Midterm 2 Flashcards

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1
Q

Bacteriuria

A

Presence of bacteria in urine
Does not necessarily imply infection
Do not treat if asymptomatic (except maybe in case of pregnancy or invasive urinary tract procedure)

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2
Q

Three most common signs of cystitis (bladder UTI)

A

Dysuria, increased frequency of urination, and increased urgency of urination

Also absence of systemic symptoms (eg no fever)

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3
Q

Conditions that mimic/mask cystitis

A

Urethritis (eg chlamydia or gonnorhea infection), vulvitis (eg HSV infection), vaginitis/bacterial vaginosis

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4
Q

Cystitis

A

UTI confined to bladder

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5
Q

Pyelonephritis

A

More invasive UTI (upper tract)
Inflammation of kidney and renal pelvis
More symptomatic symptoms, like fever, flank pain, nausea, chills, malaise, headache

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6
Q

Prostatitis

A

Inflammation/infection of prostate gland

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7
Q

Intrarenal abscess/perinephric abscess

A

Collection of pus in kidney or in the soft tissue surrounding the kidney

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8
Q

Things that would make a UTI “Uncomplicated”

A

Non-pregnant premenopausal woman of childbearing age, not chronic, no comorbidities, lower tract

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9
Q

Things that would make a UTI “Complicated”

A

Pregnant person, elderly person, male person, child, chronic, comorbid, upper tract

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10
Q

Two types of recurrent infection

A

Relapse: recurrence by same organism (may indicate therapy failure/resistance)

Re-infection: recurrence by different organism (may indicate abnormality increasing your susceptibility to infection)

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11
Q

UTI pathogenesis

A

Patients intestinal flora enter urinary tract via urethra
Catheter, nephrostomy tube, surgery, urinary stones make this more likely to happen
Organisms enter and persist in urinary tract

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12
Q

UTI risk factors

A

Aging (diabetes mellitus, urinary stasis, incontinence, impaired immmunity), urinary tract obstruction, impaired bladder innervation

Female: short urethra, sexual intercourse, contraceptives that alter normal flora, pregnancy (anatomy altered)
Males: prostatic hypertrophy, anal intercourse

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13
Q

UTI etiology

A

Usually a single pathogen
90% Enterobactales
70% E. Coli

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14
Q

E. Coli virulence factors

A

Adherence (P fimbria bind to P blood group antigen on uro-epithelial cells)
Hemolysins, Colicin V (resist complement-dependent serum bactericide)
K antigen (upper tract infection associated)
Type1 fimbria (interbacterial binding and biofilm formation)

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15
Q

Classical UTI pathogens

A

Proteus, Morganella, Providencia

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16
Q

Virulence factors of classical UTI pathogens

A

urease producing: increase urine pH, lead to crystal/stone formation, promotes biofilm formation
Highly motile
Fimbria for attachment

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17
Q

Staphylococcus saprophyticus

A

Uropathogen typically associated with younger, sexually active females, responsible for 1-5% of cystitis, identified by resistance to novobiocin
Also coagulase negative

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18
Q

Dipstick urinalysis

A

Detect nitrites (specific) and leukocytes (sensitive) —> indicators of infection

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19
Q

Urine culture

A
SBA/MacConkey agar/chromogenic agar
Commonly contaminated during collection therefore threshold for significant organism presence = 10^5 bacteria/mL (10^8/L)
# bacteria = # colonies X dilution factor
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20
Q

Urine clean catch mid stream specimen collection method

A

Most frequently used method

Urethra cleaned, first void urine allowed to pass to clear urethra, then mid-stream collected in sterile container

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21
Q

Collection bag for urine specimen collection

A

Used for children who lack bladder control, very often contaminated, most meaningful result is a negative culture

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22
Q

Urine specimen collection via indwelling catheter

A

Insert needle into catheter or through diaphragm to withdraw urine
Preferable to obtain from new catheter rather than old

23
Q

Urine specimen collection via cytoscope

A

Cytoscope is inserted into the bladder via urethra

24
Q

Urine specimen collection via subrapubic asperation/straight catheter

A

Most invasive
Specimen obtained directly from bladder
Low contamination risk therefore significance cutoff is much lower

25
Q

Urine specimen transport

A

Info needed: method and date/time of collection
Unrefridgerated: need to receive within 1-2 hours
Refridgerated: need to receive within 24 hours
If can’t get within 24 hours (e.g. lab far away), need to use Boric acid tube (maintains organism pliability but restricts growth

26
Q

Antimicrobials for uncomplicated cystitis

A
Nitrofurantoin
Fosfomycin
TMP/SMX (>24% resistance, not ideal)
Doxycycline (2nd line)
Ciproflaxin (3rd line, only if NO other oral options)
27
Q

Antimicrobials for pyelonephritis

A

Ciproflaxin (outpatient)

B-lactam + aminoglycoside (inpatient)

28
Q

MRSA

A

Staph aureus resistant to all beta lactams (usually also other drugs)
Hospital: hundreds of clonal groups, susceptible to vancomycin
Community: several clonal groups, generally susceptible to TMP/SMX, doxycycline, and clindamycin

29
Q

Mechanism of beta lactam resistance in MRSA

A
Production of novel PBP: PBP 2a, has reduced affinity for beta lactams but performs essential functions of PBPs
MecA gene (acquired through transposition, chromosomal)
30
Q

Detection of MRSA

A

Mueller-Hinton Agar + 4% NaCl (or sugar, something to increase osmotic stress) + 6ug/mL cefoxitin
Growth = Methicillin resistant

Chromogenic agar + 6ug/mL cefoxitin
Growth = methicillin resistant, purple colour = staph aureus (both = MRSA)

31
Q

How is CA-MRSA different from HA-MRSA?

