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ID Week 4 > ICL 2.30: Antibiotics > Flashcards

ICL 2.30: Antibiotics Flashcards

1
Q

which drug groups are protein synthesis inhibitors?

A
  1. macrolides
  2. clindamycin
  3. tetracyclines
  4. chloramphenicol
  5. aminoglycosides
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2
Q

what are the general steps of protein synthesis?

A
  1. 30S subunit, Initiation factors, and mRNA come together
  2. fMet-tRNA binds to mRNA
  3. 50S subunit binds to form initiation complex
  4. 2nd aminoacyl tRNA arrives at A site
  5. AA transferred from 1st tRNA to AA of new tRNA (peptide bond formed)
  6. uncharged tRNA moves to E site, then leaves
  7. translocation of ribosome puts tRNA with growing chain in P site; elongation continues
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3
Q

what’s the difference between the ribosomes of prokarytoic and eukaryotic organisms?

A

prokaryotic = 50S + 30S = 70S

eukaryotic = 60S + 40S = 80S

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4
Q

how does bacteria protein synthesis work?

A

simultaneous transcription/translation in bacteria!

even before transcription is completed, multiple ribosomes attach to mRNA creating polysomes

5’–> 3’ direction

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5
Q

what is the MOA of macrolides?

A

macrolides bind to 50S ribosome subunit

binding is reversible!

so macrolides either prevent transfer of peptide or access by next tRNA, preventing elongation

*bacteriostatic activity!

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6
Q

which drugs are macrolides?

A
  1. azithromycin
  2. clarithromycin
  3. erythromycin
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7
Q

which infections is erythromycin used for? which bacteria specifically?

A

mainly used for respiratory infections and urethral infections

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8
Q

which bacteria does erythromycin work on?

A

effective against:
1. Strep. pneumoniae

  1. Strep. pyogenes
  2. Chlamydia trachomatis
  3. Mycoplasma pneumoniae,
  4. Legionella pneumophila
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9
Q

how is erythromycin given?

A

it’s unstable in stomach acid so it’s usually given orally as a drug ester which is more stable = erythromycin ethylsuccinate or estolate

also erythromycin base is very bitter and cannot be used in oral pediatric preparations – the ethylsuccinate and estolate are tasteless

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10
Q

what are the adverse effects of erythromycin?

A
  1. liver injury –> caused only by estolate form but is reversible a few days after stopping treatment
  2. arrhythmias –> prolongation of the QT interval, increasing the risk of potentially fatal torsades de pointes-type arrhythmia
  3. temporary hearing loss: associated with doses > 4 grams/day
  4. impaired renal or hepatic function; age > 60 years
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11
Q

what are the adverse GI effects associated with erythromycin?

A

erythromycin is a motilin agonist and stimulates migrating motor complex (MMC) activity = bands of intense contractile activity of intestinal smooth muscle

GI effects are the most common adverse effect observed with erythromycin

often >50% of patients in clinical studies have complained of abdominal cramps, nausea and diarrhea

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12
Q

what can be used to treat the adverse GI effects of erythromycin?

A

antimuscarinic drugs like glycopyrrolate can be used to counteract the MMC response and therefore erythromycin-related GI problems

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13
Q

which two drugs are “newer” macrolides? what’s different about them?

A
  1. clarithromycin
  2. azithromycin

about the same antimicrobial spectrum as erythromycin, but better tolerated because of fewer G.I. effects

they are also less likely to produce the other adverse effects associated with erythromycin

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14
Q

what is azithromycin used to treat?

A

chlamydial urethritis

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15
Q

what are azithromycin and clarithromycin used to treat?

A

used to treat mycobacterial pneumonia (MAC pneumonia in AIDS patients)

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16
Q

what drug interaction do macrolides have?

A

erythromycin and clarithromycin inhibit cytochrome P450 drug metabolism in the liver –> you increase the half life of other drugs that are no longer being metabolized in the liver

azithromycin does so much less often

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17
Q

what is the MOA of clindamycin?

A

binds to 50S ribosomal subunit – similar action as macrolides

binding is reversible!

so they either prevent transfer of peptide or access by next tRNA, preventing elongation

*bacteriostatic activity!

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18
Q

clindamycin is used for the prophylaxis of what?

A

it’s used for prophylaxis of bacterial endocarditis in dental procedures for patients with valvular heart disease

a single dose of clindamycin is appropriate for prophylaxis prior to dental, oral, upper respiratory tract and esophageal procedures in at-risk, penicillin-allergic patients

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19
Q

what type of bacteria is clindamycin good at targeting?

