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Final FA review > 3/30 micro > Flashcards

3/30 micro Flashcards

1
Q

Lipoteichoic acid

  • where is it found?
  • induces what?
A

Gram (+) cell wall.

  • teichoic acids only found in gram (+)s.
  • induces TNF & IL-1.
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2
Q

Outer membrane

-whats the antigen?

A

O polysaccharide

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3
Q

Periplasm

  • where is it?
  • found in which bugs?
A
  • space btwn cytoplasmic membrane & outer membrane in gram (-) bugs.
  • this is the location of beta-lactamases.
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4
Q

dipicolinic acid

-where is this found?

A

In a spore.

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5
Q

Capsule

-gram (+) or (-)?

A

Both can have it.

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6
Q

Peptidoglycan

-gram (+) or (-)?

A

Both

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7
Q

Which bugs are pleomorphic?

A

Rickettsia & chlamydia.

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8
Q

Which bug has no cell wall?

A

mycoplasma

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9
Q

Chlamydia

-what does it lack in its cell wall?

A

muramic acid

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10
Q

Mucicarmine

-helps visualize what?

A

Capsule

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11
Q

India ink/mucicarmine stain shows bug

-think what?

A

Cryptococcus neoformans

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12
Q

Chocolate agar with factors V (NAD+) and X (hematin)

-which bug?

A

H. influenzae

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13
Q

Thayer-Martin

-whats in it?

A

VPN media

  • Vancomycin (inhibits gram-positive organisms)
  • Polymyxin (inhibits gram-negative organisms except Neisseria)
  • Nystatin (inhibits fungi)

*“to connect to Neisseria, please use your VPN client”

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14
Q

Bordet-Gengou (potato) agar

-which bug?

A

Bordetella pertussis

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15
Q

Regan-Lowe medium

-which bug?

A

Bordetella pertussis

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16
Q

Tellurite agar, Löffler medium

-which bug?

A

C. diphtheriae

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17
Q

Löwenstein-Jensen agar

-which bug?

A

M. tuberculosis

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18
Q

Eaton agar, requires cholesterol

-which bug?

A

M. pneumoniae

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19
Q

Pink colonies on MacConkey agar

-which type of bugs?

A

Lactose-fermenting enterics

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20
Q

How does E. coli look on EMB agar?

A

-colonies with green metallic sheen

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21
Q

Charcoal yeast extract agar buffered with cysteine & iron
-which bug?

A

Legionella

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22
Q

Sabouraud agar

-which bug?

A

Fungi

*“Sab’s a fun guy!”

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23
Q

Obligate aerobes

  • name them:
  • mnemonic:
A

Nocardia, Pseudomonas, & MycoBacterium tuberculosis.

*Nagging Pests Must Breathe.

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24
Q

Obligate anaerobes

  • name them:
  • mnemonic:
A

Clostridium, Bacteroides, and Actinomyces

*Can’t Breathe Air.

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25
Q

Obligate anaerobes

  • which enzymes do they lack?
  • unique characteristics?
A
  • catalase &/or superoxide dismutase

- Generally foul smelling (short-chain fatty acids), are difficult to culture, and produce gas in tissue (CO2 &H2).

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26
Q

Which type of ABx is useless against anaerobes bc it req O2 to enter bacterial cell?

A

aminoglycosides

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27
Q

Obligate intracellular

  • which bugs?
  • mnemonic:
A

Rickettsia, Chlamydia, Coxiella burnetti.

*Stay inside (cells) when it is Really Cold.

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28
Q

Encapsulated bacteria

  • name them
  • mnemonic
A

SHiNE SKiS.

  • Strep pneumoniae
  • H. influenzae type B
  • N. meningitidis
  • E. coli
  • Salmonella
  • Klebsiella pneumoniae
  • group B Strep
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29
Q

Vaccine for encapsulated bugs

-must include what?

A

-Capsule + protein conjugate serves as an antigen in vaccines.

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30
Q

Aplenic pt

-give them which vaccines?

A

Give S. pneumoniae, H. influenzae, N. meningitidis vaccines.

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31
Q

Catalase-positive organisms

  • name them
  • mnemonic:
A

You need PLACESS for your cats.

Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia.

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32
Q

Why conjugate a capsular antigen w/a protein?

