Host-parasite interactions

Содержание

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HOST-PARASITE INTERACTIONS

HOST-PARASITE
INTERACTIONS

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ECOLOGICAL RELATIONSHIPS Microbial Interactions Host-Parasite Interactions Environment

ECOLOGICAL RELATIONSHIPS
Microbial Interactions
Host-Parasite Interactions
Environment

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PATHOGEN ENVIRONMENT HOST DISEASE TRIAD Host-Parasite Interactions OTHER MICROBES Microbial Interactions

PATHOGEN

ENVIRONMENT

HOST

DISEASE
TRIAD

Host-Parasite Interactions

OTHER MICROBES

Microbial Interactions

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ECOLOGICAL RELATIONSHIPS SYMBIOSIS: neutral, antagonistic or synergistic relationship between two dissimilar

ECOLOGICAL RELATIONSHIPS
SYMBIOSIS: neutral, antagonistic or synergistic relationship between two dissimilar organisms

(SYMBIOTES, SYMBIONTS) living in close association with each other;
MUTUALISM (+/+): mutually beneficial relationship between two species
COMMENSALISM (+/0): relationship between two species in which one is benefited and the other is not affected, neither negatively nor positively
PARASITISM (+/-): relationship between two species in which one benefits (parasite) from the other (host); usually involves detriment to the host
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BASIC ECOLOGICAL DEFINITIONS FLORA; MICROBIOTA (Microbiology Definition): microorganisms present in or

BASIC ECOLOGICAL DEFINITIONS
FLORA; MICROBIOTA (Microbiology Definition): microorganisms present in or characteristic

of a special location (FLORA generically refers to plants; FAUNA generically refers to animals)
INDIGENOUS (Resident) MICROBIOTA: microbial flora typically occupying a particular niche; given diversity of environmental conditions, organisms tend to segregate
TRANSIENT FLORA: microbial flora only temporarily occupying a given niche
NICHE (ecological niche): the place of an organism within its community (ecosystem); unique position occupied by a particular species, perceived in terms of actual physical space occupied & function performed within ecosystem
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NATURAL MICROBIAL HABITATS Soil Water Air Animals and Animal Products

NATURAL MICROBIAL HABITATS
Soil
Water
Air
Animals and Animal Products

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MICROBIAL FLORA OF THE NORMAL HUMAN BODY (a.k.a., normal flora) SKIN

MICROBIAL FLORA OF THE NORMAL HUMAN BODY (a.k.a., normal flora)
SKIN
RESPIRATORY TRACT
Nose

and Nasopharynx; Mouth and Oropharynx
EYE (Conjunctivae) and OUTER EAR
INTESTINAL TRACT
Stomach and Small Intestine; Large Intestine;
Intestinal Tract of Newborn
Antibiotic Alteration of Flora
Significance of Intestinal Flora
GENITOURINARY TRACT
External Genitalia & Anterior Urethra
Vagina
BLOOD and TISSUES
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NORMALLY STERILE SITES IN THE HUMAN BODY Colonization of one of

NORMALLY STERILE SITES IN THE HUMAN BODY
Colonization of one of these

sites generally involves a defect or breach in the natural defenses that creates a portal of entry
Brain; Central nervous system
Blood; Tissues; Organ systems
Sinuses; Inner and Middle Ear
Lower Respiratory Tract: Larynx; Trachea; Bronchioles (bronchi); Lungs; Alveoli
Kidneys; Ureters; Urinary Bladder; Posterior Urethra
Uterus; Endometrium (Inner mucous membrane of uterus ); Fallopian Tubes; Cervix and Endocervix
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FACTORS CONTROLLING GROWTH OF MICROORGANISMS 1. NUTRIENT AVAILABILITY: the accessibility of

FACTORS CONTROLLING GROWTH OF MICROORGANISMS
1. NUTRIENT AVAILABILITY: the accessibility of a

necessary resource, substance or compound providing nourishment to maintain life, i.e. capable of conversion to energy and structural building blocks
Fastidious: an organism that has complex nutritional or cultural requirements, making isolation and culture more difficult
MAJOR ESSENTIAL ELEMENTS:
C, O, H, N, S, P, K, Mg, Ca, Fe, Na, Cl
MINOR ESSENTIAL ELEMENTS:
Zn, Mn, Mo, Se, Co, Cu, Ni, W
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2. PHYSICO/ENVIRONMENTAL PARAMETERS: WATER ACTIVITY/OSMOTIC PRESSURE: Water activity (aw): represents the

