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319 final > ch. 15 - Microbial Mechanisms of Pathogenicity > Flashcards

ch. 15 - Microbial Mechanisms of Pathogenicity Flashcards

1
Q

Components for the host pathogen interaction

A
  1. Invasion of the host through primary barriers
  2. Evasion of local and tissue host defenses by microbes
  3. Microbe replication, with or without spread in the body
  4. A hosts immunologic ability to eliminate or control the microbe
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2
Q

Pathology

A

study of disease

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3
Q

Etiology

A

study of the cause of disease

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4
Q

Pathogenesis

A

development of disease

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5
Q

Infection

A

multiplication of any parasitic organisms

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6
Q

Disease

A

disturbance in the state of health
- body can’t carry out all of its normal functions

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7
Q

Order of characteristics of infectious disease

A

Pathology can cause Etiology
Etiology can cause Pathogenesis
Infection can cause Disease

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8
Q

Microorganisms that can cause disease are known as

A

pathogens

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9
Q

Signs of Disease

A
  • objective and measurable
  • directly observed by a clinician
  • changes in any vital signs may be indicative of disease

ex: fever of 102, fluid-filled rash

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10
Q

Symptoms of Disease

A
  • subjective
  • felt or experienced by a patient but cannot be confirmed or measured
  • changes in any vital signs may be indicative of disease

ex: pain, fatigue

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11
Q

issue with medical professionals relying only on sign and symptoms to diagnose some diseases

A

medical professionals rely heavily on signs and symptoms to diagnose disease and prescribe treatment, however
- many diseases can produce similar signs and symptoms

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12
Q

Syndrome

A

A specific group of signs and symptoms
- e.g. chronic fatigue syndrome

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13
Q

Infectious disease

A

any disease caused by the direct effect of a pathogen/infectious agent

ex: Measles is highly infectious, caused by viral droplets. Ghonorrhea is not as contagious because transmission requires close contact

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14
Q

Noninfectious disease

A

Those not caused by pathogens.

Can be caused by genetics, the environment, poison etc.

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15
Q

Communicable or contagious diseases

A

Communicable - can be spread from host to host
Contagious - easily spread from person to person

ex: measles, hepatitis

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16
Q

Non-communicable disease

A

cannot be spread from host to host

ex: food poisoning, tetanus

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17
Q

iatrogenic disease

A

diseases that are contracted as the result of a medical procedure

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18
Q

Nosocomial disease

A

Diseases acquired in hospital settings

ex: patient, staff, visitor etc.

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19
Q

Zoonotic disease

A

transmitted from animals → humans

ex: rabies

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20
Q

Subclinical disease

A

no noticeable signs or symptoms (inapparent infection)

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21
Q

The five stages of disease

A
  1. incubation
  2. prodromal
  3. illness
  4. decline
  5. convalescence
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22
Q

stages of disease: Incubation period

A

occurs after the initial entry (infection) of the pathogen
- but before the first appearance of any signs or symptoms

→ insufficient number of pathogen particles present to cause signs and symptoms of disease
* can vary from a day or two to months

→ during this phase, the number of organisms rises in the body
* until the immune system recognizes that an invader is present

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23
Q

stages of disease: Prodromal period

A

occurs after the incubation period
* pathogen continues to multiply and host begins to experience mild symptoms
(e.g. aches and malaise)

immune system recognizes that an invader is present
* begins to attack the organism or virus

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24
Q

stages of disease: Period of illness

A
  • occurs after prodromal period
  • signs and symptoms are most obvious and severe (sore throat, fever)
  • pathogen reaches peak numbers
  • immune system is becoming more efficient at killing the pathogen
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25
Q

stages of disease: Decline Phase

A
  • occurs after period of illness
  • signs and symptoms begin to decline (e.g. fever decreases)
  • however, patients may become susceptible to developing secondary infections because their immune systems are weakened
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26
Q

stages of disease: Convalescence period

A
  • occurs after decline phase
  • patient generally returns to normal functions
  • the immune system is ready to fight future infections but
    its ability to attack the same invader will wane over the long term (years)

Typhoid fever and cholera - the convalescing person carries the pathogenic microorganism for months or even years

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27
Q

fever

A

natural reaction to infection
- sweating, shivering, and feeling cold
- protective mechanism to fight infection

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28
Q

why are high body temperatures from fevers beneficial?

