Rapid severe sepsis from Pseudomonas fluorescens/putida bacteremia due to skin and soft tissue infection - A case report.

INTRODUCTION: Pseudomonas fluorescens (P. fluorescens) and Pseudomonas putida (P. putida) are uncommon causes of skin and soft tissue infections (SSTIs). They are rarely associated with bacteremia and fatality. When presenting with sepsis/shock, patients are usually immunocompromised. Our case highlights the importance of early recognition, source control and antimicrobial choice. CASE
PRESENTATION: We present a case of an immunocompetent 57 year old female who presented with rapidly progressive septic shock in the setting of P. fluorescens/putida bacteremia. The patient continued to deteriorate despite empiric antimicrobial coverage and aggressive source control. CLINICAL DISCUSSION: P. putida and P. fluorescens are gram negative bacillus bacteria that are ubiquitous in soil and water however have been reported as an opportunistic human pathogen capable of causing nosocomial infection especially in immunocompromised patients. Patients with bacteremia and shock should initially be covered with broad antimicrobial coverage for gram positive, gram negative as well as gas producing organisms and deescalate based on cultures and sensitivities. Along with antibiotics, aggressive source control is found to be the key to successful treatment in these patients.
CONCLUSION: Our case highlights an immunocompetent patient with rapid progressive sepsis and associated multisystem organ failure. We emphasize the importance of early recognition in these patients and treatment with appropriate antimicrobial therapy followed by source control.

Introduction

Pseudomonas fluorescens (P. fluorescens) and Pseudomonas putida (P. putida) are uncommon causes of skin and soft tissue infections (SSTIs). Both are gram-negative bacillus related to P. aeruginosa and are found throughout the natural environment. Several case reports in the literature are notable for bacteremia however virulence is low and fatality is rare. A majority of the patients affected by the above mentioned are noted to be in an immunocompromised state or have comorbidities that lead to a blunted immune response [1].

Case report

A 57 year old female with no pertinent family history and a past medical history of hypertension (on amlodipine), hyperlipidemia (on atorvastatin), irritable bowel syndrome and gastroesophageal reflux disease (on famotidine) initially presented to the emergency department (ED) with complaints of right lateral ankle pain. She had reported an ankle injury 12 hours prior to presentation in her condominium non-salt water pool. Within eight hours of the injury, she developed significant pain, noted swelling on the lateral aspect and presented to the ED for further evaluation. Physical exam of the right lower extremity was notable for swelling with a 2 cm round ecchymotic lesion, limited to the lateral ankle, with limited range of motion secondary to pain, intact pulses and no other skin findings. A right leg and ankle x-ray revealed lateral malleolar edema without acute osseous findings (Fig. 1, Fig. 2). The patient was discharged home after supportive care.

Fig. 1

Initial X-ray Right leg: (2 views) with evidence of soft tissue swelling, without any noticeable fractures or osseous findings.

Fig. 2

Initial X-ray Right leg: (2 views) with evidence of soft tissue swelling, without any noticeable fractures or osseous findings.

Six hours after discharge from her initial ED visit, the patient and her husband noticed worsening swelling of her right lower extremity. The previously noticed ecchymotic lesion started to expand and become more painful. The patient then developed shortness of breath and emergency medical services were contacted. The patient had a cardiac arrest due to hypoxic respiratory failure enroute to the hospital and was intubated in the field. Upon her subsequent evaluation in the ED, her vital signs were significant for hypotension 85/57 mmHg, sinus tachycardia to 115 bpm, and she was mechanically ventilated. Her physical exam was notable for an extensive hemorrhagic lesion with associated bullous formation extending from the right foot lateral surface up to the right knee (Fig. 3).

Fig. 3

Right lower extremity 24 hours after initial injury with evidence of extensive hemorrhagic extension from the ankle to knee.

Initial laboratory findings showed a white blood cell count of 3.3 K/mm3 (3.7–10.1), hemoglobin of 8.9 gm/dL (11.6–15.4), mean corpuscular volume of 112.8 fL (80–100), platelet count of 36 K/mm3 (156–352). Her chemistry was significant for potassium 5.1 mmol/L (3.5–5.1), carbon dioxide 11 mmol/L (22–32), anion gap 33 mEq/L (3–11), creatinine 2.9 mg/dL (0.7–1.5), lactic acid 21.4 mmol/L (0.7–2.1), total bilirubin 1.7 mg/dL (0.1–1.1), aspartate transaminase 327 U/L (15–46), alanine transaminase 164 U/L (13–69), troponin of 0.110 ng/mL (0.0–0.034). Her coagulation studies revealed an elevated prothrombin time of 25.9 seconds (9.8–13.9), international normalized ratio of 2.25, fibrinogen 318 mg/dL (224–424) and a d-dimer 5200 ng/mL (0–500). Her creatinine kinase levels were noted to be at 3197 U/L (range 30–170). Her arterial blood gas findings were consistent with a metabolic acidosis with pH 6.69, pCO2 69.1 mmHg, HCO3 8.3 mmol/L (obtained on 100% fraction of inspired oxygen on mechanical ventilator). Her chest x-ray showed clear lungs with an endotracheal tube in place. A head computed tomography (CT) showed a small volume left inferior sylvian fissure subarachnoid hemorrhage. A chest CT angiography did not show evidence of pulmonary embolism.

