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| Definition of Parasite | An organism which lives in or on another organism (its host) and benefits by deriving nutrients at the other’s expense |
| Defininition of HOST | An animal or plant in which a parasitic organism lives |
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| Phylum Platyhelminths | Most primitive metazoan group that has a well developed organ system in mesodermal layer (between the epidermal layer and gut). Also has bilater symmetry and head development THREE MAJOR CLASSES 1. Turbellaria 2. Trematoda 3. Cestoda |
| Cestoda | 1. Phylum Platyhelminthes 2. Parasitic tapeworms |
| TAENIA SOLIUM | 1. Pork tapeworm 2. 2-3 metres 3. Cestoda |
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| DIPHYLLOBOTHRIUM LATUM | 1. Cestoda 2. Platyhelminthes 3. Fish or broad tapeworm 4. 10m |
| Trematoda | 1. Parasitic flukes 2. Phylum Platyhelminthes |
| SCHISTOSOMA SP. | 1. Trematoda 2. Platyhelminthes 3. Blood flukes |
| FASCIOLA HEPATICA | 1. Trematoda 2. Platyhelminthes 3. Liver fluke |
| PARAGONIMUS WESTERMANI | 1. Trematoda 2. Platyhelminthes 3. Lung flukes |
| Phylum Aschelminthes | 1. Nematodes 2. Both free living and parasitic 3. Round worms |
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| Innate immunity: Physical | Physical barriers such as the skin and mucus secreted over the epithelial cells lining the gut or respiratory tract |
| Innate immunity: Microbial | Natural microbial flora that lives externally on the body surface and within the intestinal and genital tract - important in preventing infection by pathogens through competition and release of anti-microbial substances |
| Innate immunity : Physiological | When physical barriers are breached. Defensins- soluble chemical secreted in lung tissue and gut Leukocytes |
| Leukocytes (2 types) | 1. Tissue based cells (macrophages and dendritic cells) 2. Blood borne cells (neutrophils, eosinophils, natural killer cells) |
| Use of leukocytes | Able to recognise invading organisms and kill them through phagocytosis or through the release of noxious chemicals - hydroxyl radicals or antibiotic peptides |
| What is the complement system? | Part of the innate system that helps or complements the ability of antibodies and phagocytic cells to clear pathogens from an organism |
| What are the characteristics of ‘The Complement System’ | 1. not adaptable and does not change over an individuals lifetime 2. recruited and brought into action by the adaptive immune system through 3. classical pathway, antibody mediated OR alternative pathway WHICH IS NOT ANTIBODY MEDIATED 4. Consists of a number of small proteins found in the blood synthesised by the liver |
| How does the complement system work? | When stimulated by one of several triggers, proteases in the system split specific proteins to release cytokines and initiate an amplifying cascade of further splitting |
| Response of The complement system? | End result is the massive amplification if the response and activation of the cell-killing membrane attack complex. |
| Name the three biochemical pathways that activate the complement system: | 1. Classical complement pathway 2. Alternative complement pathway 3. Lectin pathway |
| What is an Opsonin? | Any molecule that enhances phagocytosis by marking an antigen for an immune response (opsonin is Greek for ‘to prepare for eating) |
| Basic functions of complement: | Opsonization: enhancing phagocytosis Chemotaxis: attracting macrophages and neutrophils Cell lysis: rupturing membranes of foreign cells (membrane attack complex) Agglutination: clustering and bonding of pathogens together (sticking) |
| What are the two types of adaptive immunity: | Passive and reactive |
| Describe Adaptive immunity: Passive | Antibodies received from another organism e.g. passage of antibodies (Ab) from the mother to the foetus (via the placenta) it new born via milk- Confess some protection against infections for the young while the immune system is developing. Will wear off in a few weeks/ months as these Abs decline |
| Describe Adaptive immunity: reactive | Organism mounts its own response to a challenge by a pathogen |
| Whether passive or reactive, what are the three classes of responses mediated by lymphocyte s? | 1. B lymphocytes 2. T lymphocytes 3. Natural Killer (NK) lymphocytes |
| What is B lymphocytes response to stimulation? | Develop into B cells that secrete antibodies (Immunoglobulins) |
| What is T lymphocytes response to stimulation? | Regulate other immune cells or kill virus- infected cells |
| What is Natural Killer (NK) lymphocytes response to stimulation? | Kill virus-infected cells and tumour cells |
| What is the use of the adaptive immunity? | This response provides specific response to a specific antigen Lymphocytes: May become memory cells following initial exposure to pathogen |