A

anaerobes

specifically severe infections outside the CNS caused by anaerobes including Bacteroides fragilis

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20
Q

what is clindamycin used to treat?

A
  1. bacterial vaginal infections
  2. in combination with an aminoglycoside and cephalosporin for penetrating wounds of the abdomen or gut**
  3. treatment of aspiration pneumonia
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21
Q

what are the adverse effects of clindamycin?

A
  1. skin rashes, and rarely Stevens-Johnson syndrome
  2. hepatotoxicity is possible (less than 0.1% of patients)
  3. diarrhea, including Pseudomembranous colitis in up to 10% of patients
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22
Q

what is stevens-johnson syndrome?

A

a potential side effect of clindamycin

it’s a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis

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23
Q

if someone gets diarrhea/pseudomembranous colitis from clindamycin, how do you treat it?

A

metronidazole

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24
Q

what is the DOC for first episode of mild-moderate C. difficile infection?

A

metronidazole

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25
Q

which type of bacteria does metronidazole work on?

A

active only against anaerobes!

ferredoxin in sensitive bacteria chemically reduces metronidazole nitro group to produce toxic by-products which kill the bacteria!

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26
Q

what is metronidazole used to treat?

A
  1. Clostridium difficile
  2. Bacteroides fragilis
  3. Trichomonas vaginalis (protozoa)
  4. Giardia lamblia (protozoa)
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27
Q

what are metronidazole toxicities?

A

GI disturbances are the most common adverse effect

paresthesia and ataxia/convulsions may rarely occur

carcinogenic in rodents

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28
Q

what is the MOA of tetracyclines?

A

they bind to 30S ribosomal subunit and inhibits tRNA binding

this means they have a broad spectrum of activity against Gm + and Gm - bacteria

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29
Q

tetracyclines are the DOC for which diseases?

A
  1. Rickettsial infections like Rocky Mountain spotted fever
  2. cholera
  3. chlamydial infections
  4. acne
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30
Q

what are the adverse effects of tetracyclines?

A
  1. hepatotoxicity

especially in pregnancy*

characterized by high blood bilirubin (jaundice)

frequently fatal

  1. nephrotoxicity

in patients with renal disease

  1. Fanconi syndrome

in people without renal disease

  1. deposition in teeth and bones
  2. GI irritation with oral use
  3. phototoxicity
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31
Q

which tetracycline should you use in patients with renal disease?

A

doxycycline

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32
Q

what is Fanconi syndrome?

A

a possible adverse effect of tetracyclines in patients without a history of renal disease

this happens from outdated tetracyclines

it’s a disease of the proximal renal tubules of the kidney where glucose, amino acids, uric acid, phosphate and bicarbonate are passed into the urine, instead of being reabsorbed

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33
Q

which tetracyclines can cause phototoxicity?

A
  1. demethylchlortetracycline

2. doxycycline

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34
Q

what are the side effects of minocycline?

A

it’s a type of tetracycline

  1. vertigo
  2. ataxia
  3. nausea
  4. vomiting

this is all due to damage to the vestibule in the middle ear –> it’s reversible upon discontinuing the drug

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35
Q

what are the drug interactions of tetracyclines?

A

tetracyclines bind to calcium in dairy products, and calcium, magnesium or aluminum in antacids

this decreases absorption of the tetracycline

also tetracycline interferes with clotting

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36
Q

what are the contraindications of tetracyclines?

A
  1. pregnancy
  2. children 4 months to 8 years
  3. patients with renal impairment (doxycycline is the possible exception)
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37
Q

what is tigecycline?

A

a glycylcycline derivative of minocycline

it’s a tetracycline that’s only administered IV

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38
Q

which bacteria does tigecycline work against?

A

it’s NOT exported by energy dependent drug efflux pump in most bacteria

that makes it active against bacteria that have developed resistance to other tetracyclines!!

it’s active vs methicillin-resistant and vancomycin-resistant Staph. aureus

also active against enterococci and extended spectrum B-lactamase producing Gm- pathogens

it’s super broad spectrum….

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39
Q

what’s the MOA of chloramphenicol?

A

binds to 50S ribosome and prevents binding of amino acid part of aminoacyl-tRNA

it’s bacteriostatic

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40
Q

when is chloramphenicol used?

