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SP14 - Micro Immuno Exam 3 > sp14_-_micro_immuno_exam_3_20141210195229 > Flashcards

sp14_-_micro_immuno_exam_3_20141210195229 Flashcards

1
Q

What is a mucosal surface? What are some examples in the human body?

A
  • surface that interacts with air that has associated glands for secreting mucus- oral cavity, respiratory tract, reproductive/urinary tract, gastrointestinal tract
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2
Q

What are the 3 types of defense for mucosal surfaces?

A
  • innate immunity- adaptive immunity- nonspecific barrier defenses
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3
Q

Why should we study gastrointestinal diseases?

A

estimated 76 million cases of intestinal infection in the US each year; approximately 500,000 require prolonged hospitalization and 5,000 will die

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4
Q

Why should oral health care practitioners care about gastrointestinal disease?

A

transmission of gram-negative mucosal pathogens from feces to mouth

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5
Q

How are gram-negative mucosal pathogens transmitted?

A

feces to mouth via any of the “seven F’s”: feces, food, fluids, fingers, flies, fomites, and fornication

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6
Q

What is inoculum size? What is indicated about the bacteria by a small inoculum size? By a large inoculum size?

A
  • the number of bacteria needed to cause a disease- small inoculum: bacteria is probably resistant to the body’s natural defenses; usually spread directly- large inoculum: bacteria is usually more susceptible to the body’s defenses; microbe is usually growing in food or in contaminated water
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7
Q

What are the natural barrier defenses that protect us from gram-negative pathogens?

A
  • secretory substances- anatomical and physiological barriers- indigenous microbiota
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8
Q

What are the 4 mechanisms through with anatomical and physiological barriers protect us from gram-negative pathogens?

A
  • acidity: ranges from pH 1-9- motility: peristalsis- mucous layer and underlying glycocalyx (carb layer that makes it difficult for the microbe to penetrate)- tight junctions
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9
Q

Where in the GI tract are gram-positive flora found? Anaerobes? Coliforms?

A
  • gram-positive flora: increasingly as you go through the stomach, duodenum, jejunum, ileum, and colon- coliforms: in the ileum and colon- anaerobes: in the ileum and colon
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10
Q

What are the 5 secretory antimicrobial compounds? What does each do?

A
  • lysozyme: cleaves linkages between NAG and NAM- lactoferrin: bacteriostatic effects via sequestering iron- cathelicidin: disrupts bacterial membranes of gram negative and gram positive (as well as fungi)- defensins: create pores in microbes; alpha defensins are produced by neutrophils and paneth cells while beta defensins are produced by epithelial cells- secretory immunoglobulins: IgA bind/coat pathogens to make it hard to attach to mucosal surfaces
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11
Q

What are the 3 ways pathogenic bacteria overcome innate barrier defenses?

A
  • acid resistance (microbes with a low infectious dose tend to be acid resistant)- fimbriae/pili: adhere to tissue to resist being shed- bacterial structures: cationic amino acids in the cell membrane reduce effects of antimicrobial peptides and siderophores sequester iron in low iron environments
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12
Q

What type of cell is an important component of mucosal immunity and why?

A
  • macrophages- recognize microbes via pattern recognition receptors which activate the macrophages and increases the ability of the host to kill many microbes
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13
Q

What TLR is the most important for gram-negative pathogens?

A

TLR-4

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14
Q

What is the negative side to initiating the inflammatory response at mucosal surfaces?

A

inflammatory cytokines (like TNF-alpha) can disrupt tight junctions between epithelial cells which will allow in microbes of the GI tract

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15
Q

What are 2 ways bacteria can resist phagocytosis?

A
  • development of capsule to resist phagocytosis- development of mechanisms capable of neutralizing the phagocytic compartment of macrophages
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16
Q

Where are the denses clusters of lymph nodes found? What is generated by the lymph nodes?

A
  • near mucosal tissue- adaptive immune system
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17
Q

What are the two main ways to cause disease in the gastrointestinal tract?

A
  • invasive bacterial pathogens- toxin-producing bacterial pathogens
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18
Q

What are the examples of invasive GI tract bacterial pathogens discussed in class?

A
  • salmonella- shigella
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19
Q

What are the examples of toxin-producing GI tract bacterial pathogens discussed in class?

