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Invaders And Defense > Bugs And Drugs > Flashcards

Bugs And Drugs Flashcards

1
Q

These bacterial toxins are encoded by a lysogenic phage:

A

Group A strep erythrogenic toxin (think scarlet fever), Botulinum toxin, Cholera toxin, Diphtheria toxin, Shiga toxin

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2
Q

Morphology of Moraxella catarrhalis

A

GN cocci

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3
Q

Respiratory GNRs

A

Bordetella pertussis; Burkholderia; Haemophilus (HiB or NTHi); Legionella (Legionella doesn’t gram stain super well but can be visualized with silver stain)

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4
Q

Why don’t Treponema pallidum and Leptospira gram stain well?

A

They are too thin to be visualized

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5
Q

Morphology of common bacterial causes of diarrhea

A

Campylobacter, Shigella, Salmonella, E.coli… These are GNRs

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6
Q

Morphology of a bacterial species associated with food poisoning from cantaloupe and cottage cheese

A

Listeria - GPR

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7
Q

These antibiotics are generally ineffective against anaerobes because they require O2 to enter into the bacterial cell walls:

A

Aminoglycosides: gentamicin, tobramycin

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8
Q

GP rods with spores

A

Clostridium

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9
Q

Asplenics are at particular risk of infection from these pathogens:

A

Encapsulated bacteria: the capsules serve as an anti phagocytes virulence factor. Asplenics have decreased ability to opsonize bacteria, leading to a decreased ability to clear these infections. Major ones are S.pneumoniae, HiB, N.meningitidis (these three are ones for which we have vaccines), Klebsiella pneumoniae, Salmonella, E.coli, Group B strep, Pseudomonas.

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10
Q

Pathogen that causes watery diarrhea in developing countries and pathogen associated with shellfish and shark bites: morphology

A

Vibrio species (V.cholera; V.vulnificans): comma-shaped GNRs

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11
Q

This bacteria produces biofilms and is implicated in otitis media quite frequently.

A

NTHi

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12
Q

Morphology of Neisseria (N.meningitides, N.gonorrheae)

A

GN cocci

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13
Q

Define transformation.

A

Ability of bacteria to take up free DNA (often generated by cell lysis). S.pneumo, HiB, and Neisseria can do this.

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14
Q

These bacteria don’t have cell walls, so they don’t gram stain

A

Mycoplasma, Ureaplasma

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15
Q

Mechanism for vaccines against encapsulated bacteria

A

Polysaccharide capsule conjugated to carrier protein, which enhances immunogenicity by promoting T cell activation, leading to class-switching on B cells. Examples are the PCV (pneumococcal conjugate vaccine), HiB vaccine, and meningococcal vaccine.

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16
Q

Why don’t these bugs gram stain well? Legionella, Rickettsia, Chlamydia, Bartonella, Ehrlichia, Anaplasma

A

Primarily intracellular

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17
Q

These bacterial toxins cause toxic shock syndrome.

A

Super antigens from Staph aureus (Toxic shock syndrome toxin - TSST-1) and Strep pyogenes (Exotoxin A). They bind to MHC class II molecules and to TCRs outside of the usual binding site, causing overwhelming release of pro-inflammatory cytokines.

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18
Q

Important aerobic bacteria

A

Nocardia, Pseudomonas aeruginosa, Mycobacterium tuberculosis

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19
Q

This bacteria produces biofilms and is frequently implicated in infective endocarditis following dental procedures.

A

Viridans strep (strep mutans)

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20
Q

This bacteria produces a blue-green pigment.

A

Pseudomonas aeruginosa

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21
Q

This bacteria produces biofilms and is frequently implicated in catheter and prosthetic device infection.

A

Staph epidermidis

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22
Q

Define specialized transduction.

A

Lysogenic phage infects a bacterium and incorporates its DNA into the bacterial chromosome. When the viral DNA is excised, parts of the surrounding bacterial DNA are taken with it as well, and those can be transferred to another bacterium.