A

primarily used as a backup drug for β-lactams in treatment of H. influenzae or N. meningitidis meningitis in neonates and older children

it’s also used as a backup drug for tetracyclines in children 4 months-8 years, renal insufficient patients and in pregnancy (except late stages)

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41
Q

what are the adverse effects of chloramphenicol?

A
  1. BM depression; potential aplastic anemia = fatal
  2. optic neuritis which may result in blindness
  3. diarrhea, pseudomembranous colitis (because it’s a broad spectrum antibiotic)
  4. Gray baby syndrome
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42
Q

what is gray baby syndrome?

A

respiratory depression produced by high blood levels of chloramphenicol

can be fatal

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43
Q

what are aminoglycosides?

A

molecules comprised of amino sugars

they are highly polar molecules that do not distribute well into body compartments –> must be administered IV and IM only

narrow therapeutic index

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44
Q

which drugs are aminoglycosides?

A
  1. streptomycin
  2. gentamycin
  3. kanamycin
  4. tobramycin
  5. amikacin
  6. netilmicin

other drugs too

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45
Q

what’s the MOA of aminoglycosides?

A

protein synthesis inhibitors that are bactericidal!! (rare)

they transport through the wall, through peptidoglycan of G+, through porins or directly through the outer membrane (OM) in G-, disrupting the OM

they transport through cell membrane by carrier, using electrochemical gradient (uses energy)

then they covalently bind to ribosomes!!! –> aminoglycosides bind various sites on both ribosomal subunits which freezes translation after initiation step, preventing polysome formation – it also interferes with codon recognition resulting in misreading

the combination of membrane damage and inhibition of protein synthesis is bactericidal

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46
Q

how are aminoglycosides administered?

A

must be administered parenterally for systemic infections = i.v. or i.m., and tissue distribution is limited to extracellular space

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47
Q

how are aminolgycosides cleared from the body?

A

glomerular filtration

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48
Q

on which bacteria do aminoglycosides work?

A

aerobic bacteria only

they go through energy-dependent uptake which requires oxygen

therefore aminoglycosides do not work on anaerobes

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49
Q

what is streptomycin used to treat?

A

predominantly used for treatment of pulmonary tuberculosis

it’s an aminoglycoside

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50
Q

what is gentamicin used to treat?

A

aminoglycoside of first choice –> it has good cost and it’s wide spectrum than streptomycin

also hits psudomonas bacteria

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51
Q

what is tobramycin used to treat?

A

somewhat enhanced anti-Pseudomonas activity compared with gentamicin

it’s an aminoglycoside

52
Q

which two aminoglycosides have enhanced resistance to inactivating enzymes?

A
  1. amikacin

2. netilmicin

53
Q

when is amikacin used?

A

it’s active against gentamicin and tobramycin-resistant organisms

it’s only inactivated by bacterial N-acetyltransferase at the 6’position on the aminoglycoside structure

54
Q

when is netilmicin used?

A

it’s resistant to several of the bacterial enzymes that inactivate gentamicin and tobramycin

55
Q

what are the adverse effects of aminoglycosides?

A
  1. nephrotoxicity
  2. ototoxicity
  3. neuromuscular junction blockade
  4. hypersensitivity
  5. suprainfection
56
Q

how can aminoglycosides cause nephrotoxicity?

A

it can cause proximal tubular necrosis – severe toxicity in ~2% of patients

usually reversible, but sometimes permanent

there’s increased BUN, decreased creatinine clearance, generally within a week or two of treatment

concurrent administration of lop diuretics will make the renal toxicity of the aminoglycosides even worse

57
Q

how are aminoglycosides cleared from the body?

A

aminoglycosides are cleared predominantly by glomerular filtration

they are poorly protein-bound, and thus readily filtered

58
Q

how are aminoglycosides ototoxic?

A

can be permanent!!

it happens when aminoglycosides accumulate in the perilymph = the fluid between the membranous labyrinth of the ear and the bone that encloses it

can cause vestibular damage = difficulty with balance and walking, resulting in dizziness

vestibular damage may only appear several weeks after termination of treatment

cochlear = high-pitched ringing in the ears (tinnitus)

as with nephrotoxicity, ototoxicity is exacerbated by the loop diuretics.

59
Q

when can aminolgycosides cause neuromuscular junction blockade?

A

overdosage of aminoglycosides

can be reversed by neostigmine = a parasympathomimetic that acts as a reversible acetylcholinesterase inhibitor

60
Q

how do nucleic acid synthesis inhibitors work?

