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What are 6 questions we need to keep in mind when choosing antibiotics for a patient?
1. Does patient have any drug allergies? Any special circumstances (pregnancy, G6PD def, renal/hepatic insufficiency) 2. Which drug that can be used has narrowest spectrum? 3. Which is least toxic among choices of effective drug? 4. Which has least/mildest side effects? 5. Which is least costly among drugs considered? 6. How is the drug administered? How often does it need to be given. Do blood levels need to be monitored?
Name 4 special conditions that need to be considered when choosing antibiotics for a patient.
1. Pregnancy 2. Lactation 3. Genetic conditions -ex G6PD def 4. Renal or hepatic insufficiency
Should you wait until you get back culture results from specimens from a patient before starting antibiotics?
-NO! -remember that bacteria grow rapidly, so treatment should be started right away -want to get gram stain and cultures in case pt doesn't respond so then you can go back and look and see if different bug than you expected
Contrast antibiotics and antimicrobials
Antibiotics= any natural compound that inhibit or kill bacteria Antimicrobials -synthetic AND natural compounds that inhibit or kill bacteria
Define MIC
=minimum inhibitor concentration -lowest concentration of the drug that inhibits the growth of the bacteria in vitro
Define PAE
=post-antibiotic effect -persistence of growth inhibition after the antibiotic has been removed -usually assayed in vitro
Define AUC
=area under the curve -or the integrated sum from a graph of drug concentration vs time -measure of the total amount of exposure to a drug -in vivo phenomenon
Define pharmacokinetics
=absorption, distribution, metabolism, and excretion of the drug -measured using: 1. peak blood levels 2. AUC 3. urinary excretion 4. biliary exretion 5. t 1/2
Contrast bacteriostatic vs bactericidal
-drug companies highlight diff but not much clinically -based on in vitro testing -same drug can be bactericidal for one bug and bacteriostatic for another -bactericidal= used to tx endocarditis, meningitis, neutropenic pts -Bacteriostatic drug works in conjunction with host's immune system
Name 6 major mechanisms/targets of antibiotic action.
1. Cell wall synthesis -enzymes catalyzing terminal stage of cell wall synthesis -Binds D-ala-D-ala 2. Binds to cell membrane and leads to depolarization of membrane potential 3. DNA synthesis 4. RNA synthesis 5. Protein synthesis 6. Folate synthesis
True or false: most antibiotics target structures shared by offending organism and host
-false -usu target structures unique to prokaryotes
Define Beta-lactam antibiotics
-antibiotics grouped together because they share common structure (beta lactam ring) -includes 1. Penicillins 2. cepalosporins 3. monobactams 4. carbapenems -bactericidal
Describe how beta lactam antibiotics work
-permanently inhibits transpeptidases (=penicillin binding protein involved in terminal cell wall synthesis) -when transpep inhibited -> unstable cell wall -> increased osmotic press -> cell lysis -beta lactam ring resembles D-ala-D-ala substrate of transpeptidase -can also affect enzymatic actions of other penicillin binding proteins
Name 2 situations when beta lactam antibiotics are NOT bactericidal.
1. slow growing or dormant bacteria found in endocarditis, chronic osteomyelitis 2. Bacteria that downregulate autolysin activity (enterococci)
Susceptibility of gram positive bacteria to beta lactam antibiotics is determined by:
1. affinity of drug for its target PBPs 2. whether organisms produces a beta lactamase
Susceptibility of gram negative bacteria to beta lactam antibiotics is determined by:
1. affinity of drug for target PBPs 2. presence of beta lactamase 3. ability to cross outer membrane -beta lactams get in via porins
Describe the group characteristics of penicillins
=beta lactam antibiotics 1.non-toxic 2.have short t1/2 -b/c renally excreted by GFR and tubular secretion 3. Cross allergenic 4. will NOT cross intact BBB 5. Can be administered orally or IV 6. IM injections are painful and can be combined with local anesthetic
Name examples of each of the 4 generations of penicillin antibiotics.
1. 1st generation -PCN G, PCN V 2. 2nd generation -Methicillin, nafcillin, dicloxacillin, oxacillin 3. 3rd generation -amoxicillin, ampicillin 4. 4th generation -piperacillin, ticarcillin, mezlocillin, carbenicillin
Name 5 uses of 1st generation penicillins
-PCN G and PCN C 1. prevention and tx of group A strep 2. prevention and tx of syphillis 3. endocarditis (from strep viridans) 4. meningococcal 5. Actinomycosis 6. leptospirosis
Describe the group characteristics of 1st generation penicillins
=PCN G and PCN C 1. naturally occuring 2. work best against suspectible Gram positive orgn (beta hemolytic strep, treponemaa pallidum) 3. quickly excreted (t 1/2 ~ 30 min)
Describe group characteristics of 2nd generation penicillins.
-methicillin, nafcillin, dicloxacillin, oxacillin 1. made to resist inactivation by beta lactamase from staph (MSSA) 3. Stable when attacked by beta lactamases
Name 3 situations where CAN'T use 2nd generation penicillins.
=methicillin, nafcillin, dicloxacillin, oxacillin 1. MRSA 2. Listeria or enterococci 3. gram negative bacteria -also generally less active against gram positive that do NOT produce beta lactamases
Describe the group characteristics of 3rd generation penicillins
=amoxicillin and ampicillin 1. made to tx some gram negative organisms that do NOT make beta lactamases 2. Some activity against gram positives that lack beta lactamase
Describe the group characteristics of 4th generation penicillins
=piperacillin, ticarcillin, mezlocillin, carbenicillin 1. Broad spectrum of activity against gram negative bacteria (esp Pseudomonas) 2. can still be inactivated by some beta lactamases 3. ureidopenicillins can be used against enterococci a many gram + but NOT S. aureus 4. most IV drugs except indanyl carbenicillin (orally)
Name 6 adverse effects associated with penicillins
1. allergic rxns (rash); cross allergenicity 2. all cause neutropenia due to arrest of meta myelocyotes when given in high doses 3. Plt dysfxn due to coating (when given high [] of drug) 4. Na+ overload (carbenicillin, ticarcillin) 5. Hepatitis (nafcillin) 6. Allergic interstitial nephritis
Describe the bioavailability effects of Penicillins
1. most effective when concentration of antibiotic is >4x MIC for most of day 2. PCNs can cross inflamed meninges (can be used to tx meningitis) 3. high CSF levels of PCN can induce seizures 4. PCNs well distributed to all tissue except CNS, prostate, eye 5. Diff PCNs can be given IV, IM, or orally -some PCNs are better absorbed orally than others
_______ can be used to extend the half life of penicillins
=probenecid -extends half life b/c it blocks tubular secretion -esp good for 1st gen PCNs because very SHORT t1/2
Describe the group characteristics of cephalosporins
=beta lactam antibiotics -4 generations -in general successive generations more active against gram negatives and more resistant to beta lactamases -no activity against Listeria or enterococci
1st generation cephalosporins are used to target _______. An example of one would be _______.
=MSSA, strep, many enerobacteriaceae -Cefazolin
2nd generation cephalosporins are used to target ________ but are less active against _____.
=gram negative beta lactamase -S. aureus -Examples: 1. Cefotetan 2. Cefoxitin
3rd generation cephalosporins have _____ activity against ______.
-broad activity against gram negatives -includes: 1. enterobact 2. PCN resistant strep
4th generation cephalosporins can be used to treat infections by ______, _______, and _______.
Serratia Enterobacter Pseudomonas -but not completely resistant to their beta lactamases -4th generation have long t1/2 -ex. Cefepime
Name 3 adverse effects associated with cephalosporins
1. Allergy 2. Antabuse rxn -> can't take these with EtOH 3. Positive Coombs test (but no hemolytic anemia) 4. Prolonged PTT -b/c MTT side chains inhibit gamma carboxylation of glutamic acid and interfere with action of Vit K -> decreased synthesis of Vit-K dependent coag factors
Define Antabuse rxn
-assoicated with some cephalosporins -when take these drugs and drink EtOH, makes you vomit -caused by the MTT side chains -4 cephalosporins cause this: 1. cefotetan 2. cefonicid 3. Moxalactam 4. cefoperazone
Describe the bioavailability of cephalosporins
-most effective in concentrations equal to or less than 4x MIC -good tissue penetration do NOT get through inflamed meninges -can be given orally or parenterally -most cephalosporins metabolized by kidney
Why can't you use cephalothin to treat meningitis?
-b/c it gets deacetylate by liver and deacetylated form competes with active drug for uptake into liver -also deacetylated: 1. Cefotaxime 2. cephapirin
Define monobactams
=beta lactam antibiotics -one drug: Aztreonam -diff ring structure so no cross-allergenicity (can give to pts with PCN allergy)
Azteonam can be used against _______ but not against _______ or _________.
-aztreobam=monobactam 1. facultative gram negative No activity: 2. gram positive 3. obligate anaerobes
Define carbapenems
=beta lactam antibiotics -4 members 1. imipenem 2. ertapenem 3. meropenem 4. doripenem -active against almost every bug (broad spectrum) -renally excreted
Name 4 carbapenems
=beta lactam antibiotics 1. imipenem 2. ertapenem 3. meropenem 4. doripenem
Name 3 general strategies of resistance to beta lactam antibiotics
1. Mutate porins so decrease penetration of drug through outer membrane -ex. Pseudomonas 2. Alter target of antibiotic -mutations in PBPs -MRSA, S. pneumoniae 3. inactivate antibiotic with beta lactamase -klebsiella, enterobacter, psdeudomonas, B fragillis
One way to get around beta lactamases is to give a _________ in combination with beta lactam antibiotic.
