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Micro 1 Flashcards

0
Q

What organisms naturally colonize the large intestine?

A

Anaerobes - bacteroides (10^11 /g fecal mater)

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1
Q

What organisms naturally colonize the skin?

A

Yeast and gram + organisms

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2
Q

What organisms naturally colonize the mouth?

A

anaerobes - density sim to lg. intestine

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3
Q

What organisms colonize the nose and pharynx?

A

Gram + and - cocci (Neisseriae and Moraxella)
Gram + rods (Corynebacterium)

The rest of the respiratory tract is sterile

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4
Q

What organisms normally colonize the urogenital tract?

A

Urethra - transiently colonized
Vagina - changes w/ age: gram + cocci (staph, strep) before puberty; Lactobacillus Acidophilus after puberty (reduces pH and maintains uniform flora)

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5
Q

What is the procedure for gram staining?

A 
Heat fix
Crystal Violet - then rinse
Iodine - then rinse
Acetone or Isopropyl alcohol - then rinse
Safranin - rinse then dry
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6
Q

What is the mechanism of Gram staining?

A

Iodine - crystal violet complex is too large to wash out of gram +

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7
Q

Describe acid fast bacteria

A

Mycobacterium (TB)
Cell walls contain long chain fatty (mycolic) acids, do not gram stain well.
Stain w/ carbol fuchsin, decolorize w/ 3% HCl and ETOH - acid fast will remain red

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8
Q

What is lipoteichoic acid and where is it found?

A

Part of gram + cell wall - strengthens

Endotoxin - can evoke immune response from humans

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9
Q

Where are gram - toxins housed?

A

Periplasmic space - between inner cell membrane and peptidoglycan cell wall
ex: cholera toxin

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10
Q

Cell wall components

A

Disaccharide-pentapeptide subunits
N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM)
Peptide bridges between NAM cross link subunits (determine thickness of wall)
Gram +: pentaglycine links D-ala and lysine
Gram -: direct link between D-ala and diaminopimelic acid

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11
Q

What is mycolic acid?

A

Component of Acid Fast Bacteria cell wall

resistant to phagocyte killing and drying

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12
Q

What are components of gram - outer membrane?

A

Lipopolysaccharides (LPS) and phospholipids
LPS: virulence factor (endotoxin), mediates inflammation, septic shock
LPS composed of
-O antigen: repeating sugars - used for typing bacteria
-core sugars
-fatty acid moieties - bioactive portion of LPS

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13
Q

What is a bacterial capsule?

A

Both Gram + and - bacteria
High MW polysaccharides or amino acids
production depends on enviro and growth conditions
Virulence factor
Protection from complement mediated killing

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14
Q

What are pili and what are they made of?

A

proteinaceous structures extending from cell membrane
made of pilin, tipped w/ adhesins which bind host tissue (receptors) - virulence factor- antigenic
1. common type: mediate adhesion to host eukaryotic cells
2. sex type: join conjugating bacteria

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15
Q

What are flagella made of? Are they antigenic?

A

Flagellin

highly antigenic - H antigen

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16
Q

3 spore forming bacteria and assoc. diseases

A

clostridium tetani - tetanus
bacillus anthracis - anthrax
clostridium botulinum - botulism

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17
Q

How do Beta-Lactams work?

A

Inhibit final step of cell wall synthesis - transpeptidation by Penicillin Binding Proteins (PBPs)

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18
Q

What is the mechanism of penicillinase resistance in resistant penicillins?

A

Bulky side chains - sterically hinder B-lactamase binding

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19
Q

What coverage do beta-lactam / beta-lactamase inhibitor combo drugs offer?

A 
Improved gram (-) and anaerobe
MSSA
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20
Q

What classes of bacteria are highly resistant to pecinillins?

A

aerobic gram - bacilli

anaerobes

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21
Q

What are beta-lactamase inhibitors?

A

Suicide inhibitors

Bind beta-lactamase -> inactive compound

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22
Q

What are common side-effects of Penicillin drugs?