A

-A polysacc. Ag alone cannot be presented to T cells.
-Conjugating it w/a protein enhances immunogenicity by
promoting T-cell activation and subsequent class switching.

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33
Q

Pneumococcal vaccine

  • which vaccine = conjugated to protein
  • which vaccine is not?
A

-PCV (pneumococcal conjugate vaccine, i.e., Prevnar)
-PPSV (pneumococcal polysaccharide vaccine with
no conjugated protein, i.e., Pneumovax)

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34
Q

Name the conjugate vaccines:

A
  • PCV (pneumococcal conjugate vaccine)
  • H. influenzae type B (conjugate vaccine)
  • Meningococcal vaccine (conjugate vaccine)
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35
Q

Urease-positive bugs

  • name them
  • mnemonic:
A

CHuck Norris hates PUNKSS.

  • Cryptococcus
  • H. pylori
  • Proteus
  • Ureaplasma
  • Nocardia
  • Klebsiella
  • S. epidermidis
  • S. saprophyticus.
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36
Q

Protein A

  • whats it do?
  • which bug is it found in?
A
  • Binds Fc region of IgG. Prevents opsonization and phagocytosis.
  • Expressed by S. aureus.
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37
Q

Which bugs secrete IgA protease?

-mnemonic?

A

SHiN

-S. pneumoniae, H. influenzae type B, and Neisseria

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38
Q

M protein

  • whats it do?
  • which bug is it found in?
A
  • Helps prevent phagocytosis.

- Expressed by group A streptococci.

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39
Q

Exotoxin

-coded by?

A

Plasmid or bacteriophage

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40
Q

Endotoxin

-coded by?

A

Bacterial chromosome

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41
Q

Exotoxin vs endotoxin

-which one more toxic?

A

Exotoxin much more toxic.

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42
Q

Exotoxin vs endotoxin

-which one is antigenic?

A
  • Exotoxin = antigenic, induces high-titer antibodies called antitoxins.
  • Endotoxin = poorly antigenic
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43
Q

Exotoxin vs endotoxin

-vaccine available?

A
  • Exotoxin: Toxoids used as vaccines.

- Endotoxin: No toxoids formed and no vaccine available

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44
Q

toxoid

-define:

A

Exotoxin thats been partially denatured by formalin, acid, or heat.

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45
Q

Exotoxin vs endotoxin

-heat stability:

A
  • exotoxin: Destroyed rapidly at 60°C=140F (except staphylococcal enterotoxin).
  • endotoxin: Stable at 100°C=212F(=BP of water) for 1 hr.
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46
Q

A-B exotoxin

  • function of A subunit?
  • function of B subunit?
A
  • A subunit = active subunit w/toxin activity

- B subunit = binds to host, involved w/entry.

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47
Q

Which bugs’ toxin:

-Inactivate elongation factor (EF-2).

A
  • C. diphtheriae = Diphtheria toxin
  • Pseudomonas = Exotoxin A

*both = ADP ribosylating A-B toxins.

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48
Q

Which bugs’ toxin:

-Inactivate 60S ribosome by removing adenine from rRNA.

A
  • Shigella = shigatoxin
  • EHEC (including O157:H7) = shiga-like toxin

*both = ADP ribosylating A-B toxins.

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49
Q

Shiga toxin

-what can it cause?

A

-dysentery & HUS.

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50
Q

Shigella vs EHEC

-difference?

A

EHEC does not invade host cells.

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51
Q

Shiga-like toxin

-what can it cause?

A

HUS

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52
Q

EHEC: shiga like toxin

-targets which types of cells?

A

EHEC frequently causes HUS b/c the toxin targets

colonic mucosal cells AND renal endothelial cells

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53
Q

Which bugs make toxins that cause inc. fluid secretion?

A

ETEC, cholera, Bacillus anthracis.

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54
Q

ETEC:

-what are its 2 toxins & what do they do?

A

1) LT (heat-labile toxin) = inc. cAMP = Cl secretion into gut & water follows = diarrhea.
2) ST (heat-stabile toxin) = inc. cGMP = dec. NaCl & H2O resorption in gut = diarrhea.

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55
Q

ETEC: 2 toxins

-mnemonic:

A

Watery diarrhea:

-Labile in the Air (Adenylate cyclase), Stable on the Ground (Guanylate cyclase).

