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Introductory Microbiology > Microbiology of Pathogenic Factors > Flashcards

Microbiology of Pathogenic Factors Flashcards

1
Q

What is amensalism?

A
  • also called microbial antagonism
  • one organism is harmed while the other neither benefits or is harmed
  • ex. fungus secreting an antibiotic, inhibiting nearby bacteria
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2
Q

What is normal flora?

A
  • resident microbiota permanently colonize the host
  • transient microbiota temporarily colonize throughout exposure to that environment
  • do not produce disease under normal conditions
  • distribution and composition determined by various factors in the host’s environment
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3
Q

What factors determine distribution and composition of normal flora?

A
  1. Nutrients; secretory and excretory products of cells, bodily fluids, food in GI tract
  2. Physical and Chemical Factors; temperature, pH, O2, CO2, salt, sunlight
  3. Mechanical Factors; chewing, flow of saliva and peristalsis of GI tract, mucous of ciliary action of respiratory system (must be able to tolerate)
  4. Other “Host” Factors; age (quality of flora declines), nutritional status, disability, stress, personal hygiene, lifestyle, geography, occupation
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4
Q

How might gravity affect distribution of normal flora?

A

If laying down for an extended period of time, normal flora in the urogenital tract can migrate upwards and cause infection

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5
Q

Microbial Antagonism

A

Normal flora commensals benefit the host by preventing growth of pathogenic microbes; “competes” for the space by:

  • competing for nutrients
  • producing substances harmful to the pathogen
  • manipulating the host environment by altering pH levels and O2 levels
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6
Q

E. Coli and Microbial Antagonism

A
  • produces bacteriocins, proteins that inhibit the growth of closely related species of bacteria such as salmonella and shigella
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7
Q

How may the balance between normal flora and pathogenic microbes be altered?

A
  • when the balance between the normal flora and pathogenic microbes is altered (i.e. microbial antagonism fails) disease can result
  • age
  • antibiotic use
  • changes in hygiene
  • nutritional status
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8
Q

Clostridium Difficile

A
  • C. diff is a pathogen that causes a range of GI symptoms, from mild diarrhea to severe, or even fatal colitis
  • presence of normal flora in the large intestine inhibits the growth of C. diff
  • antibiotic-mediated destruction of the GI normal flora creates and environment conducive to C. diff growth, resulting in disease
  • most people colonized with this microbe
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9
Q

Opportunistic infections occur when…

A
  1. Microbes from the host normal flora move from their normal habitat, causing disease (ex. E. coli gains access to other body sites such as urinary tract or wounds causing a UTI)
  2. The host’s immune system is weakened/compromised (ex. Pneumocystis jirovecii causes pneumonia when immunocompromised, but not in a healthy person)
  3. Changes occur in the composition of the host normal flora (ex. Shift on the relative abundance of microbes due to antibiotics creates opportunity for another species to thrive and cause disease)
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10
Q

What is pneumocystis jirovecii?

A

A fungus found in ceiling tiles; has no effect on healthy persons but can cause pneumonia in those who are immunocompromised

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11
Q

What are the 5 steps in the pathogenetic process of microorganisms?

A
  1. Contact/Exposure
  2. Adherence
  3. Evasion of Host Defenses and Penetration
  4. Damage of Host Cells
  5. Transmission
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12
Q

What is the most common portal of entry for pathogens?

A

Respiratory tract - mouth and nose, lungs

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13
Q

What are 3 types of portals of entry in which we gain exposure to microbes?

A
  1. Mucous membranes - upper respiratory tract; GI tract; GU tract; conjunctiva of eye
  2. Skin - when unbroken serves as a very strong barrier, however some bacteria an enter body via natural openings in the skin such as hair follicles and sweat gland ducts (ex. MRSA)
  3. Direct deposition beneath mucous membranes or skin - trauma (punctures, wounds, cuts); surgery; invasive procedures
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14
Q

What is microbial adherence?

A
  • means by which a pathogen attaches itself to host tissues at portal of entry
  • accomplished by cell surface molecules located on the pathogen called “adhesins” binding specifically to surface “receptors” located on the cells of host tissues
  • adhesins are host and tissue specific
  • only when there is a match between adhesin and receptor that adherence and this infection can occur
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15
Q

What are the 3 types of adhesins?

