Acute renal failure in fulminant psittacosis

Acute renal failure in fulminant psittacosis

Respiratory Medicine (1994) 88, 239-240 Case Report Acute renal failure in fulminant psittacosis A. B. MASON AND P. JENKINS East Surrey Hospital Th...

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Respiratory Medicine (1994) 88, 239-240

Case Report

Acute renal failure in fulminant psittacosis A. B. MASON AND P. JENKINS

East Surrey Hospital Three Arch Road, Redhill, Surrey RH1 5RH, U.K.

Introduction Acute renal failure has been described as a rare complication of psittacosis, associated with a high mortality. We describe a further case of fulminating psittacosis complicated by acute renal failure, with a successful outcome.

Case Report A previously fit 68-year-old man was admitted with a history of an upper respiratory infection a week previously, followed after 72 h by rapidly progressive breathlessness, malaise and fever. There was no history of chest pain, sputum or haemoptysis and be denied previous respiratory symptoms. He was a non-smoker. On admission he was ill, with fever (39"9~ tachypnoea with wheeze, and central cyanosis. He was in rapid atrial fibrillation; blood pressure was 200/120. Widespread wheezes and basal crackles were present, and the chest X-ray showed bilateral patchy shadowing in the midzones. Arterial gases (on air): pH 7-49, PaCO 2 3"76 kPa, PaO 2 5.14 kPa, 0 2 saturation 78-2%. Other investigations: Hb 16"1 g d1-1, WBC 12.2 x 1091 1 (89% neutrophils), platelets 164x 1091 1, serum urea 15.6 mmol1-1, creatinine 185 #mol l - 1, sodium 133 mmol 1 2, potassium 3"7 mmol 1 1, the urine was sterile and showed 40 red cells/A 1 but no white cells. Routine blood and sputum cultures (excluding Legionella pneumophila) were negative. He was treated initially with intravenous erythromycin 1 g q.d.s. (with the addition of flucloxacillin 500 mg q.d.s, intravenously after 24 h), nebulized bronchodilators and high concentration oxygen therapy by mask, but deteriorated with increasing respiratory failure, mental confusion Received 11 March 1992and accepted in revisedform 22 October 1992. *Author to whom correspondence should be addressed at: 21 EffinghamRoad, Reigate,SurreyRH2 7JN, U.K. 0954-6111194/030239+02$08.00

and exhaustion; intermittent positive pressure ventilation was instituted 24 h after admission. At this stage he became oliguric despite high dose intravenous diuretic therapy, the urine/plasma values suggesting established renal failure. Forty-eight hours after admission the serum urea was 38.2 mmol 1-~, creatinine 559/~mol 1-1 and a decision was taken to commence haemofiltration. Despite some initial radiological progression he gradually improved sufficient to be transferred 9 days after admission to a Regional Renal Unit, where haemodialysis was commenced. His improvement continued and he was weaned from the ventilator 16 days after his initial admission. Further results availaNe at this stage included psittacosis titres at day 2 and 12 after admission showing a diagnostic rise from 1:10 to 1:80 (complement fixation test); Mycoplasma and Legionella titres were negative. Spirometry was normal; renal biopsy was not performed. He was treated with an oral course of doxycycline. His renal function continued to improve and haemodialysis was discontinued 2 weeks later. On subsequent outpatient review he remained well.

Discussion Psittacosis is an infection caused by Chlamydia psittaci, an unusual Gram-negative intracellular bacterium. The clinical syndrome in humans varies from an influenza-like illness to severe and sometimes fatal pneumonia; community-based studies have suggested that 1-5.5% of pneumonias are caused by the organisms (1,2,3). Associated cardiac (4) and neurological (5) involvement have been described and although mild renal involvement has been recognized for some time with proteinuria and oliguria the first documented cases of acute renal failure as a presenting feature of fulminant infection were reported by Byrom et al. in 1979 (6); both had a fatal outcome. As they surmise, the likely mechanism is acute 9 1994W. B. SaundersCompanyLtd.

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A. B Mason and P. Jenkhz.~

tubular necrosis, as none of the cases was at risk from hypotension or nephrotoxic drugs. The epidemiology of this infection has long been of interest. The organism was originally recognized as infecting psittacine birds, which can then disseminate the infection even as asymptomatic carriers, often on fleeting contact (7). However, as in this case, the majority of cases have no obvious source (1), and more recent evidence suggests that other vectors, including cattle, sheep and domestic cats, may be responsible (8). Man to man transmission has also been documented (9), and this may be a much underestimated source of infection (10). The case has been argued for making this infection notifiable; it remains endemic, with recurrent outbreaks, and a sufficient level of awareness is necessary to encourage its early recognition and appropriate management. Diagnosis is usually by retrospective serology, and this constitutes a further limitation; more rapid diagnostic techniques would be of value, not least in guiding choice of antibiotic t h e r a p y tetracycline is the treatment of choice. In the case described erythromycin was used initially on clinical suspicion of an atypical pneumonia, supplemented shortly afterwards by flucloxacillin in view of the early deterioration and the possibility of a preceding influenza infection. This afforded cover against Mycoplasma, Legionella, Staphylococcus aureus and Streptococcus pneumoniae; tetracycline was given on serological confirmation of the diagnosis. The choice of antibiotic therapy in community-acquired pneumonia is reviewed in detail by Harrison et at. (11). Psittacosis remains an unusual but potentially serious infection, and should be borne in mind as a cause

of any atypical pneumonia, even in the absence of any likely contact with animal vectors. Early recognition is of value in its specific management.

Acknowledgement We wish to thank Dr J. H a m m o n d and Dr M. E. Bending for their help in the management of this case.

References 1. Nagington J. Psittacosis/ornithosis in Cambridgeshire 1975 1983. J ttyg (Camb) 1984; 92: 9-19. 2. Woodhead MA. Macfarlane JT~ McCracken JS, Rose DH, Finch RG. Prospective study of the aetiology and outcome of pneumonia in the community. Lancet 1987; i: 671-674. 3. Macfarlane JT. Finch RG, Ward M J, Macrae AD. Lancet 1982~ ii: 255-258. 4. Coll R. Homer 1. Cardiac imolvement in psittacosis. BMJ 1976; 4: 35-36. 5. Cart-Locke DL. Mair HJ. Neurological presentation of psittacosis during a small outbreak in Leicestershire~ B I I J 1976; 2: 853-854. 6. Byrom NP. Walls J, Mair HJ. Fulminant psittacosis. Lancet 1979: i: 353-356. 7. Editorial. Psittacosis. BMJ 1972; 1:1 2. 8. Editorial. Psittacosis of non-avian origin. Lancet 1984; ii: 442443. 9. Shachter J. Dawson CR. Human Chlamydial Infections. Littleton, Massachusetts: PSG, 1982, 32-33. 10. Pether JVS. Noah ND. Lau YK, Taylor JA, Bowie JC. An outbreak of psittacosis in a boys' boarding school. J Ityg (Camb) 1984: 92: 337-343, I1~ Harrison BDW. Farr BM, Connolly CK, Macfarlane BM. Selkon JB, Bartlett CLR. The hospital management of community-acquired pneumonia. J R Coll Phys Lond 1987; 21: 267-269.