Anti Hypertensive Drugs Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc Brain DM, Hypokalemia DM, Hypokalemia RAAS Ihibiting Drugs Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc w NSAIDS = HTN Sympathoplegic Agents CNS α2 Agonists; Ganglionic Blockers; Neurotransmitter Depletors; α, β, Blockers Diuretics - DOC x HTN monotherapy ↓ plasma volume ECFV → ↓ VR → ↓ CO → ↓ MAP/BP → ↑ TPR (Reflex) → ↑ PRA → ↑ CO → a maintained lowered TPR; 1) ↓ intravascular volume and 2) ↓ vascula responsiveness by ↓ Na and ↓ Ca++ Drug Drug Interactions Thiazides (Hydrochlorothiazide /HydroDiuril/H2TZ) Work on Distal convoluted Tubule (descending loop of Henle?) Sexual Dysfunction, hypovolemia, Hypokalemia/alkalosi s, Hypomanesemia, Hypercalcemia, Hyperuricemia, Hyperlipidemia, Hyperglycemia w Quinidine=Torsade de Pointes; w Digoxin= Dig Toxicity; w Cotricosteroids=↑ Na Retention; w Li=↑ Plasma [Li]; w Warfarin=↓ effectiveness; w NSAIDS=HTN Elderly or dehydrated or other RxRx interactions; DM, Hypokakemia may need K supplements; ↓ in K → ↓ BP and ↑ arrythmias Along w tx HTN Diuretics (in general) are good for Edema, Dyspnea; Thiazides are good x Severe Renal Impairment w HTN Thiazide-like (Chlorthalidone/Hygr oton) Loop (Furosemide/Lasix) blocks Na/2Cl-/K on Ascending Loop of Henle so they stay in lumen Hearing Loss (just like aminoglycosides), Hypocalcemia good x tx of HTN w Renal Impairment even morese than Thiazides K-Sparring (Spironolactone, Eplerenone/inspra) Aldosterone receptor antagonist; Reduce aldosterone levels? Estrogenid SDFX/Gynecomastia b/c of steroid like sx of drug; NSAIDS, β blockers and ACE inhibitors ↑ Hyperkalemia; may lead to cardiac arrest good x tx of HTN w Hypkalemia Drug Drug Interactions ACE Inibitors (end in -pril eg Captopril) Block A I: A II conversion in lung endothelial cells; ↑ Bradykinin ↓ A-II prodx → ↓ TPR and ↓ aldosterone and ↑ Na excretion; ACE breaks down bradykinin, so if it's blocked the bradykinin can stick around longer Captorpril causes rash; hpotension, Na depletion; Dry cough → ↓ compliance, Hyperkalemia bc K not excreted bc aldosterone is inhibited; Angioedema (esp if black); Renal Failure due to ↑ GFR, Proteinuria, rashes (captopril) fever, pancytopenia, BM depression Great Results If Used w Thiazides Little sex dysfx SDFX; help manage DM; ↓ mortality if prior MI; only antihypertensive mx w/o sexual dysfx Receptor Blockers/ARB's (end in "-sartan"; Losartan, Valsartan, Irbersartan, Candesartan, Telmisartan, Block AII type I receptors → ↓ aldosterone relaease and vaeesel relaxation ↑ bradykinin → angioedema Aldosterone Receptor Blocker (Spironolactone, Eplerenone)
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Anti Hypertensive Drugs
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Brain
DM, Hypokalemia
Loop (Furosemide/Lasix) DM, Hypokalemia
RAAS Ihibiting Drugs
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
w NSAIDS = HTN
Diuretics - DOC x HTN monotherapy
↓ plasma volume ECFV → ↓ VR → ↓ CO → ↓ MAP/BP → ↑ TPR (Reflex) → ↑ PRA → ↑ CO → a maintained lowered TPR; 1) ↓ intravascular volume and 2) ↓ vascula responsiveness by ↓ Na and ↓ Ca++
Drug Drug Interactions
Thiazides (Hydrochlorothiazide/HydroDiuril/H2TZ)
Work on Distal convoluted Tubule (descending loop of Henle?)
Sexual Dysfunction, hypovolemia, Hypokalemia/alkalosis, Hypomanesemia, Hypercalcemia, Hyperuricemia, Hyperlipidemia, Hyperglycemia
w Quinidine=Torsade de Pointes; w Digoxin= Dig Toxicity; w Cotricosteroids=↑ Na Retention; w Li=↑ Plasma [Li]; w Warfarin=↓ effectiveness; w NSAIDS=HTN
Elderly or dehydrated or other RxRx interactions; DM, Hypokakemia
may need K supplements; ↓ in K → ↓ BP and ↑ arrythmias
Along w tx HTN Diuretics (in general) are good for Edema, Dyspnea; Thiazides are good x Severe Renal Impairment w HTN
Thiazide-like (Chlorthalidone/Hygroton)
blocks Na/2Cl-/K on Ascending Loop of Henle so they stay in lumen
Hearing Loss (just like aminoglycosides), Hypocalcemia
good x tx of HTN w Renal Impairment even morese than Thiazides
Estrogenid SDFX/Gynecomastia b/c of steroid like sx of drug;
NSAIDS, β blockers and ACE inhibitors ↑ Hyperkalemia; may lead to cardiac arrest
good x tx of HTN w Hypkalemia
Drug Drug Interactions
ACE Inibitors (end in -pril eg Captopril)
Block A I: A II conversion in lung endothelial cells; ↑ Bradykinin
↓ A-II prodx → ↓ TPR and ↓ aldosterone and ↑ Na excretion; ACE breaks down bradykinin, so if it's blocked the bradykinin can stick around longer
Captorpril causes rash; hpotension, Na depletion; Dry cough → ↓ compliance, Hyperkalemia bc K not excreted bc aldosterone is inhibited; Angioedema (esp if black); Renal Failure due to ↑ GFR, Proteinuria, rashes (captopril) fever, pancytopenia, BM depression
Great Results If Used w Thiazides
Little sex dysfx SDFX; help manage DM; ↓ mortality if prior MI; only antihypertensive mx w/o sexual dysfx
Angiotensin II Receptor Blockers/ARB's (end in "-sartan"; Losartan, Valsartan, Irbersartan, Candesartan, Telmisartan, Eprosartan)
Block AII type I receptors → ↓ aldosterone relaease and vaeesel relaxation
↓ CO via ↓ HR and CF; ↓ CNS; ↓ RAAS (no compensatory volume expansion
Bronchospasm (esp nonselective), Hrt Failr; Bradycardia; AV block; Peripheral Vascular Diss esp in Raynauds: Depression (not as bad as Reserpine); Vivd Dreams; Sex Dysfx
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
OK to use w β blockers
Tachycardia β blockers
All antihypertensive mx cause ↑ in RAAS (via: ↓ BP and CO → ↓ blood flow to kidney → ↑ RAAS), ↑ chance of Orthostatic Hypotension (via ↓ contractilty, volume or CF).
Dyslipidemia Drug Therapy
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Nicotinic Acid/Niacin Inhibits adipose Lipase
Type I hyperlipidemia
Drug Drug Interactions
Phenylalkylamine (Verapamil)
constipation, Hypotension, some HA, Peripheral Edema (no RE to diuretics), AV block, some CHF
β blockers; Cardiac Failure
Benzothiazipine (Diltiazem)
a little hypotension, peripheral edema, AV block (nyeh)
considered the safest Ca channel blocker
Dihydropyridines (Nefedipine et al)
Hypotension, HA, Peripheral Edema (does not RE to diuretics)
w β blockers → ↓ HR THIS IS BAD!
sublingual, short duration
highest affintiy x heart of other Ca chnl blkrs; good in ER situation
Drug Drug Interactions
Reduces esterificationof TG in liver, May reduce hepatic cholesterol formation, Reduces VLDL, TH and LDL, ↑ HDL, Effective vs Hyperlipidemia Types II-V, Cho-ol levels reduced ≈ 25% @ 3gm/day. ↓ clotting via ↑ tissue plasminogen factor and ↓ plasma fibrinogen
Bleeding of hemorrhage, easy burising, GI, Intracranial
Used during invasive cardiac procedures CABG, PTA
Inhibit fibrinopen receptor on platelets to inhibit fibrin binding and scaffold forming
Bleeding, immune reaction
Inhibit fibrinogen receptor on platelets to inhibit fibrin binding and scaffold forming
Bleeding immune reaction
Inhibit fibrinogen receptor on platelets to inhibit fibrin binding and scaffold forming
Bleeding,
Drug Drug Interactions
Heparin
Enoxaparin
Warfarin/Coumadin
Thrombolytic AgentsDissolve clots by activating the conversion of plasminogen to plasmin that hydrolyzes fibrin. Therapeutic window 2-6 hrs after ssx usu IV
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Streptokinase Activates Plasminogen Thrombo-Embolic Stroke IV ONLY
Binds to Antithrombin III thus preventing inactivation of thrombin.
HMW Heparin binds to AT III bound to factor Iia or Xa. LMW heparin binds to ATIII bound to XA only
Spontaneous hemorrhage, alopecia, HSS, fever, skin ncrosis osteoporosis/sponatneous bone brkg @ chronic doses, dangerous ↓ lvls of AT III, thrombocytopenia, antiplatelet AB's
pts w religious wishes against pork (it comes from pig glycosaminoglycans)
Do NOT Give Orally. Do NOT Give IM.
Does not cross BBB or placenta. Treat spontaneous hemorrhage w protamine sulfate
Direct Thrombin Inhibitors (Hirudin Argatroban)
Inhibit Thrombin (Factor Iia)
by inhibiting Factor Iia it stops fibrin from being made, and prevents scaffold formation; Lepirudin/Hirudin is used to replace Heparin in Heparin-Induced Thrombocytopenia; Argatroban is used to tx Heparin induced Throbocytopenia
prolongs PTT (so does Heparin)
Lepirudin is derived from leech saliva
DOC x DVT prevention after hip surgery
Stops the reduction of vit K.
Reduced vit K is crucial x turning Preprothrombin into Prothrombin thus the Ca++ on gamma Carboxyglutamic acid can't bind FIIa or FIXa to the platelets. -wiki; Warfarin is used to tx A fib, Prevent Thromboemboli stroke, acute MI, Venous Thromnosis and Pulmonary embolism.
↑ Warfarin activity if in conjunction w Cimetidine (OTC H2 blocker) via ↓ warfarin metabolism, w Phenylbutazone via ↓ binding to prots, w Aspirin = ↓ Platelet fx:: ↓ Warfarin activity if in conjunction w Cholestyramine due to ↓ absorption, Phenobarbital by inducing cyt450, w Phenytoin by inducing cyt450
pregnant women (crosses BBB and causes fetal death birth defects)
Oral (good good thing) w 100% bioavailability. Dose is calculated by finding INR PT so that PT ≈ 2.
cyto 450 metabolization; binds to prots.
