Introduction

            Host resistance--defenses possessed by the host to prevent infection

1)      Specific resistance--directed against particular microbe

2)      Nonspecific (natural) resistance

Natural Resistance

            Species resistance--resistance or susceptibility to infection by a particular

                 pathogen may vary from one host species to another

Metabolism, physiological, and anatomical differences between species

affect the ability of a pathogen to cause infection

            Racial resistance--strain or race of animal host

                        Native American--Tuberculosis

                        Black African--Malaria

                        Black American--Malaria and Yellow fever

                        Chinese--Syphilis

            Individual resistance--due to single or multiple factors

                        Age--adolescence development--acquired adult immunity

                        Nutrition

                        Occupation--societal interactions

                        Miscellaneous--gender, hygene,etc.

            Mechanical and chemical barriers of resistance

                        Skin--keratin--lactic/fatty acid secretions

                        Mucoid epithelium--respiratory, digestive, and urogenital systems

                                    lysozymes--pH

Inflammation--confines infection to site of entry (portal)

            Cardinal signs of inflammation

                        red, warm, swollen, and painful

            Caused by inducers from host tissues and plasma components

            Vasodialation followed by permeability change

                        Granular polymorphonucleocytes (neutrophils)

                                    amoeboid in tissues

            Bacterial growth sustains inflammation

            Viruses produce necrotic host cells or antigen-antibody complexes

            Pus--serum, bacteria, necrotic cells and leukocytes

            Neutrophils live 1-2 days then die (solicit macrophages)

                        Macrophages phagocytose necrotic “polys”, tissue debris and pathogens

Phagocytosis--Elie Metchnikoff  1883

            Polymorphs--front line of defense

                        antimicrobial substances and enzymes (lysosomes)

            Macrophages (monocytes) long-lived

                        may have reproductive capacity under certain conditions

                                    histiocytes, Kupffer cells, alveolar macrophages

1)      wandering  (alveolar--peritoneal)

2)      fixed  (vascular endothelium)

            Mechanisms of phagocytosis

                        preliminary attachment of microbe to phagocyte

                                    electrostatic (Ca++ and Mg++)

                                                firm attachment--opsonins (serum component)

                                    phagocyte affinity for antibody coated microbes

                        phagosome formation--lysosomal activity

                                    phagolysosome

            Complement System--small serum proteins--high stability

                        complementary to opsonization, chemotaxis, and cell lysis

                        antigen-antibody complex may cause agglutination or precipitation

                                    fairly ineffective host resistance

                        antigen-antibody binding initiates reactions of complement system

                                    enhances phagocytosis of invader  (opsonin)

                                    Gram negative bacteria--CM integrity is lost

                                    Gram positive bacteria--enhances leukocyte bind

            Interferon--nonspecific antiviral agent  (unstable in ISF)

                        inhibits intracellular viral replication

                        viral interference studies 1957 (2 unrelated virions)

                        does not react directly with the virion

                                    exert a protective intracellular mechanism

                                                nonspecific for parasitic species

                        cellular specificity relative to host cells

                                    RNA double strand virions have high inductive force

causes antiviral resistance indirectly by inducing the synthesis of an

    antiviral protein by cells exposed to two different viruses

            (host cell synthesis of antiviral protein)

Acquired Specific Immunity

            Nontoxic/noninfection antigens--pollens, chemicals, RBC’s

            Immune system promotes homeostasis and conducts surveillance

            Types of immune responses

                        first front of defense--natural nonspecific

                        second front of defense--acquired specific

            Dual response--humoral/cell-mediated  (lymphoblasts)

            Specific immunity acquired two ways:

1)      actively (clincal and subclincal infections)

2)      passively (transfer of preformed antibodies)

gammaglobulins

            Development of immune response

                        Precursors of dual responses are lymphocytes

                                    lymph nodes, spleen, bone marrow, thymus

                        Derivation of B and T lymphocytes

                                    B cells develop perhaps in GALT--Peyer’s patch

                                                20% of circulating lymphocytes

                                                lifespan--days to weeks

                                    T cells develop in thymus

                                                lifespan—months

                        Functions of B and T lymphocytes

                                    B cells--humoral response--plasma cells

                                                memory cells -- “primed” previous antigenic activity

                                                            secondary immune response--rapid

                                    T cells--cell mediated response--effector cells

                                                solicit B cells to increase humoral act.

                                                            cell cooperation

                                                memory cells--anamnestic response

                                                            natural infection or vaccination

Antigen-antibody and antigen-lymphocyte interactions

            Innumological effector system (response following complex)

                        system releases activators for cellular responses

                        Bacterial--T cells produce lymphokines (interferon, migration inhibitory

factor)

                        Viral--not directly affected by humoral responses

Immunodeficiency diseases (malfunction)

            Agammaglobulinemia--lack of immunoglobulin

                        B cell deficiency

            Ataxia-telangiectasia--lack of cell mediated immunity

                        Thymus deficiency or loss

            Swiss-type lymphopenic agammaglobulinemia

                        B cell and T cell deficiencies

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