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23
Q

Catalase-negative and/or SOD-negative anaerobes, which are generally foul-smelling due to short-chain fatty acid production

A

Clostridium, Bacteroides, Fusobacterium, Actinomyces

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24
Q

Obligate intracellular bacteria

A

Rickettsia, Chlamydia, Coxiella

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25
Q

Key spirochetes

A

Borrelia, Leptospira, Treponema pallidum

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26
Q

This bacteria produces biofilms and is frequently a major culprit in respiratory colonization in cystic fibrosis patients, as well as in contact-lens-associated keratitis.

A

Pseudomonas aeruginosa

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27
Q

What bacterial species expresses protein A, and what does protein A do?

A

Staph aureus. Protein A binds the Fc region of IgG, preventing opsonization and phagocytosis.

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28
Q

These bacterial exotoxins cause watery diarrhea: what are they, and how do they work?

A

ETEC heat-labile and heat-stabile toxins; Vibrio cholerae Cholera toxin. These over-activate adenylate cyclase, increasing cAMP, leading to increased Cl- secretion in the gut, causing H2O efflux and watery diarrhea. Heat-stabile toxin over-activates guanylate cyclase, increasing cGMP, and leading to decreased resorption of NaCl and H2O, also causing watery diarrhea.

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29
Q

Why don’t Mycoplasma (TB, etc) stain well on gram stain?

A

No cell wall

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30
Q

Define conjugation.

A

F+ plasmid contains the genes required for a sex pilus and conjugation. It will cause a sex pilus to form, which contacts the F- bacterium, leading to transfer of plasmid DNA across that bridge.

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31
Q

GP cocci, aerobic, catalase-positive, coagulase-positive

A

Staph aureus

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32
Q

Treatment for intertrigo

A

clotrimazole or nystatin, can also use barrier paste like zinc oxide

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33
Q

What bacterial species expresses M protein, and how does that help in pathogenesis?

A

Group A strep (S.pyogenes): M protein is an antiphagocytic factor with similar epitopes to various human proteins, which is what causes the autoimmune response that occurs in rheumatic fever.

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34
Q

Fungus that stains well with India ink

A

Cryptococcus neoformans

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35
Q

Diagnostic technique for scabies infection

A

Mineral oil prep: look for mites, poop, eggs. Presence of any is diagnostic, although you may treat empirically with a high index of suspicion.

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36
Q

Spore-forming bacteria

A

Bacillus, Clostridium

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37
Q

GP anaerobic branching filaments, not acid-fast

A

Actinomyces

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38
Q

Skin pain and erythema starting and the head and going across the body, with flaccid bullae that desquamate in sheets

A

Staph Scalded Skin Syndrome - due to toxin. Treat inpatient with IV antibiotics and supportive care

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39
Q

A bacterial endotoxin leads to tissue factor activation. What complication can occur?

A

This can activate the coagulation cascade, leading to DIC.

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40
Q

GP cocci in chains, beta-hemolytic

A

Group B strep agalactiae, Group A strep pyogenes

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41
Q

This bacterial exotoxin is clinically important because antibodies against it can be used to diagnose rheumatic fever. What is it, and how does it work?

A

Streptolysin O, released by Strep pyogenes. It degrades cell membranes, leading to hemolysis.

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42
Q

This bacterial exotoxin causes hemolytic-uremic syndrome.

A

Shiga toxin (Shigella) or Shiga-like toxin (EHEC). It inactivates 60S ribosome by removing adenine from rRNA. This leads to bloody diarrhea (febrile in Shigella, non-febrile in EHEC) and can cause HUS due to enhanced cytokine release.

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43
Q

Define transposition.

A

Segments of DNA can jump between plasmids and chromosomes. These are called transposons. If they jump from a chromosome to a plasmid, they can become incorporated into other bacterial genomes. This is what led to the development of vancomycin-resistant S.aureus after a plasmid containing a vancomycin resistance transposon was transferred from VRE.

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44
Q

This exotoxin is a phospholipase that causes tissue degradation. What is it and what does it lead to?

A

Clostridium perfringens alpha toxin, causes gas gangrene.

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45
Q

What are the main effects of bacterial endotoxins?

A

Endotoxins are LPS on the outer membrane of gram-negative bacteria. Their three main effects are macrophage activation via TLR-4, complement activation, and tissue factor activation.