2. PHYSICO/ENVIRONMENTAL PARAMETERS:
WATER ACTIVITY/OSMOTIC PRESSURE:
Water activity (aw): represents the available water
Osmotic

pressure (p): expressed in atmospheres; reflects the concentration of solute in an aqueous solution
OXYGEN: metabolic oxygen requirements; OBLIGATE or
FACULTATIVE, ANAEROBIC or AEROBIC, or in between, (MICROAEROPHILIC)
pH: power of hydrogen; a measurement of the amount of hydrogen
ion in solution; the logarithm of the reciprocal of the hydrogen ion concentration in an aqueous solution used to express its acidity or alkalinity (0-14)
TEMPERATURE:
Psycrophile (psychrophilic): liking cold temperatures;
Optimal growth at 15o to 20oC
Mesophile (mesophilic): liking moderate temperatures;
Optimal growth at 20o to 45oC
Thermophile (thermophilic): liking elevated temperatures;
Optimal growth at 50o to 70oC
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FACTORS CONTROLLING GROWTH OF ORGANISMS (cont.): 3. COMPETITION: the simultaneous demand

FACTORS CONTROLLING GROWTH OF ORGANISMS (cont.):
3. COMPETITION: the simultaneous demand by

two or more organisms or species for a necessary, common resource or physical space that is in limited or potentially limited supply, resulting in a struggle for survival
4. HOST IMMUNE SYSTEM: the cells and tissues involved in recognizing and attacking foreign substances in the body
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ACQUIRING INFECTIOUS AGENTS PORTAL OF ENTRY/EXIT INGESTION INHALATION DIRECT PENETRATION Trauma

ACQUIRING INFECTIOUS AGENTS
PORTAL OF ENTRY/EXIT
INGESTION
INHALATION
DIRECT PENETRATION
Trauma or Surgical Procedure
Needlestick
Arthropod Bite
Sexual Transmission
Transplacental

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ACQUIRING INFECTIOUS AGENTS (cont.) COLONIZATION: the successful occupation of a new

ACQUIRING INFECTIOUS AGENTS (cont.)
COLONIZATION: the successful occupation of a new habitat

by a species not normally found in this niche
Adherence (attachment): close association of bacterial cells and host cells generally characterized by receptors on target sites
Adhesin: structure or macromolecule located on the surface of a cell or extracellularly that facilitates adherence of a cell to a surface or to another cell; site of attachment is often a specific receptor and host cell receptors are often sugar moieties (lectin), but the adherence may also be nonspecific
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ACQUIRING INFECTIOUS AGENTS (cont.) INVASION: the entry and spread throughout the

ACQUIRING INFECTIOUS AGENTS (cont.)
INVASION: the entry and spread throughout the cells

and/or tissues of the host; specific recognition of receptor sites on target cells enhances pathogenic advantage
Invasins (invasive factors): structures or macromolecules that facilitate invasion by a pathogenic microorganism
MULTIPLICATION: the ability of a microorganism to reproduce during an infection; influenced by underlying disease, immunologic status, antibiotic treatment, nutrient availability
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TRANSMISSION OF DISEASE ENTRANCE, COLONIZATION, PENETRATION: Dependent upon Age, Sex, Nutrition,

TRANSMISSION OF DISEASE
ENTRANCE, COLONIZATION, PENETRATION: Dependent upon Age, Sex, Nutrition, Immunologic

State and General Health of Host, and Bacterial Virulence Factors
VECTOR: a carrier, especially the animal that transfers an infectious agent from one host to another, usually an ARTHROPOD
CARRIER (Carrier State): symptomless individual who is host to a pathogenic microorganim with the potential to pass the pathogen to others
NOSOCOMIAL INFECTIONS: an infection acquired in a hospital setting that was not present in the host prior to admission, generally occurring within 72 hours of admission
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EPIDEMIOLOGY EPIDEMIC: disease occuring suddenly in numbers clearly in access of

EPIDEMIOLOGY
EPIDEMIC: disease occuring suddenly in numbers clearly
in access of normal

expectancy
ENDEMIC: disease present or usually prevalent in a population or geographic area at all times
PANDEMIC: a widespread epidemic distributed or occuring widely throughout a region, country, continent, or globally
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Tuberculosis SARS* Venezuelan Equine Encephalitis Hepatitis C AIDS Enterohemorrhagic E. Coli

Tuberculosis SARS* Venezuelan Equine Encephalitis
Hepatitis C AIDS Enterohemorrhagic E. Coli
Malaria Lassa

Fever S.American Hemorrhagic Fevers
Influenza Hantavirus Pulmonary Syndrome
Lyme Disease West Nile Fever/Encephalitis*

Emerging Infectious Diseases
New diseases and diseases with increasing incidences are called emerging infectious diseases (EIDs).
EIDs can result from the use of antibiotics and pesticides, climatic changes, travel, the lack of vaccination, and insufficient case reporting.
The CDC, NIH, and WHO are responsible for surveillance and responses to emerging infectious diseases.

