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Theme 2.1 Microbiology > Host pathogen interaction > Flashcards

Host pathogen interaction Flashcards

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Biology 101 flashcards
1
Q

What are ecological relationships?

A

Ecological relationships describe the interactions between and among organisms within their environment

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2
Q

What are the types of ecological relationships?

A

MUTUALISM (+/+): the mutually beneficial relationship between two species

COMMENSALISM (+/0): the relationship between two species in which one is benefited and the other is not affected, neither negatively nor positively

PARASITISM (+/-): the relationship between two species in which one benefits (parasite) from the other (host); usually involves detriment to the host

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3
Q

What is a saphrophyte?

A

Saphrophyte – a microbe that lives off dead or decaying plant matter eg fungi living on a dead tree trunk.

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4
Q

FLORA; MICROBIOTA (Microbiology Definition):

A

microorganisms present in or characteristic of a special location

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5
Q

INDIGENOUS (Resident) MICROBIOTA:

A

microbial flora typically occupying a particular niche; given diversity of environmental conditions

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6
Q

TRANSIENT FLORA:

A

microbial flora only temporarily occupying a given niche

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7
Q

What are the Natural microbial habitats?

A
  1. Soil
  2. Water
  3. Air
  4. Animals and animal products
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8
Q

Where is microbial flora of the normal body found? (normal floral)

A
  1. SKIN
  2. RESPIRATORY TRACT
    Nose and Nasopharynx; Mouth and Oropharynx
  3. EYE (Conjunctivae) and OUTER EAR
  4. INTESTINAL TRACT
    Stomach, Small Intestine; Large Intestine;
  5. GENITOURINARY TRACT
    External Genitalia & Anterior Urethra
    Vagina
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9
Q

What are the normallly sterile sites in the body?

A
  1. Brain; Central nervous system
  2. Blood; Tissues; Organ systems
  3. Sinuses; Inner and Middle Ear
  4. Lower Respiratory Tract: Larynx; Trachea; Bronchioles; Lungs; Alveoli
  5. Kidneys; Ureters; Urinary Bladder
  6. Uterus; Endometrium (Inner mucous membrane of uterus ); Fallopian Tubes
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10
Q

On the normally sterile parts of the body what happens when we colonizationn of microbes there?

A

Colonization of one of these sites generally involves a defect or breach in the natural defenses that creates a portal of entry

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11
Q

What are the factors that control growth of micoro-organisms?

A
  1. Nutrient availability
  2. Competition
  3. Host immune system
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12
Q

How does Nutrient availability control growth of micro-organisms?

A

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

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13
Q

How does Competition control growth of micro-organisms?

A

COMPETITION: the simultaneous demand by two or more organisms or species for a common resource that is in limited supply, resulting in a struggle for survival

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14
Q

How does Host immune system control growth of micro-organisms?

A

HOST IMMUNE SYSTEM: the cells and tissues involved in recognizing and attacking foreign substances in the body

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15
Q

What does it mean to be fastidious?

A

Fastidious: an organism that has complex nutritional or cultural requirements, making isolation and culture more difficult

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16
Q

How are infectious agents acquired??

A
  1. Portals of entry and exit
  2. Colonization
  3. Invasion
  4. Multiplication
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17
Q

What is meant by Invasion?

A

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): molecules that facilitate invasion by a pathogenic microorganism

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18
Q

Invasive factors definition

A

Invasins (invasive factors): molecules that facilitate invasion by a pathogenic microorganism

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19
Q

What is meant by multiplication in acquiring infectious agents?

A

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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20
Q

What is meant by colonization in acquiring infectious agents?

A

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 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, but the adherence may also be nonspecific

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21
Q

What are the portals of entry and/or exits?

A

PORTAL OF ENTRY/EXIT

INGESTION

INHALATION

DIRECT PENETRATION
Trauma or Surgical Procedure
Needlestick
Arthropod Bite

22
Q

What are the modes of transmission of disease?

A
  1. ENTRANCE, COLONIZATION, PENETRATION
  2. VECTOR
  3. CARRIER
  4. NOSOCOMIAL INFECTIONS
23
Q
  1. ENTRANCE, COLONIZATION, PENETRATION transmission
A

ENTRANCE, COLONIZATION, PENETRATION:

Dependent upon Age, Nutrition, Immunologic State and General Health of Host, and Bacterial Virulence Factors

24
Q
  1. VECTOR transmission
A

VECTOR: a carrier, especially the animal that transfers an infectious agent from one host to another, usually an ARTHROPOD

25
Q
  1. CARRIER transmission
A

CARRIER (Carrier State): a symptomless individual who is host to a pathogenic microorganism with the potential to pass the pathogen to others

26
Q
  1. NOSOCOMIAL INFECTIONS transmission
A

NOSOCOMIAL INFECTIONS: an infection acquired in a hospital setting that was not present in the host prior to admission.

27
Q

What is meant by Nosocomial infections?

A

A nosocomial infection is an infection you get while you’re in the hospital for another reason. It’s also called a hospital-acquired infection or a healthcare-associated infection.‌ Patients and healthcare professionals bring germs inside hospitals and pass them to each other.