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46
Q

Treatment of pityriasis versicolor

A

Give oral fluconazole, exercise till sweating, then rinse off after 4 hours, and repeat in a week

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47
Q

Secondary staph aureus infection in a pre-existing skin lesion

A

Impetiginized

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48
Q

GP aerobic bacillus: what could it be?

A

Listeria, Bacillus, Corynebacterium

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49
Q

This bacterial toxin causes flaccid paralysis and “floppy baby” - what is it, and how does it work?

A

Botulinum toxin, from Clostridium botulinum: a protease that cleaves SNARE proteins, preventing release of stimulatory neurotransmitters (ACh) at the neuromuscular junction, leading to flaccid paralysis.

No stimulation -> no action potentials -> floppy.

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50
Q

A bacterial endotoxin produces a response that includes complement activation. What physiological problems occur, and why?

A

Histamine release causing hypotension and edema from C3A and C5a release, as well as neutrophil chemotaxis.

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51
Q

GP anaerobic bacillus: what could it be?

A

Clostridium

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52
Q

Bugs that stain well on Giemsa stain

A

Chlamydia, Borrelia, Rickettsia, Trypanosomes, Plasmodium

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53
Q

Fever, rash, vomiting, desquamation, end-organ failure with elevated LFTs, elevated bilirubin, associated with prolonged tampon use

A

Tampon-related S.aureus toxic shock syndrome. REMOVE THE TAMPON - source control! Very treatable in those cases.

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54
Q

GP cocci, aerobic, catalase-positive, coagulase negative

A

S.epidermidis (sensitive to novobiocin), S.saprophyticus (not sensitive to novobiocin), other Staph species

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55
Q

A bacterial endotoxin leads to macrophage activation. What cytokines are released, and what signs/symptoms occur as a result?

A

IL-1 and IL-6 lead to fever. TNF-alpha leads to fever and hypotension. Nitric oxide leads to vasodilation, leading to hypotension.

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56
Q

Second most common cause of uncomplicated UTI

A

Staph saprophyticus

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57
Q

GP aerobic branching filaments, acid-fast

A

Nocardia

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58
Q

Non-bloody diarrhea and vomiting 2-6 hours after eating contaminated food

A

Most likely due to preformed toxin from S.aureus, a heat-stable enterotoxin

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59
Q

GP cocci in chains, alpha-hemolytic

A

Viridans strep (no capsule); S.pneumoniae (encapsulated)

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60
Q

Coral red fluorescence on Woods lamp in an area of the skin subject to maceration

A

Erythrasma - Cornyebacterium minutissimum

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61
Q

Lesions in young kids that are round erosions with scale

A

Bullous impetigo - treat with oral ABX

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62
Q

Patients with chronic granulomatous disease have recurrent infections with certain catalase+ organisms: which ones, and why?

A

Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.coli, Staph, H. Pylori… This is because in CGD, patients’ disease is due to NADPH oxidase deficiency, and so they have a decreased neutrophil response to catalase-positive organisms.

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63
Q

Erythrasma treatment

A

Anti-inflammatory topical ABX or antifungals

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64
Q

Pathogen most commonly implicated in abscess formation

A

Staph aureus

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65
Q

Infection causing a raised erythematous plaque with sharply demarcated border, sometimes on the face, that occurs with fever, chills, and malaise

A

Erysipelas, caused by S.pyogenes. Treat with oral ABX.

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66
Q

GP cocci in chains, no hemolysis

A

S.bovis, enterococcus

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67
Q

Lesions with honey-colored crusting

A

Non-bullous impetigo, most commonly due to S.aureus

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68
Q

Define generalized transduction.

A

Lytic phage infects bacterium, and when the bacterium lyses, parts of its DNA are packaged in phage capsids, leading to transfer of those genes to another bacterium when it is infected by the phage.

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69
Q

Infections caused by dermatophytes

A

Tinea capitis (scalp), cruris (groin, spares the scrotum), pedis (feet), corporis (body)

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70
Q

Which generation of cephalosporins is best for treating methicillin-susceptible staph aureus?

