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Individuals live in different areas where different type of parasites are present either they are intestinal, blood, nervous system parasites and many other. And for all these parasites any other living organism is the main source for their survival because as it definition defines parasites completely relay on their hosts and at the same time they damage their host to adjust in the environment of different hosts and to process their different functions for the survival therefore host immunity responses are generated against those parasites to evade them and to get rid from that parasite. There specific parasites will be discussed along their host responses which includes intestinal parasite- Intestinal protozoans and helminths are the main agents to cause intestinal infections like Against all these parasites host activates its innate and adaptive immunity to evade them but in mostly parasitic infections eosinophils are get activated in a host body.


A life form that lives or relies upon its host and gets all the food and shelter through that host called parasites. Others create, reproduce, or assault organ structures that make their hosts weak, and causes distinctive parasitic infections. The three most regularly known classes of parasites which as a rule includes in the infection development in people, for example, Protozoa, Helminths, and Arthropodes.

? PROTOZOA: It includes,
• Entamoeba
• Giardia, Leishmania
• Balantidium
• Plasmodium

? HELMINTHS: It includes,

• Platyhelminths
• Acanthocephalins
• Nematodes
• Annelids

? ARTHROPODES: It includes the blood sucking arthropodes.

• Mosquitoes
• Ticks
• Lice
• Mites

There are specific parasites will be discussed along their invasion ways and host immunity responses, they are, Intestinal parasites, Blood parasites and Central Nervous System parasites with host responses to evade them.

Intestinal protozoans and helminths are the main agents to cause intestinal infections. Gastrointestinal infections are mostly caused by protozoan parasites as compare to helminths. Helminths contains multiple cells. There are some other important helminth parasites that usually possess in human gut, these are Cestodes, Nematodes and Trematodes… (2)
Giardia intestinalis which causes giardiasis, Entamoeba histolytica which causes amoebiasis and Cryptosporidium which causes cryptosporidiosis and are correlated to diarrhea… (3)


Entamoeba histolytica
Eh has a two-stage life cycle: it can make due as an infective cyst in environment or found as trophozoites, the nourishing and tissue abiding stage in the human colon. After excystation in the colon, Eh trophozoites for the most part sets up innocuous colonization where the parasites dwell in the gut lumen and feast upon enteric organisms by phagocytosis. Trophozoites can transform into invasive form, where parasite harmfulness factors enable it to corrupt colonic mucin and other innate epithelial barriers. Host immunity, against intrusive Eh yet at the same time this parasite can get by creating resistant avoidance procedures. Specifically, Eh cysteine proteases can cut MUC2 mucin repealing its defensive capacities enabling the parasite to break the mucus layer and connect to the basic epithelial cells. Intestinal antimicrobial peptides are likewise a vital segment of host innate immunity. Eh becomes resistant to both in place and separated antimicrobial cathelicidins in the digestive system. After amebic attack, neutrophils are the soonest in?ltrating cells however destructive Eh are e?ective in murdering, lysing, and phagocytosing neutrophils. Eh can detoxify ROS by producing H2O2. Eh trophozoites can shield themselves from neutrophil responsive oxygen properties with a 29-kDa surface protein, peroxiredoxin that has intense cancer prevention agent movement. Another immunosuppressive pentapeptide, monocyte locomotion inhibitory factor (MLIF) delivered by Eh… (5)

Evasion of Entamoeba histolytica
• Innate Immunity
Stomach HCL plays an important role through its capacity to murder acid sensitive microbes. Infective amebic cysts remains safe and survive through the acidic condition of the stomach. In the digestive tract, the following layer of natural immunity might be the mucus layer, which is thought to go about as a defensive layer, protecting E. histolytica from attacking intestinal epithelial cells (IECs). Mucin glycoproteins tie to and repress the Gal/GalNAc adherence lectin of the parasite. Trophozoites, in any case, can upset the bodily fluid layer and intestinal barrier by discharging cysteine proteases (CPs) and glycosidases to take into consideration infiltration of the colonic mucosa. Macrophages are the fundametal part in the host reaction against intestinal amebiasis. Macrophages are amebicidal after incitement with IFN-c or TNF-a. A few amebic antigens are known to activate these cells through example recognition receptors. Also, E. histolytica DNA can activates macrophages through connecting with TLR-9. Amebicidal function of macrophages is added to by the creation of nitric oxide (NO) from L-arginine, which is regulated by macrophage nitric oxide synthase. Inducible nitric oxide synthase (iNOS) to E. histolytica– initiated hepatocytic apoptosis, involving a basic part for NO in the host protection against amebiasis… (6)