A

Allergic reaction - from a rash to anaphylaxis
-may be due to B-lactam ring or to side chains

Acute Interstitial Nephritis - allergic rxn in kidney

  • fever, rash, eosinophilia
  • non-oliguric renal failure, may progress to anuria and kidney failure
  • eosinophilic cells and tubular damage seen on biopsy
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23
Q

Probenecid

A

Gout medication given to prolong effect of Penecillin - blocks renal elimination
Used for persistent infections - syphillis

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24
Q

What do cephalosporins NOT have activity against?

A

Enterococcus

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25
Q

What drugs would most likely be used to treat community acquired intra-abdominal infections or for surgical prophylaxis?

A

2nd gen cephalosporins - cephamycins

Cefotetan or Cefoxitin

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26
Q

What is the drug of choice for community acquired pneumonia (s.pneumo)?

A

Cephtriaxone - 3rd gen cephalosporin

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27
Q

What are the SPICE organisms?

A

Serratia, Providencia, Indole (+) Proteus, Citrobacter, Enterobacter

  • all have B-lactamase
  • lab may say susceptible to 3rd gen Cephalosporin, but use may select resistant strain
  • usually use cefepime or carbapenems
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28
Q

What cephalosporins have activity against anaerobic bacteria?

A

Cefotetan, Cefoxitin - 2nd gen (2B or GI) cephamycins

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29
Q

Ceftaroline

A

Advanced generation cephalosporin
Binds PBP2A and 2X
MRSA - first B-lactam w/ activity against.
Gram (-) activity between 2nd and 3rd gen

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30
Q

Cephalosporin / Penicillin cross-reactivity

A

Chance of those w/ penicillin allergy having allergy to cephalosporin
5-15% according to book, actually much lower (0-2%)
-may be due to lactam ring (unlikely) or side chains
–Ceftazadime and Aztreonam: identical side chains. Az billed as having no x-reactivity w/ Penicillins. If Cef allergic, probably Az allergic

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31
Q

What organisms are most commonly associated with ESBL?

A

ESBL - extended spectrum beta-lactamase
E.coli K.pneumoniae
Carbapenem is drug of choice

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32
Q

B-lactams and renal dosing

A

Almost all renally eliminated and need renal dosing adjustments
exceptions:
-Ceftriaxone
-Penicillinase resistant Penicillins

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33
Q

1st generation cephalosporins and what used for

A

Cephalexin, Cefazolin, Cefadroxil
Skin, lower UTI
Good gram +, Staph, MSSA, Strep (variable S.pneumoniae)
Bad gram -, no anaerobic activity
Not for use in neonates - bind Ca++ -> gallstones, biliary sludging

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34
Q

2nd Generation cephalosporins and what for

A

2A: Cephlacor, Cefuroxime - Respiratory infections
good gram(+), better S.pneumoniae,
2B: Cefotetan, Cefoxitin - cephamycins - GI infections excellent for anaerobes
community acquired intra-abdominal infections and surgical prophylaxis.

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35
Q

3rd generation cephalosporins and what used for

A

Ceftriaxone(IV), Cefotaxime, Cefixime, cefpodoxime(PO)
Ceftriaxone - DOC for CAP, DOC for CAM unless B-lactone resistant
Ceftazadime - Pseudomonas aeruginosa (PSA)
Excellent nosocomial gram(-)
Not great staph - quesionable MSSA
No PSA, no anaerobes
SPICE organisms - tendency to induce resistance

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36
Q

4th generation cephalosporins and what used for

A 
Cefepime
Good gram (+):  Strep, staph, MSSA
Good gram (-):  excellent against nosocomial infections
SPICE organsism (Serratia, Providencia, indole (+) proteus, citrobacter, enterobacter)
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37
Q

Advanced generation cephalosporin and what used for

A

Ceftaroline
Binds PBP2A and PBP2X
MRSA coverage
better S.pneumoniae, ampicillin-sensitive E.faecalis
Gram(-) is between 2nd and 3rd gen. ability

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38
Q

What is ESBL and what are most common organisms encountered?