How to treat SDFX: Mild bleeding w dose Reduction; Severe Bleeding w stopping regimen and give Vit k; BAD bleeding via all of the above w concentration or plasma
Drug Drug Interactions
Thereapeutic window 2-6hrs after ssx. Used x DVT, Acute MI
Alteplase repidly activates plasminogen bound to fibrin inthrombus (low affinity for free plasminogen); Urokinase
Thereapeutic window 2-6hrs after ssx. Used to tx MI (not better vs streptokinase), Thromboembolic Strokes(not that great); Alteplase is good @ treating MI (90 min window), Massive pulmonary embolism, Ischemic stroke (3 hr window)
GI and intracranial bleeding
Thereapeutic window 2-6hrs after ssx.
inhibits plasminogen activation
maybe intravascular thrombus
HSS, Dyspnea, Flushing, Bradycardia
Drug Drug Interactions
Nitrates (Nitroglycerin, ISDN, ISMN)
Mimics endogenous NO ↑ the cGMP pathway which relaxes myosin. Effort angina - ↓ preload, SV MVO2; Variant angina- ↑ coronary flow by relieving coronary spasm; Mixed angina - ↑ coronary blood flow ↓MVO2
Dilates the viens>>coronary aa>>peripheral aa. Used to tx Effort Angina. ↓ Venous Flow → ↓ Preload → ↓ LVEDV/P → ↓ Ventricular stretch → ↓ Systole time → ↓ Stroke Volume → ↓ MVO2/Cardiac work → ↓ Venous Return…
Flushing of face neck, Pulsating HA due dilation of meninges (esp if topical) , Postural Hypotension due to antagonism of SAS, Halitosis, Methemoglobinemia
Sublingual to bypass liver, Oral, Topical (ointment ?looks like toothpaste?) Dispensed in Lactose to prevent combustion. Should have burning sensation when placed in tongue
Keep away from air, light. Tolerance develops to low doses @ ≈ 4 wks. Stagger w drug free periods to avoid tolerance
block voltage gated Ca channels esp in aa>>vv; Verapamil - ↓ HR, CF TPR and ↑ coronary flow; Ditiazem - ↓ HR TPR & coronary flow; Nifedipine - ↓ TPR & ↑ coronary flow
Used to tx Prinzmetal angina; Effort angina refractory to NO's/ β blockers, or pts w bad SDFX to β blokrs and NO's. Only Verapamil and Ditiazem are indicated x pure effort angina.
Ditiazem - AV block, Hypotension; Verapamil - Hypotension, HA, Periph Edema, Constipation, AV block, CHF; Nifedipine - Hypotension, HA, Perip Edema
Nifedipine has ↑ contractility and ↑ HR as reflexes
only Ditiazem is safe to use w β blockers
Oral, prot bound, No Orthostatic Hypotension
Coronary Vasodialtion - D, V, N); Peripheral Vasodilation - N, V; Contractility - N ↑ (reflex), V ↓; HR - D ↓, N ↑ (reflex) , V ↓
Fatty Acid Oxidation Inhibitor (pFOXI)
Antiarrhythmic AgentsClass I Na Channel Blockers (Impede Diastolic Depolarization at some point?)
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Ia Procainamide IV
Ia Disopyramide
Ib Lidocaine IV Not as deadly as Ia
Ib Tocainide oral Not as deadly as Ia
Ib Mexiletine oral Not as deadly as Ia
Ib Phenytoin oral Not as deadly as Ia
Ic Flecanide Just as deadly as Ia
Ic Moricizine Just as deadly as Ia
Ic Propafenone Just as deadly as Ia
Class II - β Blockers
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Drug Drug Interactions
bind to open/active Na channel
↑ upstroke of AP duration (APD); ↓ K flow; ↑ phase 2, and AP depolarization
Fever, Rash, AntiNuclrAntibodies, K channel blocking, widen QRS cmplx, widen QT intervals; ≈ 20% converted to NAPA in liver so watch x NAPA toxicity, Lupus in slow acetylaters
↑ toxicity w Amiodarone Cimetidine Ranitidine Procaine
No evidence shows it works. Ia and Ic kill ppl.
bind to open/active Na channel
↑ upstroke of AP; ↓ K flow; ↑ phase 2, and AP depolarization
No evidence shows it works. Ia and Ic kill ppl.
bind to inactive/closed Na channel
↑ K flow, ↓ APDl and phase 2
Mouth numbness, Tinnitus, slurred speech, confusion, somnolescence, sxrs, CNS depression; activates K channels → ↓ AP duration from hyperpolarization
↑ toxicity w Propranolol, Verapamil Cimetidine
bind to inactive/closed Na channel
↑ K flow, ↓ APD and phase 2
activates K channels → ↓ AP duration from hyperpolarization
bind to inactive/closed Na channel
↑ K flow, ↓ APD and phase 2
activates K channels → ↓ AP duration from hyperpolarization
bind to inactive/closed Na channel
↑ K flow, ↓ APD and phase 2;
Death via Hypotension, Cardiac Failure, Asystole esp in old ppl, Teratogenesis, Gingival Hyperplasia, Hirsutism; activates K channels → ↓ AP duration from hyperpolarization
↓ upstroke of AP BIG TIME
All Class I antiaryhthmics ↓ Excitability, Responsiveness, and ischemia; also, by ↑ phase 2 they stop the cells from becoming prematurely "ready"/primed? for another contration. (except for lidocaine). Quinidine (Ia) just tells all the cells to STFU so it can reset the rhythm
Drug Drug Interactions
Non-selective (Propanolol, Sotalol, Timolol)
Propanolol - use x Atrial Tachyarrhythmias
Bronchospasm, Hrt Failure, Bradycardia AV Block, Raynauds, Depression, Sex Dysfx: see above*: Sotalol may cause Torsades de Pointes
ISA (Acebutolol)
Class II - β Blockers are GREAT x Tachyarrhthmias
Class III K+ Blockers
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Ibutilide use x A Fib/Flutter;
Dofetilide orally BID
Torsades de Pointes
Class IV Ca Antagonists (Nifedipine Is NOT an Antiarrhthmic agent)
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Verapamil AV SA Dysfx, Asystole
Diltiazem
Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine
Class V Cardiac Glycosides
Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc
Digoxin/Digitoxin?
Cardio-Selective (Atenolol, Metoprolol, Esmolol)
Atenolol DOC x something; ↓ automaticity by ↓ SAS; ↓ SAS related responsiveness of ischemic tissue; ↓ AV nodal conduction
Esmolol is new It looks like Ach, blocks the AV node and then is destroyed.
α & β blockers (Labetolol)
Drug Drug Interactions
Amiodarone (also Ia Na channel blocker and Ca channel blocker)
Delays repolarization; marked ↑ in APDuration and ERP (effective refractory period)
Good x ischemic tissue and during V Tachy to slow down excitability Hz by ↑ prolonging AP duration
Pulmonary Fibrosis (fatal), Irreversible Liver damage, Constipation, bluish discoloration, thyroid dysfx (from I's) yellow discoloraton of eyes, Torsade de Pointes Fatal arrhthmias but these are rare. Life saving prop's far outweigh.
w β blocker → inhibition of both; w α blocker → ↓ conduction velocity in all cardiac tissue; ↑ Toxicity w Procaine
Has a 30 day half life (bad)
Torsades de Pointes; Prolongs QT interval when acting as K channel blocker
use x Atrial Tachyarrhythmias, A Fib;
Torsades de Pointes, Prolongs QT interval
Sotalol (oooh also a β blocker)
use x Atrial Tachyarrhythmias
Drug Drug Interactions
↓ SA automaticity; ↓ AV nodal conduction velocity
use x Atrial Tachyarrhythmias
Don't use w Propranolol or Disopyramide
↓ SA automaticity; ↓ AV nodal conduction velocity
Drug Drug Interactions
↓ SA automaticity; ↑ ventricular Delayed After Depolarization (DAD); ↑ Excitability bc depolarize membr pot; Toxic doses have adverse effect.; Conduction velocity ↑ in atria, ↓ in AV node, ↓ in ventricles at toxic doses
use x Atrial Tachyarrhythmias
SA Bradycardia, SVT, AV Block, Jxal Tachycardia, V Tach, V Fib (20% of pts have SDFX)
Tx toxicity w K (to lvl @ 5 mEq/dL), Lidocaine to hyperpolarize, Dig Fab Fragments, DO NOTUSE PADDLES, VERAPAMIL or BRETYLIUM
Adenosine DOC x PVST Heart Transplant
Atrial Tachyarrhythmias - Tx w Propanolol, Dofetilide, Sotalol, Digoxin or Verapamil
Wolf Parkinson White (WPW) Syndrome (a ventricular pre excitation thing) - ↓ AV Node via Vagal Maneuvers, Verapamil Digoxin, Propranolol; ↓ Accessory (kent bundle) w Amiodarone QPD Flecanide Propanlolol
Torsades de Pointes - Stabilize w MgSO4 (DOC) remove causative agents (eg quinidine, amiodarone), give K to ↑ serum K lvls to 5+/- .5mEq/L
Paroxysmal Ventricular Tacnycardia (PVST) - DOC is Adenosine
↓ cAMP, ↑ gK, ↓ automaticity of SA node; Conduction velocity ↑ in atria (vagomimetic), ↓ in AV node
Flushing, SOB, Bronchospasm, HA, Hypotension, Nausea, Paraesthesia
V Tach - tx w Lidocaine (↓ V automaticity, Rapid depolarization in nml, Bidirectional block in Ischemic), Procainamide (↓ phase 0, ↑ ADP, ↑ ERP, ↓ V automaticity), Propranolol, Bretylium (↑ ADP, ↑ ERP) DC Cardioeversion (the paddles)::: None of these incr survival. HA!
Beta Lactam AntibioticsPenicillins
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
GENERALLY Staph Strep??
