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First Aid > Microbiology Bacteria > Flashcards

Microbiology Bacteria Flashcards

1
Q

Which bacterial structure protects against osmotic pressure?

A

Peptidoglycan (also gives rigid support)

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2
Q

What is peptidoglycan made of?

A

Backbone = sugar
Side chains = peptides

*you can remember this because transPEPtidases link the side chains, so the side chains must be protein

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3
Q

What is the major surface antigen of gram +? gram -? For each of these types of bacteria, what STRUCTURE induces the host response?

A

SURFACE ANTIGENS
Gram +: Cell wall
Gram -: Outer membrane

INDUCTION OF TNF and IL-1:
Gram+: Lipoteichoic acid
Gram-: Lipid A (LPS = O saccharide + lipid A)

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4
Q

Where do oxidative and transport enzymes of bacteria reside?

A

In the PLASMA membrane… which is below the cell wall in gram +’s, and below to outer membrane and little bits of peptidoglycan in gram -‘s

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5
Q

T or F: Both gram + and gram - have peptidoglycan

A

True! But gram positive have more.

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6
Q

Which ribosomal subunits do bacteria use? Humans?

A

Bacteria: 50S and 30S –>70S
Humans: 60S and 40S –> 80S

*memory: Eukaryotes are EEEven, prOOkaryotes are Odd

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7
Q

Where do beta-lactamases and hydrolytic enzyme in bacteria reside?

A

The periplasm, above the cytoplasmic/plasma membrane

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8
Q

What enzymes does the periplasmic space contain? The plasma membrane?

A

Periplasmic space: B-lactamases, hydrolytic enzymes

Cytoplasm: Oxidative enzymes, transport enzymes

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9
Q

What are bacterial piluses (used for sex/conjugation and adherence to cell surface) made of?

A

Glycoprotein

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10
Q

What are bacterial flagellum (motility) made of?

A

Protein

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11
Q

What 3 substances are bacterial spores made of?

A
  1. Keratin-like coat
  2. Dipicolinic acid
  3. Peptidoglycan

*memory: SPOons (spores) can be used for DIP (dipicolinic acid) instead of CARROTS (keratin coat)

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12
Q

What are plasmids made of?

A

DNA

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13
Q

What is the main purpose of a bacterial capsule?

A

Protection against phagocytosis

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14
Q

What is a bacterial capsule made of? Which bacteria is the exception to this?

A

Usually made of polysaccharides

Exception: Bacillus anthracis (Anthrax) contains D-glutamate

*memory: Anthrax is D (the) GLoomy (glutamate) exception

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15
Q

What bacterial structure mediates adherence to surfaces, especially catheters? What is it made of?

A

Glycocalyx (AKA “slime layer” AKA exopolysaccharide layer)

Made of polysaccharides

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16
Q

What are the gram positive bacteria?

A 
Listeria   (listen)
Staph   (stop)
Strep    (strapping)
Cornyebacterium  (corny)
Clostridium   (closets)
(in)
Mycobacterium   (my)
Propionibacterium  (proper)
Lactobacillus  (ladies)
Gardnerella  (Garden)  *gram variable
(I'm)
Actinomyces  (actually)
Nocardia  (not)
(kidding!)
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17
Q

What are the gram positive cocci?

A
  1. Staphylococcus

2. Streptococcus

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18
Q

What are the gram negative cocci?

A
  1. Neisseria

2. Moraxella catarrhalis

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19
Q

What are the zoonotic gram negative bacteria?

A
  1. Bartonella
  2. Brucella
  3. Francisella
  4. Pasteurella

*memory: Bark Bark For Pets

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20
Q

What are the 3 respiratory gram negative bacteria?

A
  1. Bordetella (whooping cough)
  2. Haemophilus
  3. Legionella (Legionairre’s, pontiac fever)
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21
Q

What are the intracellular bacteria? How do we identify them?

A
  1. Chlamydiae
  2. Rickettsiae

Identify with Giemsa stain (and Borrelia too)

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22
Q

What are the spirochetes?

A
  1. Borrelia (lyme disease)
  2. Leptispira
  3. Treponema (syphilis)
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23
Q

What are the branching filamentous bacteria? Are they gram + or -?

A
  1. Actinomyces
  2. Nocardia

Gram positive

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24
Q

Which bacteria do not gram stain well?

A

*memory; These Microbes May Lack Real Color

Treponema (these) –> dark field microscopy
Mycobacteria (microbes) –> acid-fast/carbolfuschin/ziehl-neelsen stain
Mycoplasma (May) –> ?
Legionella (Lack) –> silver stain
Rickettsia (Real) –> Giemsa
Chlamydia (Color) –> Giemsa

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25
Q

Which bacteria need Giemsa stain?

A
  1. Chlamydia
  2. Rickettsia
  3. Borrelia

and also: Trypanosomes (but use dark field for treponema syphilis), plasmodium

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26
Q

What bacteria need PAS (periodic acid-Schiff) stain? Which substance does this ID?

A

Tropheryma whipplei (Whipple disease = malabsorption, cardiac, arthritis, neurologic symptoms)

Identifies glycogen

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27
Q

What organisms need Acid fast staining? What are other names for this stain?

A
  1. Mycobacteria (TB, leprosy)
  2. Nocardia (Branching filamentous, cutaneous and pulm infection)
  3. Cryptosporidium oocytes (watery diarrhea, severe in AIDS, transmit via oocysts in water)

Other names: Carbol-fuchsin, Ziehl-Neelsen

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28
Q

What organisms need India ink stain?

A

Cryptococcus neoformans (especially for CSF. Can use mucicarmine for bronchowash)

*memory: Picture pigeons dipping their feet in india ink, and getting those indian ink drops on their foreheads

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29
Q

What organisms needs silver stain?

A
  1. Fungi (like pneumocystis and more)
  2. Legionella *memory: A Legionnairre army guy with a silver button
  3. H. pylori *memory: Helicopters are made of silver
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30
Q

What is cultured on chocolate agar?

A

H. Flu (class: and Neisseria)

*memory: Chocolate agar has factors V and X because when a kid has the FLU, mom goes to “5 and dime” (V and X) to buy CHOCOLATE

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31
Q

How do you culture Neisseria (complicated!)

A
  1. Thayer-Martin Agar
  2. Vancomycin (inhibits gram +)
  3. Trimethoprim
  4. Colistin (inhibits other gram neg organisms… no longer used in people because nephrotoxic… except for multidrug resitant pseudomonas or klebsiella)
  5. Nystatin (inhibits fungi)

*memory: THese (THayer martin) Very (vancomycin) Typically (Trimethoprim) Culture (Colistin) Neisseria (Nystatin)

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32
Q

How do you culture Bordetella Pertussis?

