Human Fascioliasis (Liver Fluke Disease) in Hawai'i: Case Report and Review of Human Fascioliasis Acquired in the United States.

Fascioliasis is a foodborne zoonotic infection caused by the trematode liver flukes: Fasciola hepatica and Fasciola gigantica (F. gigantica). Infections may cause acute and chronic hepatobiliary tract diseases in herbivore animals and humans. Fascioliasis is present worldwide, particularly in regions where sheep and cattle are raised. The global burden of human fascioliasis is estimated to be 2.7 million. Human infections are rare in the United States, and most infections were acquired abroad. In the 1950s, several human cases of F. gigantica infection were reported from Hawai'i, but no subsequent cases have been reported until the case described here. This case report describes a man from Hawai'i Island who ate raw wild watercress, and 22 days later, developed acute phase fascioliasis with fever, acute hepatitis, peripheral eosinophilia, and hypodense lesions seen on liver diagnostic imaging. Immunodiagnostic tests were positive for Fasciola species. Based on earlier reports from Hawai'i, F. gigantica infection was likely. Clinical abnormalities resolved after treatment with triclabendazole. Physicians should consider fascioliasis in immigrants and travelers from endemic areas with acute hepatitis and eosinophilia after eating raw wild watercress or chronic hepatobiliary disease. Hepatobiliary imaging and serological testing are useful for diagnosis. Oral triclabendazole is the preferred treatment. Animal fascioliasis appears to be spreading in the United States, and the popularly perceived health benefits of eating raw wild watercress and other aquatic plants may lead to more human infections. The rarity of human infections in Hawai'i suggests that it is safe to eat commercially grown watercress cultivated in Hawai'i.

Human Strongyloidiasis in Hawaii: A Retrospective Review of Enzyme-Linked Immunosorbent Assay Serodiagnostic Testing.

Human strongyloidiasis is widely prevalent in tropical and subtropical regions worldwide but is not endemic in Hawaii. Subclinical, chronic infections may be lifelong; immunosuppressive therapy, particularly with glucocorticoids, may lead to serious or fatal disseminated disease, which is preventable. We performed a retrospective analysis of patients tested for Strongyloides immunoglobulin G antibody in an academic medical center in Honolulu, Hawaii, from 2005 to 2012. Of the 475 patients tested, 78 (16%) were seropositive. The largest proportion of seropositive cases was found among Micronesians (30%), Polynesians (26%), Filipinos (13%), and Southeast Asians (11%). Among the seropositive patients, the most likely reason for clinicians to order testing was blood eosinophilia. Stool parasite examination results were available for 58% of seropositive patients of which 11% were positive for Strongyloides stercoralis larvae. Antihelminthic therapy, usually ivermectin, was ordered for 71% of patients. After treatment, blood eosinophilia and Strongyloides serology results were reassessed for 76% and 35% of patients, respectively; both tests tended to show improvement. Travelers and immigrants from Strongyloides-endemic areas, including Micronesia and Polynesia, should have serodiagnostic testing for latent strongyloidiasis, and if positive, treated empirically with ivermectin, particularly when corticosteroids or other immunosuppressive therapies are anticipated.

Hepatosplenic schistosomiasis presenting as spontaneous hemoperitoneum in a Filipino immigrant.

Hepatosplenic schistosomiasis is due to chronic parasitic trematode infections with various Schistosoma sp. The Schistosoma life cycle requires contamination of surface water by infected human or animal excreta, specific freshwater snail intermediate hosts and human skin contact with water. The disease is prevalent in many developing tropical areas, particularly in sub-Saharan Africa as well as in Southeast Asia. Deposition of Schistosoma eggs in the hepatic portal system leads to periportal fibrosis, cirrhosis and portal hypertension but little hepatocellular damage. Portal hypertension of any etiology may cause gastrointestinal varices. Rarely, ectopic varices may rupture into the peritoneal cavity and result in a hemoperitoneum. The authors describe a case of a Filipino immigrant who presented with a hemoperitoneum associated with previously unrecognized hepatosplenic schistosomiasis due to Schistosoma japonicum.

Pararenal splenosis encountered during the evaluation of a suspected pheochromocytoma.

The authors describe a patient in whom pararenal splenosis nodules were initially interpreted as probable pheochromocytoma. A 22-year-old man with chronic glomerulonephritis, hypertension and a childhood history of splenectomy was hospitalized for a hypertensive emergency. He did not improve with aggressive antihypertensive therapy. A pheochromocytoma was suspected, and a renal ultrasound and a magnetic resonance imaging showed 2 left pararenal masses. Laboratory evaluation for pheochromocytoma and aldosteronoma were negative. Biopsies of the masses were planned, but the masses were subsequently shown to be splenic tissue by a (99m)technnetium heat-damaged red blood cell scan. Ectopic splenic masses, eg, splenosis or accessory spleens, should be considered in patients with undiagnosed abdominal or kidney masses and a history of splenectomy.

Thyrotoxic periodic paralysis in a Polynesian male following highly active antiretroviral therapy for HIV infection.

Hyperthyroidism has been described after highly active antiretroviral therapy for AIDS and has been attributed to late onset immune reconstitution. The team reports a young Polynesian man with AIDS who responded to highly active antiretroviraltherapy. However, 15 months after initiation of antiretroviral therapy, he was hospitalized for hypokalemic thyrotoxic periodic paralysis, an unusual manifestation of hyperthyroidism which typically occurs in young Asian males.

Leptospirosis misdiagnosed as pulmonary-renal syndrome.

A case of leptospirosis complicated by diffuse alveolar hemorrhage, acute renal failure, and apparent hemoglobinuria was initially diagnosed and managed as a pulmonary-renal syndrome. However, renal biopsy findings were normal. Leptospirosis may manifest with severe lung injury characterized by diffuse alveolar hemorrhage, acute respiratory distress syndrome, and acute renal failure and be accompanied by high mortality rates. Leptospirosis should be considered in patients with features of pulmonary-renal syndrome, particularly in regions known to be endemic for leptospirosis. A history of potential exposure to Leptospira is an important diagnostic clue, and empiric antimicrobial therapy should be considered.