Mechanisms of Immunity in Hydatid Disease: Implications for Vaccine Development

Abstract

The Echinococcus organisms, the cause of echinococcosis (hydatid disease), are parasitic helminths with life cycles involving a carnivorous definitive host (usually dog or fox) and an intermediate host (human, ungulate, or rodent). They are complex multicellular pathogens that, despite being under constant barrage by the immune system, are able to modulate antiparasite immune responses and persist and flourish in their mammalian hosts. Understanding how the immune system deals with these parasites is a major challenge. Recent application of modern molecular and immunological approaches has revealed insights on the nature of immune responses generated during the course of hydatid infection, although many aspects of the Echinococcus-host interplay remain unexplored. This review summarizes current understanding of the immunology of echinococcosis, indicates areas where information is lacking, and shows how knowledge of host protective immunity has been translated into the design and development of anti-Echinococcus vaccines for application in intermediate hosts.

Primary spinal hydatid cyst in a patient with acquired immunodeficiency syndrome

“…Th1 and Th2 cell activation and the expression of immunoglobulin isotypes such as IgE and IgG occur at different stages of the infection and define progression of the disease and the clinical outcomes [15,16]. Failure of humoral and cellular immunity and severe immunodeficiency to antigens are seen during the AIDS course [17].…”

Efficiency Evaluation of Immunization Protocol with Echinococcus Granulosus Antigen B (Agb)

“…Consistently, a shift in the cytokine response toward a type 1expression pattern in humans or mice reduces parasite growth [32].Hence, blocking those antigens responsible for inducing host Th2 cell responses and vaccination antigens inducing a Th1cell response may be an important pointer for future vaccine design, should be necessary [33]. Zhang and McManus [34] stated that when a cyst dies naturally, is killed by chemotherapy treatment or is removed by surgery, Th2 responses drop rapidly and Th1 responses become dominant.…”

Hydatid cyst formation in male Balb/c mice following the intraperitoneal injection of live protoscoleces and activated oncospheres: a comparative study

“…Echinococcus metacestodes in suitable intermediate host are characterized by rapid growth and profuse production of protoscoleces, whereas in less suitable species growth is delayed and protoscoleces formation is impaired or absent (Zak and Sande 1999). Even different strains of mice infected with eggs, hatched eggs, or activated oncospheres of E. granulosus showed differences in susceptibility/resistance (Zhang et al 2008). In an experimental infection, CF1 white mice were infected orally with E. granulosus eggs, 66 % of mice became infected.…”

“…The factors involved in innate susceptibility/resistance (s/r) to Echinococcus infections are largely unknown. Different strains of mice which were infected with eggs, hatched eggs, or activated oncospheres of E. granulosus showed differences in s/r (Zhang et al 2008). Since Balb/c mice is a suitable experimental model for cystic echinococcosis (Rahimi et al 2011), the aim of this study was to evaluate and compare the infection rate of cyst formation in male Balb/c mice following the intraperitoneal injection of live protoscoleces and activated oncospheres.…”