Flashcards in Micro 1 Deck (145):
What organisms naturally colonize the skin?
Yeast and gram + organisms
What organisms naturally colonize the large intestine?
Anaerobes - bacteroides (10^11 /g fecal mater)
What organisms naturally colonize the mouth?
anaerobes - density sim to lg. intestine
What organisms colonize the nose and pharynx?
Gram + and - cocci (Neisseriae and Moraxella)
Gram + rods (Corynebacterium)
The rest of the respiratory tract is sterile
What organisms normally colonize the urogenital tract?
Urethra - transiently colonized
Vagina - changes w/ age: gram + cocci (staph, strep) before puberty; Lactobacillus Acidophilus after puberty (reduces pH and maintains uniform flora)
What is the procedure for gram staining?
Crystal Violet - then rinse
Iodine - then rinse
Acetone or Isopropyl alcohol - then rinse
Safranin - rinse then dry
What is the mechanism of Gram staining?
Iodine - crystal violet complex is too large to wash out of gram +
Describe acid fast bacteria
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
What is lipoteichoic acid and where is it found?
Part of gram + cell wall - strengthens
Endotoxin - can evoke immune response from humans
Where are gram - toxins housed?
Periplasmic space - between inner cell membrane and peptidoglycan cell wall
ex: cholera toxin
Cell wall components
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
What is mycolic acid?
Component of Acid Fast Bacteria cell wall
resistant to phagocyte killing and drying
What are components of gram - outer membrane?
Lipopolysaccharides (LPS) and phospholipids
LPS: virulence factor (endotoxin), mediates inflammation, septic shock
LPS composed of
-O antigen: repeating sugars - used for typing bacteria
-fatty acid moieties - bioactive portion of LPS
What is a bacterial capsule?
Both Gram + and - bacteria
High MW polysaccharides or amino acids
production depends on enviro and growth conditions
Protection from complement mediated killing
What are pili and what are they made of?
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
What are flagella made of? Are they antigenic?
highly antigenic - H antigen
3 spore forming bacteria and assoc. diseases
clostridium tetani - tetanus
bacillus anthracis - anthrax
clostridium botulinum - botulism
How do Beta-Lactams work?
Inhibit final step of cell wall synthesis - transpeptidation by Penicillin Binding Proteins (PBPs)
What is the mechanism of penicillinase resistance in resistant penicillins?
Bulky side chains - sterically hinder B-lactamase binding
What coverage do beta-lactam / beta-lactamase inhibitor combo drugs offer?
Improved gram (-) and anaerobe
What classes of bacteria are highly resistant to pecinillins?
aerobic gram - bacilli
What are beta-lactamase inhibitors?
Bind beta-lactamase -> inactive compound
What are common side-effects of Penicillin drugs?
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
Gout medication given to prolong effect of Penecillin - blocks renal elimination
Used for persistent infections - syphillis
What do cephalosporins NOT have activity against?
What drugs would most likely be used to treat community acquired intra-abdominal infections or for surgical prophylaxis?
2nd gen cephalosporins - cephamycins
Cefotetan or Cefoxitin
What is the drug of choice for community acquired pneumonia (s.pneumo)?
Cephtriaxone - 3rd gen cephalosporin
What are the SPICE organisms?
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
What cephalosporins have activity against anaerobic bacteria?
Cefotetan, Cefoxitin - 2nd gen (2B or GI) cephamycins
Advanced generation cephalosporin
Binds PBP2A and 2X
MRSA - first B-lactam w/ activity against.
Gram (-) activity between 2nd and 3rd gen
Cephalosporin / Penicillin cross-reactivity
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
What organisms are most commonly associated with ESBL?
ESBL - extended spectrum beta-lactamase
Carbapenem is drug of choice
B-lactams and renal dosing
Almost all renally eliminated and need renal dosing adjustments
-Penicillinase resistant Penicillins
1st generation cephalosporins and what used for
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
2nd Generation cephalosporins and what for
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.