Penicillin APenicillin F
Penicillin G
Penicillin V penicillinase penicillinase oral
Methicillin not used all too much staph aureus Nephrotoxic oral
Oral contraceptives lose activity if + PNC b/c gut bact activate BCPs; lose activity if + TTCCL
excreted in the urine; picks up protein at lactam ring creating a hapten leading to allergic rxn
no metabolism, drug destroying, drug can't penetrate, mutation, bioch indux, conjgx, transdx, transposition
Narrow Spectrum G+
combine w Probenicid (weak acid) to compete for excretion; Add procain (charged) to decrease absorption and incr T1/2; add phenoxyacetic acid to make acid stable and thus available orally
short T1/2 (<60 mins), renal excretion
injection b/c not acid stable
Narrow Spectrum G+
Narrow Spectrum
B lactamase resistant :-); staph aureus…damn
created to overcome the Narrow Spectr of PNC G
Broad Spectrum
Ampcl+Sulbactam (B lactamx inhibtr) x incr efficacy; BCP lose contraceptive activity w Ampcln
penicillinase; NOT active vs Klebsiella or Pseudomonas
created to overcome the Narrow Spectr of PNC G. Not much used anymore
Broad Spectrum
loses activity if + gentamycin b/c chem rxn so give staggered
Given w Na so watch Na levels
penicillinase; NOT active vs Klebsiella or Pseudomonas
Staph aureus starting to become resistant
Narrow Spectrum
B lactamase resistant :-)
Staph aureus starting to become resistant
Narrow Spectrum
B lactamase resistant :-)
Staph aureus starting to become resistant
Narrow Spectrum
B lactamase resistant :-)
Staph aureus starting to become resistant
Narrow Spectrum
B lactamase resistant :-)
Amox+Clavulinic acid (B lactamx inhibtr) x incr efficacy
oral (better vs Ampicillin)
prodrug (ampicilin is active compound
Geocillin (Carbenicillin Inodyl)
Narrow Spectrum, G-
Pseudomonas (best vs Psuedomonas of PNCs), G-
Pseudomonas AND klebsiella G-
Not an Antibacterial
D-Cycloserine (2ry tx of TB (1 of 4))
Cephalosporins
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
GENERALLY excreted in the urine cross rxn w PNC allergy oral?
inhibit beta lactamase (no antibacterial activity by themselves)
Clavulanic Acid + Ticarcillin or Amoxicillin; Sulbactam + Ampacillin; Tazovactam + Pipercillin/Mezclocillin (combos needed x activity)
cell wall sythesis inhibtr via binding D-ala D-ala
(staph aureus, C. diff, commonly used x PNC resistant drugs)
Red Man SSx, (hives, HoTN, flushing, rush, chest pain); ototoxic, injx site irritation,, rash, chest pain, hypotension, synergistic w Nephrotoxic drugs (AG)
AG + vanc = Synergistic Nephrotoxicity
Bact chg the D-ala D-ala so drug has nowhere to bind
IV (IM) via slow infusion to avoid Red Man SSx, oral x gut bact (e.g C. diff)
(staph infx that don't RE to PNC meth, oxa naf or cloxacillins)
Nephrotoxic if given IV (less so if given orally)
Synergistic w other nephrotoxc drugs
topical intrathecal/pleural (IV/IM)
detergent, cell membr disruption
detergent, cell membr disruption
Circumoral paresthesias if IV, nephrotoxic
Drug Drug Interactions or Combos
Broad Spec (G+ cocci, G- cocci/rods
compeltes with paba for coupling enzyme so bact can't make vit. B9. free drug is active drug; pH dependant (will crystalize out at low pH so drink lots of water
none but alt x (UTI, nocardiosis, shigella, trachoma, chlamydia, pneumocystis jirovechi)
StvJonSSx (from long lasting sulf Rx), decr vit K synth(by wiping out gut bact), hypoglycemia/GI, hepatitis, crytalluria, CNS-rare-,
incr warfarin activty (wfn is bumped off plasma prot by sulfmds causing unwanted bleeding); hydantoin (same as wfn but is an anticonvulsant), incr T1/2 Phenytoin (competes x micrsomal enzx),
good distribution, bound to plasma prot making it difficult to metabolize, renal excretion (unchanged), acetylation in liver loses activity but retains toxicity, T1/2 depends on kidny fx
gluc6phos DH defx (NADPH is depleted and can't reduce G6PDH-causes hemolytic anemia), AIDS, kernicterus (new borns; bumps off bilirubin and causes mental retardation), allergic to SO2 (e.g. Celexa)
Minocycline Tetracycline Lyme teeth discoloration not good for UTIs
Drug Drug Interactions or Combos
G+, G-, Broad Spectrum
stop ribosomal complex from moving, disrupt aa binding
G+, Bacteriostatic (cidal @ high doses but w toxicities
Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation
Mycoplasma pneumonia, Legionella, Diphtheria, also used to tx bacterial bronchitis, otitis media, acne(topical). Prophylax endocarditis colon/oral surgx [2ry Staph Strep, tetanus, chlamydia, lyme; some G- N. Meningitidis, H. flu, B. pertussis]
ERTHX + Clindamycin is antagonistic; ERTHX + PNC = syng renal damage; decr cytochrome P450 activity so other Rx/herbs have more activity Chloramphenicol+Erythromycin=antagonism by 50S competition
concentrated in the liver, bile excretion
Induced resistance, 50S ribosome mutation, efflux pumps, hydrolysis/destrx of Rx; cross resistance to other macrolides and clindamycin
must coat tablet to protect it from stomach pH, so it dissolves in duodenum; good body distr
Broad Specturm
Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation
H. flu, mycobacterium avium (AIDS pts usu), H. pylori
decr cytochrome P450 activity so other Rx/herbs have more activity
Broad Specturm
Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation
GI (staph enteritis could cause superinfx), hypersstvy, photosenstvy, liver damage, renal damage, dizzy/vertgo, damage to teeth/bones causes discolored teeth
Chelates heavy metals (Ca, Mg…) which reduces absorption; TTCCL decreases activity of BCPs via killing gut bact needed for BCP activation; PNC+TTCL=antagonistic
Lower dose if kidney disfx. Excretion depends on GFR (except for minocycline and doxycycline); kids <10 preg fem
Gradual reisistance via R factor and efflux, overuse. Cross resistance w streptomycin, erythromycin, ampicillin, chloramphenicol, oxacillin, and cephalosporins. G- usu have cross resistance w chloramphenicol (not G+)
oral not so good absorption, IM/IV
Broad Specturm G+, G-
30S inhibition previnting t-aminoacyl binding
oral not so good absorption, IM/IV
Doxycycline Tetracycline Lyme teeth discoloration oral good absorption
Tetracycline ssti, intra-abdominal infx GI, N/V/D IV ONLY
Chlorapmphenicol lower dose if liver disease oral
Aminoglycosides
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
GENERALLY Aminoglycosides
Streptomycin Aminoglycosides TB (must combo); plague mutation of 30S subU IM (no CSF distribution)
unchgd excreted form by kidny via GFR; short T1/2, low TI, dosing schedule is tricky so instead of lots of small doses Rx is a few heavy doses instead of lots of small doses
renal disfx incr plasma lvls so lower dose; synergistic renal tox w other renal toxic drugs
resistance via R factor transfor; mutation of 30S subU; adenylation in kanamycin streptomycin, gentamycin, tobramycin; phosphorylation in kanamycin, streptomycin; acetylation in kanamycin, neomycin, tobramycin, amikacin, gentamycin strreptoycin
IM, subQ, oral (x gut infx; bad absorption in gut), intrathecal, topical
inhibits fMet binding; inhibits translocation step (aminoacyl binding to tRNA); require O2 for transport thru cell walll
vestibular system disruption, hearing loss if high doses, peripheral neuritis, facial paresthesia, NMJ blocked in high doses, rash/hives, kidny damage
Must combo w other TB drugs; strpmcn + PNC to tx enterococci; DO NOT GIVE ALONE b/c resistance develops quickly; synergistic activity w Erhthromycin to tx Strep faecalis endocarditis
Broad Spectrum
E. coli, Proteus, Shigellae,, Klebsiella; prophylactic x bowel surgx (staph enterocolitis)
Nephrotoxic ototoxic, contact dermatits
NOT effective x Pseudomonas or Bacterioides
topical oral x gut infx,
Pseudomonas resistant to Polymyxin B(Klebsiella, Proteus , G- rods causing meningitis; E. coli, ); Plague
Quinupristin streptogramin G+ 50S inhibitor combo drug w Dalopristin oral
Linezolid Oxazoladinone G+ GI, HA, MAOI inhibition poor people
Netilmycin Oxazoladinone
Antifungal Drugs
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
Polyenes
Nystatin Polyene N/A
Amphtericin B Polyene N/A
Imidazoles/Triazoles
Ketoconazole
VR E. faecium, bactremia, URI caused by MRStaph/Strep PNC resistant Strep pneumoniae
joint muscle pain, decr cytoP450
R factor transmits binding site mutation
multi-drug resistant organisms
Drug Drug Interactions or Combos
yeasts and fungi
binding to ergsterol causes cell membrane leakage
Candida albicans; Moniliasis (oral or topical) (Cryptococcus, Histoplasma, Blastomyces, Trichophytion, Epidermophyton, Microsporum; sometimes mycoplasma bact),
none unless given systemically (oral - mild N/V, diarrhea; IV - hemolytic anemia, kidny damage)
topical, oral (excreted in feces) vaginal tablets,
.3 mg <MIC< 1 mg. Dose is 2x MIC that lab gives you.
