Fluid collections develop around renal allografts in 20% to 51% of cases.1 These may be lymphoceles, hematomas, urinomas, or abscesses. Lymphoceles usually form weeks to months after transplantation surgery and are due to disruption of recipient iliac lymphatics with variable contributions from lymphatics of the allograft kidney.2 Urinomas arise from urine leakage due to ureteral ischemia and necrosis or acute leakage at the anastomotic site.3 Abscesses may arise from extension of surgical wound infections or from secondary infection of lymphoceles, hematomas, or urinomas; they account for 2% to 30% of all aspirated fluid collections in the early posttransplant period.1 The most common bacterial etiologies of periallograft renal abscesses include Staphylococcus aureus, enteric gram-negative bacilli and bacteroides species.4 This report describes what we believe is the first case of P. multocida bacteremia and periallograft abscess in a patient who had undergone renal transplantation.
A 67-year-old man with kidney failure secondary to Goodpasture syndrome underwent renal transplantation in November 2004 from a living, unrelated donor. His pretransplantation panel-reactive-antigen was 17%, and he shared a 4-antigen match with the donor. After transplantation, he was maintained on mycophenolate, cyclosporine, and prednisone for chronic immunosuppression but did not receive induction therapy. He did well until 5 months posttransplantation, when his serum creatinine was noted to have increased to 1.7 mg/dL from a posttransplant baseline of 1.3 mg/dL. Ultrasound imaging of the transplanted kidney revealed an adjacent fluid collection measuring 13.2 × 7.6 cm, and he was admitted to the hospital. His only complaint at that time was fatigue during the previous 2 weeks. His medications included mycophenolate (1 g BID), cyclosporine (150 mg BID), and prednisone (15 mg daily). He was a healthy-appearing man with normal vital signs. The physical examination was unremarkable, with a completely healed abdominal surgical incision. Laboratory data at admission were as follows: white blood cell count, 14,700/μL (90% granulocytes and 10% lymphocytes); hemoglobin level, 8.3 g/dL; platelet 431,000/μL; serum urea nitrogen, 45 mg/dL; and creatinine, 1.7 mg/dL. The rest of a serum chemistry panel, including liver-associated enzymes, was normal. A chest radiograph was normal. A computerized tomographic (CT) scan of the abdomen showed a 13 × 9-cm fluid collection anteromedial to the allograft kidney (Fig. 1). The CT-guided needle aspiration of the collection yielded purulent fluid, which led to immediate placement of a percutaneous drainage catheter. A creatinine level measured in this fluid was identical to that of serum. Piperacillin/tazobactam and ciprofloxacin were started empirically. Gram-negative coccobacillary forms were noted on Gram stain of the aspirated fluid and routine cultures of this and a blood culture grew P. multocida. Minimum inhibitory concentrations for penicillin, ceftriaxone, and levofloxacin were 0.25, less than or equal to 0.12, and less than or equal to 0.25 μg/mL, respectively. The antibiotic regimen was subsequently changed to intravenous ceftriaxone and ciprofloxacin. Purulent material continued to drain from the percutaneous catheter and repeated CT scans of the abdomen showed little change in the abscess, which measured 9.3 × 7.8 cm at the end of the second week of catheter drainage. Open surgical drainage of the abscess was then performed without complications, and the patient was discharged on the second postoperative day. Fluid obtained at surgery was negative for bacteria on Gram stain and growth on routine cultures. Follow-up CT scans showed slow resolution of the residual fluid collection, and intravenous ceftriaxone was continued for a total duration of 8 weeks. A final CT scan at the end of this antibiotic course eventually confirmed complete resolution of the abscess. The patient's serum creatinine returned to its posttransplant baseline. He remains well 9 months after completion of therapy. Subsequent to the isolation of P. multocida, the patient gave additional history that he owned a diabetic cat and had sustained a scratch to his arm while giving the cat an insulin injection approximately 2 weeks before hospitalization.
Pasteurella species are nonmotile gram-negative coccobacilli that grow on blood agar without hemolysis and do not grow on MacConkey agar. They are part of the normal oral and gut flora of many wild and domestic animals, with carriage rates highest among cats and dogs.5-7
Human infection by P. multocida takes 3 forms. The most common is local wound infection at the site of an animal bite or scratch, which usually manifests as cellulitis, soft tissue abscess, tenosynovitis, or osteoarticular infection.8 Second, respiratory tract infection or colonization can occur in persons with chronic lung diseases (bronchiectasis, chronic bronchitis, or lung cancer) and extensive exposure to animals carrying P. multocida.9,10 The third form of pasteurellosis is bacteremia with or without metastatic infection. This systemic disease has been reported most often in immunocompromised patients, including those with cirrhosis of the liver and malignancies.11,12
Our patient's presentation was consistent with that of an immunocompromised host in that he was relatively asymptomatic despite the presence of bacteremia and a large abscess. His immunosuppressive therapy may also have prevented a local inflammatory reaction at the site of the cat scratch. We postulate that a subclinical superficial infection, probably related to the cat scratch, lead to a transient P. multocida bacteremia, which seeded a previously sterile fluid collection adjacent to the renal allograft. This fluid collection likely originated as a lymphocele as suggested by its creatinine level identical to that of serum. The resulting periallograft abscess then caused a secondary bacteremia detected at the time of his presentation. The elevated creatinine could have resulted from partial ureteral obstruction by the abscess, prerenal azotemia related to sepsis and dehydration, or both.
Pasteurella multocida infections in the transplant population are rare, with only 2 previous reports in the English-language literature of renal transplant recipients who had been exposed to dogs or cats. The first13 was that of a 9-year-old girl who developed a psoas muscle abscess 6 months after renal transplantation, and the second2 was of a 40-year-old woman who developed an infected lymphocele 10 months after nephrectomy of a transplanted kidney. These infections, however, may become more common with increasing numbers of patients undergoing organ or bone marrow transplantation. Although there is no clinical trial evidence to prove that infection of animal bites or scratches14 is prevented by postexposure antibiotic prophylaxis, it is recommended in certain circumstances, especially for severe wounds or immunocompromised patients. Amoxicillin/clavulanic acid is the drug of choice and has excellent activity against P. multocida and other bite-associated organisms.15
Although immunocompromised individuals are at increased risk for serious zoonotic infections,16 the health benefits of pet ownership are thought to outweigh these risks, provided that patients take appropriate precautions. The Centers for Disease Control and Prevention's Healthy Pets, Healthy People web site offers immunocompromised and other patients advice for preventing animal borne infections, including avoidance of bites and scratches.17 Probably because of its rare occurrence, however, P. multocida is mentioned neither here nor in recent provider guidelines.18 Transplant patients who have pets should be counseled to minimize potentially traumatic physical contact with animals and to report promptly bites or scratches, however minor, to their providers. Postexposure antibiotic prophylaxis should be considered.
We have presented the first case of P. multocida renal allograft perinephric abscess. Although rare, P. multocida infections should be considered in the differential diagnosis of bacterial infections in the immunocompromised host, especially when a history of pet ownership or animal contact is elicited.
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