JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
A CASE OF GANCICLOVIR-RESISTANT CMV IN A DONOR NEGATIVE/RECIPIENT NEGATIVE LIVER TRANSPLANT PATIENT
LEPTOSPIROSIS: A CAUSE OF SOUTH AMERICAN TROPICAL FEBRILE INFECTION
G. Handley, MD; C. McIntyre, MD; D. Kitchell, MD Department of Medicine, Ochsner Medical Center, New Orleans, LA
S. Igbinedion, MD; K. Patel, MD; H. Samant, MD Department of Medicine, LSU Health Sciences Center-Shreveport
Introduction: Worldwide incidence of leptospirosis stands at over 1 million cases per year, typically from tropical climates. Outbreaks occur after heavy rainfall or flooding. Additional risk factors include immersion or consumption of contaminated water. While usually asymptomatic, 90% of clinical infections present as a self-limiting febrile illness. Initial symptoms include severe headache, chills, myalgia, nausea, vomiting, diarrhea, abdominal pain, and cough. Conjunctival suffusion is characteristic, but not always present, while the skin rash seen in other tropical febrile infections is rare. Case: A 36-year-old man from the United States presented with fevers, night sweats, chills, severe headache, paresthesias, diffuse symmetric arthralgias, myalgias and auditory hallucinations after a 4-day hike along the coast near Mendellin, Colombia. Activities included hostel stays, camping, freshwater swimming, mosquito bites, and ingestion of water from local sources purified by commercial tablets. He received yellow fever and typhoid vaccinations prior to departure, and took atovaquone/proguanil malaria prophylaxis. Conjunctival suffusion and skin rashes were absent. Initial lab work revealed hemoglobin 13.5, platelets 108, ALT 72. Ultrasound revealed mild hepatosplenomegaly. Serological studies for HIV, Dengue, Zika, and Chikungunya were non-reactive, and no Malaria parasites were seen on thick and thin smears. Leptospira IgM antibodies returned positive and a 7 day course of oral doxycycline was prescribed. Discussion: Though occurring in only 10% of clinical illness, progression to the second or immune phase of Leptospirosis can include renal and liver failure, known as Weil Disease, with case- fatality ratioapproaching5-15%. Apulmonaryhemorrhagic form exists with case-fatality ratio > 50%. Because leptospirosis often presents as a biphasic illness after a temporary improvement in fever and symptoms, early detection and treatment remains critical. Doxycycline is the drug of choice, but alternatives include ampicillin or amoxicillin. Severe cases require penicillin 1.5MU IV every 6 hours or IV ceftriaxone. Exposure avoidance remains themainstay for prevention. Thoughnot recommended, chemoprophylaxis with doxycycline 200mg weekly may prevent clinical disease in short-term exposures. Physicians should recognize leptospirosis as a cause of tropical febrile illness to prevent progression to more severe disease.
Introduction: Cytomegalovirus (CMV) disease in liver transplant patients with donor-seronegative and recipient seronegative (D-/R-) status is a rarity. Ganciclovir-resistant CMV disease in this population is even much rarer and has never been reported. Case: A 62-year-old man with a past medical history of cirrhosis secondary to hepatitis C with complications of slight ascites and grade 2 esophageal varices s/p banding underwent orthotopic liver transplant from a cadaveric donor. The patient had a donor-seronegative and recipient-seronegative (CMV D-/R-) status. He was on tacrolimus, mycophenolate, prednisone and valganciclovir therapy. The patient completed valganciclovir therapy 90 days after transplant. Patient presented 4 months after transplant with a history of acute diarrhea ongoing for a week. Physical exam revealed non-thrombosed external hemorrhoids. Labs showed a white cell count of 9.3, baseline hemoglobin of 11.1 g/dl, potassium 4.4 mmol/L, and significant rise in creatinine from 0.91 to 2.8 mg/dl, AST 311, ALT 521, Alkaline phosphatase 290, Total Bilirubin 0.4 mg/dl. The patient tested negative for Clostridium difficile infection. CMV DNA quantitative pattern returned positive at 14,900 IU/ml. Flexible sigmoidoscopy showed erythematous mucosa in the sigmoid colon, no ulcers seen. Biopsies obtained revealed increase in inflammatory cells within the lamina propria, minimal neutrophilic inflammation, apoptotic debris and occasional viral inclusions within endothelial and fibroblast cells within the lamina propria. Immunohistochemical stain for CMV returned positive. These findings correlated with a diagnosis of CMV colitis. Liver biopsy was negative for CMV hepatitis. Genotype studies showed mutations in CMV UL 97 and resistance to ganciclovir indicative of infection with ganciclovir-resistant (GanR) CMV. The patient was started on IV Foscarnet. Repeat follow-up after a month showed patient with CMV PCR negative status with normalization of liver enzymes. Discussion: Toourknowledge, therehasbeennodocumentation of a case of GanR CMV in the CMV D-/R- population. Our case of Ganciclovir-resistant CMV in this population is the first documented. This presentation should alert gastroenterologists about the danger of the liberal use of CMV prophylaxis in the CMV D-/R- population
J La State Med Soc VOL 170 MARCH/APRIL 2018 59
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