The Gal/GalNAc lectin is the major amebic surface adhering particle and initiates the binding to the colonic mucus layer and sugar determinants on an assortment of host cells including epithelial cells. The Gal/GalNAc lectin contains the carbohydrate recognition domain (CRD) that results binding. Against E. histolytica, IgA antibodies against Gal/GalNAc lectin corresponded with assurance. Mucosal IgA coordinated at the CRD space was related with assurance of kids from E. histolytica contamination and illness. On the other hand, serum hostile to lectin IgG was not related with assurance, but rather was related with an expanded recurrence of new E. histolytica contaminations. Cell-interceded interferon gamma (IFN-c) seems to give security from amoebiasis through its capacity to initiate neutrophils and macrophages to murder the parasite.
Complement may act to protect from spreading of trophozoites and extra intestinal sickness. Once amebae activates the complement system, membrane attack complexes (MACs) shape and lyse the parasites. The parasite has no less than two strategies to oppose complement. Gal/GalNAc lectin, which shares arrangement closeness antigenic cross-reactivity with the MAC-inhibitory protein CD59, hinders the development of the C5b-9 complex, and therefore prevents lysis by MACs… (7)

Blood borne parasites are found in the bloodstream of a host body and that blood parasite further spreads to healthy person by an infected person through vectors. The blood parasitic diseases are caused by vector-borne Protozoa which includes Trypanosomes, Plasmodium, Babesia and Theileria. Plasmodium which causes malaria, Babesia which causes babesiosis, and Trypanosoma brucei causes African sleeping sickness. The blood parasites directly attack on red blood cells of a host body, causes anemia and other blood disorders, blood clotting, organ failure and death… (8)


Trypanosoma brucei
This parasitic protozoan completes their life cycle in to two hosts that is insect to human. At the time of their life cycle, the morphological and physiological characters of these parasites get changes to adjust in the environment of different hosts and to process their different functions for the survival. T. brucei, an extracellular and hemoflagellate which circulates in a bloodstream. The life cycle of this parasite requires a mammalian host (such as humans) and a blood-sucking insect (tsetse fly) for completion. In the mammalian host, T. brucei shows three distinct cell types: slender form, intermediate form, and stumpy forms. The slender form is the only cell type capable of division in the blood circulation of the mammalian host. However, it can be differentiated into the stumpy form via the intermediate form, using a number of mechanisms that are driven by both the host and the parasite itself. The stumpy form is the terminal stage of this parasite in the mammalian host and the only stage that can infect the insect vector thus, it is analogous to the terminally differentiated mammalian cell. Before infecting the insect host, the stumpy parasites arrest cell proliferation but will die if they are trapped in the mammalian host for a significant period… (9)


Evasion of Trypanosoma brucei

• Host Humoral Immunity

Trypanosomes instigate diseases with variable side effects relying upon the infective host, trypanosome species and serodeme. For the most part, trypanosomosis is portrayed by fever, iron deficiency, decreased profitability, and infertility and, if left untreated. The infected creatures display a progression of trypanosome waves communicating distinctive variable surface glycoproteins (VSG). The VSG qualities encode a group of proteins that show broad heterogeneity at the N ends, yet are genuinely comparable at the C ends. The C terminus is covalently bound to dimyristyl-phosphatidylinositol, which is responsible for anchoring it to the membrane… (10)
These parasites are evade by opsonization which is performed by macrophages. Despite the effectiveness of the anti-VSG-specific antibodies, complete elimination of trypanosomes is hampered by the rapid appearance of those with different variable surface antigens to which the host has not mounted an immune response. Due to over host immune response, the raised levels of IgM and IgG immunoglobulins happening in African trypanosomosis are particular to the tainting serodeme/strain in perspective of the way that contaminating trypanosomes can ingest 85-100% of the produced immunoglobulins. Counter acting agent reaction to non-VSG invariant antigens additionally happens amid trypanosome contamination. In spite of the fact that these reactions have no immediate connection to the control of parasitaemia, it has been demonstrated that a prevalent IgG reaction to a cysteine protease, warm stun protein (hsp 70/BIP) and enigmatic VSG epitope could be related with resilience to trypanosome disease. This would propose a part for invariant antigens in balancing the disease… (11)