3rd generation cephalosporins and what used for
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
4th generation cephalosporins and what used for
Good gram (+): Strep, staph, MSSA
Good gram (-): excellent against nosocomial infections
SPICE organsism (Serratia, Providencia, indole (+) proteus, citrobacter, enterobacter)
Advanced generation cephalosporin and what used for
Binds PBP2A and PBP2X
better S.pneumoniae, ampicillin-sensitive E.faecalis
Gram(-) is between 2nd and 3rd gen. ability
What is ESBL and what are most common organisms encountered?
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*****
What are the carbapenems and what do they cover?
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***
What do carbapenems not cover?
ampicillin resistant enterobacteria
C.diff (can cause c.diff)
What is the biggest side effect of carbapenems?
Not likely, though.
Prob related to cilastatin (added to increase half-life)
More likely w/ high dose.
Cross-reactivity w/ penicillins 1-50%
Used for empiric treatment of gram (-) organisms in patients w/ Penicillin allergy
PSA activity, but not great
No ESBL, no x-reactivity w/ penicillins
What drugs are useful against Acinetobacter baumannii?
DOC: ampicillin/sulbactam - given for sulbactam alone
Imipenem, Meropenem, Doripenem - decreasing effectiveness
How do aminoglycosides work?
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
What are the individual aminoglycosides and what are they used for?
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.
Mechanisms of aminoglycoside resistance
1. Addition of side chains by Transferase enzymes - prevent drug binding
2. 30s modification
3. Efflux pumps / decreased porin production -> decreased intracellular concentration
Aminoglycoside adverse events
Nephrotoxicity - most common. Minimize trough concentrations
Vestibular/ Ototoxicity - assoc. w/ total drug exposure (irreversible)
Neuromuscular Blockade - additive w/ other drugs (myasthenia gravis)
What are the floroquinalone drugs and what are they used for?
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)
Floroquinolone side effects
CNS toxicity: headache, dizziness, insomnia, seizures
Damage to growing cartilage: no use w/ peds
Cardiac arrhythmia / torsades (min risk unless prone to arr. or on QT prolonging drugs - Moxi highest risk
What drug interactions are floroquinalones prone to
Chelation effect: Reduced absorption when taken w/ divalent cations (Ca++, Mg++, Fe++)
What is Red Man Syndrome?
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
What are the treatment options for VRE?
Quinupristin / dalfopristin (E. faecium only)
Tigecyclin (other tetracyclines maybe)
What is the mechanism of Vancomycin resistance in Enterococci and Staph A?
D-ala D-ala becomes D-ala D-lac or D-ser
Vancomycin can't bind
What is the "erm" gene?
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
How do you deal with yeast in the blood?
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
Yes -> Echinocandin
No -> Fluconazole
What mechanisms do microorganisms employ to avoid ciliary action of the respiratory system?
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
What organisms are most associated with skin infections?
What is impetigo?
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
What is Erysipelas?
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
What is cellulitis?
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
What is a carbuncle?
Multiple furuncles in a confined area forming a large confluent, suppurative infection.
Patients are often acutely ill and require surgery and systemic antibiotics
What organisms are involved in fasciitis and myonecrosis?
Strep pyogenes, Staph aureus, Vibrio vulnificus (if seawater exposure), Clostridia (gas gangrene)
What causes Scarlet Fever?
Strep pyogenes - primary infection in pharynx - sore throat
Streptococcal pyrogenic exotoxins produced
strawberry tongue, diffuse rough red rash, desquamation of skin on recovery
What is the cause of Toxic Shock Syndrome?
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
What usually causes hot tub folliculitis?
Psuedomonas infect dilated pores in under-chlorinated hot tub.
What organism is associated with animal bites?
Penicillin works well.
What causes Whitlow?
Herpes symplex virus - finger infection assoc. with healthcare workers, esp. dentists.
What organism causes gangrene?
Cowdry Type A nuclear Inclusion - suggestive of what?
Herpes Symplex Virus - if seen in a cervical smear
Cytomegalovirus - if seen in respiratory cell
binucleate epithelial cells with perinuclear halo is suggestive of what?