-beta lactamase inhibitor 1. clavulanic acid 2. sulbactam 3. tazobactam -do not work against chromosomally encoded beta lactamases
Define vancomycin
=glycopeptide antibiotic that inhibits cell wall synthesis -blocks polymerization of N-acetyl murmamic acid backbone of PDG cell wall by binding to D-ala-D-ala -bacteriocidal -can only be given IV
Inhibitors of cell wall synthesis are active against ______ but are not active against _______.
Active 1. gram positives -including MRSA and PCN resistant pneumococci Not active 1. gram negatives -b/c cannot get past outer membrane
Name 3 adverse effects associated with vancomycin
1. Red Man syndrome -not allergy -rapid infusion causes HM release from mast cells 2. ototoxicity 3. Neprotoxic -esp when given with aminoglycosides
Name 2 strategies of resistance to vancomycin
1. decreased penetration of antibiotic to its target -gram negatives instrinsically resistant -vancomycin can't get past outer membane 2. Alter target of antibiotic -enterococci
Name 5 types of inhibitors of protein synthesis
1. Aminoglycosides -streptomycin -gentamycin 2. Tetracyclines -doxycycline -minocycline 3. MSL group -macrolide: erythromycin -long acting macrolide: azithromycin -lincosamides: clindamycin -streptogramins (synercid) 4. Chloramphenicol 5. Oxazolidinones -linezolid
Define aminoglycoside
=protein synthesis inhibitor antibiotic -bind to S12 protein on 30s ribosomal subunit -> block normal initiation complex -bacteriocidal -active against bacteria with with ETC
Name 3 aminoglycosides
1. Streptomycin 2. gentamycin 3. tobramycin 4. amikacin
True or false: blood levels of aminoglycosides need to be monitored
-true -b/c low toxic to therapeutic ratio
Define tetracyclines
=antibiotics that are inhibitors of protein synthesis -block tRNA binding to ribosome by binding 30s subunit -usually bacteriostatic -can NOT be given to kids or pregnant women
Name 5 tetracycline
=protein synthesis inhibitor antibiotics 1. tetracycline 2. oxytetracycline 3. minocycline 4. doxycycline 5. tigecycline
Define the MSL group of antibiotics
=protein synthesis inhibitor antibiotics -bind 50s ribosomal subunit and interact with 23s rRNA -> block chain elongation -bactericidal or bacteriostatic depending on organism
Name the members of the MSL group of antibiotics
=protein synthesis inhibitors 1. Macrolide: erythromycin 2. Long acting macrolide: clarithromycin & azithromycin 3. Lincosamide: clindamycin 4. Streptogramins: synercid
Define erythromycin
=protein synthesis inhibitor (MSL group) -activity: gram positives (GAS, Legionella, Mycoplasma, syphyllis, diptheriae) & gram negative (pertussis, C. jejuni) -NOT cross-allergenic -safe in pregnancy -inhibits P450 enzymes
Name 5 toxicities associated with Clarithromycin
1. teratogenic (do NOT use w/pregnant women) 2. fewer GI problems vs erythormycin 3. Ototoxic (tinnitus, vertigo) 4. Inhibits P450 enzymes -> drug interactions 5. Can precipitate C. difficile colitis -b/c broad spectrum antibiotic
Name 4 uses of azithromycin
=protein synthesis inhibitor antibiotic -long-acting macrolide 1. respiratory tract pathogens and strep throat 2. prevent MAC(opporunistic infection with mycobacterium avium complex) in AIDS 3. Shigellosis 4. non-gonococcal urethritis
________ causes a significant risk of pseudomembranous colitis due to the overgrowth of C. difficile
Define streptogramins
=protein synthesis inhibitor antiobiotics; MSL group -bind 50s ribosomal subunit -Synercid is main drug -can be used to tx MRSA and VRE (vancomycin resistant enterococci) but other drugs are more favorable b/c of side effect of Synercid
Define Thlithromycin
=protein synthesis inhibtor; MSL grou -keotolide -binds 50s ribosomal subunit -> inhibit protein synthesis -higher affinity for ribosomal binding site than macrolides -good against staph and strep resistant to macrolides and clindamycin (except enterococci)
Define chloramphenicol
=inhibitor of protein synthesis antibiotic -binds to 50s ribosomal subunit and inhibits translocation of peptide chain from A site to P site -broad spectrum antibiotics -not used in US b/c of side effects
Define oxazolidinones
=protein synthesis inhibitor antibiotic -inhibits protein synthesis by binding to 50s ribosomal subunit ->block peptide transfer activity -major drug is Linezolid -Active against all gram positive cocci and P. multocida (good for VRE, MRSA, and beta lactamase pneumococci) -also MAO inhibitor (watch tyramine levels)
Name 2 types of antibiotics that are inhibitors of DNA synthesis
1. Quinolones -Ciproflaxcin, levofloxacin, trovafloxacin) 2. Metronidazole and Tinidazole
How do quinolones work?
-DNA synthesis inhibitor antibiotics -interfere w/DNA gyrase (essential enzyme) -also prevent winding of DNA helix into supercoiled form -bactericidal
How does metronidazole work?
=antibiotic inhibitor of DNA synthesis -in reducing environment, gets reduced to substance that inhibits bacterial DNA synthesis -action is bactericidal -limited use to anaerobic organisms
Name 2 types of antibiotics associated with antabuse rxns
-make you vomit if you take this drugs and drink EtOH 1. some cephalosporins 2. metronidazole
Define Rifamycins
=antibiotic inhibitors of RNA synthesis -inhibit DNA dependent RNA polymerase by binding to the beta subunit and inhibiting initiation of txn -bactericidal -Major drug: rifampin -effective TB drug -can turn urine, tears, sweat orange
Define Daptomycin
=antibiotic cell membrane toxin -cyclic lipopeptide -activity limited to gram positive pathogens -[] dependent bactericidal activity -disrupts multiple plasma membrane fxns (PDG synthesis, lipotecheic acid synthesis, bacterial membrane potential)
Define Sulfonamides
=antibiotic inhibitors of folate metabolism -competitively inhibit folate synthesis ->inhibit DNA synthesis -often given with trimethoprim b/c act synergistically and bactericidal in combo -several uses -several adverse effects (including allergy) -metabolized in liver, renally excreted
Define Trimethoprim
=antibiotic inhibitor of folate metabolism -competitively inhibits bacterial dihydrofolate reductase -> inhibit DNA synthesis -often given with sulfonamides b/c synergistic and bactericidal in combo -several uses -several adverse effects -renally excreted -
Contrast acute vs subacute endocaridits
Acute -rampant infection caused by organisms of high virulence -rapid destruction of heart valves -may be lethal -days-weeks Subacute -slow infection due to organisms of low virulence -weeks-months
Name 3 bacteria that can cause acute endocarditis
1. S. aureus (including MRSA) -causes most severe disease 2. Pneumococci 3. gonorocci
Name 4 bacteria that can cause subacute endocarditis
1. Streptococcus -60-80% of cases 2. Strep viridans 3. Enterococci 4. Other strep
True or false: all of the leading causes of infective endocarditis are gram positive organsims
-true -some produce dextran and/or fimbriae that make it easier to stick to heart
Describe infective process of endocarditis
-damaged endothelium results in fibrin-plt thrombus -> microorganisms colonize thrombus -> vegetation -hallmark is constant bacteremia with little change in colony counts over time -low virulence microorganisms in bloodstream can form immune complexes with circulating antibodies
Name 4 signs and symptoms of infective endocarditis
1. fever 2. NEW heart murmur 3. evidence of embolic phenomenon 4. higher grade or persistent bacteremia -can also see in course of disease 1. loss of appetite/weakness 2. anemia 3. splenomegaly
Name 3 mechanisms by which infective endocarditis can cause tissue damage:
1. local invasion by the organism 2. peripheral embolization of vegetation fragments 3. circulating immune complexes
Name some risk factors that predispose to infective endocarditis.
1.valvular heart disease 2. mitral valve prolapse with regurg 3. congenital heart disease 4. coartation of aorta 5. Marfan's syndrome 6. PDA 7. VSD but NOT ASD 8. Perpipheral arteriovenous fistulas 9. Idiopathic hypertrophic subarotic stenosis 10. Prosthetic valves 11. IV drug use
Name 2 things required for infective endocarditis to form
1. lesion on vascular endothelium susceptible to infection -causes: turbulent flow, high pressures, traumatic injury, structural defects 2. Circulating organisms (ex bacteremia) that can infect endothelium
True or false: invasive procedure lea to transient bacteremia.
-true -examples: 1. almost any dental procedures 2. bronchoscopy 3. EGD 4. colonoscopy 5. prostatectomy -prophylactic antibiotics to prevent endocarditis only needed in high risk individuals (prosthetic heart valves, prior endocarditis)
Name some effects of local invasion in infective endocarditis.
