Abstract:
We report a reare case of leptospirosis who developed Jurish – Herxheimer reaction after initiation of treatment. The mechanism of this reaction and its pathophysiology are reviewed.
Key words: Jarisch-Herxheimer, Leptospirosis
Introduction:
Lleptospirosis is caused by Leptospira interrogans (e.g. serogroup L. icterohaemorrhagiae). Spread is bny contact with infected rat urine, e.g. while swimming, taking pond bath. They usually present with fever, jaundice, headache, red conjunctivae, tender legs (myositis), purpura, hemoptysis, hematemesis, or any bleeding, Meningitis, myocarditis and renal failure may develop.
Case Report:
A 32 year old male presented in August 2002, with a 7day history of fever, headache, myalgia and nausea. He had always been fit and well. On examination he was hemodynamically stable, pyrexia, and had meningism, and mild abdominal tenderness, without hepatosplenomegaly. Blood tests showed 9.6 x 109/L neutrophils, 125 x 109/L platelets, but no other abnormalities. We started intravenous cefuoxime 1.5gm twice daily and oral doxycycline 100mg twice daily, to cover meningococal, streptococcal, salmonella and other gram negative and typical pathogens. Blood tests 12 hr. later after admission showed urea and creatinine normal aST 110/U/Lt, ALT 176 U/L. Tests for malaria parasite was negative, widal test negative abdominal sonogram revealed no abnormality. Blood for culture and sensitivity was sent.
The patient became increasingly breathless and hypoxaemic. A chest rediograph showed mild cardiomegaly and an electrocardiograph (ECG) showed low voltage with widerspread ST segment changes. A transthoracic echocardiogram showed mold dilation of left ventricle. Pre-existing cardiac or pulmonary disease was considered unlikely in this otherwise healthy male. The patient was started on intravenous dexamethasone, dopamine infusion and oxygen inhalation. His condition improved over next 48 hours. The report ECG and transthroacic echocardiogramon day 5 showed complete resolution of previous abnormalities. He was discharged after finishing a week’s course of the antibiotics, and soon returned to work. He is doing well since then when last seen in Dec. 2002.
We subsequently diagnosed acute leptospirosis by a leptospira spp. 1gM antibody titre of 1:2560, from blood sample taken on day 8 of admission (negative on the first day of hospitalization). The patient’s acute deterioration after antibiotic treatment was probably due to a Jarisch-Herxhemier reaction.
Discussion:
Cardiovascular involvement can occur in both the septicaemic and immune phases of Leptospira infection. Minor ECG changes and pulmonary edema have been reported in the first week of illness, but cardiomegaly is unusual.
The Jarisch Herxheimer reaction is a recognized complication of antimicrobial treatment of spirochaetal infections. Lysed bacteria releasel LPS, triggering release of cytokines including tumour necrosis factor- and iL-6 & 8. Antibiotics, including tetracyclines, -lactams and cephalosporins trigger LPS release from bacteria. LPS induces NO mediated vasodilation resulting in systemic hypotension. LPS can also induce pulmonary hypertension.
Conclusion:
Leptospirosis is relatively uncommon condition in this part of Orissa; Milder cases are underdiagnosed.
It is not possible to predict which patients might develop a Jarisch Herxhemier reaction after starting treatment. Physicians should know that this reaction can include systemic gypotension. And acute pulmonary edema and that most patients recover fully with appropriate supportive therapy.
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