Staphylococcus virulence factors
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)
What is quorum sensing?
Alteration of gene expression according to density of local cell population
- upreg. coagulase at low cell density - colonization
- upreg. staphylokinase at high density - spread
Scalded skin syndrome
Caused by staph a. exfoliative toxin in neonates and children.
Bullous impetigo is localized SSS
Staph aureus identification
gram + cocci in clusters
positive catalase (diff. from strep)
positive coagulase (diff staph epidermidis and staph saprophyticus)
Virulence factors of strep pyogenes
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,
What is post-streptococcal glomerulonephritis?
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
What causes Toxic Shock-like syndrome?
Group A strep
Streptococcal pyrogenic exotoxin A is responsible - SUPERANTIGEN
Fever, hypotension, rash, renal impairment, respiratory failure, diarrhea
Streptococcus pyogenes identification
gram + cocci in chains
B-hemolytic on blood agar (SLO, SLS)
Lancefield group A antigen
What is propionibacterium?
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
animal bite bacteria
gram - rod
Gram + rod, anaerobic, spore producing
Gram + rod, spore producing, anaerobic
What is indicated by chronic candidiasis
Causes sporotrichosis - subQ infection
Fungal infection after thorn prick or gardening injury - causes pyogenic and granulomatous reaction
What are Dermatophytes?
Fungi that commonly infect skin -> tinea
-epidermophyton, trichophyton, microsporum
->ringworm, athlete's foot, jock itch
Invasion of nail bed -> malformed growth
What are the alphaherpesviruses?
HSV1,2 and Varicella-Zoster Virus
What are the betaherpesviruses?
Human Herpes Virus 6 (A and B),7 and Cytomegalovirus
What are the gammaherpesviruses?
Epstein-Barr Virus, Human Herpes Virus 8 (Karposi's Sarcoma assoc. Herpesvirus)
What is the structure of Herpes Symplex Virus?
Large encapsulated (icosahedral) DNA virus (dsDNA)
152k BPs, 70-80 genes
3 phases of viral gene expression
Immediate gene expression : adapt cell for virus replication
Early gene expression: vDNA replication
Late gene expresson: structural proteins
What do antiherpes virus drugs require for activation? What is method of action?
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.
Where are latent VZV infections established?
Dorsal Root Ganglion
What cells are infected by beta herpesviruses?
HHV 6A and B: Tcell tropic. Also monocytes and macrophages
Cytomegalovirus: myeloid cells.
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
What disease is HHV 8 associated with?
usually older men of mediterranean ancestry and HIV patients
Non-enveloped icosahedral - small
circular dsDNA (8-10 genes)
HPV-16 transforming genes and major capsular protein
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
What HPV viruses are most closely associated with cervical cancer?
HPV 16 and 18
2 HPV vaccines and approved ages for admin.
Gardasil - age 9 - 26 (types 6,11, 16, 18)
Cervarix - age 10-15 (types 16, 18)
Picornaviurs - description and example
Small, non-enveloped, single strand +RNA
Coxsackievirus: tends to occur in outbreaks
-hand, foot and mouth
-most common source of aseptic meningitis
What is coxsackie virus?
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
Necotizing fasciitis is most commonly associated with what organism?
also - CA-MRSA (does not respond to methacillin or cefazolin normally given for skin infections)
In presentation of scalded skin syndrome there is the presence of large vessicles or bullae. What organism is likely? What is less likely?
More likely: S.aureus
Less likely: S. pyogenes
If a person develops blistering dermatitis after swimming in the ocean, what organism would be of concern?
-also assoc. w/ raw or undercooked oysters
-high mortality rate
What is the treatment for impetigo?
Topical abx (mupirocin) or oral abx
What is dermatitis/arthritis syndrome?
Dermatitic lesions with accompanying joint pain
-in sexually active young adult - Think Neisseria gonorrhoeae
-spreads through lymph and blood
What antibacterials are known for false elevation of creatinine, elevated INR (w/ warfarin), and hyperkalemia?