A

More virulent than HA, but easier to treat than HA (resistant to fewer drugs)

32
Q

CA-MRSA clinical presentation

A
Boils or draining pimples
“Spider bites” or “bug bites”
Sores that won’t heal
Abscesses
Systemic infections (e.g. pneumonia, blood infections) - uncommon but serious
33
Q

Genetics of MRSA

A

MecA gene complex carried on staphylococcal cassette chromosome (SCC)
Five types of SCC-mec (I-V)
HA-MRSA = types I, II, or III SCC-mec, multidrug resistant
CA-MRSA = type IV SCC-mec, usually only resistant to beta lactams and erythromycin

34
Q

PVL toxin

A

Panton-Valentine lecocidin
Cytotoxin present in <5% of MRSA
Rare in HA-MRSA
Encoded by two genes, lukS-PV and lukF-PV
Destroys WBCs, causes severe tissue damage
Associated with necrotic skin lesions/severe necrotizing pneumonia

35
Q

VRE

A

Enterococci resistant to vancomycin

Intrinsic glycopeptide resistance

36
Q

Identifying enterococcus

A

Glucopyranoside positive and yellow pigment = E. casseliflavus
Glucopyranoside positive and no pigment = E. gallinarum
Glucopyranoside negative and ampicillin resistant = E faecium
Glucopyranoside negative and ampicillin sensitive = E. faecalis

37
Q

Vancomycin mechanism of action

A

Complexes with D-Ala-D-Ala to inhibit cell wall synthesis

38
Q

Mechanism of resistance in VRE

A

Change D-Ala to D-lac to prevent vancomycin binding

Rare, requires a full operon mutation (Van X, Van H, VanA ligase)

39
Q

VRE genotypes

A

VanA: high resistance to Vancomycin and Teicoplanin, common in E. faecium and faecalis (more faecium than faecalis though)
VanB: low to high resistance to vancomycin and susceptible to Teicoplanin, common in faecium and faecalis
VanC: low resistance to vancomycin, susceptible to Teicoplanin, common in E. gallinarum, casseliflavus, flavrscens

40
Q

ESBLs

A

Extended spectrum beta lactamases
Plasmid borne, inhibited by clavulinic acid
Activity against penicillins and 1st/2nd/3rd gen cephalosporins
Do not hydrolyze cephamycins or carbapenems
Most common in E. coli and Klebsiella spp.
Detection: >5mm difference between zone of inhibition of cetroaxin disc and cetroaxin+cavulinic acid disc = positive for ESBL

41
Q

AmpC beta lactamases

A

Inducible or de-repressed
Not inhibited by clavulinic acid
Chromosomal, but de-repressed ampC has mobilized on plasmids
Enterobacter spp., Citrobacter spp., K. Aerogenes, Serratia

42
Q

5 big carbapenemases

A

KPC, NDM (big threat), VIM, OXA-48, IMP

43
Q

Detection of carbapenemase production

A

Modified carbapenem inactivation method

  1. Incubate meropenem disc in broth
  2. Place disk on susceptible E. Coli culture, as well as dry disc
  3. Smaller/no inhibition zone = positive for carbapenemase production
44
Q

Pneumonia

A

inflammatory condition of the lung primarily affecting alveoli

45
Q

Signs and symtoms of pneumonia

A

Fever, cough (productive or dry), chest pain, shortness of breath

46
Q

S. pneumoniae

A

Most common bacterial RTI cause
Small gram positive diplococci, alpha hemoluytic, bile soluble, optochin S (other viridans strep are bile insoluble and optochin R), growth often enhanced in CO2 atmosphere, most are encapsulated

Colonizes the nasopharynx (throat swabs useless for diagnosis, need swab from lower tract for it to mean anything)

47
Q

S. Pneumoniae virulence factors

A

Most important is the capsule (aids in phagocytic escape, adherance and colonization)

Pneumolysin (hemolysin): destroys ciliated epithelial cells, activates classical complement pathway, suppresses oxidative burst by phagocytic cells

Secretory IgA protease

48
Q

Pneumovax

A

Pneumococcal vaccine
23 different serotypes account for 90% of invasive strains
Protection wanes with time and age
Indications: advanced age, splenectomy, HIV/AIDS, lymphoma, myeloma, alcoholism, diabetes

49
Q

PREVNAR

A

Conjugate vaccine for pneumococcus

Indicated for use in infants and adults

50
Q

Pneumonia treatment

A

Historically penicillin (now resistance), cephalosporins (most often), macrolides, fluroquinolones (severe disease), vancomycin

Amoxicillin is ok for mild-moderate disease

51
Q

Two most common pathogens associated with COPD

A

H. Influenzae = #1, S. Pneumoniae = #2

52
Q

COPD

A

Chronic obstructive pulmonary disease
Umbrella term for progressive lung diseases like emphysema, chronic bronchitis, refractory asthma, and some forms of bronchiectasis

Characterized by increasing breathlessness (main problem is breathing OUT, not in)

53
Q

H. Influenzae

A

Most common cause of AE-COPD
Small gram negatve bacilli
Requires X factor (Haem) and V factor (NAD) for growth
Will grow on chocolate agar (5% CO2)
May be encapsulated (meningitis risk)
Type b (Hib) responsible for most invasive disease (meningitis, epiglottitis), Hib vaccine has made this rare
Majority of mucosal disease due to non-encapsulated strains

54
Q

Treatment of RTI

A

Amoxicillin-clavulanate very effective (high dose)
Fluoroquinolones very active, but contraindicated in children
Newer macrolides reasonable activity
2nd/3rd gen cephalosporins effective