A

1st gen (cefazolin, Cephalexin) or 2nd gen cefuroxime.

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71
Q

Tinea workup on KOH prep

A

Branching septate hyphae

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72
Q

Topical treatment for tinea infections

A

Clotrimazole or terbinafine

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73
Q

This bacterial toxin causes spastic paralysis and “lockjaw” - what is it, and how does it work?

A

Tetanospasmin, from Clostridium tetani. Protease that cleaves SNARE proteins. Prevents release of inhibitory neurotransmitters (GABA, glycine) from cells in spinal cord, leading to tetany.

No inhibition -> tons of action potentials -> tetany.

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74
Q

Rash in groin, under breasts, skin folds, involving scrotum, with satellite pustules and papules

A

Intertrigo - caused by Candida

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75
Q

Serpiginous burrows, very itchy, often in web spaces, wrist, penis, scrotum, breast

A

Scabies

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76
Q

First-line therapy for MRSA

A

Vancomycin

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77
Q

KOH prep of Malassezia furfur

A

Spaghetti and meatballs - hyphae and spores

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78
Q

First-line therapy for streptococci

A

Penicillins - Penicillin G (IV) or V (oral), aminopenicillins

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79
Q

Patient presents with pharyngitis and fever. A gram stain from a swab of the pharynx reveals gram-positive cocci in chains. The patient has, in the past, developed urticaria after taking amoxicillin. What is the best choice of treatment for this patient?

A

Allergic to penicillins, so this patient should be given a macrolide, which is second-line therapy for streptococci (this patient has an infection with S.pyogenes). Macrolides include erythromycin, azithromycin, clarithromycin.

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80
Q

A patient presents with symptoms of meningitis, and gram stain and culture of the patient’s CSF reveal penicillin-resistant strep pneumo. What is your first choice of drug for this patient?

A

Vancomycin - inhibits peptidoglycan synthesis.

81
Q

Pathogen causing pityriasis versicolor (light or dark or salmon-colored plaques on skin, transmitted via direct contact - think young adults at the gym)

A

Malassezia furfur

82
Q

First-line therapy for MSSA

A

Semi-synthetic penicillins: oxacillin, nafcillin, dicloxacillin

83
Q

This cephalosporin can be used to treat MRSA.

A

Ceftaroline - 5th generation cephalosporin with broad gram positive and gram negative coverage, including MRSA. Does not cover pseudomonas.

84
Q

Your hospital has discovered a few patients with a strain of MRSA that is also resistant to vancomycin. How would you treat it?

A

Linezolid or daptomycin

85
Q

Why don’t Mycobacteria gram stain well?

A

Their cell wall has high lipid content

86
Q

Is penicillin V/G bacteriocidal or bacteriostatic in GPRs, GPCs, GNCs, and spirochetes?

A

Bacteriocidal

87
Q

List the classes of antibiotics that interfere with peptidoglycan crosslinking.

A

Penicillins - penicillinase sensitive (penicillin G and V, ampicillin, amoxicillin) and penicillinase resistant semi-synthetics (Oxacillin, nafcillin, dicloxacillin), as well as the anti-pseudomonas ones (piperacillin, ticarcillin)
Cephalosporins
Carbapenems (imipenem, meropenem, doripenem, ertapenem)
Monobactams (aztreonam)

88
Q

What are first-line therapies for enterococcus, and what allows them to be bacteriocidal?

A

Penicillin + gentamicin, and then second line is ampicillin + gentamicin. The gentamicin is an aminoglycoside that makes this treatment bacteriocidal rather than bacteriostatic.

89
Q

List the penicillins that will kill pseudomonas.

A

Piperacillin and ticarcillin, which are second-line therapy for pseudomonas

90
Q

When treating an infection with piperacillin or ticarcillin, if you suspect the bug may produce a beta-lactamase, what should you do?

A

Add a beta-lactamase inhibitor (clavulanate, etc) because these drugs are susceptible to penicillinases.

91
Q

What are the key beta lactamase inhibitors?

A

Clavulanate, tazobactam

92
Q

Why are semi-synthetic penicillins able to work in bacteria that produce penicillinases?

