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antimicrobials targeting folic acid synthesis (DNA methylation)

Sulfonamides (sulfadiazine, sulfamethoxazole, sulfisoxazole) and trimethoprim


antimicrobials targeting DNA topoisomerases

fluroquinolones (ciprofloxazin and levofloxacin)


antimicrobials damaging DNA



antimicrobials targeting peptidoglycan synthesis

glycopeptides (bacitracin and vancomycin)


antimicrobials targeting peptidoglycan cross linking

penicillnase sensitive penicillins (amoxicillin, amplicillin, and penicillin G, V), penicillnase resistant penicillins (dicloxacillin, nafcillin, oxacillin), antipseudomonals (piperacillin, ticarcillin), cephalosporins (1st- cefazolin, 2nd cefoxitin, 3rd ceftriaxone, 4th cefepime, 5th ceftaroline), carbapenems (doripenem, ertapenem, imipenem, meropenem), monobactams (aztreonam)


antimicrobials targeting mRNA synthesis (RNA polymerase)



antimicrobials targeting 50s subunit

chloramphenicol, clindamycin, linezolid, macrolids (azithromycin, clarithromycin, erthromycin), streptogramins (dalfopristin, quinupristin)


antimicrobials targeting 30s subunit

aminoglycosides (amikacin, gentamicin, neomycin, streptomycin, tobramycin) and tetracyclines (doxycycline, minocycline, tetracycline)


penicillin G, V mechanism of action

bind penicillin binding proteins (transpeptidases). Block transpeptidase cross-linking of peptridoglycan in cell wall. Activate autolytic enzymes.


penicillin G, V clinical use

mostly gram positive organisms (S. pneumoniase, S. pyogenes, Actinomyces). Also gram negative cocci (mainly N. meningitidis) and spirochetes (Namely T. pallidum). Bactericidal for gram positive cocci, gram positive rods, gram negative cocci, and spirochetes. Penicillinase sensitive


penicillin G, V toxicity

hypersensitivity reactions, hemolytic anemia


penicillin G, V resistance

penicillnase in bacteria (a type of beta-lactamse) cleaves Beta-lactam ring


amoxicillin, ampicillin (aminopenicillins) mechanism of action

same as penicillin but with wider spectrum; penicillinase sensitive penicillins. Also combined with clavulanic acid to protect against destruction by beta lactamase. amOxicillin has better Oral bioavailability than ampicillin.


amoxicillin, ampicillin (aminopenicillins) clinical use

extended spectrum penicillin. In addition to penicillin coverage [mostly gram positive organisms (S. pneumoniase, S. pyogenes, Actinomyces). Also gram negative cocci (mainly N. meningitidis) and spirochetes (Namely T. pallidum). Bactericidal for gram positive cocci, gram positive rods, gram negative cocci, and spirochetes. Penicillinase sensitive], also covers H. influenzae, H. pylori, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci).


amoxicillin, ampicillin (aminopenicillins) toxicity

hypersensitivity reactions, rash, pseudomembranous colitis.


amoxicillin, ampicillin (aminopenicillins) resistance

penicillnase in bacteria (a type of beta-lactamse) cleaves Beta-lactam ring


dicloxacillin, nafcillin, oxacillin mechanism of action

same as penicillin. narrow spectrum, penicillinase resistant because of bulky R group blocks access of beta lactamase to beta lactam ring.


dicloxacillin, nafcillin, oxacillin clinical use

S. aureus (except MRSA; resistant because of altered penicillin binding protein target site). Use Naf for staph


dicloxacillin, nafcillin, oxacillin toxicity

hypersensitivity reactions, interstitial nephritis.


piperacillin, ticarcillin (antipseudomonals) mechanism of action

same as penicillin but with extended spectrum


piperacillin, ticarcillin clinical use

pseudomonas spp. and gram negative rods; susceptible to penicillinase; use with beta lactamase inhibitors


piperacillin, ticarcillin (antipseudomonals) toxicity

hypersensitivity reaction


beta lactamase inhibitors

clavulanic acid, sulbactam, tazobactam. often added to penicillin to protect it from destruction by beta lactamase (penicillinase).


cephalosporins mechanism of action

beta lactam drugs that inhibit cell wall sythesis but are less susceptible to penicillinases. bactericidal.


organisms not covered by cephalosporins

they are LAME. Listeria, Atypicals (Chlamydia, mycoplasma), MRSA, and Enterococci. Exception: ceftaroline covers MRSA.


