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Leptospirosis induced pulmonary alveolar hemorrhage.

Background

Leptospirosis, is a worldwide zoonosis with protean clinical manifestations caused by the spirochete Leptospira interrogans. We report a case of pulmonary alveolar hemorrhage caused by leptospira in a young immunocompetent male.

Case Report

A 19 year old previously healthy male presented with a two day history of cough, low grade temperatures, frontal headache (10 out of 10), photophobia, nausea and non-bilious vomiting. He noticed some blood on blowing his nose but denied frank hemoptysis. Evaluation at a local emergency room revealed the patient to be febrile (temperature of 100.1F) with anemia, thrombocytopenia, elevated liver enzymes, and acute renal failure with radiological findings concerning for pneumonia. He was subsequently transferred to a tertiary care hospital for further evaluation and management. The patient also reported a rash around his mouth after recent exposure to citric acid containing foods.

His past medical history was significant for Attention Deficit Hyperactivity Disorder (ADHD), allergy to sulfa medications causing severe rash, and allergy to "acidic" foods causing perioral rash. He was not taking any medications on a regular basis.

The patient smoked 1 pack per day for 4 years. He was drinking mostly on weekends. He worked off and on, doing paint jobs for construction companies. He had 2 dogs and 2 cats as pets. He denied any sick contact, recent travel, sexually transmitted diseases, known tuberculosis contact, recent tick or insect bites. He did report multiple female sexual partners.

[FIGURE 1 OMITTED]

On examination, the patient was sitting holding his head and appeared to be in moderate distress. The blood pressure was 140/78 mm Hg, pulse 100 beats per minute, temperature 36.5C, and respirations 20 breaths per minute with oxygen saturation of 94% on two liters. Perioral crusted skin lesions were present with no mucosal involvement. He had few bilateral crackles with decreased aeration in the lower lung zones. Photophobia was present with no focal neurological deficits. He was alert and oriented to time, place and person.

Lab work revealed a white cell count of 14,600/[micro]L with 79% neutrophils, 5% bands, 1% metamyelocytes, 11% lymphocytes. hemoglobin was 9.2 g/dL, platelets 75,000/[micro]L. He had hyponatremia with sodium of 131 mmol/L. BUN and creatinine were elevated at 51 and 5.5 mg/dL respectively. Total bilirubin was 1.7 mg/dL, conjugated bilirubin 0.6 mg/dL, AST 53 U/L, ALT 47 U/L, alkaline phosphatase 63 U/L, LDH 179 U/L. An HIV test was negative. Blood and urine cultures were negative. Chest X-ray revealed innumerable poorly defined pulmonary nodules bilaterally, most in the range of 0.5 cm in diameter (Figure 1). CT brain revealed no acute intracranial process or space-occupying lesion. A lumbar puncture was performed showing no red blood cells, 15 white blood cells/[micro]L, glucose of 90 mg/dL and protein of 25 mg/dL.

[FIGURE 2 OMITTED]

Patient was started initially on Ceftriaxone 1g every 24 hours and azithromycin 500 mg every 24 hours intravenously. Vancomycin and Doxycycline were added empirically and Ceftriaxone dose increased to 2g every twelve hours. Infectious Diseases service was consulted and additional history was obtained. The patient reported swimming in the local river 6 days prior to onset of illness. He underwent a bronchoscopy and required intubation and ventilator support post procedure due to severe hypoxia.

Serial chest imaging showed development of bibasilar consolidation (Figure 2.). A CT chest done 10 days after procedure showed diffuse areas of dense consolidations bilaterally, more so in the dependent portions of the lungs, hazy areas of airspace opacity in the upper lobes and a nodular appearing area of airspace opacity at the right apex. (Figure 3A,B). Bronchoscopy revealed diffuse tracheo-bronchitis with severe pulmonary alveolar hemorrhage. Bronchial wash cytology showed scattered alveolar macrophages, inflammatory cells, and reactive respiratory epithelial cells with no Pneumocystis jerovecii on staining. Endobronchial biopsy showed mild inflammation. P-ANCA, C-ANCA and anti glomerular basement membrane antibody were negative. Mycoplasma, Rickettsia, Ehrlichia, and Legionella serologies were negative. Leptospira antibody (IHA) was positive with a titer of 1: 200 with repeat testing 1 week later showing titers at 1: 800.

The patient was initially started on high dose methylprednisolone. His antibiotic regimen was simplified to Doxycycline and Ceftriaxone for a total 14-day course. During the course of hospitalization, he also developed mild steroid induced gastritis, suspected ventilator associated pneumonia (treated empirically with linezolid and piperacillin/tazobactam for 7 days), worsening elevation of liver enzymes secondary to propofol use, and right basilic vein thrombosis owing to presence of intervenous lines. He was intubated for a total of 14 days and was eventually discharged to a nearby rehabilitation facility for recuperation.