binding to sterol causes cell membrane leakage
severe deep fungal infx (e.g. meningitis, bone, pnemonia…); topical
VERY TOXIC: NEPHROTOXIC, hypersensitivity, chills, fever, phlebitis, HA, anemia, anorexia, decr renal fx HoTN, hepatic failur, jaundice, hepatocullular disfx,
Use only in hospital w fatally ill pts and make sure pt is "healthy" enough to take th Rx. Daily dose not to exceed 1.5 mg/kg; AmphoB allows Rifampicin (usu bact Rx) to penetrate fungal cell wall and kill fungi, but is toxic to host); intrathecal administration causes chemical meningits
DO NOT EXCEED 4g else renal damage, do LFT's, renal fx test b/f tx
topical, IV (low doses long time, .5mg/kg)
Broad Spectrum
Inhibition of ergosterol syths causing membr disruption
systemic infx (coccidiomycosis, paracoccidiomycosis, histoplasmosis-formally txd w Amph B
inhibits cytchrP450 (disrupts steroid hormone metbz and other drug metabz), elevates LFT's
Deaminated to 5fluoracil (active cmpd) which replaces U in mRNA resulting in screwy peptides. Also converted to 5fluorodeoxyriboseMonoPhos. Which inhibits thymidylate synthase. Basically commits suicide
Candida albicans (Cryptococcus)
Fatal Bone Marrow Depression, diarrhea, AIDS pts have trouble tolerating
Usefulness lmtd b/c cytopls membr not permeable to 5Flu, so AmphoB potentiates 5-flu effectiveness (tx x Candida & cryptococcus infx)
HIGH lots of things become resistant
binds to cell membr, kills(?) growing fungi by disrupting mitotic spindle. Binds to host keratin creating an environment where fungi can't grow and the fungi is shed w natural shedding process
skin and nail infx, athletes foot. (Microsporum, trichophyton, Epidermophyton; athletes foot and stuff): (systemic x candida albicans)
mild; HA (gone in a few days), memory probs, GI
Gris + PHB decr Gris lvls by decr absorption; Gris + warfarin decr warfarin activity by induction; Gris induces prophyrin synths causing porphyria attack to those pts w porphyrias
oral (good absorption if eaten w fats), IV. Up to 12 mos to treat dermatophytes
Broad Spectrum
Inhibition of ergosterol syths causing membr disruption
HA, diarrhea, dyspepsia, abd pain; chg in tast patterns; incr LFT (severe hepatotoxicity rare)
T1/2=16 days, liver metabolizes, inactive cmpd excreted in feces kidny
Inhibits beta 1-3 glucan syths
Aspergillosis after AmphoB has failed
Drug Drug Interactions or Combos
Streptomycin Aminoglycosides 1ry for all TB tx: oral;
Cycloserine 2ry must be given w B6
Ethionamide GI, HoTN, liver toxicitiesLevofloxacinViomycin AG 2ry prot syths inhibitor 2ry TB ototoxicityKanamycin AG 2ry prot syths inhibitor 2ry TB ototoxic nephrotoxicAmikacin AG
Rifabutin/Rifampin 1ry induces P450 from RNA pol mutation
Capreomycin peptide
Aminosalicyclic acid folic acid synths
Ciprofloxacin
Isoniazid TB combo
Ethambutol excreted in urine/feces DO NOT use in kids oral
inhibits fMet binding; inhibits translocation step (aminoacyl binding to tRNA); require O2 for transport thru cell walll
Ototoxicity, nephrotoxicity (all AG do)
INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem
Start to see improvement of morbidity in 2 weeks
Seizures (esp if predisposed), peripheral neuorapothy
ppl w seizures, depression (exacerbated)
inhibits RNA polymease (initiation step)
TB combo, active systemic TB, TB mingitis,eradication of meningiococcal carrier state; Mycobacterium avium
reare hepatitis, turns host fluids orange, flu like ssx
must combo; maybe can use AmphoB to let rifampin into fungal infx; Rifampin + AminosAcid block the absorption of the other from gut (bad thing); INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem
INH+Rifampin have additive liver toxicity <-toxicity; causes loss of BCP activity
2ry agent when 1ry no longer useful
ototoxicity, renal toxicity (not as bad as AG)
2ry b/c of GI probs
bad diarrhea b/c of high dose (8g)
Rifampin + AminosAcid block the absorption of the other from gut (bad thing); BCPs lose effectiveness; induction of liver;
requires 8g per day
1ry TB tx, NO G-/+ activity
isonicotinic acid uses up causing OH buildup in cell; interferes w mycolic acid synths causing cell wall damage
INH metabolit causes toxicity B6 defx, peripheral neuropathy; liver toxicity esp w EtOH (death); szr if prone;
INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem; give w B6; INH inhibits metbz of Phenytoin
prodrug (active cmpd is converted by catalase to isonicotinic acid); LONG T1/2 you can give; acetylation inactivates; P450 metabolism
Treat <20yos. DO NOT TREAT if >35yos
mutation of catalase TB has high mutation rate so selectivity is common :(
oral good absorption; prophylaxis x 9 mos if evidence of expossed (only prophylaxic tx
1ry TB tx, NO G-/+ activity
mycolic acid inhibition ro RNA syths inhibtion
TB combo, mycobacterium avium cmplx
retrobulbar neuritis @ high doses (decr visual acuity, red green color blindness)
INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem
Pyrazinamide 1ry reinfection
Dapsone Leprosy use 3-4 leprosy mx to startClofazimine Leprosy use 3-4 leprosy mx to startAmithiozone Leprosy use 3-4 leprosy mx to start
Thalidomide Leprosy teratogen use 3-4 leprosy mx to start
Ethionamide 2ry Leprosy use 3-4 leprosy mx to start
AntiViral Drugs
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
HIV Drugs- 1PI + Ritonavir + 2NRTI (specific combo) = 4 drug Tx; or NRTI (combo)+ NNRTI = 3 Drug Tx
Liver Toxicity TOXICITY MANDATES hospitalization
INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem
HIGH if tx w/o other drugs
pregnant women (day 20-50 cuases seal limbs in fetus)
Drug Drug Interactions or Combos
Amantadine and Rimantadine (better mx)
prophylactic tx of Flu A2 in elderly (parkinson)
nervousness, depression, epilepsy esp if prone to psychosis
do not use w bactrim, antihistamines (causes neurotoxicity; esp in older ppl, hmmm)
NOT USED CURRENTLY B/C OF RESISTANCE IN ALL STRAINS OF FLU
decr dose in elderly b/c of decr renal fx
Idoxuridine (historical significance only)
antimetabolite; DNA synths inhibitor by stopping DNA elongation; incorporated into DNA causing DNA breakage, muation rate incr; selectivity due to rapid rate of virus replication
(herpes keratitis from herpes type I, if nothing else left)
photosensitivity, edema causing lacrimal duct occlusion; slows down healing process
topical, (systemic-HARDLY)
(DNA viruses via decr synthesis)
replaces adening to stop DNA synths
(herpes keratitis from herpes type I, if idoxuridine not available); chicken pox, herpes encephalitis via systemic; ocular herpes infx
at high doses stops host DNA synths (polymerase); carcinogen, teratogen, mutagen
systemic - allopurinol + vida causes decr activity of gout mx
deamination causes inactivity; prodrug
topical, (systemic-HARDLY); acyclovir is better
inhibit virus binding by binding to virus; inhibit at all steps of virus rep
Chronic Hepatitis (B, C) (Karposis sarcoma, melanoma)
neurotoxic, flu like ssx usu resolves in days, bone marrow suppresion, exacerbate depression/suicide
inhibits viral DNA polymerase; syths inhibition
Herpes (all kinds and manifestations)
inactivated if taken w allopurinol
Zidovudine NRTI @ low lvls or monothpy
Lamivudine NRTI @ low lvls or monothpy
Emtricitabine NRTI @ low lvls or monothpy
Tenofovir NRTI NOT prodrug @ low lvls or monothpy
Efavirenz NNRTI HIV @ all stages; teratogen cytP450 indux preg fem, liver disfx @ low lvls or monothpy
Atazanavir Protease inhibitor
Fosamprenavir Protease inhibitor
Lopinavir Protease inhibitor
Ritonavir Protease inhibitor inhibits cytP450
Enfuvirtide Fusion inhibitor; peptide binds to gp41 HIV @ all stages don't give if allergic injx
AntiParasitic DrugsAntiMalarial
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
GENERALLY
Chloroquine Aminoquinolone
incorporation into DNA causing early DNA termination and slow replx by blocking reverse transcriptase
HIV @ all stages; prophylaxis x exposure and newborn
damage tissue that are constantly turning over via mt toxicity; lactose acidosis, liver failure low platelets
combo Lamivudine+Zidovudine
prodrug concerted to nucleotide
incorporation into DNA causing early DNA termination and slow replx by blocking reverse transcriptase
HIV @ all stages; prophylaxis x exposure and newborn
damage tissue that are constantly turning over via mt toxicity; lactose acidosis, liver failure low platelets
combo Lamivudine+Zidovudine
prodrug concerted to nucleotide
incorporation into DNA causing early DNA termination and slow replx by blocking reverse transcriptase
HIV @ all stages; prophylaxis x exposure and newborn
damage tissue that are constantly turning over via mt toxicity; lactose acidosis, liver failure low platelets
combo Tenofovir + Emricitabine
prodrug concerted to nucleotide
incorporation into DNA causing early DNA termination and slow replx by blocking reverse transcriptase
HIV @ all stages; prophylaxis x exposure and newborn
damage tissue that are constantly turning over via mt toxicity; lactose acidosis, liver failure low platelets, renal insfx
combo Tenofovir + Emricitabine
nonompetetive inhibitor of reverse transcriptase
inhibit final prot metabz of HIV prot
HIV @ all stages; prophylaxis x exposure and newborn
long lasting DM, hyperlipidemia, diarrhea
combo w low dose Ritonavir, then combo w NRTI
@ low lvls or monothpy; cross resistance
inhibit final prot metabz of HIV prot
HIV @ all stages; prophylaxis x exposure and newborn
long lasting DM, hyperlipidemia, diarrhea
combo w low dose Ritonavir, then combo w NRTI
@ low lvls or monothpy; cross resistance
inhibit final prot metabz of HIV prot
HIV @ all stages; prophylaxis x exposure and newborn
long lasting DM, hyperlipidemia, diarrhea
combo w low dose Ritonavir, then combo w NRTI
@ low lvls or monothpy; cross resistance
inhibit final prot metabz of HIV prot
HIV @ all stages; prophylaxis x exposure and newborn
long lasting DM, hyperlipidemia, diarrhea inhibits cytP450
combo b/c incr T1/2 of other drugs; but contraindicated if pt taking other mx
@ low lvls or monothpy; cross resistance
painful injx; incr chance of bact pneumonia
@ low lvls or monothpy; cross resistance
Drug Drug Interactions or Combos
sulfa drugs, trimethoprim, quinolones
DNA replication disruption; B9 syths inhibition
Binding to DNA inhibits nucleic acid synths
use during erythrocytic phase of maria cycle; schizonticide;
GI, HA, malaise, vertigo, blurry vision.
Coadministration w Primaquine is required to tx /prevent relapse;
Excreted in tears absorbed by corneal epithlm causing edema and opacifications of cornea (retinal aa constrx causes retinal ischemia and visual impairment)
if Plasmodium sp can't concentrate in cell then mx won't work; falciparum is chloroquine resistant and reqs cinchona and anti-folates
as prophylactic tx must be given x 6 mos straight after leaving endemic area.; as suppressive therapy 2.5 g orally w/in 3 days, IM if necessary;
Mefloquine
Hydroxychloroquine
Quinine Cinchona alkaloid
Primaquine 8-Aminoquinolone ppl w Gluc 6 P DH defx
Chloroquanide
Pyrimethamine
Trimethoprim
ppl w Gluc 6 P DH defx
Sulfa
Amebicides, AntiProtozoal Drugs
Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration
Metronidazole teratogenic
Diloxanide furoate
blood schizonticide
blood schizonts of P falciparum, vivax, Prophylactic ovale, malariae
interference with w fine coordination and spatial discrimination
not active vs P falciparum; pts w epilepsy or on psychiatric mx; pregn
prophylactic vs chloroquine resistant falciparum, ovale, vivax;
Actinomycosis-1)Cervicofacial-most common, usu follows dental caries and happens after trauma 2)Thoracic-pulmonary inf may be initiated by extentision or inspiration. Maybe spread to CNS 3)Abdominal-usus due to perforation of intestinal wall e.g. appdx rupture. ss(x) follow infd organ. 4)Genital-common in femms, usu w/ IUDs, ss(x) similar to PID, usu subclinical
75% of cases in Males unk reasons. 50% of cases to immunocompr, AIDS, EtOHics, cancer, chrnc pulmonary inf. Orgsms are wrdwde, soil and aquatic.
Nocardiosis-Pulmonary inf as transitory or chronic, rarely necrtizing, w/ many large abscesses. 2)May disseminate to organs w/ predilection to brain
M>F b/c of more exposure. Sub/tropical, Sudan, Mxco, usu soil dwellers.
Actinomycetoma-SubQ inf 1)Swollen lesion usu on foot/hand suppurating abscesses w/ grains (same as eumycetoma)
1)Modes of Inf-Passage through birth canal, infection in utero, contact during manifestation, blood transfusion 2)Adolescent to adults
Syphillis-1)Primary Stage-Hard chancre nonpainful (genitals-males cervix-fems) 2)Secondary Stage-Flu like ssx, skin lesions, mucous membrane lesions 3)Latent Period 4)Late Period/Tertiary Stage-Neurosyphilis:Asymptomatic or Symptomatic-Meningovascular, Parenchymatous (paresis, Tabes Dorsalis). Late Benign Syph-Gumma Formation
Pinta-Looks like skin is peeling, or becoming unpigmented
Bejel/Endemic-Mouth lesions, skin lesions, granulomatous lesions on skin nasophrx, bones
Borrelia recurrentis, hemsii, turicatae, parkerii
Relapsing Fever Tick Born (B. recurrentis)-More relapses but less severe. Louse born (B. hermsii, turicatae, parkerii)-Usu only one severe febrile episode
Leptospirosis-usu subclinical may cause fevers, conjuctivitis, Icterus jaundice Kidney/Liver dss
Bact of supragingiva is mostly G(+) sp. Bact of subgingiva is mostly G(-) sp. Disruption of these proportions → disease.