A

high body temperatures can help our immune system function better
- can also inhibit microbial growth

note: ideal growth temperature for many microbes is 37 degrees C

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29
Q

Pyrogens

A

substances that cause fever
- chemicals released by the immune system that cause the body temperature to rise, resulting in a fever
- fevers are meant to create an unfavorable environment for the pathogen

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30
Q

Acute disease

A

symptoms develop rapidly
ex: common cold

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31
Q

Chronic disease

A

disease develops slowly
ex: Tuberculosis

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32
Q

Subacute disease

A

symptoms between acute and chronic

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33
Q

Latent disease

A

disease with a period of no symptoms
- when the causative agent is inactive (dormant)

ex: cold sore produced by a reactivated herpesvirus hiding latent in nerve cells

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34
Q

Koch’s postulate

A

method for determining whether a particular microorganism was the cause of a particular disease

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35
Q

Koch’s postulates criteria

A
  1. the suspected pathogen must be found in every case of disease but not present in healthy individuals
  2. the suspected pathogen must be isolated from the diseased organism and grown in pure culture
  3. a healthy test subject infected with the suspected pathogen must develop the same signs and symptoms of disease as seen in postulate 1
  4. the pathogen must be re-isolated from the new host and must be identical to the pathogen from postulate 2
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36
Q

Limitations to Koch’s postulate

A
  • it assumes pathogens are only found in diseased individuals, which is not true
  • assumes all healthy tests subjects are equally susceptible
  • assumes all pathogens can be grown in pure culture
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37
Q

Molecular Koch’s postulates

A
  • Stanley Falkow proposed a revised form of Koch’s postulates in 1988
  • relies not on the ability to isolate a particular pathogen, but rather to identify a gene that may cause the organism to be pathogenic
  • usual harmless bacteria, such as E. coli, can acquire genes that now make them pathogenic
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38
Q

molecular Koch’s postulates criteria

A
  1. the phenotype (sign or symptom of disease) should be associated only with pathogenic strains of a species
  2. inactivation of the suspected gene(s) associated with pathogenicity should result in a measurable loss of pathogenicity
  3. reversion of the inactive gene should restore the disease phenotype
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39
Q

molecular Koch’s postulates criteria applied to Enterohemorrhagic E. coli (EHEC)

A
  1. EHEC causes intestinal inflammation and diarrhea, whereas nonpathogenic strains of E. coli do not
  2. one of the genes in EHEC encodes for Shiga toxin, a bacterial toxin (poison) that inhibits protein synthesis
    - inactivating this gene reduces the bacteria’s ability to cause disease
  3. by adding the gene that encodes the toxin back into the genome (e.g. with a phage or plasmid), EHEC’s ability to cause disease is restored
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40
Q

Pathogenicity

A

ability of a pathogen to cause disease

factors that pathogenicity depends on:
- virulence
- attenuation

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41
Q

Virulence

A

intensity of the disease produced by the pathogen

  • avirulent (not harmful)
  • virulent (harmful)
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42
Q

Attenuation

A
  • weakening of the disease-producing ability of the pathogen
  • attenuated vaccines contain crippled viruses or bacteria that are injected into a host to stimulate an immune response
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43
Q

Two indicators of virulence

A

1. median infectious dose (ID50)
- measured by determining how many microbes are required to cause disease symptoms in 50% of the experimental group of hosts

2. Median lethal dose (LD50)
- number of bacteria or virus particles (virions) required to kill 50% of an experimental group of animal hosts

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44
Q

actual infective dose for an individual depends on what factors?

