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217 Cards in this Set
- Front
- Back
Gram positive rods (3)
|
Bacillus
Clostridium Listeria |
|
Gram positive filaments (2, tests)
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Acid fast aerobe - Nocardia
Acid fast negative anaerobe - Actinomyces |
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Gram positive cocci (2 major classes, 1 additional differentiator)
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Catalse + -> Staph (coagulase + -> s. aureus)
Catalase -> Strep |
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Streptococcus hemolysis classes
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Alpha: s.pneumoniae (capsulated, optochin sens), viridance strep (no capsule, optochin resist)
Beta - Group A s.pyogenes (bacitracin sens), Group B s. agalactiae (bacitracin res) Gamma - enterococci |
|
S. Pneumoniae causes . . . (4)
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MOPS
Meningitis Otitis media Pneumoniae Sinusitis |
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S. Pyogenes causes - pyogenic, toxigenic, immunologic (2,3,3)
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Pyogenic - pharyngitis, cellulitis, impetigo
Toxigenic - toxic shock-like syndrome, scarlet fever Immunologic - rheumatic fever, glomerulonephritis |
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Protein A (organism, MOA)
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S. aureus
Binds Fc of Ig -> blocks opsonization and phagocytosis |
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IgA protease (organisms (3), MOA)
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S. pneumo, H.influenza B, Neisseria
Cleaves IgA to allow colonization of respiratory mucosa |
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M protein (organism, mechanism)
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Group A strep (s. pyogenes)
Prevents phagocytosis |
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Clostridium (4 species and key feature for each)
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Gram positive rod
C. tetani -> spastic paralysis C. botulinum -> flaccid paralysis C. perfringens -> gangrene C. difficule - diarrhea, 2/2 abx use |
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Macrophages vs neutrophils (where, life span, killing)
|
Macs: long-lived, in tissues, not much O2 dependent killing
Neutrophils: short-lived, circulating, vigorous respiratory burst |
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Phagocytic receptors (3)
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Integrin and complement - recognize C3b coated organism
Fc receptors - bind IgG if preformed Ab exist Lectins - recognizes specific carbohydrates |
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Phagocytic activating receptors
|
Classical - innate inflammatory response: TLR, TNF, iFN, IL-1
Alternative - late response, non inflammatory: IL-4, IL-13, Th2 mediated |
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Fever path (5)
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Exotoxin (eg LPS) ->
Leukocyte activation -> Pyrogenic cytokines (TNFa, IL-1β -> Circumventricular organs -> Prostaglandins -> Heat retention -> rise in core body Temp |
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Acute phase response (7)
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Lethargy
incr CRP, decr albumin Inhibition of bone formation Decr serum Fe and Zn (to keep away from pathogens) Incr WBC and platelets Decr RBC |
|
5 non-infectious causes of fever
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Malignancy
Granulomatous disease (sarcoid) Collagen vascular disease (SLE, RA) Drug reactions (dilantin) Fictitious |
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Toxins: phospholipases (1 example)
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Cleave phosphatidylcholine (lecithin)
Eg. c.perfringens alpha toxin |
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Toxins: superantigens
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Staph and strep -> toxic shock syndrome
Activate 1 in 5 T cells -> massive cytokine release |
|
Cholera toxin
|
Turns Gsalpha permanent only
G protein that -> adenylate cyclase -> incr cAMP -> decr Na absorption and incr Cl absorption -> WATER LOSS -> "rice-water" stool |
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Tetanus and botulism toxins
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Tet: blocks release of GABA -> spastic paralysis
Bot: blocks Ach -> flaccid paralysis |
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C. difficile toxin
|
Rho GTPases keep tight junctions b/w epithelial cells
Toxin blows apart junction |
|
Gram negative cocci (2, one test)
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Neisseria:
Maltose fermenter -> meningitidis Maltose nonfermenter -> gonorrhoeae |
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Gram negative coccoid rods (2)
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H. Influenza
Bordella pertussis |
|
Gram negative comma shaped (2, 2 tests)
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All are oxidase positive
42deg -> campylobacter Alkaline -> vibrio cholera |
|
Gram negative rods classes
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Lactose fermenters: klebsiella, e.coli
Lacose nonfermenters: Oxidase + : pseudomonas Oxidase - : shigella, salmonella, proteus |
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Gram negative comma shaped, oxidase +, grows at 42
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Campylobacter
|
|
Gram negative comma shaped, oxidase + grows in alkaline media
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Vibrio cholera
|
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Gram negative rod, lactose nonfermenter, oxidase +
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Pseudomonas
|
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Gram negative rod, lactose nonfermenter, oxidase -
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Shigella
Salmonella Proteus |
|
Main differences b/w gram neg and gram pos (2)
|
Gram pos have thick peptidoglycan
Gram neg have thin peptidoglycan and an inner AND outer lipid membrane |
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Spirochetes (3)
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Borrelia - Lyme
Treponema pallidum - Syphillis Leptospira |
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Respiratory Gram negatives (4)
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Bordetella
Haemophilus Legionella Pseudomonas in immunocompromised |
|
Common microbes in heart infections (3)
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S. aureus -> ABE
Viridans strep -> SBE Enterococcus -> SBE |
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Anaerobic abscesses
|
Bacteroides fragilis - a normal gut flora
Intestines leak into peritoneal cavity -> b. fragilis follows -> other facultative anaerobes consume O2 so b. fragilis can thrive |
|
Normal flora (skin, nose, oropharynx, dental plaques, colon, vagina)
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Skin - Staph epidermidis (Staph aureus)
Nose - Staph epidermidis, staph aureus Oropharynx - viridans strep Dental plaque - strep mutans Colon - bacteroides fragilis > e. coli Vagina - lactobacillus, e. coli, group b strep) |
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Staphylococci durability features (4)
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Non-spore forming
Facultative anaerobes Dessication/heat resistant High salt concentration resistant |
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Differentiator for S.aureus and S.epidermidis
|
S.aureus is yellow on MSA plate
|
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S. aureus (encounter, entry, multiplication)
|
Carried in 30% of pop on skin, nares
Entry via trauma, surgery Extracellular multiplication |
|
S. aureus virulence factors (2)
|
1. Protein A binds Fc to block phagocytosis
2. TSST-1 superantigen |
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S. aureus toxin-related disease (3)
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Toxic shock syndrome - fever, rash, hypotension
Food poisoning: short onset, caused by enterotoxins Staph scalded skin syndrome: intraepidermal blisters, in neonates and children, by exfoliative toxin |
|
S. aureus resistance and Rx
|
Many staph are have B-lactamase, resistant to 1st line penicillins
Use B-lactamase resistant B-lactam: nafcillin If resistant to nafcillin -> vancomycin (+gentamicin) |
|
MRSA (CA vs HA acquired, 1st line Rx)
|
usually Hospital acquired
Community acquired has more soft skin and tissue infections Vancomycin is first line Rx |
|
Acute bacterial endocarditis most common cause
|
S. aureus
|
|
S. epidermidis
|
Normal skin flora
Infects prosthetics and catheters |
|
S. saprophyticus
|
UTI
|
|
Novobiocin positive
|
S. saprophyticus (as opposed to the other coagulase negative s. epidermidis)
|
|
Strep agalactiae (class, main cause, mnemonic)
|
Group B, beta hemolytic
Normal in female genital tract -> neonatal sepsis, meningitis, pneumonia (use prophylactic penicillin) Group B, Baby, Brain |
|
Strep bovis (class, main causes (2)
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Group D Strep
Normal gut flora -> correlates w/ colon cancer when found in blood Subacute endocarditis |
|
Enterococci (class, 2 features, 1 main cause)
|
Group D Strep
Normal GI flora Lots of resistance --> endocarditis |
|
Strep pyogenes (class, encounter, localized vs systemic infections, main antigen)
|