A
  1. Bacterial structures - fimbriae/pili, flagella
  2. Adherence proteins - M protein, Opa protein, etc.
  3. Glycocalyx - capsule, slime layer
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16
Q

How do bacterial structures aid in adherence?

A
  • adhesins present on the fimbriae and flagella of many bacteria
  • P-fimbriae on pyelonephritogenic E. coli adhere to a specific galactose disaccharide founding the surface of uroepithelial cells, responsible for 90% of UTIs
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17
Q

How do adherence proteins aid in adherence?

A
  • M proteins produced by streptococcus pyogenes (GAS) appear as hair-like projections from cell surface
  • mediates attachment of bacteria to epithelial of the host - many subtypes
  • some subtypes more strongly associated with specific diseases than others
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18
Q

How does glycocalyx aid in adherence?

A

Two types:

  • capsule (if well organized and firmly attached to cell wall)
  • K1 capsule associated with some strains of Neisseria meningitidis type b (causes meningitis); will bind to epithelial cells of the ventricles and vascular endothelium of the brain
  • slime layer (unorganized and loosely attached to cell wall); facilitates the formation of biofilms
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19
Q

What are biofilms?

A
  • colony of bacteria that adheres to surfaces (living and non-living), embedded in an extracellular slime layer that surrounds neighboring organisms
  • can bind to teeth, medical catheters, heart valves, hip replacements, contact lenses, food equipment, etc.
  • may involve multiple bacterial species and consist of many layers
  • involved in many bacterial infections in humans,especially CHRONIC infections
  • highly resistant to disinfectants and antibiotics
  • shelters microorganisms from host immune system
  • few treatments available (i.e. enzymatic bacteriophages), surgery often required
20
Q

How do capsules also contribute to evasion of host defences?

A
  • impairs phagocytosis, preventing immune cells from adhering to microbe and increasing virulence of the pathogen
  • by the time antibodies are produced against the capsule, infection has already occurred
  • bacteria needs a capsule to create an infection (ex. S. pneumoniae)
21
Q

How does the cell wall contribute to evasion of host defenses?

A
  • M proteins increase virulence by helping bacteria resist phagocytosis by WBC (ex. Streptococcus pyogenes)
  • Mycolic acid present in the cell wall of mycobacterium tuberculosis increases virulence by resisting digestion by phagocytosis
22
Q

What two enzymes are important for bacterial evasion of the host?

A
  • coagulase and kinase

- don’t always have both

23
Q

How does coagulase assist in evasion of the host?

A
  • coagulates fibrinogen in the blood to form fibrin
  • fibrin clot protects the bacteria from phagocytosis and isolates the microbe from other defenses; allows it to “hide”
  • can be negative or positive
  • ex. Staphylococci spp.
24
Q

How does kinase assist in evasion of the host?

A
  • degrades fibrin and digests clots formed by the body to isolate the wound
  • will also degrade clot made by bacteria so that it can leave in great numbers
  • also facilitates microbe’s entry into host tissues
  • streptokinase produced by Streptococcus pyogenes
  • staphylokinase produced by Staphylooccus aureus
25
Q

What mechanisms allow facultative intracellullar bacteria to live inside immune cells?

A

1) Escaping phagosomes before fusing with host cell lysosomes
2) Preventing phagosome-lysosome fusion
3) Reducing effectiveness of toxic compounds within lysosome
4) Producing cell walls resistant to lysosomal proteases

26
Q

How can the ability for bacteria to live in immune cells be problematic?

A
  • can travel to other places via immune cells travelling through circulation
27
Q

What is hyaluronidase?

A
  • degrades hyaluronic acid, a polysaccharide that holds host cells together, and allows bacteria to penetrate deeper into host tissues
28
Q

What is collagenase?

A
  • degrades collagen fibers at the base of superficial tissues and allows bacteria to move deeper into tissue
29
Q

What are invasins?

A
  • rearrange actin filaments in epithelial cells of the intestinal lumen
  • disruption of cytoskeleton induces “membrane ruffling” of the host cell - bacterium sinks into the ruffle and is engulfed by the host cell
  • used by Salmonella spp. and E. coli spp. to enter host cells that are not phagocytic
30
Q

What is membrane ruffling?