A
  1. route of entry
  2. age
  3. health of the host
  4. immune status of the host
  5. environmental factors
  6. pathogen-specific factors
    - e.g. susceptibility to the acidic pH of the stomach
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45
Q

what are the types of pathogens

A
  • primary pathogen
  • opportunistic pathogen
46
Q

Primary pathogen

A

always cause disease
- regardless of the hosts’s resident microbiota or immune system

47
Q

Opportunistic pathogen

A

can only cause disease when the host’s defenses are compromised

48
Q

Stages of Pathogenesis

A
  1. exposure or contact
  2. adhesion
  3. invasion
  4. infection
  5. pathogen exit
49
Q

stages of pathogenesis: Adhesion

A

the capability of pathogenic microbes to attach to the cells of the body

e.g.
Glycocalyx produced by bacteria in a biofilm allows the cells to adhere to host tissues and to medical devices such as the catheter
- glycocalyx is an adhesin

50
Q

Adhesins/Ligands

A

both bind to receptors on host cells
- adhesins help ligands bind to receptors

Adhesins: any microbial factor that promotes attachment
- they also help form biofilms

examples of adhesins:
- Type I Fimbriae
- Type IV Pili
- cell wall components
- virus envelope receptors

ex:
1. Glycocalyx: Streptococcus mutans
2. Fimbriae: Escherichia coli
3. M protein (on fimbriae): *Streptococcus pyogenes
- helps with evading phagocytosis

51
Q

stages of pathogenesis: Invasion

A

the entry of a pathogen into a living cell, where it then lives
- once adhesion is successful, invasion can proceed

Invasion involves the dissemination of a pathogen
- throughout local tissues or the body

ex: H. pylori is able to invade the lining of the stomach by producing virulence factors that allow it to pass through the mucin layer covering epithelial cells
- i.e. releases urease

52
Q

Invasiveness

A

the ability of a bacterial pathogen to spread rapidly through tissues

53
Q

Infection

A

multiplication of the pathogen

54
Q

Portals of exit

A

generally the same as the portals of entry

  • mucous membranes
  • skin
  • respiratory
  • urogenital
  • GI tract
55
Q

Once organisms enter a host, how do they cause disease?

A

virulence factors
- pili
- enzymes that harm the host or prevent detection
- proteins that disrupt normal cellular function
- capsule
- enzymes that inactivate antibiotics

Pathogenicity island: a genomic island that contains virulence factors

56
Q

Intracellular pathogens

A

avoid immune mechanisms
- by living inside host cells

57
Q

Facultative intracellular pathogens

A

can invade host cells but can also survive outside the host cell

ex: Salmonella, Shigella, Listeria

58
Q

Obligate intracellular pathogens

A

invade and reproduce inside a host cell only

ex: Rickettsia, Coxiella, Bartonella

59
Q

what do pathogens produce to invade host cells

A
  • exoenzymes
  • toxins
60
Q

exoenzyme

A

enzymatic virulence factors that help bacteria invade tissue and evade host defenses
- e.g. S. aureus produces coagulase, blood clot protects bacteria, also produces streptokinase which dissolves clot and releases bacteria to invade

four classes mentioned:
1. glycohydrolase
2. nuclease
3. phospholipases
4. proteases

61
Q

exoenzymes: Glycohydrolases

A

degrades hyaluronic acid (i.e. hyaluronan) that cements adjacent cells together in the epidermis
- promotes spreading through tissues

e.g. Hyaluronidase S in S. aureus

62
Q

hyaluronidase S in Staphylococcus aureus

A

hyaluronidase S = glycohydrolase (exoenzyme)
- allows for passage between cells that would otherwise be blocked (deeper tissues)

hyaluronidase produced by S. aureus degrades hyaluronan (hyaluronic acid) in the extracellular matrix

note: S. pyogenes also has hyaluronidase

63
Q

exoenzyme: Phospholipases

A

degrades phospholipid bilayer (membrane) of host cells
- causing cellular lysis, and degrade membrane of phagosomes
- enables escape into the cytoplasm

e.g. Phospholipase C of Bacillus anthracis

64
Q

exoenzyme: Nucleases

A

degrades DNA released by dying cells that can trap the bacteria,
- thus promoting spread

e.g. DNAse produced by S. aureus

65
Q

exoenzyme: Proteases

A

degrades collagen in connective tissues to promote spread
- exoenzyme

e.g. Collagenase in C. perfringens

66
Q

Toxin

A

substance produced by pathogen, contributes to pathogenicity
- allows microorganisms to colonize and damage the host tissues

e.g. patient with edema
- bacteria causes the release of pro-inflammatory molecules from immune cells
- these molecules cause an increased permeability of blood vessels, allowing fluid to escape the bloodstream and enter tissue

