Normal Flora Flashcards

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1
Q

How do humans associate with microorganisms?

A

– Colonization: host tolerates the microbe, Normal Flora

– Elimination: killing or removal of the microbe, requires a defence system (immune system)

– Infection: pathological harm to the host becomes evident as microbes invades host tissue- Pathogenesis/Pathology

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2
Q

What is COLONIZATION and how does it develop?

A

– the presence of microorganisms at any body site without evident disease
– Starts at birth
– Follows:
•contact with the birth canal & feeding •contact with others, environment & surfaces

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3
Q

What are Normally Colonized Body Sites and examples?

A
  • surface tissues constantly in contact with the environment eg. skin
  • Surfaces lined with mucous membranes:
    – conjunctiva
    – nose
    – external ear
    – nasopharynx
    – axilla
    – mouth
    – large intestine
    – anterior urethra
    – vagina
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4
Q

What are Body Sites that are not Normally Colonized?

A

• internal tissues not in contact with the environment
– blood
– brain
– muscle
– bone

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5
Q

What are normal body flora?

A

Aka colonizers

• NORMAL BODY FLORA is the mixture of microorganisms regularly found at certain anatomical sites in the body of all healthy /normal person

• The microbes are not associated with diseases
• They colonize certain anatomical body sites
• aka-
– normal microbial flora
– indigenous microbiota

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6
Q

How can normal flora be classified?

A

CLASSIFCATION OF NORMAL FLORA

  1. Based on duration of association with the anatomical site
    a. Transient b. Permanent

Based on relationship to the host:
2.a) Mutualism (Symbiotic)-Both host and bacteria are thought to derive benefit from each other

b) Opportunistic- normal flora in their host cause endogenous diseases as a result of weakness in the host defences or transfer to a different body site

c) Commensal- no apparent benefit or harm to either organism following their association

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7
Q

How can normal flora be classified?

A

CLASSIFCATION OF NORMAL FLORA

  1. Based on duration of association with the anatomical site
    a. Transient b. Permanent

Based on relationship to the host:
2.a) Mutualism (Symbiotic)-Both host and bacteria are thought to derive benefit from each other

b) Opportunistic- normal flora in their host cause endogenous diseases as a result of weakness in the host defences or transfer to a different body site

c) Commensal- no apparent benefit or harm to either organism following their association

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8
Q

What are the FACTORS INFLUENCING THE TYPE OF MICROBES AT ANY ANATOMIC SITE?

A

FACTORS INFLUENCING THE TYPE OF MICROBES AT ANY ANATOMIC SITE
Human factor:
– genetics
– age
– Sex
– Stress
– nutrition and diet
– Temperature
–pH
– Hormonal state

Microbial factor:
– Tissue tropism (Lactobacilus)
– Specific adherence
– Biofilm formation

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9
Q

BENEFICIAL EFFECTS OF NORMAL BODY FLORA

A
  1. Synthesis vitamins-enteric bacteria secrete Vitamin K and Vitamin B12, and lactic acid bacteria produce certain B-vitamins
  2. Prevention of colonization by pathogens
  3. Antagonism & killing of other
    bacteria-Bacteriocin production
  4. Stimulation of the development of certain tissues-caecum and certain lymphatic tissues (Peyer’s patches) in the GI tract
  5. Stimulation of the production of natural antibodies.- IgA, cross-reacting
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10
Q

What is cross reaction?

A

A situation here an antibody produced in response to a specific antigen binds sign another antigen

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11
Q

What are the HARMFUL EFFECTS OF NORMAL BODY FLORA?

A
  1. Bacterial synergism
  2. Competition for nutrients
  3. Induction of a low grade toxaemia
  4. Agents of disease= Opportunistic Pathogens
  5. Transfer to susceptible hosts
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12
Q

What is the CLINICAL SIGNIFICANCE OF NORMAL FLORA?

A

• Difficulty in interpretation of culture results
• Applicable specimens
– throat swab
– eye swab
– urogenital specimens
– skin and ulcer specimen
– sputum
– nasopharygeal and nasal specimen
– faeces and rectal swabs
– Urine
• Knowledge of patients clinical condition is vital

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13
Q

What is Pathogenesis?

A

Pathogenesis is a series of changes occurring between contact with an infective agent and manifestation of a disease

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14
Q

What is Pathogenicity?

