International Journal of Health & Allied Sciences

: 2015  |  Volume : 4  |  Issue : 3  |  Page : 181--184

Coexisting anicteric leptospirosis and pulmonary tuberculosis in a farmer

Nayyar Iqbal1, Stalin Viswanathan2,  
1 Department of Internal Medicine, Pondicherry Institute of Medical Sciences, Kalapet, India
2 Department of General Medicine, Indira Gandhi Medical College and Research Institute, Kadirkamam, Pondicherry, India

Correspondence Address:
Stalin Viswanathan
Department of General Medicine, Indira Gandhi Medical College and Research Institute, Kadirkamam, Pondicherry - 605 009


Leptospirosis and tuberculosis (TB) are widely prevalent in the tropics, with the former presenting acutely ranging from a flu-like illness to severe hepatorenal dysfunction (Weil�SQ�s disease) and hemorrhage. TB is a smoldering illness, which rarely presents acutely as community-acquired pneumonia or acute lung injury. We present a 35-year-old farmer who had acute onset breathlessness and oliguria following a short febrile illness, which required mechanical ventilation and renal replacement therapy. His diagnostic workup revealed concomitant pulmonary TB and anicteric leptospirosis which improved with appropriate antibiotics and supportive care.

How to cite this article:
Iqbal N, Viswanathan S. Coexisting anicteric leptospirosis and pulmonary tuberculosis in a farmer.Int J Health Allied Sci 2015;4:181-184

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Iqbal N, Viswanathan S. Coexisting anicteric leptospirosis and pulmonary tuberculosis in a farmer. Int J Health Allied Sci [serial online] 2015 [cited 2023 Oct 4 ];4:181-184
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Leptospirosis is the most prevalent zoonosis in the world. [1] Tuberculosis (TB) causes 1.8 million deaths worldwide every year. [2] Leptospirosis is a significant cause of acute renal failure (ARF) in developing countries. [3] About 44-67% of patients with leptospirosis can have a renal failure that is generally associated with Weil's disease (severe leptospirosis). [4] TB can occasionally present acutely in the form of meningitis, miliary TB or community acquired pneumonia (CAP) associated with respiratory failure or with acute respiratory distress syndrome (ARDS). [2],[5] We report a young farmer who presented during the rainy season with coexistent TB and leptospirosis-related anicteric ARF and acute respiratory distress.


This 35-year-old male was referred from another hospital with oliguria and acute onset breathlessness of 1-day's duration. He had presented to the referring hospital with 1-week's symptoms of high-grade fever, headache, dysuria, myalgia, and bilateral flank pain. He had tachypnea (40/min), tachycardia (120 bpm), normotension (110/70 mmg) and bilateral chest crackles with desaturation in room air (SpO 2 85%). With a provisional diagnosis of acute pyelonephritis and ARF and probable acute lung injury, he was administered piperacillin-tazobactam pending results. Investigations revealed deranged renal parameters with hypokalemia [Table 1], normal liver function tests (LFT), neutrophilic leukocytosis, bilateral upper lobe infiltrates on chest radiograph [Figure 1]a-c, and PaO 2 /FiO 2 of 212.5 (85/0.4). Urinalysis revealed pyuria with no casts or hematuria. Next day, his respiratory failure worsened with the onset of hypotension and metabolic acidosis, following which he was intubated, mechanically ventilated and infused dopamine and soda bicarbonate; continuous veno-venous hemodialysis was initiated. His endotracheal aspirate was positive for acid-fast bacilli (AFB) and he was commenced on modified doses of antituberculous therapy on the 3 rd day. The patient was weaned to a T-piece on day 4. On the same day, his serologies revealed positive Leptospira IgM (PanBio) and negative results for scrub typhus, dengue and systemic lupus. With a modified Faine score of 30, ceftriaxone 2 g and doxycycline 100 mg BD (for other rickettsioses, endemic in our area) were immediately initiated. He developed pericarditis and worsening breathlessness, but stabilized with another sitting of hemodialysis and one unit of RBC transfusion. He was extubated on 5 th day. Computed tomography [Figure 1]d-f on the 6 th day showed bilateral upper lobe cavities and asymmetrical bilateral pleural effusion. Pleural fluid was exudative (protein 4.5 g/dL) with a predominance of lymphocytes (total count 410; lymphocytes 68%) and ADA of 38 U/L. Melioidosis was also considered in view of bilateral cavities, pleural effusion, and renal failure, but Burkholderia was not isolated. Esophagogastroscopy done on 9 th day for malena showed fundal and corporal gastritis. His urinary AFB was negative and he was unwilling for a renal biopsy. Between 5 th and 14 th days, his creatinine remained elevated [Table 1] but stable, and he was discharged on the 15 th day with antituberculous therapy. He was lost to follow-up thereafter.{Figure 1}{Table 1}


