Biology2 1. A. A pathogen is defined as an organism capable of causing disease in the host. A host provides a warm, moist and nutrient-rich environment for the parasite. The human host besides maintaining a uniform temperature also renews itself and thus is an appropriate habitat for pathogenic microorganisms where they can live, reproduce and evolve(Alberts, et al., 2002). B. Methicillin resistantStaphylococcus aureus(MRSA) is a resistant bacterium that is a normal flora of the skin and nasal cavity but it can cause septicemia if it gains entry into tissues and causes an infection which is rather difficult to treat because it is resistant to most antibiotics. It usually causes sores or boils on the skin but it can also infect the lungs and the urinary tract. Norovirus or the Norwalk-like virus causes an infection that causes nausea, vomiting, abdominal pain and watery diarrhoea. The virus is very contagious and can cause infection through contaminated food and water and is common in crowded places like schools, cruises, nursing homes and child care centres. Athlete's foot or tinea pedis occurs due to a infection by a fungus.Trichophyton mentagrophytesis the caustaive organism. It causes vesicular infections or often appears as a toe web. The infection appears suddenly often due to prolonged warmth and moisture but can be treated quickly. Malaria is caused by the pathogenPlasmodium, a protozoan. Species of Plasmodium that can infect human beings areP. vivax, P. ovale, P.malariaeand P.falciparum.P. falciparumis known to cause a rather severe form of malaria.
Biology3 (CDC, 2018). The femaleAnopheles culicifaciesmosquito carries the pathogen and infects human beings when it bites through the sphorozoites of the protozoan into the human blood stream. The malaria parasite causes fever with chills and apathy in the patient. Transmission of malaria occurs when a mosquito bites an infected person and transfers the pathogen contained in the blood sucked from infected person and bites a healthy individual where the pathogen gets lodged. C.S. aureusis a gram positive bacterium and the cell wall comprises of a thick peptidoglycan cell wall. It occurs as spherical colonies in clusters that are usually arranged in two planes and this bacterium is devoid of flagella. The norovirus is a non-enveloped virus that has an icosahedral geometry. The diameter of the capsid can vary between 23 to 40 nm. The capsids are composed of about 60 VP1 proteins and the surface of the capsid has an amorphous surface structure and can be visualized under an electron microscope. The structure of the fungus that causes Athlete's foot has septate hyphae and the fruiting body is a branched conidiophore. Some strains may even have spiral-shaped or coiled hyphae. Chlamydospores may also be found in some cases. The Plasmodium lives in the red blood corpuscles of man as an intracellular parasite and in an adult form it is called the trophozoite which is amoeboid, has a single nucleus with a vacuolated and granular cytoplasm.
Biology4 D. Route of entry Pathogens gain entry into a susceptible human body to cause infection. The mucus membrane, the skin, the respiratory, the urogenital and the gastrointestinal tracts are the routes of entry or portals of entry for disease causing micro-organisms. Contact with clean disinfected, clean surfaces can reduce the chance of entry. 2.A. Resident flora are the microorganisms that reside on a particular site on the human body. These are about 10 times more numerous than a person's own cells. Some microorganisms are present on the body from a few hours to a few weeks and are called transient flora. 2.B. Resident flora prevent infection by offering competition for space and nutrition to the invading pathogenic organisms if any. So, the host remains protected due to the presence of the resident flora. There are several benefits of normal resident microflora. These organisms synthesize and excrete vitamins and these are absorbed and utilized by host organisms. Enteric bacteria that are normal residents of the human intestine secrete Vitamin K and Vitamin B12. Lactic acid bacteria also produce some B-vitamins. The normal flora offer competition in terms of attachment sites and nutrients to pathogenic bacteria in the oral cavity, the skin, the vaginal epithelium and the intestine. Intestinal bacterial flora produce bacteriocins that kill other bacteria. They may also produce peroxides and nonspecific fatty acids that inhibit or even kill other bacteria. Normal flora induce an immunological response which is an antibody-mediated immune response. This helps in preventing infections because the low levels of antibodies may cross react with certain pathogens and thus prevent infections.