A

They have a bulky R group that blocks access of the beta-lactamase to the beta-lactam ring.

93
Q

Which antibacterials interfere with folic acid synthesis and reduction, therefore interfering with DNA methylation?

A

Sulfonamides (sulfamethoxazole, etc) - block DHFR. Trimethoprim blocks THFR.

94
Q

What antibacterial interferes with mRNA synthesis by inhibiting DNA-dependent RNA polymerase?

A

Rifampin (RNA pol inhibitor, ramps up microsomal cytochrome p450, red-orange body fluids - non-hazardous side effect, rapid resistance if used alone)

95
Q

What is the risk of monotherapy with rifampin in TB patients?

A

High risk of resistance if used alone

96
Q

TB prophylaxis

A

Isoniazid

97
Q

What is the standard set of four drugs used to treat TB?

A

Rifampin, isoniazid, pyrazinamide, ethambutol

98
Q

What infections should be treated with metronidazole?

A

Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (including C.diff), H.pylori (with PPI+clindamycin)

99
Q

What is the MOA of an antibacterial that is good for treating anaerobic infections below the diaphragm?

A

Metronidazole - forms toxic free radical metabolites that lead to DNA damage. It is bacteriocidal and anti-protozoal.

100
Q

These bactericidal drugs require O2-dependent active transport to get into cells, where they irreversibly bind to the 30S subunit. They don’t have any activity alone against strep or enterococci, and need to be used in combo with a beta-lactam in those organisms in order to be able to penetrate the cell wall. What are they?

A

Aminoglycosides - gentamicin and tobramycin.

Can’t be used for anaerobes, abscesses, atypical bacteria.

101
Q

What are the major side effects of aminoglycosides?

A

Reversible nephrotoxicity, irreversible oto toxicity due to loss of hair cells, risk of neuromuscular blockade, and teratogenic.

Give in once-daily doses to decrease toxicity, and monitor if treating for more than 5-7 days.

102
Q

These drugs bind to the 30S subunit and prevent attachment of AA-tRNA. They are bacteriostatic. What are they?

A

Tetracyclines - tetracycline, doxycycline, minocycline.

103
Q

How does resistance to tetracyclines develop?

A

Decreased uptake of the drug or increased efflux of the drug due to transport pumps encoded on plasmids.

104
Q

Do tetracyclines have activity against pseudomonas or anaerobes?

A

No!

105
Q

What organisms can be treated with tetracyclines?

A

Staph aureus, Strep pneumo, GPRs, atypical bacteria, zoonotics, malaria. Can treat intracellular pathogens!

Used for CAP, skin and soft tissue infection, Lyme disease, other tick-borne illnesses (think Erlichia and Anaplasma especially), STIs

106
Q

This member of the lincosamide class of antibiotics reversibly binds to the 50s ribosomal subunit, blocking peptide translocation. It is good for treating anaerobic infection above the diaphragm.

A

Clindamycin

107
Q

This drug is helpful for treating lung and oral abscesses, or for treating strep in combo with a beta-lactam, but it has a high risk of C.diff infection following its use.

A

Clindamycin

108
Q

What is the MOA of linezolid and other oxazolidinones?

A

Inhibits protein synthesis by binding to the 50S ribosome, inhibiting formation of the initiation complex and 70S ribosome. It is bacteriostatic… But kills them slowly.

109
Q

What is the clinical use of linezolid?

A

MRSA, VRE, other highly resistant gram positives.

110
Q

Can linezolid be used for GNs?

A

No! Can’t be used for GNs, anaerobes, atypicals.

111
Q

What are the major side effects of linezolid?

A

Bone marrow suppression, especially thrombocytopenia; peripheral neuropathy; serotonin syndrome

112
Q

What are the major side effects of macrolides?

A

GI motility issues, QTc prolongation, hepatitis, reversible ototoxicity

113
Q

What classes of drugs are used to treat atypical CAP?

A

Tetracyclines, macrolides, fluoroquinolones

114
Q

What are some mechanisms by which bacteria can develop resistance to macrolides?