• Host Cell Mediated Immunity
When the trypanosoma interacts with host body, trypanosome-actuated macrophages and T cells prompts up-direction of interferon-gamma (IFN?) discharge by CD8+ T cells with consequent concealment of interleukin-2R (IL-2R) articulation on both CD8+ and CD4+ T cells. This impact can be switched by a 40-45 kDa protein got from T. brucei. Erythrophagocytosis by the actuated macrophages might be a main consideration in the acceptance of extravascular sickliness. Moreover, macrophages create tumor putrefaction factor-alpha (TNF-?). The T cells deliver an assortment of cytokines which, when bound to particular cell surface receptors, adjust the development, separation or capacity of the receptor-bearing cells. IL-2 and IFN-? are discharged by the proliferative lymph hub cells amid disease. IFN-? is known to empower macrophage action and to advance surface articulation of significant histocompatibility complex (MHC) class I and II on different cell composes to evade blood parasites… (12)


Parasites those attack the central nervous system are considered as the most damaging and dangerous and that condition can be resulted prolong. Many protozoan and helminth parasites can attack on CNS. In some cases the parasite may have a tropism for the central nervous system (CNS) and this represents the primary affect of the pathogen. In many cases, though, the pathogen does not exhibit a specific tropism for the CNS and affects many other organs and tissues. And the clinical manifestations depend on the invasion of the CNS. The chronic stage is initially characterized by invasion of the lymphatics. The parasites will later cross the blood brain barrier and invade the CNS, is associated with various neurological impairments, if it’s not treated well or misdiagnosed it may cause comma or death. These are the parasites which can affect nervous system; Toxoplasma gondii, Echinococcus granulosus, Schistosomes, and Taenia solium etc… (13)


Taenia solium
T. solium includes the pig and human as their hosts. People wind up tainted by ingesting undercooked or crude pork contaminated with the cyticercus arrange. The cysticercus is involved a liquid filled bladder and a rearranged scolex (i.e., head). Cysticerci are discharged in the stomach and the scolex everts and joins to the mucosa of the small digestive system. Connection is intervened by suckers and a line of snares on the scolex. Proglottids are segmental units which will stretch out down the small digestive system with the more develop proglottids being further from the scolex. The most terminal proglottids are most develop and contain irresistible embryonated eggs. These egg-loaded proglottids separate and are passed in the defecation. Pigs end up tainted by ingesting sustenance or water polluted with eggs or proglottids. The embryonated eggs incubate in the wake of going through the stomach of the pig and the developing life known as the oncosphere is discharged. Oncospheres infiltrate the mucosa of the stomach or small digestive system and are spread hematogenously to the muscles and different tissues of the pig. Once in the tissues the oncosphere forms into a cysticercus… (14)


Evasion of Taenia solium

• Host Response
Parasitic attack, the host mounts an intrinsic and in the end a versatile insusceptible reaction. A noteworthy segment to the host’s guard against the parasite is an incendiary reaction. On account of neurocysticercosis, there are particular cellular writes related with irritation in the focal sensory system (CNS). These incorporate B and T lymphocytes, plasma cells, macrophages, and pole cells. By dissecting the diverse cell composes exhibit, plainly the host mounts a natural and versatile insusceptible reaction. Contingent upon the area of the cysticerci, diverse immunoglobulin isotypes and cytokines will be discharged. If cysticerci is found in the cerebrospinal liquid (CSF), then it increases the levels of IgG, IgM, IgE, and cytokines IL1? and IL6… (15)

Parasites either they are intestinal, blood, and nervous system parasites, they damage their respective hosts to adjust in the environment and to get all the nourishments from the host to survive. Severity of causing diseases by these parasites depend on their invasion strategies and also on their site of an infection but host almost responses the same at any parasitic infection like to limit the damage done by an invading parasite, a host’s immune system must respond in a balanced and well-regulated manner by activating its innate and adaptive immunity which includes macrophages, eosinphils, cytokines ,special host enzymes, inflammatory responses, and antibodies according to the type of a parasite and some other humoral responses to evade or to remove that parasite.

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