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56
Q

Bacillus anthracis

  • whats its toxin that causes fluid secretion?
  • hows it work?
A

Edema factor = mimics cAMP = Likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax.

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57
Q

Vibrio cholerae

  • toxin?
  • mech?
A

Cholera toxin = permanently activates Gs = inc. cAMP = inc Cl secretion into the gut = diarrhea.

*Voluminous “rice-water” diarrhea.

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58
Q

Bordetella pertussis

  • whats its toxin?
  • whats it do?
A

Pertussis toxin = disabled Gi = inc. cAMP = impairs phagocytosis to permit survival of microbe.
-Whooping cough: the toxin may not be the cause of the cough.

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59
Q

Bordetella pertussis

  • what are the 3 stages?
  • in which one is pt most contagious?
  • in which stage are the “whoops”.
A

1) Catarrhal = most contagious.
2) Paroxysmal = whooping cough
3) Convalescent stage

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60
Q

Bordetella pertussis

  • where does it infect?
  • does it cause productive or non-productive cough?
A
  • Invades resp. tract & attaches (via filamentous hemagluttinin) to ciliated epithelium of trachea/bronchi.
  • Evades immune response and destroys the ciliated cells causing whooping cough.
  • non-productive cough bc cilia is destroyed.
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61
Q

Does bordetella pertussis invade the body?

A

No.

  • It attaches to ciliated epithelial cells of the bronchi and then releases its exotoxins.
  • The FHA, a pili rod extending from its surface, is involved in this binding. Antibodies directed against the FHA prevent binding and disease, and thus they are protective.
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62
Q

Bordetella pertussis

-how does it damage the ciliated cells?

A

Tracheal cytotoxin: This toxin destroys the ciliated epithelial cells, resulting in impaired clearance of bacteria, mucus, and inflammatory exudate. This toxin is probably responsible for the violent cough.

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63
Q

Which bugs have exotoxins that inhibit release of NTs?

A

C. tetani & C. botulinum.

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64
Q

C. tetani & C. botulinum

  • which one causes flaccid paralysis?
  • which one causes spastic paralysis?
A
  • Tetani = spastic
  • Botulinum = flaccid

*if botox was spastic, it would be against the point cuz then you’d get wrinkles. Whole point is to make the muscle remain flaccid.

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65
Q

Presentation of botulinum poisoning?

A
  • Initially = diplopia & dysphagia.

- Followed by general muscle weakness, which rapidly leads to sudden respiratory paralysis and death.

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66
Q

Which bugs have exotoxins that lyse cell membranes?

-what are their toxins called?

A
  • C. perfringens = Alpha toxin = Phospholipase(lecithinase)

- S. pyogenes = Streptolysin O = lyses RBCs

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67
Q

What will WBC count look like in pertussis infection?

A

It will look like a viral infection = more lymphocytes than neutros.

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68
Q

Which bugs have superantigens that can cause shock?

-name the toxins:

A
  • S. aureus = Toxic shock syndrome toxin (TSST-1)

- S. pyogenes = Exotoxin A

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69
Q

How do superantigens work?

-what chemicals do they cause to be released?

A

-Bring MHC II and TCR in proximity to outside of antigen binding site to cause overwhelming release of IFN-γ and IL-2 => shock.

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70
Q

Toxic shock syndrome:

-Sxs:

A

Fever, rash, shock.

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71
Q

How does endotoxin lead to DIC?

-activates what mediator?

A

Activates tissue factor

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72
Q

Tissue factor

  • aka?
  • which coag. pathway does it activate?
A
  • aka thromboplastin

- Extrinsic pathway.

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73
Q

Which bugs use transformation more than most?

  • mnemonic:
  • what else do these bugs have in common?
A

SHiN

  • S. pneumoniae
  • H. influenzae type B
  • Neisseria

*these all have IgA protease.

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74
Q

Bacterial Conjugation: F+ × F–

  • whats transferred?
  • are chromosomal genes transferred?
  • is plasmid transferred?
A
  • plasmid is replicated and transferred.
  • no chromosomal genes are transferred.

*key = plasmid is replicated first, so after conjugation, both bugs are F+.

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75
Q

If F+ plasmid is incorporated into bacterial chromosomal DNA, what do you call it?