1. disturbance in conduction 2. CHF 3. valve perforation 4. MI
Name some effects of peripheral embolization in infective endocarditis
-embolization caused by vegetation fragments 1. mycotic aneurysm formation 2. septic infarction of organs including -kidneys -spleen and liver -stroke (CNS involved)
What are some effects of circulating immune complexes in infective endocarditis
-seen when low virulence bugs bind circulating Ab and form complexes 1. peteciae in nail beds and conjunctivae 2. Litten spots (roth spots) -retinal hemorrhages -associated w/# of conditions 3. Osler's nodes 4. Janeway lesions 5. Arthritis 6. Glomerulonephritis 7. Myocarditis
Name 3 major complicatins of infective endocarditis
1. Valve perforation/destruction 2. Cerebral embolization and/or hemorrhage 3. heart failure
Define SIRS
=systemic inflammatory response syndrome -widespread inflamm response to variety of severe clinical insults -need 2 or more of: 1. Temp >38 C or <36 2. Heart rate >90 bpm 3. RR >20 breaths/min or PaCO2 < 32 mmHg 4. WBC > 12,000 cells/mm3 or <4000 cells/mm3 with >10 % bands (immature)
Define sepsis
=systemic response to infection -if pt has sepsis that have clinical signs of SIRS w/concrete evidence of infection
Define severe sepsis
=associated with organ dysfxn, hypoperfusion, hypotension. -clinical signs of hypoperfusion include: 1. lactic acidosis 2. oliguria 3. acute alteration in mental status
Define septic shock
=sepsis with hypotension despite adequate fluid resuscitation combined with perfusion abnormalities (lactic acidsosi, oliguria, acute alteration in mental status) -pts that need inotropic or vasopressor support despite fluids are in septic shock -inflammatory response to bacterial products -> maladaptive responses to overwhelming infection -wide spread tissue injury and systemic inflammation
Define hypotension
=systolic BP <90 mmHg or a reduction of >40 mmHg from baseline in absence of other causes for the fall in BP
Define multiple organ failure
=presence of altered organ fxn in acutely ill pt such that homeostasis cannot be maintained w/out intervention
Define bacteremia
=presence of viable bacteria in the blood
Name 10 signs and symptoms of septic shock
1. Feeling of impending doom 2. Hyperventilation 3. Fever 4. Hypotension due to low SVR 5. Accumulation of lactic acid -hyperventilation may mask by lowering pCO2 6. Organ damage -due to hypoperfusion and DIC -kidney, lung, liver, gut, heart 7. DIC 8. Leukopenia ---Leukocytosis 9. Activation of neuroendocrine axis (ex produce ACTH) 10. Cyotkine induction
Describe the group characteristics of septic shock
-750,000 cases/year -30-50% mortality -characterized by: 1. increased CO 2. decreased peripheral vascular resistance -skin will be warm and dry -does NOT require positive blood culture -about 50% of pts with septic shock have bacteremia
Name some bacterial products capable of causing septic shock
1. LPS 2. Lipotechoic acid 3. Flagellin 4. glucan 5. bacterial DNA (CpG islands)
Name the 3 most common sites for infections leading to septic shock
1. lungs 2. abdomen 3. urinary tract
Name some predisposing factors to sepsis
1. aggressive cancer therapy 2. corticosteroids and immunosuppressive therapy 3. anti-microbial resistant organisms 4. increased use of invasive devices 5. longer lives of people predisposed to sepsis (elderly, diabetes, cancer pts)
Name 3 receptors involved in binding LPS
1. LPB (LPS binding protein) -plasma protein 2. CD14 (GPI anchored protein on mphage and neutrophils) -no transmembrane domain so can't signal 3. TLR-4
Name 5 cytokines induced in septic shock
-binding of bacterial products to TLRs induces cytokine production -cytokines induced include: 1. IL-1, IL-6, IL-10, IL-12, TNF, INF gamma -cytokines can activate 1. activation of coag cascade 2. PG, LT synthesis 3. complement activation
True or false: septic shock is characterized by an early inflammatory response followed by a later anti-inflammatory response
Define Toll-like proteins
-family of 11 proteins -have similar intracellular domains -extracellular domains are distinct-> specificity of bacterial products -form heterodimers -some activate cells by forming molecular aggregates on cell surface -> activate intracellular cascade -various locations 1. cell surface 2. intracellular -bind to RNA and DNA
Name the bacterial products that bind to: -TLR2 -TLR2, TLR6, Dectin - TLR3, CD14 -TLR4, MD2, CD14 -TLR 4, CD14 -TLR5 -TLR9
TLR2: PDG, lipotechoic acid, some types of LPS TLR 2, TLR 6, dectin: fungal glucan TLR 3: viral RNA TLR 4: LPS TLR4 etc: minimally oxidized LDL TLR5: flagellin TLR9: bacterial CpG DNA
Name 3 important cell types in sepsis.
1. Macrophages -activation -> activate NFkB -> changes in gene expression -make cytokines, ROS, tissue factor 2. Endothelial cells -make cytokines, NO -upregulate ICAM, VCAM 3. Epithelial cells
Name some other responses to sepsis besides the cellular response
-activation of clotting cascade-DIC -activation of complement cascade -activation of pituitary to produce ACTH -activation of sympathetic and parasympathetic nervous system -activation of liver to produce acute phase proteins
Define DIC
=disseminated intravascular coagulation -activation of coag sequence: thrombi throughout microcirculation -consumption of plts and coag factors to subhemostatic levels -activation of fibrinolysis -tissue hypoxia: microinfarcts -hemorrhage from trauma due to consumption of clotting factors and fibrinolysis destroying clots -can be seen in septic shock
True or false: about 40% of the time we don't have a microbiologic diagnosis of septic shock
-ie what is causing the septic shock -true
Name 5 types of patients at higher risk for sepsis
1. central venous catheter 2. malignancy, esp hematologic 3. Over 65 4. HIV infected 5. Requiring transfusion
How do we treat septic shock
1. Fluid replacement and vasopressors to keep BP > 90 2. broad spectrum antibiotics (after cultures taken)
True or false: many anti-inflammatory drug trials for treating septic shock have been successful
-false -most have failed EXCEPT activated protein C (but this can only be given to certain pts)
Define Activated protein C
=anti-thrombin compound that breaks up clots -tx can be helpful in septic shock but can't be given to everyone -also inhibits activation of endothelial cells by bacterial products
Name 3 major complications of uncontrolled sepsis cascade
1. DIC 2. Multi-organ failure -lungs: ARDS -kidneys: acute tubular necrosis -liver: hepatitis -heart: decreased contractility -brain: confusion 3. Death
Define PAMPs
=pathogen associated molecular patterns =bacterial products that can cause an inflammatory response -includes: 1. LPS 2. lipoproteins 3. PDG 4.flagellin
Define URI
=upper respiratory infection -nasal congestion -+/- pharyngitis -+/- cough
Define laryngitis
=inflammation of the larynx, leading to a change in speaking voice
Define bronchitis
=inflammation of the bronchi -characterized by excessive mucus production
Define bronchiolitis
=inflammation of the bronchioles, often leading to airway obstruction
Define bronchiectasis
=dilation of the bronchi and terminal bronchioles, often due to combination of obstruction and infection
Define Pneumonia
=Infection of the lung parenchyma -Infection may primarily involve: 1. air spaces themselves (alveolar pattern) 2. interstitum of the lung (interstitial pattern)
Define pleurisy
=inflammation of the pleura leading to chest pain on inspiration
Define empyema
=infection of the pleural space
True or false: pneumonia is the most lethal nosocomial infection
Name 5 normal host defense mechanisms against pneumonia.
1. upper airway filters 2. gag reflex 3. cough 4. tracheobroncial clearance 5. alveolar macrophages
Name 6 predisposing factors to developing pneumonia
1. Depressed cough 2. Depressed gag/disorders of swallowing 3. Injury to the mucociliary apparatus 4. Interference with phagocytic fxn of alveolar macrophages 5. Pulmonary congestion 6. Accumulation of secretions
How do we classify pneumonia?
1. By Organism category -bacterial -mycobacterial -fungal -viral 2. By specific organism -pneumococcal -mycoplasma -legionella 3. By presentation -community acquired vs nosocomial -classical vs atypical -acute vs chronic -normal host vs immunocompromised
Name the top 4 bacteria that cause community acquired classical pneumonia
-in order of prevalence 1. S. pneumoniae 2. H. influenzae 3. S. aureus 4. Gram negative bacilli -Other causes of community acquired pneumonia 1. Atypical bugs 2. Viruses 3. Aspiration
Name 3 bacterial that cause atypical community acquired pneumonia
1. Legionella 2. Mycoplasma pneumoniae 3. Chlamydia pneumonia
True or false: sputum gram stain should not be used in diagnosis of pneumonia
-false! -want to use b/c rapid, reliable, non-invasive, and cheap -but have to make sure get an adequate sample (true sputum which will show lots of polys vs saliva which will show mouth bacteria)
Name 4 bacteria that cause classical pneumonia
1. Pneumonoccal pneumonia 2. Staphylococcal pneumonia 3. Klesbsiella pneumonia 4. Streptococcal pneumonia
Describe pneumococcal pneumonia
-most common bacterial pneumonia -disease of the elderly -usu follows URI -abrupt onset of fever, shaking, chills, purulent sputum -may see leukocytosis and hypoxia -classic "lobar" pneumonia on xray -high incidence of bactermia -Dx by sputum gram stain and culture
How do we treat pneumococal pneumonia?
1. Penicillin G 2. 3rd generation cephalosporin
Describe staphylococcal pneumonia
=frequent cause of nosocomial pneumonia -rare cause of community acquired pneumonia except in influenza outbreaks -inhalation and hematogenous routes -causes parenchymal necrosis -acute presentation, pt ill-appearing, purulent sputum -leukocytosis -xray varies -dx sputum gram stain and culture, blood cultures
How do we treat staphylococcal pneumonia?
1. vancomycin 2. semisynthetic PCN
Describe Klebsiella pneumonia
=Community acquired in alcoholics, diabetics, and those w/underlying lung disease -acute presentation, severe illness -"current Jelly" sputum -leukopenia with left shift or leukocytosis -chest xray: bulging fissure/lobar consolidation with parenchymal necrosis -dx: sputum gram stain and culture, blood cultures
How do we treat Klebsiella pneumonia?
1. Cephalosporins 2. Quinolones
Current jelly sputum is characteristic of which type of pneumonia?
-Klebsiella pneumonia
Describe streptococcal pneumonia
-caused by beta hemolytic strep -rare cause of community acquired but outbreaks can occur -acute presentation with shaking, fever, chills, chest pain -pleural effusion common early in infection -empyema common in those with WBC > 20,000 -dx: sputum gram stain and culture (gram positive chains), blood culture, ASO titer
How do we tx streptococcal pneumonia?