first generation cephalosporins clinical use

cefazolin and cephalexin- gram positive cocci (staph and strept), Proteus mirabilis, E coli, Klebisella pneumoniase (PEcK). Cefazolin is used prior to surgery to prevent S. aureus wound infections.


second generation cephalosporins clinical use

cefoxitin, cefaclor, cefusoxime- gram positive cocci, Haemophilus infleunzae, enterobacter aerogenes, Neisseria spp, Proteus mirabilis, E coli, Klebisella pneumoniase, Serratia marcescens (HEN PEcKS).


third generation cephalosporins clinical use

ceftriaxone, cefotaxime, ceftazidime- serious gram negative infections resistant to other beta lactams. Ceftriaxone- menigitis, gonorrhea, disseminated lyme disease. Cetazidime- pseudomonas.


fourth generation cephalosporins clinical use

cefepime- gram negative organisms with increased activity against Pseudomonas and gram positive organisms.


fifth generation cephalosporins clinical use

ceftaroline- broad gram positive and gram negative spectrum, including MRSA; does not cover pseudomonas


cephalosporins toxicity

hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram like reaction, vitamin K deficiency. Exhibit cross reactivity with penicillins. increased nephrotoxicity of aminoglycosides.


cephalosporins resistance

structural changes in penicillin binding proteins (transpeptidases).



imipenem, meropenem, ertapenem, doripenem


carbapenems (imipenem, meropenem, ertapenem, doripenem) mechanism of action

Imipenem is a broad spectrum, beta lactamase resistant carbapenem, Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.


carbapenems (imipenem, meropenem, ertapenem, doripenem) clinical use

gram positive cocci, gram negative rods and anaerobes. wide spectrum but significant side effects limit use to life threatening infections or after other drugs have failed. Meropenem has a decreased risk of seizures and is stable to dehydropeptidase I.


carbapenems (imipenem, meropenem, ertapenem, doripenem) toxicity

GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.





monobactams (aztreonam) mechanism of action

less susceptible to beta lactamases. prevents peptidoglycan cross-linking by binding to penicillin binding protein 3. Synergistic with aminoglycosides. No cross allergenicity with penicillin.


monobactams (aztreonam) clinical use

gram negative rods only. no activity against gram positives or anaerobes. For penicillin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.


monobactams (aztreonam) toxicity

nontoxic, GI upset


vancomycin mechanism

inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Not susceptible to beta lactamases.


vancomycin clinical use

gram positive bugs only- serious, multidrug resistant organisms, including MRSA, S epidermidis, sensitive Enteroccocus species, and C diff (oral dose for pseudomembranous colitis).


vancomycin toxicity

well tolerated in general but not trouble free. Nephrotoxicity, ototoxicity, thrombophlebitis, diffuse, flushing-- red man syndrome (can largely prevent by pretretment with antihistamines and slow infusion rate).


vancomycin mechanism of resistance

occurs in bacteria via amino acid modification of D ala D ala to D ala D lac.



gentamicin, neomycin, amikacin, tobramycin, streptomycin


aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin) mechanism of action

bactericidal, irreversible inhibition of intiation of comples through binding of the 30s subunit. can cause misreading of mRNA. Also block translocation. require O2 for uptake; therefore ineffective against anaerobes.


aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin) clinical use

severe gram negative rod infections. Synergistic with beta lactam antibiotics. Neomycin for bowel surgery.


aaminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin) toxicity

nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics). Teratogen


aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin) mechanism of resistance

bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation


tetracyclines (tetracycline, doxycyline, minocycline) mechanism of action

bacteriostatic, bind to 30s and prevent attachment of aminoacyl tRNA; limited CNS penetration. Doxycyline is fecally eliminated and can be used in patients with renal failure. Do not take tetracyclines with milk (Ca), antacids (Ca or Mg), or iron containing preparations because divalent cations inhibit drugs absorption in the gut.


tetracyclines (tetracycline, doxycyline, minocycline) clinical use

Borrlia burgdorferi, M pneumoniase. Drugs' ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia. Also used to treat acne.


tetracyclines (tetracycline, doxycyline, minocycline) toxicity

GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.


tetracyclines (tetracycline, doxycyline, minocycline) mechanism of resistance

decreased uptake or increased efflux out of bacterial cells by plasmid encoded transport pumps


chloramphenicol mechanism of action

blocks peptidyltransferase at 50s ribosomal subunit. bacteriostatic.