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PATHOGENICITY vs. VIRULENCE PATHOGENICITY: the quality of producing disease or the

PATHOGENICITY vs. VIRULENCE
PATHOGENICITY: the quality of producing disease or the ability

to produce pathologic changes or disease
VIRULENCE: a measure of pathogenicity; a measurement of the degree of disease-producing ability of a microorganism as indicated by the severity of the disease produced; commonly ascertained by measuring the dosage required to caused a specific degree of pathogenicity; one general standard is the LD50 (lethal dose 50%)
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PATHOGENICITY vs. VIRULENCE (Definitons) DOSAGE: the number of pathogenic microorganisms entering

PATHOGENICITY vs. VIRULENCE
(Definitons)
DOSAGE: the number of pathogenic microorganisms entering the

host
LD50 = the number of microorganisms required to cause lethality (death) in 50% of the test host
TRUE PATHOGEN: any microorganism capable of causing disease; an infecting agent
OPPORTUNISTIC PATHOGEN: a usually harmless microorganism that becomes pathogenic under favorable conditions causing an opportunistic infection
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INFECTION vs. DISEASE INFECTION: the colonization and/or invasion and multiplication of

INFECTION vs. DISEASE
INFECTION: the colonization and/or invasion and multiplication of pathogenic

microrganisms in the host
with or without the manifestation of disease
DISEASE: an abnormal condition of body function(s)
or structure that is considered to be harmful to the affected individual (host); any deviation from or interruption of the normal structure or function of any part, organ, or system
of the body
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INFECTION vs. DISEASE (Definitons) BENIGN: a non-life or non-health threating condition

INFECTION vs. DISEASE
(Definitons)
BENIGN: a non-life or non-health threating condition
MALIGNANT:

a disease tending to become progressively worse (MORBIDITY = illness) and potentially result in death (MORTALITY = death)
CONTAGIOUS: capable of being transmitted from one host to another; communicable; infectious
INFECTIOUS DOSE: number of pathogenic organisms required to cause disease in a given host
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KOCH'S POSTULATES Four criteria that were established by Robert Koch to

KOCH'S POSTULATES
Four criteria that were established by Robert Koch to identify

the causative agent of a particular disease, these include:
1. the microorganism (pathogen) must be present in all cases of the disease
2. the pathogen can be isolated from the diseased host and grown in pure culture
3. the pathogen from the pure culture must cause the same disease when inoculated into a healthy, susceptible laboratory animal
4. the pathogen must be reisolated from the new host and shown to be the same as the originally inoculated pathogen
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Bacterial Virulence Mechanisms Adherence (Colonization) Invasion Degradative enzymes Exotoxins Endotoxin Induction

Bacterial Virulence Mechanisms
Adherence (Colonization)
Invasion
Degradative enzymes
Exotoxins
Endotoxin
Induction of excess inflammation
Evasion of phagocytic &

immune clearance
Byproducts of growth (gas, acid)
Superantigen
Resistance to antibiotics
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MICROBIAL PATHOGENICITY VIRULENCE FACTORS COLONIZATION FACTORS: specific recognition of receptor sites

MICROBIAL PATHOGENICITY
VIRULENCE FACTORS
COLONIZATION FACTORS: specific recognition of receptor sites on target

cells enhances pathogenic advantage
1. CAPSULE: nonspecific attachment
2. SURFACE RECEPTORS/TARGET SITES: Receptors on both bacteria (adhesins) and host (target)
Examples include:
i) fimbriae (formerly known as pili) of Enterobacteriaceae
ii) Chlamydia binds host N-acetyl-D-glucosamine which is a cell surface lectin (polysaccharide target receptor)
iii) Protein adhesin of Mycoplasma located in specialized tip structure; adheres to sialic acid-containing cell receptors
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VIRULENCE FACTORS (cont.) INVASIVE FACTORS (invasins): enable a pathogenic microorganism to