1. Penicillin 2. Clindamycin
Describe hemophilus pneumonia
-usu not type B -often in pts with COPD -sometimes difficult to distinguish from chronic bronchitis -Sx: increased SOB, fever, increased cough, increased sputum, mild leukocytosis -dx: sputum gram stain, culture-if no other pathogen present -
How do we treat pneumonia due to Hemophilus?
1. Ampicillin 2. Cephalosporin
Name 4 causes of atypical pneumonia
1. Mycoplasma pneumonia 2. Chlamydia pneumonia 3. Legionella pneumonia 4. viral pneumonia
Describe mycoplasma pnuemonia
-second most common cause of community acquired pneumonia -causes atypical pneumonia -grows aerobically and anaerobically -can be isolated on supplemented medium but slow growth -No PDG -Can attach to respiratory epithelium (TLR-2)
Describe the pneumonia caused by M. pneumoniae
-atypical pneumonia -spread by resp. droplets -Avg incubation 3 weeks -younger population than pneumococcal pneumonia affected -Ab to glycolipid Ag cross react with human RBCs and brain cells
Describe the clinical presentation of pneumonia due to mycoplasma pneumoniae
Sx -headache -malaise -low grade fever -intractable, non-productive cough -ear pain w/bullous myringitis Extrapulmonary manifestations -Rash (severe-> Steven-Johnson syndrome) -Hemolysis (IgM to RBC I Ags) -CNS disease
How do we diagnose mycoplasma pneumonia and treat it?
Dx -culture possible but not often done -PCR of secretions -Ag detection by EIA -Beside and lab "cold agglutinin" test -Ab detection from EIA Rx -tetracyclines -macrolides -quinolones
Describe pneumonia due to chlamydia
2 species cause pneumonia 1. C. pneumoniae 2. C. psittaci (zoonosis) -elderly affected -also common 18-30 yo -atypical pneumonia -gradual onset of sx (pharyngitis, hoarseness, sinusitis)
How do we diagnose and treat pneumonia due to chlamydia
-intracellular parasite so culuture usu not done -Dx: serology, DFA, PCR Tx: TCN or macrolides
Who gets pneumonia due to legionella?
1. smokers w/COPD 2. transplant pts 3. those receiving steroids 4. CMI deficient
Describe legionella pneumoniae
-cause of atypical pneumonia -aerobic, gram negative bacteria -attachment via pili/ flagella -found in water -multiply intracellularly and prevent phagosome-lysosomal fusion -Virulence factors: 1. Mip (macrophage infectivity potentiator protein) -promotes phagocytosis so can multiply intracellularly 2. DOT 3. ICM -2 & 3 prevent phago-lysosomal fusion
Describe the clinical presentation of pneumonia due to legionella
-atypical pneumonia -gradual onset of sx -non-productive F/B cough -GI complaints frequent -high fever -relative bradycardia -hyponatremia -hematuria -proteinuria -mild leukocytosis Chest Xray -patchy, nodular infiltrates, ill-defined borders -pleural or perihilar spaces
Legionella can be cultured on ________ culture media
-charcoal yeast extract -can use cultures to diagnose atypical pneumonia
Define aspiration pneumonia
-aspiration of oral flora -indolent infection w/ low grade fever, putrid, foul smelling sputum -Chest xray shows cavitary lesions in dependent lung segments -dx: sputum gram stain, aspirate -rx should cover both aerobes and anaerobes
Who is most likely to develop aspiration pneumonia?
1. Bad teeth 2. Alcoholics 3. Those with altered consciousness
Name 5 poor prognostic factors for community acquired pneumonia
1. Age ( > 65 yrs) 2. Coexisting disease -diabetes, CHF, chronic lung disease 3. Clinical findings -RR >30 -altered mental status -extrapulmonary infection 4. Lab tests -WBC too high or too low -hypoxemia -renal failure 5.certain Microbial pathogens -S. pneumoniae -legionella -S. aureus
Name 3 bacteria that are common offenders for nosocomial pneumonia
1. S. aureus 2. Pseudomonas 3. enteric gram negative rods (ex Klebsiella)
Name some risk factors for nosocomial pneumonia.
1. altered consciousness 2. mechanical ventilation 3. H2 blockers 4. NG tubes 5. thoracic or abdominal surgery 6. obesity -nosocomial pneumonia may be difficult to diagnose (often diagnosed by change in status)
Name 7 complications of pneumonia
1. empyema 2. ARDS 3. Immunologic phenomena -hemolytic anemia 4. Meningitis 5. Septic arthritis 6. Abscesses 7. osteomyelitis
Name 3 preventative measures for pneumonia
1. pneumovax 2. influenza vaccine 3. aspiration precautions
Name 4 "other" causes of pneumonia
1. Mycobacterium hominis 2. pathogenic fungi 3. norcardia 4. viruses
Name the 5 first-line anti-TB drugs
1. INH 2. rifampin 3. pyrazinamide 4. streptomycin 5. ehtambutol
True or false; the mechanism of drug resistant strains of Mycobacterium tuberculosis is plasmid-mediated
-false -it's due to choromsomal mutations 1. INH resistance
How do we treat latent TB infections identified by positive PPD test?
1. INH (6-9 months) -increased risk of inducing hepatitis if over age 35 2. rifampin (4-9 months)
Define BCG
=TB vaccine -innoculate w/low virulence strain of M. bovis -given in countries with endemic TB but not low TB countries (reduced efficacy there and messes up ability to detect TB infection with PPD skin test) -good at reducing severity of disease in children and prevent TB meningitis -variable efficacy
Name 3 ways to diagnose tuberculosis
1. Acid fast stain or fluorescent auramine-rhodamine smears of sputum -show acid fast bacilli 2. Culture -preferred 3. Nucleic acid assays
True or false: the risk of TB infection is proportional to the intensity of exposure
Who spreads TB infections?
-people with active (cavitary) disease -M. tb is exclusively a human pathogen -spread bty respiratory droplets that become aerosolized
True or false: TB infection usually does not lead to disease
-true -Exceptions: 1. infants 2. immunocompromised -both have high rate of active and severe disease following exposure
Name an animal pathogen mycobacteria that produces disease indistinguishable from TB
=M. bovis -M. bovis and M. tb can't be distinguished by nitrate test (both able to reduce nitrate)
True or false: M. tuberculosis and M. bovis can be distinguished by a nitrate test
-false -both are able to reduce nitrate
Name the major groups in the genus mycobacterium
1. Mycobacterium tuberculosis complex -m. tb, m. bovis, m. microti, m. africanum 2. Nontuberculous mycobacteria -runyon groups 1-4 3. Mycobacterium leprae 4. Myrcobacterium ulcerans
Describe Mycobacterium tuberculosis
1. short, slim unencapsulated rod 2. acid fast 3. irregular beading due to vacuoles, polyphosphate granules 4. obligate aerobe but contains enzymes for anaerobic metabolism 5. Grows on Lowenstein Jensen media (complex media for growth required) 6. Slow growing (doubling time 18 hrs) 7. multiples intracellularly in phagosomes and prevents phagosome-lysosome fusion
How does mycobacterium tuberculosis acquire iron?
1. Exochelin steals iron from host ferritin 2. mycobacitin in cell envelope takes iron from exochelin
Name 3 bacteria that contain mycolic acid
=complex, long chain FA 1. Mycobacteria 2. Norcardia 3. Corynebacterium
Name 8 group characteristics of mycobacteria
1. slim shaped rod organisms that are 1-10 microns long 2. Non-motile and non-spore forming 3. obligate aerobes 4. slow growing 5. contain mycolic acid (complex long chain FA) 6. Cell wall with high lipid content 7. catalase positive -some exceptions 8. Stain acid fast
Describe pathogenesis of a TB infection
1. host inhales aerosolized respiratory droplets containing M. tb from person w/cavitary tb 2. mphages engulf M. tb from inhaled droplets 3. M. tb prevent phagosome-lysosomal fusion 4. M. tb multiply intracellularly w/in phagosomes 5. when multiplied enough, mphage is killed, dead cell ingested by other mphages, M. tb now ingested by other cells 6. Infected mphages produce cytokines and chemokines that attract phagocytes and inflammatory cells
True or false: M. tb infections can eventually disseminate in body via lymph nodes and bloodstream
-true -can seed in: 1. liver 2. spleen 3. kidney 4. bone 5. brain 6. meniges 7. other parts of lung
How does the host immune system respond to acute TB infection
-T cell mediated response -develops 2-6 weeks after infection -in 90% of people, able to clear the TB infection without progressing to disease -form granulomas (walls off infection but still contains viable M. tb that could later reactivate) -will show positive PPD skin test
When is TB most likely to reactivate?
-within 5 years of the primary infection -result of persistent bacteria in the host suddenly proliferating -some people at a higher risk of reactivating than others -reactivation infections likely to occur in apex of lung
Name 7 factors that increase risk of reactivating TB infection
1. Very young or very old 2. pregnant women 3. immunosuppressed individuals -ex post-transplant, AIDs 4. post measels 5. malnourished 6. alcoholics 7. other comorbid diseases (renal disease, diabetes)
Name some groups of people who are at increased risk of getting TB
-those living in TB endemic areas 1. prison 2. homeless 3. elderly 4. foreign born (ex high rates among Mexican Americans) -people with difficulty dealing with infection 1. immunocompromised -esp AIDs
Why do we do the PPD skin test?