Group A Strep
Encounter - normal skin/mucosal flora in 5-25%; pharyngitis from inhalation (cool climate); impetigo from touch (warm climate) Pharyngitis and impetigo are localized infections Necrotizing fasciitis is systemic M protein (blocks phagocytosis by binding complement factor H) |
|
Fever, white exudate on tonsils, rash on limbs and trunk
|
S. pyogenes
|
|
S. pyogenes disease not caused by exotoxins (3 w/ rx)
|
Impetigo - superficial skin infection w/ fragile vesicles (rx - antibiotics)
Cellulitis and erysipelas - deeper skin infection that spreads rapidly w/ systemic sx (rx - oral abx) Necrotizing fasciitis - rx aggressive abx + surgery |
|
Pharyngitis w/ strawberry tongue and rash
|
Caused by GAS (pyogenes) exotoxin
|
|
Strep pyogenes disease caused by exotoxins
|
Scarlet fever
Toxic shock syndrome |
|
Non-infectious complications of s. pyogenes
|
Glomerulonephritis - immune complex deposition
Acute rheumatic fever -> valvular heart disease |
|
S. pyogenes Rx
|
Penicillin for 10 days
|
|
Strep pneumoniae risk factors (3) and Rx (1)
|
Pre-existing lung damage (smokers)
Immunocompromised Splenectomy (loss of spleen -> incr risk of infection from encapsulated organisms) Rx - ceftriaxone |
|
Osteomyelitis (what is it, common spread/sites, dx)
|
Progressive inflammatory destruction of bone, necrosis, new bone formation
Hematogenous spread to distal femur and prox tibia common in children Bone biopsy = gold standard |
|
Osteomyelitis major pathogens (3 age groups)
|
Neonates - S. aureus, strep
Infants - S. aureus Later in life - S. aureus, mixed infections |
|
Osteomyelitis minor pathogens (4)
|
Sickle cell -> salmonella
Cat/dog bites -> pasteurella multocida Vertebral -> TB (Pott's disease) |
|
Septic arthritis (3 clinical)
|
Sudden articular pain
Tenderness/swelling/warmth in joints Knee > hip > shoulder |
|
Septic arthritis common organisms (3)
|
S. aureus > strep > n.gonorrhoeae
|
|
Gonococcal septic arthritis (2 presentations)
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Monoarticular septic arthritis
Dermatitis-septic arthritis: traid of dermatitis, migratory polyarthralgias, tenosynovitis + fever |
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Bacteremia primary vs secondary
|
Primary: direct invasion of blood stream (nosocomia, ivdu, trauma)
Secondary: infection at other site leads to bugs invading blood (pyelonephritis, pneumonia) |
|
Infective endocarditis: acute vs subacute
|
Acute - invasive, pathogenic organisms w/ toxic course
Subacute - less pathogenic bacteria -> more indolent course |
|
Bacteremia clinical (2 main, 3 specifics)
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Fever
Lethargy/mental status If skin: cellulitis If pneumonia: pleuritic CP or cough If pyelo: back pain |
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Infective endocarditis predisposing factors (4)
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Valvular heart disease (RHD, CHD, MVP)
Idiopathic hypertrophic subaortic stenosis Prostethics IVDU |
|
Infective endocarditis path (6 and 1 hallmark)
|
Turbulence/trauma to valvular endothelium -> platelets-fibrin -> nonbacterial thrombotic endocarditis -> THEN trauma and bacteremia -> adherence/colonization -> VEGETATION
|
|
Infective endocarditis clinical (5)
|
Constitutional symptoms
Back pain FEVER Murmur Emboli |
|
Osler nodes
|
Small painful nodes on pads of fingers/toes
Caused by circulating immune complexes Infective endocarditis |
|
Janeway lesions
|
Hemorrhagic, painless macules on palms/soles
Infective endocarditis |
|
Consequences of vegetations in infective endocarditis (5)
|
Distal site infections (myocardial abscess)
Host response w/ proinflamm cytokines -> fever, sweats, chills Tissue destruction by organism Emboli Immune complex formation -> glomerulonephritis |
|
Beta lactams MOA and resistance mechanisms
|
Bactericidal
Inactivate transpeptidases (penicillin binding proteins, PBPs) required for peptidoglycan synthesis Beta lactamase inactivates |
|
Beta lactams classes (4)
|
Penicillins
Cephalosporins Monobactams Carbapenems |
|
Oxacillin (class, 1 use, 2 tox)
|
Penicillin beta lactam
Staph aureus Hypersensitivity, interstitial nephritis |
|
Ampicillin/Amoxicillin(oral) (class, use, 3 tox)
|
Intermediate spectrum Aminopenicilin beta lactam
Penicillinase sensitive Gram pos and neg rods (h.flu, listeria, e.coli, salmonella, proteus) Hypersensitivity, ampicillin rash, pseudomembranous coliits |
|
Penicillin (class, 2 main use, 2 tox)
|
Beta lactam
Gram positive (s. pneumo, s.pyo, actinomycyes), SYPHILIS Hypersensitivity, hemolytic anemia |
|
Clavulinic acid use
|
Combine w/ amoxicillin/ampicillin
Inhibits beta lactamases |
|
Piperacillin/Ticarcillin (class, 2 uses, 1 tox)
|
Extended spectrum beta lactam
Pseudomonas, enterobacter Hypersensitivity |
|
What two cephalosporins penetrate CSF?
