Micro/id Set 4

Front 1

What is R?

Back 1

R – The Reproductive Number. The number of new infectious organisms (or infected cells) produced during each period of replication of the organism

Front 2

What is the relationship between drug resistance and R?

Back 2

A resistant organism is one whose R value is >1 in the presence of an antimicrobial drug. Eventually the resistant organism will outgrow the wild-type organism and establish a new steady-state. The resistant organism has a growth advantage in the presence of the drug

Front 3

Name 3 ways bacteria can exchange genetic information

Back 3

Transformation – segments of DNA from donor bacteria are taken up from the extracellular environment by recipient bacteria and integrated into the recipient genome by recombination; Transduction – DNA is moved from one bacterial cell to another by a virus (bacteriophage); Conjugation – transfer of genetic material between bacteria through direct cell to cell contact

Front 4

What is primary drug resistance?

Back 4

Predates drug therapy; Drugs promote growth of resistant organisms by providing the necessary selective pressure; Effective therapy = treatment with a drug to which the organism is known to be sensitive, treatment with a combination of drugs where at least one drug component will reduce R to <1.0; Mostly due to improper use (or overuse) of antibiotics

Front 5

What is secondary drug resistance?

Back 5

Acquired resistance; Occurs during drug therapy; Some resistance mutations occur during therapy; If an effective drug is being taken correctly, R wil be <1.0 and secondary resistance will be unlikely to occur; If an effective drug is being taken irregularly/incorrectly, drug concentrations will decrease to levels adequate for survival and continued replication of resistant organisms; Low drug concentration provides the necessary selective pressure for the emergence of mutant variants with R>1.0; Most secondary resistance exists because of non-adherence to a prescribed drug regimen (usually involving multiple drugs)

Front 6

Which major drug classes are susceptible to inactivation of drug as a mechanism of resistance?

Back 6

Beta-lactams: Penicillins, Cephalosporins, Carbapenems, Monobactams

Front 7

Which major drug classes are susceptible to inavtivation by target inactivation?

Back 7

Glycopeptide Antibiotics, Clindamycin, Macrolides, Fluoroquinolones, Rifampin, Vanc

Front 8

Which major drug classes are susceptible to inavtivation by efflux?

Back 8

tetracyclines, beta lactams, fluroquinolones (less common), macrolides, dalfopristin

Front 9

Define “virion”.

Back 9

The virus particle; made up of viral nucleic acid and viral structural proteins; The structural proteins serve as the payload vehicle to deliver the nucleic acid

Front 10

How are viruses classified?

Back 10

Nucleic acid in the virion (RNA or DNA); Symmetry of the Capsid; Presence/absence of an envelope; Dimensions of the virion and the capsid

Front 11

What are viral ‘quasispecies’ and how do they evolve?

Back 11

Subsets of a given virus population that retain the same general architecture and genome and function the same way but differ slightly with respect to actual genetic sequence and coat protein structure (on account of mutation in genetic sequence); Subpopulations of viruses that are different than infecting virus; They evolve as a result of the rapid evolution of viruses, which stems from the large numbers of progeny produced by a given virus (increasing the number of opportunities for a mutation to arise, recombination/reassortment to occur) and the lack of a proofreading function of viral RNA polymerases (low fidelity replication leading to greater likelihood of mutation)

Front 12

What are the major obstacles that a virus has to overcome to survive efficiently?

Back 12

How to get all of the information necessary for replication into a small genome, How to be maintained in a population and not die out, How to have a structure that allows sufficient stability for transmission, but sufficient instability for cell infection

Front 13

Describe interferon induction and action and list clinical side effects associated with interferon (either endogenous or exogenous)

Back 13

Induction and Action: Sense viral nucleic acids (recognized as foreign because of unique nature – dsRNA, ssDNA – not found in host cells), Interferons bind to IFN receptors, which signal through the JAK-STAT pathway to induce antiviral protein genes; Clinical Side Effects FLU-LIKE: Fever (antiviral effect on most viruses), Malaise, Fatigue, Muscle Pain,

Front 14

What are “neutralizing antibodies?