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Biology5 If the mucosal surfaces are breached, infection of the host by normal flora are possible. Dental caries, periodontal disease, abscess, release of foul smelling discharge and even endocarditis can be caused by normal resident flora. At times impairment of the host or the host immune system, such as, in patients of leukaemia, immuno-suppression, irradiation therapy or chemotherapy can cause the normal resident flora to cause disease or the normal flora may fail to suppress the growth of transient pathogenic organisms and they could cause infections and the host may get infected and suffer from disease. 3.C. Skin and the mucus membrane play an important part in the protection of the body from pathogens. Often the first line of defence of the body is formed by the skin, tears and mucous. Tears and mucous contain the enzyme lysozyme that kills bacteria. The skin has its own resident microflora that offer competition to pathogenic strains that may try to colonize the skin or the underlying tissues. 4. Blood clotting occurs when a blood vessel ruptures and several circulating components of blood get converted into an insoluble gel that plugs the site of rupture and prevent the loss of blood from tissues or organs. It comprises of two systems, the first system involves platelets that help to form a thrombus or a blood clot. The second system is mainly dependent on the clotting factors that act to form a fibrin clot. The clotting factors are formed in the liver, and utilize calcium ions from the blood and the phospholipids which are platelet cell membrane components(Thrombocyte, n.d.).
Biology6 Injured tissue: exposure of endothelial cells When a blood vessel gets injured it gets exposed to foreign substances, following this, collagen adheres to the broken surface. The interrupted endothelium exhibits specific cell membrane receptors where the platelet adhesion happens. Platelets play an important role in blood clotting. The von Willebrand factor (vWF) that is released from the platelets and the injured endothelial cells mediates the adhesion between the platelets and the collagen fibrils that get exposed due to injured endothelial cell lining. Narrowing of blood vessels
Biology7 Blood vessel narrowing or vasoconstriction occurs when injury occurs in order to reduce blood loss. The walls of vessels have smooth muscles that contract when injury occurs and cause vasoconstriction. The reduced diameter of the vessel at the site of injury helps in minimising the loss of blood. Blood vessels of intact vessels do not allow clotting to occur because of a fibrinolytic heparin molecule and the thrombomodulin. Together these two prevent platelet aggregation. But when injury occurs and the endothelium is disrupted, the von Willebrand factor is secreted, the vasoconstriction follows as a brief contraction to decrease blood flow to the area. This is the first step in restoring haemostasis at the injury site. Activity of platelets The contents of the granules stored inside the platelets are also released and this causes the aggregation of platelets. The platelet glycoprotein is linked to the collagen and this activates the integrin protein of the platelets. As a result the platelets bind tightly to the extracellular matrix. The release of granules into the blood plasma is accompanied by ADP, vWF, serotonin and the platelet-activating factor. These accelerate the activation of more and more platelets into the blood system. When many platelets clump together at the site of the injury, it is known as platelet aggregation. The mechanism that leads to the activation of a protein receptor that increases the concentration of calcium in cytosol of the platelets. The calcium plays a role in the activation of protein kinase C. This culminates in the activation of a particular kind of phospholipase. The phospholipase enzyme modifies the integrin of the glycoprotein of the cell membrane. This cross linking between the platelets and fibrinogen
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Biology8 increases its ability to bind to fibrinogen. This increases the aggregation of platelets. This is the first step towards establishing haemostasis. Activity of clotting factors Clotting factors are the part of the cascade that results in the formation of the clot. There are 12 clotting factors that are given common names and assigned Roman numerals. Vitamin K is an essential part of the cascade that culminates in the formation of a clot. It helps in post translational carboxylation of clotting factors. There are two pathways of coagulation, the intrinsic and the extrinsic pathway. The extrinsic pathway leads to formation of the activation of the Factor X while the intrinsic pathway amplifies the generation of the Factor Xa. The two pathways converge at Factor Xa that plays a centrally important role in the coagulation pathway. The membranes of the TF (Tissue Factor) -bearing cells and platelets are the sites where coagulation factors get activated through a process that involves initiation, amplification and fibrin formation. As soon as vascular injury occurs, initiation occurs when cells having the TF bind to Factor VII, thus causing its activation. A small amount of thrombin then formed from the prothrombin. The thrombin so produced, activates platelets. The formation of the prothrombinase complex occurs, it is made up of Factor Xa and co-factors associated with platelets. The complex once formed causes a burst of thrombin production. This is called the amplification. This is followed by several protease reactions that convert the soluble fibrinogen protein into the insoluble fibrin. This leads to the formation of the thrombus. Thrombin plays a role in activation of Factor XII which helps in the cross-linking of fibrin. The fibrin mesh so formed entangles cellular components like the platelets and the red blood corpuscles.