chloramphenicol clinical use

meninigitis (haemophlus influenzae, Neisseria meningitidis, Streptococcus pneumoniase) and Rocky mountain spotted fever (rickesttsia rickettsii) Limited use owing to toxicities, but often still used in developing countries


chloramphenicol mechanism of resistance

plasmid encoded acetyltransferase inactivates the drug


clindamycin mechanism of action

blocks peptide transfer (translocation) at 50s ribosomal subunit. Bacteriostatic


clindamycin clinical use

anaerobic infections (e.g. Bacteroides sp, Clostridium perfringens) in aspiration pneumonia, lung abscesses and oral infections. Also effective against invasive group A streptococcal infection. Treats anaerobic infections above the diaphragm vs. metronidazole (anaerobic below the diaphragm).


clindamycin toxicity

pseudomembranous colitis (C diff), fever, diarrhea


oxazolidinones (linezolid) mechanism of action

inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex


oxazolidinones (linezolid) clinical use

gram positive species including MRSA and VRE


oxazolidinones (linezolid) toxicity

bone marrow suppresion (especially thrombocytopenia), peripheral neuropathy, serotonin syndrome


oxazolidinones (linezolid) mechanism of resistance

point mutation of rRNA



azithromycin, clarithromycin, erythromycin


macrolides (azithromycin, clarithromycin, erythromycin) mechanism of action

inhibition of protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S subunit. Bacteriostatic


macrolides (azithromycin, clarithromycin, erythromycin) clinical use

Atypical pneumonias (mycoplasma, chlamydia, legionella), STIs (chlamydia), gram positive cocci (streptococcal infections in patients allergic to penicillin), B. pertussis.


macrolides (azithromycin, clarithromycin, erythromycin) tocixity

MACRO: gastrointestinal Motility, Arrhythmia caused by prolong QT interval, acute Cholestatic hepatitis, Rash, eOsinophilia. Increases serum concentration of theophyllines, oral anticoagulants. Clarithromycin and erthromycin inhibit cytochrome P-450.


macrolides (azithromycin, clarithromycin, erythromycin) mechanism of resistance

methylation of 23S rRNA binding site prevents binding of drug


trimethoprim mechanism of action

inhibits bacterial dihydrofolate reductase. Bacteriostatic


trimethoprim clinical use

used in combination with sulfonamides (TMP-SMX), causing sequential block of folate synthesis. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis


trimethoprim toxicity

megloblastic anemia, leukopenia, granulocytopenia (may alleviate with supplemental folinic acid. TMP Treats Marrow Poorly.


sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine) mechanism of action

inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacterostatic (bacteriocidal when used with TMP). Dapsone, used to treat lepromatous leprosy, is closely related drug that also inhibits folate synthesis.


sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine) clinical use

gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.


sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine) toxicity

hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infant, displace other drugs from albumin (e.g. warfarin)


sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine) mechanism of resistance

altered enzyme (bacterial dihydropteroate synthase), decrease uptake or increase PABA synthesis.



ciprofloxacin, norfloxacin, levofloxacin, olfoxacin, mociflocacin, gemifloxacin, enoxacin


fluoroquinolones (ciprofloxacin, norfloxacin, levofloxacin, olfoxacin, mociflocacin, gemifloxacin, enoxacin) mechanism of action

inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV. bactericidal. Must not be taken with antacids.


fluoroquinolones (ciprofloxacin, norfloxacin, levofloxacin, olfoxacin, mociflocacin, gemifloxacin, enoxacin) clinical use

gram negative rods of urinary and GI tracts (including pseudomonas), Neisseria, some gram positive organism.


fluoroquinolones (ciprofloxacin, norfloxacin, levofloxacin, olfoxacin, mociflocacin, gemifloxacin, enoxacin) toxicity

GI upset, superinfections, skin rashes, headache, dizziness, Less commonly, can cause leg cramps and myalgias. Contraindicated in pregnancy, while nursing, and children under 18 years due to possible cartilage damage. Some may prolong QT interval. May cause tendonitis or tendon rupture in people over 60 and in patients taking prednisone. Fluoroquinolones hurt attachments to your bones.


fluoroquinolones (ciprofloxacin, norfloxacin, levofloxacin, olfoxacin, mociflocacin, gemifloxacin, enoxacin) mechanism of resistance

chromosome encoded mutation in DNA gyrase, plasmid mediated resistance, efflux pumps.