Streptococcus mutans, Lactobacillus acidophilus
Everybody everywhere is susceptible (babies falling asleep w/ bottle, ↓ salivary rate, late weaning). Brushing, Fluoride, Peridex (.12% chlorohexidine)etc etc. helps to prevent. ↑[L. acidophilus]≈[caries]. S. mutans main cause of oral infs.
Dental Caries-Decalcification of inorganic and organic portions of tooth via acids produced when bact act on CHOs
Legionella and BartonellaGeneral Features 1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus
Etiology Epidemiology Manifestations
Legionella pneumophilia
Bartonella bacilliformis
Bartonella quintana
Bartonella henselase
1)Microbial-brkdwn of epithelial wall provides entry, G(-) rods increase, tissue damage due to endotoxins of G(-) bact 2)Immunologial-allergic rxn of gingiva to mouthwash/toothpast, pemphigus vulgaris, lichen planus, neoplastic dss, carcinoma 3)Traumatic-blunt trauma, plaques, chemical (aspirin is caustic to epithelial tissue)
1)Bartonellosis-Acute anemia → verruga Anemia caused by removal of infd sensitized RBC's, HA Myalgia. Anemic phase ends when humoral RE induced Chronic Bartonellosis w/ cutaneous lesions1-2cm for years
1)Spread via human louse Pediculus humanus
1)"Trench Fever"-Fevers at 5day intervals 2)Most commonly HA, xtrm wkns tibial pain Varies fr ass(x) to debilitating 3)Angiomatosis
1)Car Scrath Dss-Lymphadenopathy at site of inf 2)SBE 3)Bacillary Angiomatosis
Parasites
Etiology Epidemiology Manifestations
Entamoeba histolytica
Giardia lablia
Balantidum coli
Plasmodium falciparum
↓↓↓SubKingdom Protozoa↓↓↓
Reservoir: Only Humans thus human-human transmission only via fecal contaminated H2O w/ cysts. Flying bugs can transport feces cysts from feces to food Common in Tropics 1)Prot defx, Pregnant, immdfx Inf≠Dss, but may → assx carriers.
1)Amoebic Dysentery-abd pain, cramps, colitis w/ diarrhea→Bloody stools w/ 25poops/day. (R lobe of liver may be inf→rupture→lung inf. Length of illness days-yrs
WrdWde Childrn<10yo e.g. daycare centers Homosexual Males Reservoir:dogs, muskrats, sheep, lakes, rivers aka "backpackers dss" Transmission fecal-oral cyst is infective form Flying bugs can transport feces cysts from feces to food
1)Giardia-mild drrha to malabsorption syndrm, foul dirrha, abd cramps, farting, steatorrha Malnutrition b/c G. lamblia absorbs fat sol. stuff like beta carotene, B12 exacerbating malabsorption syndrm
WrdWde, Fem Mosquito is vector. Mosqo ingests diff sex sp., male matures to magetes female into macrogamete, fertilization forming zygote/ookineate/oocyst, oocyst turns to haploid sporozites, sporozites goto mosqo saliva glands, inf humans. In humans sporozites goto hepatocytes to become merozoites, release, inf RBC's, mature into trophozoites, merozoites, rupture, release more merozoites
Africa Tse Tse fly is vector 1)African Sleeping Sickness
More Notes↓↓↓SubKingdom Metazoa↓↓↓
General FeaturesEtiology Epidemiology Manifestations
Ascaris lumbricoides
Enterobius vermicularis
Stronyloides stercoralis
Wucheria bancrofti
Phylum Platyhelminthes Class ↓↓Trematodes↓↓ General Features Nutrient uptake via absorption Nonsegmented
Etiology Epidemiology Manifestations
Coccidian parasite, Cat is vector and reservoir. Immcprsd and pregnant are at risk. Cat eats cyst, cyst turns into trophozit, trophozit turns to oocyst, cat poops, humans ingest oocyst, oocyst turns into sporozit, inf and dss
1)Toxoplasmosis-Acute:chills, fever, HA fatigue, lmphadenitis, myalgia Chronic:rash, encephlitis, myocarditis
Children under 5, Americas Kissing bug is vector, inf but poops on human skin causing irritation, human scratches inf into skin, inf. Trypomastigotes invade phagocytic cells, develp into amastigotes, multiply, ruputure, mature to trypomastigit form, inf new RBC's (get picked up by new Kissing bug). Many reservoirs.
1)Chagas Disease-Inflamntn, swelling, facial rash/edema, death bea CNS damage (esp in chldrn) and myocarditis
Trypanosoma grucie g, rhodosaiense
Phylum ↓↓Nematodes↓↓
1)Found in 2/3 of world esp (sub)tropics and areas w/ ↓ sanitation 2)Most prevalent in Asia SthEast USA 3)4-14yos 4)Access to hlthcr, hygeine, soc.ec cond's also factors
1)Adult worms no acute ss(x) 2)GI obstr, abdom pain oral expulsion 3)Lung phase w/ pulmonary ss(x) (Ascaris coming out of anus?)
1)Temperate climates 2)5-10yos 3)Adults inhabit cecum Most common helminthe inf in USA
1)Enterobiasis-usu ass(x) but ss(x) = perianal pruritus at night, anorexia irritability abdom pain Sometimes fem w/ vulvovaginitis or peritoneal granulomas
1)Indigenous to S.E. USA (KY, TN, FL LA etc) esp veterans
1)Skin-Larva currens (fast advancing skin lesion usu on perineum or trunk 2)GI-bloating, anorexia nausea 3)Pulmonary-nonspcfc
1)inhabit lymph syst and subq tiss Larva is inf agent Tropical
Fasciolopsis buski Asia Metacercariae is inf agent
↓↓Class Cestodes↓↓General Features Head w/ scolex suckers, hermaphroditic, no gut, nutrients via abosrption aka Tapeworms
Etiology Epidemiology Manifestations
Taenia solium
Taenia saginata
Rickettsia and EhrlichiaI) Rickettiosis
Etiology Epidemiology Manifestations
Rickettsia prowazekii
R. typhi
Rickettsia rickettsii
wrldwde Humans only definitve host T saginata no hooks Larval cyst in undercooked meat is inf agent High in Latin America/Africa low in USA
1)T solium-passing of gravid proglottids >13branches/glottid thus major concern is develping cystercosis 2)cystercosis-depends on where cyst is Neuro is fatal
wrdwde High in Latin america low in USA T solium has hooks, Eggs of undercooked beef are inf agents
1)T sagomata-abd pain, passing proglottids 15-20branches/glottid 2)cystercosis-depends on where cyst is, Neurocyst can be fatal
Cystic echinococcosis Hydatid Cysts Can Be Found In Liver
Human/Rat Louse (or flea) (respectively) is vector/reservoir, Louse dies b/c of inf, Africa, S. America. No person-person transmission G(-)
A)Typhus Fever 1)Epidemic/Louse bornTyphus-Fever HA myalgia, rash on 4th day (1st on trunk then limbs usu not face), Maculopapular rash w/ petechia, CNS dsf(x)(stupor delerium), uremia Brill's Disease is remanifestation usu mild w/o rash
Texas G(-)
2)Endemic Flea Born Typhus-Same as Epidemic but less severe Rash first on appendages THEN trunk
E. USA, campers/hikers. Roden/Dog ticks are vectors. Ticks are vecrtor and reservoir. Ticks not killed by inf G(-)
B)Spotted Fever 1)Rocky Mt. Spotted Fever-incubation x 5days, HA fever myalgia, maculopapular rash w/ petechia on 4th day on hands feet then trunk face. Death via circulatory collapse/kidney failure
2)Boutennese Fever milder form of RMSF Rash first on trunk then appendages
Transmitted by mite bite of house mouse G(-)
3)Rickettsialpox Rash first on trunk then appendages
SE Asia, Australia. Transmitted by chigger G(-)
C)Scrub Typhi Rash first on trunk then appendages
Farm/Rural area, Slaughterhouse workers
D)Q Fever Rash first on trunk then appendages
Actinomycetes
No Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic
Key Diagnostics Treatment Notes
Spirochetes
Spiral shaped, Nonsporulating, Motile
Key Diagnostics Treatment Notes
1)examin sputum, pus tissue, cervical exudates for granules and filaments >1mcmtr side. 2) Culture ID via morph, gram stain (+) and fimaments. 3)Facultative anaerobes
1)PNC 2)tetracycline, clindamycin, sulfonamides. 3)surgery to drain lesions
Part of normal flora. Propylactics used by
dentists and after trauma.Nonsporeforming
1)Distinguish from TB 2)Exam sputum for G+ orgs 3)Culture ID via morph, Aerobic growth, partial acid fast
1)SFM-TMP 2)surgery
20-30% fatal 1)Log phase more virulent vs stationary phase. Virulence due to penetrating growing tip.
Effect lysozome fx. Virulent forms grow out of
macrophage
1)Examine pus for granule and verify size, color, G+ w/ bact filaments<fungal filmts 2)Culture ID via morph, cell wall composition, use for verification
NonVenereal ss(x)-Yaws, Pinta, Bejel Dg(x) via demonstration of orgsm T(x)=PNC (or Ttrcycl or Erythrmc) 2)Virulence-Outer membr prots for adherence, hyaluronidase for tissue invasion, fibronectin for mimic, antiphagocytosis (reason for undetectable) 3)May cause still born or late abortion
Skin to skin
Skin to skin
Oral Microbiology
Key Diagnostics Treatment Notes
…?
Transmission via mouth-mouth contact Usu not fatal
Borrelia in blood, stain w/ Giemsa. Must take sample DURING febrile stage.
1)Ttrcycln, Erythromycin 2)JH rxn
Tick born is Endemic. Louse Born is Epidemic. Relapses progressively
milder. Death via CV probs
1)Clinical exam-"Bullseye erythema"(75% of p(t)) 2)Serological tests ELISA, Immunoflrsc Ab
1)Early Inf-Doxycycline or Amoxycilin 2)Late-Ceftriaxone
Only spirochete resistant to envrnmnt outside body thus is the only spirochete that can be cultivated. Transmission via soil, H2O, food, inf tissue, congenital(rare)
Bact of supragingiva is mostly G(+) sp. Bact of subgingiva is mostly G(-) sp. Disruption of these proportions → disease.
1)Caries excavation. Restore missing s(x)
Legionella and Bartonella1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus
Key Diagnostics Treatment Notes
Gentamycin
Gentamycin
None
1)Flurosc antibody staining 2)Culture fr lung
1)Erythromycin 2) Rifampin
G(-) rods Stain better w/ silver stain Antiphagocytic Antibodies≠killing Cytotoxin inhibits PMN respiratory bursts Macrophages may kill Orgs produce B-lactamase Two other Legionella spp w/ diff DNA but same ss(x)
1)Can be found w/o dss.