A

-termed high-frequency recombination (Hfr) cell.

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76
Q

Bacterial Conjugation: Hfr × F–

  • whats transferred?
  • are chromosomal genes transferred?
  • is plasmid transferred?
A
  • Replication of incorporated plasmid DNA may include some flanking chromosomal DNA.
  • Transfer of plasmid and chromosomal genes.
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77
Q

Transposition

-how can this lead to ABx resistance spread?

A
  • Segment of DNA (transposon) that can “jump” (excision and reintegration) from one location to another, can transfer genes from plasmid to chromosome and vice versa.
  • When excision occurs, may include some flanking chromosomal DNA, which can be incorporated into a plasmid and transferred to another bacterium.
  • Examples include antibiotic resistance genes on R plasmid.
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78
Q

Genes for the following 5 bacterial toxins are encoded in a lysogenic phage:
-mnemonic:

A

ABCDE

  • ShigA-like toxin
  • Botulinum toxin (certain strains)
  • Cholera toxin
  • Diphtheria toxin
  • Erythrogenic toxin of S. pyogenes (scarlet fever)
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79
Q

Gram (+) rods

  • name them
  • mnemonic:
A

from CC to MLB - Grant uses a rod (baseball bat).

  • Clostridium (anaerobe)
  • Corynebacterium
  • Listeria
  • Bacillus (aerobe)
  • Mycobacterium
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80
Q

Bile soluble

-does it survive in bile?

A

No

-its lysed in bile.

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81
Q

Which bug grows in 6.5% NaCl?

A

Enterococcus

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82
Q

α-hemolytic bacteria

-what color ring in blood agar?

A

green

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83
Q

β-hemolytic bacteria

-what color ring in blood agar?

A

clear area

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84
Q

Coagulase

  • how does it cause coagulation?
  • what does coagulase allow the bug to do?
A
  • Activates prothrombin.

- form a fibrin clot around itself => abscess.

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85
Q

S. Aureus

-commonly colonizes where?

A

Nose

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86
Q

Minor skin infections are usually caused by which bugs?

A

Almost exclusively caused by either S. pyogenes (GAS) or by S. aureus.

87
Q

Scalded skin syndrome

  • which bug?
  • which toxin?
  • mechanism?
  • which disease has similar process going on?
A
  • S. aureus = exfoliative toxin
  • Toxin cleaves desmoglein in desmosomes of skin, which attach keratinocytes together in stratum spinosum.

*Pemphigus vulgaris = IgG against desmoglein.

88
Q

S. aureus

  • toxic shock: which toxin?
  • why were women getting this disease more than men?
A

-tampons and TSST-1 from staph aureus.

89
Q

MRSA

-how did it gain resistance to methicillin & nafcillin?

A

Altered penicillin-binding proteins (PBPs)

-transpeptidase = PBP

90
Q

S. Aureus

-problems caused by exotoxin release:

A
  • gastroenteritis
  • toxic shock
  • scalded skin syndrome
91
Q

Endocarditis of artificial heart valves

  • which bug?
  • Tx:
A

S. epidermidis

-vanco

92
Q

Strep Pneumo

  • main disease it causes:
  • mnemonic:
A

MOPS

  • meningitis
  • otitis media (in children)
  • pneumonia
  • sinusitis
93
Q

Strep Pneumo

-whats it look like?

A

lancet-shaped, gram (+) diplococci.

  • encapsulated
  • IgA protease
94
Q

Strep pneumo has no virulence w/o its _______.

A

Capsule

95
Q

Strep viridans:

-which one causes dental caries?

A

Streptococcus mutans

96
Q

Strep viridans:

  • which one causes subacute bacterial endocarditis at damaged valves?
  • what allows it to infect the cardiac valves?
A

S. sanguinis

  • These bacteria produce an extracellular dextran which bind to fibrin-platelet aggregates on damaged heart valves.
  • dextrans also allow binding to tooth enamel.
97
Q

Which bug synthesizes dextrans from glucose?

-and what does it allow it to bind to?

A

Strep. viridans => S. sanguinis

  • which bind to fibrin-platelet aggregates on damaged heart valves.
  • also allows binding to tooth enamel.

*this is why it causes subacute endo, needs fibrin aggregates to attach to the valves. So need previous
damage.

