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Immuno mikro eng > First Pass Miss - Micro Exam 2 > Flashcards

First Pass Miss - Micro Exam 2 Flashcards

1
Q

What are the symptoms of the toxic shock syndrome exerted by LPS, and what induces similar physiologic responses?

A

Hypotension, fever, and disseminated intravascular coagulation (blood clotting / thromboses) mostly mediated via IL-1 / TNFalpha

Staphylococcal / streptococcal superantigens have a similar effect

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2
Q

What are three types of cis-acting regulatory regions?

A
  1. Promoter - DNA sequence recognized via RNA polymerase
  2. Operator - near promotor, binds repressor protein and reduces transcription when bound (i.e. lac repressor)
  3. Activator - near promotor, binds activator protein to increase transcription (i.e. CRP protein)
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3
Q

What is an attenuator?

A

mRNA secondary structure which modulates transcription (i.e. hairpin loop)

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4
Q

Would lacI be cis-acting or trans-acting?

A

Trans-acting since it creates the protein which binds the cis-acting lacO

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5
Q

What is an R factor and their two subunits?

A

R(esistance) factor is a conjugative episome which encodes for Abx resistance

  1. RTF - resistance transfer factor, coding autonomous replication and conjugal transfer
  2. Resistance determinant - composed of 1+ transposons, which carries the antibiotic resistance gene
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6
Q

What is the inducer of the lac operon?

A

Allolactose (indicates lactose presence), binds lac repressor to inactivate it, increasing transcription

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7
Q

What is lysogenic conversion, and what are some examples?

A

Change in bacterial phenotype after phage infection (bacterial virulence factors carried by specialized transduction)

Examples:
Diphtheria toxin, botulinum toxin, cholera toxin, exotoxin A (S. pyogenes), Shigatoxin

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8
Q

What penicillin class has the highest chance of kidney damage, and what symptoms are associated?

A

an be seen with all penicillins, but methicillin most common. Cause:
Acute interstitial nephritis

Triad: Fever, Rash, Eosinophilia which can lead to renal failure

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9
Q

What is the first line empiric treatment for bacterial meningitis?

A

3rd generation cephalosporins like ceftriaxone and ceftazidime which penetrate the BBB well, then if it’s like listeria you can switch to ampicillin

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10
Q

Why do we worry about SPICE organisms when treatment with 3rd generation cephalosporins? What should we do instead?

A

All have a beta lactamase which can be selected for during therapy, so against these it is best to use cefepime or carbapenems for invasive / critically ill infections

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11
Q

What does Avibactam do?

A

It is a non-betalactam b-lactamase inhibitor which can restore ceftazidime activity against organisms which produce b-lactamases and carbapenemases

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12
Q

What is the only monobactam and what is its claim to fame?

A

Aztreonam (beta-lactam with no side chain)

Used for empiric nosocomial gram negative coverage in patient with penicillin allergy (zero cross-reactivity)

Covers P. aeruginosa but NO ESBL (not quite carbapenem)

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13
Q

What are the only Beta-lactams which are not renally cleared and thus you don’t have to think about dosing?

A
  1. Ceftriaxone
  2. Penicillinase-resistant penicillins - i.e. Nafcillin

Have a major contribution of biliary secretion

Explains why ceftriaxone can’t be used in infants / neonates - biliary sludging

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14
Q

What is changed about the gram + and gram - activity of 3rd gen cephalosporins?

A

Gram + - Enhanced S. pneumoniae activity (good against Community-acquired pneumonia and bacterial meningitis), but worse MSSA activity (use first class)

Gram - - Good against nosocomial gram negative (PEK), but no Pseudomonas coverage

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15
Q

What is Streptolysin O analogous to in S. aureus?

A

It is a cytolysin which forms pores in RBCs, analogous to alpha toxin of S. aureus

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16
Q

What is TSST analogous to in S. pyogenes?

A

SpeA-E, inducing fever, rash, and hypotension. They are Streptococcal pyrogenic exotoxins

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17
Q

What do hydrolytic enzymes like streptokinase cause?

