To the editor: Immunosuppression associated to transplant involves a risk of infection.1
A 69-year-old female patient with a history of CRF secondary to adult polycystic liver and kidney disease who had been on HD since 1982 is reported. She was implanted a cadaveric kidney graft in 1986. Baseline immunosuppression consisted of cyclosporine, azathioprine, and steroids. Other relevant history data included HBP, chronic virus C hepatitis, and allergy to quinolones.
In 2007, the patient attended the emergency room complaining of fever, dry cough, and some abdominal discomfort.
On physical examination, the patient was found to be in a good general condition, with a baseline SatO of 94%, BP
values of 130/60 mmHg, and a temperature higher than 38 ºC. The only remarkable findings in cardiopulmonary
auscultation were crackling sounds, particularly in the left base. Cysts of her underlying disease were palpated in the abdomen.
Results of blood laboratory test son admission included: Creatinine 1.5 mg/dL, WBC 5090 (82% neutrophils),
platelets 95,000, prothrombin activity 55%. Results of all other blood tests and urine analysis were normal.
Chest X-rays showed blurring of left base, and patient was admitted to hospital with a diagnosis of left basal pneumonia.
After collecting samples for culture (blood, urine, sputum), empirical treatment was started with cefotaxime.
At 24 hours of admission, the patient experienced impairment of her general condition, severe arterial hypotension,
oliguria, and coagulopathy, requiring hemodynamic support with dopamine and colloids, furosemide infusion, and
vitamin K treatment. A CT scan of the abdomen and pelvis found no added disease to cysts.
Because of severity of the condition, cefotaxime was replaced by imipenem and clarythromycin. Blood culture results reported isolation of penicillin-resistant and imipenem-susceptible Hafnia alvei.
Measures taken achieved clinical stability and improvement of the patient. Immunosuppression, necessary to
prevent rejection of transplanted organs, implies a predisposition to experience severe infection.1 Rubin et al
reported a calendar of infections depending on the transplant period: hospital-acquired infections are common in the first month, opportunistic infections predominate between the first and sixth months, and any community-
acquired infection may occur after 6 months.2
A community-acquired H. alvei infection occurring in a kidney transplant patient 20 years after transplant is reported here.
Members of the Hafnia genus are Gram-negative bacilli belonging to the family Enterobacteriaceae that occasionally
cause infection in humans. Though this species has been known since 1954, for decades it was considered to belong to the genus Enterobacter, and was therefore called «Enterobacter hafniae» or «Enterobacter alvei». Recent DNA and biochemical studies defined these organisms as members of a separate genus with a single species, Hafnia alvei.3
The gastrointestinal tract of humans and animals, particularly mammalians, but also birds, may be a reservoir for Hafnia.3 Epidemics of H. alvei infection related to the poultry industry are well documented in the literature.4 In our case, the patient was questioned again and said that she was in continuous contact with poultry, but had no awareness that her animals were ill.
Most patients colonized or infected by H. alvei have underlying diseases such as cancer (particularly hematological
tumors), surgery, trauma, pulmonary disease, cirrhosis, hepatitis, or pancreatitis.5 In the case reported, CRF for polycystic liver and kidney disease, chronic virus C hepatitis, and immunosuppression also existed. In this patient,
comorbid conditions and repeated contact with poultry may have promoted infection development.
Very little is known about this microorganism as a pathogen in animals and humans. It may cause a great variety of
systemic infections, including septicemia and pneumonia.
A literature review revealed that half the patients with bacteremia were immunocompromised because of tumors,
hepatic disease, or HIV infection. 3 In transplant patients, association was only found with liver6 and stem cell transplant.7 Our case is the first reported in a kidney transplant patient.
In conclusion, immunosuppression associated to transplant and underlying diseases predispose to uncommon infections. A first description of an H. alvei infection in a kidney transplant patient whose main clinical manifestation
was septicemia is given.
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Sepsis induced by hafnia alvei in a kidney transplant patient
Sepsis por hafnia alvei en una paciente con trasplante renal
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La inmunosupresión asociada al transplante conlleva un riesgo de padecer infecciones 1. Mujer de 69 años con antecedentes de IRC secundaria a enfermedad poliquística hepatorrenal del adulto, en programa de HD desde 1982. Recibió un injerto renal de cadáver en 1986. La inmunosupresión basal fue ciclosporina, azatioprina, y esteroides. Otros antecedentes relevantes eran HTA, hepatopatía crónica por virus C y alergia a quinolonas.
To the editor: Immunosuppression associated to transplant involves a risk of infection.1 A 69-year-old female patient with a history of CRF secondary to adult polycystic liver and kidney disease who had been on HD since 1982 is reported. She was implanted a cadaveric kidney graft in 1986. Baseline immunosuppression consisted of cyclosporine, azathioprine, and steroids. Other relevant history data included HBP, chronic virus C hepatitis, and allergy to quinolones.
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