98
Q

Scalded skin syndrome = from which bug?

A

S. aureus

99
Q

Scarlet fever = from which bug?

A

Strep. pyogenes.

100
Q

M-protein

  • seen in which bug?
  • function?
  • Abs to it: pros & cons?
A
  • Strep. pyogenes
  • prevents phagocytosis
  • Abs against M-protein enhance host defense BUT can give rise to rheumatic fever bc they’re very similar to cardiac myocyte myosin chain = molecular mimicry.
101
Q

ASO titers

-good for detecting what?

A

Recent S. pyogenes infection

-these Ab titers only high during during infection.

102
Q

Strep. pyogenes: rheumatic fever

-what are criteria for Dx rheumatic fever?

A

J♥NES criteria for rheumatic fever

  • Joints—polyarthritis
  • ♥—carditis
  • Nodules (subcutaneous)
  • Erythema marginatum
  • Sydenham chorea
103
Q

PSGN

-preceded by what?

A

strep pyogenes pharyngitis OR impetigo.

*Impetigo more commonly precedes glomerulonephritis than pharyngitis.

104
Q

rheumatic fever

-preceded by what?

A

strep pyogenes pharyngitis

105
Q

Scarlet fever

  • which bug?
  • mechanism?
  • Sxs:
A
  • strep pyogenes
  • Exotoxin (pyrogenic/erythrogenic) = produces fever (so it is pyrogenic) and causes a scarlet-red rash.
  • The rash begins on the trunk and neck, and then spreads to the extremities, sparing the face. The skin may peel off in fine scales during healing.
  • scarlet rash with sandpaper-like texture, strawberry tongue, circumoral pallor.
106
Q

Scarlet fever

-how does the erythrogenic toxin cause the rash/desquamation?

A

Erythrogenic toxin is known to damage the plasma membranes of blood capillaries under the skin and produce a red skin rash.

107
Q

Scarlet fever vs Kawasaki

-what does kawasakis have that scarlet fever doesnt?

A

Kawasakis has bilateral conjunctivitis.

108
Q

Neonatal meningitis vs adult meningitis

-difference in presentation?

A

neonatal meningitis may not present w/stiff neck.

109
Q

GBS

-what diseases can it cause?

A

Pneumonia, meningitis, strep.

110
Q

Mucormycosis

-affects what type of pts?

A

DKA & immunosuppressed.

-ie. leukemic pts.

111
Q

Aspergillus vs Mucor

-diff in appearance?

A
  • Mucor = 90 degree angles, non-septate.

- Aspergillus = 45 degree angles, septate.

112
Q

EHEC: verotoxin

-aka?

A

shiga-like toxin

113
Q

Neonatal meningitis: 0-3 months

-#1 cause?

A

GBS

-followed by E.coli & Listeria.

114
Q

Meningitis: > 3 months old (infants and adults)

-cause?

A
  • Strep pneumo

- N. meningitidus

115
Q

Rubeola

-aka?

A

Measles

116
Q

Measles

  • Sxs:
  • mnemonic:
A

3 C’s
-Cough. coryza, conjunctivitis.
+ koplik spots.

117
Q

Coccidio vs histo

-distinguishing the spherule vs macro.

A
  • coccidio = spherule filled w/endospores = much LARGER than RBC.
  • histo = macro filled w/histo = smaller than RBC.
118
Q

Rotavirus

-which family of viruses?

A

Reovirus

119
Q

Most common cause of acute gastroenteritis in industrialized countries:

A

campylobacter

120
Q

Negative sense RNA viruses:

-what must they carry w/them in order to be infectious?

A

RNA-dependent RNA-polymerase.

121
Q

recurrent C.dif colitis

-what drug = oral w/little systemic absorption?

A 
fidaxomicin = bacteriocidal
*vanc = bacteriostatic.
122
Q

Which ones the pinworm?

-Tx:

A

Enterobius vermicularis

  • scotch tape one.
  • albendazole or pyrantel pamoate.
123
Q

environmental influences permitting toxin synthesis

-which bugs?

A

gram (+) spore forming rods

  • Bacillus & clostridium
  • once spores germinate they can start making spores.
  • Need proper environment to germinate.
124
Q

Why is primaquine added to chloroquine tx of P.vivax/ovale?

