Around 25% of the global population suffer from one or more parasitic infections, of which food and vector-borne parasitic zoonotic diseases are the major concern. Additionally, in recent years, zoonoses and communicable diseases common to man and animals have gained increasing attention worldwide. Great changes in the climatic conditions, cropping pattern, demography and food habits, increasing international travels, marketing and trades, deforestation and urbanization play vital roles in the emergence and re-emergence of parasitic zoonoses. Although, underestimated, however, collected burden of food and vector-borne parasitic diseases is attributed to ~60 million Disability Adjusted Life Years (DALYs). Of the 20 Neglected Tropical Diseases (NTDs) listed by World Health Organization (WHO) and Centres for Disease Control and Prevention (CDC), 13 diseases are of parasitic origin. Besides, there are about 200 zoonotic diseases where WHO enlisted eight diseases as Neglected Zoonotic Diseases (NZDs) in the year 2013, of them four diseases namely cysticercosis, hydatidosis, leishmaniasis and trypanosomiasis are caused by the parasite. In this review, we discussed global burden and impacts of food and vector-borne zoonotic parasitic diseases.

Ticks are notorious blood-sucking ectoparasites affecting both humans and animals, and serve as a unique vector of various deadly diseases. Ticks are pool feeder and extensive tissue damage is a common feature in hosts’ skin during their feeding. Here, we have elegantly shown the roles of the receptor for advanced glycation end-products (RAGE) during repeated tick infestations. Initially (day1), ticks attached hypostome into the skin making a notch on the epidermis associated with cellular damage and infiltrations, and there were no hemorrhagic changes. In advanced stages (day5), a large blood pool developed, which was flooded with blood (RBC). The hemorrhagic zone was surrounded by the presence of inflammatory cells. Very few inflammatory cells were detected around the zone of hemorrhage in the primary infestation. In the primary infestation, we found very few eosinophils up to day4 of feeding. At day5 of post attachment, eosinophil infiltration a little bit increased at the periphery of blood pool. Infiltrations of inflammatory cells increased in the subsequent infestations and reached to the highest level in the 3 rd infestation in wild type (wt) mice, but not in RAGE-/- mice, which was comparable to the non-infested control mouse skin. RAGE was highly expressed in the 3 rd infestation in wt mice. Interestingly, in the tertiary infestation, infiltration of innate lymphoid cells type 2 (ILC2s), expression of S100A8 and S100B, and peripheral eosinophil counts significantly increased at the biting sites of ticks in wt, but not in RAGE -/- mice. Taken together, our study revealed that RAGE-mediated inflammation and eosinophils played crucial roles in the tick induced inflammatory reactions.

Abstract Ticks are notorious blood-sucking ectoparasites affecting both humans and animals, and serve as a unique vector of various deadly diseases. Here, we have shown the roles of the receptor for advanced glycation end-products (RAGE) during repeated infestations by the tick, Haemaphysalis longicornis using RAGE-/- mice. In primary infestation, a large blood pool developed which was flooded with numerous RBC, especially during the rapid feeding phase of the tick both in wild type (wt) and RAGE-/- mice. Very few inflammatory cells were detected around the zones of hemorrhage in the primary infestations. However, number of inflammatory cells gradually increased in the subsequent tick infestations and at the 3 rd infestations number of inflammatory cells reached to the highest level (350.3±16.8 cells/focus), and the site of attachment was totally occupied by the inflammatory cells in wild type (wt) mice whereas very few cells were detected at the ticks’ biting sites in RAGE-/- mice. RAGE was highly expressed in the 3 rd infestation in wt mice. In the 3 rd infestation, infiltration of innate lymphoid cells type 2 (ILC2s), expression of S100A8 and S100B significantly increased at the biting sites of ticks in wt, but not in RAGE -/- mice. Also, peripheral eosinophil counts significantly increased in wt but not in RAGE -/- mice. Taken together, our study revealed that RAGE-mediated inflammation and eosinophils played crucial roles in the tick induced inflammatory reactions.

Ascaridia galli is the largest gut-dwelling helminth of chickens which confers adverse effects on meat and egg production and thus, on the animal protein supply and the economy. Both adult and immature parasites affect the gut health, but larval stages play the major role in pathology. The larvae cause excessive mucus production, damage to the intestinal gland, hemorrhage, anemia, diarrhea, and malnutrition. The adult worms can cause death by intestinal obstruction and intussusception. Although both cellular and humoral immunity are involved in fighting against ascaridiasis, the role of naturally acquired immunity is poorly defined. In cellular immunity, Th-2 cytokines (IL-4, IL-5, IL-9 and IL-13), goblet cells (mucin), GALTs (gut -associated lymphoid tissues), CD8α+ intraepithelial cells, TCRγδ+T cells, and TGF-β4 form a protective band. Type 2 immunity provides protection by forming a network of eDAMP (endogenous damage-associated molecular pattern), chitin, and parasitic antigens. Among antibodies, IgY is the most prominent in chickens and provides temporary humoral protection. During parasitic infection, infiltration of various immune cells is evident, especially in the intestinal epithelium, lamina propria, and crypts of the duodenum and jejunum. In chickens older than 3 months, gradual reduction of worm burden is more successful. Female chickens exert a short-lived but higher level of protection by passing IgY to chicks in the form of egg yolk antibodies (EAB). In laying condition, immunity differs greatly between breeds. This review provides a good overview of the silent but inevitable pathological changes induced by A. galli; and the interaction of host immunity with the parasite.