| What are the step of adaptive immunity? | 1. Memory cells are produced by initial exposure of pathogen, secondary exposure causes mass expansion of specific lymphocytes resulting in more rapid and effective immune responses THIS IS DONE BY 2. B lymphocytes produce antibodys 3. Antibodies produced become specific to a particular antigen molecule on or produced by the pathogen (parasite) |
| Antibodies produced by the adaptive immune system does not directly harm a pathogen... but | Binding can tigger potent responses against the invader |
| What are the binding responses triggered by the adaptive immune system | 1. Soluble immunoglobulins attach to antigens and thereby make them recognisable to phagocytic cells as objects to be phagocytosis. Process called OPONISATION. 2. Immunoglobulins bund to antigens and ‘clump’ them to increase their size and increase the chances of phagocytosis 3. Immunoglobulins bind to certain toxins to render them non-toxic |
| Binding of antibodies to antigens inactivates antigens by: | Enter text here... |
| What is the use of cell mediated immunity | Controlled by T lymphocytes (T-cells) have a set of receptors on their membranes that are able to bind to other receptor molecules on host cells THESE ARE KNOWN AS MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) |
| What is MHC good for? | Important mechanism for host immune system to distinguish self from on self |
| MHC Class 1 | Detected by sub types of T lymphocytes, cytotoxic T cells and NK cells. These cytotoxic cells carry surface glycoproteins CD8 therefore known as CD8 positive cells (CD8+be) Cytotoxic T cells an natural killer cells are able to bind are able to bind MHC 1 of the infected host cell and destroy in by releasing PERFORIN |
| What does perforin do? | Causes the formation of a pore on the infected cell membrane allowing the entry of factors generated by cytotoxic T cells destroying the infected cell (and the pathogen) |
| MHC Class II | detected by sub types of T lymphocytes known as T helper cells (CD4+ve cells). Antigens are present mai king on the surface of B lymphocytes, macrophages and dendritic cells (antigen presenting cells) |
| What are the three sub sets of T helper lymphocytes | 1. T helper cell 1 (Th1) 2. T helper cell 2 (Th2) 3. T helper cell 17 (Th17) |
| T helper cells don’t directly kill pathogens but... | Regulate other immune responses through the release of cytokines (such as the interleukins) |
| How is the immune response to helminth different to Protozoa? | Helminths cannot be ingested by phagotic cells such as macrophages (too large) |
| Describe LEISHMANIA MAJOR (Protozoa) and how the immune response responds | Protozoan, single cellular parasite invades host macrophages. Immunity based on T helper 1(Th1) response. This activated neutrophils and macrophages stimulating the production of nitric oxide to kill the parasites |
| What parasite causes malaria disease? | Plasmodium spp. |
| Structure of malaria parasite | Apicomlexan structure |
| Four main species casing malaria in humans | P. falciparum, p. ovale, p. vivax, p. malariae |
| Immune response to malaria parasite | 1. inter-cellular location 2. expression of antigens on the surface of the infected erythrocyte provide a target for the hosts immune system 3. parasite counters by altering the structure of the presented surface molecules into antigentically distinct forms 4. PfEMP1 (Erythrocyte membrane protein-1) is switched structerally to evade the host immune system |
| How much antigenic switching occurs each generation of malaira parasite? | 2% per generation -but increases with immune pressure from the host |
| Immunity to Malaria | 1. people in endemic regions develop immunity to infection 2. subjects always show symptoms of infection following initial exposure but subsequent exposure results in reduced symptoms 3. Immunity slow to develop due to parasitic antigenic variation mechanisms 4. Ab binding - may block cell invasion by the merozoite or initiate Ab cytotoxic killing of the parasite 5. no current vaccine |
| What anti-malaria drugs are there? | Chloroquine - fast acting blood schizontocide (not effective against falciparium due to developed resistance) Primaquine - effective against liver stage. mainly used to treat P. vivax or P. ovale malaria Arteminsin - located from plant and used in Chinese traditional medicine Severe p. falciparum treated with i.v. 'dug cocktail' |
| Malaria control strategies | Chemophrophylaxis - used on people travelling to endemic areas Mosquito nets and insecticidal sprays |
| 4 main classes of insecticides | Organophosphates, cabamates, pyrethroids and DDT |
| Malaria Vaccine | RTS,S - Mosquirix protein based malaria vaccine 27 - 46% efficacy |
| Parasitic Protozoa (kineoplastids) Cutaneous and Visceral Leishmaniasis | Causes by Leishmaniasis species Located in topical and sub-tropical regions throughout the world Transmitted by Sand fly vector (genus Phlebotomus) |
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