1)Can be found w/o dss 2)may cause SBE
1)Blood ID esp in immcmpr pts 2)Cultures NOT helpful b/c too few orgs available due to cell mdtd RE
1)Now reduced in AIDS pts b/c of t(x) for M tb inf
1)Metronidazole (flagyl) follwd by iodoquinol 2)t(x) for carriers w/ luminal amoebiasis iodoquinol, furamide and paromomycin 3)Improve sanitation
Phylum Sarcomastigaphora Class Sarcodina NOT
commensal, Amoebic cysts can form in liver maybe
fatal, Reportable dss in Tx Asexual reprodx. Cyst
Ingestion→Stomach→HCl to release trophozoites in dudnem→Attachment to host cell and destruction
1)Exmn stool x trophozits (fresh smple) usu billions of trophzits, Smple at diff time intervals b/c neg sample ≠inf, Cysts are 11μm long commonly found in solid samples and survive for ≈2wks 2)String test, Ab test w/ 98% accuracy
1)Metronidazole, furazolidine, quinacrine. T(x) of contacts
Phylum Sarcomastigaphora Class Mastigaphora
Cyst*chlorine resistant* Ingestion→Stomach→HCl to release trophozoites in
dudnem and jjnm→trophzits attach to
intstn villi via ventral suckers and absorb
semidigstd food through body, usu encyst in colon, onset of dss b/c of intstn
inflmmtn.
1)Exmn RBC's for rings 2)PCR or Ag detction
1)Mefloquin-orally Quinine-IV both to treat blood and liver
↓↓↓SubKingdom Metazoa↓↓↓
Key Diagnostics Treatment Notes
Phylum Platyhelminthes Class ↓↓Trematodes↓↓ Nutrient uptake via absorption Nonsegmented
1)Thk/Thn blood films for trypomastigotes 2)Biopsy-of nodes, spleen, liver for amastigotes 3)xenodiagnosis-inf clean kissing bug w/ p(t) blood
1)Nifurtimox (has little affect on tissue inf) 2)Na Stibogluconate w/ Meglumine antimoniate
Kissing bug eradication as control method
Phylum ↓↓Nematodes↓↓
1)Microsc ID of eggs in stool 2)Poor growth
1)Albendazole PO (mebendazole later to treat whipworm), Mebendazole avoid vermifuges 2)VitA to improve growth devl't
1)Fem > Male 2)15-35cm long Creamy white Cuticle w/ fine circular striations 3)Adult lives in upper sm
intest
1)Nocturnal observation 2)Scotch tape test of anal area and view micrscp for eggs (≈50mcrmetrs)
1)Albendazole PO (mebendazole later to treat whipworm), Mebendazole 2)treat whole family and school chums
1)F>M 2-13cm Yellow, Fem w/ pointed tail 2)Gravid fem migrates to anus to deposit
eggs 3)Hygeine preventative
1)Eosinophilia as hallmark of helminthe inf 2)Larva in stool 250μm orgnsm=intestinal inf 600μm orgnsm=hyperinf 3)Larva in sputum = hyperinf 4)Culture in beef broth
1)Ivermectin or Thiabendazole, but usu too late by the time p(t) seeks t(x)
1)Symptoms can occur if p(t) put on corticostrds 2)worms don't need to leave body to finish life cycle Can also be free
living 3)↑ prodx of steroids → ↑ virulence
1)Microsc ID of mcrofiliariae of blood sampls at night 2)ICT for Ab-Ag rxn.
1)interruption of dss w Albendazole+Ivermectin(or Diethylcarmazine) for 5 yrs Alleviate/prevent-lymphedema mngnmt
blood/tisse parasite Mosqo vector
↓↓Class Cestodes↓↓Head w/ scolex suckers, hermaphroditic, no gut, nutrients via abosrption aka Tapeworms
Key Diagnostics Treatment Notes
Rickettsia and EhrlichiaI) Rickettiosis
Key Diagnostics Treatment Notes
eggs w/ spine in feces
Praziquantel (incr cell membr permeability) Oxamniquine no longer available in USA
vaccine dev'lt against Sm p80 would be nice avoids inf via surf membr renewal
elliptoid shaped eggs in stool or vomit
Praziquantel (incr cell membr permeability)
1)worm inf dgx via eggs in stool 3mos post inf ID of progolittid for speciation 2)cystercosis-cysts in involved organ Eggs in feces Ag-Ab tests
1)Praziquantel for worm inf. 2)Albendazole or Praziquantel for cystercosis 3)Surgy to remove calcified cysts
cysticercosis ingestion can happen in populations that don't eat pork. b/c a carrier can contaminate the nonpork meal e.g. jews eating food from a dirty pork eater
1)worm inf dgx via eggs in stool 3mos post inf ID of progolittid for speciation 2)cystercosis-cysts in involved organ Eggs in feces Ag-Ab tests
1)Praziquantel for worm inf. 2)Albendazole or Praziquantel for cystercosis 3)Surgy to remove calcified cysts
Imaging Serological tests should be used b/f invasive methds, Immunoassys
Surgry w/ postop Albendazole
Flea born Typhus-Rash on arms/legs THEN trunk Tick born-Rash on trunk first then legs/arms, serology
Ttcycl, Chloramphenicol w/in 7 days onset
30%fatal Flea born Typhus is wrdwde Not fatal for fleas. Fatal for louse
Ttcycl, Chloramphenicol w/in 7 days onset
Ttcycl, Chloramphenicol w/in 7 days onset
inf in tick is everywhere, <60%fatal w/o t(x). Rickettsia live in nucl of cell 2 and 3 caused by diff sp vs 1)
Key Diagnostics Treatment Notes
Ttcycl, Chloramphenicol w/in 7 days onset
Ttcycl, Chloramphenicol w/in 7 days onset
Ttcycl, Chloramphenicol w/in 7 days onset
Ttcycl, Chloramphenicol w/in 7 days onset
Ttcycl, Chloramphenicol w/in 7 days onset
Severity of dss b/c of high [endotoxin] Vector control important esp for human lice and rats Vaccine available
Superficial InfectionsGeneral Features No Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic
Etiology Epidemiology Manifestations
Trichosporon beigelii
Exophiala werneckii
Malassezia furfur
Cutaneous Infections (Dermatophytosis)
General Features
Etiology Epidemiology Manifestations
M. audouinii
T. tonsurans
common in Mediterranean
M. audouinii children, worldwide
usu males. Favors humidity
Trichophyton
usu occurs w/ tinea pedis
More Notes:
Subcutaneous InfectionsGeneral features Introduced via traumatic implantation. Some occur worldwide w/ endemic areas, Several sp may cause same ss(x)Etiology Epidemiology Manifestations
Pedraia hortai Black Piedra-Black gritty nodules in hair shaft
Temperate climates, sporadically in S. U.S.
White Piedra-soft, mucilaginous, light colored nodules on hair
Teenagers, female, U.S. Gulf Coast, FL, warmth of Caribbean
Tinea nigra-Chronic asymptomatic infection of stratum corneum usu of palm
Normal skin/scalp flora. Ds(x) hightest in tropics. Found equally in wo(men). Recurrent. Excess perspiration, corticosteroids, malnutrition and hydrophobic cmpds on skin.
Pityriasis versicolor-Chronic, mildly asymptomatic non-inflammatory infection of stratum corneum. Lesions covered w/ sharply delineated furfuraceous scales, w/ variable pigmentation, may be single or coalesed.
usu caused by 1) Trichophyton (rubrum, tonsurans, mentagrophytes) 2) Epidermophyton floccosum or 3) Microsporum (canis, gypseum, audouinii). colonize keratized tissue. Found on humans, animals, and in soil. Inf fr nml flora are more chronic/mild. Inf fr soil/animals more acute, more sensitive to t(x) and less likely to reoccur. same sp can cause more than one ss(x), more than one sp can cause same ss(x).
childhood disease. Spread frm Mexico to U.S.
Tinea capitus-1) Epidemic a. Grey patch caused by M. audouinii b. Black dot caused by T. tonsurans 2) Nonepidemic more severeTinea favosa-yellow cup shaped crusts called scutula
occurs in adult males, acquired from animals
Tinea barbae-mild irritation to folliculitis
Tinea corpus-ringworm on body w/ scaling to inflammatory lesions of glabrous skin
Tinea crurus (jock itch)-Lesions are sharply demarcated raised erythematous border
Most common, affects millions worldwide
Tinea pedis (athletes foot)-…often begins on 4th/5th digit
Tinea manum-infection of hand
Tinea unguium-nail infection
Transmission my contact, either fr soil, lesions, or indirect (pool, shower, comb, etc) Microsporum sp:macroconidia, Epidermophyton floccosum:macroconidia, Trichophyton sp:microconidia. Temp sensitive limits inf to surface. Fatty acids on scalp after puberty help limit grey patch to pre-puberty.
Sporothrix schenckii
Rhinosporidium seeberi
Loboa loboi
Entomophthoromycosis (C/B?)
Systemic Infections
General Features
Etiology Epidemiology Manifestations
Found worldwide, endemic areas in Brazil, Mxco, Zimbabwe. 75% of cases male, in U.S. associated w/ horticulture/gardening as occupational hazard.
Sporotrichosis-4 clinical types: 1) cutaneous lymphatic-75% of cases. Leads to necrotic lymph nodules progressing along lymph vessels 2) cutaneous non-lymphatic-"fixed" form, found in endemic areas
Pseudallescheria boydii
1ly in males b/c of exposure. Wolrdwide w/ endemic areas in Sudan, Mxco. Orgms usu live in soil.
Mycetoma (Eumycetoma)-localized, swollen, lesion with pus on foot or hand. Pus contains grains. Looks like random lesions on body with dark, crusty draining blotches.
Worldwide, more in Tropics. Males>Femes. Usu a soil orgnsm. Inf via traumatic implantation
Chromo(blasto)mycosis-SubQ, localized chronic inf of skin and subq tissues leading to verrucoid, ulcerated, crusted l(x)s. Starts as small red macule then black stuff on skin, then HUGE swollen warts.
Phaeohyphomycosis cerebral-1)SubQ Phaeo is subQ cysts (1"x1") red, black 2)Cerebral Phae is cerebral inf w/ abscess, fatal 3)inf of paranasal sinuses
Aquatic parasite. Occurs in children/young men > femes. Most cases in Sri Lankan divers/fisherman
Rhinosporidosis-looks like huge wart on/near nose
Affects males, usu S. America. Dolphins may be resorvouir
Lobomycosis-chronic inf may spread peripherally w/ verrucous ulcerated lesions. Develops over 20-30 yrs
Conidiobolus coronatus or Basidiolus ranarum
1)Occur in nml hlthy peeps, asymptomatic/subclinical 2)1ly pulmonary inf that may spread via blood 3)immunit to reinf 4)geographically restricted or in endemic areas 6)localized outbrx from exposure to common source
Coccidioides immitus, Coccidioides posadasii
white females, immunocompromised (AIDS). Disseminated form occurs in men w/ pigmentation and pregn femms (3rd trimester). Found in Sonoran Life Zone/Desert (e.g. El Paso) SW U.S., Mexico. C immitus in San Joaquin Valley. C posadassi elsewhere. Thermly dimorphic mold-soil.