-identify people with latent TB infection -want to tx people with latent infection that would benefit -want to identify people with increased risk of active TB disease (infants, immunocompromised)
What defines a positive PPD test
1. Normal immune system 10 mm induration after 48-72 hours 2. HIV infected -5 mm induration after 48-72 hours -Positive test tells you: 1. individual is infected with TB 2. individual infected with nontb mycobacteria (includes BCG, used as vaccine against TB)
Name 5 proposed virulence factors for mycobacterium tuberculosis
1. mycolic acid glycolipids 2. trehalose -very pro-inflammatory -released from cell wall 3. Catalase, peroxidase, lipoarabinomannan -resist host cell oxidative burst 4. lipoarabinomannan -also induces cytokine production and help prevent apoptosis
True or false: mycobacterium is often cultured on solid agar for diagnostic purposes
-false -b/c slow growing -often use liquid culture b/c sensitive and grows more quickly
Name 3 tests to distinguish mycobacterium tuberculosis from other mycobacteria
1. Niacin test -M. tb produces lots of niacin 2. Catalase test 3. Nitrate test M. tb can reduce nitrate. But so can M. bovis
Describe the group characteristics of fungi.
1.Eukaryotes 2. Rigid cell wall w/ unique components (chitin, glucan, polysaccharide protein complexes) 3. Heterotrophys 4. Facultative or obligate aerobes 5. Ubiquitous environmental organisms 6. Digest and ingest dead organic matter 7. Non-motile
Name the 3 components of the cell wall of fungi
1. Chitin 2. Glucan 3. Polysaccharide protein complexes -act as cement -immunodeterminant groups of cell wall Ag Chitin + glucan form crystalline skeleton that gives strength to wall
How are fungi classified?
2 different morphological groups 1. Molds -multicellular 2. Yeast -single-cell Can be further classified as dimorphic or monomorphic
Define dimorphic fungi
=fungi that grow as yeast in infected tissue and mold when in culture media -many are primary pathogenic fungi -Examples 1. Coccidiodes immitis 2. Histoplasma capsulatum 3. Sporothrix schenckii
Define primary pathogen
=pathogen capable of causing invasive disease in individuals with normal immune systems
Define monomorphic fungi
=fungi that grow only as mold or only as yeast whether they are grown on artificial media or within infected tissue
Name 2 major monomorphic molds
=fungi that grow only as molds in both culture and in body -opportunistic pathogens 1. Aspergillus 2. Mucor and Rhizopus
Name the 3 dimorphic fungi
-primary pathogens 1. Coccidiodes immitis 2. Histoplasma capsulatum 3. Sporothrix schenckii
Define Zygomycetes
=class of fungi -opportunistic pathogens -unique characteristics: 1. Non-septated mycelia 2. Asexual spores contained w/in sporangia borne on spoangiophores -Includes: 1. Mucor 2. Rhizopus
Define mold
=multiceullar form of fungi -components 1. Hypha 2. Mycelia
Define hyphae
=tubular structure that is characteristic component of mold (fungi) -grows by elongation -can be: 1. septated -have septa that divides into individual cells 2. Non-septate -lack divisions -Mycelium are produced as hyphae grows
Define Mycelium
=intertwining strands that are part of mold -branch out of the growing hyphae -mycelium enlarge and eventually produce a visible colony (thallus)
Define yeasts
=unicellular fungi -3-5 microns in diameter -vary in shape -typical colony resembles bacteria
Define pseduohyphae
=elongated buds produced by Candida albicans on solid media =elongated yeasts
True or false: fungi undergo both sexual and asexual reproduction
-true -have different characteristic morphologies and reproductive structures in asexual vs sexual stage -however, since we don't know the sexual forms for some fungi, classification is based on asexual reproduction characteristics
Contrast how molds and yeasts reproduce
Yeasts: budding Molds: form spores
Define conidia
=all asexual reproductive fungal spores -spores are how molds reproduce -lightweight and can be airborne -These are the infectious elements that may be inhaled or implanted into the skin of pts -can be subclassified 1. Sporangiospores 2. arthroconidia 3. macroconidia
Define sporangiospores
=fungal spores that are contained inside sac-like structures (sporangia)
Define Rhizopus and Mucor
=monomorphic molds 1. Zygomycetes 2. Non-septate 3. Sporangiospores 4. Acquired through inhalation 5. opportunistic pathogens
How do we distinguish rhizopus and mucor?
-both are nonseptate monomorphic molds 1. Rhizopus has roots (rhizoids) 2. Mucor does NOT have roots
Define Aspergillus fumigatus
=monomorphic mold 1. Septated hyphae that branch at acute angles 2. Conidia come off top 1/2 of conidiophore 3. mature colonies gray-green color 4. ubquitous in environment and esp compost heaps 5. Acquired by inhalation 6. opportunistic infections -neutropenic pts -chronic granulomatous disease
Name 3 types of infections caused by Aspergillus fumigatus
1. Invasive pulm infections and sinus infectious -immunocompromised 2. Allergic pulm syndromes -asthma pts 3. Pulmonary aspergillioma =fungus ball -in people with pre-existing pulm cavity (ex tb)
Name 3 types of Aspergillus
1. Aspergillus fumigatus 2. Aspregillus flavus 3. Aspergillus niger
Describe the group characteristics of Aspergillus
1. monomorphic molds 2. opportunistic pathogens 3. Ubiquitous in air 4. All produce extracellular proteases
Name 3 groups of people who get infections caused by rhizopus and mucor
-opportunistic pathogens -infections are rapidly fatal 1. Invasive disease in neutropenics 2. Rhibocerebral infarction in diabetics w/metabolic acidosis -associated w/impaired transferrin binding 3. disease in other immunosuppressed (organ transplants, AIDs)
Define Coccidiodes immitis
1. Dimorphic mold 2. Primary pathogen fungi 3. Culture form= arthroconidia w/in mycelia 4. infected tissue form: spherules that contain endospores 5. Found in soil in SW US and Mexico 6. Acquired as mold by inhalation and transforms into spherules in lung
Name 3 types of infections caused by Coccidiodes immitis
=dimorphic mold that's a primary pathogen 1. Asymptomatic infection or subclinical pneumonia 2. Disseminated disease -meninges, bone, skin 3. Meningitis
A ________ immune response is necessary to control infection from Coccidiodes immitis
-T cell mediated
Define Histoplasma capsulatum
=Dimorphic mold that's a primary pathogen 1. Culture form=makes both microconidia and tuberculate macroconidia 2. Tissue form=small yeast 3. Found in Ohio and Miss River valley in soil, also in soil w/bird and bat feces 3. Acquired by inhalation of the microconidia -> transforms to yeast 4. Infections usu asymptomatic or self-limited 5. May cause disseminated infections -esp to GI mucosa -esp immunocompromised and kids
True or false: antibodies generated against histoplasma capsulatum are protective
Define Blastomyces dermatitidis
=dimorphic fungi 1. Environmental form=oval/pear shaped conidia on short conidiophores 2. Tissue form=double walled yeast 3. Found in soil in Midwest -esp hunters and woodsmen 4. Acquired by inhalation 5. Mostly causes disseminated disease (skin, bones/joints, GU tract)
Define Sporothrix schenckii
=dimorphic mold that's a primary pathogen 1. Culture=hyphae with triangular pigmented macrospores 2. Tissue form=cigar shaped yeasts 3. Found in soil enriched w/vegetable matter -Disease seen in gardeners, floral word, christmas tree farmers 4. Acquired by inoculation of organism into skin 5. Usu causes erythematous nodule or subcutaneous nodules 6. malnutrition, alcoholism, immunosuppression predispose to infection
Define Cryptococcus neoformans
1. Monomorphic round yeast 2. Primary pathogenic fungi 3. Grows as mold in its sexual state 4. 2 variants -var. neoformans: associated w/pigeons and found worldwide -var. gattii associated w/eucalyptus trees. Found in So Cal and Australia 5. Acquired by inhalation 6. Has a capsule 7. Grows at 37 degrees C
Name some factors that allow Cyrtococcus neoformans to cause disease in humans
1. Antiphagocytic capsule 2. Urease 3. Phenol oxidase 4. can grow at 37-39 degrees C 5. Produces mannitol -> causes cerebral edema and inhibits phagocyte fxn
Name 2 infections caused by Cryptococcus neoformans
1. Pneumonia 2. Fungal meningitis Although primary pathogen, most cases in immunocompromised pts
Name 4 species of Candida
Monomorphic yeast 1. Candida albicans 2. Candida krusei 3. Candida parapsilosis 4. Candida tropicalis
True or false: infections caused by nontuberculosis mycobacterium are rarely spread person to person
True or false: nontuberculous mycobacteria are INH sensitive as a group
-false -they are INH resistant as a group
How does mycobacterium tuberculosis spread?
Exclusive human pathogen 1. Ingestion of infected meats or milk 2. Inhalation of aerosolized respiratory secretions from person w/ cavitary TB
True or false: Mycobacterium leprae can be grown in culture
Define Mycobacterium kansasii
=nontuberculous mycobacterium 1. Photochromogen (runyon class 1) 2. Causes lung disease clinically similar to TB -esp in immunocompromised 3. Seen in midwest states 4. Long, banded beaded "barber pol" yellow bacillus 5. Reduces nitrate
Define Mycobacterium marinum
=nontuberculous mycobacterium 1. Photochromogen 2. Causes infection in people w/ fish tanks (granulomas, abscesses) -lesions heal poorly 3. Organism grows more readily at lower temp 4. Inhabits both salt and freshwater
Define Mycobacterium scrofulaceum
=nontuberculous mycobacterium 1. scrotochromogen 2. Causes granulomatous cervical adenopathy in kids (scrofula)
Define Mycobacterium avium intracellulare complex (MAC)
=nontuberculous mycobacterium 1. Nonchromogen 2. Pleomorphic 3. May produce pigment in absence of light 4. Bind and invade oropharyngeal and GI cells 5. Cause disease in immunocompetent hosts and especially in immunocompromised hosts
Name 4 syndromes caused by MAC in immunocompetent hosts
1. TB like disease -white, middle aged smokers w/COPD, bronchiecstasis 2. Lung infection in pts w/ bronchiecstasis 3. Persistent cough + interstitial changes in non-smoking women over age 50 -AFB in sputum smear is diagnostic
An AIDS pt presents with fever, fatigue, malaise, anorexia, and weight loss. His CD4 T cell count is below 100. What is he likely infected with?