A

Extended Spectrum Beta-Lactamase
E.coli and K.pneumoniae - can be transferred to other enterobacteria
Renders resistance to all penicillins, cephalosporins and aztreonam
Carbapenems are DOC**

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39
Q

What are the carbapenems and what do they cover?

A 
group 1:  Ertapenem - DOC for ESBL organisms
good gram (+)
great gram (-) except APE:  acinetobacter, PSA, enterobacter

group 2: Imipenem, Meropenem, Doripenem
good gram (+)
great gram (-): ESBL, PSA, A.Baumanii (decreasing effectiveness)
anaerobes: excellent, but no c.diff
in general - used for multi-drug resistant organisms*

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40
Q

What do carbapenems not cover?

A 
MRSA
ampicillin resistant enterobacteria
stenotrophomonasmaltophilia
KPC (carbapenemase)
C.diff (can cause c.diff)
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41
Q

What is the biggest side effect of carbapenems?

A 
Seizures 
Not likely, though.
Prob related to cilastatin (added to increase half-life)
More likely w/ high dose.
Cross-reactivity w/ penicillins 1-50%
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42
Q

Aztreonam

A

Used for empiric treatment of gram (-) organisms in patients w/ Penicillin allergy
PSA activity, but not great
No ESBL, no x-reactivity w/ penicillins

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43
Q

What drugs are useful against Acinetobacter baumannii?

A

DOC: ampicillin/sulbactam - given for sulbactam alone

Imipenem, Meropenem, Doripenem - decreasing effectiveness

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44
Q

How do aminoglycosides work?

A

Bind 30s ribosomal subunit - inhibit protein synthesis
BacterioCIDAL, concentration dependent killing (high dose preferred)
Oxygen dependent transport - so no activity vs. anaerobes
Note: no oral absorption, high conc. in urine - good for UTI

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45
Q

What are the individual aminoglycosides and what are they used for?

A

Gentamycin: staph and enterococcus in comb. w/ B-lactam
-also eye ointment
Tobramycin / Amikacin: Empiric nosocomial (double coverage)
-sometimes definitive as well. Ami: mycobacterial
Neomycin: Oral - GI decontam pre-op. Topical - neosporin
Streptomycin: enterococcal infection when gentamycin resistant.
-mycobacterial infection

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46
Q

Mechanisms of aminoglycoside resistance

A
  1. Addition of side chains by Transferase enzymes - prevent drug binding
  2. 30s modification
  3. Efflux pumps / decreased porin production -> decreased intracellular concentration
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47
Q

Aminoglycoside adverse events

A

Nephrotoxicity - most common. Minimize trough concentrations
Vestibular/ Ototoxicity - assoc. w/ total drug exposure (irreversible)
Neuromuscular Blockade - additive w/ other drugs (myasthenia gravis)

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48
Q

What are the floroquinalone drugs and what are they used for?

A

Moxifloxacin, Levofloxacin, Ciprofloxacin, Gemifloxacin and Norfloxacin
Respiratory: Levo and Moxi: Excellent against all CAP
PSA: Cipro and Levo: also enteric gram (-)
Anaerobes: Moxi (some B.fragilis activity)

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49
Q

Floroquinolone side effects

A

CNS toxicity: headache, dizziness, insomnia, seizures
Damage to growing cartilage: no use w/ peds
Dysglycemia
Cardiac arrhythmia / torsades (min risk unless prone to arr. or on QT prolonging drugs - Moxi highest risk

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50
Q

What drug interactions are floroquinalones prone to

A

Chelation effect: Reduced absorption when taken w/ divalent cations (Ca++, Mg++, Fe++)

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51
Q

What is Red Man Syndrome?