A
  • vibrio (v. cholerae)- entertoxigenic E. coli (ETEC)
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20
Q

What are the examples of “hybrid” misfit GI tract bacterial pathogens discussed in class?

A
  • enterohemorrhagic E. coli (EHEC)- enteropathogenic E. coli (EPEC)
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21
Q

What is the difference between invasive, hybrid, and toxin-producing GI tract bacterial pathogens in large intestine vs. small intestine?

A
  • invasive: large intestine- toxin-producing: small intestine- hybrid: small and upper large intestine
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22
Q

What is the difference between invasive and toxin-producing GI tract bacterial pathogens in volume of stool?

A
  • invasive: small volume of stool- toxin-producing: copious amounts of watery stool
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23
Q

What is the difference between invasive, hybrid, and toxin-producing GI tract bacterial pathogens in bloodiness of stool?

A
  • invasive: bloody stool- toxin-producing: no blood in stool- hybrid: blood in stool (and possibly in urine with EHEC)
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24
Q

What is the difference between invasive and toxin-producing GI tract bacterial pathogens in presence of leukocytes in stool?

A
  • invasive: leukocytes in stool- toxin-producing: no leukocytes in stool
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25
Q

What is the difference between invasive, hybrid, and toxin-producing GI tract bacterial pathogens in tissue ulcerations?

A
  • invasive: tissue ulcerations- toxin-producing: no tissue damage- hybrid: colonization causes attaching and effacing lesion
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26
Q

What is the most severe Shigella species? The most prevalent in the US?

A
  • most severe: S. dysenteriae- most prevalent: S. sonnei
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27
Q

For Shigella, is the inoculum size small or large? Is it resistant to acid?

A
  • small inoculum- acid resistance
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28
Q

Where will Shigella usually multiply/colonize? How are the virulence genes activated?

A
  • in the colon- the anaerobic environment of the colon activates the virulence genes
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29
Q

How does Shigella invade the cells of the colon?

A
  • the M cells in the colon naturally sample what is in the lumen of the large intestine so they take in the Shigella via Shigella’s INVASION PLASMID ANTIGENS- while the mucosal surfaces is resistant to infection, the basal surface is not so Shigella invades via the basal surface- in the lamina propria, Shigella is ingested by macrophages which produces the inflammatory response that causes the illness- epithelial cells will ingest the bacteria, facilitated by bacterial factors- bacterial proteins lyse the phagosomal vesicle- intracellular spread facilitated by IcsA (an ATPase that causes actin polymerization)
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30
Q

What is the purpose of invasion plasmid antigens? What is the purpose of IcsA? What bacteria possesses these proteins?

A
  • help bacteria to invade M cells- ATPase that causes actin polymerization which allows the bacteria to go from one cell to the next without leaving the cell- Shigella
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31
Q

What damage is caused by Shigella?

A

ulcer (invaded cells die and slough off)

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32
Q

What type of Shigella is different? How so?

A
  • Shigella dysenteriae type 1- S. dysenteriae type 1 produces the Shiga toxin which kills intestinal epithelial and endothelial cells and disrupts sodium absorption; produces a larger volume of stool that is more watery and bloody
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33
Q

What are the 2 major diseases caused by Salmonella?

A
  • gasteroenteritis: S. typhimurium and S. enteritidis- typhoid fever: S. typhi and S. paratyphi
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34
Q

How is Salmonella transmitted? Is a small or large inoculum needed? Acid resistant?

A
  • fecal (human or animal) to oral transmission- relatively large inoculum required- more acid-sensitive than shigella
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35
Q

What induces the expression of virulence genes in Salmonella?

A

low pH induces the expression of at least 40 proteins found on the pathogenicity islands on large virulence plasmids

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36
Q

How does Salmonella invade cells?

A
  • when Salmonella approaches the cell’s surface, they induce an activity of cell signalling pathways and cause an increase in the cellular calcium concentration- this increase induces surface “ruffles” and uptake of the organism (microbe-directed phagocytosis)- Salmonella remains within the cell vesicles for many hours (unlike Shigella)- Salmonella is released into the lamina propria; somehow this induces NaCl loss from host cells- macrophages engulf most Salmonella but some escape to cause a transient bacteremia (the typhoid serovars will survive and grow within the macrophages)
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37
Q

How does Salmonella typhi differ from other Salmonella in terms of where it invades?