A
  1. BORDET-Gengou agar
  2. Potatoes *memory: BORD leo up like a POTATO
  3. Regan-Lowe medium *then go to LOWes
  4. Charcoal *to get some CHARCOAL
  5. Blood
  6. Antibiotic
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33
Q

How do you culture Cornyebacterium diptheriae?

A
  1. Tellurite agar
  2. Loffler medium

*memory: DIP into your courage and TELL her OFF

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34
Q

How do you culture mycobacterium TB?

A

Lowenstein-Jensen agar

*memory: TBT to Dr. Jensen

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35
Q

How do you culture Mycoplasma pneumoniae?

A
  1. Eaton agar
  2. Cholesterol
    * memory: Mycoplasma EATs cholesterol because its so skinny it doesnt have its own cell wall
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36
Q

What does MacConkey agar do? Which organisms is it useful for?

A

Turns colonies of lactose-fermenting enterics pink

macConKEES = 
Citrobacter
Klebsiella
E. Coli
Enterbacter
Serratia
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37
Q

What agar is used to grow E. Coli?

A

Eosin-methylene blue (EMB). E coli shows up black with metallic green sheen.

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38
Q

What 3 things are used to grow Legionella?

A
  1. Charcoal yeast extract agar
  2. Cysteine
  3. Iron

*memory: A french LEGIONAIRRE with a SILVER helmet (silver stain), sitting around a fire with CHARCOAL, holding his IRON dagger. He is no SISSY (cysteine)

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39
Q

What agar is used for Fungi?

A

Sabouraud agar

*memory: Sab’s a Fun Guy

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40
Q

What are the obligate aerobes?

A
  1. Nocardia
  2. Pseudomonas
  3. Mycobacterium TB

*memory: Nagging Pests Must Breathe

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41
Q

Which bacteria is seen in burn patients?

A

Pseudomonas (obligate aerobe)

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42
Q

Which bacteria are obligate anaerobes?

A
  1. Fusobacterium
  2. Clostridium
  3. Bacteroides
  4. Actinomyces

*memory: Frankly Cant Breathe Air

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43
Q

Which antibiotic is NEVER effective against anaerobes?

A

Aminoglycosides. They need O2 to be taken up.

*memory: Amin-O2-glycosides

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44
Q

What 4 properites do anaerobic bacteria have?

A
  1. Foul smelling (due to short chain fatty acids)
  2. Difficult to culture
  3. Produce gas in tissues (CO2 and H2) *memory: remember clostridium perfingens is gas gangrene, and clostridium is anaerobic
  4. Susceptible to oxidative injury (dont have catalse or superoxide dismutase)
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45
Q

What are the 3 steps of the oxidative burst?

A
  1. O2 -> O2- (NADPH oxidase)
  2. O2- -> H2O2 (superoxide dismutase)
  3. H2O2 -> HOCl (myeloperoxidase)
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46
Q

What does catalase do?

A

H2O2 -> H2O + O2 (allows bacteria to dismantle H2O2, after they use their superoxide dismutase to turn O2- to H2O2)

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47
Q

What does glutathion peroxidase do?

A

OH- -> H2O

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48
Q

Which bacteria are considered “ATP parasites” because they rely on host mitochondria to make it?

A

The intracellular bacteria (Rickettsia, chlamydia, coxiella)

*memory: stay INtracellular when its Really CHilly and COld

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49
Q

Which bacteria are facultative intracellular?

A

*memory: Some Nasty Bugs May Live FacultativeLY

Salmonell  (some)
Neisseria  (Nasty)
Brucella  (Bugs)
Mycobacterium  (May)
Listeria  (Live)
Francisella (Facultative...)
Legionalla (L)
Yersina pestis (Y)
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50
Q

What are the encapsulated bacteria?

A

*memory: SHiNE SKiS

Strep PNEUMO
H. INFLUENZA TYPE B
(i)
Neisseria MENINGITIDIS
E. COLI
Salmonella TYPHI
Klebsiella PNEUMONIAE
Strep GROUP B
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51
Q

Does group A strep have a capsule?

A

Nope. Just Group B strep and strep pneumo

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52
Q

Why are vaccine containing polysaccharide capsule antigens usually conjugated to a carrier protein?

A

Only proteins, NOT polysaccharide antigens, can be presented to T cells. If there is a conjugate protein, the cell can chew it up and present it on MHC to a T cell. This allows the B cells - which have developed antibodies from the polysaccharide part of the vaccine - to class switch and form memory cells.

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53
Q

What are the conjugated and non-conjugated pneumococcal vaccines?

A

Conjugated: PCV (stands for pneumococcal conjugate vaccine) = Prevnar

Unconjugated: PPSV (stands for pneumococcal polySaccharide vaccine) = Pneumovax

*memory: PneumoVAX needs to get its FACTS straight… its just not as good

NOTE: I think Prevnar will form long lasting IgG and IgE antibodies, wherease pneumovax will form short lasting IgM antibodies

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54
Q

Besides the pneumococcal vaccines, what 2 other vaccines do we have?

A
  1. H. Flu type B (made of polyribosyl phosphate [PRP] conjugated to diptheria toxin)
  2. Neisseria Meningitidis (also conjugated… although I think there is a polysacch version that should not be given to kids)
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55
Q

What are the urease positive organisms?

A

*memory; CHuck norris hates PUNKSS

Cryptococcus
H. Pylori
(uck norris hates)

Proteus
Ureaplasma
Nocardia
Klebsiella
Staph epidermis
Staph saprophyticus
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56
Q

What are the catalase positive organisms?

A

*memory: cats Need PLACESS

Nocardia
Pseudomonas
Listeria
Aspergillus
Candida
E. Coli
Staph
Serratia
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57
Q

Which bacteria produce a yellow pigment?

A
  1. Actinomyces
    • > Note: Yellow “sulfur” granules (made of filaments of bacteria) in a pus-forming lesion is basically diagnostic for actinomyces
  2. Staph Aureus
    • > Yellow means gold
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58
Q

Which bacteria produces a blue-green pigment?

A
  1. Pseudomonas aeruginosa *memory: AERUGula is green

2. E. Coli produces black colonies with a green-meallic sheen on EMB agar

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59
Q

Which bacteria produces a red pigment>

A

Serratia marcescens *memory: red MARASCENO cherry

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60
Q

Which bacteria produces protein A? What is the action of protein A?

A

Staph Aureus *memory: Call it “protein Aureus”

Binds the Fc region of IgG, to flip it around and prevent opsination and phagocytosis

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61
Q

Which bacteria produce protein M? What is the action of protein M?

A

Strep Pyogenes *memory: Don’t eat (phagocytosis) My (M protein) pie (pyogenes)

Helps prevent phagocytosis. Also, is the reason molecular mimcry results in acute rheuMatic fever

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62
Q

Which bacteria produce IgA protease?