Back 14

Neutralizing antibodies – antibodies that prevent the virus from infecting the host cells, Achieve this by blocking viral attachment (via steric interference, capsid stabilization, inducing structural changes), blocking endocytosis, and/or blocking viral uncoating (via capsid stabilization or fusion interference)

Front 15

Why are neutralizing antibodies important in viral infections?

Back 15

Prevent against viral reinfection, clear virus from fluids, and downregulate intracellular virus replication

Front 16

T/F: RNA polymerases lack proofreading functions

Back 16

T

Front 17

T/F: RNA virus infections in humans are more likely to harbor viral quasi-species than DNA viral infections

Back 17

T

Front 18

T/F: DNA viruses must get into the nucleus of the cell to make use of the DNA polymerase of the host cell.

Back 18

TRUE (RNA viruses need only penetrate the cytoplasm)

Front 19

T/F: HCV infection is an example of an acute viral infection

Back 19

FALSE – example of a persistent infection

Front 20

T/F: HIV infection is an example of a latent viral infection

Back 20

FALSE – example of a persistent infection

Front 21

T/F: Herpes Simplex Virus is an example of a latent viral infection

Back 21

T

Front 22

T/F: Varicella zoster virus infection is an example of an acute viral infection

Back 22

FALSE (latent)

Front 23

Which hepatitis class (A,B,C,D,E) is most likely transmitted fecal-oral?

Back 23

A,E

Front 24

Which hepatitis class (A,B,C,D,E) is most likely transmitted by sex?

Back 24

B,D

Front 25

Which hepatitis class (A,B,C,D,E) is most likely transmitted by blood?

Back 25

B,C,D

Front 26

Which hepatitis class (A,B,C,D,E) is most likely transmitted perinatally?

Back 26

B,D

Front 27

Which is the most likely method of transmission for hepatitis A virus?

Back 27

Fecal-oral

Front 28

Which is the most likely method of transmission for hepatitis B virus?

Back 28

Sexual, blood, perinatal

Front 29

Which is the most likely method of transmission for hepatitis C virus?

Back 29

Blood

Front 30

Which is the most likely method of transmission for hepatitis D virus?

Back 30

Sexual, Blood, perinatal

Front 31

Which is the most likely method of transmission for hepatitis E virus?

Back 31

Fecal-oral

Front 32

T/F: Hepatitis C has a longer incubation period than hepatitis A (acute)

Back 32

TRUE (6-300 days versus 2-6 days)

Front 33

T/F: Hepatitis B is the most likely hepatitis virus to persist

Back 33

FALSE (Hepatitis C – 70% versus 5% for B)

Front 34

T/F: Hepatitis B is the most common cause of acute Hepatitis in the US

Back 34

FALSE (Hepatitis A)

Front 35

T/F: Jaundice is most frequently associated with HAV infection

Back 35

TRUE (30-70% vs 20-40% for B, 15-25% for C)

Front 36

T/F: The capsid protein of HAV elicits protective antibodies (can immunize against Hep A)

Back 36

T

Front 37

T/F: There is limited HCV diversity following infection

Back 37

FALSE – HUGE amount of diversity post-infection

Front 38

T/F: The body may clear hepatitis C infection without help

Back 38

FALSE – huge diversity leads to persistence of HCV RNA

Front 39

T/F: Interferon is used to treat HAV infection

Back 39

FALSE – Interferon used to treat chronic hepatitis caused by HBV, HCV infection. No tx for acute Hep.

Front 40

T/F: Sub-Saharan Africa and Far East Asia have very high Hepatitis B prevalence

Back 40

T

Front 41

T/F: Hepatitis D cannot cause Hepatitis without the presence of Hepatitis B co-infection

Back 41

T

Front 42

T/F: A vaccine against hepatitis A is available

Back 42

T

Front 43

T/F: A vaccine against Hepatitis B is available

Back 43

T

Front 44

T/F: A vaccine against Hepatitis C is available

Back 44

FALSE – Wide genetic variability and high viral mutability make developing a vaccine prohibitively difficult

Front 45

What other infections can cause hepatitis?

Back 45

Generally, toxins, medication, and other infection can cause hepatitis in addition to viruses; Infections: Systemic viruses (cytomegalovirus, mononucleosis, EBV, measles, varicella zoster, adenovirus, HSV, coxsackievirus, HIV), Spirochetes (syphilis, leptospirosis), Toxoplasma, Rickettsia (Rocky Mountain spotted fever)

Front 46

Which hepatitis virus is most often associated with fatality during pregnancy?