A

1) alter the target site by methylation of 23S (encoded by the erm gene)
2) enhanced efflux pumps (mef gene on a transposon)
3) mutate 50s binding site
4) drug inactivation by an enzyme

115
Q

What is the MOA of macrolides?

A

Inhibits protein synthesis by binding to the 23S part of the 50S ribosomal subunit, interfering with tRNA attachment and peptide elongation.

116
Q

Are macrolides bacteriocidal or bacteriostatic?

A

Bacteriostatic?

117
Q

First-line therapy for pseudomonas

A

Cefepime, ceftazidime

118
Q

This antibacterial drug only reaches adequate concentrations in urine. What is it?

A

Nitrofurantoin - used for treatment of UTIs. Inhibits protein synthesis, DNA synthesis, cell wall synthesis, etc. Good for GNRs, especially E.coli, with moderate activity against enterobacter. Does not work well against pseudomonas or anaerobes.

119
Q

These drugs inhibit DNA topoisomerases, causing DNA supercoiling. They are bactericidal. What are they?

A

Fluoroquinolones - ciprofloxacin, levofloxacin, moxifloxacin

120
Q

Which fluoroquinolone has the best activity against pseudomonas?

A

Ciprofloxacin. Levofloxacin has some at high dose. Moxifloxacin does not.

121
Q

Which fluoroquinolone has poor/no activity against GP and anaerobes?

A

Ciprofloxacin

122
Q

A mutation in DNA gyrase or topoisomerase IV will cause resistance to which class of antibacterial drugs?

A

Fluoroquinolones

123
Q

What are the major adverse effects associated with fluoroquinolones?

A

C.diff, GI effects, tendinitis and tendon rupture, CNS symptoms, peripheral neuropathy, hepatitis. Only use these when there’s not really another good treatment option!

124
Q

This class of antibiotics can turn urine and other bodily fluids orange.

A

Rifampin (of the rifamycin class). This is a harmless side effect.

125
Q

What are the major side effects of rifamycin?

A

GI, hepatitis, P450 drug interactions, orange urine

126
Q

What are the major side effects of metronidazole?

A

Bad taste, GI effects, peripheral neuropathy, vomiting if taken with alcohol.

127
Q

What organisms is TMP-sulfa useless for?

A

Pseudomonas, anaerobes, atypicals

128
Q

What is a consequence of long-term use of trimethoprim?

A

Folate deficiency

129
Q

How do beta-lactams enter GP bacteria?

A

Diffuse directly across the peptidoglycan cell wall

130
Q

How do beta-lactams enter GN bacteria?

A

Pass through porins in the cell wall

131
Q

Clinical uses of natural penicillins

A

Streptococci, enterococci, meningococcus, syphilis, gas gangrene (used with clindamycin), periodontal infection

132
Q

This is used as a treatment for HiB due to 30% prevalence of making beta-lactamases.

A

Amox+clavulanate

133
Q

Which beta-lactam can cause neutropenia?

A

Oxacillin

134
Q

Which generations of cephalosporins are good for streptococci?

A

All of them!

135
Q

Clinical uses of cefazolin and Cephalexin:

A

GPC, plus Proteus, E.coli, Klebsiella.

136
Q

Clinical uses of 2nd generation cephalosporins:

A

Add anaerobes! GPC, Proteus, E.coli, Klebsiella, but also Hflu, Enterobacter, Neisseria, Serratia

137
Q

Clinical uses of 3rd gen cephalosporins:

A

Ceftriaxone for meningitis, gonorrhea, disseminated Lyme disease
Ceftazidime for pseudomonas

138
Q

Clinical uses of 4th gen cephalosporin (cefepime)

A

Pseudomonas…. But also other GNs, GPs

139
Q

Clinical uses of ceftaroline (5th gen cephalosporin)

A

Broad GP and GN coverage, including MRSA. Does not cover Pseudomonas.

140
Q

Cefepime has good CNS penetration, but this leads to an adverse effect. What is it?

A

Altered mental status in the elderly

141
Q

Which cephalosporins have good CNS penetration?

A

Ceftriaxone, ceftazidime, cefepime

142
Q

What is a problematic side effect of ceftriaxone?

