For a fungal pathogen to successfully infect, colonize and spread inside a susceptible host, it must have overcome the host immune responses. The early recognition of the fungal pathogen-associated molecular patterns (PAMPS) by the host’s pattern recognition receptors (PRRs) results in the establishment of anti-fungal immunity. Although, our immune system has evolved several processes to combat these pathogens both at the innate and adaptive immune levels. These organisms have developed various escape strategies to evade the recognition by the host\'s innate immune components and thus interfering with host immune mechanisms. In this chapter, we will summarize the major PRRs involved in sensing fungal PAMPS and most importantly the fungal tactics to escape the host\'s innate immune surveillance and protective mechanisms.
Part of the book: Fungal Reproduction and Growth
Anthelmintic, ectoparasiticides (insecticides, acaricides), and antiprotozoal chemotherapeutic drugs target parasites. Chenopodium oil like alkaloids, arsenic compounds, cupric sulfate, nicotine, and cupric silicate were used to destroy nematodes. Unfortunately, these chemicals were less effective and less safe for livestock. The four major groups of broad-spectrum antinematodal compounds are macrocyclic lactones such as milbemycins/ivermectin, benzimidazole/pro-benzimidazole, tetrahydro pyrimidines such as morantel, pyrantel tartrate, and imidazothiazoles such as tetramisole and levamisole. The various factors responsible for gastrointestinal (GI) parasitism make it difficult to develop effective control measures, to the best of our knowledge. Hence, an effective strategy for the control of parasitic diseases that do not solely rely on anthelmintic therapies needs to be developed at the regional level, based on the epidemiology of the disease. This book chapter aims to elaborate on the various other ways to control parasitic diseases due to Anthelmintic drug resistance.
Part of the book: Parasitic Helminths and Zoonoses