Coccidiomycosis-1)1ry inf is generally inapparent, benign (60%) or mild-severe URI. 2)2ry inf (a)benign chronic pulmonary-thin walled cavities or granulomas (b)progressive pulmonary form-may follow 1ry or from reactivation. May disseminate to skin depending on health status
Histoplasmosis capsulatum
Incidence: Symptomatic pulmonary disease 75% Men. 1:1 sex ration in chldrn. Mildly chronic cases are 75-90%male. Immunocompromised p(x) at risk or mortatlity 70% dissemination and mortality in AIDS p(x). Sexual bias in disease but not exposure Geography: Worldwide, endemic areas E of Misspi, incldng Rio Grande areas. Mold-soil microconidia-irrittion on inhalation. Animals as reservoir.
Histoplasmosis-1)pulmonary inf 95%subclinical. Leaves cavitary lesions in peeps w/ underlying lung probs 2)Disseminated disease may leave lesions b/c infd retic.edoth cells freely disseminate even in ass(x) p(x). Oropharyngeal cancer due to mildly chronic disase (recurrent over 10-20yrs). 3)African Histoplasmosis disese of skin and bones
Blastomyces dermatitidis
Incidence: males>femms AfroAmrcns> All ages but more in 30-50yo's In small epidemics-no sex bias, mostly children inf, usu pulmonary inf. Geography: Thermally dimorphic, Africa, Mxco, Venzla, Israel, India, East U.S. Coast. Lives in soil. Animals (dogs) as reservoir.
Blastomycosis-Inhalation of conidia → 1)Pulmonary inf w/ variety of ss(x). 2)Chronic cutaneous disease is 80% of presentation w/ 50% having pulmonary ss(x) 3)Disseminated disease generalized w/ bone, UG tract, and CNS as extrapulmonary sites.
Paracoccidioides brasiliensis
Incidence:No sexual bias w/ 5-25% of pop skin test +. Symptomatic disease are 90%male ag wrkrs. 11:1 male:femm b/c estrogen inhibits mold to yeast morph. Geography:Central and S. Amrca. Avoids the Amazon Thermally Dimorphic
Paracoccidiomycoses 1)Pulmonary inf asymptomatic, self limiting, may become latent, few develop ss(x) after exposure. 2)Chronic Progressive Inf occurs following latency in 90% cases w/ dissemination to mucosal and gingival srfcs, may have chronic pulmonary disease and some both Dissemination to other organs also observed 3)Acute progressive form (10%of cases) in children and adults fatal in weeks
Opportunistic InfectionsGeneral Features 1)Inf of immunocompromised 2)becoming more frequent 3)pathogenic ones are ubiquitous 4)any fungus or shroom may cause inf
Etiology Epidemiology Manifestations
Cryptococcus neoformans va grubii
Incidence:most children in NY cty skin test +, 1000cases/yr in nonAIDS pop. Maybe 3:1 male:femms. 50%in healthy peeps, 50% 2ry to DM, AIDS, bone cancer, 4th most common disease in AIDS p(x) Geography:worldwide types B-tropical, type C-S. Calif, type AandD-soil and pigeon guano (pigeon as reservoir) Yeast is inhaled and forms capsule after infection
Cryptococcosis-1)1ry Pulmonary inf usu ass(x) to mild ss(x) thus not often diagnosed 2)Disseminated disease-meningitis in U.S., skin/bone inf-Euro.
Candida albicans, and other sp
1)Nml flora of mouth, GI, vagina, skin 2)immunocompromised, trauma experience e.g. burn, leukemias, endocrine factors e.g. DM/DI, AIDS are all predisposing factors. Also iatrogenic 3)Plaque made of (an)aerobe leading to microenvironment. Deep seated plaque required physical scraping for removal. Biofilm helps colony grow. Abiotic surfaces e.g. dentures, help biofilm adhesion and device deterioration
Candidasis-Thrush, Vaginitis, Intertrigginous, Onychomycosis, Diaper rash 2)Systemic inf 4th most common nosocomial blood stream inf and is life threatening. 3)Endocarditis 4)Recurrent Eye inf 5)Random skin rashes/lesions after sepsis 7)UTI 8)chronic mucocutaneous candidiasis involved cell mediated immunity. epithelial lesions are verrucous and warty
Aspergillus fumigatus and other sp.
Adults, males-unkown sex bias 2)similar predisposing factors as Candida. 3)Worldwide in soil-mold, decaying vegetation, can be aerosolized
Aspergillosis-1)Allergic RE (IgE) as asthma, allergic bronchopulmonary aspergillosis (most common RE), IgG RE for nonatopic inf 2)noninvasive colinization-aspergilloma in preexisting cavity e.g. pulmonary pleura, asymptomatic may lead to fatal hemmorrage, nonpulmonary colonization in head cavities w ss(x) of otitis, sinusitis etc. 3)Invasive disease occurs as 1ry pulmonary inf of compromised host seen as a fatal necrotizing pneumonia, dissemination may spread to GI, liver kidney etc
Pneumocystitis jiroveci
More Notes
Rhizopus orysae, Absidia, Rhizomucor, Mucor
Predisposing factors: Acidosis-rhinocerbral inf, Leukemia Steroids Immunosupprsant-thoracic form Geography:Worldwide on decaying vegetation-mold, soil, H2O. Produce sporangiospores (conidia)
Muromycosis-1)Cerebral form looks like bells palsy, death w/in 1 week if untreated 2)Thoracic form is usu pulmonary inf.
Immunocompr, AIDS p(x), Ubiquitous, Worldwide, nml flora, animals as reservoir 30-40%mortality in infants, 10% mortality in AIDS p(x)
Pneumocystitis jiroveci Pneumonia-Diffuse pneumonia 1)debilitates infants w/ subtle infant, Bcell and Lymphocyte infiltration 2)immnocopmr p(x) manifest ofver several weeks w/ fever, recurrent/breakthrough tachypnea, massive # of orgnsms invading alveolar spaces.
Nosocomial inf x2 fr 1980-1990 at 4/1000 discharge. Candida albicans 60%, Candida sp. 20%, Torulopsis, Aspergillus.Inf of UTI, surgical wound, pneumonia, fungemia, IV catheter most likely cause for inf. Infectious, and expensive. Other opportunistic sp: Trichosporon (see white piedra), Geotrichum, Penicillium
Superficial InfectionsNo Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic
Key Diagnostics Treatment Notes
Hair cut (or Terbinifine)
Cutaneous Infections (Dermatophytosis)
Key Diagnostics Treatment Notes
Subcutaneous InfectionsIntroduced via traumatic implantation. Some occur worldwide w/ endemic areas, Several sp may cause same ss(x)
Key Diagnostics Treatment Notes
Direct exam shows hair shaft w/ nodules. Under scope shows fungi
These are types of Piedra
1)Examine skin scrapings for pigmented hyphae. 2)Culture for verification
lipophilic, hypopigmentation due to interference of fungal melanin synths
mentagrophytes) 2) Epidermophyton floccosum or 3) Microsporum (canis, gypseum, ). colonize keratized tissue. Found on humans, animals, and in soil. Inf fr nml flora are more chronic/mild. Inf fr soil/animals more
acute, more sensitive to t(x) and less likely to reoccur. same sp can cause more than one ss(x), more than one sp can cause same ss(x).
USEFUL FOR MOST: 1)chronicity 2)reoccurence 3)severity 4)spread to others 5)pets/animals 6)distinguish fr C.albicans. Some sp fluoresce so use "wood's lamp". Examine hair for spores (endo/ecto(thrix). Skin/nail scraping for hyphae. Culture ID via color, txtr, topography etc)
Transmission my contact, either fr soil, lesions, or indirect (pool, shower, comb, etc) Microsporum sp:macroconidia, Epidermophyton :microconidia. Temp sensitive limits inf to surface. Fatty acids on scalp after puberty help limit grey
Surgery
Systemic Infections
Key Diagnostics Treatment Notes
Lesions along lymphatics is pathognomonic. Direct exam for cigar shaped yeast. Culture ID of thermally dimorphic (grows as: mold in soil, yeast at 37º. Serology not helpful
Orally-KI (in milk), Itraconazole Topical-Amphotericin B (for lymphatic relapse or 1ry pulmonary inf, Heat
1) looks like cysts on skin following lymphatics 2) looks like you put your skin through a meat grinder. Dissemination is rare. Pulmonary inf is becoming common in hospitals
Direct exam of pus for granule of certain size, color, filaments >1mcromter. Culture for verification based on morphology and asexual conidial formation
1)Longterm antib(x): Ampho B, topical Nystatin, KI (all w/ little success). 2)Surgery to clean abscess. 3)Amputation.
Actinomycetoma is due to bact. yeast grows faster vs mold
Direct exam reveals pigmented branching hyphae w/ sclerotic bodies (spore). Culture ID of dark pigmented colonies looking for asexual reproduction
1)Surgery successful if early 2)Itraconazole 3)Antibacterials for 2ry inf 4)AmphoB-partial cure w/ relapse
Direct exam of tissue shows pigmented fungal elements Culture ID via morphology and conidial formation
Drugs w/ variable success. Surgery for certain manifestations
Cerebral Phaeo diagnosed after death.
6-330 mcrmtr sporangium (filled w/ endospores) No culture available
1) Surgery 2) various drugs tried
Direct exam of tissue for chain of bout 4 lemon shaped cells bout 9micrmeters. No culture
Similar to chromomycosis
Spontaneous resolution
1ly pulmonary inf that may spread via blood 3)immunit to reinf 4)geographically localized outbrx from exposure to common source
Skin test. Differentiate from other URI's. Take travel h(x). Direct exam of sputum for sporangia or spherules. Thermly dimorphic grows as spherule-tiss. Culture ID for arthrospores in filament (also exoantigen and DNA probe)
1)bed rest for 1ry ss(x) 2)disseminated w/ AmphoB or Fluconazole (use Fluc in AIDS p(x)) 3)cavities removed surgcly
HIGHLY INFECTIOUS. Possible terrorist agent. Virulence due to protease, estrogen binding prot, Tcell mediated RE in reinf, alkalinazation of phagosomeallergies to 1ry inf is good b/c it indicates immune RE.
1)Direct exam of sputum, biopsy, blood for intracellular yeast. Culture ID takes 28 days shows spores w/ spikes. Use DNA probe nstead 2)animal inoculation to obtain tissue for ID. Blood test also helpful for d(x) and pr(x)
1ry Pulmonary-treat ss(x) only. Acute cases use AmphoB or Itraconazole w/ Ketoconazole and fluconazole as alternatives. Surgery to remove pulm lesions
moderate chronic disseminated disease fatal if untreated (6-12 mos) Fulminant disease may occur in infants and adults. Resistant to oxidative burst
1)Direct exam of sputum, biopsy, pus, for broad based budding yeast 2)Culture ID yeast-tissue mold-nature 3)DNA test, exoantigen
1)AmphoB Itrazonazole 2)2hydorxystilbamine 3)Ketoconazole-mixed results 4)Itraconazole for HIV suppression
virulenc factors: morphogenesis, cell wall, anti macrophage adhesion
1)Direct exam of mucosal scrapings for "pilots wheel" yeast 2)Culture ID mold-nature yeast-tissue, ID via yeast form 3)serolgy for diagnosis/prognosis
1)Sulfa drugs x 3-5yrs 2)Imidazoles, oral kitoconazole (possiblity of relapse) Itraconazole 3)AmphoB for inpatient
Skin test shows no sex bias for symptomatic disease Virulence factors:morphogenesis, estrgn binding prot, cell wall, immune suppression
Opportunistic Infections1)Inf of immunocompromised 2)becoming more frequent 3)pathogenic ones are ubiquitous 4)any fungus or shroom may cause inf
Key Diagnostics Treatment Notes
1)Direct exam of sputum or CSF in India ink for capsule 2)Culture ID-cells examined for capsule Phenol oxidase test used for ID 3)Serologic test for capsular antigen.