VIRULENCE FACTORS (cont.)
INVASIVE FACTORS (invasins): enable a pathogenic microorganism to enter

and spread throughout the tissues of the host body; specific recognition of receptor sites on target cells enhances pathogenic advantage
DEGRADATIVE ENZYMES: a class of protein capable of catalytic reactions; bacterial and host enzymes both play roles in the disease process
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VIRULENCE FACTORS (cont.) TOXIGENICITY: the ability of a microorganism to cause

VIRULENCE FACTORS (cont.)
TOXIGENICITY: the ability of a microorganism to cause disease

as determined by the toxin it produces which partly determines its virulence
1. ENDOTOXIN: a complex bacterial toxin that is composed of protein, lipid, and polysaccharide (LPS) which is released only upon lysis of the cell
2. EXOTOXINS: a potent toxic substance formed
and secreted by species of certain bacteria
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BASIC EFFECTS of ENDOTOXIN FEVER: any elevation of body temperature above

BASIC EFFECTS of ENDOTOXIN
FEVER: any elevation of body temperature above normal
LEUKOPENIA/LEUKOCYTOSIS:

abnormal reduction in number of leukocytes in blood, (<5000/mm3) / abnormally large number of leukocytes in blood, as during hemorrhage, infection, inflammation, or fever (>12,000mm3)
METABOLIC EFFECTS : pathogenic organisms can affect any of the body systems with disruptions in metabolic processes, e.g.,hypotension, hypoglycemia, etc.
RELEASE OF LYMPHOCYTE FACTORS: agranular leukocyte concentrated in lymphoid tissue; active in immunological responses, including production of antibodies
CELLULAR DEATH:
SEPTIC SHOCK: associated with overwhelming infection resulting in vascular system failure with sequestration of large volumes of blood in capillaries and veins; activation of the complement and kinin systems and the release of histamines, prostaglandins, and other mediators may be involved
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): disorder characterized by a reduction in the elements involved in blood coagulation due to their utilization in widespread blood clotting within the vessels; late stages marked by profuse hemorrhaging
ORGAN NECROSIS: the sum of morphological changes indicative of cell death and caused by the progressive degradative action of enzymes
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EXOTOXINS TWO-COMPONENT (BIPARTITE) A-B TOXINS with INTRACELLULAR TARGETS: conform to general

EXOTOXINS
TWO-COMPONENT (BIPARTITE) A-B TOXINS with INTRACELLULAR TARGETS: conform to general structural

model; usually one component is a binding domain (B subunit) associated with absorption to target cell surface and transfer of active component across cell membrane, the second component is an enzymatic or active domain (A subunit) that enzymatically disrupts cell function
BACTERIAL CYTOLYSINS (a.k.a. Cytotoxins)
with CELL MEMBRANE TARGETS: hemolysis, tissue necrosis, may be lethal when administered intravenously
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EXAMPLES of BIPARTITE A-B TOXINS with INTRACELLULAR TARGETS Diphtheria toxin -

EXAMPLES of BIPARTITE A-B TOXINS
with
INTRACELLULAR TARGETS
Diphtheria toxin - ADP-ribosylation inhibits

cell protein synthesis by catalyzing transfer of ADP- ribose from NAD (nicotinimamide adenine nucleotide) to EF-2 (elongation factor- 2)
Pseudomonas aeruginosa toxin - similar action as DT
Cholera toxin - A-subunit catalyzes ADP-ribosylation of the B-subunit of the stimulatory guanine nucleotide protein Gs; profound life-threatening diarrhea with profuse outpouring of fluids and electrolytes
Enterotoxigenic Escherichia coli (ETEC) heat-labile enterotoxin - similar or identical to cholera toxin
Tetanus neurotoxin - less well understood; binding domain binds to neuroreceptor gangliosides, releases inhibitory impulses with trismus
Botulinum neurotoxin - among most potent of all biological toxins; binding domain binds to neuroreceptor gangliosides, inhibits release of acetylcholine at myoneural junction resulting in fatal paralysis
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BACTERIAL CYTOLYSINS with CELL MEMBRANE TARGETS Three Major Types: 1. Hydrolyze

BACTERIAL CYTOLYSINS
with
CELL MEMBRANE TARGETS
Three Major Types:
1. Hydrolyze membrane phospholipids (phospholipases); e.g.,