A

Strep pneumo, H flu, Neisseria (meningitidis AND gonorrhoeae)

*memory: IgA protease is noSHiN Igceptionally (Ig) special, because 2 bacteria have it

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63
Q

What is a type 3 secretion system?

A

AKA injectisome. Allows direct delivery of toxins from gram negative bacteria (like pseudomonas, salmonella, shigella, E. coli) into host cells.

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64
Q

Which types of bacteria have exotoxins?

A

Both gram neg and gram positive

endotoxins = only gram neg

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65
Q

Exotoxin vs. Endotoxin: Where are the genes for each location

A

Exotoxin: Plasmids, bacteriophages (Phage toxins = ABCDE… shigA, Botulinum,Cholera, Diptheria, Erthrocyte lysis strep pyogenes)

Endotoxin: Bacterial chromosome

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66
Q

Exotoxin vs. Endotoxin: Which is secreted from the cell?

A

Exotoxin

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67
Q

Exotoxin vs. Endotoxin: Which has a higher toxicity?

A

Exotoxin

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68
Q

Exotoxin vs. Endotoxin: Which is more antigenic (induces more antibodies)?

A

Exotoxin. Endotoxins are poorly antigenic.

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69
Q

How do endotoxins such as Lipid A on gram negatives cause problems?

A 
Induce...
IL-1 --> Fever
TNF-A--> Fever
NO --> Hypotension
C3a --> Edema (mast cells?)
C5a --> Attract neutrophils
Tissue factor --> DIC
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70
Q

Exotoxin vs. Endotoxin: Which can be used as a vaccine?

A

Exotoxin

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71
Q

Exotoxin vs. Endotoxin: Which is stable at 100 deg C for 1 hour?

A

Endotoxin (exception: Staph aureus is an exotoxin that causes food poisoining and is resistant up to 120 deg C. All other exotoxins are destroyed by the time tepm reaches 60 deg C)

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72
Q

What type of toxin does tetanus (clostridium tetani) have?

A

Exotoxin (its a gram positive, so it CANT do endotoxin!)

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73
Q

What type of toxin does Neisseria meningitidis have?

A

Endotoxin

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74
Q

What are the 6 categories of EXOTOXIN mechanisms and the bacteria in each?

A
  1. Protein synthesis
    - Shigella
    - EHEC
    - Pseudomonas aeruginosa
    - Diptheria
    * memory: will is PRecious (protein synthesis) but he SHould (shiga) Experiment (EHEC) with PSEUDO (pseudomonas) DIP (diptheria
  2. Increased fiuid secretion
    - ETEC (heat labile and heat stable)
    - Anthrax
    - Cholera
  3. Inhibit Phagocytic activity
    - Bordetella/whooping cough
  4. Inhibit NT release
    - Tetanus
    - Botulinum
  5. Lyse cell membranes
    - C. Perfringens/Gas gangrene
    - Strep pyogenes
  6. Superantigens
    - Strep pyogenes
    - Staph Aureus
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75
Q

How does Diptheria toxin work?

A

Inactivates EF2 (like pseudomonas) to cause pharyngitis, pseudomembranes in the throat, ad bull neck

*memory: EF up your throat

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76
Q

How does pseudomonas aeruginosa’s toxin (‘Exotoxin A’) work?

A

Inactivates EF2 (like diptheria) to cause host cell death

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77
Q

How does Shigella’s toxin (Shiga toxin) work?

A

Inactivates 60S ribosome by removing adenine from rRNA, which causes GI mucosal damage and HUS

*memory: SHixty (60) S inactivation

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78
Q

How does Enterohemorrhagic E coli (EHEC)’s toxin work?

A

Inactivates 60S ribosome by removing adenine from rRNA (like Shiga toxin. So its called Shiga-like toxin).

This results in HUS. Prototype: O157:H7

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79
Q

What is the difference between Shiga Toxin and Shiga-like Toxin?

A

Shiga-like toxin, produced by E. coli, does not invade host cells. HOWEVER, it still causes bloody diarrhea because it causes necrosis and inflammation

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80
Q

How does Enterotoxigenic E Coli (ETEC)’s toxin work?

A

It has 2 toxins that both cause watery diarrhea:

  1. LT (heat labile) : Overactive cAMP –> Cl- secretion
  2. ST (heat stable): Overactive cGMP –> decreased NaCl resoprtion
  • memory: Labile (LT) in the Air (AMP) moves stuff more (Cl secretion)
  • memory: Stable (ST) on the Ground (GMP) moves stuff less (decreased NaCl resoprtion)
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81
Q

How does Bacillus anthracis toxin work?

A

Mimics cAMP to cause an edematous border of black eschar in Anthrax skin lesions.

Thats why its called “Edema Toxin”

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82
Q

How does Vibrio cholerae’s toxin (Cholera toxin) work?

A

Permanently activates Gs –> overactive cAMP –> Cl- secretion

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83
Q

How does Bordetella pertusses’s toxin (Pertussis toxin) work?

A

Disables Gi –> overactive vAMP –>impaired phagocytosis –> “100 day cough” in adults and “whoop” inspiration cough in children

*memory: I cAMPed out too much in the library and disabled by immune GuYs, so I got a bad cough

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84
Q

How does clostridium tetani’s toxin (Tentanospasmin) work?

A

Cleaves SNARE proteins required for release of GABA and Glycine neurotransmitters from RENSHAW CELLS of the spinal cord –> spasticity, risus sardonicus, lockjaw, opisthotonos (back muscle contraction), violent painful contracts after loud noise

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85
Q

How does clostridium botulinum (Botulinum toxin) work?

A

Cleaves SNARE proteins requires for release of Acetylcholine at neuromuscular junctions –> flaccipd paralysis, floppy baby, normal nerve conduction but decreased muscle compound action potential

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86
Q

Which toxin is NOT an A-B toxin (B component binds to host cell, A component attaches ADP-ribosyl to disrupt host cell proteins)?

A

ETEC’s heat stable toxin

*memory: this toxin is stable; it doesnt do any weird reaching over and activation stuff

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87
Q

How does clostridium perfringens toxin (Alpha toxin) work?

A

It is a phospholipase (lecithinase) –> degrades tissues and cell membranes –> myonecrosis “gas gangerene”, hemolysis “double zone” on blood agar, edema

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88
Q

How does strep pyogenes erythrogenic toxin, Streptolysin O, work?

A

Degrades cell membranes –> Lyses RBCs and causes Beta-hemolysis

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89
Q

How is strep pyogenes’ eryhtrogenic toxin helpful in diagnosing rheumatic fever?

A

ASO antibodies = antibodies against streptolysin O, there are used to diagnose rheumatic fever

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90
Q

How does strep pyogenes’ non-ertyhrogenic toxin, Exotoxin A, work?

