Title : Is plasmapheresis the future treatment for Leptospirosis? Case report of a 75-year-old patient with complete recovery after plasmapheresis therapy
Abstract:
Leptospirosis is a zoonotic disease produced by spirochetes of Leptospira, with an incidence ten times higher in tropical regions like Puerto Rico, in comparison to the rest of the world. The principal reservoir are rats, dogs, cats and farm animals with excreted infected urine, contaminated soil or water that produces the disease through direct contact of broken skin, mucosa or conjunctivas. During the first infective phase, Leptospira are found in blood and cerebrospinal fluid and the course is asymptomatic, followed by an immune phase where Leptospira are excreted in the urine. Ten percent or less progress to septic shock and multi-organ dysfunction (Weil’s Disease) presenting with acute kidney injury, pulmonary hemorrhage, acute respiratory distress syndrome (ARDS), bleeding diathesis, impaired hepatic functions, jaundice, thrombocytopenia, circulatory collapse or even death. This is the case of 75-year-old female with major depressive disorder with psychotic features, who arrived with fever of 400 C, decreased appetite and lower extremities myositis, who practiced daily farming and rose gardening and had direct contact with horses, cats, dogs and recently found dead animals. Upon admission, the patient was acutely ill, awake, alert, oriented and was tachycardic, with a blood pressure of 84/50 mm Hg, and a negative Tourniquet test. Within 24 hours, marked deterioration was noted and she was admitted to intensive care unit (ICU) for suspected leptospirosis and viral syndrome. Acute kidney injury (AKI), sepsis, leukocytosis of 14,500 10^3/uL, moderate thrombocytopenia, elevated transaminases, hyperbilirubinemia, severe dehydration, and moderate hyponatremia developed, therefore empiric intravenous antibiotic was started. After four hours in the ICU, she was intubated and thirty six hours later developed ARDS and pulmonary hemorrhage. Jaundice, increased leukocytosis of 24.5K, severe thrombocytopenia of 29K, elevated liver enzymes and AKI stage 3 were present, therefore hemodialysis was started. By day eleven Leptospira DNA PCR was confirmed. During hospitalization, a total of seven plasmapheresis, six hemodialysis, one fresh frozen plasma, seven platelet transfusions, and three packed red blood cell transfusions were given. By day ten, after clinical and renal improvement the patient was extubated successfully. Plasma exchange may interrupt the mechanisms causing tissue damage in severe sepsis. Renal injury in leptospirosis might be caused by activation of toll-like receptors (TLR) 2 and 4 by lipopolysaccharides (LPS) causing interstitial edema and a tubulointerstitial nephritis with cellular infiltrate. Also, lung injury is thought to be induced by deposition of IgM, IgA, IgG and C3 in the alveolus. The outer membrane of Leptospira shares characteristicsof both Gram-positive and Gram-negative bacteria and the binding of LPS to TLR4 on the surface of B lymphocytes results in the activation of B-cells and the production of IgM against the LPS of Leptospira. Activation of B-cells and T-cells, which promote the killing of Leptospira, also produces pro-inflammatory cytokines and tissue inflammation. Plasma exchange may prevent immune complex-mediated tissue injury. As a result, anytime a patient with septic shock and multi-organ failure with a history of dead animals or suspected infected water contact is revealed, leptospirosis should be considered, and plasma exchange could be the preferred therapy.