|
3rd gen - Ceftriaxone
4th gen - Cefipime |
|
Cephalosporins (activity, resistance, excretion, 1 pearl)
|
Bactericidal
Inhibit cell wall synth but less susceptible to penicillinase Renal excretion Less allergy Only 5th gen has activity against enterococci |
|
Cefazolin (class, use (4))
|
1st gen cephalosporin
Penicillin-resistant S. aureus that is not MRSA (gram pos cocci) Proteus, E.coli, Klebsialla |
|
Cephalosporins (5 gens)
|
1st - cefazolin
2nd - cefuroxime 3rd - ceftriazone 4th - cefipime 5th - ceftaroline AZ - U - TRI - IPI TAR |
|
Cefuroxime (class, uses (5))
|
2nd gen cephalosporin
Gram pos cocci Proteus, E.coli, Klebsiella, H.flu |
|
Ceftriazone (Class, uses (3), 1 key feature)
|
3rd gen cephalosporin
Serious gram neg resistant to other beta lactams N. Meningitis/Gonorrhoeae, S. Pneumo Penetrates CNS |
|
Ceftazidime (class, use)
|
3rd gen cephalosporin
Pseudomonas |
|
Cefepime (class, use)
|
4th gen cephalosporin
Gram pos and pseudomonas |
|
Ceftaroline (class, use)
|
5th gen cephalosporin
MRSA and gram neg except pseudomonas |
|
Cephalosporins toxicity (2)
|
Less hypersensitivity than PCN (DON'T GIVE TO PT W/ KNOWN SEVERE RXN TO PCN)
Nephrotoxicity |
|
Aztreonam (class, use)
|
Monobactam cell wall synth inhibitor
B lactamase resistant Gram neg rods Low tox |
|
Imipenem/Cilastatin (class, use, tox (2))
|
VERY broad spectrum B-lactamase resistant carbapenem
(Cilastatin inhibits drug inactivation in renal tubules) Seizures, nephrotoxic |
|
Vancomycin (Class, use (3), tox (3))
|
Glycopeptide cell wall inhibitor - binds d-ala d-ala portion of precursors (not PBP)
No x-resistance w/ beta-lactams Gram pos serious resistant organisms: MRSA, C.difficile, enterococci Tox: Red-man diffuse flushing (block w/ antihistamines), nephro, ototox |
|
Daptomycin (moa/class, use, tox)
|
Lipopeptide cell wall inhibitor via formation of K channel
Gram pos: mrsa, s. pyo, VRE Tox: skeletal muscle |
|
Pneumonia: modes of infection
|
Aspiration of fine particles: TB
Inhalation of droplets: influenza, meningococci Aspiration from nasopharynx: pneumococci, legionella, gram neg enterics |
|
Pathogens causing community acquired pneumonia (2 typical, 3 atypical)
|
Viruses
Pneumococcus (40%) Atypicals: Mycoplasma in young Chlamydia Legionella (most lethal) Enteric gram neg rods in elderly |
|
Contrast bacterial and viral pneumonia (nature, sputum, ausc, xray, wbc)
|
Bacterial: consolidating, purulent/rusty sputum, fremitus, focal consolidation, elev wbc)
Viral: nonconsolidating/diffuse, no sputum, normal ausc, diffuse xray, normal wbc) |
|
Legionairre test
|
Urinary antigen
|
|
Strep pneumoniae test
|
Urinary antigen
|
|
CAP Rx (3)
|
Macrolides
Quinolone - elderly Doxycycline |
|
Pathogens causing pneumonia in immunocompromised (2 classes, 5 pathogens)
|
Decr cell-mediated (HIV):
Pneumocystis Fungi Mycobacteria CMV Humoral immunity (CVID) Encapsulated (S.pneumo) |
|
Hospital acquired pneumonia pathogens (entry,class of paths w/ one eg, dx)
|
Entry - aspiration b/c gram negs colonize pharynx
Gram negative rods (pseudomonas) Dx - culture |
|
HAP Rx
|
Broad spectrum beta lactam
|
|
4 pathogens that cause nosocomial pneumonia and risk factors
|
S. aureus - coma/diabetes/renal failure
Legionella - high dose steroids Pseudomonas - steroids Acetinobacter - steroids |
|
Acetinobacter (risks, site of disease, rx)
|
Invasive procedures
Pneumonia and bacteremia Lots of resistance |
|
Pseudomonas aeruginosa (class, 3 high risk patients, toxin)
|
Gram neg rod, oxidase positive
Nosocomial, burns, cystic fibrosis Exotoxin A inactivates EF-2 |
|
How does pseudomonas grow in CF lung?
|
Starts as piliated non-mucoid and progresses to non-piliated mucoid via alginate capsule
|
|
Pseudomonas Rx
|
Aminoglycoside + extended spectrum penicillin - piperacillin
|
|
Legionella identification
|
Fastidious growth
Charcoal medium Gram negative rod |
|
Legionella (encounter, entry, spread)
|
Grow in amoeba biofilms in water coolers, spas . .