A

Binds to MHC2 and TCR and cross links them –> Tons of IL-1, IL-2, IFN-gamma, TNFalpha –> shock (same as staph aureus TSST-1 toxin)

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91
Q

How does staph aureus Toxic shock syndrome toxin (TSST-1) work?

A

Binds to MHC2 and TCR and cross links them –> Tons of IL-1, IL-2, IFN-gamma, TNFalpha –> shock (same as strep pyogenes Exotoxin A)

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92
Q

What is “transformation”?

A

Ability to take up naked DNA from the environment. Also called “competence”.

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93
Q

Which bacteria are “competent”?

A

S. pneumo, H. flu, Neisseia (SHiN)

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94
Q

Adding what to the environment would prevent bacteria from doing “transformation” (taking up naked DNA)?

A

Deoxyribonuclease… because this degrades naked DNA

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95
Q

What is F+ x F- conjugation vs. Hfr X F- conjugation?

A

FxF: PLASMID DNA (a single strand of it) is transferred across the mating bridge

HfrXF: PLASMID AND CHROMOSOMAL bacterial DNA is transferred when plasmid DNA is incorporated into the bacterial chromosomal DNA and then replicated

(Hfr = high frequency recombination)

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96
Q

What is transposition?

A

When transposons (segments of DNA) “jump” from plasmids to chromosomal DNA and mix up the genes in the process. They can then transfer genes from one bacteria to another

(ex: Vancomycin resistant staph got the VanA gene from vancomycin-resistant enterococcus)

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97
Q

What is generalized vs. specialized transduction?

A

Generalized: “A packaging accident”
- Lytic phage infects bacteria -> bacterial chromosomal DNA cleaved -> bacterial chromosomal DNA packaged into viral capsid -> phase infects another bacteria and transfers it

Specialized: “An excision accident”
- Lytic phage infects bacteria -> viral DNA incorporates into bacterial chromosme -> viral DNA is excised along with some flanking bacterial DNA -> bacterial DNA gets packaed with virus -> virus can infect another bacteria and transfer it

98
Q

What are the 5 bacterial exotoxins that are encoded on lysogenic phages?

A

*memory: ABCDE

shigA
Botulinum
Cholera
Diptheria
Erythrogenic toxin of strep pyogenes
99
Q

What is the first way we divide up gram + bacteria?

A
  1. Cocci (staph, strep)
  2. Rods (lots)
  3. Branching filamentous (Actinomyces, Nocardia)
100
Q

How do we narrow down Gram + cocci?

A

It’s either staph or strep. Staph are catalase +, strep are not.

101
Q

How do we narrow down Gram+ rods?

A

No clear cut way. We can pull out clostridium as an anerorobe, listeria as a facultative intracellular

102
Q

How do we narrow down branching filamentous?

A

It’s either actinomyces or nocardia. They are both gram positive. Actinomyces is obligate anaerobe, Nocardia is obligate aerobe. Also, nocardia is acid fast.

103
Q

How do we narrow down types of staph?

A

First with coagulase:
coag+: Staph aureus
coag-: Staph epidermis, Staph saprophyticus

Then with Novobiocin: *memory: NO SRES
nov sensitive: Staph epidermis (SR)
nov resistant: Staph saprophyticus (ES)

104
Q

How do we narrow down types of strep?

A

First with types of hemolysis:

Alpha hemolyis = partial hemolysis = green surrounding

  • Strep pneumo
  • Viridian strep

Beta hemolysis = complete hemolysis = clear surrounding

  • Strep pyogenes (group A)
  • Strep agalactiae (group B)

No hemolysis = red surrounding

  • Strep enterococcus (group D)
  • Strep nonenterococcus (group D)
105
Q

How do we narrow down something that is a Gram+ cocci that is catalase negative with alpha hemolysis?

A

Gram+ cocci = staph or strep
Catalase negative = strep
Alpha hemolysis = Strep pneumo or strep viridians

Next step: optochin

  • Strep viridians: Optochin resistant (lives in the mouth because not afraid op-to-chin)
  • Strep pneumo: Optochin sensitive *OVRPS (optochin, viridian resistant, pneumo sensitive)
106
Q

How do we narrow down something that is a Gram+ cocci that is catalase negative with alpha hemolysis

A

Gram+ cocci = staph or strep
Catalase negative = strep
Beta hemolysis = strep pyogenes or strep agalactiae

Next step: Bacitracin *memory: BRAS

  • group B strep: resistant
  • group A strep: sensitive
107
Q

What are the 4 types of bacteria that can do beta hemolysis?

A
  1. Group A strep (bacitracin sensitive)
  2. Group B strep (bacitracin resistant)
  3. Staph aureus (catalase and coagulase +)
  4. Listeria (tumbling motility, meningitis in newborns, unpasteurized milk)
108
Q

What diseases can staph cause?

A
  • Skin infection
  • Organ abscess **Forms fibrin clot around self
  • Pneumonia after influenza virus infection**
  • Endocarditis
  • Septic arthritis
  • Osteomyelitis **treat with clindamycin
  • Toxic shock syndrome **TSST-1 binds MHC2 and T cells
  • Scalded skin syndrome **exfoliative toxin ETa and ETb attack desmoglien
  • Rapid onset food poisoning **Enterotoxin stable to 130 deg, nonbloody diarrhea and vom after 2-6 hrs
  • Nosomial infection **MRSA. Use Vancomycin, Ceftaroline, Linezolid, or Daptomycin
109
Q

How does staph TSS present differently than strep pyogenes TSS?

A

Staph: Fever, vomiting, rash, desquamination, shock, organ failure. Vaginal tampons, nasal packing.

Strep: Painful skin infection (I guess vomiting is the main difference? And the fact that its not due to tampons)

BOTH caused by an exotosin (TSST-1 in staph, Exotoxin A in strep) and BOTH due to MHC2 binding to T cells

110
Q

Which bacteria should be suspected with infections of prosthetic devices (ex: hip implant, heart valve) and IV catheters? HOW does it do this? HOW can it be confirmed?

A

Staph epidermis. Produces adherent biofilm. Confirm with novobiocin sensitivity. (*memory: NO SRES… Novobiocin, Saphrophyticus resistant, Epidermis sensitive)

111
Q

If a young woman has an UTI and its NOT due to E. Coli, what bacteria should we suspect? How could we confirm in a lab?

A

Staph saprophyticus (#2 cause of UTI in young women). Confirm w/ novobiocin resistance (*memory: NO SRES… Novobiocin, Saprophyticus resistant, epidermis sensitive)

112
Q

Is strep pneumo alpha hemolytic, beta hemolytic, or neither?

A

Alpha hemolytic (will have green area around it)

113
Q

Which of the strep are encapsulated?

A

Only strep pneumo

114
Q

What is strep pneumo the most common cause of?