A

Histamine response to rapid infusion of vancomycin - not a true allergic reaction
non-specific mast cell degranulation

infusion should not exceed 1g/hr. pretreatment w/ diphenhydramine

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52
Q

What are the treatment options for VRE?

A

Linezolid
Daptomycin
Quinupristin / dalfopristin (E. faecium only)
Tigecyclin (other tetracyclines maybe)

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53
Q

What is the mechanism of Vancomycin resistance in Enterococci and Staph A?

A

D-ala D-ala becomes D-ala D-lac or D-ser

Vancomycin can’t bind

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54
Q

What is the “erm” gene?

A

Confers MLS resistance to S.aureus (Macroside, Lincosamide, Streptogramin)
- all 3 work at same ribosome site
If isolate says erythromycin resistant and clindamycin susceptible
D test to check for MLS before using clindamycin

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55
Q

How do you deal with yeast in the blood?

A 
Confirm not at risk for Cryptococcus (immunosuppressed, HIV)
Is almost always Candida
-Albicans > Glabrata
Risk for fluconazole resistance?
-recent exposure or known colonizer of C.glabrata
Critically ill?
Yes -> Echinocandin
No -> Fluconazole
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56
Q

What mechanisms do microorganisms employ to avoid ciliary action of the respiratory system?

A

Development of strong adhesins
-Rhinovirus: capsid protein attaches to ICAM-1
-Mycoplasma pneumonia attaches to neuraminic acid on host respiratory epithelium
Paralysis of ciliary action
-Bordatella pertussis - tracheal cytotoxin
-Influenza virus -> ciliated cell disfunction

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57
Q

What organisms are most associated with skin infections?

A

S. aureus

S. pyogenes

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58
Q

What is impetigo?

A

Skin infection commonly caused by S.aureus or S.pyogenes
More common in children
Intraepithelial vesicles w/ surrounding erythema - weeping yellow crusty lesions.
Patients irritable, uncomfortable, afebrile
S.pyogenes infections can lead to glomerulonephritis

59
Q

What is Erysipelas?

A

Skin infection usually caused by Streptococcus pyogenes - involves epidermis and dermis
Bright red, inflamed w/ sharp borders, painful. Usually face and lower limbs. Patients often febrile

60
Q

What is cellulitis?

A

Skin infection usually caused by S.aureus involving epidermis, dermis, and subcutaneous tissue
Patients often febrile, involved skin is edematous, erythmatous, warm, tender, and painful with bullae common. Ecchymosis

61
Q

What is a carbuncle?

A

Multiple furuncles in a confined area forming a large confluent, suppurative infection.
Patients are often acutely ill and require surgery and systemic antibiotics

62
Q

What organisms are involved in fasciitis and myonecrosis?

A

Strep pyogenes, Staph aureus, Vibrio vulnificus (if seawater exposure), Clostridia (gas gangrene)

63
Q

What causes Scarlet Fever?

A

Strep pyogenes - primary infection in pharynx - sore throat
Streptococcal pyrogenic exotoxins produced
strawberry tongue, diffuse rough red rash, desquamation of skin on recovery

64
Q

What is the cause of Toxic Shock Syndrome?

A

S. aureus produces TSST-1 (toxin) during infection on minor skin wound, female genital tract (tampon), post-influenza pneumonia.
Hematogenous spread of toxin -> very high fever, hypotension, multi-organ damage, diffuse erythmatous rash

65
Q

What usually causes hot tub folliculitis?

A

Psuedomonas infect dilated pores in under-chlorinated hot tub.

66
Q

What organism is associated with animal bites?

A

Pasturella multocida

Penicillin works well.

67
Q

What causes Whitlow?

A

Herpes symplex virus - finger infection assoc. with healthcare workers, esp. dentists.

68
Q

What organism causes gangrene?

A

Clostridium spp

69
Q

Cowdry Type A nuclear Inclusion - suggestive of what?

A

Herpes Symplex Virus - if seen in a cervical smear
or
Cytomegalovirus - if seen in respiratory cell

70
Q

binucleate epithelial cells with perinuclear halo is suggestive of what?