A
  • enters the lymphatic system- multiplication in macrophages in the liver, spleen, and bone marrow
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38
Q

Where does Salmonella typhi colonize in an asymptomatic carrier?

A

gall bladder

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39
Q

What is similar between Shigella and Salmonella?

A
  • both are invasive so they body cause bloody stool with leukocytes in the stool- both are able to respond to environmental changes
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40
Q

What is different between Shigella and Salmonella?

A
  • inoculum size- bacteremia (in Salmonella typhi?)- species that cause severe disease are very dissimilar
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41
Q

How are invasive enteric pathogens (Shigella and Salmonella) diagnosed? How are they treated?

A
  • identified based on symptoms and stool cultures- oral rehydration- antibiotic resistance first identified in Shigella so fluroquinolones are used- gall bladder removal (for infection with S. typhi)- vaccine to the capsule of S. typhi
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42
Q

What Vibrio species was discussed in class?

A

Vibrio cholerae

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43
Q

What are the two types of cholera? How do they differ?

A
  • El Tor- Classical- El Tor mutated the O1 antigen so that there is a new LPS serotype, it is encapsulated, and it affects all age groups
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44
Q

What are the virulence factors of V. cholerae?

A
  • flagella- pili: adhere to mucosal tissue; shift from salt water to reduced ion levels found in the body leads to expression of pili and the toxin- cholera toxin: phage encoded
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45
Q

What is the mechanism of the cholera toxin?

A

toxin constiutively activates adenylate cyclase so that cAMP is being made constantly; cAMP accumulates which makes the cell stop absorbing Na and secrete Cl which leads to the loss of water and diarrhea

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46
Q

What E. coli is associated with secretory diarrhea? Dysentery-like? Urinary tract infections?

A
  • secretory diarrhea: ETEC and EPEC- dysentery-like: EHEC- urinary tract infections: UPEC
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47
Q

Does ETEC have a large or small inoculum? Acid resistant?

A
  • large inoculum- not resistant to gastric acid
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48
Q

How does ETEC adhere to mucosal tissue?

A

colonization factor antigens (cfa)on fimbrae

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49
Q

What toxins are produced by ETEC? What is the mechanism of each?

A
  • heat-labile toxin (LT): similar to cholera toxin in that it also activates adenylate cyclase to increase cAMP to decrease Na absorption, increase Cl secretion, and produce diarrhea- heat-stable toxin (ST): same end effect as the heat-labile toxin but activates guanylate cyclase to increase cGMP
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50
Q

How is secretory diarrhea bacteria identified?

A
  • rule out Vibrio cholerae (more severe): eaten shellfish, been in endemic area, agar plating, agglutination test, or serological testing- inoculate plates with diluted stool samples without a rich medium and in aerobic incubation
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51
Q

How is secretory diarrhea (Cholera and ETEC) treated?

A
  • oral rehydration: mix of sugar and salt- antibiotics can help shorten the duration or reduce the severity (tetracyclines for Vibrio and flouroquinolones for ETEC)
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52
Q

What age is most commonly infected with EPEC? What is the symptom of an EPEC infection?

A
  • prevalent in newborns- noninflammatory secretory diarrhea
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53
Q

Where does EPEC infect? Large or small inoculum?

A
  • distal small intestine- large infectious dose
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54
Q

What is characteristic about EPEC? Describe it.

A
  • characteristic intimate adherence pattern (AKA attaching and effacing lesion)- bundle-forming pili (bfp) assist in adherence from a relative long distance; syringe-like secretion system (called Type III secretion) injects Tir into host cell; Tir binds to intimin on EPEC resulting in pedestal formation
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55
Q

What causes diarrhea in an EPEC infection?

A

no toxin production; malabsorption due to microvilli disruptions and disruption of epithelial tight junctions

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56
Q

What is similar and different between EPEC and EHEC?

A
  • EHEC has a set of EPEC genes so it also produces an attaching effacing lesion- EHEC also produces a toxin that can lead to hemolytic uremic syndrome (which is much more serious)
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57
Q

What is the most notorious EHEC?

A

E. coli O157:H7

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58
Q

What are the two resulting diseases from the shiga-like toxin of EHEC?