Back 46

HEV

Front 47

A patient presents with elevated liver function tests (ALT and AST). HAV IgG positive, HAV IgM negative; Hepatitis B surface antigen positive; Hepatitis B surface antibody negative; Hepatitis B core IgG positive; Hepatitis C IgG positive; Hepatitis C PCR negative. Which of the following statements is/are true: a)The patient has acute Hepatitis A b)The patient has chronic Hepatitis A c)The patient was previously infected with Hepatitis A d)The patient has active Hepatitis B infection (Chronic) e) The patient has a previous Hepatitis B infection but he cleared the infection f) The patient has a previous Hepatitis C infection but he cleared the infection g)The patient has active Hepatitis C infection

Back 47

C, D,F

Front 48

On a routine workup, a patient is found to have normal liver function tests. The physician, for some reason, orders a Hepatitis B surface antibody (IgG) and it is positive. Which of the following is/are true? a)The patient has active hepatitis B infection b)The patient has chronic Hepatitis B infection c)The patient had a past infection with hepatitis B that they cleared (possible – need to check for HBc antibodies) d)The patient never had hepatitis B but was previously vaccinated with the Hepatitis B vaccine

Back 48

D

Front 49

T/F: Parvovirus can only replicate in dividing cells

Back 49

T

Front 50

T/F: Transmission is via the gastrointestinal route (fecal-oral)

Back 50

FALSE -- respiratory

Front 51

T/F: The first phase of infection, no matter the host, is the viremic phase

Back 51

T

Front 52

T/F: The manifestations of the second phase of the infection depend on who the host is (immunocompromised, sickle cell patient, etc.)

Back 52

T

Front 53

T/F: An IMMUNOCOMPETENT adult usually gets transient arthritis and maybe a little anemia (and very occasionally an evanescent rash)

Back 53

T

Front 54

T/F: An IMMUNOCOMPETENT child usually gets a rash (slapped cheeks in appearance) and maybe a transient anemia.

Back 54

T

Front 55

T/F: Someone with sickle cell disease may get a more severe anemia

Back 55

TRUE (transient aplastic crisis – severe acute anemia)

Front 56

T/F: An IMMUNOCOMPROMISED adult (advanced HIV or transplant) may get severe anemia that requires transfusion and occasionally the use of IVIG (intravenous immunoglobulin which contains preformed antibodies against parvovirus B19) for treatment

Back 56

TRUE (pure red cell aplasia – chronic anemia)

Front 57

T/F: Hydrops fetalis is a devastating consequence of fetal infection

Back 57

T

Front 58

T/F: The greatest risk of ParvoB19 infection in pregnant women is in the 3rd trimester

Back 58

FALSE (1st and 2nd)

Front 59

T/F: HPV transmission is via the respiratory route

Back 59

FALSE – wart abrasion or mucous membrane

Front 60

T/F: HPV is the most prevalent STD in the world today

Back 60

T

Front 61

T/F: Low risk types of HPV (e.g. 6 and 11) cause cancer

Back 61

FALSE – high-risk types (16,18) cause cancer

Front 62

T/F: High risk types of HPV (16 and 18) cause warts

Back 62

FALSE – LOW RISK types cause warts

Front 63

T/F: Acquisition of HPV occurs very shortly after sexual debut

Back 63

T

Front 64

T/F: HPV L1 and L2 proteins are involved in replication

Back 64

FALSE – L1 = major capsid protein; L2 = minor capsid protein

Front 65

T/F: HPV E6 and E7 proteins are responsible for transformation

Back 65

TRUE – E7 inhiits pRB (induces its degradation), removing check on transcription; E6 inhibits p53 by targeting it for ubiquitin mediated proteolysis

Front 66

T/F: HPV is responsible for some cases of anal, vulvar, and penile cancers

Back 66

T

Front 67

T/F: Neutralizing antibodies against HPV LI are protective

Back 67

T

Front 68

T/F: There is a virus-like particle vaccine that has been approved for HPV recently but one of its side effects is the possibility of developing cancer