A

To prevent recurrence by killing the dormant hypnozoites in the liver.

125
Q

P. vivax & P. ovale

-how often does the fever occur?

A

every 48 hrs.

126
Q

Prevention of neonatal tetanus:

A

vaccinating the pregnant mother.

-IgG will cross placenta.

127
Q

Central catheters

-is the femoral vein a good place for them?

A

NO

-avoid femoral placement!

128
Q

acute rheumatic fever

-can it occur after GAS impetigo?

A

No

-just pharyngitis.

129
Q

Pyrrolidonyl arylamidase (PYR) test:

  • replaced what other test?
  • which bug is (+)?
A
  • replaced bacitracin test.

- S. pyogenes = PYR (+).

130
Q

Pseduohyphae

-think what?

A

candida

131
Q

Kinesin

-direction:

A

anterograde (takes vesicles from neuron soma to axon terminal).
(-) => (+)

  • (+) end of MT is at axon terminal.
  • (-) end of MT is in neuron soma
132
Q

Dynein

-direction

A

retrograde

+) => (-

133
Q

2 most common causes of hematogenous osteomyelitis

A 
#1 = s. aureus
#2 = strep. pyogenes
134
Q

What skin lesion can pseudomonas cause?

-in which type of pts?

A

-ecthyma gangrenosum in immunocompromised pts.

135
Q

What is CAMP factor and who makes it?

A
  • GBS makes CAMP factor.

- enlarges area of hemolysis formed by s. aureus.

136
Q

What week of gestation do women get screened for GBS?

-if positive, when do they get which ABx?

A
  • Screen pregnant women at 35–37 weeks.

- Patients with (+) culture receive intrapartum penicillin prophylaxis.

137
Q

GBS strep

-main virulence factor

A

capsule

138
Q

Enterococci

-which lancefield group?

A

D

139
Q

Group D strep: non-enterococci

-name it:

A

strep. bovis

140
Q

Subacute endocarditis in colon cancer patients

-which bug?

A

Group D strep

  • strep bovis.
  • or enterococcus s/p GU/GI operations.
141
Q

Group D strep

-how to differentiate enterococci vs strep bovis?

A

Only enterococci can grow in 6.5% NaCl, bovis can not.

-both can grow in bile.

142
Q

Corynebacterium diphtheriae

  • how does it get its exotoxin?
  • mechanism of exotoxin?
A
  • β-prophage

- Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2.

143
Q

Diphtheria

  • if toxin gets into blood, what cells are preferentially damaged?
  • what can this lead to?
A

Heart & neural cells.

-myocarditis, arrythmias,

144
Q

Dx of diphtheria

  • culture will show what?
  • Is there a certain test that can help?
A
  • Gram-positive rods with metachromatic (blue and red) granules.
  • Black colonies on cystine-tellurite agar.
  • Elek test for toxin.
145
Q

Diphtheria

-prevention:

A

-Toxoid vaccine prevents diphtheria (against beta-subunit of toxin).

146
Q

Diphtheria

-Tx:

A

1) Antitoxin
2) penicillin/macrolide
3) DPT vaccine.

147
Q

Elek test

-what is it?

A

differentiates btwn toxic and

non-toxic strains.

148
Q

How do you kill spores?

A

Autoclave: steaming at 121°C for 15 minutes.

149
Q 
Spore forming bugs:
-what class are they?
A
  • gram (+) rods
  • Bacillus, clostridium.
    • coxiella burnetti
150
Q

Autoclave: why is pressure necessary?

A

-pressure necessary or all water will evaporate and it will be dry. water will germinate them and make them easier to kill.

151
Q

Tetanus

-how is Dx made?

A

Clinically made: good Hx & physical.

152
Q

Botulinum toxin

-heat labile or heat stabile?

A
  • Labile

* only real heat labile exotoxin = staph aureus enterotoxin.

153
Q

Botulism

-is there a difference in mechanism of adults getting it vs. babies?

A
  • adults get sick from ingesting pre-formed toxin, not from ingesting the actual bug/spore b/c the bug is outcompeted by our normal flora.
  • babies lack the robust intestinal flora to keep c. botulinum at bay = so they can get sick from the spores.
154
Q

botulinum toxin commonly found in:

A

Honey & canned goods.