A

They dissolve fibrin to facilitate spread of bacteria, and are responsible for runny, thin pus. (pyoderma / streptococcal impetigo)

Can be used therapeutically to dissolve blood clots

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18
Q

When does erysipelas occur and what does it progress to? What are the associated symptoms?

A

Occurs on face, especially following strept throat. Can rapidly spread infection to deeper layers and cause necrosis + septicemia.

Associated with edema, fever, and lymphadenopathy

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19
Q

What limits the spread of tinea infections? What do chronic infections mean?

A

Rapid shedding of keratinized layers due to advanced skin growth which is induced by infection.

Cell mediated immunity is important and delayed-type (Type 4) hypersensitivity will result

Chronic infections: impaired T cell and lack of DTH reaction

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20
Q

What is the purpose of M protein? What is it responsible for?

A

Antiphagocytic, does molecular mimicry with antigen variation via N terminus (>80 serotypes)

Mediates binding to epidermis

Responsible for post-streptococcal sequelae, including acute glomerulonephritis, rheumatic heart disease

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21
Q

What are complications of roseola?

A

High fever, aseptic meningitis, hepatitis, mononucleosis-like syndrome

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22
Q

What is the structure of papillomaviruses?

A

Non-enveloped icosahedral

Circular dsDNA with 8-10 genes

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23
Q

What is the structure of Picornaviruses and what is one example?

A

Small, non-enveloped viruses with ssRNA (+) genomes

example: Coxsackieviruses (especially A)

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24
Q

What are two diseases caused by picornaviruses?

A
  1. Hand, Foot, and Mouth Disease - blisters / ulcers on all these areas, typical in Asia
  2. Herpangina - includes only the mouth lesions
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25
Q

What is one difference between HFM disease and when the lesions clear vs Roseola?

A

Typically, Roseola lesions do not actually appear until the fever is actually gone.

HFM lesions appear immediately and are gone in 1-5 days

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26
Q

What are levofloxacin and moxifloxacin also called and why?

A

Respiratory fluoroquinones -> good against all streptococcus, and all CAP organisms

Should not be relied on vs Staph / Enterococcus due to easy mutation

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27
Q

What is B. fragilis and what fluoroquinone is good against it?

A

An anaerobe commonly targeted in therapies

Only moxifloxacin

Unfortunately, it lacks anti-pseudomonal activity, also it’s not good versus UTI’s because it’s not renally cleared

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28
Q

What are the common fluoroquinolone side effects?

A

CNS toxicity - headaches, seizures, neuropathies
Tendon ruptures due to cartilage damage
Dysglycemia
Cardiac arrythmias / prolonged QT, especially moxifloxacin

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29
Q

What are daptomycin’s issues and when is it absolutely contraindicated?

A

Causes CPK elevations and rhabdomyolysis (muscle breakdown)

Irreversibly binds pulmonary surfactant, avoid in pneumonia

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30
Q

What is the clinical application of Linezolids?

A

VRE infections - but keep in mind it’s only static

MRSA - pneumonia (when vanco-resistant, dapto can’t be used)

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31
Q

What are VRE and what is the most common species for it? How is it typically treated?

A

Vancomycin-resistant enterococcus

Common in Enterococcus faecium

Treated via Linezolid / Daptomycin usually

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32
Q

What are the macrolides mostly active against?

A

Respiratory pathogens, including pneumococcus, Hemophilus, mycobacterium

Also: Chlamydia / gonorrhea
Mycobacterium avium complex seen in HIV

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33
Q

What is Azithromycin used for? Why is it chosen most often?

A

Chlymadia, gonorrhea, non-TB mycobacteria, and 1st line for CAP

It has a long half life, allowing for shorter drug course, has fewest CYP3A4 interactions, causes diarrhea least in class

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34
Q

What are doxycycline / minocycline typically used for?

A

Respiratory tract infections, including CAP
Skin infections, especially when CA-MRSA is a concern

Good against animal bites / lyme disease

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35
Q

What is minocycline emerging as good for?