1)AmphoB 2)Combo AmphoB+5-Fluorocytosine 3)Fluconazole (esp in AIDS p(x) to prevent relapse)
1)only fungus w/ capsule 2)Meningitis fatal if untreated 3)Virulence factors:Mating type, growth at 37 degr, capsule is antiphagocytic, immune suppression
1)Direct exam of sputum, pus, tissue for yeasts, pseudohyphae 2)Culture ID looks for germ tubes, chlamydospores. Yeast ID via physio rxns 3)Isolation from skin/vaginal mucosa to confirm. Significance in urine 'pends on other factors Isolation fr sterile site significant. 4)Serology ineffective
1)Topicals for Cutaneous-Nystatin, Miconazole, Clotrimazole(OTC x vaginitis), Ketoconazlole. 2)Thrush t(x) lozenges 3)Esophegitis AmphoB, Fluconazole 4)Systemic-AmphoB, Fluconazole, Ketoconazole (sometimes combo w/ Miconazole IV and 5-Flurocytosine 5)t(x) of predisposing factors helps in t(x)
1)can be acute/chronic, disseminated/superficial/deepseated 2)Concern of esophigitis in AIDS 3)Virulenc Factors:yeast morph chgs, protease phospholipase, adhesins, laminin collagen, macrophage evasion, immune supression, Th1 response and Th2 susceptibility
1)Direct exam of sputum, biopsy for septate hyphaew/ acute angle branching 2)Culture ID based on colonial morphology and pattern. Fast growth (white center, green cortex) +blood culture should be considered significant since even invasive cultures can be - Serologic test best in noninvasive disease
1)Treat allergy ss(x) 2)AmphoB w/ 5Fluorocytosine or surgery for Aspergilloma 3)Must treat invasive disease aggressively b/c it's fatal. AmphoB or Itraconazole
1)ubiquitous so may be contaminate in culture so repeated cultures used. 2)Virulence:protease phospholipase, adhesins laminin, gliotoxin (immunosuppresant) endotoxin
1)Direct exam of sputum, biopsy for NON-septate hyphae, usu few to see 2)Culture ID via colony morphgy and sporangial formation
1)Direct exam-Infant looks emaciated, X-rays show diffuse lung cavity 2)sputum, Biobsy (for asci, spores ameboid shaped yeast, 3)No culture available
1)Acute t(x) Trimethoprim-sulfamethozoasole 2)Propylaxis for AIDS via TMP-SMX.
Fungus related to ascomycetes. Atypical chrtcs, used to be thought as parasite. Virulence:adhesins to Type I pneumocytes, disruption of blood-air barrier (lung)
Candida albicans 60%, Candida sp. 20%, Torulopsis, Aspergillus.Inf of UTI, surgical wound, pneumonia, fungemia, IV catheter most likely cause for inf. Infectious, and expensive. Other opportunistic sp: Trichosporon (see white
Dipylidium caninum Cysticercus Ingestion of infected fleas
Schistosoma species Direct penetration of skin by free-swimming cercaria
Cysticercus, embryonated egg or proglottid
Ingestion of infected pork; ingestion of egg (cysticercosis)
Echinococcus granulosus
Ingestion of eggs from infected canines
Echinococcus multilocularis
Ingestion of eggs from infected animals, fecal-oral route
Ingestion of infected beetle larvae in contaminated grain products
Table 8-4. Transmission and Distribution of Pathogenic Parasites
Distribution
Intestinal ProtozoaWorldwide
WorldwideWorldwideWorldwideWorldwideWorldwide
North America, EuropeUrogenital Protozoa
WorldwideBlood and Tissue Protozoa
Worldwide
Tropical and subtropical areasNorth America, EuropeWorldwideTropical and subtropical areasNorth, Central, and South AmericaAfrica
NematodesWorldwide
Areas of poor sanitationWorldwideWorldwideTropical and subtropical areas
Tropical and subtropical areas
Tropical and subtropical areas
WorldwideTropical and subtropical areasTropical and subtropical areasAfricaAfrica and Central and South AmericaAfrica and Central and South AmericaAfrica, AsiaJapan, Australia, United States
TrematodesChina, Southeast Asia, India
WorldwideChina, Japan, Korea, Vietnam
Asia, Africa, India, Latin America
Africa, Asia, India, Latin America
Cestodes
WorldwideWorldwide
WorldwideWorldwide
Worldwide
Pork-eating countries: Africa, Southeast Asia, China, Latin America
Sheep-raising countries: Europe, Asia, Africa, Australia, United States
PSGN - Follows group A β hemolytic strep infx, usu due to bad hygiene, ↓ C3, ASO or antiDNAse B positive, shows "lumpy bumpy" on subepithelium w IF, large hypercellular glom
RPGN - Crescents → deposition of fibrin in bowman space, monocytes, large pale kidneysType I - Anti GBM IgG complexes → complex deposits on GBM → smooth linear appearance on
immunofluroscence. e.g Goodpasteurs
Type II - Immune complex mediated → "lumpy bympy" glomerular BM on immunofluorescence. e.g. Bergers Disease
Type III - ANCA associated aka Pauci immune shows nothing on GBM w immunofluorescence but PMNs have either c-ANCA or p-ANCA. Usu a RE to Wegener Granulomatosis or vasculitis'.
Alport Disease - mutation of α 5 Type IV collagen → nephritis, nerve deafness, and ocular problems and splitting of lamina densa
Hypercellular
Perihilar
Collapsing
Tip Lesion
Lupus NephropathyType I - no ssx
Type II - IgGs and C3 in mesangial matrix, Proteinuria, hematuria. Just uncomfortable
Membranous Glomurlonephropathy/MN/Membranous Nephropathy/MGN - subepithelial immune complex disease vs GBM but NO Ig's in ciruculation, epimembranous spike and dome appearance, Autoimmune states or heavy metals can predispose
Membranoproliferative Glomerulonephritis/MPGN - basement membrane alterations, glomerular cell proliferation, WBC infiltration,Tram Track appearance due to GBM duplication
Type I - Subendothelial IgG and complements, Prominent Tram Track appearance, ↑ mesangial cells, ganular complement deposits w IF, Ig complexes circulating
Type II - Dense Deposit Disease shows some tram trac appearance, C3 next to dense deposists, ↓ serum C3, no Ig's in BM complexes, IgG vs C3 convertase, ribbon like deposits w/in capillary,
nephrotic and nephritic ssx both present
Diabetic Nephropathy - Early stage has large kidneys (later has small granular kidneys), EM shows thick holey GBM, thin lamina rara interna and externa, tubular atrophy
Type III - Focal Proliferative has extenseive damage, ↓ complement, few pts w nephrotic ssx, segmental necrosis, mesangial deposits
Type IV - Diffuse Proliferative is most severe form, combo of nephritic and nephrotic ssx, 100% glomeruli involved, scarring, wire loop abnormalities, subendothelial depostis of Ig's and C3 and
Fibrin
HIV Associated Nephropathy - Black Drug users affected, Tamm Horsfall prots
IgA Nephropathy/Berger Disease - IgA deposits in medangium, recurrent hematuria
Amyloidosis - large kidneys, low BP, congo red stain positive
Hypertensive Nephrosclerosis - Black ppl w uncontrolled HTN, proteinuria
AnticonvulsantsDrugs That Work On Na+ Channels
Drug MOA SDFX Source T(x) For
Carbamazepine
Oxcarbazepine Same as CBZ but less frequency notes
Lamotrigine Inactivates Voltage gated Na+ channels notes
Drugs That Work On T-type Ca++ ChannelsDrug MOA SDFX Source T(x) For
Zonisamide notes
Hepatic Toxicity
Phenytoin (Fosphenytoin is broken down into Phenytoin)
Decrease Influx. Increase Efflux of Na+, Ca2+ and K+ channels in open state
StvnJohns Sx, Contraindicated in ppl w/ allergies to sulfonamid AB
Adjunct thpy for Partial Szrs as induction NOT long term use
Valproic Acid (GABA synth inducer)
At low conc. Blocks voltage Na+ channels. High conc slows influx of Ca++. Increases activity of GABA making enzm (glutamic acid decarbxlylse) and inhibits GABA metabolism.
At low conc. Blocks voltage Na+ channels. High conc slows influx of Ca++. Increases activity of GABA making enzm (glutamic acid decarbxlylse) and inhibits GABA metabolism.
Generalized Epilepsy Sx. Absence Szr
Partial Szr 3rd line x refractory cases
Inhibits Na+channels from inactive state, incr Cl- flux thru GABA receptors (diff from BZD binding site)
alters ion channel leading to decr in NE, 5HT reuptake
Bipolar reduces cycling and depression NOTHING for mania
CarbamazepineSlows recovery rate of inactive Na+ Channels, preventing the PDS. Metabolite also active. paroxysmal depolarizing shift
Hepatic induction leading to need for MASSIVE dosages. Dizzines, diplopia, nausea, ataxia, blurred vision. Aplatstic anemia, Agranulocytosis, Thrombocytopenia, StvJohnson Sx
Spirochetes actively proliferate at entry site, spread over body
1. Chancre present at inoculation site
2. Regional lymphadenopathy
Primary Latent
Variable over period of 5 years (Latent periods with recurrences)
1. Skin and mucosal lesions
Skin and mucosal lesions rich in spirochetes (highly infectious)2. Generalized
lymphadenopathy
Few months to a lifetime (average 6 to 7 years)
Variable-rest of patients life
Related to organ system diseased
Paucity of spirochetes in classic lesion
SyphillisDiagnosis Tissue Change
b)Fluorescent antibody
Chancre present
2. STS positive
STS Positive
1. Infection active
2. STS Positive
STS Positive
1. Gumma
2. Special silver stains 2. Healing3. Scarring
4. Tissue distortion
Identification of T. pallidum
Chancre appears at inoculation site
a) Dark-field microscopy
1. Dark-field microscopy of chancre
None demonstrable; Chancre has healed with little scarring
1. Dark-field microscopy
2. Resolution spontaneous
1. STS positive or negative
Actinomycetes
Gr(-) rods. .5>filaments>1mcmtr. Cell wall w/ peptidoglycan, a.a. Streptomyces-are large family of bact. found in soil, H2O, organic debris-primary source for antibiotics.
Etiology Epidemiology Manifestations Treatment Key Diagnostics NotesActinomycosis Normal flora of GI tract, oral cavity.