In this study, the efficacies of chemotherapy employing nitazoxanide (NTZ), albendazole (ABZ), and a NTZ/ABZ-combination against alveolar echinococcosis (AE) were investigated in an experimental murine model. Following secondary infection, meaning i.p. injection of 20 Echinococcus multilocularis metacestodes, the drugs were administered by intragastric inoculation on a daily bases for a period of 5 weeks. Treatment was started either immediately on the day of infection, or at 2 months p.i., respectively. Application of the NTZ/ABZ-combination starting at 2 months p.i. was proven to be most effective in terms of reducing parasite weight (from 4.42+/-1.03 to 1+/-0.05 g; P=0.01). Inspection of treated parasites by transmission electron microscopy showed that ABZ- and NTZ-treated metacestode tissues, respectively, were heterogeneous in that both largely intact parasites as well as severely altered metacestodes could be observed. NTZ/ABZ-combination treatment induced the most severe ultrastructural alterations, including massive reduction in length and number of microtriches, severely damaged tegumental architecture, and progressive loss of viability of the germinal layer, associated with encapsulation by host connective tissue. A comparative pharmacokinetic study in mice revealed that the application of ABZ and NTZ in combination resulted in a two- to four-fold increase of albendazole sulfoxide serum levels for the period of 4-8 h following drug uptake compared to application of ABZ alone. In a third experiment, mice were orally infected with E. multilocularis eggs, and treated with NTZ starting at 2 months p.i. This resulted in a significantly lower lesion number in treated versus untreated mice (P=0.01). This investigation indicates the potential value for NTZ and/or a combined ABZ/NTZ chemotherapy against AE.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ijpara.2004.01.006DOI Listing

Publication Analysis

Top Keywords

alveolar echinococcosis
8
starting months
8
application abz
8
secondary primary
4
primary murine
4
murine alveolar
4
echinococcosis combined
4
combined albendazole/nitazoxanide
4
albendazole/nitazoxanide chemotherapy
4
chemotherapy exhibits
4

Similar Publications

Alveolar echinococcosis (AE) is a serious parasitic infectious disease that is highly invasive and destructive to the liver and has a high mortality rate. However, currently, there is no effective targeted imaging and treatment method for the precise detection and therapy of AE. We proposed a new two-step targeting strategy (TSTS) for AE based on poly(lactic--glycolic acid) (PLGA).

View Article and Find Full Text PDF

Cystic and alveolar echinococcosis are severe zoonotic diseases characterized by long asymptomatic periods lasting months or years. Viable Echinococcus spp. eggs released into the environment through the feces of canids can infect humans through accidental ingestion via hand-to-mouth contact or consumption of contaminated food or water.

View Article and Find Full Text PDF

The first case of alveolar echinococcosis from southern Croatia: progressive course of the disease in an immunocompromised patient.

Germs

September 2024

MD, PhD, Infectious Diseases Department, University Hospital of Split, HR-21000 Split, Croatia, and University of Split School of Medicine, HR-21000 Split, Croatia, and University Department of Health Studies of the University of Split, HR-21000 Split, Croatia.

Introduction: Alveolar echinococcosis is one of the most pathogenic zoonoses caused by the larval forms of . It is endemic in central Europe, but from 2001 to 2018, eight European countries reported their first cases of alveolar echinococcosis. These numbers testify to unprecedented spread of the infection.

View Article and Find Full Text PDF

Inhibition of the MyD88 signaling pathway could upregulates Ghrelin expression to synergistically regulate hepatic -infected progression.

Front Immunol

January 2025

State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.

Introduction: AE and whether the inhibition of the MyD88 inflammatory pathway can enhance Ghrelin expression to collaboratively modulate AE progression remains unclear.

Methods: In this study, we evaluated Ghrelin serum levels and changes in TLR4/MyD88/NF-κB pathway proteins and inflammatory factors in AE patients and mouse models at different stages of infection (-4, -8, and -12 weeks). Additionally, we administered the MyD88 inhibitor TJ-M2010-5 intraperitoneally to infected mice to evaluate alterations in inflammation and Ghrelin levels, as well as disease progression.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!