Back 68

T

Front 69

T/F: Up to 90% of HPV infections in young girls clear on their own by two years after infection

Back 69

T

Front 70

T/F: Malignant transformation occurs in HPV when integration disrupts E2 which controls the expression of E6 and E7

Back 70

T

Front 71

T/F: Most infections with high-risk types of HPV are symptomatic

Back 71

FALSE – most are asymptomatic

Front 72

T/F: The Pap smear has been an effective tool to decrease the rate of cervical cancer in the US

Back 72

T

Front 73

T/F: HIV+ patients infected with a high risk HPV are at higher risk of developing cancer than HIV negative patients

Back 73

TRUE – takes them longer to clear the infection

Front 74

Sexual transmission: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 74

Hepatitis C virus, HPV 16

Front 75

Respiratory transmission: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 75

HPV 16, Parovirus B19

Front 76

High-risk type: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 76

HPV 16

Front 77

Transient aplastic crises: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 77

Parvovirus B19

Front 78

Pure red cell aplasia: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 78

Parvovirus B19

Front 79

Hepatocellular carcinoma: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 79

Hepatitis B Virus, Hepatitis C Virus

Front 80

Fifth disease: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 80

Parvovirus B19

Front 81

Slapped cheek: 1. Hepatitis B Virus, 2. Hepatitis C virus, 3. HPV 16, 4. Parvovirus B19?

Back 81

Parvovirus B19

Front 82

What are differences between negative and positive strand viruses?

Back 82

Positive Strand Virus – has genome that can be sensed by immediately be sensed by ribosomes, translated; Negative Strand Virus – have genome that is “opposite polarity” – genome it not initially accessible to ribosome (need to first convert – strand to a + strand that can be sensed by ribosome); Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell.; Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA polymerase before translation.; Purified RNA of a positive-sense virus can directly cause infection though it may be less infectious than the whole virus particle.; Purified RNA of a negative-sense virus is not infectious by itself as it needs to be transcribed into positive-sense RNA; however each virion can be transcribed to several positive-sense RNAs

Front 83

What are the mechanisms behind antigenic drifts and shifts observed in influenza?

Back 83

If different flu strains infect the same cell (one bird strain and one human strain infecting a pig cell, which is a permissive host for both, for example), the genetic material can replicate and then undergo reassortmet, which results in a virus with different external glycoproteins but internal machinery that allows for replication in human cells; Minor mutations of viral genome as a result of high replication rate and error prone RNA polymerase result in antigenic “drift” – functional glycoproteins but different enough structurally to allow for evasion of antibody binding because epitope that was recognized is altered.

Front 84

What are hemagglutinin and neurominidase?

Back 84

HA – trimeric protein with globular head on a stalk that binds cellular receptor sialic acid and mediates fusion of viral envelope with the host cell membrane; NA – tetrameric surface protein that cleaves sialic acid residues on the host cell surface, enabling viral exit

Front 85

What are the clinical features of influenza?

Back 85

Transmission: Respiratory, Seasonal, primarily winter; Symptoms: Appear 1-4 days post infection, HA, fever, myalgias, nonproductive cough, sore throat, no rhinorrhea, Last 3-7 days, Likely caused by local production of IFN and IL-1

Front 86

What are some complications of influenza?

Back 86

Primary virus infection – interstitial pneumonitis; Secondary bacterial pneumonia, Facilitated by damage to innate immune system (destruction of ciliated epithelial cells, abnormal macrophage function)

Front 87

Compare and contrast seasonal influenza to H1N1 2009 infection.

Back 87

VIRUS SHEDDING – prolonged compared to seasonal flu (4.5 days versus 107 hrs for mean time to 50% samples with viable virus), H1N1 2009 -- Shift from older to younger age groups for infection, hospitalization, mortality compared to seasonal flu, Shift in hospitalization from youngest (0-4 yrs) and oldest (65+ years) for seasonal flu to <49 years for H1N1 2009, Similar age shifts for illness and mortality compared to seasonal flu, Older age cohorts demonstrated pre-existing immunity to H1N1 2009 (usually not the case in seasonal flu), BUT – both causes influenza virus, caused similar symptoms

Front 88

What kind of protection does the inactivated influenza vaccine provide? Killed (Inactivated) Vaccine (primarily HA, NA): Reformulated annually, WHO lab network isolates, identifies viruses

Back 88

Strains reported to reference lab, Panel makes recommendation on viruses to include in upcoming year’s vaccine, Recommended for health care workers and population at high risk of morbidity and mortality, Provides PARTIAL protection, Decreases incidence of influenza 30-70%, Decreases morbidity and mortality 60-90%

Front 89

What kind of protection does the live attenuated intranasal vaccine provide?