Daptomycin mechanism of action

lepopeptide that disrupts cell membrane of gram positive cocci


Daptomycin clinical use

S aureus skin infections (especially MRSA), bacteremia, endocarditis, VRE. Not used for pneumonia (avidly binds to and is inactivated by surfactant).


Daptomycin toxicity

myopathy, rhabdomyolysis


Metronidazole mechanism of action

forms toxic free radical metabolites in bacterial cell that damage DNA. Bactericidal, antiprotozoal


Metronidazole clinical use

treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. diff). Used with a proton pump inhibitor and clarithromycin for triple therapy for triple therapy against H. Pylori. Treats anaerobic infections below the diaphragm vs clindamycin.


M tuberculosis prophylaxis



M tuberculosis treatment

Rifamin, Isoniazid, Pyrazinamide, Ethambutol (RIPE for treatment)


M avium- intracellulare prophylaxis

azithromycin, rifabutin


M avium- intracellulare treatment

more drug resistant than M tuberculosis. Azithromycin or clarithromycin plus ethambutol. Can add rifabutin or ciproflaxacin


M leprae treatment

long term treatment with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form



rifampin rifabutin


rifamycins (rifampin, rifabutin) mechanism of action

Inhibit DNA dependent RNA polymerase


rimfampin's four R's

RNA polymerase inhibitor, ramps up microsomal cytochrome P-450, red/orange body fluids, rapid resistance if use alone. Rifampin ramps up cytochrome P450 but rifabutin does not.


rifamycins (rifampin, rifabutin) clinical use

M. tuberculosis; delay resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B.


rifamycins (rifampin, rifabutin) toxicity

Minor hepatotoxicity and drug interactions (increase cytochrome P450); orange body fluids. Rifabutin favored aver rifampin in patients with HIV infections due to less P450 stimulation.


rifamycins (rifampin, rifabutin) mechanism of resistance

mutations reduce drug bindint to RNA polymerase. Monotherapy rapidly leads to resistance.


Isoniazid mechanism of action

decrease synthesis of mycolic acids. bacterial catalase peroxidase (encoded by KatG) needed to convert INH to active metabolite


Isoniazid clinical use

Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB. Different half lives depending on fast vs slow acetylators


Isoniazid toxicity

Neurotoxicity, hepatotoxicity, Pyridoxine (B6) can prevent neurotoxicity. INH Injures Nephrons and Hepatocytes.


Isoniazid mechanism of resistance

Mutations leading to underexpression of Kat G


Pyrazinamide mechanism of action

mechanism uncertain. Is a prodrug that is converted to active compound pyrazinoic acid.


Pyrazinamide clinical use

Mycobacterium tuberculosis


Pyrazinamide toxicity

Hyperuricemia, hepatoxicity


Ethambutol mechanism of action

decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferae


Ethambutol clinical use

Mycobacterium tuberculosis


Ethambutol toxicity

optic neuropathy (red- green color blindness)


spherical (coccus) gram positive bacteria

staph and strep


spherical (coccus) gram negative bacteria

moraxella catarrhalis, neisseria


rod (bacillus) gram positive bacteria

bacillus, clostridium, corynebacterium, gardnerella, lactobacillus, listeria, mycobacterium (acid fast), propionibacterium


rod (bacillus) gram negative enteric bacteria

bacteroides, camylobacter, e coli, enterobacter, helicobacter, klebsiella, proteus, pseudomonas, salmonella, serratia, shigella, vibrio, yersinia


rod (bacillus) gram negative respiratory bacteria

bordetella, haemophilus (pleomorphic), legionella (silver stain).


rod (bacillus) gram negative zoonotic bacteria

bartonella, brucella, francisella, pasteurella


branch filamentous gram positive bacteria

actinomyces, nocardia (weakly acid fast)


pleomorphic gram negative bacteria

chlamydia (giemsa), rickettsiae (giemsa)


spiral gram negative bacteria

borrelia (giemsa), leptospira, treponema


no cell wall bacteria

mycoplasma, ureaplasma (contain sterols, which do not gram stain)


bacteria that do not gram stain well

treponema, mycobacteria, mycoplasma, legionella pneumophila, rickettsia, chlamydia