67
Q

Toxigenicity

A

ability to produce a toxin

68
Q

Toxemia

A

presence of toxin in the host’s blood

69
Q

Toxoid

A

inactivated toxin used in a vaccine
- tetanus

70
Q

Antitoxin

A

antibodies against a specific toxin

71
Q

Exotoxins

A

toxic substances (proteins) produced inside pathogenic bacteria and are released outside the cell
- most commonly Gram-positive bacteria, as part of their growth and metabolism

exotoxins are secreted into the surrounding medium
- done during log phase

e.g. Clostridium botulinum which is a Gram-positive bacteria that produces exotoxins

72
Q

Endotoxins

A

the lipid A portion of the lipopolysaccharides (LPS) that are part of the outer membrane of the cell wall of Gram-negative bacteria
- endotoxins are released when the bacteria die and the cell wall breaks apart

  • fever, clotting factors, vasodilation, shock, and death may result when endotoxin is released into the blood

e.g. Salmonella typhimurium is a Gram-neg bacteria that produces endotoxins

73
Q

exotoxin vs. endotoxin

A

exotoxins are proteins which are released from the cell
- endotoxins are composed of lipids and are part of the cell membrane

74
Q

characteristics of endotoxins:

A

the source of endotoxins are Gram-negative bacteria
- it is found in the outer membrane (lipid A part of the lipopolysaccharide)

endotoxins have the ability to produce a fever
- unable to be neutralized by antitoxin

LD50 (lethal dose 50%) level is relatively large
- it is also relatively stable

the effect on tissues are non-specific
- cannot convert to a toxoid or be used as one

75
Q

characteristics of exotoxins:

A

found in mostly Gram-positive bacteria
- they are protein by-products of the growing cell

exotoxins are unable to cause a fever
-they have a highly specific effect on tissues
- the LD50 (lethal dose median) is small

unstable
- they denature at temperatures above 60 degrees C
- UV can also denature them

converted to a toxoid by heat or chemical treatment
- the toxoid can be used against the toxin
- or can be neutralized by an antitoxin

76
Q

what are the highly specific effects that exotoxins can do

A

1. plasma membrane disruption
2. cytoskeleton alterations
3. protein synthesis disruption
4. cell cycle disruption
5. signal transduction disruption
6. cell-cell adhesion disruption
7. vesicular trafficking
8. exocytosis

e.g. E. coli binds to the villus and secretes toxins that disrupt normal function (plasma membrane disruption)

77
Q

exotoxin categories

A

grouped into three categories based on their target:
1. intracellular-targeting toxins
- A-B exotoxins
2. membrane-disrupting toxins
3. superantigens

78
Q

Superantigens

A
  • exotoxins that trigger an excessive activation of the immune and inflammatory response
  • high fevers, low blood pressure, multi-organ failure, shock, and death
  • e.g. pyrogenic (fever-producing) toxins of S. aureus such as toxic shock syndrome and S. pyogenes
79
Q

A-B exotoxins

A

type of intracellular-targeting toxins (exotoxin) comprised of two components:
- A subunit and B subunit

A subunit
* A subunit is for activity and is toxic
* The A subunits of some AB toxins posses an ADP-ribosyltransferase enzymatic activity → changes specific host cell functions (e.g. diphtheria toxin)

B subunit
* B subunit binds host cell receptors → delivers the A subunit to the host cell
* Many B subunits are complexes of 5 units arranged as a ring

80
Q

AB subunit mechanism

A
  1. The B component binds to the host cell by interacting with specific cell surface receptors
  2. the toxin is brought in through endocytosis
  3. once inside the vacuole, the A component separates from the B component
    - A component gains access to the cytoplasm
    - B subunit remains in the vacuole
81
Q