Back 89

Live attenuated intranasal vaccine (FluMist): Replication restricted to nasopharynx, Cold adapted – grows best at intranasal temp(25C), Temperature sensitive – restricted replication at 37C, Reformulated annually, Approved for use in healthy people 5-49 YO

Front 90

Do parmyxoviruses undergo epidemiologically important antigenic change?

Back 90

No

Front 91

Is there a natural reservoir for paramyxoviruses?

Back 91

No natural reservoir, Maintained in population by continuous person to person spread,

Front 92

How are parmyxoviruses spread?

Back 92

Spread by respiratory route

Front 93

Which proteins are present in parmyxoviruses?

Back 93

Proteins: H – mediates receptor binding, F -- mediates fusion, M – required for assembly, Located at inner face of viral envelope, N – encapsidates genome, L – major catalytic subunit of polymerase, P – polymerase subunit, Genome

Front 94

Describe the genome of parmyxovirus.

Back 94

Nonsegmented – NPMFHL protein coding regions, mRNAs generated by polymerase reinitiation

Front 95

Describe the surface glycoproteins of parmyxoviruses.

Back 95

Surface Glycoproteins – carbohydrates attached during transit through ER and Golgi, Usually 2 proteins: Cell attachment protein (Binds attachment protein, Elicits neutralizing antibody, H, HN, G) Fusion Protein (F, To be active, F has to be cleaved into F1, F2 by intracellular proteases, Activation needed for virion infectivity)

Front 96

Describe the replication cycle of parmyxoviruses.

Back 96

Entry (Virions fuse at cell membrane (neutral pH)) Intracellular replication (All RNAs synthesized in cytoplasm, H/F transported thru ER/Golgi to PM), Exit (Nucleocapsids assemble below H/F, Virion assembly mediated by matrix protein, Virion budding from cell membrane OR: Fusion with adjacent cell, Surface proteins are fusogenic at neutral pH on cell membrane, Multinucleated giant cells seen in culture and in tissue)

Front 97

What are common themes for parmyxoviruses? (look at viral seasons slide) (bad question)

Back 97

Common Themes: Cause seasonal outbreaks, Cause severe diseases in young children and elderly, Infections recur throughout life, Disease less severe in older children/adults, Vaccines under development for some, Diagnosis: Direct visualization of antigens in specimens with fluorescent monoclonals, Culture (except human metapneumovirus), Nucleic acid amplification

Front 98

What diseases does RSV cause?

Back 98

In winter, respiratory disease; Generally, otitis media, bronchitis, bronchiolitis, croup, and pneumonia, Most severe disease in young infants

Front 99

How do you catch RSV?

Back 99

Come into direct contact with respiratory secretions

Front 100

How does RSV spread?

Back 100

Requires direct contact with respiratory secretions, Contact isolation prevents nosocomial transmission; Begins as upper respiratory infection, but can progress in severity – progressive dyspnea, increase RR, hypoxemia

Front 101

Describe the epidemiology of measles infection.

Back 101

Geographic distribution: Worldwide; incidence depends on vaccination rates, Epidemic – countries with high vaccine coverage, Endemic – countries with poor vaccination rates; Age – dist’n has changed in countries with high vaccination rates; Routes of transmission – respiratory, aerosol; Attack rate – 99.9%; Mortality rate – In developing countries, 30% in infants 6-9 months

Front 102

Describe the pathogenesis of measles.

Back 102

Systemic replication: First site – respiratory epithelium, Second site – local lymph nodes, Dissemination by infected monocytes departing from respiratory LNs (primary viremia), Epithelial/endothelial cells infected throughout body release virus into blood (secondary viremia)

Front 103

Describe the clinical symptoms of measles.