-MAC -blood cultures are diagnostic -more likely to cause disseminated disease in immunocompromised
Name 2 rapid growing mycobacteria
Grow colonies in 5 days Do NOT produce pigment 1. M. chelonae 2. M. fortuitum -usu complication of surgery, etc -highly drug resistant
Define Mycobacterium leprae
=nontuberculous mycobacterium 1. can NOT be cultured 2. Can be grown in armadillos, mouse foot pad 3. Grows best on the cooler parts of body (skin and peripheral nerves) 4. Only 10% infected will develop leprosy (5-7 year incubation period) 5. 2 forms of the disease -tuberculoid form -lepromatous leprosy forms
Describe the 2 forms of leprosy due to Mycobacterium leprae
1. Tuberculoid form -granulomas formed -anesthetic skin plaques, asymmetric peripheral nerve trunk involvement 2. Lepromatous leprosy -poor cell mediated immune response -granulomas poorly formed -symmetric skin nodules, leonine facies, plaques, loss of eyelashes and body hair, testicular dysfxn
Define mycobacterium ulcerans
=nontuberculous mycobacterium 1. Causes Buruili ulcers 2. Causes infection in immunocompromised 3. presents as small, painless subcutaneous nodule -skin adjacent to lesion and whole limb can become edematous -ulcer can widen and deepen -> destroy adjacent structures and bone 4. Tx = surgical debridement
Define Legionella
=common cause of community and nosocomial pneumonia -facultative -intracellular -gram negative -difficult to stain -grows on Charcoal yeast extract agar (w/iron and cysteine) -Catalase positive -gelatinase positive -beta lactamase positive -high proportion of branched-chain FA by gas-liquid chromatography -motile -40 differ species
Describe the growth requirements for Legionella
1.Buffered Charcoal yeast extract agar 2. iron 3. cysteine
Describe the life cycle of Legionella pneumophilia
1. Gets tagged with complement C3 2. phagocytosed by alveolar macrophages and monocytes 3. During coiling phagocytosis, sorts membrane proteins so phagosome has lots of complement R and few MHC I or II R 4. Inhibits phagolysosomal fusion 5. Legionella multiples w/in phagosome 6. Keeps multiplying until host cell destroyed
Describe the host defense against legionella
=cell-mediated immunity 1. Activated lymphocytes secrete cytokines that activate mphages -> activated mphages inhibit intracellular multiplication of Legionella a. downregulate complement Rs -> less endocytosis legionella b. down regulate transferrin R -> limit iron uptake -> inhibit legionella multiplication 2. PMNs secrete apolactoferrin to help limit iron supply 3. Antibodies don't help
The most likely time to get pneumonia due to Legionella is _______.
-summertime (air conditioning)
All of the following are risk factors for legionella infection EXCEPT a. Age> 30 b. immunocompromised status c. cigarette smoking d. women e. alcohol abuse
-women -men are more likely to get legionella infection
How is legionella spread?
1. NO person-person spread 2. inhalation of organism in a mist -air ocnditioners or equipment -nebulizers or humidifiers -shower heads -whirlpools -mist generators
Name 3 types of Legionella infections
1. Asymptomatic infection -induces high antibody titer 2. Legionnaire's disease 3. Pontiac fever -incubation period 1-2 days -febrile illness w/out pneumonia -mild and nonfatal Also extrapulmonary disease
Define Legionnaire's disease
=severe, often fatal pneumonia caused by legionella -incubation period 2-10 days -Stages 1. mild illness that presents w/flu-like sx 2. moderately serious pneumonia 3 multilobar pneumonia
How do we diagnose and treat Legionella?
Dx 1. Fluorescent staining or gene probe of sputum or tissue 2. ELISA to look for Legionella Ag in urine 3. Retrospective serology Tx Community acquired 1. Erythromycin 2. Long acting macrolides Nosocomial/immunocompromised 1. azithromycin 2. fluroquinolone
Define Rickettsia
-gram negative bacteria -obligate intracellular parasite -contain 70S ribosomes -tend to gram stain poorly -transmitted by arthropods
Define zoonosis
=disease of animals that can be transmitted to humans
Define vector
=a carrier that transfers the pathogen from one host to another -ex Rickettsia, etc the vector is an arthropod
Describe 2 types of vector borne transmission of pathogens
1. Mechanical vector transmission -vector transmits pathogen from one host to another but is NOT essential for life cycle of pathogen 2. Biological -pathogen develops or multiplies in body of vector before it can pass the pathogen to other species
Define resevoir of infection
=the permanent host or carrier of the pathogen from which the vector acquires the infection
Define transovarian transmission
=infection of progeny via their mother -all progeny of infected mother will also be infected w/the organism -in the case of arthropods, lots of progeny -> big increase number of infected progeny
Define transtadial transmission
=infection of an arthropod through its different life stages -will still be infected even after it goes through metamorphosis
Name the resevoir and vector for Rickettsia
Resevoir 1. mammal 2. arthropod Vectors 1. arthropod
How does Rickettsia cause disease?
-get disseminated in bloodstream -parasitize endothelial cells -> damaged endothelium -> vasculitis, obstruction, capillary leaks, thrombosis -> rash, organ damage and potentially shock
How do we diagnose infection w/Rickettsia?
-clinical diagnosis -look for triad of: 1. fever 2. headache 3. rash
Define Rocky Mountain Spotted Fever
-infection caused by Rickettsia -clinical diagnosis of triad of: 1. fever 2. headache 3. rash -if suspect, treat first w/antibiotics, then confirm w/ serology -high mortality rate if untxed
How does Rickettsia invade endothelial cells?
1. Adhere as a slime layer to XOL R on endothelial cells 2. Escape from phagolysosome via phospholipase 3. Can get around the cell on actin (like Shigella) -> get into neighboring cells 4. Or multiply and lyse the cell
Define Rickettsia prowazekii
=bacteria that causes epidemic typhus -gram negative obligate intracellular pathogen
What pathogen causes epidemic typhus?
=Rickettsia prowazekii Resevoir: 1. humans 2. flying squirrel Vector: 1. Body louse (lice) 40% mortality Brill-Zinsser disease =mild form in a previously infected person that gets reactivated
Define Rickettsia typhi
=gram negative intracellular pathogen -causes murine typhus -lower mortality associated w/untreated disease
A delirious pt is lying in the ER with a high fever, chills, a rash spreading from the chest everywhere, and severe headache. The man was homeless and lice were found in his house and clothing. What does he have?
=epidemic typhus caused by Rickettsia prowazekii
What is the cause of murine typhus?
=Rickettsia tyhpi -disease found in subtropical regions 1. Ca-Texas border 2. Hawaii Resevoirs 1. Rats 2. Opossums 3. Rat fleas Vectors 1. Cats 2. Rat fleas Low mortality if untxed (vs epidemic typhus)
What causes Rocky Mountain Spotted Fever?
=Rickettsia rickettsii Vector 1. American Dog tick (Dermacentor) Resevoir 1. Ticks (transovarial and transtadial) 2. mammals Oklahoma and N. Carolina highest rates of disease infections in summer
A patient presents to the hospital on Friday with fever, severe headache, and a petchial rash. He had been backpacking in the woods in North Carolina the weekend before with some friends. What does he have?
=Rocky Mountain spotted fever caused by Rickettsia rickettsii
Define Orientia tsutsugamushi
=gram negative obligate intracellular pathogen -causes scrub typhus -distributed throughout Pacific rim Resevoir 1. Mites 2. Rats Vector: 1. Mites (chiggers)
Define Coxiella brunetti
=gram negative obligate intracellular pathogen -has hearty "spore-like" body that resists dying -usu acquired by inhalation -carriers =sheep and cattle -can live and replicate w/in phagolysosome -causes Q fever -causes both acute and chronic infections
What causes Q fever?
=Coxiella brunetti Acute 1. pneumonia 2. +/- pericarditis 3. +/- myocarditis 4. +/- severe headache 5. +/- aseptic meningitis 6. +/- encephalitis Chronic infections 1. Endocarditis 2. hepatitis -usu acquired by inhalation
Define Ehrlichia
=obligate intracellular gram negative bacteria -no LPS -can make ATP -cause ehrlichiosis Ticks act as both vector and resevoir
What is a disease that resembles Rocky Mountain Spotted fever?
=ehrlichiosis -caused by ehrlichia -can infect granulocytes or monocytes -cause leukopenia -start on doxycycline RIGHT AWAY -low mortality infection -Can have serious complications -2 major types 1. HME 2. HGE/HGA
Name some serious complications of Ehrlichiosis
1. meningoencephalitis 2. ARDS 3. toxic shock like illness Vulernable pts 1. immunocompromised 2. elderly 3. asplenic pts
Define Human monocytic ehrlichiosis
=disease caused by Ehrlichia chaffeensis -Seen in: 1. rural SE US 2. south central Resevoir: white tailed deer Vector: tick Pathology 1. perivascular lymphohistiocytic infiltrates 2. no vaculitis 3. tissue infiltration by phagocytes 4. noncaeseating granulomas 5. hypercellular BM
Define Human granulocytic ehrlichiosis
=human granulocytic anaplasmosis -infection caused by ehrlichia -transmitted by ticks -resevoirs: small mammals and mice
What causes at scratch disease?
-Bartonella -often acquired from scratch of a young cat -infects endothelial cells -can spread to lymph nodes ->sx 1. low grade fever 2. malaise 3. painful, tender lymph node Bartonella transmitted from cat to cat by fleas
Define Bartonella
-gram negative intracellular pathogen -diseases 1. cat scratch disease 2. bacillary angiomatosis (AIDs pts) -invades and lives in endothelial cells -slow growing on media -best visualized with silver stain
What causes bacillary angiomatosis?