A

they target enzymes required for nucleic acid synthesis

61
Q

which drug groups are nucleic acid synthesis inhibitors?

A
  1. fluoroquinolones

2. rifamycin

62
Q

what do fluoroquinolones do?

A

they’re nucleic acid synthesis inhibitors

they inhibit enzymes that maintain the supercoiling of closed circular DNA

63
Q

what do rifamycins do?

A

they’re nucleic acid synthesis inhibitors

they block prokaryotic RNA polymerase from initiating transcription

64
Q

what is nalidixic acid?

A

a first generation quinolone used for
treatment of urinary
tract infections

65
Q

which bacteria does nalidixic acid work on?

A
  1. E. coli
  2. Klebsiella
  3. Enterobacter
  4. Proteus spp.
66
Q

what is ciprofloxacin?

A

a second generation fluoroquinolone useful for
treatment of many systemic infections

broad spectrum relative to nalidixic acid

67
Q

what is levofloxacin?

A

third generation fluoroquinolone

specifically a respiratory fluoroquiniolone

68
Q

which fluoroquinolones are fourth generation?

A
  1. moxifloxacin
  2. gatifloxacin

respiratory fluoroquinonlones

69
Q

what is the MOA of quinolones and fluoroquinolones?

A

DNA gyrase (topoisomerase II) relieves tension in double-stranded DNA, relaxes supercoils

topoisomerase IV separates and unlinks DNA for the following DNA replication

Qs and FQs inhibit both enzymes so they inhibit DNA replication

70
Q

are Qs and FQs bacteriastatic or bactericidal drugs?

A

bactericidal drugs

71
Q

which bacteria are fluoroquinolones active against?

A

FQs enter into the host cells and therefore are active against intracellular pathogens:

  1. Legionella
  2. mycoplasma
  3. chlamydia

they’re really broad spectrum too though so they’re rapidly bactericidal against many Gm+ and Gm- bacteria

72
Q

is resistance a problem with fluoroquinolones?

A

yeahhh

resistance developes radpidly –> resistance to one fluoroquinolone usually means resistance to all of them

for example, with M. tuberculosis, the MfpA protein mimics DNA

in general, anaerobes are intrinsically resistant

73
Q

which bacteria are intrinsically resistant to fluoroquinolones?

A

anaerobes

but moxifloxacin and gatifloxacin will hit anaerobes

74
Q

what are fluoroquinolones used to treat?

A
  1. UTIs
  2. diarrhea caused by Campylobacter, E. coli, Salmonella, or Shigella
  3. gonococcal infections
  4. Prophylaxis of anthrax
  5. respiratory tract infections
75
Q

which FQs are used to treat gonococcal infections?

A
  1. ciprofloxacin

2. ofloxacin

76
Q

which FQs are used for prophylaxis of anthrax?

A
  1. ciprofloxacin

2. levofloxacin

77
Q

which FQs are used to treat respiratory tract infections?

A

for gram (-) bacteria use ciprofloxacin or levofloxacin

for anaerobes or pneumococcus use 4th generation FQs like gatifloxacin and moxifloxacin

78
Q

what is ciprofloxacin used for?

A

it’s the most potent of the fluoroquinolones for P. aeruginosa

it has a long post-antibiotic effect and is well absorbed in GI

***it’s a potent CYP450 inhibitor

79
Q

how is ciprofloxacin administered?

A

orally or IV

excreted in urine

80
Q

what are the drug interactions associated with FQs?

A
  1. antacids containing Ca2+, Mg2+, Zn2+, Bi2+, or Al3+ may reduce the oral bioavailability of fluoroquinolones
  2. fluoroquinolones may increase the anticoagulant effect of warfarin
  3. hepatotoxicity
  4. hyper/hypoglycemia
  5. allergic reaction
81
Q

what is a potential complication associated with FQs inhibiting CYP450 enzymes?

A

due to inhibition of the CYP450 enyzmes, fluoroquinolones may increase the plasma concentration of theophylline

this can increase BP and heart rate

theophylline = drug used in therapy for respiratory diseases such as COPD and asthma

82
Q

which FQ is linked to hepatotoxicity?

A

trovafloxacin

has been linked with 14 cases of liver failure

83
Q

how do FQs mess with blood sugar?

A

can cause hypoglycemia in elderly diabetics

and can cause hyperglycemia in non-diabetics

especially gatifloxacin which is contraindicated in diabetes mellitus

84
Q

what are some of the adverse effects of both quinolones and fluoroquinolones?

