ABSTRACT
Although other hantaviruses are associated with renal manifestations, hantavirus cardiopulmonary syndrome (HCPS) has not been associated with such sequelae. The HCPS survivors were prospectively evaluated for renal complications. Subjects underwent yearly evaluation, laboratory studies, and 24-hour urine collection. Thirty subjects were evaluated after recovery from HCPS with the first follow-up at a median of 7.4 months after discharge. Subjects were a wide age range (18-51) but had an equal gender composition. Eighteen of 30 (60%) returned for > 1 evaluation. Half (15/30) had a 24-hour urine collection with > 150 mg of total protein and 6 had > 300 mg. Seven had a Cockcroft-Gault creatinine clearance (CrClCG) < 90 mL/min/1.73 m2 and 2 were < 60. Fifty-three percent met the definition of chronic kidney disease. Those treated with extracorporeal membrane oxygenation had less renal sequelae (P = 0.035). Our data suggest that renal sequelae may occur in HCPS. Further study of renal complications of New World hantavirus infections are needed.
Subject(s)
Hantavirus Pulmonary Syndrome/complications , Kidney Diseases/diagnosis , Kidney Diseases/etiology , Adolescent , Adult , Chronic Disease , Extracorporeal Membrane Oxygenation , Female , Orthohantavirus/pathogenicity , Hantavirus Pulmonary Syndrome/virology , Humans , Kidney/pathology , Male , Middle Aged , Severity of Illness Index , Young AdultABSTRACT
West Nile virus (WNV) myocarditis has been documented pathologically in birds and mammals but has rarely been reported in human clinical syndromes. We describe myocarditis associated with WNV.
Subject(s)
Myocarditis/virology , West Nile Fever/diagnosis , Aged , Animal Diseases , Animals , Birds/virology , Humans , Male , Mammals/virology , Myocarditis/veterinaryABSTRACT
Since 1999, there have been nearly 20,000 cases of confirmed symptomatic West Nile virus (WNV) infection in the United States, and it is likely that more than 1 million people have been infected by the virus. WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will likely remain an important cause of neurological disease for the foreseeable future. Clinical syndromes produced by WNV infection include asymptomatic infection, West Nile Fever, and West Nile neuroinvasive disease (WNND). WNND includes syndromes of meningitis, encephalitis, and acute flaccid paralysis/poliomyelitis. The clinical, laboratory, and diagnostic features of these syndromes are reviewed here. Many patients with WNND have normal neuroimaging studies, but abnormalities may be present in areas including the basal ganglia, thalamus, cerebellum, and brainstem. Cerebrospinal fluid invariably shows a pleocytosis, with a predominance of neutrophils in up to half the patients. Diagnosis of WNND depends predominantly on demonstration of WNV-specific IgM antibodies in cerebrospinal fluid. Recent studies suggest that some WNV-infected patients have persistent WNV IgM serum and/or cerebrospinal fluid antibody responses, and this may require revision of current serodiagnostic criteria. Although there is no proven therapy for WNND, several vaccines and antiviral therapy with antibodies, antisense oligonucleotides, and interferon preparations are currently undergoing human clinical trials. Recovery from neurological sequelae of WNV infection including cognitive deficits and weakness may be prolonged and incomplete.