Discussion

Leptospirosis, a zoonosis with protean manifestations caused by the spirochete, Leptospira interrogans, occurs worldwide. Wild or domestic animals are its reservoir. (1) Humans become infected after direct contact with the urine of infected animals or from exposure to contaminated soil, water, or other matter. The spirochetes enter the host through a breech in skin or mucous membranes and travel to the liver where they reproduce. This is followed by leptospiremia two to thirty days later, causing the organism to spread to all parts of the body including the meninges. (2) The organism is thought to cause disease through a toxin-mediated vascular injury, resulting in small-vessel vasculitis. (3-6)

Two general clinical patterns of disease, anicteric and icteric forms are recognized. Pulmonary symptoms can occur in both the nonicteric and icteric forms. These include cough, hemoptysis, and chest pain which could be secondary to myositis or have a more pleuritic character. (7)

Radiographic findings can include small "snowflake-like" nodular densities corresponding to areas of alveolar hemorrhage, large confluent consolidations, or a diffuse, ill-defined ground-glass pattern that may represent resolving hemorrhage.8-11 Serial radiographs may show progression from a nodular pattern to confluent consolidation, as seen in this patient (Figures 2,3).

A good epidemiological history usually clinches the diagnosis. Early in the disease, cultures of blood, urine, and cerebrospinal fluid can grow the organism in special media. Presence of IgM-class antibodies or a fourfold rise in IgG titers between acute and convalescent sera is diagnostic. (12) Penicillin is the usual therapy, but doxycycline is effective in shortening the illness and for prophylaxis. (13)

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Conclusion

Leptospira interrogans should be considered as an important infectious cause of pulmonary alveolar hemorrhage in the appropriate epidemiological setting.

References

(1.) Goldstein EJC. Household pets and human infections. Infect Dis Clin North Am 1991 Mar;5(1):117-30

(2.) Farr RW. Leptospirosis. Clin Infect Dis 1995 Jul;21(1):1-6; quiz 7-8.

(3.) Arean VM. The pathologic anatomy and pathogenesis of fatal human leptospirosis (Weil's disease). Am J Pathol 1962 Apr;40:393-423.

(4.) Arean VM, Sarasin G, Green JH. The pathogenesis of leptospirosis: toxin production by Leptospira icterohaemorrhagiae. Am J Vet Res 1964 May;25:836-43.

(5.) Miller NG, Allen JE, Wilson RB. The pathogenesis of hemorrhage in the lung of the hamster during acute leptospirosis. Med Microbiol Immunol 1974;160(4): 269-78.

(6.) De Brito T, Bohm GM, Yasuda PH. Vascular damage in acute experimental leptospirosis of the guinea-pig. J Pathol 1979 Aug;128(4):177-82.

(7.) Martinez Garcia MA, de Diego Damia A, Menendez Villanueva R, Lopez Hontagas JL. Pulmonary involvement in leptospirosis. Eur J Clin Microbiol Infect Dis 2000 Jun;19(6):471-4.

(8.) Im JG, Yeon KM, Han MC, Kim CW, Webb WR, Lee JS, Han YC, Chang WH, Chi JG. Leptospirosis of the lung: radiographic findings in 58 patients. Am J Roentgenol 1989 May;152(5):955-9

(9.) Luks AM, Lakshminarayanan S, and Hirschmann JV. Leptospirosis presenting as diffuse alveolar hemorrhage: case Report and literature review. Chest. Feb 2003;123:639-643.

(10.) Primack SL, Miller RR, and Muller NL. Diffuse pulmonary hemorrhage: clinical, pathologic, and imaging features. Am J Roentgenol Feb 1995;164:295-300.

(11.) Albelda SM, Gefter WB, Epstein DM, and Miller WT. Diffuse pulmonary hemorrhage: a review and classification. Radiology 1985 Feb;154:289-297.

(12.) Levett PL. Leptospirosis. Clin. Microbiol. Rev., Apr 2001;14:296-326.

(13.) Edwards CN, Levett PN. Prevention and Treatment of Leptospirosis. Expert Rev Anti Infect Ther. 2004 Apr;2(2):293-8.

Sharjeel Ahmad, MD

Staff Physician, Infectious Diseases Associate Director, Adult Medicine Community Health Services, Inc Hartford, CT

Arif R. Sarwari, MD

Associate Professor, Section of Infectious Diseases, Department of Medicine, West Virginia University, Morgantown, WV
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Title Annotation:Scientific Article
Author:Ahmad, Sharjeel; Sarwari, Arif R.
Publication:West Virginia Medical Journal
Article Type:Case study
Geographic Code:1USA
Date:Nov 1, 2010
Words:1394
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