A

*memory: MOPS

Meningitis *Note: Even though Neisseria has a strain called meningitidis, strep pneumo causes it more often!
Otitis media
Pneumonia
Sinusitis

115
Q

What bacteria is associated with rusty sputum?

A

Strep pneumo

116
Q

What bacteria is associated with sepsis in sickle cell disease?

A

Strep pneumo

117
Q

Is strep pneumo still virulent with no capsule?

A

Nope! Even though it still has IgA protease, with no capsule, its hopeless. Will get eaten up right away.

118
Q

Where is it normal to find strep viridians?

A

The oropharynx *memory: strep viridians live in the mouth because its not afraic of-the-chin (op-to-chin resistant)

119
Q

Which bacteria causes dental caries?

A

Strep viridians (streptococcus mutans type)

120
Q

Which bacteria can cause endocarditis?

A
  1. Staph Aureus
  2. Strep viridians (strep sanguinis. ONLY at damaged heart valves!)
  3. Strep enterococci (group D - after GI/GU procedures)
  4. Strep bovis/gallolyticus (also assoc. w/ colon cancer)
121
Q

How does streptococcus sanguinis bind to damaged heart valves?

A

It makes dextrans using sucrose as a substrate. Dextrans allow it to bind fibrin, which is bound to platelets at damaged heart valves.

So basically strep sanguinis can ONLY bind where there is fibrin-platelets aggregates (clots)

122
Q

What disease does group A strep (pyogenes) cause?

A
  • Pharyngitis (strep throat)
  • Cellulitis/Erysipelas
  • Impetigo (although in derm we learned that usually staph aureus)
  • Scarlet fever (scarlet rash with sandpaper-like texture, strawberry tongue, circumoral pallor, and desquamation)
  • Toxic shock syndrome (Exotoxin A superantigen)
  • Necrotizing fasciitis
  • Rheumatic fever **due to immune response to M protein *memory: dont eat My Pie (phagocytosis, M protein, Pyogenes)
  • Acute glomerulonephritis
123
Q

If you want to confirm a diagnosis of group A strep pyogenes in your patient but dont have time to culture it, what other test can you run?

A

PYR (pyrrolidonyl arylamidase) test - will turn bright pink/cherry red if positive. Strep pneumo has this enzyme.

*memory: Pies (pyogenes) are my peers (PYR+)

124
Q

How can we detect a recent strep pyogenes infection?

A

ASO (anti-streptolysin O) antibody titers. Can be helpful for diagnosing rheumatic fever.

125
Q

What are the 5 major criteria for rheumatic fever?

A 
*memory: JONES
Joints (polyarthritis)
O (heart shape) (carditis - esp. the valves)
Nodules (subcutnaeous)
Erythema marginatum (itchy rash)
Sydenham chorea (involuntary movement)
126
Q

What are the 2 scary results of strep pyogenes pharyngitis?

A
  1. Glomerulonephritis
  2. Rheumatic fever

*memory: PHaryngitis, nePHritis, PHever, PHyogenes

127
Q

Impetigo from strep pyogenes is most likely to result in what?

A

Glomerulonephritis (then secondly pharyngitis)

128
Q

What is scarlet fever? What causes it?

A

Red rash with sandpaper-like texture, strawberry tongue, circumoral pallor, and later desquamation

Caused by Group A strep (pyogenes) – which is alpha hemolytis, bacitracin sensitive

129
Q

When would we see strawberry tongue in a child?

A
  1. Kawasaki disease

2. Scarlet fever

130
Q

When would see strawberry cervix?

A

Trichomonas (a protozoal anaerobic vaginal infection with green yellow discharge. Treat w/ metronidazole and treat partner, pH>4.5, diagnose with quick wet prep before they die)

131
Q

What disease does group B strep cause?

A
  • pneumonia
  • meningitis
  • sepsis
132
Q

What population does group B strep mainly affect?

A

Babies

133
Q

Which bacteria produces a substrate that enlarges the area of beta hemolysis made by staph aureus? What other enzymes does this bacteria have that is useful in lab testing?

A

Group B strep (agalactiae). It produces CAMP factor (unrelated to cAMP!), which enlarges hemolysis around staph aureus.

Also is Hippurate test +

134
Q

When are pregnant women screened, and how are they treated, for group B strep?

A

35-37 weeks (because babies get it as they are delivered, not through the placenta)

Treat with intrapartum penicillin prophylaxis

135
Q

Which 4 bacteria can cause necrotizing fasciitis?

A
  1. Strep pyogenes
  2. Staph Aureus
  3. Clostridium perfringens (‘gas gangrene’)
  4. Pseudomonas (ecthyma gangrenosum)

*memory: Stop Strapping Closets to my necrotic legs PleaSe!

136
Q

Which bacteria are group D strep (enterococci) resistant to?

A

Penicillin G

137
Q

Which diseases do group D strep (enterococci) cause?

A
  • UTI
  • biliary tract infection
  • endocarditis after GI/GU procedures
138
Q

What is streptococcus grouping (A, B, D, etc) based on?

A

The carbohydrate on the cell wall

139
Q

How is VRE treated?

A

Linezolid or Daptomycin

140
Q

How is MRSA treated?

A

Vancomycin, Ceftaroline (5th gen), Linezolid, or Daptomycin

141
Q

Which bacteria can grow in 6.5% NaCl and bile?

A

Group D strep (separated from other strep because they are gamma hemolytic, AKA no hemolysis)

Group D enterococci: Bile and NaCl growth
Group D nonenterococci: only NaCl growth

142
Q

Which bacteria is associated with colon cancer?

A

Strep gallolyticus (strep bovis biotype 1)

*memory: Bovis in the Blood means Cancer in the Colon

143
Q

What diseases does cornyebacterium diptheriae cause?

A

“Diptheria”, which is characterized by:

  • pseudomembranous pharyngitis (grayish-white membrane in back of throat that can obstruct it)
  • lymphadenopathy
  • myocarditis
  • arrhythmias
144
Q

How is cornyebacterium diptheriae diagnosed on lab tests?

A

Its a gram positive anaerobic rod with:

  • Metachromatic blue-red granules (on microscopy, they look like little cigars)
  • Elek test positive for diptheria toxin
  • Black colonies on cystine-tellurite agar
145
Q

What is used to make the diptheria vaccine?

A

Diptheria toxoid

146
Q

Which species of bacteria form spores?

A

Bacillus, Clostridium, and Coxiella

147
Q

How can we kill spores?

A

Autoclaving - steam at 121 deg C for 15 minutes

148
Q

How can we treat clostridium tetanus?

A

Antitoxin +/- vaccine booster, and diazepam for muscle spasms

149
Q

Which form of clostridium botulinum affects adults vs. babies?

A

Adults: Preformed toxins
Babies: Spores in honey

150
Q

How can we treat clostridium botulinum?

A

Antitoxin

151
Q

What do the toxins of C. Diff do?