A
  • hemorrhagic colitis (colon)- hemolytic uremic syndrome (HUS) (kidneys)
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59
Q

What does the shiga-toxin affect?

A

attach small blood vessels in the mucosal surfaces of the large intestine; this can be intensified when inflammatory cytokines are present

60
Q

How is a EHEC infection usually diagnosed?

A
  • bloody stool with edema of the ascending colon- EHEC cannot ferment sorbitol- detection of Shiga-like toxins
61
Q

What is the usual treatment for EHEC?

A
  • CDC says no antibiotics because inflammation makes the toxin more potent- supportive therapy: rehydrate if necessary- dialysis if in kidneys (HUS)
62
Q

What is the most common form of bacterial infection of an organ system (not including the mouth) and the most frequent cause of doctor’s visits by adults?

A

urinary tract infection

63
Q

What is cystitis?

A

inflammation in the bladder

64
Q

How does the prevalence of UTI’s differ between males and females?

A
  • females: have increasing chance from age 10 and on- males: have a very low chance until age 45 when the prostate gland is less active and then have an increasing chance
65
Q

What is the difference between an uncomplicated and complicated UTI?

A
  • uncomplicated UTI: all normal defense mechanisms are intact; no recent hospital admissions; disease limited to lower urinary tract- complicated UTI: some structural abnormality in the urinary tract; recently admitted to the hospital; disease most likely will spread to kidneys; immune system repressed
66
Q

What are some natural defenses found in the urinary tract?

A
  • complete voidance of bladder- peristalsis- ureterovesicle valves- mucous layer- normal microbiota (lactobacillus)- pH (low pH due to lactobacillus)
67
Q

What are the 2 ways in which UPEC adheres to uroepithelial cells through fimbriae?

A
  • acute cystitis associated with fimbrial antigen FimH; colonizes the bladder- pyelonephritis is associated with the expression of P fimbriae; colonizes the kidney
68
Q

What does UPEC produce to aid its virulence?

A

production of aerobactin and hemolysin (associated with pyelonephritis (kidney infection)); hemolysin has the ability to lyse host cells

69
Q

What types of bacteria cause uncomplicated UTIs? Complicated UTIs?

A
  • uncomplicated UTIs: E. coli, Proteus mirabilis- complicated UTIs: Proteus mirabilis, Klebisella
70
Q

Which bacteria causes a more severe UTI: E. coli or Proteus mirabilis?

A

Proteus mirabilis

71
Q

What are the 5 virulence factors of Proteus mirabilis?

A
  • flagella: to allow Proteus to swim up ureters- adhesin on fibriae: to allow attachment in the urinary epithelium- hemolysins- IgA protease: to degrade IgA- urease: enzyme that raises the pH of the urine; toxic to renal cells; enhances formation of struvite (urinary stones) which can lead to chronic infection
72
Q

How are UTIs diagnosed?

A
  • difficult to positively ID the causative agent of the UTI- count bacteria in urine- Proteus diagnosed by consistently alkaline urine and production of urease
73
Q

What is the treatment for UTIs?

A
  • variety of antimicrobials- trimethoprim-sulfamethoxazone
74
Q

What is the appearance of Klebsiella?

A

large, mucoid colonies due to large capsule

75
Q

What are the 4 virulence factors of Klebsiella?

A
  • pili: type 1 for adherence in urinary tract (“I gotta go #1!”) and type 3 for adherence in the respiratory tract- enterotoxin similar to ST and LT of ETEC (induces secretory diarrhea)- aerobactin: an iron sequestering protein- antiphagocytic capsule: PRIMARY VIRULENCE FACTOR because the lungs have many alveolar macrophages so they need to resist phagocytosis
76
Q

What is one of the most prevalent gram-negative GI bugs?

A

Helicobacter pylori

77
Q

How is Helicobacter pylori transmitted? Where is it found in the body?

A
  • transmitted oral-to-oral (unique!) and fecal-to-oral- only found in the mucous overlying the mucous secreting cells of the stomach
78
Q

What does Helicobacter pylori do in the body for virulence?