A

Carbapenem-resistant A. baumannii

treated with Sulbactam or Imipenem/doripenem/meropenem before with little else

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36
Q

What are the two big problems with tigecycline?

A
  1. Highly lipophilic - poor for treating blood, lung, and urine infections
  2. Causes nausea/vomiting in 20% of patients
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37
Q

What is the spectrum of tigecycline activity? When is it used clinically?

A

Very broad in both gram positive and negative, just misses PP = pseudomonas and proteus

Used as last line for resistant gram-negative like Acetinobacter and Klebsiella

Used often in POLYMICROBIAL WOUNDS including MRSA or VRE

TPP = tigecycline misses pseudomonas and proteus

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38
Q

What should be done if something is found to be erythromycin resistant but clindamycin susceptible?

A

Special “D test”, since resistance may be latent and inducible - bacteria likely has the erm gene

39
Q

What is the major clinical role for TMP/SMX?

A

Outpatient UTIs, good against MRSA but poor for Strept (not good for skin infections)

Also PJP pneumonia and S. maltophilia pneumonia

40
Q

What can Trimethoprim cause? Sulfa?

A

Hyperkalemia -> blocks K+ excretion, so beware with K+ sparing diuretics

Also anemia, leukopenia, and granulocytopenia

Increased bleeding when given with warfarin

Sulfa: Hypersensitivity mostly, + rise in plasma creatinine although just by blocking secretion (unlike daptomycin which causes muscle breakdown and increased CPK)

41
Q

What are three main uses of metronidazole?

A
  1. Empiric anaerobic coverage for intra-abdominal infections
  2. Drug of choice for mild-moderate C. difficile
  3. Trichomonas vaginalis coverage
42
Q

What is the major side effect of metronidazole?

A

Peripheral neuropathy if given cumulatively

Also warfarin reaction (increase) + disulfiram-like reaction with alcohol consumption

43
Q

What is Rifampin’s spectrum of activity?

A

Good against all gram +, including MRSA, but not used as a monotherapy

Ineffective against gram negative unless in combination

Excellent against TB

44
Q

Give two reasons why Rifampin is not typically used

A
  1. Hepatotoxicity
  2. Induces multiple Cytochrome P450 enzymes, including CYP3A4. Contraindicated in many HIV meds because it causes subtherapeutic levels of the drugs (quicker metabolism)
45
Q

How does Polymyxin B work and why did it stop being used?

A

Cationic detergent which destroys outer cell membrane LPS by displacing divalent cations

Stopped being used due to nephrotoxicity, only works against gram negative but works great

46
Q

Why is polymyxin used clinically?

A

Last line treatment against multi-drug resistant gram negative:

P. aeruginosa, A. baumanii, K. pneumoniae, E. coli

47
Q

What is nitrofurantoin used for, and its main contraindication?

A

Urinary tract organisms (gram negative, narrow spectrum)
Contraindicated if GFR < 60 mL/min (compromised kidney function)

Can be used in place of TMP/SMX or Keflex or Cipro

48
Q

What is the mechanism of action of dapsone and when is it used?

A

antagonist of PABA
Used in prevention and treatment of pneumocystic pneumonia when patient has sulfa allergy (can’t used TMP/SMX)

causes Hemolysis worse with G6PDH deficiency

49
Q

What is the primary virulence factor of Group D Streptococcus / Enterococcus?

A

Multiple, high-level resistances to a wide variety of antibiotics

Includes VRE

50
Q

What is used for malaria prophylaxis?

A

Atovaquone / Proguanil = Malarone

51
Q

How is Aspergillus identified in culture?

A

Branched, septate hyphae (mold form). Blood cultures will be negative, biopsy of infected tissue is necessary (unlike Candida).

52
Q

What are the symptoms of babesiosis? How does it resolve?

A

Fever, not periodic
Myalgia, anemia, hepatosplenomegaly, renal dysfunction

Resolves spontaneously within a few week, but very dangerous in asplenic individuals

53
Q

What is one major CNS complication of IE? One more? hehe

A

Mycotic aneurysm formation in arterial wall (abscess formation of vasovasorum)

Will be silent until rupture occurs causing subarachnoid hemorrhage

Also fibrin plates can break off and cause cerebral emboli

54
Q

What are three main causes of osteomyelitis?