Mechanism of diphtheria AB toxin

A

inhibits protein synthesis
- A subunit inactivates elongation factor 2 (EF-2) by transferring an ADP-ribose
→ this stops protein elongation, inhibiting protein synthesis, and killing the cell

type of A-B subunit that exhibits ADP-ribosyltransferase enzymatic activity
- which changes specific host cell functions

82
Q

Primary infection

A

acute infection
- causes the initial illness

83
Q

Secondary infection

A

opportunistic infection
- after a primary (predisposing) infection

occurs during decline stage of disease
- immune system susceptible to secondary infections here

84
Q

Local infection

A

Pathogens are limited to a small area of the body

85
Q

Systemic infection

A

an infection throughout the body

86
Q

Focal infection

A

systemic infection that began as a local infection

87
Q

Sepsis

A

toxic inflammatory condition
- arising from the spread of microbes → bloodstream,
- especially bacteria or their toxins, from a focus of infection

88
Q

Bacteremia

A

bacteria in the blood

89
Q

Septicemia

A

growth of bacteria in the blood
- causes sepsis

90
Q

Viremia

A

viruses in the blood

91
Q

virulence factor: immune evasion

A

evading the immune system is important to invasiveness
- specifically evading phagocytosis by cells of the immune system

examples:
- capsules formed around bacteria cells
- proteases break down host antibodies to evade phagocytosis

92
Q

immune evasion (virulence factor): proteases

A

antibodies normally function by binding to antigens (molecules on surface of pathogenic bacteria)
- phagocytes bind to antibody → initiate phagocytosis

some bacteria can produce proteases (exoenzyme)
- they break down host antibodies → evasion of phagocytosis

93
Q

immune evasion (virulence factor): fates of bacterial pathogens inside phagosome

A

a bacterial pathogen attaches to a host cell membrane
- pathogen induces phagocytosis
- once inside the phagosome, pathogen has 1 of 3 fates, depending on the pathogen:

fate 1: pathogen undergoes phagosome-lysosome fusion
- differentiates into a form that is able to replicate in the phagolysosome
- results in inclusion bodies
e.g. Coxiella burnetii

fate 2: no fusion of phagosome with lysosome
2a: pathogen prevents fusion with lysosome (e.g. Salmonella)
2b: phagosome moves to host membrane and expels pathogen into extracellular space (e.g. Salmonella Typhi)
2c: bacterium can be engulfed by a microphage and survive within the phagosome
2d: the macrophage travels to regional lymph nodes and disseminate the organism through the circulatory system

fate 3: pathogen lyses phagosome before fusion with lysosome
- and then moves throughout the cytoplasm into adjacent cells by forming actin tails
e.g. Shigella and Listeria

94
Q

viral virulence: antigenic variation

A

changing surface antigens so that they are no longer recognized by the host immune system
- occurs in certain types of enveloped viruses
- this includes influenza viruses

exhibits two forms of antigenic variation
- antigenic drift
- antigenic shift

95
Q

antigenic drift

A

form of slight antigenic variation
- occurs because of point mutations in the genes that encode surface proteins

96
Q

antigenic shift

A

form of major antigenic variation
- occurs because of gene reassortment

97
Q

Antigenic drift in influenza virus

A

mutations in the genes for the surface proteins neuraminidase and/or hemagglutinin
- result in small antigenic changes over time

98
Q

Antigenic shift in influenza virus

A
  • simultaneous infection of a cell with two different influenza viruses results in mixing of genes
  • resultant virus possess a mixture of the proteins of the original viruses

process:
virus A & virus B both infect same host cell → mixing of genes
- A & B have different influenza viruses
- resultant virus has mixture of proteins from original viruses
(e.g. virus C has hemagglutinin from B and neuraminidase from A)

influenza pandemics can be traced back to antigenic shifts

99
Q

protozoa: Antigenic Masking

A

protozoans coat themselves in host antigens
- to avoid detection by the immune system

100
Q

protozoan pathogenesis: Antigenic Variation

A

some protozoans can alter their surface antigens to prevent antibody binding
- just like viruses and bacteria,

example: Trypanosoma brucei - the causative agent of sleeping sickness,
- contains hundreds of silent variant surface glycoproteins (VSG) genes that can become activated one at a time → different antigen with each VSG gene