Activities related to farming, fishing, sewage and veterinary practice are at risk for leptospirosis. [4] Leptospira live in the kidneys of natural hosts and may persist in genital tracts of domestic animals. [1] Transmission is by contact with infected urine or other tissues. [4] Leptospira spread hematogenously after entry into skin/mucosa. [4] Underestimation of disease occurs due to the nonspecific nature of symptoms, unawareness, poor access to reliable, and inexpensive lab facilities. [6] Conjunctival suffusion and calf tenderness are relatively specific findings, [6] neither of which were observed in our patient. Myalgia can be seen in almost all patients, but creatine kinase [Table 1] elevation is observed in <60% patients. [3]

Pulmonary involvement is seen in about 20-70% of leptospirosis, with cough, hemoptysis and ARDS being observed. [6] In our case, acute lung injury was contributed partly due to TB, because lung infiltrates in leptospirosis are predominantly in the lower zones and are nonsegmental and pleural effusions are rare. [7] Contributions to respiratory distress may have also been due to leptospirosis-related ALI, metabolic acidosis and uremic pericarditis. Respiratory distress improved with mechanical ventilation and antibiotics. Depending on the case series, the incidence of tuberculous CAP can be seen up to 60% of microbiologically confirmed pneumonias. [2] Reactivation, primary or postprimary TB, or atelectasis due to enlarged nodes can cause acute presentation of TB. [2] Pleural effusion, immunocompromised states, normal WBC counts, contact with other patients may be some clues to TB masquerading as CAP. [2] It is possible that our patient had a reactivation of latent TB due to severe leptospirosis and renal failure. A large population-based study from Taiwan showed that acute kidney injury (AKI) requiring dialysis increases the risk of acquiring TB. [8]

Both mild and severe leptospirosis lead to renal dysfunction. [9] Vasodilation related hypotension, and hypovolemia related to diarrhea, vomiting and fever cause renal injury. [3] Hypotension generally precedes renal and pulmonary complications. [10] All renal components including the tubules, interstitium, glomeruli and vascular structures can be affected. [10] Tubulointerstitial inflammation is mainly responsible for the renal failure. [4] Renal failure is generally nonoliguric, unlike in our patient. Uremia and oligoanuria are seen during the 2 nd week of illness. [4] Acute interstitial nephritis is detected earlier than acute tubular necrosis. [3] Hypokalemia [Table 1] is the typical finding in leptospiral ARF. [3]

In a study from Turkey, 92% of cases of leptospirosis were anicteric and renal involvement was in the form of leukocyturia, hematuria or proteinuria singly or in combination. [11] Hurst et al. showed that patients with leptospiral renal failure requiring dialysis had no associated jaundice or hemorrhage. [12] In India, flooding during monsoons can lead to leptospirosis, which is mostly anicteric. [3] Hence, the notion that renal disease is generally seen in severe leptospirosis (Weil's disease) needs to be dispensed when patients have associated thrombocytopenia or travel to endemic area. Isolated thrombocytopenia (not in our case) occurs commonly and often correlates with renal failure. [13]

Mimics of leptospirosis include Hantavirus infection, rickettsioses, and malaria. [14] Infectious causes of renal failure include the hepatitis viruses B and C, HIV, Hantavirus, legionella, listeria, and rickettsia. [14] Acute reno-pulmonary manifestations can be due to infections like rickettsioses, malaria, HIV and inflammatory disorders such as SLE, Wegener's granulomatosis, and sarcoidosis. We did not have facilities to check for Hantavirus, legionella and listeria. Serological testing for hepatitis B and C, HIV was nonreactive. Testing for c-ANCA and angiotensin converting enzyme (ACE) were not performed due to a conclusive diagnosis and recovery following antibiotics and supportive care.


Leptospirosis can concurrently exist with other infections. Association of leptospirosis with dengue, Hantavirus, hepatitis E, malaria (both falciparum and vivax), melioidosis and herpes simplex have been reported in the literature. [15],[16] In one report, two viruses (hepatitis E and dengue) have coexisted with leptospirosis. [16] There are seven instances of concomitant scrub typhus and leptospirosis, reported primarily from Taiwan and Thailand due to their endemicity. [17] Our patient had leptospirosis coexisting with TB, which has never been previously reported in medical literature. Health care providers in the tropics need to be on the vigil, to detect common tropical diseases, which may coexist and confuse the clinical picture.

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