A
  • producer of urease: makes neutral pH in stomach- inflammatory effector molecules: cause epithelial cells to produce IL-8 (acts as chemokine to recruit neutrophils)- cytotoxin is associated with peptic ulcer disease (induces vacuolation and apoptosis of epithelial cells)- down regulation of somatostatin-producing D-cells
79
Q

How can Helicobacter pylori cause cancer?

A

down-regulates somatostatin-producing D cells; somatostatin normally inhibits gastrin (gastrin leads to cell proliferation); with gastrin unregulated, cell proliferation increases

80
Q

How is Helicobacter pylori treated?

A
  • first line: proton pump inhibitor; antibiotic cocktail- second line: proton pump inhibitor; many antibiotics
81
Q

Is Neisseria gram-negative or positive? Motile? Aerobic or anaerobic? What is their reservoir?

A
  • gram-negative- non-motile (twitching motility from pili)- aerobic (but can grow anaerobically)- humans are their only reservoir
82
Q

What disease is caused by Neisseria?

A

gonorrhea

83
Q

How is Neisseria diagnosed?

A
  • cultured on chocolate agar in the presence of CO2- modified Thayer-Martin agar- catalase and oxidase reactions both positive- sugar fermentations
84
Q

What are the 2 major species of Neisseria? What are the major differences between them?

A
  • N. meningitidis: invades throat; large capsule; have blebs on the surface- N. gonorrhoeae: invades male urethra or female cervix; no capsule; phase/antigenic variation; smoother surface
85
Q

What is the encounter and entry process of Neisseria meningococci?

A
  • reservoir is human nasopharynx- attach to nasopharyngeal epithelial cells and invade mucous membranes- invasion of the blood stream only occurs in individuals deficient in complement component- Type IV pili (attach organism to meninges in CNS)- lipooligosaccharide (LOS) damages host tissue by eliciting inflammatory response, resulting in hemorrhaging of blood into the skin and mucous membranes
86
Q

What is the encounter and entry process of Neisseria gonococci?

A
  • human reservoir (asymptomatic carriers greater among women)- upon introduction, attach to columnar epithelia of cervix or urethra via pili and surface proteins- adhesins controlled by phase variation (presence/absence) and antigenic variation (composition)
87
Q

How does phase variation in E. coli work?

A

promoter inversion: expression of gene product is turned on or off at a high frequency based on the direction in which the promoter is facing

88
Q

How does phase variation in N. gonorrhoeae work?

A

slipped strand mispairing: controls surface proteins (colony opacity-associated opa genes) as well as LPS for whether or not the genes are expressed

89
Q

How does antigenic variation in N. gonorrhoeae work?

A

reassortment and recombination of the pilS loci changes the composition or structure of surface molecules

90
Q

How does Neisseria spread and multiply?

A
  • gonococci multiply rapidly and are shed in genital secretions (do not have flagella and are not motile)- they attach to non-ciliated cells that have microvilli- ciliated cell motility slows and ceases- ciliated cells die and slough from epithelial surface- non-ciliated microvili engulf bacteria; they are internalized by “parasite-directed endocytosis”- intracellular replication within vacuoles- intracellular traffic (vacuoles fuse with the basement membrane)- exocytosis in which the vacuoles discharge the bacteria into subepithelial connective tissueKNOW THIS
91
Q

What protease does Neisseria possess? What does it do?

A
  • extracellular IgA1 protease- removes the Fc-receptor end of the IgA1 antibody to enable escape from phagocytosisKNOW THIS
92
Q

What damage is done by Neisseria?

A
  • does not secrete exotoxins- LPS (LOS - lipooligosaccharides) and other cell wall components cause cell damage; induce tumor necrosis factor alpha (TNF-alpha) which leads to sloughing of ciliated cells and non-ciliated cell lysis which releases factors that cause inflammation
93
Q

What do antibodies target on Neisseria? How does Neisseria evade it?

A
  • LPS (LOS), protein I of the outer membrane, as well as other surface proteins- strains alter LPS with host-derived sialic acid which is a surface component of RBCs so they are able to camoflauge; this also leads to the possibility of self recognition
94
Q

What is the difference between the disease caused by N. gonococci and N. meningococci? Why do these differences exist?