101
Q

antigenic variation in Typanosoma brucei

A

T. brucei coated with one type of variant surface glycoprotein (VSG) antigen (“green”)
- eventually, antibodies build up that can attack the green form of VSG and kill the cells

however, a few protozoa will begin expressing a different VSG (“blue”) that the antibody does not recognize
- these variants survive and repopulate the blood

this cycle continues because the T. brucei genome contains hundreds of silent VSG genes that can become activated
- one at a time is activated

102
Q

protozoa: Intracellular Location

A

protozoans have found ways to live inside the host cell to prevent detection
- just like some bacteria

example:
* Toxoplasma species use an actin-myosin motor of their own
- to forcibly drive themselves into a host cell

103
Q

protozoa intracellular location: Toxoplasma

A
  1. Toxoplasma approaching a host cell uses MIC proteins to attach to host cell membrane
  2. the myosin motor propels the organism through the membrane
    - without forming a phagocytic vacuole
  3. a protease located at the parasite’s posterior cleaves the adhesin
    - allows internalization
104
Q

protozoa: Immunosuppression

A

Some protozoans induce the secretion of anti-inflammatory cytokines
- to reduce the innate immune response

e.g. Plasmodium makes a protein that mimics human macrophage inhibitory factor
- this malarial protein alters the blend of cytokines

105
Q

Medically important fungi include

A

Trichosporon species
- can infect hair, skin, and nails

Malassezia species
- infect skin to produce hyper pigmented patches
- a disease called tinea versicolor

106
Q

Systemic fungal pathogens cause

A

diseases in:
- central nervous system
- GI tract
- tissues
- respiratory system (serious)

note: diseases all around the body

107
Q

examples of pathogenic fungi that can produce virulence factors similar to bacterial virulence factors

A

Candida albicans is an opportunistic fungal pathogen
- produces adhesions (surface glycoproteins) → assist in spread and tissue invasion
- produces proteases and phospholipases → increases ability of the fungus to invade host tissue

Cryptococcus’ main virulence factor is capsule production
- causes pneumonia and meningitis

Histoplasma and Blastomyces are thermally dimorphic fungi
- most grow as hyphae at 25 degrees C
- when temperature rises to 37 degrees C (body temperature), they grow as yeast which is the most pathogenic form

108
Q

human host defense mechanisms and fungal virulence factors

A

X. H: human host defense → F: fungal virulence factor
- aspect of fungal virulence factor
H: human, F: fungi

  1. H: toxic compounds production → F: robustness/stress resistance
    - cell wall
    - detoxification
  2. H: recognition and phagocytosis → F: immune evasion
    - masking of PAMPs: capsule, pigments
    - escape from immune cells
  3. H: inflammation → F: damage
    - physical forces
    - secreted enzymes
    - toxins
  4. H: epithelial barriers → F: adhesion/invasion
    - biofilm formation
    - translocation
  5. H: nutritional immunity → F: growth in the host
    - 37 degrees C (some forms of fungi can survive at body temp)
    - host derived nutrients
    - adaptation to niches
  6. H: danger response → F: morphological transition
    - yeast ↔ hypha
    - spore ↔ yeast
    - spore ↔ hypha
109
Q

Mycotoxins

A

Fungal toxins

  • Claviceps purpurea, a fungus that grows on rye and related grains,
  • produces a mycotoxin called ergot toxin, an alkaloid responsible for the disease known as ergotism
110
Q

Aflatoxin

A

virulence factor produced by the fungus Aspergillus
- type of mycotoxin

  • enter the body via contaminated food or by inhalation
  • chronic pulmonary disease aspergillosis
111
Q

who is at highest risk for fungal infections

A

immunocompromised patients

Candida albicians can cause opportunistic infections if they breach normal innate defense mechanisms

112
Q

host injury during most fungal infections is due primarily to…

A

collateral damage produced by the immune system
- as a result of fighting the infection

319 final (6 decks)

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