Protozoa immunization

D. increases the body s natural immune response to the protozoa... 

Other contributions to this book have taken a molecular view of parasitic nematodes, yet molecules make only a rather brief appearance here. This chapter has tried to show that parasitic nematodes are fascinatingly and tantalizingly diverse at a phenotypic level. It has focused particularly on diversity in phenotypes that are apparent in response to environmental conditions within or outside a host. The interaction of parasites with within-host factors is a major current research effort. However, helminth immunology is particularly notable for its inattention to diversity, especially when compared with the immunology of parasitic protozoa (Read and Viney, 1996). Observations of the interaction of host immunity with subsequent development in S. ratti show the potential power of such interactions. It is also clear that a principal mechanism of the action of host immune responses is against nematode fecundity (Stear et al., 1997). This is likely to be a molecularly complex interaction. Understanding this interaction, as well as variation in the interaction is interesting, but could also form the basis of control by transmission-reduction rather than eradication per se. 

IFN-y may also prove valuable in treating a variety of other conditions, and clinical trials for various indications are currently underway. This cytokine shows promise in treating leishmaniasis, a disease common in tropical and subtropical regions. The causative agent is a parasitic protozoan of the genus Leishmania. The disease is characterized by the presence of these protozoa inside certain immune cells, particularly macrophages. IFN-y appears to stimulate the infected macrophage to produce nitric oxide, which is toxic for the parasite. 

The immune system protects humans and animals from microbial infections by such infectious agents as bacteria, yeasts and fungi, viruses and protozoa. These differ greatly not only in their size but in their structural and molecular properties, as well as in the ways in which they seek to infect our bodies. Some of these pathogens infect bodily fluids, some penetrate tissues and some even survive and multiply within individual host cells. These intracellular pathogens include viruses, some parasitic protozoa (such as Plasmodium, the causative agent of malaria, which infects erythrocytes) and... 

About 10-20% of all transmembrane proteins that are targeted to the ER and subsequently enter the secretory pathway are subject to post-translational modification with glycosylphosphatidyl-inositol (GPI). Proteins bearing the GPI anchor are involved in signal transduction, immune response, cancer cell invasion, and metastasis and the pathobiology of trypanosomal parasites. The structure of the GPI anchor has been analyzed for mammals, protozoa, and yeast. The general structure of the glycolipid structure is shown in Scheme 4. 

Humoral Immune Response in Chronic Inflammatory Processes. The specificity of the diagnostically relevant intrathecal antibodies depends on the underlying cause of the disorder. In the case of chronic infective processes, the antibodies are exclusively targeted against the causative organism (F5). Increased IgC levels are found in about 30% of patients with chronic meningitis or encephalitis from various causes, such as bacteria, virus and protozoa, and in diseases like polyradiculitis, sarcoidosis, and chronic myelopathy (LI). 

Our bodies are under constant attack by viruses, bacteria, protozoa, and metazoan parasites. Persons bom without an immune system adequate to fight off these invaders die very quickly unless heroic measures are taken. We have learned to cooperate with our immune systems by immunizing ourselves against some bacteria and viruses. At other times we may fight a stubborn battle with our own defense systems against allergic reactions and a variety of autoimmune responses.1... 

Chagas disease in humans can be divided in two main phases the acute phase and the chronic phase. The acute phase may have no symptoms or have very mild symptoms. When present, the symptoms can include diarrhea, vomiting, headache, fever, edema, rashes, swollen lymph glands, enlarged liver or spleen, and myocarditis and/or meningoencephalitis. This phase is characterized by the presence of the protozoa in the patient s blood and can be severe and /or fatal in infants, children, and in people with weakened immune systems. In this phase, morbidity and clinical symptoms are directly associated with the parasitemia level. Chagas disease manifestations in the acute form are very common when T. cruzi is acquired by via the oral route. 

In addition to malaria, several other serious infections may occur in humans due to parasitic invasion by protozoa.2,44 Severe intestinal infections (dysentery) produced by various protozoa occur quite frequently, especially in areas where contaminated food and drinking water are prevalent. Infections in tissues such as the liver, heart, lungs, brain, and other organs may also occur because of protozoal infestation. As mentioned in this chapter s introduction, individuals with a compromised immune system may be especially susceptible to these intestinal and extraintestinal infections.2,70... 

Interferons were originally discovered as proteins that interfered with virus replication. When mice were injected with antibodies to interferons, they became markedly susceptible to virus-mediated disease, including virus-related tumour induction. Interferons can be detected at low levels in most human tissues, but amounts increase upon infection with viruses, bacteria, protozoa, and exposure to certain growth factors. Interferons were initially classified according to the cellular source, but recent nomenclature is based primarily on sequencing data. Thus leukocyte interferon (a mixture of proteins) is now known as interferon alfa, fibroblast interferon as interferon beta, and immune interferon as interferon gamma. 

Al-Khodor, S., Kalachikov, S., Morozova, I., Price, C., Abu Kwaik, Y. The PmrA/PmrB two-component system of Legionella pneumophila is a global regulator required for intracellular replication within macrophages and protozoa. Infect Immun 77 (2009) 374-386. 

Inflammatory and infectious diarrhoea. Examples of pathogens frequently associated with infectious diarrhoea include bacteria, Salmonella, E. coli, Campylobacter, viruses, rotaviruses, coronaviruses, parvoviruses (canine and feline), norovirus and protozoa, coccidia species, Cryptosporium and Giardia. The immune response to inflammatory conditions in the bowel contributes substantively to development of diarrhoea. Activation of white blood... 

The immunocytes are all involved in specific types of immune response that are generally divided into two types (1) cell-mediated, i.e., specifically sensitized T cells (derived from the thymus) which are associated with graft rejection, resistance to certain viruses, bacteria, fungi, and protozoa, and delayed-type hypersensitivity and (2) humoral-mediated, i.e., B cells (bursa equivalent) which produce specific antibodies after the body is exposed to a specific antigen. 

Mechanisms to control parasitic protozoa are similar to those utilized for other infectious agents they can be divided into non-specific mechanism(s) and specific mechanism(s) involving the immune system. The best studied non-specific mechanisms include those that affect the entry of parasites into the red blood cell. The sickle cell haemoglobin trait and lack of the Duffy factor on the erythrocyte surface make the red cell more resistant to invasion by Plasmodium. These traits are commonly found in populations from malaria-endemic regions. A second example of a non-specific factor is the presence of trypanolytic factors in the serum of humans which confer resistance to T. brucei, Although nonspecific factors can play a key role in resistance, usually they work in conjunction with the host s immune system. 

The protozoa can elicit humoral responses in which antigen-antibody complexes are formed and these can trigger coagulation and complement systems. Immune complexes have been found circulating in serum and deposited in the kidneys where they may contribute to conditions such as glomerulonephri-... 

TNFa is released in response to bacteria (endotoxins and LPS), viruses, protozoa, cytokines (GM-CSF, IL-1, IL-2, IFNy, and TNFa itself), immune complexes, complement component C5a, neuropeptide substance P, and reactive oxygen intermediates. Unhlce TNFa, sources of preformed TNFp have not been identified. ... 

The disease is caused by a coccidian like protozoa, Cryptosporidium spp. and is widespread in animals, though only in immune-compromised humans. Cryptosporidium has been shown to be the main cause of respiratory infections in turkeys and chicken [54,55]. 

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