A
  • N. gonococci: localized inflammation; rarely lethal (even when spread to the blood stream)- N. meningococci: colonize nasopharynx with no local symptoms; creates 3 general diseases (uncomplicated bacteremic process, metastatic infection of the meninges, and overwhelming systemic infection)difference in diseases because meningococci are heavily encapsulated and produce hemolysin
95
Q

What is Pelvic Inflammatory Disease in females? In males? What bacteria causes this?

A
  • females: gonococcal infection of female upper reproductive tract; inflammation of the uterus and fallopian tubes; scarring of upper tract and adjacent organs- males: epididymitis; ascent of organism into upper reproductive tract of men- Neisseria gonococci
96
Q

What is Disseminated Gonococcal Infection? What bacteria causes this?

A
  • can result from Pelvic Inflammatory Disease due to endotoxin; pustular lesions of the skin; inflammation of tendons and joints; suppurative arthritis; more common in women- Neisseria gonococci
97
Q

What is Purpura Fulminans? What bacteria causes this?

A
  • disseminated intravascular coagulation (DIC) due to the ability to survive in the bloodstream; skin manifestations, meningitis, shock, death; response to LOS mediated by TNF-alpha and IL-1; the higher the response, the greater the damage and risk of death- Neisseria meningococcus
98
Q

How is a Neisseria infection treated?

A
  • high resistance to antibiotics- antimicrobial chemoprophylaxis of close contacts is the primary means of preventing secondary cases of sporadic meningococcal disease
99
Q

How is a Neisseria infection prevented?

A
  • behavioral: condoms, partner notification, early diagnosis and treatment- vaccines to gonococci are difficult to produce (antigenic and phase variation, protective intracellular components)- vaccine to meningococci (quadrivalent derived against capsular polysaccharide, tetravalent is a polysaccharide-protein conjugate)KNOW THIS
100
Q

Is a vaccine available against Neisseria gonococci? Against Neisseria meningococci?

A
  • vaccines to gonococci are difficult to produce (antigenic and phase variation, protective intracellular components)- vaccine to meningococci (quadrivalent derived against capsular polysaccharide, tetravalent is a polysaccharide-protein conjugate)KNOW THIS
101
Q

Is Haemophilus gram positive or negative? Aerobic or anaerobic?

A
  • gram-negative- aerobic (some anaerobic)
102
Q

Where does Haemophilus colonize?

A
  • colonizes upper respiratory tract of almost everyone- H. influenzae probably only infects 1-2% of healthy children, but does NOT cause influenza (which is actually caused by a virus)
103
Q

What is required for Haemophilus influenzae to grow? For other Haemophilus species?

A
  • H. influenzae requires hemin (X factor) and NAD+ (V factor) for growth; access to these factors require lysed blood (chocolate agar) rather than whole-blood (blood agar)- other Haemophilus species require only NAD+; can grow on blood agarKNOW THIS
104
Q

What are the two types of Haemophilus influenzae strains?

A
  • typeable: have 7 antigenically distinct capsular polysaccharides- non-typeable: unencapsulatedKNOW THIS
105
Q

What is the most virulent type of H. influenzae? What does it cause?

A
  • H. influenzae type b (Hib) is the most virulent- bacteremia (bloodstream) and meningitis in children younger than 2
106
Q

What types of diseases are caused by non-typeable strains of H. influenzae?

A

respiratory tract diseases

107
Q

What are the 4 virulence factors of H. influenzae?

A
  • polyribosyl ribitol phosphate (PRP) capsule: resistance to phagocytosis (as long as antibody is not present); basis for the Hib vaccine- endotoxin: causes pathogen-directed endocytosis- IgA1 protease: similar to Neisseria!- pili and outer membrane proteins: similar to Neisseria!KNOW THIS
108
Q

How is the human host able to defend against H. influenzae?

A
  • antibodies against the capsule- immunization of infants: pure Hib PRP polysaccharide vaccine is NOT immunogenic in infants; PRP-conjugated diptheria toxoid (adjuvant) produces good antibody responses in infants
109
Q

Why are antibodies not effective in a N. gonococci infection?

A

N. gonococci doesn’t have a capsule

110
Q

What is the treatment for a H. influenzae infection?

A
  • many H. influenze are resistant to beta-lactam antibiotics because they produce beta-lactamase- chloramphenicol is the drug of choice- third-generation cephalosporins
111
Q

Is Pseudomonas aeruginosa gram positive or negative? Where is it found?