A

Toxin A: Binds to brush border of the gut.

Toxin B: Depolarizes actin so bacteria can get into cell

152
Q

What disease does C. Diff cause?

A
  • Pseudomembranous colitis (scoping shows yellow pseudomembranes)
  • Diarrhea
153
Q

What antibiotics predispose to C. Diff?

A
  1. Clindamycin
  2. Ampicillin

*memory: CLINDAmycin CLEANS you out, ampCIllin secretely does the same

154
Q

How do we diagnose C. Diff?

A

PCR for one or both toxins (toxin A and B)

155
Q

How do we treat C. Diff?

A

Metronidazole (excellent for anaerobes below the diaphragm) or oral vancomycin (excellent for gram positives).

*memory: VANKO took the METRO to go C DIFFerent people

156
Q

How do we treat recurrent C. Diff?

A

Repeat prior regimen, OR give fidaxomicin (new macrolide specifically made for C. Diff), OR give fecal transplant

157
Q

What is special about Bacillus anthracis’s capsule?

A

It is the only bacteria with a polypeptide, not polysaccharide capsule. It contains D-glutamate

*memory: Antrhax is D-GLoomy exception

158
Q

What are the symptoms of cutaneous anthrax?

A

Starts as a papule surrounded by vesicles, then becomes an ulcer/necrosis with black eschar/crust and an edematous rim (because edema toxin, which mimcs cAMP to inclrease Cl- secretion)

Painless throughout. Can progress to bactermia and death, but rarely.

159
Q

What are the symptoms of pulmonary anthrax? What is this caused by?

A

Flu-like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, shock.

Caused by inhalation of spores.

160
Q

What diseases does bacillus cereus cause?

A

Food poisoning, either emetic or diarrheal….

  • Emetic: Nausea and vomiting 1-5 hours after eating rice and pasta
  • Diarrheal: Watery diarrhea and GI pain 8-18 hours after eating
161
Q

What toxin causes bacillus cereus emetic type food poisoning?

A

Cereulide, a preformed toxin

162
Q

Why is bacillus cereus cause “reheated rice syndrome”

A

Because the spores survive cooking and then keeping the rice warm results in germination of spores and enterotoxin formation

163
Q

How can Listeria monocytogenes be acquired?

A
  • Unpasteurized dairy
  • Cold deli meats
  • Through the placenta
  • Vaginal transmission during birth
164
Q

Which bacteria forms “rocket tails” to shoot from cell to cell, thereby avoiding antibodies and also causing cellular damage? What are these tails made of?

A

Listeria monocytogenes

Tails made of actin polymerization

NOTE: This produces a characteristic “tumbling motility” seen on… microscopy? idk

165
Q

What is the only gram positive organism to produce endotoxin?

A

Listeria monocytogenes

166
Q

What diseases can Listeria monocytogenes cause?

A

Pregnant women

  • Amnionitis
  • Septicemia
  • Spontaneous abortion

Neonates

  • Granulomatosis infantiseptica (surviving neonates of mothers with Listeria get pyogenic granulomas all over body)
  • Neonatal meningitis

Immuncompromised patients
- Meningitis

Healthy
- Mild gastroenteritis

167
Q

How do we treat Listeria monocytogenes?

A

If healthy person: Nothing, its self limited

If baby, elderly, or immunocompromised: Ampicillin

*memory: Its part of HHELPSS (H. influenza, H. pylori, E. coli, Listeria, Proteus, Salmonella, Shigella)

168
Q

Actinomyces vs. Nocardia: How are they told apart on lab test?

A

They are both gram + branching filamentous bacteria that resemble fungi, BUT:

Actionmyces = obligate anerobe
Nocardia = obligate aerobe, acid-fast (weak)
169
Q

Where is actinomyces usually found? Nocardia?

A

Actinomyces: Oral flora (its a dental procedure thing)
Nocardia: Soil (not normal in the human body)

170
Q

What diseases does actinomyces usually cause?

A

Oral/facial abscesses that drain through sinus tracts, forming yellow “sulfure granules” of bacteria. Actinomycosis = “lumpy jaw”

171
Q

What diseases does nocardia usually cause?

A

Immunocompetent: Cutaneous infections after trauma

Immunocompromised; Pulmonary infections

172
Q

how do we treat actinomyces and nocardia?

A

*memory: treat them in a SNAP (and they look like branches, which you can just SNAP)

Sulfonamides for Nocardia

Actinomyces gets Penicillin

173
Q

How does primary TB infection normally present?

A

A “Ghon complex”

  • Ghon focus in lower-middle lobes
  • Calcified hilar nodes
174
Q

how does secondary TB (either reactivation of latent TN, or reinfection of a partially immunized host) normally present?

A

Lesion of fibrosis and caseous necrosis in the upper lobes (TB is an obligate aerobe so it goes up to where it can find more O2)

175
Q

Once a Ghon complex forms from primary TB infection, how does it usually heal?

A

By fibrosis. Then the host has immunity and hypersensitivity to TB. Their PPD test (purified Tuberculin injection) will be positive.

176
Q

What are the 4 outcomes of primary TB infection?

A
  1. Healing
  2. Death from lung disease (HIV, malnutrition)
  3. Miliary TB/bactermia
  4. Dormant TB in several organs… reactivates later
177
Q

What can cause a false positive TB test?

A

BCG vaccine for TB (used in non-US)

178
Q

What can cause a false negative TB test?

A
  1. Steroids (poor immunity)
  2. Malnutrition (poor immunity)
  3. Immunocompromised
  4. Sarcoidosis
179
Q

If someone gets a +PPD test and says they have gotten the BCG vaccine, what further workup can you do?

A

IGRA (interferon gamma release assay). This test will have fewer false positives from the BCG vaccine.

180
Q

When should AIDS patients receive prophylaxis for Mycobacterium avium, and what is the prophylaxis?

A

When: CD4

181
Q

What 4 types of mycobacterium can cause disease?

A
  1. M. TB - Lungs
  2. M. avium - Lungs
  3. M. scrofulaceum - cervical lymphadenitis in children
  4. M. marnum - hand infection in aquarium handlers
182
Q

An aquarium handler has a hand infection. What does he have?

A

Mycobacterium marinum

183
Q

What are the symptoms of TB?

A 
Fever
Night sweats
Weight loss
Cough (can be productive or not)
Hemoptysis
184
Q

What are the 2 mycobacterium virulence factors?

A
  1. Cord factor
    - Inhibits macrophage maturation
    - Induces TNFalpha
    * memory: draw a CORD across a doorway to STOP people
  2. Sulfatides (surface glycolipids)
    - Inhibit phagolysosome fusion; so can proliferate intracellularly
    * memory: SSSulfatides stop fuSSSion

NOTE: part of “Some Nasty Bugs May Live FacultativeLY”

  • Salmonella
  • Neisseria
  • Brucella
  • Mycobacterium
  • Listeria
  • Francisella
  • Legionella
  • Yersina pestis
185
Q

Which bacteria causes “glove and stocking” loss of sensation, and why?

