Regression of alveolar echinococcosis after chronic viral hepatitis C treatment with pegylated interferon alpha 2a

Abstract

We present a case of 53 years old patient with transplanted kidney, chronic hepatitis C and alveolar echinococcosis who was treated with pegylated interferon α which resulted in regression and calcification of Echinococcus multilocularis loculi. Patient had been diagnosed with chronic hepatitis C two years after kidney transplantation. Hepatitis was left untreated because of immunosuppressive treatment and satisfactory graft function. Nine years after transplantation the patient was diagnosed with alveolar echinococcosis and treated with mebendazole 2 × 200 mg daily for 6 months. Cessation of temporary treatment resulted in echinococcosis progression with appearance of secondary loculi and a small ascites after which mebendazole was restarted. Ten years after transplantation, kidney graft failure occurred and the patient was started on hemodialysis in conjunction with pegylated-interferon alpha 2a for treatment of chronic viral hepatitis C. Complete early viral response was observed 3 months after therapy initiation while a follow-up CT scan after 4 months did not document any changes in the number or size of E. multilocularis loculi. A completed course of antiviral therapy resulted in sustained viral response while a subsequent second follow-up CT scan 6 months after cessation of antiviral therapy documented regression and calcification of main E. multilocularis loculi along with resolution of secondary loculi and ascites.

EmTIP, a T-Cell Immunomodulatory Protein Secreted by the Tapeworm Echinococcus multilocularis Is Important for Early Metacestode Development

“…This general picture is supported by previous studies which compellingly showed that the resistance of murine [11] – [13] or human [14] , [15] hosts to E. multilocularis metacestodes is associated with a Th1-dominated immune response whereas a Th2-dominated immune response occurs as E. multilocularis metacestodes thrive in these murine [16] , [17] or human [15] , [18] , [19] hosts. In agreement with a parasitocidal role for Th1 responses during AE, administration of Th1-inducing immune-stimulants like Bacillus Calmette–Guérin (BCG) [20] – [23] , IL-12 [13] , IFN-α-2a [11] , [24] and IFN-γ [25] , [26] have all been shown to restrain parasite establishment, proliferation or dissemination in rodents experimentally infected with E. multilocularis larvae. Conversely, Th2-dominated immune responses have been tightly associated with progressive forms of AE both in humans [15] , [19] and mice [16] , [17] with compelling evidence pointing at an underlying expansion of regulatory T-cells [27] , [28] .…”

Diagnostics of Echinococcus granulosus particles in hepatic cysts punctate of seropositive patients

“…In human medicine, infection with three species of tapeworm presents a significant health problem: E. granulosus, with dogs and some other canids as definitive hosts and humans, sheep, goats, cattle, pigs and horses as intermediate hosts and carriers of larval stage (Markell et al, 2000). Other form is alveolar echinococcosis caused by E. multilocularis, with foxes, dogs and catsas definive hosts, small rodents as intermediate hosts and humans as intermediate (accidental) hosts (Dražilová et al, 2012) These two forms are of special importance due to wide distribution and serious medical and economic impact. Third form, polycystic echinococcosis caused mainly by E. vogeli, with bush dogs and dogs as definitive hosts, rodents as intermediate hosts and man and other mammals as accidental hosts is less frequent and restricted to Central and South America (Neva et al, 1994.;Garcia, 2007).…”