28
Q

EPIDEMIC define

A

disease occurring suddenly in numbers clearly

in excess of normal expectancy

29
Q

ENDEMIC define

A

disease present or usually prevalent in a population or geographic area at all times

30
Q

PANDEMIC define

A

a widespread epidemic distributed or occurring widely throughout a region, country, continent, or globally

31
Q

Differentiate between True pathogen and Opportunistic pathogen.

A

TRUE PATHOGEN: any microorganism capable of causing disease in most cases; an infecting agent

OPPORTUNISTIC PATHOGEN: a usually harmless microorganism that becomes pathogenic under favorable conditions causing an opportunistic infection

32
Q

Pathogenicity vs Virulence

A

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 cause a specific degree of pathogenicity

33
Q

Why virulence is more important than pathogenicity?

A

In crude terms, you look at how many microbes are required to kill an animal.

Few highly virulent microbes will kill it versus a microbe with low virulence (many microbes required before death)

34
Q

What are the Bacterial virulence mechanisms? (9)

A

Adherence (Colonization)

Invasion

Degradative enzymes

Exotoxins

Endotoxin

Induction of excess inflammation

Evasion of phagocytic & immune clearance

Superantigen

Resistance to antibiotics

35
Q

WHAT ARE THE MICROBIAL PATHOGENICITY VIRULENCE FACTORS?

A
  1. Colonization factors
  2. Invasive factors (invasins)
  3. Degradative enzymes
  4. Toxigenicity
36
Q

MICROBIAL PATHOGENICITY VIRULENCE FACTOR: Colonization factors

A

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)

Example:
i) fimbriae (formerly known as pili) of Enterobacteriaceae

37
Q

MICROBIAL PATHOGENICITY VIRULENCE FACTOR: Invasive factors

A

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 the pathogenic advantage

38
Q

MICROBIAL PATHOGENICITY VIRULENCE FACTOR: Degradative enzymes

A

DEGRADATIVE ENZYMES: a class of protein capable of catalytic reactions; bacterial and host enzymes both play roles in the disease process

39
Q

MICROBIAL PATHOGENICITY VIRULENCE FACTOR: Toxigenicity

A

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
40
Q

Endotoxin vs Exotoxin

A
  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
41
Q

WHAT ARE THE BASIC EFFECTS of ENDOTOXINS?

A
  1. Fever
  2. Leukopenia/Leukocytosis
  3. Metabolic effects
  4. Release of lymphocyte factors
  5. Cellular death : Septic shock, Organ necrosis, Disseminated intravascular coagulation)
42
Q

what do endotoxins basically cause?

A

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:
1. 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 and prostaglandins

  1. 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;
    ORGAN NECROSIS: host cell death that results in organ failure
43
Q

WHAT ARE THE EFFECTS OF EXO-TOXINS?

A
  1. TWO-COMPONENT (BIPARTITE) A-B TOXINS with INTRACELLULAR TARGETS: usually one component is a binding domain (B subunit) and transfer of active component across cell membrane, the second component is an enzymatic or active domain (A subunit) that enzymatically disrupts cell function
  2. BACTERIAL CYTOLYSINS (a.k.a. Cytotoxins)
    with CELL MEMBRANE TARGETS: hemolysis, tissue necrosis, may be lethal when administered intravenously
44
Q

EXAMPLES of BIPARTITE A-B TOXINS
with
INTRACELLULAR TARGETS

A
  1. Diphtheria toxin - inhibits cell protein synthesis, host cells die and cause a Pseudomembrane in throat.
  2. 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
  3. Tetanus neurotoxin - less well understood; binding domain binds to neuroreceptor gangliosides, Patient gets spasms and trismus
  4. 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
45
Q

How do bacteria build RESISTANCE TO HOST DEFENSES?

A
  1. ENCAPSULATION and
    ANTIGENIC MIMICRY, MASKING or SHIFT

CAPSULE, GLYCOCALYX or SLIME LAYER
Polysaccharide capsules = Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, etc.

  1. 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

  1. RESISTANCE to HUMORAL FACTORS
  2. RESISTANCE to CELLULAR FACTORS
46
Q

How do bacteria cause DAMAGE TO HOST?

A
  1. DIRECT DAMAGE
    (Tissue Damage from Disease Process):
    Toxins
    Enzymes
  2. INDIRECT DAMAGE
    (Tissue Reactions from Immunopathological Response):
    Damage Resulting from Vigorous Host Immune Response
    Hypersensitivity Reactions (Types I - IV)
47
Q

What are the host defense mechanisms?

A
  1. External (primary)
  2. Internal (secondary)
  3. Cellular immune response
  4. Humoral immune response
48
Q

EXTERNAL (PRIMARY) defense mechanism

A

EXTERNAL (PRIMARY): Physical barrier e.g., skin and endothelial lining 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)

49
Q

INTERNAL (SECONDARY) defense mechanism

A

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.

50
Q

CELLULAR IMMUNE RESPONSE defense mechanism

A

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

51
Q

HUMORAL IMMUNE RESPONSE defense mechanism

A

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

Theme 2.1 Microbiology (10 decks)

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