A

Mycobacterium leprae, because it likes cool temperatures so it infects the skin and superficial nerves at the extremities

186
Q

Why can’t mycobacterium leprae grow in vitro?

A

Because it only grows in cool temperatures

187
Q

What is the animal reservoir for leprosy?

A

Armadillos

188
Q

What are the 2 forms of leprosy?

A

Lepromatous

  • Diffuse
  • Lion-like facies
  • communicable!!
  • Low cell immunity, can only do Th2

Tuberculoid (more mild)

  • Hairless plaques, just a few
  • High cell immunity, good Th1 response
  • memory: Th2, stay away from YOU (communicable)
  • memory: Th1, I’d rather have that ONE
189
Q

How do we treat leprosy?

A

Tuberculoid (mild form): Dapsone + Rifampin
Lepromatous (sever): Dapsone + Rifampin + Clofazimine

*memory: For the severe form, you have to bring out the CL

Note: Rifampin turns urine orange
Note: Dapsone also used for PCP prophylaxis
Note: Clofazimine specific to leprosy

190
Q

How do we first distinguish gram negatives?

A
  1. Diplococci (Neisserria,moraxella catarrhalis)
  2. Coccoid rods (H. Flu, bordetella, brucella, pasteurella)
  3. Rods (Klebsiella, E Coli, Salmonella, Proteus, Shigella, etc)
  4. Comma shaped & oxidase+ (campylobacter, vibrio, helicobacter)
191
Q

How do we distinguish between the gram negative, comma shaped, oxidase positive gram negatives?

A

Campylobacter grows in 42 deg *CAMPy likes the hot CAMPfire

Vibrio cholerae grows in alkaline media *Basic viBritch (basic bitch)

Helicobacter pylori produces urease *remember we can do the urease breath test

192
Q

How do we distinguish between gram negative diplococci?

A

See if it ferments maltose…

Neisseria MMMeningitidis: Ferments MMMaltose
Neisseria gonorrhoeae: Does not ferment maltose

193
Q

How do we distinguish the coccoid rods from each other?

A

No great laboratory test except for H. Flu, which needs Factor V (NAD+) and factor X (hematin) [presesent on chocolate agar or with co-culture with staph aureus which provides factor V]

Pasteurella: Think animal bites
Bordetella pertussis: Whooping cough
Brucella: Brucellosis… lifelong disease with sweating, joint pain, abdominal pain

194
Q

What is the first step to distinguish between all the different gram negative rods?

A

Lactose fermenting on MacConkey agar.

Lactose fermenters (pink colonies):   *memory: maConKEES
Citrobacter
Klebsiella
E. Coli
Enterobacteria
Serratia
NON-lactose fermenters (white colonies/yellow):
Pseudomonas (ox +)
Shigella (H2S-)
Salmonella (H2S+)
Proteus (H2S+)
Yersina (H2S+)
195
Q

E. Coli is a lactose fermenter (part of maConKEES). What other enzyme does it have? Why is this clinically significant?

A

B-galactosidase… breaks down lactose –> glucose + galactose

Significant because people with galactosemia can get E. Coli sepsis… E. Coli makes their accumulation of galctose even worse.

NOTE: Galactosemia =

  • AR deficiency in galactose-1-phosphate-uridyltransferase [classically] or galactokinase [more mild]
  • Get infantile cataracts, jaundice, hepatomegaly, intellectual disability, E. Coli sepsis. Treat by excluding galactose and lactose from diet)
196
Q

What bacteria grows on EMB (Eosin-methylene blue) agar?

A

E. Coli. Grows as black colonies with a green metallic sheen.

*NOTE: Pseudomonas is the only bacteria that grows as actual GREEN colonies, on regular agar

197
Q

How do we identify pseudomonas on lab tests?

A
  • Gram negative rod
  • Non-lactose fermenter
  • Oxidase positive

This is enough, but it ALSO is

  • catalase positive
  • produces green colonies
198
Q

How do we narrow down gram negative rods that are non-lactose fermenters, and are oxidase negative?

A

H2S production

Does not produce H2S: Shigella *memory: There only enough “SH”it for one word… if its SHigella, it cant make H2S
Produces H2S: Salmonella, Proteus, Yersina

199
Q

Gram negative diplococci means…

A

Neisseria!! (or moraxella… but probably neisseria)

200
Q

Neisseria gonorrhoeae vs. meningitidis: Which ferment glucose?

A

Both

*memory: MeninGococci, Gonococci (both have G for glucose, only mening has M for maltose)

201
Q

Neisseria gonorrhoeae vs. meningitidis: Which ferment maltose?

A

Only meningitidis

*memory: MeninGococci, Gonococci (both have G for glucose, only mening has M for maltose)

202
Q

Neisseria gonorrhoeae vs. meningitidis: Which produce IgA protease?

A

Both

NOTE: And Strep pneumo (pnuemo only!) and H. Flu *mmeory: SHiN

203
Q

Neisseria gonorrhoeae vs. meningitidis: Which is more often intracellular (they can both be facultatively intracellular)?

A

Gonorrhoeae. Often within neutrophils.

*memory: Gonorrhoeae is like a Gofer, it digs a hole and stays in there

204
Q

Neisseria gonorrhoeae vs. meningitidis: Which has a capsule?

A

Only meningitidis

*memory: Meningitidis has a Metal plate around it

205
Q

Neisseria gonorrhoeae vs. meningitidis: How is each transmitted?

A

Gonorrhoaeae: sexual, perinatal
Meningitidis: Respiratory, oral

206
Q

What diseases does N. Gonorrhoeae cause?

A
  • Gonorrhea (burning urination + yellow urethral discharge)
  • Septic arthritis
  • Neonatal conjunctivitis
  • PID (along with chlamydia is most common cause)
  • Fitz-Hugh-Curtis syndrome (infection of the liver causing violin string adhesions from peritoneum to liver)
207
Q

What disease does M. Meningitidis cause?

A
  • Meningitis
  • Meningococcemia (non-blanching rash)
  • Waterhouse-Friderichsen syndrome (adrenal hemorrhage -> adrenal insufficiency, DIC, and shock most often seen in children)
208
Q

What prevents neonatal transmission of N. Gonorrhoaeae?

A

Erythromycin ointment

209
Q

What prevents sexual transmission of N. Gonorrhoeae?

A

condoms

210
Q

How do we treat N. Gonorrhoae?

A

Ceftriaxone (plus azithromycin OR doxycycline for possible co-infection with chlamydia)

  • memory: uniCEF for those who are GON-ers
  • meory: DOGs (doxycycline) and AZTECS (azihromycin) are good at CLimbing (chlamydia)
211
Q

How do we prevent spread of N. meningitidis?