A

papilloma virus

71
Q

Staphylococcus virulence factors

A

alpha toxin: Complement like pore forming cytolysin - kills erythrocytes and leukocytes.
TSST-1: exotoxin. super-antigen cross-links Tcell receptor to MHC class II of host -> cytokine release.
Exfoliative toxins (scalded skin syndrome): intercellular splitting at desmosome
Exoproteins - allow spreading: hyaluronidase (hydrolyzes CT) staphylokinase (fibrinolysis)
Antiphagocytics: Protein A (binds Fc), Coagulase (surface polymerization of fibrin - resist phagocytosis), Catalase (resist H2O2)

72
Q

What is quorum sensing?

A

Alteration of gene expression according to density of local cell population
Staph a.
- upreg. coagulase at low cell density - colonization
- upreg. staphylokinase at high density - spread

73
Q

Scalded skin syndrome

A

Caused by staph a. exfoliative toxin in neonates and children.
Bullous impetigo is localized SSS

74
Q

Staph aureus identification

A 
gram + cocci in clusters
positive catalase (diff. from strep)
positive coagulase (diff staph epidermidis and staph saprophyticus)
75
Q

Virulence factors of strep pyogenes

A

M protein: mediates binding to epidermis. anti-phagocytic. variable. cross-reactive Ab -> glomerulonephritis
Protein F: adhesin - mediates fibronectin binding at wound site
Streptolysins O and S - cause B- hemolysis on blood agar
SLO: oxygen labile, sulfhydryl activated cytolysin. Antibodies against -> self immunity
Streptococcal pyrogenic exotoxins (Spe A-C): Superantigens
-Spe A produced by bacteriophage carrying Grp. A Strep
-induce cytokine release -> fever, rash, Tcell stim, endotoxin sensitivity -TSST like
Hydrolytic enzymes - responsible for thin runny pus
streptokinase dissolves fibrin,

76
Q

What is post-streptococcal glomerulonephritis?

A

Caused by cross-reaction with M-protein
-M-protein / Ab immune complexes deposit in glomerulus
Edema, hypertension, hematuria, proteinurina about 3 weeks post-infection
Rare in US. More in developing countries

77
Q

What causes Toxic Shock-like syndrome?

A

Group A strep
Streptococcal pyrogenic exotoxin A is responsible - SUPERANTIGEN
Fever, hypotension, rash, renal impairment, respiratory failure, diarrhea

78
Q

Streptococcus pyogenes identification

A 
gram + cocci in chains
B-hemolytic on blood agar (SLO, SLS)
Pyogenic
Catalase negative
Lancefield group A antigen
79
Q

What is propionibacterium?

A

Causes acne
predominant anaerobe of normal skin flora
breaks down lipids in sebum
Acne vulgaris - inflammation of hair follicle associated with sebaceous glands
keratin + sebum + bacteria -> blackhead
can cause infections in severely immunocompromised
endocarditis, contam prosthetic valves, cerebrospinal shunts
can contam blood cultures - must diff. from true pathogen

80
Q

Pasteurella multocida

A

animal bite bacteria

gram - rod

81
Q

Clostridium perfringens

A

Gram + rod, anaerobic, spore producing

gas gangrene

82
Q

Clostridium Tetani

A

Gram + rod, spore producing, anaerobic

Tetanus

83
Q

What is indicated by chronic candidiasis

A

Tcell deficiency

84
Q

Sporothrix shenckii

A

Causes sporotrichosis - subQ infection

Fungal infection after thorn prick or gardening injury - causes pyogenic and granulomatous reaction

85
Q

What are Dermatophytes?

A

Fungi that commonly infect skin -> tinea
-epidermophyton, trichophyton, microsporum
->ringworm, athlete’s foot, jock itch
Invasion of nail bed -> malformed growth

86
Q

What are the alphaherpesviruses?