Trimethoprim - hyperkalemia
SMX/TMP = Bactrim
How is Viridians Strep identified?
Lacks lancefield group and any specific surface markers
Biochemical testing for definitive identification
How are Group D strep and enterococci clinically identified?
Gram +, catalase -
Serologic test for group D antigen
Enterococci grow in 6.5% NaCl, hydrolyze esculin in 40% bile
How is candida identified in the lab in the setting of a systemic or blood stream infection?
KOH or Gram stain - budding round oval yeast cells w/ hyphae
How is aspergillus identified in the setting of a systemic or bloodstream infection?
Blood culture returned negative
Biopsy of infected tissue
Aspergillus cultured in lab - branched septate hyphae
Describe the plasmodium lifecycle
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.
What is a hypnozoite?
Dormant form of Plasmodium
-P.vivax, P.ovale only
-responsible for long term relapses.
What are the erythrocyte receptors for P.vivax and P.falciparum?
P.vivax: Duffy receptor on reticulocyte
P.falciparum: glycophorin A on all red cell types.
How is malarial fever induced?
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)
What is the effect of HbS on the spleen?
Person can become functionally asplenic -> increased susceptibility to encapsulated bacteria
What provides natural resistance to malaria?
Lack of Duffy receptor (P.vivax)
- cells prevent parasite from rearranging actin to form adhesin -> decreased 'stickiness' of infected erythrocyte.
How are plasmodia organisms identified in clinical practice?
-thick smear: diagnose parasitemia
-thin smear: identify Plasmodia species
ELISA: Ab detection
gene probes, PCR for P.falciparum
How is Babesia microti spread?
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.
What organism is the main cause of eye infections?
Infection of eyelid margin / sebaceous gland
Inflamation of lacrimal sac
Infection of aqueous or vitreous humor
Requires ulceration or penetrating injury to compromise cornea and sclera
How is S.pneumoniae identified clinically?
Gram stain: gram +, lancet shaped diplococci
No Lancefield grouping
Quelling reaction - anti-capsule Ab -> capsular swelling
Optochin (P disk) susceptibility
for Haemophilus influenzae b - most virulent strain
-given to infants (@2 mos) since 1990
How is H.influenzae identified in a clinical setting?
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
How does Pseudomonas aeruginosa Exotoxin A work?
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.
What is the primary cause of corneal penetration in a Pseudomonal eye infection?
protease works on elastin, IgG, IgA, collagen, complement
How is pseudomonas identified in a clinical setting?
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
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
Diseases caused by Histoplasma capsulatum
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
How is Histoplasma capsulatum identified?
Very slow growth on blood agar or Sabouraud agar from blood culture
Usually via biopsy- culture and identify bimorphic fungus
What is the drug of choice for Lyme disease?
What valve of the heart is most frequently involved in endocarditis?
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%
What organisms are most frequently involved in bacterial endocarditis?
80% aerobic gram (+): S.viridians, S.aureus, enterococcus, etc.
20% unusual others: E.coli, yeast
What is mycotic aneurism?
Aneurysm due to infection - complication of infective endocarditis.
-occur at bifurcation points
-bacteria from IE - direct invation, embolic occlusion, or immune complex deposition
What are conjunctive petechiae?
Marker of acute endocarditis
small pieces of vegetation break off - embolize in small vessels of conjunctiva
What are Osler's Nodes and Janeway's Lesions?
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.
What abnormal lab results are associated with infective endocarditis?
Anemia - 70-90%
Thrombocytopenia - 5-15%
Leukocytosis - may be absent
Elevated sedimentation rate -almost always (70-90%)
How are blood cultures ordered in the setting of suspected infective endocarditis?
3 sets over the course of 24 hours - each a separate venopuncture
What is HACEK group endocarditis?
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
What is the most common cause of osteomyelitis?
What is the preferred therapy for an animal bite? IV and PO
What about penicillin allergic patient?
IV: ticarcillin / clavulanic acid
PO: Amoxicillin/clavulanic acid
Penicillin allergic: Doxycycline, Moxifloxacin