Inhaled aerosols -> lyses amoeba and enters macrophages to multiply Disease localized to lungs |
|
Legionella (risk factors, 2 diseases)
|
Immunosuppresion, dialysis, cancer, alcohol
Legionnaire's - immunocomprosimed,fever, pneumonia w/ 15% mortality Pontiac fever - healthy, self-limiting fever |
|
Legionella Rx
|
Erythromycin
|
|
Protein inhibitors (cidal or static, moa, resistance)
|
Bacteristatic
Inhibit 30S or 50S Resistance - target site mod, active efflux, enzyme inactivation |
|
Protein Synthesis Inhibitors (6)
|
Aminoglycosides - bacteriCIDAL
Tetracyclines Chloramphenicol Macrolides Linezolid Clindamycin |
|
Linezolid (class, use, 2 tox)
|
Protein synth inhibitor
Resistant gram positive Bone marrow suppression Reversible thrombocytopenia |
|
Tetracyclines (class, uses (6), 1 tox)
|
Protein synth inhibitors
Accumulates intracellularly so used: Chlamydia, Rickettsia, Gonorrhoeae Borrelia, H.pylori, M. pneumo Avidly binds teeth and bones -> yellow discoloration in children/pregants |
|
Tigecycline (class, 1 use)
|
Tetracycline protein synth inhibitor
Resistant gram neg and pos rods - PSEUDOMONAS |
|
Gentamicin (class, 2 uses, 2 tox)
|
Aminoglycoside protein synth inhibitor
Not taken up by anaerobes Gram neg facultative rods Synergy w/ beta lactams Tox: nephrotox, ototox (esp incombo w/ loop diuretics) |
|
Aminoglycoside resistance and one other key point
|
transferase enzymes inactivate drug
Concentration dependent killing -> once daily dosing and post antibiotic effect |
|
Chloramphenicol (class, 1 use, 2 tox)
|
Protein synth inhibitor
Meningitis Aplastic anemia and gray baby syndrome |
|
Macrolides (class and 3 examples)
|
Protein synth inhibitors
Eyrthomycin Clarithromycin Azithromycin |
|
Erythromycin (class, 1 use, 2 tox)
|
Macrolide protein synth inhibitor
Atypical pneumonias (chlamydia, mycoplasma, legionella) Tox: GI and QT prolongation |
|
Azithromycin and clarithromycin (class, uses)
|
Macrolide protein synth inhibitors developed to be have less tox and longer t1/2 than erythromycin
Same use: atypical pneumonias |
|
Clindamycin (class, 1 use, 1 tox)
|
Lincosamide protein synth inhibitor
Anaerobic infections (b.fragilies, clostridium perfringens) in abscesses Tox: c.difficile -> colitis |
|
Which protein synth inhibitors aren't bacteristatic?
|
Aminoglycosides are bactericidal
|
|
Secretory diarrhea (2 pathogens, description, location)
|
V. cholera
ETEC Copious, watery, no tissue invasion Small bowel |
|
Dysentery (2 pathogens, description, location)
|
Shigella
Entamoeba Small volume w/ blood/mucus/pus, invasion Large bowel |
|
Hemorrhagic colitis (1 pathogens, description, location)
|
EHEC
Medium volume, bloody, no invasion Large bowel |
|
Secretory bloody diarrhea (3 pathogens, description, location)
|
Salmonella
Campylobacter Yersinia Copious, watery, bloody, pus, sometimes tissue invasion Ileum and colon |
|
Contrast upper and lower bowel pathogens (volume, invasion, systemic sx, fecal wbc, blood)
|
Upper: fluid loss, no systemic systems, no fecal wbc, not bloody
Lower: small, volume, invade mucosa (shigella, campylo), systemic sx, fecal WBC, bloody |
|
Enterotoxigenic E. Coli (ETEC) (type of diarrhea, toxin)
|
Water diarrhea, Traveler's
Heat-labile toxin similar to cholera toxin |
|
Shigella (type of diarrhea, entry and multiplication)
|
Gram neg, non lactose fermenting rod
Bloody diarrhea (dysentery), like EIEC Enter M cells -> multiply in cytoplasm of epithelials and macs Actin-comet tail |
|
Shigella toxins (3)
|
Type III secretion - cell invasion and apoptosis
Actin nucleation protein - cell-cell spread Shiga Toxin - A-B toxin that inhibits protein synth |
|
Enterohemorrhagic E. Coli (EHEC) (type of diarrhea, 2 toxins and their damages)
|
Hemorrhagic colitis (bloody medium volume)
Shiga-like toxin -> HUS Attaching and effacing lesions via type III secretion system, intimin, and tir |
|
Salmonella (type of diarrhea, identifier, 2 types of disease based on 2 different serotypes)
|
Secretory, bloody diarrhea
Produce H2S Typhoid fever - salmonella invades intestinal epi --> lymph nodes -> seeds organs -> fever, abd pain, rose spots Gastroenteritis -> most common: nausea, abd pain |
|
Salmonella: enteric vs typhoid fever
|
Typhoid fever - fever, diarrhea, headache