Biology9 Factor Xa with Factor V as a co-factor causes the activation of prothrombin (Factor II) to thrombin (Factor IIa). Each Factor Xa molecule can catalyse the formation of 1000 thrombin molecules. Normal blood flow is restored when plasminogen breaks down the thrombin and restoration of structural integrity of blood vessel is complete. 5. Macrophages play a role in preventing infection in multifarious ways. The differentiation of macrophages occurs from the monocytes that migrate into tissues and differentiate in a tissue specific way. When monocytes differentiate in the presence of the cytokine interferon- γ, they form the microbial invaders and such macrophages are called as the classically activated macrophages. When monocytes differentiate in the presence of glucocorticoids and prostaglandins, the resulting macrophages are known to play a role in immune regulation. While wound healing macrophages differentiate in response to the cytokine interleukin-4. The macrophages that play a role in immune regulation produce the cytokine interleukin-10 that suppresses the immune system and limits inflammation in the later stages of the immune response. .
Biology10 6. Mechanisms of acquisition of immunity Naturally acquired immunity Artificially acquired immunity Passive ImmunityImmunity acquired through antibodies from breast milk or through the placenta. IgG antibodies are the only isotype that can cross the placenta. The IgA antibodies pass that are transferred through the breast milk also provide passive immunity to the new born baby and protect from bacterial infections in the gut until the newborns can synthesize antibodies by themselves. Immunity acquired through antibodies taken from another animal or person. This type of immunity protects from pathogen or poison once but there is no immune memory associated with this type of immunity. A person is at risk if the same pathogen is encountered a second time. Active ImmunityImmunity gained after getting an infection and recovery from the infection. This type of immunity confers protection during subsequent infections if the pathogen is encountered again due to memory of the immune response. Second response is usually faster and antibodies have higher affinity for the antigens. Immunity acquired due to vaccination. Vaccines have been developed against the measles virus, chicken pox virus, polio virus, diphtheria and several infectious diseases and provide life- long protection against pathogens. 7. Differences between antigens and antibodies-
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Biology11 Antibodies are synthesized by the body to defend the body against antigens while antigens are substances that stimulate the immune system to elicit a response by forming antibodies. Antibodies are always proteins called immunoglobulins while antigens could be proteins, lipopolysaccharides or lipoproteins. The structure of antibodies is Y-shaped, but antigens can vary in shape. The structure of the antibody molecule is always Y-shaped. And antibodies are polymeric protein molecules that are secreted by the plasma cells. The immune system employs the antibodies to neutralize pathogens such as, bacteria and virus that have infected the host. The recognition of the pathogen occurs through the antigen and antibody that can bind together, if complementarity is established. The mechanism involved in recognition is extremely precise. At times the antibody may tag a microbe and block its function required for invasion and survival. At other times the antibody may recruit other cells such as, natural killer cells or macrophages to eliminate the pathogen. The antibodies are able to communicate with other components of the humoral or cellular response through its Fc region which is located at the base of the 'Y'. Since antibodies are polymeric proteins, they are made up of two light chain polypeptides and two heavy chain polypeptides. The heavy and light chains are held together by disulfide bonds.
Biology12 also called immunoglobulins, Y-shaped molecules are proteins manufactured by the body that help fight against foreign substances calledantigens.Antigensare any substance that stimulates the immune system to produceantibodies. There are five isotypes of antibodies- Immunoglobulin G, Immunoglobulin D, Immunoglobulin E are monomeric, Immunoglobulin A is dimeric in nature and Immunoglobulin M is pentameric. each polypeptide of the antibody molecule has a constant and a variable region. The amino acid sequence of the variable region confers specificity on the antibody and it can bind to the antigen complimentarily. Heavy chains Each isotype of antibody has a different type of heavy chain. Five types of mammalian immunoglobulin heavy chain are named α in IgA, δ in IgD, ε in IgE, γ in IgG and μ in IgM antibodies. The size and the composition of the heavy chains is different, α and γ heavy chains are composed of 450 amino acids while the ε and μ heavy chains have 550 amino acids. The constant part of the heavy chain is identical in all antibodies of one isotype. Heavy chains for IgA, IgG and IgE have three immunoglobulin domains and a hinge region that adds flexibility while the heavy chains of IgM and IgE have four immunoglobulin domains in
