Acute lung injury and multi-organ dysfunction; an unusual manifestation of leptospirosis
Rotherham, UK
* E-mail: shankarsubash{at}yahoo.co.uk
Editor—Leptospirosis is a zoonosis—an infection that can be transmitted from animals to humans—and is primarily a disease of tropical regions. It is an uncommon, but notifiable, disease in the UK, <1 patient million–1 yr–1,1 yet two to three people in England and Wales die every year from the disease. Severe forms are associated with a very high mortality rate. Diagnosis is based on epidemiological history, clinical features, and investigations. It is often missed and easily overlooked because of the lack of awareness and the inability to obtain early laboratory confirmation. Adequate antibody titres appear only after a period of 5–7 days2 and, in the UK, the specimen needs to be sent to the reference laboratory at Hereford. Leptospirosis should be a differential diagnosis in an acutely ill patient with appropriate risk factors and symptomatology. We present a patient of an uncommon presentation of leptospirosis.
A 59-yr-old male attended the hospital with a 5-day history of fever, lethargy, body pain, headache, productive cough, and decreased appetite. He lived independently, smoked 30 cigarettes a day, and was keen on fishing in the nearby canal. He was in good health with no significant past medical or surgical history and had not recently travelled outside the UK.
On examination, he was alert, oriented, and icteric. Temperature was 37.7°C, heart rate 109 beats min–1, arterial pressure 93/53 mm Hg, and well-perfused peripheries. His ventilatory frequency was 19 min–1 with an oxygen saturation of 96% on room air. On auscultation, his heart sounds were normal and air entry were equal on both lungs with occasional scattered wheeze.
Initial investigations revealed a white cell count of 7.0 x 109 litre–1, platelets 52 x 109 litre–1, haemoglobin 13.2 g dl–1, urea 22.5 mmol litre–1, creatinine 262 µmol litre–1, bilirubin 30 µmol litre–1, GGT 83 IU litre–1, and CRP of 339 mg litre–1. ECG showed normal sinus tachycardia and chest X-ray revealed mildly increased bronchoalveolar markings. An initial diagnosis of sepsis with lower respiratory tract infection and acute renal impairment was made and he was transferred to a medical ward.
Within a few hours, his condition detoriated; he became breathless, hypoxic, and hypotensive (arterial pressure 80/50 mm Hg) despite a litre of colloid and crystalloid infusion. His arterial gases were, pH 7.47, PaCO2 3.3 kPa, base excess –4 mmol litre–1, bicarbonate 17 mmol litre–1, PaO2 8.6 kPa, SaO2 94% on oxygen 15 litre min–1. He was transferred to a critical care ward.
Facial continuous positive airway pressure (CPAP) and invasive monitoring was initiated. Noradrenaline infusion was started to maintain a mean arterial pressure (MAP) of 
70 mm Hg. Despite these measures, his condition worsened rapidly. Within 2 h, he became exhausted, more hypoxic, and acidotic (blood gas, FIO2 0.9, pH 7.34, PaCO2 4.8 kPa, base excess –6.4 mmol litre–1, bicarbonate 19.4 mmol litre–1, PaO2 7.7 kPa, SaO2 84%). Investigations and chest X-ray were repeated. Repeat chest X-ray revealed an extensive bilateral alveolar shadowing (Fig. 1), simulating acute respiratory distress syndrome (ARDS). At this point, his trachea was intubated.
Repeat investigations revealed worsening of renal (creatinine 338 µmol litre–1, urea 26.2 mmol litre–1) and hepatic (bilirubin 114 µmol litre–1, GGT 98 IU litre–1, alkaline phosphatase 131 IU litre–1, albumin 22 g litre–1, aspartate transferase 59 IU litre–1) function. Platelets fell to 23 x 109 litre–1, activated partial thromboplastin time was 35.5 s, prothrombin time 10.4 s, and lactate 1.2 mmol litre–1. Abdominal ultrasound revealed no abnormalities, and a cardiac echo showed a dilated and poorly contracting right ventricle with normal left ventricular function. With the background history of fishing, along with hepatic and renal impairment, leptospirosis was suspected and appropriate samples sent to the reference laboratory. Samples were also sent for atypical screening.
Treatment was initially commenced with amoxicillin, later changed to benzylpenicillin. Platelets were transfused. Pressure control ventilation (PEEP 10 cmH2O, peak airway pressure 27 cmH2O, FIO2 0.9) was instituted, maintaining a PaO2 of 8.1 kPa. High-dose noradrenaline (0.8 µgm kg–1 min–1 ) was required to maintain an MAP of 70 mm Hg. He had clinically adequate filling pressure and was started on a diuretic infusion to good effect. There was significant pulmonary bleeding for the first 4 days and his platelets were low; hence, activated protein C was not considered. He required sedation, and ventilatory support with lung protection strategy for 7 days before sedation and noradrenaline were able to be weaned off. A percutaneous tracheostomy was performed on day 7. Chest X-rays were compatible with ARDS and started to improve after 1 week. He was weaned slowly after more than 19 days and discharged to a medical ward on day 26.
The initial result for leptospirosis was negative. We sent a second specimen after 6 days, which resulted positive for leptospirosis, MAT positive at 1:640, ELISA IgM positive at 1:1280, and the infecting organism was reported as Leptospiro icterohaemorrhagiae. The appropriate health authorities were informed.
Leptospirosis is transmitted to humans usually by contact with soil or water contaminated with the urine of rats, cattle, rodents, and other wild animals. The disease usually presents as flu-like illness with mild hepatic and renal impairment. Severe forms of leptospirosis are characterized by severe hepato–renal dysfunction, mental status changes, haemorrhagic diathesis, and rarely with multi-organ dysfunction. Pulmonary involvement is not uncommon (20–70%),3 but symptoms are usually mild without sequelae. ARDS requiring artificial ventilation is very rare and has a high mortality rate of up to 51%.4 This is often associated with pulmonary haemorrhage because of endothelial damage.56 In our patient, the progression to haemorrhagic ARDS was very rapid. Early recognition and institution of appropriate antibiotics is known to reduce the mortality.7
To conclude, clinicians need to be aware of the possibility of leptospirosis even if the illness presents with unusual clinical features. Elicitation of good history from the patient and a high level of suspicion are paramount in identifying this rare but potentially fatal disease. This condition should be considered in the differential diagnosis of all acutely ill patients with relevant history, and clinical manifestation and appropriate antibiotics should be started early.
References
1 www.hpa.org.uk/infection/topics_az/zoonosis/gen_info.htw.
2 Paul N Levett. (2001) Leptospirosis. Clin Microbiol Rev 14:296–326.
3 Bethlem EP and Carvalho CRR. (2000) Pulmonary leptospirosis. Curr Opin Pulm Med 6:436–41.[CrossRef][Medline]
4 Vieira SR and Brauner JS. (2002) Leptospirosis as a cause of acute respiratory failure: clinical features and outcome in 35 critical care patients. Brazil J Infect Dis 6:135–9.
5 Nicodemo AC, Duarte MIS, Alves VAF, et al. (1997) Lung lesions in human leptospirosis: microscopic, immunohistochemical and ultrastructural features related to thrombocytopenia. Am J Trop Med Hyg 56:181–7.
6 Emmanouilides CE, Kohn OF, Garibaldi R. (1994) Leptospirosis complicated by Jarisch–Herxheimer reaction and adult respiratory distress syndrome: case report. Clin Infect Dis 18:1004–6.[Web of Science][Medline]
7 Bal AM. (2005) Unusual clinical manifestations of leptospirosis. J Postgrad Med 51:179–83.[Medline]
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