junii as a rare opportunistic pathogen can cause significant bloodstream infections in patients with substantial comorbidities. Continued reporting of such cases will help clarify the epidemiology, clinical spectrum, and optimal management of A. junii infections.