  • canned goods = anaerobic environment.
  • clostridium = anaerobes.
155
Q

Hyphae

-only seen in which form of a fungus?

A

Mold

-Yeast are unicellular fungi that do not grow as hyphae.

156
Q

Diphtheria toxin

-mech:

A

ADP-ribosylation of EF-2: inhibits protein synthesis.

157
Q

Polar granules that stain deeply w/aniline dyes:

A

C. diphtheria

158
Q

EF-2: what does it do?

A

Necessary for tRNA to insert new AAs into growing protein chain during translation.

159
Q

Pseudomonas

  • shape:
  • gram stain:
  • lactose fermenting?
  • oxidase +/-?
A
  • gram (-) rod
  • non-lactose fermenting.
  • oxidase +
160
Q

E. coli

-lactose fermenter?

A

yes

161
Q

Salmonella + Shigella

  • lactose fermenters?
  • oxidase +/-?
A
  • None lactose fermenters

- oxidase (-)

162
Q

H2S prod

  • what color on TSI or Hektoen agar?
  • shigella or salmonella?
A
  • Black on TSI or Hektoen agar

- salmonella

163
Q

Where are peyers patches located?

A

ileum

164
Q

Shigella

-was makes it cause so much disease? invasion or toxin?

A

Invasion

*nontoxigenic strains have also been found that cause significant disease.

165
Q

Secondary bacterial pneumonia after viral URI

-causative agent:

A 
#1 = strep pneumo
#2 = staph aureus
166
Q

Normal CD4 count for healthy adults?

A

400-1400 cells/uL

167
Q

Do protozoans incite an eosinophilic response?

A

No, only invasive helminths.

168
Q

bacterial vaginosis

-caused by:

A

gardnerella vaginalis

169
Q

Gas gangrene

-Tx:

A

-IV penicillin G

170
Q

Double zone of hemolysis: beta & alpha

-seen in which bug?

A

C. perfringens

171
Q

Anaerobic hemolytic bug:

A

C. perfringens

172
Q

C. perfringens

-besides hemolysis & gas gangrene, what can it cause?

A

Late onset food poisoning.
-we are NOT ingesting preformed toxin here like c. botulinum for example. Here, we ingest the spore, wait for it to germinate, produce toxins, and then we get the diarrhea.

173
Q

C. dif

  • name the 2 toxins & what they cause:
  • how do they cause cell death?
A

-exotoxin A => watery diarrhea
-exotoxin B => pseudomembranous colitis
*these exotoxins both induce APOPTOSIS of epithelial
cells of colonic mucosa.

174
Q

C. dif

-How to Dx?

A
  • Diagnosed by detection of one or both toxins in stool.
  • lots of pts are colonized w/c. dif but not all of those are strains that produce the toxin. So you check for the toxin, not the bug.
175
Q

What is unique about bacillus anthracis capsule?

-whats it made of?

A

The only bacterium with a polypeptide capsule.

-contains d-glutamate.

176
Q

Bacillus anthracis

  • what are the 2 toxins?
  • can they cause pathology on their own?
A
  • lethal factor (LF) and edema factor (EF).

- both toxins must be present to cause symptoms.

177
Q

Bacillus anthracis

-edema factor: mechanism?

A

-acts as adenylate cyclase, inc. cAMP intracellularly.

178
Q

Bacillus anthracis

-lethal factor: mechanism?

A
  • exotoxin that acts as a protease and cleaves MAP KINASE.
  • Map kinase = controls cell growth.
  • So LF responsible for tissue necrosis. This causes tissue necrosis thats seen in the black eschar.
179
Q

Bacillus anthracis

-Tx:

A

fluoroquinolones or doxycycline

180
Q

Cutaneous anthrax

-black eschar: is it painful?

A

No - its painless.

181
Q

Pulmonary anthrax

-what will CXR show?

A

Widened mediastinum on CXR in the 2nd phase.

182
Q

Bacillus cereus

-whats the pre-formed toxin called that causes the N/V?

A

Cereulide

183
Q

Bacillus cereus

  • emetic type:
  • diarrheal type:
A
  • Emetic type = N/V w/in 1–5 hr.

- Diarrheal type = watery, nonbloody diarrhea and GI pain within 8–18 hr.