Clostridium, Staphylococcus
2. Thiol-activated cytolysins (oxygen-labile) alter membrane permeability by binding to cholesterol; e.g., Streptococcus, Clostridium
3. Detergent-like activity on cell membranes; e.g., Staphylococcus, rapid rate of lysis
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MICROBIAL PATHOGENICITY (cont.) RESISTANCE TO HOST DEFENSES ENCAPSULATION and ANTIGENIC MIMICRY,

MICROBIAL PATHOGENICITY (cont.)
RESISTANCE TO HOST DEFENSES
ENCAPSULATION and
ANTIGENIC MIMICRY, MASKING or

SHIFT
CAPSULE, GLYCOCALYX or SLIME LAYER
Polysachharide capsules Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, etc.
Polypeptide capsule of Bacillus anthracis
EVASION or INCAPACITATION of PHAGOCYTOSIS and/or IMMUNE CLEARANCE
PHAGOCYTOSIS INHIBITORS: mechanisms enabling an invading microorganism to resist being engulfed, ingested, and or lysed by phagocytes/ phagolysosomes
RESISTANCE to HUMORAL FACTORS
RESISTANCE to CELLULAR FACTORS
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MICROBIAL PATHOGENICITY (cont.) DAMAGE TO HOST DIRECT DAMAGE (Tissue Damage from

MICROBIAL PATHOGENICITY (cont.)
DAMAGE TO HOST
DIRECT DAMAGE
(Tissue Damage from Disease Process):
Toxins
Enzymes
INDIRECT

DAMAGE
(Tissue Reactions from Immunopathological Response):
Damage Resulting from Vigorous Host Immune Response (a.k.a, immunopathogenesis; autoimmune hypersensitivy)
Hypersensitivity Reactions (Types I - IV)
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HOST RESISTANCE The degree to which a host can limit the

HOST RESISTANCE
The degree to which a host can limit the effects

of an infection, ranging from:
TOLERANCE in which symptoms are suppressed or unusually large doses of a drug, toxin, or protein are able to be endured
HYPERSENSITIVITY in which only a few cells surrounding the infected cell(s) are affected or an increased susceptibility to an antigen, such as an allergic reaction to a previous exposure to an antigen, the extreme case being anaphylactic shock
IMMUNITY in which the microorganisms do not multiply due to any one or a combination of host immune factors or the biological condition by which a body is capable of resisting or overcoming an infection or disease
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HYPERSENSITIVITY REACTIONS TYPE I: ANAPHYLACTIC REACTION (ANAPHYLAXIS, ANAPHYLACTIC SHOCK): a life-

HYPERSENSITIVITY REACTIONS
TYPE I: ANAPHYLACTIC REACTION (ANAPHYLAXIS, ANAPHYLACTIC SHOCK): a life- threatening

immediate hypersensitivity reaction to a previously encountered antigen, characterized by respiratory distress, vascular collapse, and shock; allergy or atopic diseases
TYPE II: CYTOTOXIC REACTION: a specific destructive action against certain cells by an invading agent; humorally mediated, autoimmune diseases, cytotoxic diseases, antibody diseases
TYPE III: IMMUNE COMPLEX REACTION: serum sickness diseases
TYPE IV: CELL-MEDIATED IMMUNE RESPONSE: delayed-type hypersensitivity, cell- mediated cytotoxic diseases, granulomatous diseases
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IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS Type I Hypersensitivity Reactions: Anaphylactic Reaction

IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS
Type I Hypersensitivity Reactions:
Anaphylactic Reaction (Anaphylaxis;

Anaphylactic shock)
IgE-mediated: Cross-linking of cell-bound IgE antibodies by antigen with degranulation of mast cells or basophils
Life-threatening immediate hypersensitivity reaction to a previously encountered antigen, characterized by respiratory distress, vascular collapse, and shock
Allergy or atopic diseases
Atopy: hereditary hypersensitivity to common environmental antigens
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IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS Type II Hypersensitivity Reactions: Humorally-Mediated Autoimmune

IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS
Type II Hypersensitivity Reactions:
Humorally-Mediated Autoimmune Diseases
Interaction

of cross-reactive antibody with host cell surface antigen; Autoantibodies and immune complexes
Cytotoxic reaction (antibody-mediated) (ADCC): Specific destructive action against certain cells presenting antigens from an invading agent
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IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS Type III Hypersensitivity Reactions: Immune Complex

IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS
Type III Hypersensitivity Reactions:
Immune Complex Reaction
Antibody-mediated
Deposition

of circulating immune complexes in small vessels with complement activation causing damage to vessels
Serum sickness diseases
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IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS Type IV Hypersensitivity Reactions: Cell-Mediated Immune

IMMUNOPATHOLOGICAL RESPONSE with TISSUE REACTIONS
Type IV Hypersensitivity Reactions:
Cell-Mediated Immune Response
T

cells sensitized to “self” antigens secrete lymphokines that either do direct damage to host cells (e.g., TNF) or indirect damage enhancing the inflammatory response
Delayed-type hypersensitivity (TB test) (CD4+ mediated)
Cell-mediated cytotoxic diseases (CD8+ mediated)
Granulomatous disease
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HOST DEFENSE MECHANISMS EXTERNAL (PRIMARY): Physical barrier of gross surface area;

HOST DEFENSE MECHANISMS
EXTERNAL (PRIMARY): Physical barrier of gross surface area; e.g.,

skin, respiratory tract, gastrointestinal tract, genitourinary tract
Mechanical and Physical Factors: sweat, fatty acids, pH, indigenous competitive flora (microbial antagonism), peristalsis, hair, cilia, urinary flushing, mucus, [tears, nasal secretions, saliva (lysozyme)], semen (spermine), mucosal secretory antibody (IgA predominant)
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HOST DEFENSE MECHANISMS (cont.) INTERNAL (SECONDARY): When an infecting parasite succeeds

HOST DEFENSE MECHANISMS (cont.)
INTERNAL (SECONDARY): When an infecting parasite succeeds in

penetrating the skin or mucuos membranes, cellular defense mechanisms include local macrophages and blood-borne phagocytic cells. Mononuclear phagocytes (monocytes and macrophages) and polymorphonuclear leukocytes (PMNs) are the most important phagocytic cells targeting bacterial infections.
MONONUCLEAR PHAGOCYTE SYSTEM (formerly Reticular Endothelial System): total pool of monocytes and cells derived from monocytes; predominantly macrophages (phagocytic cells)
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HOST DEFENSE MECHANISMS (cont.) OTHER: NON-SPECIFIC: oxygen metabolites (superoxide anion radical,

HOST DEFENSE MECHANISMS (cont.)
OTHER:
NON-SPECIFIC: oxygen metabolites (superoxide anion radical, hydrogen peroxide,

hydroxyl radicals, halide radicals), kinin forming system related to clotting
HOST-GENERATED PROTEINS: complex array of humoral and cellular mediators; e.g., lysosomal enzymes, lipid mediators, prostaglandins, histamine, heat-shock proteins (stress proteins)
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HOST DEFENSE MECHANISMS (cont.) CELLULAR IMMUNE RESPONSE: any immune response directed

HOST DEFENSE MECHANISMS (cont.)
CELLULAR IMMUNE RESPONSE: any immune response directed at

the cellular level; includes INFLAMMATION and PHAGOCYTOSIS processes
INFLAMMATORY RESPONSE: a protective response of tissues affected by disease or injury characterized by redness, localized heat, swelling, pain, and possibly impaired function of the infected part
PHAGOCYTOSIS: the process by which certain phagocytes can ingest extracellular particles by engulfing them; particles OPSONIZED with antibody are more rapidly and efficiently ingested
T-LYMPHOCYTES and CYTOKINES
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HOST DEFENSE MECHANISMS (cont.) HUMORAL IMMUNE RESPONSE: the sum total of

HOST DEFENSE MECHANISMS (cont.)
HUMORAL IMMUNE RESPONSE: the sum total of components

of the immune response circulating in the blood or body fluids ; includes ANTIBODY and COMPLEMENT systems
COMPLEMENT PROTECTIVE SYSTEM: a protein system in serum that combines with antibodies to form a defense against cellular antigens
B-LYMPHOCYTES and
ANTIBODY PRODUCTION: a class of proteins produced as a result of the introduction of an antigen that has the ability to combine with the antigen that caused its production
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REVIEW

REVIEW

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PATHOGEN ENVIRONMENT HOST DISEASE TRIAD Host-Parasite Interactions OTHER MICROBES Microbial Interactions REVIEW

PATHOGEN

ENVIRONMENT

HOST

DISEASE
TRIAD

Host-Parasite Interactions

OTHER MICROBES

Microbial Interactions

REVIEW

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ACQUIRING INFECTIOUS AGENTS PORTAL OF ENTRY/EXIT INGESTION INHALATION DIRECT PENETRATION Trauma