giemsa stain

chlamydia, borrelia, rickettsia, trypanosomes, plasmodium


PAS stain

stains glycogen, mucopolysaccharides; diagnosis whipple disease


ziehl-neelsen (carbol fuchsin) stain

acid fast bacteria (nocardia, mycobacteria, protozoa (cryptosporidium oocysts). auramine rhodamine stain is an alternative


india ink stain

cryptococcus neoformans (mucicarmine can also be used to stain think polysaccharide capsule red)


silver stain

fungi (pneumocystis), legionella, H pylori


chocolate agar

H influenzae and Neisseria. Has factor V (NAD+) and X (hematin)


thayer-martin agar

N. gonorrhoeae, N meningitidis. Contains vancomycin (inhibits gram positive organisms), trimethoprim, colistin (inhibits gram negative organisms except neisseria), and Nystatin (inhibits fungi)


bordet gengou agar

B pertussis, contains potato


regan lowe medium

B pertussis, contains charcoal, blood, and antibiotic


tellurite agar and loffler medium

c diphtheriae


lowenstein jensen agar

m tuberculosis


eaton agar

m pneumoniae, requires cholesterol


MacConkey agar

lactose fermenting enterics, fermentation produces acid, causing colonies to turn pink


Eosin methylene blue agar

E coli, colonies with green metallic sheen


charcoal yeast extract agar buffered with cysteine and iron



Sabouraud agar




Nocardia, Pseudomonas aeruginosa, and mycobacterium tuberculosis. reactivation of M tuberculosis (eg after immunocompromise or TNF-alpha inhibitor use) has a predilection for the apices of the lung which have the highest pO2.



fusobacterium, clostridium, bacteroides, and actinomyces. They lack catalase and/or superoxide dismuase and are thus susceptible to oxidative damage. Generally foul smelling (short chain fatty acids), are difficult to culture and produce gas in tissue (CO2 and H2). They are normal flora in GI tract, typically pathogenic elsewhere. Aminoglycosides are ineffective against anaerobes because these antibiotics require O2 to enter into bacterial cell.


obligate intracellular bacteria

rickettsia, chlmydia, coxiella (C burnetti, Q fever). relay on host ATP


facultative intracellular bacteria

salmonella, neisseria, brucella, mycobacterium, listeria, francisella, legionella, yersinia pestis.


encapsulated bacteria

hamophilus influenzae type B, neisseria meningitidis, Escherichia coli, salmonella, klebsiella pneumoniae, and group B strep. their capsules serve as an antiphagocytic virulence factor. Capsule plus protein conjugate serves as an antigen in vaccines. They are opsonized then cleared by spleen. Asplenics have decreased opsonizing ability and thus increase risk for severe infections. Give S. pneumoniae, H influenzae, N meningitidis vaccines.


encapsulated bacteria vaccines

some vaccines containing polysaccharide capsule antigens are conjugated to a carrier protein, enhancing immunogenisity by promoting T cell activation and subsequent class switching. A polysaccharide antigen alone cannot be presented to T cells. examples include pneumococcal, H influenzae type B, meningococcal vaccine.


Usease positive organisms

cryptococcus, H pylori, Proteus, Ureaplasma, Nocardia, Klebsiella, S epidermidis, S saprophyticus.


catalase positive organisms

catalase degrades H2O2 into H2O and bubbles of O2 before it can be converted to microbicidal products by the enzymes myeloperoxidase. People with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with certain catalase positive organisms. Examples include Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E coli, Staphylococci, Serratia


bacteria that produces yellow sulfur granules



bacteria that produces yellow pigment

S aureus


bacteria that produces blue green pigment

pseudomonas aeruginosa


bacteria that produces red pigment

serratia marcescens


protein A virulence factor

binds Fc region of IgG. Prevents opsonization and phagocytosis. Expressed by S aureus.


IgA protease virulence factor

enzymes that cleaves IgA. Secreted by S pneumoniae, H influenze type B and Neisseria in order to colonize respiratory mucosa.


M protein virulence factor

helps prevent phagocytosis. Expressed by group A streptococci. Shares similar epitopes to human cellular proteins (molecular mimicry); possibly underlies the autoimmune response seen in acute rheumatic fever.