A
  • occurs when invasins disrupt the cytoskeleton of a cell
  • allows bacteria to sink into the ruffle and become engulfed by cell
  • once inside host, bacteria becomes enclosed in a vesicle and will induce an inflammatory response
  • can move from the epithelial cells into the bloodstream (causing sepsis), or enter phagocytes where they reproduce and grow
31
Q

What advantage do bacteria gain from living within host cells?

A
  • abundance of nutrients, protected from immune system, partially protected from antibiotics
32
Q

By what mechanisms do host cells experience damage from microbes?

A

1) Appropriating host nutrients
2) Causing direct damage to tissues surrounding site of invasion
3) Producing toxins
4) Inducing hypersensitivity reactions (allergy)

33
Q

Organisms that result in death of the host…

A
  • are failures; they die with the host

- need us to be symptomatic to spread but still tolerate disease

34
Q

How do microbes appropriate host nutrients?

A
  • most pathogenic bacteria require iron to grow
  • in humans, iron is tightly bound to iron transport proteins
  • microbes can become iron deficient
  • employ several strategies to obtain iron from host
35
Q

How do bacteria obtain iron from the host?

A

1) Siderophores: receptors on bacteria bind more tightly to iron than host transport proteins; have a greater affinity
2) Direct binding to host iron-binding proteins: loosens bond and allows bacteria to take iron
3) Producing toxins: toxins destroy host cells, releasing the iron stores of the host

36
Q

How do bacteria cause direct damage to tissues surrounding the site of invasion?

A
  • as intracellular bacteria and viruses metabolize and multiply in host cells, the host cell typically ruptures to facilitate their release, destroying host cell
  • once released, pathogens spread to other tissues in great numbers
37
Q

How do toxins cause damage to host cells?

A
  • alter normal metabolism of host cells
  • inhibit protein synthesis, destroy RBCs and blood vessels, and disrupt nervous system function
  • effects are unique
38
Q

What are exotoxins?

A
  • enzymatic proteins produced INSIDE some living bacteria as a normal part of growth and metabolism
  • actively secreted into the environment, or released during cell lysis
  • soluble in bodily fluids
  • rapidly transported throughout the host, highly toxic in nature , exposure can be fatal
  • diseases associated with exotoxin-producing bacteria are caused by the toxins, not the pathogen
39
Q

What is botulism?

A
  • disease caused by ingestion or exposure to botulinum exotoxin
  • food poisoning
  • requires antitoxin to treat
40
Q

What are A-B exotoxins?

A
  • consist of A and B polypeptides
  • Part A is the ACTIVE enzymatic component
  • Part B is the BINDING component
  • ex. Bordetella pertussis produces a toxin that increases cAMP in respiratory epithelial cells, causing increased mucous and coughing (whooping cough)
41
Q

What are membrane disrupting toxins?

A
  • induce cell lysis via formation of protein channels (i.e. leukocidins, hemolysins) or disruption of phospholipid layer of membrane (i.e. phospholipases)
42
Q

What are superantigens?

A
  • provoke an intense immune response
  • similar to endotoxins; same capacity to produce shock
  • not processed inside macrophages
  • bind directly to MHC Class II proteins on macrophage surface, “skipping” steps in the immune response
  • result in excessive IL-2, TNF, and TF production
  • causes fever, N/V, diarrhea, shock and sometimes death
  • only this type of Gram positive toxin causes fever
  • ex. staphylococcal toxic shock syndrome
43
Q

What are endotoxins (Lipid A)?

A
  • stored in cell wall
  • released when Gram negative bacteria are killed (or multiply)
  • cell wall lyses, liberating the endotoxin
  • stimulate macrophages to release high levels of IL-1
  • all endotoxins produce the same signs and symptoms regardless of pathogen
  • chills, fever, weakness, generalized aches
  • increased production of tissue factor; activates extrinsic and intrinsic coagulation
  • will see disseminated intravascular coagulation (DIC); obstructive clots in capillaries, inducing tissue death
  • shock and death of host in severe cases
44
Q

How do endotoxins produce fever?

A
  • IL-1 released by macrophages in response to endotoxins travels to the hypothalamus
  • induces the hypothalamus to produces prostaglandins, which induce fever
45
Q

How are microbes transmitted from host to host?

A
  • leave the body via specific portals of exit in secretions, excretions, discharges or shed tissue
  • portal of exist are generally the same as the portals of entry
  • respiratory tract
  • GI tract
  • GU tract
  • skin, conjunctiva, blood, etc.

Introductory Microbiology (11 decks)

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