=disease in AIDs pts 1. Bartonella henselae 2. Bartonella quintana -pathogen spreads to angioblasts -> angioproliferation -> hemangioma lesions in liver/spleen or skin/bone
What causes trench fever?
-Bartonella quintana -transmitted by human body louse (lice) -affects homeless, chronic alcoholics -high fever, pain on moving eyeballs, headache, muscle soreness, hyperasthesias of shin
What causes Carrion's disease?
=Bartonella baciliformis -vector: sandflies -Endemic in Peru, Colombia, Equador -biphasic course disease 1. Acute septicemic phase -fever, headache, anorexia, malaise -days-weeks 2. Chronic phase -eruptive hemangioma skin nodules (verruga peruana)
Define Leptospira
=Spirochetes -can be cultured, but grow slowly -250 diff. serovars -infection dx by serology -cause leptospirosis
How do humans get infected with leptospira?
-by exposure to urine of infected animals w/leptospirosis -usu via soil or water contaminated w/infected animal urine -can be transmitted by lots of diff animals (may or may not show signs of infection)
Define Leptospirosis
-infection caused by Leptospira -incubation 2 days-4 weeks -variable presentation and can be asymptomatic -Biphasic disease 1. Headache, muscle aches, vomiting, diarrhea, then recovery 2. (if it occurs) kidney or liver failure, meningitis -dx by serology -self-limited (3 weeks or longer) disease; NO antiobiotics needed
Define infective endocarditis
=infection of the lining of the heart chambers and heart valves caused by bacteria, fungi, or other infectious organisms
Name the 2 requirements for infective endocarditis
1. Lesion on vascular endothelium susceptible to infection 2. Circulating organisms
Name some predisposing factors to endocarditis
1. Valvular heart disease 2. Mitral valve prolapse or regurg 3. Prosthetic valves 4. IV drug use 5. Most congenital heart defects (except ASD b/c low flow) 6. Marfan's 7. Recent invasive procedure (ex dental procedure) -cause transient bacteremia
Name 3 organisms that cause acute endocarditis
1. S. aureus -includes MRSA 2. Pneumococci 3. Gonococci
Name 3 organisms that subacute endocaridits
-note: other strep species than pneumococci account for 60-80% of subactue 1. S. viridans 2. Enterococci 3. Other strep
What do you suspect if the blood culture for endocarditis come back negative?
1. Prior administration of antibiotics that transiently sterilize the blood 2. Fungi 3. Other bacteria (coxiella, chlamydia, legionella, etc)
How does infective endocarditis develop?
1. Endothelial damage to endocardium 2. Fibrin/platelet thrombus forms on lesion 3. Circulating microorganisms colonize thrombus -> vegetation -hallmark is constant bacteremia w/little change in colony counts over time
True or false: all leading causes of infective endocarditis are gram positive organisms
Name 4 major signs/sx of infective endocarditis
1. Fever 2. NEW heart murmur 3. evidence of embolic phenomenon 4. High grade or persistent bacteremia
What are some complications of infective endocarditis
1. Peripheral embolization of vegetation fragments -mycotic aneurysm -septic infarcts 2. Circulating immune complexes -lesions (petechiae, Roth spots, Osler nodes) -arthritis -glomerulonephritis -myocarditis 3. local invasion by organism -valve perforation -disturbance in conduction -MI -heart failure
______% of patients with septic shock have bacteremia
=50% Common offenders: 1. Gram negative rods 2. gram positive organisms 3. mixed infection 4. fungi
Name 3 groups of people at increased risk of developing sepsis
1. elderly 2. diabetics 3. cancer pts -b/c of use of corticosteroids and immunosuppressive therapies
How does sepsis develop?
1. Microbial products interact with circulating proteins -> initiate a pro-inflammatory cascade 2. Pro-inflamm state mediated by TNF, IL-1, IL-6, IL-12 and complement activation 3. Also get activation of a pro-coagulant state (activate coag proteins and inactivate fibrinolysis) 4. Activation of iNOS in endothelium -> NO -> relaxation of arteriolar SM 5. Pro-coag state results in DIC, ischemia, hypoperfusion -> tissue injury
True or false: sepsis also involves some anti-inflammatory pathways.
-true -while initially it is an overwhelming pro-inflamm state, body starts to initiate some anti-inflamm pathways to mitigate -Secrete IL-10 (anti-inflamm), soluble inhibitors of pro-inflamm cytokines -later, anti-inflamm dominants -> increased risk of opportunistic infection
Name 3 proteins LPS can bind to:
1. LPB (LPS binding protein) -plasma protein -when binds LPS, enhances cell response to it -elevated LBP levels in sepsis -catalyzes binding to CD 14 2. CD14 -LPS can bind but no intracellular signal 3. TLR-4 -signal transducing R for LPS -forms complex w/CD 14 -intracellular signaling -> activation gene txn
Define CD 14
=cell surface R -acts as a pattern recognition R -can bind: 1. LPS 2. PDG 3. heat shock proteins -found of Mphages and PMNs -GPI anchored protein w/no transmembrane domain -> no signal transduction
Define TLR proteins
=Family of heterodimer protein Rs -similar intracellular domain but extracellular specific for a different bacterial product -activate 2 intracellular cascades (Myd88 -> NFkB; Tram/Trip) -> activate gene tx -have different locations (cell surface vs intracellular)
Name some common TLRs
1. TLR 4= LPS, heat shock proteins 2. TLR 5= flagellin 3. TLR 9= CpG DNA 4. TLR 2=lots of stuff
Name 3 fxns of the bacterial cell wall
1. gives bacteria its shape 2. provides structural support 3. prevents bacteria from swelling up and popping
Vancomycin acts on the __________ rxn of cell wall synthesis while beta lactam antibiotics work on the __________ rxn.
Vancomycin=transglycosylation Beta lactam =transpeptidation
How does Vancomycin work?
=cell wall synthesis inhibitor - Normally, last 2 AA are targets of transpeptidase rxn: terminal D-alanine is cleaved off and another AA is substituted for another amino group on another pentapeptide chain -> cross-link VA binds to terminal D-ala-D-ala end of the peptide VA physically blocks transglycosylation and cross-linking b/c so big End result: can’t make larger polymer structure, just stick with short 5 unit chains -> interrupts cell wall synthesis
Why does Vancomycin not work against gram negative infections?
-b/c it's too big to fit through porins to get to the peptide components of the transglycosylation rxn that it inhibits -does work well against gram + esp those resistant to beta lactam antibiotics (ex. MRSA/serious infections)
What is resistant to vancomycin? How does it work?
-Enterococci -plasmid carries gene for enzymes that will make D-ala-D-lac instead of D-ala-D-ala -now, cell wall synthesis has been changed and vancomycin can no longer bind to its substrate
True or false: cell wall synthesis inhibiting antibiotics are bactericidal
-true -b/c cell wall is integral to bacterial survival -Includes: 1. Beta lactams 2. vancomycin
Vancomycin is a _______.
cell wall synthesis inhibitor 1. but NOT a beta lactam
Beta lactams are _______.
=cell wall synthesis inhibitor
How does the beta lactam ring of beta lactam antibiotics help it do its job?
Beta lactam ring holds antibiotic in a 3-D configuration that resembles the D-ala-D-ala terminal peptide, which fits into active site of the transpeptidation enzyme. -So beta lactam antibiotics can fit into the active site of the transpeptidase and act as a noncompetitive inhibitor (beta lactam gets cleaved by the transpeptidase and covalently attaches to AA in active site of transpeptidase -> enzyme is out of commission). Therefore, beta lactam antibiotics irreversible inhibitors of cell wall synthesis (even if wash out antibiotics, bacteria can’t start growing again b/c enzymes are altered)
True or false: different beta lactams target different penicillin binding proteins in bacteria
-true -there are lots of PBP that are involved in the transpeptidation rxn of cell wall synthesis -diff beta lactam antibiotics have diff affinities for various PBP, and result in diff effects on the cell -doesn't really matter what happens b/c all inhibit cell wall synthesis and are bactericidal
Why does PCN not work against gram negative infections?
-b/c it can't get across the outer membrane/porins to get to the site of cell wall synthesis -but other PCN derivatives can do this
Name 2 major factors that influence susceptibility to beta lactam antibiotics
1. Physiologic factors -growth (most sensitive when actively growing) -osmotic pressure (high osmotic press in kidney decreases sensitivity) 2. Intrinsic bacterial factors -Affinity for PBPs -Presence of beta lactamases -Outer membrane of gram negatives
Define beta lactamases
=enzymes produced by the bacteria as a resistance mechanism to beta lactam antibiotics -hydrolyze ring of beta lactam -> inactive the antibitocs -> drug resistance -found at site of cell wall synthesis 1. Gram += periphery of cell 2. Gram -= periplasmic space
Name 3 mechanisms of beta lactam antibiotic resistance
1. Chromosomal mutations that decrease permeability of porins (gram negatives, pseudomonas) 2. Acquisition of new or mutant PBP w/poor affinity for beta lactams (MRSA, pneumococci) 3. Acquisition of genes for beta lactamases (gram neg enterics; Pseudomonas)
Describe beta lactam resistance in S. aureus
1. Penicilinase (beta lactamase) acquired on plasmid -initially, only resistance mechanism so still sensitive to other beta lactams that penicillinase had low affinity for (ex methicillin) 2. Chromosomal mutation at mec locus -encodes for new PBP w/low affinity for beta lactams -provides resistance to all beta lactams (methicillin, cephalosporins) -STILL sensitive to vancomycin!
Describe beta lactam resistance in S. pneumoniae
1. Acquired by DNA transformation for new PBP genes -provides partial resistance -resistance often acquired stepwise from low -> high -many partially resistant strains are sensitive to ceftriaxone -highly resistant can't be treated w/beta lactams
What do we use to treat MRSA?