A
  • Rifampin *turns urine orange
  • Ciprofloxacin
  • Ceftriaxone
212
Q

How do we treat N. meningitidis?

A

Ceftriaxone

Penicillin G

213
Q

How is H. Flu transmitted?

A

Aerosol

214
Q

Which type of H. Flu are the most common causes of otitis media, conjunctivitis, bronchtis, and invasive infection?

A

Non-typeable strains. Because we have a vaccine for capsular type B now.

215
Q

What virulence factor does H. Flu produce?

A

IgA protease (Strep pneumo, H flu, and both types of Neisseria all produce this)

216
Q

Which bacteria will grow with staph aureus and why?

A

H. Flu, because staph aureus prodives factor V (NAD+) through the hemolysis of RBCs (its beta hemolytic… clear rim of hemolysis)

217
Q

What diseases does H. Flu cause?

A 
*memory: haEMOPhilus
Epiglottitis
Meningitis
Otitis media
Pneumonia
218
Q

What are the signs of epiglottitis?

A
  • H. Flu culture (chcolate agar, factors V and X)
  • cherry red epiglottis
  • “thumbprint” sign on x-ray: Thickening of the epiglottis on lateral view
219
Q

How do we treat H. Flu mucosal infection (epiglottitis, otitis media)?

A

Amoxicillin +/- clavulonic acid
*remember amoxicillin and ampicillin are usually given with clavulonic acid (or sulbactam or tazobactam) because they are susceptible to beta-lactamases

220
Q

How do we treat H. Flu meningitis?

A

Ceftriaxone (and give Rifampin to their close contacts for prophylaxis)

221
Q

What is the H. Flu vaccine made of?

A
  1. Polyribosylribitol phosphate (PRP) — (the tybe B capsular polysaccharide)
  2. Diptheria toxoid (or tetanus or other protein)

Ex Q: A patient with antibodies to ribose, ribositil, and phosphate is immune to H. Flu

222
Q

At what age do we give the H. Flu vaccine?

A

2 months - 18 months

223
Q

How do we diagnose Legionella?

A

Antigen in urine

224
Q

How is Legionella transmitted?

A

From environmental water sources (air conditioning systems, hot water tanks)

NOT person to person

225
Q

What are the signs of a Legionella infection?

A

Legionaire’s disease:

  • Severe pneumonia (usually lobar)
  • Fever
  • GI symptoms (diarrhea, N/V)
  • CNS symptoms (just due to low O2, non specific)
  • Hyponatremia sometimes

Pontiac fever:
- Mild flu

226
Q

How does Legionella survive?

A
  1. its resitant to chlorine and can grow on inanimate objects
  2. Once in the body, its a facultative intracelllular. Uses type IV secretion system to make a home out of macrophages before it goes in
227
Q

What substance causes pseudomonas to have a blue-green pigment?

A

Pyocyanin

228
Q

What odor does pseudomonas ave?

A

Grape-like

229
Q

What toxins does pseudomonas produces?

A
  1. Endotoxin (because gram neg) –> Fever, shock

2. Exotoxin A –> inactivates EF2 –> host cell death

230
Q

What diseases is pseudomonas associated with?

A

*meomry: PSEUDDO is a BECH

Pneumonia
Sepsis
otitis Externa (swimmer's ear)
UTIs
Drug use
Diabetes
Osteomyelitis (from puncture wounds)

Burn victims *wound infection
Ecthyma gangrenoum *immuncompromised
CF patients *b/c biofilms
Hot tubs **b/c often found in water

231
Q

Why is pseudomonas associated with CF pneumonia?

A

May form biofilms, allowing it to persist longer

232
Q

What is ecthyma gangrenosum?

A

A rapidly progressive necrotic cutaneous lesion caused by pseudomonas. May be a large ulcer with necrotic regions in it.

Usually only seen in immunocompromised patients.

233
Q

How do you treat pseudomonas?

A

FIRST LINE

  1. Piperacillin, Ticarcillin (4th gen pseudomonals)
  2. Cefepime, Ceftazidine (extended cephalosporins, 3rd and 4th generation)
  3. Fluoroquinolones (ciprofloxacin)
  4. Aminoglycosides (gentamicin, tobramycin)

THEN…

  1. Aztreonam (a monobactam) - If pencillin allergy OR too renal insufficient for aminoglycoside
  2. Imipenem, meropenem (carbapenems) - If serious infection and not afraid of seizure, skin rash, GI
  3. Colistin, polymyxin B - if drug resistant
234
Q

What virulence factors does E. Coli have?

A
  1. Fimbriae (cystitis, pyelonephritis)
    * memory: Ureters look like fimbriae
  2. K Capsule (pneumonia, neonatal meningitis)
  3. LPS endotoxin (septic shock)
235
Q

What are the 4 types of E. Coli?

A
  1. EIEC (invasive… bloody diarrhea)
  2. ETEC (Travelers diarrhea)
  3. EPEC (Pediatrics…. diarrhea in children)
  4. EHEC (Hemolytic uremic syndrome, bloody diarrhea)
236
Q

Which type of E. Coli causes manifestations similar to Shigella?

A

EIEC (invasive): Invades the intestinal mucosa and causes necrosis and inflammation –> dysentery

EHEC (hemolytic); Produces Shiga-like toxin that inactivates 60S ribosome by removing adenine from rRNA –> dysentery

237
Q

Which type of E. Coli produces the heat-lable (LT) and heat-stable (ST) toxins?

A

ETEC (Traveler’s).

These toxins increase Cl- secretion to produce watery diarrhea (non bloody because no inflammation or vasion).

LT: Increases cAMP –> increased Cl- secretion
ST: Increases cGMP –> decreased NaCl resorption

238
Q

Which type of E. Coli produces diarrhea in children? What pathologic changes does it produce?

A

EPEC (pediatric). Causes flattening of villi and prevents absorption. Adheres to apical surface.

239
Q

Which type of E. Coli is the one that has an O157:H7 strain?

A

EHEC (hemolytic). The one that produce shiga-like toxin.

240
Q

How can EHEC be distinguished from other E. Coli on lab tests?

A

Does not ferment sorbital

*memory: EHEC “sold it all” to have its own hemolytic uremic thing

241
Q

What is hemolytic uremic syndrome?

A

Triad:

  1. Anemia
  2. Thrombocytopenia
  3. Acute renal failure

Pathogenesis

  1. Blocking 60S damages the endothelium of blood vessels
  2. Microthrombi form on endothelium
  3. RBCs get lysed into schistocytes (mechanically cant fit through vessels as well)
  4. Platelets get consumed (in the microthrombi)
  5. Renal blood flow decreases (because the thrombi)

First Aid (7 decks)

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