A

Recent trauma (hematologic spread) - common in young people
Surgery (local spread)
Diabetes - poor vasculature / insufficiency / necrosis

55
Q

What time scale defines chronic osteomyelitis, and what is the main difference from acute?

A

> 3 months duration, often following acute OM

Main difference: chronic can be polymicrobial (acute is usually monomicrobial)

56
Q

What are the major risk factors for septic arthritis?

A

Poor health indicators (low SES, diabetes, IDU)
rheumatoid arthritis
joint prostheses / history of steroid injections to joints

57
Q

What joints are commonly affected in septic arthritis vs reactive arthritis? What disease processes do they follow?

A

Septic arthritis - usually monoarticular of knees or ankles, follows UTI
Reactive arthritis - usually four or fewer joints, asymmetrical, of back or lower limb, follows UG or GI infection

58
Q

What are some extra-articular manifestions of reactive arthritis?

A

Anterior uveitis, conjunctivitis, keratoderm blennorrhagicum (psoriasis-like, often on feet)

59
Q

What are involucrum and sequestrum?

A

Sequestrum - necrotic bone in osteomyelitis

Involucrum - ectopic bone overgrowth

60
Q

What is the first line treatment for aspergillus? What azole is not active against it?

A

Voriconazole

Only fluconazole is not active against it

61
Q

What is the clinical application of itraconazole?

A

Non-life threatening cases of endemic mycoses

62
Q

What are posaconazole / isuvaconazole used for?

A

Mucormycoses, with isuvaconazole’s niche to be determined

63
Q

What organisms are echinocandins good against?

A

All candida species, considered first line for all, except maybe C. parapsilosis

Aspergillus - used in combination therapy if patient is intolerant to voriconazole or amphotericin

64
Q

When would you know to use echinocandins vs fluconazole for yeast infection?

A

If patient is not critically ill and this is new, use fluconazole

If recent azole exposure, known colonizer with C. glabrata, or critically ill, use echinocandins

65
Q

What is the spectrum for cidofovir and when is it used?

A

HSV, VZV, CMV

Used for CMV when CMV is resistant to ganciclovir / foscarnet

66
Q

When is foscarnet used and what are its big side effects?

A

Only for CMV when ganciclovir is not available

Side effects: Nephrotoxicity, CNS effects, potential chelator of divalent cations in blood (hypokalemia - bananas, hypocalcemia - milk, hypomagnesia - magnets)

67
Q

What are the major neuraminidase inhibitors and what is one side effect?

A

Zanamivir (IV), oseltamivir (PO)

Zanamivir can exacerbate COPD if inhaled

68
Q

What are the side effects of flucytosine?

A

Dose-dependent bone marrow suppression

69
Q

What is the mainstay of therapy for animal bites?

A

Beta-lactam / beta-lactamase inhibitors which hit both gram positive and gram negative infections -> i.e. augmentin

Can still use doxycycline / ceftriaxone though

70
Q

What drug of the cephalosporin class is good against S. pneumoniae?

A

1st generation cephalosporins are not good against it (all other streptococci they are fine against)

ceftriaxone is the drug of choice for CAP because of this coverage

71
Q

What is a common saying for Clindamycin / Metronidazole?

A

Clindamycin above the diaphragm, metronidazole below

Clindamycin is good at treating Bacteriodetes and anaerobic species from mouth anaerobes leading to aspiration pneumonia

Metronidazole is good at treating anaerobic species in the gut and pelvis (C. difficile, Trichomonas)

72
Q

What is the drug of choice for enterococccal endocarditis?

A

Ampicillin 4 weeks, gentamacin can be added

If amp-resistant, 6 weeks Vanco

Do at least 8 weeks if VRE (use daptomycin)

73
Q

What is the empiric therapy for infected diabetic foot ulcers?