A

HSV1,2 and Varicella-Zoster Virus

87
Q

What are the betaherpesviruses?

A

Human Herpes Virus 6 (A and B),7 and Cytomegalovirus

88
Q

What are the gammaherpesviruses?

A

Epstein-Barr Virus, Human Herpes Virus 8 (Karposi’s Sarcoma assoc. Herpesvirus)

89
Q

What is the structure of Herpes Symplex Virus?

A 
Large encapsulated (icosahedral) DNA virus (dsDNA)
152k BPs, 70-80 genes
90
Q

3 phases of viral gene expression

A

Immediate gene expression : adapt cell for virus replication
Early gene expression: vDNA replication
Late gene expresson: structural proteins

91
Q

What do antiherpes virus drugs require for activation? What is method of action?

A

Phosphorylation by virus encoded thymodine kinase
acyclovir -> acyclovir monophosphate
cellular kinases -> acyclovir triphosphate -> inhibition of virus encoded DNA polymerase
- triphosphorylated drug embeds in viral DNA acting as chain terminators.

92
Q

Where are latent VZV infections established?

A

Dorsal Root Ganglion

93
Q

What cells are infected by beta herpesviruses?

A

HHV 6A and B: Tcell tropic. Also monocytes and macrophages

Cytomegalovirus: myeloid cells.

94
Q

Exanthm subitem

A

Roseola - common childhood infection
Caused by HHV 6B, sometimes 7.
Fever and rash on trunk and face spreading to legs.
Complications: fever >40C, neurological involvement - seizures, aseptic meningitis, hepatitis, mono-like symptoms

95
Q

What disease is HHV 8 associated with?

A

Kaposi’s sarcoma

usually older men of mediterranean ancestry and HIV patients

96
Q

Papillomavirus morphology

A 
Non-enveloped icosahedral - small
circular dsDNA (8-10 genes)
97
Q

HPV-16 transforming genes and major capsular protein

A

E6: p53 tumor suppressor protein destruction
E7: Inactivation of Rb tumor suppressor protein

L1 protein: major surface marker - target for antiviral Ab and component of Gardasil HPV vaccine

98
Q

What HPV viruses are most closely associated with cervical cancer?

A

HPV 16 and 18

-relatively uncommon

99
Q

2 HPV vaccines and approved ages for admin.

A

Gardasil - age 9 - 26 (types 6,11, 16, 18)

Cervarix - age 10-15 (types 16, 18)

100
Q

Picornaviurs - description and example

A

Small, non-enveloped, single strand +RNA
Coxsackievirus: tends to occur in outbreaks
-hand, foot and mouth
-most common source of aseptic meningitis

101
Q

What is coxsackie virus?

A

Picornavirus
Prone to occur in outbreaks - most common in infants and children
Hand food and mouth disease, aseptic meningitis
- fever, sore throat, headache, anorexia
- vomiting and convulsions - usually in children
- w/in 2 days - lesions of mouth, tonsils, soft palate
- healing in 1-5 days
faster resolution than HSV

102
Q

Necotizing fasciitis is most commonly associated with what organism?

A

S.pyogenes

also - CA-MRSA (does not respond to methacillin or cefazolin normally given for skin infections)

103
Q

In presentation of scalded skin syndrome there is the presence of large vessicles or bullae. What organism is likely? What is less likely?

A

More likely: S.aureus

Less likely: S. pyogenes

104
Q

If a person develops blistering dermatitis after swimming in the ocean, what organism would be of concern?

A

Vibrio

  • also assoc. w/ raw or undercooked oysters
  • high mortality rate
105
Q

What is the treatment for impetigo?

A

Topical abx (mupirocin) or oral abx

106
Q

What is dermatitis/arthritis syndrome?

A

Dermatitic lesions with accompanying joint pain

  • in sexually active young adult - Think Neisseria gonorrhoeae
  • spreads through lymph and blood
107
Q

What antibacterials are known for false elevation of creatinine, elevated INR (w/ warfarin), and hyperkalemia?