What do we use against partially beta lactam resistant S. pneumoniae?
-ceftriaxone (cephalosporin)
Name 2 strategies developed by researchers to overcome beta-lactamases and antibiotic resistance?
1. Design beta lactams not degraded by beta lactamases -carbapenems 2. Develop beta lactamase inhibitors
How do quinolone antibiotics work?
DNA synthesis inhibitors -target DNA gyrase and topoisomerases (enzymes impt to keep bacterial DNA in right 3-D conformation so can be replicated) -causes double strand DNA breaks -bactericidal
Ciproflaxin is a _______.
=fluroquinolone =DNA synthesis inhibitor Use: 1. Gram negatives (pseudomonas) 2. Gram positives (B. anthracis)
What are respiratory quinolones?
=DNA synthesis inhibitor antibiotics -more active against pathogens of upper and lower respiratory tract infections -ex more active against gram positives (pneumococci)
Fluroquinolones are active against what types of bacteria?
=DNA synthesis inhibitors 1. most gram positives and gram negatives 2. mycoplasma 3. intracellular pathogens (chlamydia, rickettsia) 4. mycobacteria
What kinds of bacteria are fluroquinolones NOT good against?
1. Some anaerobes 2. syphillis
Name the only quinolone active against pseudomonas?
Describe resistance to quinolones
-Usu several stepwise genetic mutations 1. mutations in target enzymes (topoisomerases) 2.permeability/efflux pumps Now some plasmid mediated resistance 1. Qnr genes protect DNA gyrase from quinolone inhibition 2. aminoglycoside modifying enzymes may inactivate quinolones
What bacteria have quinolone resistance plasmids? Why do we care?
1. Enterobacteriaceae 2. Pseudomonas -dangerous b/c 1. potential to develop high resistance 2. can spread resistance of other types of bacteria
Rifampin is a ________
=RNA synthesis inhibitor
Sulfonamides/sulfa drugs are __________
=inhibitors of folate metabolism -> indirectly inhibit DNA synthesis -often given in combo with trimethoprim (another folate metab antagonist) b/c actions are synergistic
Trimethoprim is a ________.
=folate metabolism antagonist -indirectly inhibits DNA synthesis -often given in combo w/sulfa drugs b/c actions are synergistic -Active against: 1. S. aureus (MRSA) 2. Enterobacteriaceae (UTIs) 3. Pneumocystis resistance by plasmids encoding enzymes not recognized by the drugs
How do Protein synthesis inhibitors work?
-bind to 30s or 50s ribosomal subunit of -generally target ribosomal RNA at several sites -widespread plasmid resistance b/c of heavy use
Tetracyclines are ___________.
=Protein synthesis inhibitors -bind to 30S ribosomal subunit -Bacteriostatic -Active against: 1. Gram positive 2. Most gram neg -Lots of resistance 1. efflux pumps
What kinds of bacteria are tetracyclines active against?
=protein synthesis inhibitors (30S) 1. Most gram + 2. Most gram - NOT: pseudomonas, enterobacter, nosocomial 3. Most anaerobes 4. Mycoplasma 5. Intracellular pathogens (Rickettsia, Chlamydia, Brucella) 6. Spirochetes 7. Bartonella
Tigecycline is a ________.
-tetracycline=protein synthesis inhibitor (30S) -circumvents acquired resistance mechanisms -restores tetracycline use for bacteria w/intrinsic susceptibility -NOT active against: 1. Nosocomial pathogens (pseudomonas, enterobacter, acinetobacter) 2. M. tb complex 3. serious staph infections
Aminoglycosides are _________.
=protein synthesis inhibitors -amino sugars linked together by a glycoside -active against extracellular bacteria w/ ETC 1. Facultative gram neg 2. Pseudomonas 3. S. aureus -bactericidal
What are aminoglycosides NOT good against?
1. Things w/out ETC -streptococci -some anaerobes 2. Intracellular bugs (b/c can't penetrate eukaryotic cells)
Streptomycin is a __________.
=aminoglycoside=protein synthesis inhibitor
Name 2 mechanisms of aminoglycoside acquired resistance
1. Chromosomal mutation -Streptomycin ONLY 2. Plasmid encoding inactivating enzymes -ALL aminoglycosides -strategy to overcome is design new aminoglycoside w/fewer sites that could be targeted by inactivating enzymes Don't forget about intrinsic resistance (no ETC or intracellular pathogen)
Macrolides are _________.
=protein synthesis inhibitors -bind to 23S ribosomal RNA in 50S subunit -NOT reliably bactericidal (depends on individual macrolide and individual bacteria)
What kinds of bacteria are ALL macrolides active against?
=protein synthesis inhibitors 1. Most gram positive 2. Campylobacter 3. Mycoplasma 4. Rickettsia 5. Chlamydia 6. Legionella Not able to get across gram negative outer membrane of gram negatives
Clarithromycin and azithromycin are __________.
=macrolides -have additional activity 1. Upper resp tract gram neg (H. influ, Moraxella) 2. Helicobacter 3. MAC
Name 2 macrolide resistance phenotypes
1. M phenotype -due to efflux pump -common in US -bacteria STILL sensitive to telithromycin and clindamycin 2. MLS phenotype -due to 23S ribosomal methylation -> blocks drug from binding -if this resistance, then resistant to macrolides AND clindamycin
Chloramphenicol is a _________.
=50S protein synthesis inhibitor -"the chlorine" -Broad spectrum antibiotic 1. gram + 2. gram - 3. anaerobes -clinical use limited by rare but severe side effects
Which protein synthesis inhibitor antibiotics act on the 50S subunit? The 30S?
=CLEan TAG; CLEan lies over the base (inhibits 50S); TAG lies beneath the base (inhibits 30S) CLEan C=Chloramphenicol, clindaymcin L=Linezolid E=Eryhtromycin TAG T=Tetracycline AG=Amino glycoside
Which protein synthesis inhibitor is the only one that can't be absorbed orally?
=aminoglycosides (note: Tigecycline, a tetracycline derivative, also can't be given orally)
Name 2 situations where you would use chloramphenicol.
=protein synthesis inhibitor antibiotic whose use is limited by rare but severe side effect -give when can't give alternate antibiotic 1. Bacterial meningitis but pt is allergic to PCN, cephalosporins 2. Young children or pregnant women with Rocky Mtn spotted fever (can't give tetracycline)
Name some side effects of chloramphenicol
=protein synthesis inhibitor -think of it pouring chlorine in your bones 1. Anemia -reversible 2. Aplastic Anemia -irreversible; fatal 3. Gray baby syndrome
Which antibiotic causes gray baby syndrome?
=chloramphenicol -b/c baby can't fully conjugate the drug in the liver ->toxicity -> shock, cynanosis, abd distension
Clindamycin is active against what types of bugs that make it especially useful?
=anaerobes! -also active against gram + -no use against gram -
Name some uses of clindamycin
=50S protein synthesis inhibitor 1. Anaerobic infections -aspiration pneumonia -lung abscesses -perforated bowel -septic abortion -vaginosis 2. Acne
Use of which antibiotic is associated w/pseudomembranous colitis?
=clindamycin -other antibiotics also cause
Name 2 antibiotics that can be used to treat pseudomembranous colitis.
=bloody, pus diarrhea caused by C. difficile 1. Vancomycin -goes unabsorbed in GI tract so is very concentrated by the time it gets to the colon 2. Metronidazole
Linezolid is a ________.
=50S protein synthesis inhibitor ="Godzilla lizard" -stamps out gram + resistant bugs 1. MRSA 2. VRE 3. hospital acquired pneumonia
Side effects of linezolid include: a. damage to your wallet b. BM suppression c. headaches d. GI irritation e. all of the above
-all of the above
Name some side effects associated w/macrolides
=50S protein synthesis inhibitor antibiotics -erythromycin associated w/most 1. GI irritation -gastroparesis 2. Cholestatic hepatitis 3. Prolonged QT syndrome
Tetracycle/doxycycline are __________/
=30S protein synthesis inhibitors =Tet offensive 1. Venereal disease by Chlamydia 2. Mycoplasma pneumoniae 3. Brucella and Rickettsia 4. Acne
Which of the following are side effects of doxycline? a.GI irritation b. phototoxic dermatitis c. renal and hepatic toxicity d. discolored teeth and depressed bone growth (kids) e. all of the above
=all of the above
Aminoglycosides are used against_______
1. gram neg enterics (including Pseudomonas aeruginosa) -often used for hospital infections
Name the adverse effects of aminoglycosides
"A MEAN Guy" 1. otoxicity -irreversible hearing loss 2. renal toxicity 3. neuromuscular blockade
If an antibiotic has the ending "-floxacin" then it is a ______.
=fluroquinolone =DNA synthesis inhbitors
Name some adverse effects associated w/ fluroquinolones
=DNA synthesis inhibitors 1. GI irritability 2. Cartilage damage (avoid in kids b/c they have more cartilage) 3. Tendonitis and tendon rupture (Cipro) 4. rare CNS side effects 5. increased risk of C. difficile infection
Fluroquinolones are best against _________
=gram negative bugs (including pseudomonas)
Which antibiotic causes red man syndrome?
=vancomycin -rapid infusion -> non-allergic release of HM -> red, itchy rash over torso -can be prevented by infusing slowly or giving antihistamine
Which antibiotics cause side effects almost exclusively in AIDs pts?
=trimethoprim and sulfa drugs -cause rash, BM suppressor -also DON'T give to anyone taking warfarin!
Post-infectious arthritis occurs after which of the following infections? a.C. trachomatis urethritis b. Campylobacter gastroenteritis c. Yersinia gastroenteritis d. Shigella gastroenteristis e. all of the above
=all of the above -HLA-B27 is a major risk factor for developing it post-infectious
Methylation of a 23S ribosomal RNA confers resistance to _________.

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