184
Q

Actinomyces vs. Nocardia

-gram + or -?

A

gram (+)

185
Q
  • Where is actinomyces found?

- Where is nocardia found?

A
  • actinomyces = normal flora of mouth.

- nocardia = soil.

186
Q

Nocardia

-what does it cause in immunocompromised?

A

-Pulmonary infections in immunocompromised.

187
Q

Nocardia

-what does it cause in immunocompetant?

A

-Cutaneous infections after trauma in immunocompetent.

188
Q

PPD (+) if:

A

-current infection, past exposure, or BCG vaccinated.

189
Q

PPD (-) if:

A

-no infection or anergic (steroids, malnutrition, immunocompromise) and in sarcoidosis.

190
Q

What the most specific TB test?

-why is it more specific?

A

Interferon-γ release assay (IGRA) is a more specific test; has fewer false positives from BCG vaccination.

191
Q

TB

-which virulence factor allows it intracellular bacterial prolif? AKA which ones allow it to survive the phagolysosome?

A

-sulfatide (surface glycolipids) inhibit phagolysosomal fusion.

192
Q

reactivation TB

-seen in which part of lung?

A

apex

-b/c oxygen tension is highest at apex of lung due to dec. pulm circulation there, and TB = ob. aerobe

193
Q

TB

-is it intracellular? if so, which cells does it invade?

A

yes. macros.

194
Q

M. avium–intracellulare

-prophylaxis:

A

azithromycin

195
Q

M. avium–intracellulare

-grows best in what condition?

A

grows best at 41 C.

196
Q

Which agar grows TB best?

A

Löwenstein-Jensen agar

197
Q

Cord factor

  • what bug is it in?
  • what does it do?
A

-Virulent strains of TB
-inhibits macrophage maturation and induces release of
TNF-α.

198
Q

TB

-what is its main virulence factor?

A

Cord factor.

199
Q

Why would cord factor want to induce release of TNF-alpha?

A

the cord factor induces the macro to release TNF-alpha which is pro-inflammatory. Why would the bug want to inc. inflammation/macrophage activation? Isn’t that bad for the bug? No, because although it wont be able to spread, the bug knows that we will form a granuloma around it, which it can survive and lay dormant in.

200
Q

Mycobacterium leprae

  • which tissues does it invade?
  • why?
A

Likes cool temperatures (infects skin and superficial nerves—“glove and stocking” loss of sensation).

201
Q

Mycobacterium leprae

-can it be grown in vitro?

A

Can NOT be grown in vitro.

202
Q

Mycobacterium leprae

-whats its reservoir in the U.S.?

A

Reservoir in United States: armadillos.

203
Q

Leprosy

-aka?

A

Hansen disease

204
Q

Lepromatous leprosy:

  • better or worse than tuberculoid?
  • whats the primary immune defense?
A
  • worse

- characterized by low cell-mediated immunity with a humoral Th2 response.

205
Q

Tuberculoid leprosy

  • better or worse than lepromatous?
  • whats the primary immune defense?
A
  • better

- characterized by high cell-mediated immunity with a largely Th1-type immune response.

206
Q

Tuberculoid leprosy

-Sxs:

A

-limited to a few hypoesthetic, hairless skin plaques.

207
Q

Lepromatous leprosy:

-Sxs:

A

-presents diffusely over the skin, with leonine (lion-like) facies, and is communicable.

208
Q

Lepromatous leprosy:

-Tx:

A

Dapsone, rifampin, and clofazimine for 2–5 years for lepromatous form.

209
Q

Tuberculoid leprosy

A

Dapsone and rifampin for 6 months for tuberculoid form.

210
Q

clofazimine

-what is it?

A

Used to treat lepromatous leprosy.

211
Q

Tuberculoid v Lepromatous

-Will their biopsies differ?

A
  • If you biopsy Tuberculoid lesions = small amnts of bacteria, b/c its contained.
  • If you biopsy Lepromatous lesions = lots of bacteria present
212
Q

Lepromatous

-fertility issues?

A

-Internal testicular damage => infertility.

213
Q

Leposy

-most commonly involved nerves?

A

The most frequently enlarged nerves are those closest to the skin-the greater auricular, the ulnar (above the elbow), the posterior tibial, and the peroneal (over the fibula head).

Final FA review (52 decks)

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