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Pathogen entry into the host depends on cell adhesion and the infectious dose.
• The portal of entry is the route an exogenous pathogen uses to enter the body.
• The infectious dose is the number of microbes entering the body.
• Many pathogens have adhesins that allow them to adhere to specific tissues.
Many pathogens enter at specific, natural portals of entry because these microbes contain on their surface “sticky” factors, called adhesins, that allow pathogens to adhere to appropriate tissue sites. A variety of adhesins often are associated with bacterial capsules, flagella, or pili.
Breaching the host barriers can establish infection and disease.
• Invasiveness is the ability of a pathogen to penetrate tissues and spread.
• Many pathogens use phagocytosis by body cells to enter cells or pass through defenses.
Some staphylococci produce coagulase to form a blood clot that protects them from phagocytosis.
• Others produce streptokinase, which dissolves fibrin clots and allows dissemination of the bacteria.
• Hyaluronidase enhances pathogen penetration through tissues.
• Leukocidins disintegrate neutrophils and macrophages.
• Hemolysins dissolve red blood cells.
Pathogens must be able to leave the host to spread disease.
• Pathogens or toxins leave the host through a portal of exit
Nosocomial infections are serious health threats within the health care system.
• Health care-associated infections (HAIs) occur as a result of receiving treatment for another condition.
• Nosocomial infections are associated with hospitals.
• They occur as a result of chains of transmission.
Defense against parasites; part of allergic reactions
Release of chemical mediators of inflammation; part of allergic reactions
Phagocytosis and intracellular killing of pathogens; initiate acquired immunity
Activate lymphocytes; initiate acquired immunity
The outer cortex and germinal centers are sites rich in B cells while the deep cortex and medulla contain large numbers of T cells.
The process of phagocytosis is the internalization of bacteria with the use of pseudopodia. Bacteria is internalized in a phagosome. The enzyme lysosome is combined with the phagosome creating phagolysosome. The phagolysosome kills and digest the bacteria. The bacteria is than egested.
Formation of Neutrophil Extracellular Traps (NETs)
• Some neutrophils transform into extracellular fibers (NETs).
• Nuclear envelope and granule membranes disintegrate and mix.
• Pathogens get caught in NET fibers.
• Antimicrobials degrade and kill pathogens.
• Tissue macrophages initiate phagocytosis and secrete cytokines.
Capillary walls dilate, causing edema, heat, redness and pain.
More phagocytes come to site of injury.
• Fibrin wall forms around injury preventing the spread of the pathogens.
Natural killer cells recognize and kill abnormal cells.
• NK cells are formed in the bone marrow, and migrate to: tonsils, lymph nodes, spleen
• When activated, they produce cytokines that trigger response by macrophages and other cells.
• Then they move into blood and lymph where they kill: cancer cells, virus-infected cells
When an NK cell recognizes a cell as “nonself” it releases cytotoxic perforins and granzymes.
Interferon Puts Cells in an Antiviral State
• Interferons (IFNs) are protein cytokines that trigger:
• macrophage activation.
• production of substances to interfere with RNA viral reproduction
The ability to eliminate pathogens requires a multifaceted approach.
• Antigens are microbes or microbe parts that provoke an immune response.
• The immune system recognizes unique antigenic determinants (epitopes).
• Immune deficiency is the loss of the body’s ability to respond to antigens and epitopes.
An antigen may have numerous epitopes. For example, a structure such as a bacterial flagellum may have hundreds of epitopes, each having a characteristic and distinct three-dimensional shape. It is the ability of acquired immunity to recognize these specific microbial “fingerprints” and generate the specificity needed.
In B cells, IgD's function is to signal the B cells to be activated. By being activated, they are ready to take part in the defense of the body in the immune system. T Cells are distinguished by their TCRs. In T cells, the receptor protein is composed of two antibody-like chains of glycoproteins.
Activation of the appropriate B cells begins when antigens enter a lymphoid organ, bringing the antigenic determinants close to the appropriate B cells. Antigenic determinants must bind with B cell receptor proteins. This, along with chemical stimulation from T cells, triggers B cells to divide and form a clone; that is, a population of genetically identical B cells with the same receptors for the antigen that is present.
In Primary Response, B cells are activated and effector cells, the plasma cells, start producing and secret- ing antibody. IgM are the first on the scene, but they are soon replaced by a longer-lasting IgG response. During the primary antibody response, memory cells also are produced, which provide the immunological memory needed for subsequent encounters with the same antigen.
A second or subsequent infection by the same pathogen or antigen produces a more powerful and longer lasting secondary antibody response. Due to the presence of memory cells, a rapid response to antigen leads to the production of IgG, the principal antibody. The secondary antibody response occurs faster and is more vigorous than the primary response. It also provides a much lon- ger period of resistance against disease.
Thus, the formation of antigen-antibody complexes may result in death to the microorganism possessing the antigen, inactivation of the antigen, or increased susceptibility of the antigen to other body defenses. Each of the process enhance phagocytosis.
*Learn the individual complexes and components
Membrane Attack Complex
This complex forms pores in the membrane, increasing cell membrane permeability and inducing the cell to undergo lysis through the unregulated flow of salts and water.
Acquired immunity can result by actively producing antibodies to an antigen.
• Active immunity occurs when the body’s immune system responds to antigens by producing antibodies and lymphocytes.
• Naturally acquired active immunity follows illness or pathogen exposure or through IgG transmission from mother to newborn
The process, called titration, may be used to the physician’s advantage because the dilution series is a valuable way of determining the titer of antibodies. The titer is the most dilute concentration of serum antibody yielding a detectable reaction with its specific antigen
Precipitation requires the formation of a lattice between soluble antigen and antibody.
• Precipitation reactions involve antigens and antibodies cross-linked in a huge lattice.
• In fluid, the molecules diffuse until they reach the ideal/concentration (the zone of equivalence).
• In immunodiffusion, antigens and antibodies diffuse through a gel until they reach the zone of equivalence.
• In immunoelectrophoresis, diffusion is combined with electrophoresis.
Agglutination involves the clumping of antigens.
• A visible reaction requires less antibody or antigen if they are clumped together.
• In passive agglutination:
• antigens are adsorbed onto a surface.
• antibodies are added.
• agglutination is observed
Hemagglutination is used to:
• determine blood type.
• detect viruses that cause agglutination of red blood cells.
Complement fixation can detect antibodies to a variety of pathogens.
• Labeling methods are used to detect antigen–antibody binding.
• A fluorescent antibody technique can detect antigen–antibody binding by labeling antibodies with a fluorescent marker
In the lab, antibodies recognizing one epitope (monoclonal Abs) are produced using myelomas.
• Myeloma cells are fused to an activated B cell to form a hybridoma.
• A hybridoma producing the desired mAb can be cloned.
• mAbs can be used in:
• disease prevention., immunomodulation (controlling overactive inflammatory responses).
•Type I IgE-mediated hypersensitivity, which is a process involving IgE, mast cells, basophils, and cell mediators inducing smooth muscle contraction;
•Type II cytotoxic hypersensitivity, which involves IgG, IgM,
•Type III immune complex hypersensitivity, which involves IgG, IgM,
The fourth type is a delayed hypersensitivity, where a cell-mediated immune response develops over
• Type I hypersensitivity is induced by allergens.
• The sensitizing dose is the first dose of antigen.
• The immune system responds as it would a pathogen.
• The person is sensitized as IgE antibodies attach to mast cells and basophils
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