A
  1. abnormalities of bone and cartilage formation
  2. photosensitivity
  3. tendonitis/tendon rupture
  4. CNS issues
  5. cardiac effects
85
Q

what bone/cartilage abnormalities can Qs and FQs cause?

A

can cause cartilage damage in weight bearing joints in animal studies

bow legs in babies!

so because of this Qs and FQs are contraindicated in children under 18 and pregnant women

86
Q

how do Qs and FQs cause CNS complications?

A

confusion, insomnia, fatigue, depression, drowsiness, seizures

they seizures are caused by binding to gamma-aminobutyric acid (GABA) receptors

87
Q

what cardiac effects can Qs and FQs cause?

A

they prolong the QTc interval, increasing the risk of ventricular tachy-arrhythmias

88
Q

which drugs are inhibitors of RNA synthesis?

A
  1. rifampin
  2. rifamycin
  3. rifampicin
  4. rifabutin

all bactericidal!!

89
Q

what is the MOA of inhibitors of RNA synthesis?

A

these antimicrobials bind to DNA-dependent RNA polymerase and inhibit initiation of mRNA synthesis

90
Q

what is the spectrum of activity of inhibitors of RNA synthesis?

A

broad spectrum but is used most commonly in the treatment of tuberculosis

resistance is common so combination therapy is often needed

91
Q

what is the MOA of antimetabolites?

A

competitive inhibition by substance that resembles normal substrate of enzyme

ex. sulfa drugs

92
Q

what is the MOA of folic acid synthesis inhibitors?

A

competitive inhibition by substance that resembles normal substrate of enzyme

ex. sulfamethoxazole is a sulfonamide

93
Q

what does trimethoprim do?

A

it’s a folic acid synthesis inhibitor

trimethoprim inhibits bacterial dihydrofolate reductase

94
Q

what is a bactrim?

A

sulfonamid + trimethoprim

sulfonamides used to be mainstays of antimicrobial therapy, but now mainly used in combination with dihydrofolate reductase inhibitors (e.g. trimethoprim) for susceptible organisms

95
Q

what are the adverse effects of sulfonamides?

A
  1. hypersensitivity
  2. blood disorders (e.g. aplastic anemia)
  3. crystalluria (the presence of crystals in the urine)
  4. jaundice and kernicterus of the newborn
96
Q

what are the general characteristics of mycobacterium tuberculosis?

A

gram-positive aerobic rod-shaped bacilli

lack of spore formation and toxin production

no capsule, flagellum (non-motile)

“acid fast” bacteria

generation time of 18- 24 hours but requires 3-4 weeks for visual colonies

97
Q

what are the pathological features of mycobacterium tuberculosis?

A

principle cause of Human Tuberculosis

intracellular pathogen (alveolar macrophages)

waxy, thick, complex cellular envelope

produces tubercles = localized lesions of M. tuberculosis

98
Q

how do you treat TB?

A

combination of first and second line drugs for the first 2 months which could include:

  1. isoniazid
  2. rifampicin
  3. pyrazinamide
  4. streptomycin or ethamcutol

next 4 months, a combination of:

  1. isoniazid
  2. rifamicpin
99
Q

what is isoniazid used for?

A

used for active disease in combination with other drugs & used alone for prophylaxis

it decreases mycolic acid synthesis

100
Q

what’s the spectrum of isoniazid?

A

narrow antimycobacterial spectrum: only hits M. tuberculosis and M. kansasii

101
Q

how is isoniazid given?

A

orally available & widely distributed including CNS and caseous lesions

metabolism is different in fast vs slow acetylators

102
Q

what is the MOA of isoniazid?

A

Isoniazid is a prodrug and must be activated by a bacterial catalase-peroxidase enzyme that in M. tuberculosis is called KatG

mutation of KatG peroxidase provides high level resistance

103
Q

what are the adverse effects of isoniazid?

A

overall it’s relatively safe

  1. but can cause peripheral neuritis which can be prevented with bitamin B6
  2. hepatitis - rare in individuals <35 years old
  3. hypersensitivity
104
Q

what environment does pyrazinamide require?

A

it’s a nicotinamide analog like isoniazid

requires acidic environment

it’s only effective vs intracellular mycobacteria that express the pncA gene –> mutation in the pncA gene causes resistance

105
Q

what are the adverse effects of pyrazinamide?