A

Biliary sludging

143
Q

What are some adverse reactions associated with cephalosporins as a class?

A

Hypersensitivity reactions, cross-reactivity with penicillins, diarrhea, vitamin K deficiency

144
Q

Which carbapenem does not have good pseudomonas coverage?

A

Ertapenem

145
Q

What is the spectrum of use for carbapenems?

A

GP cocci, GNRs, anaerobes, including pseudomonas.

146
Q

What bacteria are not covered by carbapenems?

A

MRSA, MRSE, E.faecium, VRE, C.diff, Burkholderia. Ertapenem does not cover pseudomonas or Acetinobacter

147
Q

Side effects associated with carbapenems:

A

Rash, diarrhea, CNS toxicity lowering seizure threshold

148
Q

This antibacterial is not very susceptible to beta-lactamases, binds to PBP3 and prevents peptidoglycan cross-linking, and does not have cross-allergenicity with penicillins. What is it?

A

Aztreonam (a monobactam)

149
Q

Spectrum of activity of aztreonam

A

GNRs only. This will work for pseudomonas

150
Q

This drug inhibits peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors, and is bacteriocidal against most bacteria, except C.diff (static).

A

Vancomycin

151
Q

What side effects are associated with vancomycin?

A

Nephrotoxicity, ototoxicity, thrombophlebitis, Red man syndrome

152
Q

A patient being treated for a MRSA infection inpatient is receiving his medications intravenously when he gets concerned because he is flushed and appears bright red. What drug is he most likely receiving, and how can this problem be fixed?

A

Vancomycin - slow the infusion rate!

153
Q

This drug is a cyclic lipopeptide that inserts itself into the bacterial cell wall and essentially blows up the cell. What is it, and what kinds of infections can it not be used for?

A

Daptomycin - rapidly cidal. Can’t be used for lung infections because the drug is inhibited by pulmonary surfactant

154
Q

What is a major side effect of daptomycin?

A

Myopathy, rhabdomyolysis

155
Q

This rapidly cidal drug is used to treat MRSA skin infections, bacteremia, endocarditis, and VRE, but not pneumonia.

A

Daptomycin

156
Q

This TB prophylactic agent can also cause drug-induced lupus.

A

Isoniazid

157
Q

This drug is used for prevention of gonococcal conjunctivitis in newborns. What is its mechanism of action?

A

Erythromycin - binds to the 23S part of the 50S subunit and prevents translocation of ribosomes.

158
Q

Prophylaxis in HIV patients for pneumocystis jirovecii

A

TMP-sulfa

159
Q

This antifungal binds ergosterol and forms membrane pores in the fungi.

A

Amphotericin B

160
Q

Side effects associated with Amphotericin B

A

EVERYTHING. Fever/chills, hypotension, nephrotoxicity, anemia, arrhythmias, IV phlebitis.

161
Q

Topical drug that works like Amphotericin B

A

Nystatin

162
Q

These antifungals inhibit ergosterol synthesis

A

Azoles - clotrimazole, fluconazole, intraconazole, etc

163
Q

What kind of fungal infection is treated with terbinafine?

A

Dermatophyte infections (tinea)

164
Q

How do echinocandins work?

A

Inhibit synthesis of beta-glucan

165
Q

What drugs are used to treat Trypanosoma brucei?

A

Suramin and melarsoprol (suramin w/o CNS involvement)

166
Q

What drug is used to treat Trypanosoma cruzi?

A

Nifurtimox

167
Q

This drug is used for treatment of malaria but resistance to it builds up in P.falciparum.

A

Chloroquine

168
Q

Treatment for P.falciparum

A

Atovaquone/proguanil

169
Q

These drugs are used for influenza prophylaxis and treatment. What are they and how do they work?

A

Oseltamivir, zanamivir. Block release of virus by inhibiting influenza neuraminidase.

170
Q

What are the limitations of adamantanes (amantadine, rimantadine)?

A

These drugs interfere with viral uncoating in influenza A, but don’t work for influenza B. They are not used to to adverse effects and the rapid emergence of resistance, as well as the fact that they are limited to influenza A only.