Type III secretion system

also known as injectisome. needle like protein appendage facilitating direct delivery of toxins from certain gram negative bacteria (eg pseudomonas, salmonella, shigella, E coli) to eukaryotic host cell.



secreted by certain species of gram positive and gram negative bacteria, composed of polypeptide, gene located on plasmid or bacteriophage. Highly toxic. Induces high titer antibodies called antitoxins. Toxoids are used as vaccines. Destroyed rapidly at 60 degrees C (except staph enterotoxin). Typical disease include tetanus, botulism, diphteria.



outer cell membrane of most gram negative bacteria. Composed of lipopolysaccharide (structural part of bacteria; released when lysed). Gene located within bacterial chromosome. Low toxicity. Can cause fever, shock, and activates tissue factor leading to DIC. Activates macrophages to release TNF alpha (fever and hypotension), IL-1 (fever), IL-6, and nitric oxide (hypotension). Activates complement C3a leading to hypotension and edema and C5a leading to neutrophil chemotaxis. Poorly antigenic. No toxoids formed and no vaccine available. Stable at 100 degrees C for 1 hour. Typical diseases include meningococcemia, sepsis by gram negative rods. O-antigen


Diphtheria toxin

released by cornebacterium diphtheriae. Inactivate elongation factor (EF-2). Causes pharyngitis with pseudomembranes in throat and severe lymphadenopathy (bull neck).


exotoxin A

released by pseudomonas aeruginosa. Inactivate elongation factor (EF-2). Causes host cell deathe


Shiga toxin (ST)

released by shigella spp. inactivates 60S ribosome by removing adenine from rRNA. GI mucosal damage causes dysentery; ST also enhances cytokine release, causing hemolytic-uremic syndrome (HUS).


Shiga like toxin (SLT)

released by enterohemorrhagic E coli (EHEC). inactivates 60S ribosome by removing adenine from rRNA. SLT enhances cytokine release, causing HUS (prototypically in EHEC serotype O157:H7). Unlike shigella, EHEC does not invade host cells.


Heat labile toxin (LT)

released by enterotoxigenic E coli (ETEC). Overactivates adenylate cyclase (increases cAMP) leading to increase Cl secretion in gut and H2O efflux. Causes watery diarrhea. Labile in the Air (Adenylate cyclase).


Heat stable toxin

released by enterotoxigenic E coli (ETEC). Overactivates guanylate cyclase (increases cGMP) leading to decrease resorption of NaCl and H2O in gut. Causes watery diarrhea. Stable on the Ground (guanylate cyclase).


Edema toxin

released by bacillus anthracis. Mimics the adenylate cyclase (increases cAMP). Likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax.


Cholera toxin

released vibrio cholerae. Overactivates adenylate cyclase (increases cAMP) by permanently activating Gs leading to increase Cl secretion in gut and H2O efflux. Causing voluminous rice water diarrhea.


Pertussis toxin

released by bordetella pertussis. Overactivates adenylate cyclase (increases cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe. May not be the cause the cough in whooping cough. can cause 100 day cough in adults.



released by Clostridium tetania. A protease that cleaves SNARE (soluble NSF attachment protein receptor), a set of proteins required for neurotransmitter release via vesicular fusion. Causes spasticity, risus sardonicus and lock jaw; toxin prevents release of inhibitory (GABA and glycine) neurotransmitters from Renshaw cells.


Botulinum toxin

released by clostridium botulinum. A protease that cleaves SNARE (soluble NSF attachment protein receptor), a set of proteins required for neurotransmitter release via vesicular fusion. Causes flaccid paralysis, floppy baby; toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions leading to flaccid paralysis.


alpha toxin

releasing Clostridium perfringens. Phospholipase (lecithinase) that degrades tissue and cell membranes. Causes degradation of phospholipids leading to myonecrosis (gas gangrene) and hemolysis (double zone of heomlysis on blood agar).


streptolysin O

released by streptococcus pyogenes. A protein that degrades cell membrane. Causes lyses RBCs; contributes to beta- hemolysis; host antibodies against toxin (ASO) used to diagnose rheumatic fever (do not confuse with immune complexes of poststreptococcal glomerulonephritis).


Toxic shock syndrome toxin (TSST-1)

released by staphylococcus aureus. Binds to MCH II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-gamma, TNF-alpha leading to shock. Causes toxic shock syndrome: fever, rash, shock,; other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin).


Exotoxin A

released by streptococcus pyogenes. s. Binds to MCH II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-gamma, TNF-alpha leading to shock. Causes toxic shock syndrome: fever, rash, and shock.



takes up naked DNA from environment.



plasmid becomes incorporated into host.