A
  • gram negative- ubiquitous (found in soil and water)
112
Q

Is Pseudomonas motile? Aerobic or anaerobic?

A
  • motile: one or several polar flagella; polar pili (twitching)- aerobic (this species - some strains are anaerobic when grown on nitrate)
113
Q

What is produced by Pseudomonas aeruginosa? What does it smell like?

A
  • colonies produce water-soluble pigments that function as antibacterials- fruity or grape-like odor to colonies (or near wounds)
114
Q

What is required for growth of Pseudomonas aeruginosa?

A
  • grows rapidly, very robust- minimal nutritional requirement (need only acetate and ammonia for C and N sources)- can survive in hand creams, soaps, and dilute antiseptics
115
Q

What virulence factors does Pseudomonas aeruginosa possess that aids in its persistance?

A
  • mucoid polysaccharide capsule (alginate): shields from the immune system- siderophores- elastase- exotoxin A- phospholipase C
116
Q

What virulence factors does Pseudomonas aeruginosa possess that aids in its dissemination?

A
  • toxin A- spreading factors (collagenase, elastase, and exoenzymes)- flagella- heat-stable hemolysin- tissue damage by proteases and toxins
117
Q

What does Pseudomonas aeruginosa use siderophores for? Phospholipase C?

A
  • siderophores: iron binding compounds that compete with transferrin for iron; iron limitation causes increased production of elastase and exotoxin A which damages tissues or creates conditions that make iron more accessible- phopholipase C: hydrolyzes phospholipids (lecithin) in the eukaryotic membrane, releasing usable phosphate
118
Q

How is Pseudomonas aeruginosa encoutered?

A
  • adheres to vegetables and plant matter- in water taps, drains, and wet surfaces (otitis externa - swimmer’s ear)- in hot tubs (“hot tub rash”)
119
Q

How does Pseudomonas aeruginosa enter the body?

A
  • opportunistic pathogen; needs a local or systemic breach of the immune system or immunocompromised patients- organism does not adhere well to healthy epithelium; can enter through abrasions, cuts, etc.; usually need a large inoculum in order to cause infection
120
Q

What are the 2 things that Pseudomonas’ ability to spread and multiply depend upon?

A
  • avoiding phagocytosis- successful adherence to a surfaceKNOW THIS
121
Q

What mediates Pseudomonas’ adherence to epithelia?

A

flagella and pili (interctions with glycolipid which creates a receptor for Type 4 pili on host cells and TLR-5)KNOW THIS

122
Q

What is the function of the polysaccharide capsule of Pseudomonas?

A
  • major adhesin and component of biofilm in cystic fibrosis patients- production is highly regulated
123
Q

What damage is created by the LPS of Pseudomonas?

A
  • adhesin- lipid A: endotoxin; interacts with the host TLR4 to initiate inflammatory response- core oligosaccharide interacts with CFTR (an ATP-binding cassette transporter; cystic fibrosis transmembrane conductance regulator); bacterial internalization and initiation of immune response- long O-antigen side chains: responsible for resistance to human serum, antibiotics and detergents
124
Q

What damage is caused by the exotoxins of Pseudomonas?

A
  • cause local inflammation- some kill host cells (exotoxin A)
125
Q

What damage is caused by multifunctional enzymes (proteases) such as elastase and LasA in Pseudomonas?

A
  • elastase: cleaves elastin and collagen (direct tissue damage), cleave proteinase inhibitors, cleaves immune system components (complement and immunoglobulins)- LasA: serine protease that works with elastase to degrade elastin
126
Q

What damage is caused by the Type III Secretion System of Pseudomonas?

A
  • delivers virulence factors directly into host cells (transfer from bacterial cytosol to host cytoplasm)- similar to flagella- targets specific proteins on host cells- induced by host cell contact or low calcium levels
127
Q

What factors are predisposing to a Pseudomonas infection?

A
  • local breach of the immune system- systemic illnesses (ex. diabetes, premature infants, etc.)- both systemic and local (ex. burns)
128
Q

What disease was discussed in class to be associated with Pseudomonas aeruginosa?

A

cystic fibrosis

129
Q

Why are people with cystic fibrosis more at risk of a P. aeruginosa infection?