A

Initially IV therapy with vancomycin +/- ceftriaxone to cover gram negative in case of deep tissue infiltration

DONT WAIT FOR ULCER TO FULLY HEAL TO STOP

74
Q

What are three major virulence factors of S. pneumoniae?

A
  1. Polysaccharide capsule - primary, avoids complement-mediated phagocytosis and lysis
  2. Pneumolysin, a membrane-damaging cytolysin related to SLO of S. pyogenes
  3. Cell wall teichoic acid / peptidoglycan promote inflammation
75
Q

What are two other names for S. pneumoniae?

A

Pneumococcus or diplococcus (gram positive diplococci)

Same morphology as group B strep

76
Q

What are the three primary virulence factors of P. aeruginosa?

A
  1. Exotoxin A
  2. Elastase
  3. Adhesin
77
Q

What does elastase do? How does it relate to eye pathology?

A

Cleaves elastin and human Igs, collagen, and complement

It is the primary cause of corneal perforation in eye infection

78
Q

What is the Quellung reaction?

A

One of the biochemical tests (other than capsular serotyping and P disk susceptibility testing) to test for P. pneumoniae

It checks if there is capsular swelling on addition of anti-capsule antibodies

79
Q

What biochemical test is diagnosis of P. aeruginosa?

A

High levels of cytochrome oxidase -> positive oxidase test

80
Q

What are the two stages of Chlamydia trachomatis?

A
  1. Elementary body - infectious, expresses adhesins

2. Reticulate body - replicative, intracellular

81
Q

What is inclusion conjunctivitis?

A

Chlamydia eye infection of the neonate from direct contact with cervical secretions during delivery. (perinatal)

Marked by acute, mucopurulent discharge ~7 days post-partum

82
Q

What is chronic follicular conjuncitivitis also called and who does it typically affect?

A

Trachoma - typically chronically infects people in the developing world of lower SES

Can cause blindness if complicated by trichiasis

83
Q

What is seen on retinoscopy for Candida enophthalmitis?

A

Following injury, a white cotton ball expanding on retina or floating in vitreous humor

84
Q

How are humans typically infected via histoplasma?

A

Inhalation of infectious conidia while handling bird (i.e.. chicken) or bat droppings

85
Q

What are the two forms of Acanthamoeba species?

A
  1. Trophozoites - free-living and tissue-invading

2. Cysts - infectious stage, often get in following mild corneal trauma and improper contact lens sterilization

86
Q

What is the primary virulence factor of GBS and how does it work? How does it create pneumonia?

A

Polysaccharide capsule with sialic acid moiety on terminal sugar, limiting C3b deposition and decreasing phagocytosis

Has a beta-hemolysin as well which injures lung epithelial cells and helps it penetrate BBB (E. coli K1 uses invasins)

87
Q

How is E. coli K1 meningitis contracted?

A

Via low BW and pre-term babies (GBS meningitis contracted via same group + in moms with no IgG against GBS capsule)

88
Q

What will Listeria most likely cause if contracted perinatally?

A

Septicemia + meningitis (third leading cause as a neonate)

Treat with IV Ampicillin

89
Q

What do infants born with T. gondii often show? (if not aborted or stillbirthed)

A

Microcephaly, hydrocephaly, psychomotor disturbances, and convulsions (CNS involvement)

90
Q

What forms are the Hep A and Hep B vaccines?

A

Hep A - inactivated, given around 12 months

Hep B - given to all high risk adults as recombinant surface antigen (subcellular)

91
Q

What is Pneumovax?

Prevnar13?

A

Pneumococcal vaccine, conjugated vaccine covering 23 pneumococcal capsular types

Recommended in adults >65 yo and high risk individuals >2 yo

Prevnar13: 13 types, recommended in all children <5

92
Q

What does Rotavirus cause? When should you get the vaccine?

A

Severe acute gastroenteritis

Recommended between ages 2-6 months

93
Q

What is the meningococcal vaccine?

A

Vaccine with capsular polysaccharides A, C, Y, and W-135. B was not immunized previously (due to sialic acid autoimmune risk) but is now

Immuno mikro eng (56 decks)

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