A
  • Pathogenicity is the ability to produce disease in a host organism
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15
Q

What is a Pathogen?

A
  • is a microorganism, macroorganism or foreign body capable of infecting & inducing a disease upon contact with a susceptible host
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16
Q

What is Pathology?

A

Pathology
– Morphological changes, indicative of deviation from normal, seen in an infected/diseased tissues/organ

– A branch of medicine, study of processes and changes seen in an infected/diseased tissues/host

17
Q

Virulence

A

is the degree of pathogenicity of the microbe

18
Q

Invasiveness

A

Invasiveness is the ability of microbes to penetrate deep into host cell/tissues

19
Q

Toxigenesis

A

Toxigenesis is the ability to produce toxins

20
Q

Attributes of Pathogenic Organisms

A
  1. Transmittability
  2. Adhesiveness
  3. Invasiveness
  4. Toxigenicity
  5. Host immune system evasion
  6. Production of host tissue degrading enzymes
21
Q

What is Transmittability?

A

The ability of infectious microorganisms to move from a colonized, infected or reservoir host to a new susceptible host

22
Q

What are the modes of transports for pathogens?

A

Contact
Direct
Indirect

Droplet
large particle droplets (> 5 microns) generated during coughing, sneezing, talking or tracheal suctioning,
pneumonias, pertussis, diphtheria, influenza type B, mumps, and meningitis

Airborne
Evaporated droplet <5 micron, remain suspended in the air for long periods of time
Pulmonary tuberculosis (TB), measles, chicken pox, pulmonary plague and haemorrhagic fever with pneumonia

Common vehicle transmission
food, water, therapeutic devices, hospital equipment

23
Q

Maintenance of Transmittability

A
  1. Animal Reservoir
  2. Common vehicle-water, food, fomites
  3. Human carrier-asymptomatic state
  4. Common portal of entry-mouth, ears, airways, genitalial opening
  5. Clinical symptom-sneezing, coughing
24
Q

What is ADHERENCE?

A

Ability of the micro organisms to attach to host cells and tissue

25
Q

TYPES OF ADHERENCE

A

Nonspecific adherence
Specific adherence

26
Q

Nonspecific adherence

A

reversible attachment of the bacterium to the eucaryotic cell surface (sometimes called “docking”)
involves nonspecific attractive forces which allow approach of the bacterium to the eucaryotic cell surface
hydrophobic interactions
electrostatic attractions
atomic and molecular vibrations resulting from fluctuating dipoles of similar frequencies
Brownian movement
recruitment and trapping by biofilm polymers interacting with the bacterial glycocalyx (capsule)

27
Q

Specific adherence

A

Irreversible, permanent attachment of the microorganism to the eucaryotic cell surface (sometimes called “anchoring”)
involves permanent formation of specific lock-and-key bonds between complementary molecules on each cell surface
Complementary receptor and adhesin molecules must be accessible and arranged in such a way that many bonds form over the area of contact between the two cells.

28
Q

What is INVASIVENESS?

A

The ability of microorganisms to penetrate the host cells or tissues, penetration beyond the point of attachments

29
Q

Types of invasiveness?

A

Active - induced by the pathogen: Neisseria gonorrhoea

Passive- induced by the host cell/ tissue: Listeria monocytogen

Actin
internalin

30
Q

What is TOXIGENICITY?

A

The ability to produce toxins

31
Q

Toxin

A

substances produced by microbes with lethal effects on eukaryotic cells

32
Q

Types of Bacterial Toxins

A

Exotoxins are released from bacterial cells and may act at tissue sites or remote from the site of bacterial growth

Endotoxins (aka- Endotoxin, LPS )
are cell-associated substance.
released from growing bacterial cells and lysed cells (lysozyme, antibiotics)

33
Q

What is HOST IMMUNE SYSTEM EVASION?

A
34
Q

Types of HOST IMMUNE SYSTEM EVASION

A
  1. Antigenic heterogeneity
  2. Antigenic variation
    a. Antigenic drift
    b. Antigenic shift
  3. Capsule production
  4. IgA protease production
  5. Prevention of intracellular killing
    a. Avoiding entry into vagosome
    b. Avoiding phagosome-lysosome fusion
    c. Inactivation of lysosomal enzymes
    d. Development of resistance to lysosomal enzymes