A

Sulfamethoxazole
Trimethoprim - hyperkalemia

SMX/TMP = Bactrim

108
Q

How is Viridians Strep identified?

A

Blood culture
Gram +
Lacks lancefield group and any specific surface markers
Biochemical testing for definitive identification

109
Q

How are Group D strep and enterococci clinically identified?

A

Blood culture
Gram +, catalase -
Serologic test for group D antigen
Enterococci grow in 6.5% NaCl, hydrolyze esculin in 40% bile

110
Q

How is candida identified in the lab in the setting of a systemic or blood stream infection?

A

Blood culture

KOH or Gram stain - budding round oval yeast cells w/ hyphae

111
Q

How is aspergillus identified in the setting of a systemic or bloodstream infection?

A

Blood culture returned negative
Biopsy of infected tissue
Aspergillus cultured in lab - branched septate hyphae

112
Q

Describe the plasmodium lifecycle

A

Anopheles mosquito bites host
Sporozoite -> blood -> Liver - form schizont - asexual reproduction -> merozoite -> blood
Merozoite enters RBC: Trophozoite -> schizont -> merozoite -> cell ruptures
Some cells for gametocytes -> mosquito for sexual reprod.

113
Q

What is a hypnozoite?

A

Dormant form of Plasmodium

  • P.vivax, P.ovale only
  • responsible for long term relapses.
114
Q

What are the erythrocyte receptors for P.vivax and P.falciparum?

A

P.vivax: Duffy receptor on reticulocyte

P.falciparum: glycophorin A on all red cell types.

115
Q

How is malarial fever induced?

A

Produced by asexual blood schizont. RBC ruptures -> release of:
-malarial metabolites, hemozoin (from hemoglobin): pyrogenic, antigenic,
-cytokines: IL-1, TNF
Fever is initially sporadic, then cyclical corresponding w/ parasitic replication cycles (48-72 hour bouts)

116
Q

What is the effect of HbS on the spleen?

A

Person can become functionally asplenic -> increased susceptibility to encapsulated bacteria

117
Q

What provides natural resistance to malaria?

A

Lack of Duffy receptor (P.vivax)
HbS heterozygous
HbC
- cells prevent parasite from rearranging actin to form adhesin -> decreased ‘stickiness’ of infected erythrocyte.

118
Q

How are plasmodia organisms identified in clinical practice?

A 
Blood smears
-thick smear:  diagnose parasitemia
-thin smear: identify Plasmodia species
ELISA:  Ab detection
gene probes, PCR for P.falciparum
119
Q

How is Babesia microti spread?

A

Tick-bourne.

1-4 week incubation. Usually flu-like: Fever, myalgia, hepatosplenomegaly, hemolytic anemia,renal dysfunction
Spontaneous resolution in a few weeks.
Can be life threatening in asplenic patients.

120
Q

What organism is the main cause of eye infections?

A

S. aureus

121
Q

Infection of eyelid margin / sebaceous gland

A

Blepharitis

122
Q

Inflamation of lacrimal sac

A

Dacrocystitis

123
Q

Infection of aqueous or vitreous humor

A

Endophthalmitis

Requires ulceration or penetrating injury to compromise cornea and sclera

124
Q

How is S.pneumoniae identified clinically?

A

Gram stain: gram +, lancet shaped diplococci
No Lancefield grouping
Capsular serotyping
Quelling reaction - anti-capsule Ab -> capsular swelling
Optochin (P disk) susceptibility

125
Q

Hib vaccine

A

for Haemophilus influenzae b - most virulent strain

-given to infants (@2 mos) since 1990

126
Q

How is H.influenzae identified in a clinical setting?

A

Gram (-) rod - very small
Requires blood products for growth (grows on chocolate, but not blood agar)
Hematin (X factor) and/ or NAD (V factor) needed for growth

127
Q

How does Pseudomonas aeruginosa Exotoxin A work?