The patient was admitted to the intensive care unit for workup and treatment of septic shock. Intravenous fluids with 0.9% normal saline was initiated. Blood cultures were obtained prior to initiation of intravenous antibiotics and general surgery was emergently consulted for evaluation of necrotizing fasciitis. She was initiated on empiric coverage with intravenous vancomycin (15mg/kg every 8 hours), meropenem (1 gm every 8 hours) and clindamycin (600mg every 8 hours) for necrotizing fasciitis coverage. A bedside fasciotomy of her right lower extremity (RLE) was performed followed by a bedside below the knee guillotine amputation for aggressive source control given her clinical deterioration. Tissue cultures were obtained and sent for bacterial, fungal and acid fast bacillus. A second set of blood cultures were obtained after amputation. The patient continued to have progression of her acidosis and nephrology was consulted for initiation of continuous renal replacement therapy (CRRT).

Unfortunately, her clinical status continued to deteriorate with worsening acidosis, requiring multiple pressors, and the patient shortly expired despite aggressive resuscitative efforts on the second hospital day due to multisystem organ failure. On the second day, blood cultures and tissue cultures grew P. fluorescens and P. putida. Both organisms were sensitive to piperacillin/tazobactam, gentamicin, tobramycin and meropenem.

Discussion

P. putida and P. fluorescens are gram negative bacillus bacteria that are ubiquitous in soil and water however have been reported as an opportunistic human pathogen capable of causing nosocomial infection especially in immunocompromised patients. Clinical data on both organisms is lacking owing to the rarity and relatively low virulence rate [2]. A series of case reports by Yang et al. described P. putida related infections and only 5% were SSTIs of which 80% were associated with trauma [3]. In 2017, Nishimura et al. identified three case reports of P. fluorescens infections related to contaminated infusions and an immunocompromised oncology patient [4]. Both P. fluorescens and P. putida rarely result in bacteremia, shock or mortality hence risk factors for all patients should be identified. Immunosuppression, contaminated blood product infusions or catheter related bloodstream infections as the most common cause of infections with these isolates [3]. Pseudobacteremia secondary to contamination of blood cultures during venipuncture, in the preparation of culture media, or during laboratory processing of the culture has been reported and should be considered. Blood cultures should be repeated to establish a true blood stream infection [5].

When presenting with bacteremia and associated shock, signs and symptoms related to organ hypoperfusion should be identified. These include but are not limited to tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, and cool, clammy skin. Signs of end organ dysfunction should be evaluated. Progressive shock can lead to irreversible organ damage, multiorgan failure (MOF), and death. During this stage, anuria and acute renal failure develop, acidemia further depresses cardiac output, and hypotension becomes severe and recalcitrant to therapy [6]. Diagnosis can be made with blood cultures and tissue samples from the suspected source of SSTI. Other laboratory work should include a complete blood count, comprehensive metabolic panel, lactic acid levels, an arterial blood gas as well as other labs indicated based on patients presenting symptoms.

Patients with bacteremia and shock should initially be covered with broad antimicrobial coverage for gram positive, gram negative as well as gas producing organisms and deescalate based on cultures and sensitivities. A study by von Graevenitz et al. looked at patients with positive cultures for P. putida and P. fluorescens which showed sensitivity of the two species to polymyxin colistin, aminoglycosides, tetracycline, higher generation cephalosporins, piperacillin/tazobactam and carbapenems [2]. However, there have been studies that show multi drug resistant species to carbapenems exist [2]. Along with antibiotics, aggressive source control was found to be the key to successful treatment in these patients [7]. Our patient underwent a bedside fasciotomy followed by an above the knee amputation. For worsening acidemia combined with acute renal failure nephrology was consulted and CRRT was initiated.

Although there is lacking data, literature identifies two lethal cases of bacteremia from P. fluorescens and P. putida. Both patients were noted to be immunocompromised or have various other comorbidities [1,4]. When diagnosed early, treatment with appropriate antibiotics and source control leads to improved outcomes. However, patients with multisystem organ failure tend to have a poor prognosis. Despite aggressive source control and broad antimicrobial coverage, our patient expired due to the severity of her illness and associated multisystem organ failure.

Conclusion

P. fluorescens and P. putida are uncommon causes SSTIs rarely resulting in bacteremia and fatality. Very few cases have been reported and most respond well to appropriate antimicrobial therapy. A few lethal cases have been identified however patients were reported to be immunocompromised. Our case above highlights an immunocompetent patient with rapid progressive sepsis and associated multisystem organ failure. We emphasize the importance of early recognition in these patients and treatment with appropriate antimicrobial therapy followed by source control.

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All authors contributed to this manuscript. P. Singh is the article guarantor.

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