Back 103

Arise during VIREMIA, Prodrome – fever, cough, corzya, conjunctivitis, Koplik spots, Maculopapular rash arises with immune response, Manifestation of cellular response

Front 104

Describe how measles can be prevented.

Back 104

Live attenuated vaccine, Given to infants 12-15 months of age, Has changed age dist’n of infection, Now very young infants and older children/young adults (10-22 years)

Front 105

Describe the clinical manifestations of mumps.

Back 105

Clinical Manifestations: Infection of glandular epithelial cells, Parotitis, orchitis most commonly recognized, Pancreatitis and ovarian infection occur, but infrequently recognized, Meningitis ~10% of cases

Front 106

Describe prevention of mumps.

Back 106

Live attenuated vaccine

Front 107

How do you get rabies?

Back 107

Via saliva from bite of infected animal

Front 108

What are the symptoms and signs of rabies?

Back 108

Prodrome – fever, malaise, parathesias at bite site, Later – anxiety, aggressive behavior, seizures, hypertonia, paralysis

Front 109

How do you prevent rabies?

Back 109

Inactivated vaccine, Long incubation period allows for post-exposure use, Pre-exposure immunization in vocations with high risk of exposure (veterinarians, wildlife managers)

Front 110

Why is a single anti-tubercular drug useful to treat a patient with latent TB infection but not so to treat active TB?

Back 110

Viral load! 1 in 106-108 organisms resistant, latent viral load only 104-105

Front 111

How do mycobacteria acquire drug resistance?

Back 111

Chromosomal mutation, not plasmids or transposable elements. Non-compliance!

Front 112

What is the mechanism of action of isoniazid (INH)? What is the mechanism of resistance to INH? What are its toxicities?

Back 112

Mechanism: Bacteriacidal when dividing, nicotinamide analog, inhibits synthesis of mycolic acids, higher conc. Inhibit glycolysis, form O free radicals. Resistance: katG: enzyme that activates drug; inhA: binds nicotinamide and synthesizes mycolic acid. Toxicity: hepatitis, peripheral neuropathy, hypersensitivity rxns, drug-induced lupus

Front 113

What is the mechanism of action of rifampin (RIF)? What is the mechanism of resistance to RIF? What are its toxicities? (very similar to Rifabutin)

Back 113

Mechanism: inhibitor of bacterial DNA-dependent RNA polymerases, bacteriacidal against most gram+, some gram-, . Resistance: RNA polymerase mutations, arises fast as single agent. Toxicities: orange discoloration of urine, sweat, tears, soft contact lenses; hepatitis; hypersensitivity rxns (flu-like); Light-chain proteinuria in >50% of patients; Drug-drug interactions (Potent enzyme inducer)

Front 114

What is the mechanism of action of Pyrazinamide (PZA)? What is the mechanism of resistance to PZA? What are its toxicities? Is it effective in treating latent TB infection?

Back 114

Mechanism: bacteriacidal, nicotinamide analog like INH, active in acidic pH, good for intracellular TB. Resistance: mutation in pyrazinamidase enzyme (pncA) which activates drug. Toxicities: hepatotoxicity, hyperuricemia >50% ptns, photosensitivity dermatitis (rare). Not effective at latent/dormant TB

Front 115

What is the mechanism of action of Ethambutol (EMB)? What is the mechanism of resistance to EMB? What are its toxicities?

Back 115

Mechanism: bacteriostatic, inhibits RNA synthesis and mycolic acid metabolism . Toxicities: peripheral neuropathy, retrobulbar optic neuritis, color blindness, peripheral vision loss

Front 116

What are some principles of antimycobacterial therapy that allow DOT?

Back 116

Slow growth of mycobacteria and characteristics of bactericidal drugs allows intermittent therapy. Administered 2-3x per week

Front 117

What is the mechanism of action of Dapsone? What is it used to treat? What are its toxicities.

Back 117

Mechanism: sulfone (sulfanilamide analog), inhibits folate synthesis, resitance extensive. Use: Pneumocystis carinii/jiroveci. Toxicities: hemolytic anemia, methemoglobinemia & subclinical hemolysis, hypersensitivity rxns (rash, fever), agranulocytosis & fatal mono-like syndrome (rare), reversal rxns & erythema nodosum leprosum during intiation