Segment of DNA that can jump from one location to another. Can transfer from plasmid to chromosome or vice versa.



generalized transduction occurs when lytic phage infects bacterium, leading to cleavage of bacterial DNA. Specialized transduction occurs when a lysogenic phage infects bacterium; viral DNA incorporates into bacterial chromosome. when phage DNA is excised and can infect another bacterium. Shiga like toxin, botulinum toxin, cholera toxin, diphteria toxin, and eythrogenic toxin are encoded in lysogenic phages.


identifying staphlycocci

with novobiocin, saprophyticus is resistant and epidermidis is sensitive


identifying streptococci

with optochin, viridans is resistant; pneumoniae is sensitive. With bacitracin, group B are resistant; group A strep are sensitive.


alpha hemolytic bacteria

form green ring around colonies on blood agar. Includes the following organisms: Streptococcus pneumoniae (catalase negative and optochin sensitive), Viridans streptococci (catalase negative and optochin resistant).


beta hemolytic bacteria

form clear area of hemolysis on blood agar. Includes the following organisms: Staphylococcus aureus (catalase and coagulase positive), Streptococcus pyogenes- group A strep (catalase negative and bacitracin sensitive), Streptococcus agalactiae- group B strep (catalase negative and bacitracin resistant), and Listeria monocytogenes (tumbling motility, meningitis in newborns, unpasteurized milk).


Staphylococcus aureus

Gram +, cocci in clusters, catalase +, coagulase +, β-hemolytic, forms yellow/golden colonies (aurei="golden"). gram positive cocci in clusters. protein A (virulence factor) binds Fc-IgG, inhibiting complement activation and phagocytosis. Commonly colonizes the nares.


diseases caused by staphylococcus aureus

Inflammatory disease- skin infections, organ abscesses, pneumonia (often after influenza virus infection), endocarditis, septic arthritis, and osteomyelitis. Toxin mediated disease- toxic shock syndrome, scalded skin syndrome (exfoliative toxin), rapid onset food poisoning (enterotoxins). MRSA (methicillin resistant S aureus) infection- important cause of serious nosocomial and community acquired infections; resistant to methicillin and nafcillin because of altered penicillin binding protein. TSST is a superantigen that binds to MHC II and T cell receptor, resulting in polyclonal T cell activation. Staphylococcal toxic shock syndrome (TSS) presents as fever, vomiting, rash, desquamation, shock, end organ failure. Associated with prolonged use of vaginal tampons or nasal packing. Compare with Streptococcus pyogenes TSS (a toxic shock like sydrome associated with painful skin infection). S aureus food poisoning due to ingestion of preformed toxin leading to short incubation period (2-6hrs) followed by nonbloody diarrhea and emesis. Enterotoxin is heat stable, cannot be destroyed by cooking. Staph aureus makes coagulase and toxins. Forms fibrin clot around self leading to abscess.


Staphylococcus epidermidis

Staphylococcus epidermidis is a catalase-positive, coagulase-negative, urease-positive, non-hemolytic with white colonies, gram-positive cocci that grows in clusters. infects prothetic devices (eg hip implant, heart valve) and intravenous catheters by producing adherent biofilms. Component of normal skin flora; contaminates blood cultures. Novobiocin sensitive.


Staphylococcus saprophyticus

Staphylococcus saprophyticus is a facultative anaerobe, urease-positive, gram-positive, catalase-positive coccus. secound most common cause of uncomplicated UTI in young women (first is E coli). Novobiocin resistant.


Streptococcus pneumoniae

Streptococcus pneumoniae is a facultative anaerobic, optochin-sensitive gram-positive diplococci. most common cause of meningitis, otitis media (in children), pneumonia, sinusitis. lancet shaped, gram positive diplococci. Encapsulated. IgA protease. Most are optochin sensitive. Pneumococcus is associated with rusty sputum, sepsis in sickle cell disease and splectomy. No virulence without capsule.


Viridans group streptococci

alpha hemolytic. They are normal flora of the oropharynx that cause dental caries (streptococcus mutans) and subacute bacterial endocarditis at damaged heart valves (S sanguinis). Resistant to optochin, differentiating them from S pneumoniae, which is alpha hemolytic but optochin sensitive. S sanguinis makes dextrans, which bind to fibrin platelet aggregates on damaged heart valve. Viridans group strep live in the mouth because they are afraid of the chin (opto-chin resistant).