|
|
Clostridium difficile disease (5)
|
Watery diarrhea
Fever Loss of appetite Nausea Abd pain/tenderness |
|
Pseudomembranous colitis (pathogen, path, 2 causes)
|
Caused by C.difficile toxins
Destruction of enterocyte cytoskeleton 2/2 clindamycin or ampicillin |
|
Top 3 pathogens causing UTIs
|
E. coli
Staph saprophyticus Klebsiella pneumoniae |
|
Cystitis sx (3) and rx
|
Dysuria
Urgency Frequency Nitrofurantoin or TMP-SMX 3-5 d |
|
Pyelonephritis sx (4 and rx)
|
Fever
Chills Flank pain (CVA) / tenderness Incr WBC Quinolone 7-14 d or Beta-lactam + gentamicin |
|
Pyuria
|
WBC in urine
Abscence of WBC rules out UTI but not presence does not equal infection |
|
2 types of recurrent UTI
|
Relapses - interval b/w recurrence is less than 2 wks, image if multiple relapses
Reinfections - interval b/w recurrence > 2wks, most UTIs |
|
When to treat asymptomatic bacteruria
|
Pregnant women (7d TMP-SMX
Newborns (due to reflux) Urologic manipulation (cytoscopy) |
|
Bacterial infections requiring bactericides (3)
|
Endocarditis
Osteomyelitis Meningitis |
|
Meningitis symptom triad
|
Fever, stiff neck, headache
|
|
6 encapsulated organisms and what main disease they can cause
|
MENINGITIS
S. Pneumo H. Flu N. Meningitidis E. Colie K1 Group B strep in neonates Cryptococcus neoformans |
|
3 CSF profiles in meningitis
|
Purulent - PMNs, low glucose ->bacterial (acute)
Lymphocytic low glucose -> TB, fungal, spirochetal, listeria, sarcoidosis (acute or subacute) Lymphocytic normal glucose -> viral (subacute) |
|
Anatomic differences b/w purulent and lymphocytic low glucose profiles
|
Purulent - cranial surface
Lymphocytic low glucose - base of brain -> CN palsies |
|
Risk groups for meningitis pathogens (4 groups)
|
Neonate: Group B strep, E. coli, Listeria
Young adult: N. Meningitidis > S. Pneumo Older: S. Pneumo > N.Meningitidis Immunosuppressed: Cryptococcus, Listeria |
|
Drug-induced meningitis (3)
|
NSAIDs
TMP-SMX IVIG |
|
Key lymphocytic low glucose meningitis pathogen not to miss
|
TB
|
|
Chlamydia trachomatas pneumonia (epi, encouter, entry, rx)
|
Infants
Encounter - infected mother's birth canal Entry - conjunctivitis/nasopharyngeal into phagocytes, lives intracellularly in vacuole of epithelials Self-limiting disease (almost everyone has been infected) |
|
N. Gonorrohoeae (toxins and agar)
|
No toxins, damage done by immune response
Chocolate agar |
|
N. Gonorrohoeae (entry, spread, virulence)
|
Colonized mucosal surfaces so secretions all carry Gc
Can penetrate mucosal layers -> pelvic inflammatory disease and occasionally disseminates Evades immune system via pili antigen variation |
|
N. Gonorrohoeae Rx
|
3rd gen cephalosporin - Ceftriaxone
Assume chlamydia coinfection and treat w/ doxycycline or azithromycin |
|
Syphilis organism
|
Treponema pallidum spirochete
|
|
Syphilis stages
|
Primary - chancre, painless 3wk post exposure, SERONEGATIVE
Secondary - disseminated disease w/ maculopapular rash on palms and soles, systemic disease and contagious Tertiary - 1/3 secondary progress 30 yr later, noncontagious, arteritis, neurosyphilis, granulomatous inflammation |
|
Syphilis Dx
|
Can't isolate
PCR or serological |
|
DNA and metabolic toxins (3 classes and their basic MOA)
|
Quinolones - inhibit DNA gyrase and topoisomerase
Metronizadole - metabolites directly damage DNA Sulfa derivatives - inhibit bacterial and protozoal folate synth |
|
Fluoroquinolones (cidal or static? 3 examples. MOA, resistance)
|
Bactericidal
Ciproflaxacin, levofloxacin, moxifloxacin Block bacterial DNA gyrase Resistance: active efflux, dna gyrase mutation |
|
Ciprofloxacin, levofloxacin, moxifloxacin
|
Fluoroquinolone DNA gyrase inhibitors
|
|
Fluoroquinolones (use, SE (3))
|
Gram neg rods
DONT USE W/ ANTACIDS Cartilage damage -> don't use in children or pregnant women Tendonitis |
|
Metronidazole (moa, 4 uses, 3 se)
|
Metabolites damage DNA
Giardia, Entamoeba, Trichomonas, Anaerobes SE: GI, metallic taste, disulfiram like reaction w/ alcohol |
|
Sulfonamides (cidal or static?, moa, 2 resistance, 4 se)
|
Bacteriostatic
PABA antimetabolites inhibit dihydropteroate synthetase Resistance: widespread via target side mod, increased PABA synth SE: Kernicterus, drug interactions, hemolytic anemia if GP6D, Stevens Johnson |