ACQUIRING INFECTIOUS AGENTS
PORTAL OF ENTRY/EXIT
INGESTION
INHALATION
DIRECT PENETRATION
Trauma or Surgical Procedure
Needlestick
Arthropod Bite
Sexual Transmission
Transplacental

REVIEW

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PATHOGENICITY vs. VIRULENCE PATHOGENICITY: the quality of producing disease or the

PATHOGENICITY vs. VIRULENCE
PATHOGENICITY: the quality of producing disease or the ability

to produce pathologic changes or disease
VIRULENCE: a measure of pathogenicity; a measurement of the degree of disease-producing ability of a microorganism as indicated by the severity of the disease produced; commonly ascertained by measuring the dosage required to caused a specific degree of pathogenicity; one general standard is the LD50 (lethal dose 50%)

REVIEW

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INFECTION vs. DISEASE INFECTION: the colonization and/or invasion and multiplication of

INFECTION vs. DISEASE
INFECTION: the colonization and/or invasion and multiplication of pathogenic

microrganisms in the host
with or without the manifestation of disease
DISEASE: an abnormal condition of body function(s)
or structure that is considered to be harmful to the affected individual (host); any deviation from or interruption of the normal structure or function of any part, organ, or system
of the body

REVIEW

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KOCH'S POSTULATES Four criteria that were established by Robert Koch to

KOCH'S POSTULATES
Four criteria that were established by Robert Koch to identify

the causative agent of a particular disease, these include:
1. the microorganism (pathogen) must be present in all cases of the disease
2. the pathogen can be isolated from the diseased host and grown in pure culture
3. the pathogen from the pure culture must cause the same disease when inoculated into a healthy, susceptible laboratory animal
4. the pathogen must be reisolated from the new host and shown to be the same as the originally inoculated pathogen

REVIEW

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Bacterial Virulence Mechanisms Adherence (Colonization) Invasion Degradative enzymes Exotoxins Endotoxin Induction

Bacterial Virulence Mechanisms
Adherence (Colonization)
Invasion
Degradative enzymes
Exotoxins
Endotoxin
Induction of excess inflammation
Evasion of phagocytic &

immune clearance
Byproducts of growth (gas, acid)
Superantigen
Resistance to antibiotics

REVIEW

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BASIC EFFECTS of ENDOTOXIN FEVER: any elevation of body temperature above

BASIC EFFECTS of ENDOTOXIN
FEVER: any elevation of body temperature above normal
LEUKOPENIA/LEUKOCYTOSIS:

abnormal reduction in number of leukocytes in blood, (<5000/mm3) / abnormally large number of leukocytes in blood, as during hemorrhage, infection, inflammation, or fever (>12,000mm3)
METABOLIC EFFECTS : pathogenic organisms can affect any of the body systems with disruptions in metabolic processes, e.g.,hypotension, hypoglycemia, etc.
RELEASE OF LYMPHOCYTE FACTORS: agranular leukocyte concentrated in lymphoid tissue; active in immunological responses, including production of antibodies
CELLULAR DEATH:
SEPTIC SHOCK: associated with overwhelming infection resulting in vascular system failure with sequestration of large volumes of blood in capillaries and veins; activation of the complement and kinin systems and the release of histamines, prostaglandins, and other mediators may be involved
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): disorder characterized by a reduction in the elements involved in blood coagulation due to their utilization in widespread blood clotting within the vessels; late stages marked by profuse hemorrhaging
ORGAN NECROSIS: the sum of morphological changes indicative of cell death and caused by the progressive degradative action of enzymes

REVIEW

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EXOTOXINS TWO-COMPONENT (BIPARTITE) A-B TOXINS with INTRACELLULAR TARGETS: conform to general

EXOTOXINS
TWO-COMPONENT (BIPARTITE) A-B TOXINS with INTRACELLULAR TARGETS: conform to general structural

model; usually one component is a binding domain (B subunit) associated with absorption to target cell surface and transfer of active component across cell membrane, the second component is an enzymatic or active domain (A subunit) that enzymatically disrupts cell function
BACTERIAL CYTOLYSINS (a.k.a. Cytotoxins)
with CELL MEMBRANE TARGETS: hemolysis, tissue necrosis, may be lethal when administered intravenously