A

liver damage is possible at only slightly higher than usual therapeutic doses

also causes urate retention & therefore may precipitate gout attacks –> allopurinol can be used for treatment of gout

106
Q

what is the MOA of ethambutol?

A

inhibits mycolic acids attachment to D-arabinose residues and form mycolyl-arabinogalactan-peptidoglycan complex in the cell wall of M. tuberculosis

107
Q

what is the spectrum of ethambutol?

A

M. tuberculosis and some atypical mycobacteria

not as potent as isoniazid, rifampin or pyrazinamide

108
Q

what are the pharmacokinetics of ethambutol?

A

not widely distributed

but does cross inflamed meninges

109
Q

what are the adverse effects of ethambutol?

A
  1. optic neuritis = decreased visual acuity

2. urate retention

110
Q

what is the MOA of rifampin?

A

inhibits RNA polymerase

111
Q

what are the characteristics of rifampin?

A

has a broader spectrum than isoniazid

widely distributed, including CNS

usually well tolerated

*turns body fluids orange

induces expression of cytochrome P450

112
Q

what are the adverse effects of rifampin?

A
  1. hepatotoxicity
  2. hypersensitivity

usually well tolerated though

113
Q

what is rifabutin used to treat?

A

used to treat tuberculosis in AIDS patients

compared with rifampin, it causes less induction of cytochrome P450

114
Q

what are the benefits of using rifapentine vs. rifampin?

A

longer half-life than rifampin, therefore can be administered twice weekly

115
Q

how do you treat MAC respiratory infections?

A

MAC = mycobacterium avium complex

MAC respiratory infection is a real danger for immunocompromised patients (ex. AIDS)

treat with azithromycin or clarithromycin macrolide antibiotics & either ethambutol or rifabutin

116
Q

which drugs can be used to treat leprosy?

A
  1. dapsone
  2. rifampin
  3. clofazimine

used when the disease is resistant to dapsone and rifampin, or if the latter are not tolerated

MOA is unknown

117
Q

what is the DOC for leprosy?

A

dapsone

it’s a dihydropteroate synthetase inhibitor

major toxicities are related to blood = methemoglobinemia & hemolytic anemia

118
Q

what is methemoglobinemia?

A

a disorder characterized by the presence of a higher than normal level of methemoglobin in the blood

heme group is in the Fe3+ (ferric) state, not the Fe2+ (ferrous) of normal hemoglobin so methemoglobin cannot bind oxygen

methemoglobin is an oxidized form of hemoglobin that has a decreased affinity for oxygen, resulting in an increased affinity of oxygen to other heme sites and overall reduced ability to release oxygen to tissues

119
Q

why is tuberculosis naturally resistant to certain antibiotics?

A

M. tuberculosis: naturally resistant to certain antibiotics due to presence of:

  1. drug-modifying enzymes
  2. drug-efflux systems
  3. hydrophobic cell wall
120
Q

is antibiotic resistance a problem with TB?

A

yeah….

mycobacteria undergo natural mutations which can lead to development of drug resistance

so TB has to be treated with combination chemotherapy which decreases probability of development of drug resistance

development of increasingly resistant strains is mainly due to patient non-compliance

121
Q

what does poly-resistant TB mean?

A

resistance to more than one drug, but not the combination of isoniazid and rifampicin

122
Q

what is MDR TB?

A

multi-drug resistant TB

resistance to at least isoniazid and rifampicin

123
Q

what is XDR TB?

A

extensively drug-resistant TB

MDR plus resistance to fluoroquinolones and at least 1 of the 3 injectable drugs (amikacin, kanamycin, capreomycin)

124
Q

where are MDR and XDR TB most prevalent?

A

MDR and XDR-TB rates are higher in developed nations with access to anti-TB drugs.

MDR and XDR-TB: uncommon in developing nations lacking TB drugs (high drug-susceptible TB rates)

125
Q

TB is related to which other virus?

A

HIV/AIDS

people with latent TB have a 10-20% of developing active TB in their lifetime

people with HIV and latent TB are 100 times more likely to develop active TB –> HIV infection can cause latent M. tuberculosis infection to become reactivated

a person with HIV/AIDS will have a harder time fighting off the M. tuberculosis infection due to a compromised immune system

126
Q

which drugs are used to treat TB?

A
  1. isoniazid
  2. rifampin
  3. pyrazinamide
  4. ethambutol

ID Week 4 (6 decks)

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