Biology13 the constant region. The variable region, as the name suggests, differs based on the B cell that produced it. All antibodies produces by the same B cell have the same amino acid sequence. The variable region of the heavy chain of the antibodies is made of 110 amino acids and has one immunoglobulin domain. The light chains of the immunoglobulins in mammals have just two types- the κ and λ chains. Each light chain has two domains, one domain is constant while the other is variable. A light chain can be 211-217 amino acids in length. Each antibody has two of these and both are identical(Abcam, n.d.). Humoral immunity is the immune response that involves B cells that are able to recognize antigens of pathogens that have entered the blood or the lymph and are exogenous in origin. The antigens bind to the B cells and interleukins or T helper cells cause the co-stimulation of B cells. The B cells get activated and B cell proliferation also begins. Upon proliferation the B cells form plasma cells. Antibodies specific to the antigens encountered are borne by the plasma cells. The released antibodies circulate through the body and bind to antigens. These could include cells that have been invaded by pathogens, tumour cells or even transplanted cells. The cell mediated response involves T cells and responds to cells that carry a display of aberrant Major histo-compatibility complex markers or the MHC markers. The antigen presenting cells or the APCs bind to T cells. The T cells then proliferate and produce cytotoxic T cells. Cytotoxic T cells display the antigens. This occurs when MHC I are displayed on cells. In case of MHC II and exogenous antigens displayed on the plasma membrane, T cells proliferate to produce T helper cells which release interleukin and stimulate B cells to produce antibodies. Once antibodies bind to antigens, non specific Natural killer cells and macrophages are stimulated to destroy the antigens(Cliffnotes, n.d.).
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Biology14 8. According to the clonal selection theory, the immunological memory allows a rapid response to occur when a second exposure to antigen happens(Klinman, 1996). Vaccinations are used to artificially induce immunological memory, while infections and recovery allow for naturally induced memory.B cells have specific antibody as a cell surface receptor. When a soluble antigen is encountered it binds to the antibody displayed on the B cell surface that has the correct specificity leading to the formation of clones that are the antibody-producing plasma cells, also called the memory cells. B cells that are specific to the antigen can secrete antibodies. Low levels of soluble antibodies can be produced after one week of exposure to an antigen. But a second exposure to an antigen elicits a much faster response. The levels of antibodies are several orders higher in magnitude than the first response. The binding affinity of the antibodies for antigens during the second response is about 1000 times higher. This happens due to somatic mutations in the variable regions of heavy and light chains of memory cells. It is a random process but the binding affinity to antigens can be higher and only those clones that have a higher affinity proliferate while those with inactive antibodies die.
Biology15 The inability of the immune system to distinguish between self and non-self forms the basis of autoimmune response. The production of B- cell clones that produce antibodies that destroy self-antigen displaying cells causes destruction of the body's own tissue and causes diseases such as Type 1 diabetes, rheumatoid arthritis and rheumatic carditis. Rheumatic carditis occurs when antibodies directed against the M protein of Group A streptococcus begin to cross react with the cardiac myosin. This leads to inflammation and acute damage. This can lead to impaired heart valve function. Polyclonal activators might at times activate B cells. Due to a repetitive structure, multiple B cell receptors can get activated and result in cross linking. Autoantibodies can be produces by cross reactive antigens. Epitopes on an auto- antigen may be recognised by B cells as also on a foreign antigen as a co-incidence. When B cells present an auto-antigen there is no response from T helper cells that are auto-reactive. But when there is a cross reactive antigen the T helper cells get tricked into launching an auto immune response that leads to proliferation and production of antibody producing clones.
Biology16 References Abcam, n.d.antibody-structure-and-isotypes.[Online] Available at:http://www.abcam.com/protocols/antibody-structure-and-isotypes [Accessed 12 May 2018].
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Biology17 Alberts, B. et al., 2002.Molecular Biology of the Cell.4th ed. s.l.:Garland Science. CDC, 2018.parasites.html.[Online] Available at:https://www.cdc.gov/malaria/about/biology/parasites.html [Accessed 22 May 2018]. Cliffnotes, n.d.humoral-and-cell-mediated-immune-responses.[Online] Available at:https://www.cliffsnotes.com/study-guides/anatomy-and-physiology/the-immune- system-and-other-body-defenses/humoral-and-cell-mediated-immune-responses [Accessed 12 May 2018]. Klinman, N., 1996. The “Clonal Selection Hypothesis” and the current concepts of B cell tolerance. Immunity,Volume 5 , p. 189–195. Thrombocyte, n.d.process-of-blood-coagulation/.[Online] Available at:http://www.thrombocyte.com/process-of-blood-coagulation/ [Accessed 17 May 2018].