|
Kernicterus
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Sulfa adverse effect
CNS injury due to toxic effects of high concentrations of bile pigments in infants Sulfa displace bilirubin from albumin -> incr free bilirubin |
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Sulfa drug resistance
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Decreased permeability, and mutant target site
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Lyme Rx
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Doxycycline
Ceftriaxone |
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Ehrlichiosis (disease, type of organism, transmitted by)
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Human monocytic ehrlichiosis
Rickettsia Transmitted by Amblyomma |
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Anaplasmosis (disease, type of organism, transmitted by)
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Human granulocytic anaplasmosis
Rickettsia Transmitted by Ixodes (like B.Burg) |
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Ehrlichiosis and Anaplasmosis (clinical and rx)
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Nonspecific fevers chills
HME (ehr) -> maculopapular or petechial rash Rx - doxycycline or tetracycline |
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Babesiosis (where does it multiply, transmitted by, 2 clinical, 1 key dx)
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Intra-erythrocytic parasite
Transmitted by Ixodes Fever, hemolytic anemia Maltese cross on smear |
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Rocky Mountain Spotted Fever (organism, clinical triad, 1 epi)
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Rickettsia rickettsii
Rash on palms, soles (migrating to trunk), headache+fever Endemic to east coast |
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Bordetella Pertussis (class, agar plate, encounter, multiplication)
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Gram neg coccobacillus
Fastidious -> CCBA plate Encounter - respiratory droplets Adheres to ciliated bronchial epithelial cells -> multiplies extracell and inhibits mucociliary clearance |
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CCBA plate
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Bordetella
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Bordetella Pertussis Toxin
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Pertussis toxin - ADP ribosylating A-B toxin
Increases cAMP by inhibiting Gsa which normally inhibits adenylate cyclase |
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Bordetella Pertussis Rx and Prevention
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Rx - Azithromycin (resistant to penicillin)
Vaccine - pertussis proteins |
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H. pylori (class, epi, toxin)
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Gram negative curved/spiral
Fastidious Infections are widespread and clinically silent Cag type 4 secretion system |
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H. pylori stages of damage
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D-wk: superficial gastritis
wk-mo-yr: chronic gastritis mo-yr: MALT lymphoma, adenocarcinoma |
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H. Influenza type B (class, causes, colonizes)
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Gram neg coccobacillus
Causes meningitis and pneumonia in < 5 yo Colonizes upper respiratory tract |
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N. Meningitis (normal flora?, rx, prevention)
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Normal flora in upper resp tract (compared to N. Gono NOT normal)
Ceftriaxone Vaccine for college students |
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Functions of normal flora (6)
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Produce+secrete B12 and vitK
Digest food (carb, proteins, FA) Digest endogenous (urea, bilirubin,bile salts) Drug metabolism (warfarin Educate immune system Suppress other pathogens (c.diff) |
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Which fungi is human commensal?