171
Q

When should you initiate influenza treatment with neuraminidase inhibitors?

A

Ideally within 24hours, but ASAP

172
Q

These drugs are used in treatment of HSV and VZV. What are they and how do they work?

A

Acyclovir, famcyclovir, valacyclovir. They are nucleoside analogues that inhibit viral DNA polymerization, blocking replication of the virus.

173
Q

Why do acyclovir, famcyclovir, and valacyclovir not work in CMV infection?

A

CMV lacks the thymidine kinase that phosphorylates those drugs in HSV/VSV infection, so the drugs would be ineffective. Use ganciclovir/valganciclovir instead.

174
Q

What are side effects of nucleoside analogues used in treatment of HSV/VSV?

A

Nephrotoxicity (from crystalline nephropathy - prevent with proper hydration), headache

175
Q

This drug can be used to substantially reduce subclinical viral shedding in HSV infection.

A

Acyclovir

176
Q

Side effects of ganciclovir/valganciclovir

A

Bone marrow suppression causing leukopenia and pancytopenia, renal toxicity, may impair fertility

177
Q

What causes ganciclovir resistance, and what drugs should you use instead?

A

Mutations in UL97 prevent activation of ganciclovir by phosphorylation. In this case, treat with cidofovir or foscarnet.

178
Q

What’s a serious side effect of cidofovir?

A

It’s very nephrotoxic

179
Q

What are side effects of foscarnet?

A

Nephrotoxicity and electrolyte wasting

180
Q

What are the 5 classes of drugs typically used in HIV HAART, and list a few examples of each

A

NRTIs - abacavir, tenofovir, zidovudine. These are nucleosides that competitively inhibit nucleotide binding to reverse transcriptase. NNRTIs - efavirenz. These bind to RT at a different site, inhibiting it. Protease inhibitors - navir. These prevent maturation of new viruses by inhibiting HIV-1 protease (pol gene) f. Integrate inhibitors - elite graver. Fusion inhibitors: enfuvirtide, maraviroc.

181
Q

Typical components of cART regimen

A

3 drugs or more, typically 2 are NRTIs and often one is an integrase inhibitor. The use of multiple drugs is to prevent resistance.

182
Q

This antiretroviral binds gp41, inhibiting viral entry.

A

Enfuvirtide

183
Q

This antiretroviral prevents HIV entry through CCR5.

A

Maraviroc

184
Q

Chronic watery diarrhea in HIV+ patient

A

Cryptosporidium

185
Q

EBV presentation in HIV patients with CD4 count <500

A

Oral hairy leukoplakia

186
Q

Pneumonia in HIV patient

A

Pneumocystis jirovecii- ground-glass opacities on CXR

187
Q

Cavitation or infiltrates on CXR of AIDS patient, presenting with hemoptysis

A

Aspergillus infection

188
Q

Meningitis with an encapsulated yeast that stains with India ink and has capsular antigen, in an HIV+ patient

A

Cryptococcus neoformans

189
Q

Cotton-wool spots on fundus copy in an HIV+ patient

A

CMV retinitis - treat with valganciclovir or ganciclovir

190
Q

Ring-enhancing CNS lesion that is solitary in an HIV patient

A

CNS B-cell lymphoma from EBV

191
Q

Oval yeast cells within macrophages, and presentation of fever, weight loss, fatigue, cough, dyspnea, etc

A

Histoplasmosis

192
Q

Multiple ring-enhancing lesions on brain MRI

A

Toxoplasma gondii causing brain abscesses

193
Q

Reheated rice food poisoning, that starts quickly and ends quickly

A

B.cereus

194
Q

Pneumonia in an alcoholic, currant jelly sputum

A

Klebsiella

195
Q

Meningitis in a newborn

A

Group B strep, E.coli, listeria

196
Q

Osteomyelitis with no pertinent history

A

Staph aureus

197
Q

Vaginal infection with fishy odor, thin white discharge, clue cells, no inflammation, elevated pH

A

Bacterial vaginosis

198
Q

Slapped cheek rash

A

Parvovirus B19 -ssDNA virus

Invaders And Defense (4 decks)

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