A
  • Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is dysfunctional in cystic fibrosis patients- without CFTR, there is a decreased sialylation of surface glycolipids so P. aeruginosa can bind these epithelial cells better than it would in a healthy individual- there is also dehydration of respiratory secretions so there is a thick mucus that impairs the mucociliary system- mucoid exopolysaccharide also shields the organisms from the immune systemKNOW THIS
130
Q

What is sepsis? How can sepsis be triggered by Pseudomonas?

A
  • sepsis: severe systemic illness marked by hemodynamic derangements and organ malfunction brought about by the interaction of certain microbial products with host reticuloentothelial cells- LPS endotoxin mediated (specifically the lipid A moiety)- triggers production of Tumor Necrosis Factor (TNF) which stimulates macrophages to produce IL-1
131
Q

What is MODS (Multi-Organ Dysfunction Syndrome)?

A
  • high cardiac output, lowered blood pressure- distributive shock (lack of perfusion of selected vascular beds)
132
Q

What are the 3 requirements of sepsis?

A
  1. large population of infecting/colonizing organisms2. presence of bacterial products that stimulate release of host cytokines3. widespread dissemination of microbial products to host’s reticuloendothelial system
133
Q

Upon what does the mortality of sepsis depend?

A
  • nature and severity of infection- host defense state- promptness and efficacy of treatment
134
Q

How is a Pseudomonas infection usually diagnosed? Treated?

A
  • easily cultured and identified- antibiotic treatment depends on the geographic location (in some hospitals, certain antibiotic resistant strains predominate); frequently requires antibiotic synergism to treatKNOW THIS
135
Q

Is Lysteria gram positive or negative?

A

gram positive

136
Q

Where is Listeria monocytogenes found?

A
  • intestinal tract of vertebrates, sewage, soil, and water- food-borne pathogen (aided by its exceptional heat resistance and ability to grow at refrigerator temperatures)
137
Q

What are the 2 types of Listeria monocytogenes motility?

A
  • peritrichous flagella- actin polymerization
138
Q

What is Listeriosis?

A
  • infections of fetus, immunocompromised, elderly, and pregnant people- can result in systemic infections such as bacteremia and meningitis- 5-10% of adults are asymptomatic carriers
139
Q

What are the 3 virulence factors of Listeria?

A
  • internalins: mediate adherence and invasion of cells- listerlysin O: enables escape from vacuoles; responsible for beta-hemolytic pattern- phospholipases: aid in escape from vacuoles; movement through the cell via actin polymerization; can cross the placenta
140
Q

How does Listeria spread from cell to cell?

A
  • bacteria enters the cell via phagocytosis- bacteria escapes the vacuole- bacteria uses actin polymerization to push its way into the neighboring cell while still having the cell membrane of the original cell around it; it never needs to go into the extracellular space again
141
Q

How is Listeria prevented?

A

control of growth in food supply (avoid unpasteurized milk and juices; pregnant and immunocompromised individuals are advised to avoid deli foods, raw meats, and soft cheeses)

142
Q

How is Listeria treated?

A

antibiotics are effective if diagnosed in time

143
Q

Is Clostridia aerobic or anaerobic? Gram positive or gram negative?

A
  • strictly anaerobic- gram positive
144
Q

Where is Clostridium found? What does it produce?

A
  • found in the environment (soil, water, and animal wastes)- produce endospores- produce proteinaceous toxins that are responsible for disease symptoms
145
Q

What are the 4 species of Clostridium?

A
  • C. difficile: pseudomembranous colitis- C. perfringens: cellulitis, gas gangrene, food poisoning- C. botulinum: botulism- C. tetani: tetanus
146
Q

What are the major diseases caused by Clostridia?

A
  • botulism (food poisoning, infant botulism, and wound botulism)- tetanus- pseudomembranous colitis- gas gangrene- suppurative wounds and abscesses
147
Q

What is a bacterial endospore? What causes a spore to form? What makes it germinate?

A
  • metabolically inactive state in which organisms can remain viable for hundreds of years- resistant to adverse conditions (extreme heat, drying, radiation, most chemical disinfectants)- spore induction caused by unfavorable environmental conditions- spores will readily germinate when conditions become favorable for vegetative growth

SP14 - Micro Immuno Exam 3 (1 decks)

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