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C. albicans
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How do fungi typically cause host damage? (4)
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Usually self-limiting, mild damage
Don't produce toxins Destroy tissues by invasion Fungus ball occlude arteries, veins, bronchi |
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Coccidioidomycosis (where?, 4 clinical, histopath)
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Epi: SW US
Pneumonia, meningitis, rash Disseminates in immunocompromised -> Histopath: spherule w/ endospores |
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Spherule filled w/ endospores
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Cocciodiomycosis
SW US |
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Candida albicans (entry, 3 clinical)
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Opportunistic normal flora
Oral and esophageal thrush, diaper rash Disseminates to any organ |
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Cryptococcus neoformans (key feature, common clinical scenario, 1 clinical presentation)
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ENCAPSULATED
Most people are resistant AIDS patients -> meningitis Umbilicated papules |
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Cryptococcal meningitis Dx
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CSF cryptococcal antigen
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Fungus ball
Septate hyphae 45deg angle branches |
Aspergillus
More common in cancer than HIV |
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Amphotericin B (moa, 2 se)
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Antifungal binds ergosterol
SE: infusion-related - cytokines -> fever/chills nephrotox |
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Fluconazole (moa, se)
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Inhibits ergosterol synthesis by inhibiting CYP P450
SE: drug interactions |
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Flucytosine (moa, se)
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Interrupts DNA and protein synth
SE: bone marrow suppression |
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Echinocandins (moa, organism, tox)
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Antifungals inhibit cell wall synth
Aspergillus Low tox |
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Basic antifungal Rx principles
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Local: fluconazole or ketoconazole
Systemic: amphotericin B |
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Opportunistic fungi (3)
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Aspergillus
Candida Cryptococcus |
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If infected w/ HIV and TB, what is the chance of active infection each year? What is it for non-HIV?
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8% per year
5-10% lifetime |
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TB pathogenesis
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Inhale aerosol ->
No host reaction b/c bland capsule -> Multiplies in macs -> hilar lymph nodes -> Silent bacillemia -> lung apices and latent TB |
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Progressive primary and miliary TB
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In newborns or immunosuppresed infection is not contained by CMI
Progressive primary -> pneumonia Miliary -> disseminates through blood to all sites |
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Where is recrudescent TB most commonly found?
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Lung apex
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TB path
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Caseating necrotizing granulomas w/ giant cells
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TB clinical presentation 5
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Cough, fever, night sweats > 3 wks
Weight loss Hemoptysis Apical cavitary lung lesions |
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Extrapulmonary TB in HIV
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Hilar lymphadenopathy
Pleural effusions Rarely miliary disease |
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Contrast atypical mycobacteria to TB (encounter, virulence, PPD, drugs)
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Atypical: from environment, lower virulence, usually neg PPD, not the same as TB
TB: human to human, virulent, PPD pos, TB drugs |
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TB drugs: primary vs secondary resistance
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Primary - bug already resistant pre therapy
Secondary - resistance develops during therapy |
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1st line TB drugs and early bacteriocidal activity
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Rifampin
Isoniazid Ethambutol Pyrazinamide I > E > R > P So treat with INH immediately |
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Isoniazid (moa, activity, 2 tox 1 antidote)
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1st line TB
Inhibits mycolic acid synth Activity depends on host acetylation speed Tox: neuro and hepato, rx neurotox w/ pyroxidine B6 |
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Rifampin (moa, 3 tox)
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Inhibits DNA-dependent RNA pol
Tox: hepatic, induces P450, stains contact lens orange |
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Pyrazinamide (use, activity, 2 tox)
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Anti TB
Active in acid pH (macrophage phagolysosomes) Tox: hepatic, uric acid |
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Ethambutol (use, 1 tox)
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Anti TB
Used to prevent resistance developing to other drugs Tox: retrobulbar neuritis |
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MDR TB (which drugs?)
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Resistant to at least INH and Rifampin
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XDR TB (which drugs?)
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MDR TB (INH and rifampin) + kanamycin, amikacin or capreomycin plus any fluoroquinolone
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Honey crusts, vesicles, pustules (2 pathogens)
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Impetigo
S. pyo S. aureus |
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Papules and pustules around hair folliculitis (2 pathogens)
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Folliculitis
S. aureus Pseudomonas |
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Tender, fluctuant mass w/ overlying erythema (2 pathogens)
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Abscess
S. aureus Non TB mycobacteria |
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Painless erythematous target like (1)
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Lyme
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Pustules w/ ulceration extending along lymphatic drainage channel
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Sporothrix "Rose Gardener's Disease"
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Umblicated skin lesion
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Cryptococcus or molluscum
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