A

ADP-ribosylation of Elongation Factor 2
NAD + EF2 ADPribose-EF2 (inactive) + nicotinamide + H+
same activity as diphtheria toxin

Inactivates protein synthesis - promotes tissue invasion and evasion of immune response.

128
Q

What is the primary cause of corneal penetration in a Pseudomonal eye infection?

A

Elastase

protease works on elastin, IgG, IgA, collagen, complement

129
Q

How is pseudomonas identified in a clinical setting?

A

Gram - rod, motile on wet mount
Mostly aerobic, but facultative anaerobe
Fruity odor on solid media
Blue-green fluorescence under UV light (phyocyanin, pyoverdin)
High levels of cytochrome oxidase - pos. oxidase test

130
Q

Trachoma

A

caused by Chlamydia trachomatis - chronic follicular conjunctivitis
Usually passed mother - child, mostly in less developed african/asian countries
Trichiasis - inward growth of eyelashes - corneal scraping
Recurrent infection, roughening of inner eyelid, can produce blindness

131
Q

Diseases caused by Histoplasma capsulatum

A

Chorioretinitis - disseminated disease from primary respiratory infection
Presumed Ocular Histoplasmosis Syndrome - small areas of inflamation and scarring of retina - circular - if affects macula may produce blind spot

132
Q

How is Histoplasma capsulatum identified?

A

Very slow growth on blood agar or Sabouraud agar from blood culture
Usually via biopsy- culture and identify bimorphic fungus

133
Q

What is the drug of choice for Lyme disease?

A

Doxycycline

134
Q

What valve of the heart is most frequently involved in endocarditis?

A 
Mitral - L. side of heart:  more pressure -> more turbulence
M - 28-45%
Aortic - 5-36%
M&A combined - 0-35%
Tricuspid - 0-6%
Pulmonic - <1%
135
Q

What organisms are most frequently involved in bacterial endocarditis?

A

80% aerobic gram (+): S.viridians, S.aureus, enterococcus, etc.
20% unusual others: E.coli, yeast

136
Q

What is mycotic aneurism?

A

Aneurysm due to infection - complication of infective endocarditis.

  • occur at bifurcation points
  • bacteria from IE - direct invation, embolic occlusion, or immune complex deposition
137
Q

What are conjunctive petechiae?

A

Marker of acute endocarditis

small pieces of vegetation break off - embolize in small vessels of conjunctiva

138
Q

What are Osler’s Nodes and Janeway’s Lesions?

A

Both appear on hands and feet of individuals w/ infective endocarditis
Osler’s: caused by immune complex deposition -> inflamation / necrosis. Painful.
Janeway: caused by septic emboli - microembolism - flat, necrotic, painless.

139
Q

What abnormal lab results are associated with infective endocarditis?

A

Anemia - 70-90%
Thrombocytopenia - 5-15%
Leukocytosis - may be absent
Elevated sedimentation rate -almost always (70-90%)

140
Q

How are blood cultures ordered in the setting of suspected infective endocarditis?

A

3 sets over the course of 24 hours - each a separate venopuncture

141
Q

What is HACEK group endocarditis?

A

infective endocarditis caused by: Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominus, Eikinella corrodens, Kingella kingae

Sub-acute course. Fastidious - req. 2-3 weeks to grow.
If suspected, give lab special instructions - suppliment media and hold cultures longer

142
Q

What is the most common cause of osteomyelitis?

A

S. Aureus

143
Q

What is the preferred therapy for an animal bite? IV and PO

What about penicillin allergic patient?

A

IV: ticarcillin / clavulanic acid
PO: Amoxicillin/clavulanic acid

Penicillin allergic: Doxycycline, Moxifloxacin

144
Q

What is the treatment for bone/joint pseudomonal infection. How long?

A 
IV B-lactam, 4 weeks joint, 6 weeks bone
Use Aminoglycoside (G,T, A) or FQ (Cip, Lev) for 2 weeks

M2 (19 decks)

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