REVIEW

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BACTERIAL CYTOLYSINS with CELL MEMBRANE TARGETS Three Major Types: 1. Hydrolyze

BACTERIAL CYTOLYSINS
with
CELL MEMBRANE TARGETS
Three Major Types:
1. Hydrolyze membrane phospholipids (phospholipases); e.g.,

Clostridium, Staphylococcus
2. Thiol-activated cytolysins (oxygen-labile) alter membrane permeability by binding to cholesterol; e.g., Streptococcus, Clostridium
3. Detergent-like activity on cell membranes; e.g., Staphylococcus, rapid rate of lysis

REVIEW

Слайд 63

REVIEW

REVIEW

Слайд 64

MICROBIAL PATHOGENICITY (cont.) RESISTANCE TO HOST DEFENSES ENCAPSULATION and ANTIGENIC MIMICRY,

MICROBIAL PATHOGENICITY (cont.)
RESISTANCE TO HOST DEFENSES
ENCAPSULATION and
ANTIGENIC MIMICRY, MASKING or

SHIFT
CAPSULE, GLYCOCALYX or SLIME LAYER
Polysachharide capsules Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, etc.
Polypeptide capsule of Bacillus anthracis
EVASION or INCAPACITATION of PHAGOCYTOSIS and/or IMMUNE CLEARANCE
PHAGOCYTOSIS INHIBITORS: mechanisms enabling an invading microorganism to resist being engulfed, ingested, and or lysed by phagocytes/ phagolysosomes
RESISTANCE to HUMORAL FACTORS
RESISTANCE to CELLULAR FACTORS

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MICROBIAL PATHOGENICITY (cont.) DAMAGE TO HOST DIRECT DAMAGE (Tissue Damage from

MICROBIAL PATHOGENICITY (cont.)
DAMAGE TO HOST
DIRECT DAMAGE
(Tissue Damage from Disease Process):
Toxins
Enzymes
INDIRECT

DAMAGE
(Tissue Reactions from Immunopathological Response):
Damage Resulting from Vigorous Host Immune Response (a.k.a, immunopathogenesis; autoimmune hypersensitivy)
Hypersensitivity Reactions (Types I - IV)

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HYPERSENSITIVITY REACTIONS TYPE I: ANAPHYLACTIC REACTION (ANAPHYLAXIS, ANAPHYLACTIC SHOCK): a life-

HYPERSENSITIVITY REACTIONS
TYPE I: ANAPHYLACTIC REACTION (ANAPHYLAXIS, ANAPHYLACTIC SHOCK): a life- threatening

immediate hypersensitivity reaction to a previously encountered antigen, characterized by respiratory distress, vascular collapse, and shock; allergy or atopic diseases
TYPE II: CYTOTOXIC REACTION: a specific destructive action against certain cells by an invading agent; humorally mediated, autoimmune diseases, cytotoxic diseases, antibody diseases
TYPE III: IMMUNE COMPLEX REACTION: serum sickness diseases
TYPE IV: CELL-MEDIATED IMMUNE RESPONSE: delayed-type hypersensitivity, cell- mediated cytotoxic diseases, granulomatous diseases

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HOST DEFENSE MECHANISMS (cont.) CELLULAR IMMUNE RESPONSE: any immune response directed

HOST DEFENSE MECHANISMS (cont.)
CELLULAR IMMUNE RESPONSE: any immune response directed at

the cellular level; includes INFLAMMATION and PHAGOCYTOSIS processes
INFLAMMATORY RESPONSE: a protective response of tissues affected by disease or injury characterized by redness, localized heat, swelling, pain, and possibly impaired function of the infected part
PHAGOCYTOSIS: the process by which certain phagocytes can ingest extracellular particles by engulfing them; particles OPSONIZED with antibody are more rapidly and efficiently ingested
T-LYMPHOCYTES and CYTOKINES

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HOST DEFENSE MECHANISMS (cont.) HUMORAL IMMUNE RESPONSE: the sum total of

HOST DEFENSE MECHANISMS (cont.)
HUMORAL IMMUNE RESPONSE: the sum total of components

of the immune response circulating in the blood or body fluids ; includes ANTIBODY and COMPLEMENT systems
COMPLEMENT PROTECTIVE SYSTEM: a protein system in serum that combines with antibodies to form a defense against cellular antigens
B-LYMPHOCYTES and
ANTIBODY PRODUCTION: a class of proteins produced as a result of the introduction of an antigen that has the ability to combine with the antigen that caused its production

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