Disease caused by Streptococcus pyogenes (group A streptococci)

group A strep causes: pyogenic- pharyngitis, cellulitis, impetigo, and erysipelas. Toxigenic- scarlet fever, toxic shock like syndrome, necrotizing fasciitis. Immunologic- rheumatic fever, acute glomerulonephritis.


Streptococcus pyogenes (group A streptococci)

Streptococcus pyogenes (Group A Strep, GAS) is a facultative anaerobic, β-hemolytic, gram-positive cocci. bacitracin sensitive, pyrrolidonyl arylamidase (PYR) positive. Antibodies to M protein enhance host defenses against S pyogenes but can give rise to rheumatic fever. ASO titer detects recent S pyogenes infection. Pharyngitis can result in rheumatic fever and glomerulonephritis. Impetigo more commonly recedes glomerulonephritis than pharyngitis.


criteria for acute rheumatic fever

caused by Streptococcus pyogenes (group A streptococci). Jones: joints- polyarthritis, heart- carditis, nodules (subcutaneous), erythema marginatum, sydenham chorea.


Scarlet fever

caused by Streptococcus pyogenes (group A streptococci). Scarlet rash with sandpaper like texture, strawberry tongue, circumoral pallor, subsequent desquamation.


Streptococcus agalactiae (group B streptococci).

Streptococcus agalactiae (GBS, Group B streptococcus) is a catalase negative gram-positive cocci with beta hemolysis on blood agar. bacitracin resistant, colonizes vagina; causes pneumonia, meningitis, and sepsis, mainly in babies. Produces CAMP factor, which enlarges the area of heomlysis formed by S aureus. Hippourate test positive. Screen pregnant women at 35-37 weeks of gestation. Patients with positive culture should receive intrapartum penicillin prophylacxis. Group B for babies.


Enterococci (group D streptococci)

Enterococci (E faecalis and E faecium) are normal colonic flora that are penicillin G resistant and cause UTI, biliary tract infections, and subacute endocarditis (following GI/GU procedures). Lancefield group D includes the enterococci and the nonenterococci group D streptococci. Variable hemolysis. VRE (vancomycin resistant enterococci) are an important cause of nosocomial infection. Enterococci, hardier than nonenterococcal group D, can grow in 6.5% NaCl and bile. Entero= intestine, faecalis=feces, strepto= twisted (chains), coccus=berry.


Streptococcus bovis (group D streptococci)

Streptococcus gallolyticus (formerly S. bovis) is catalase-negative, gram-positive coccus. colonizes the gut, but not apart of regular flora. S gallolyticus (S bovis biotype 1) can cause bacteremia and subacute endocarditis and is associated with colon cancer.


Corynebacterium diphtheriae

Corynebacterium diphtheriae is an aerobic, non-sporeforming gram-positive bacillus. causes diphtheria via exotoxin encoded by beta-prophage. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2. Symptoms include pseudomembranous pharyngitis (grayish-white membrane) with lymphadenopathy, myocarditis, and arrhythmias. Lab diagnosis based on gram positive rods with metachromatic (blue and red) granules and a positive Elek test for toxin. Toxoid vaccines prevent diphtheria. Coryne=club shaped. Black colonies on cystine-tellurite agar. ABCDEFG: ADP-ribosylation, Beta-prophage, Corynebacterium, Diphtheriae, Elongation factor 2, Granules.


Bacterial spores

formed when nutrients are limited. They are highly resistant to heat and chemicals. Have dipicolinic acid in their core. Have no metabolic activity. Must autoclave to potentially kill spores by steaming at 121 degrees Celsius for 15 min. Species and diseases include: Bacillus anthracis (anthrax), Bacillus cereus (food poisoning), Clostridium botulinum (botulism), Clostridium difficile (antibiotic associated colitis), Clostridium perfringens (gas gangrene), Clostridium tetani (tetanus), Coxiella burnetii (Q fever).



gram positive, spore forming, obligate anaerobic bacilli.


Clostridia tetani

gram positive, spore forming, obligate anaerobic bacilli. Produces tetanospasmin, an exotoxin causing tetanus. Tetanus toxin (and botulinum toxin) are proteases that cleave SNARE proteins for neurotransmitters, GABA and glycine, from Renshaw cells in spinal cord. Causes spastic paralysis, trismus (lockjaw), risus sardonicus (raised eyebrows and open grin). Prevent with tetanus vaccine. Treat with antitoxin with or without vaccine booster, diazepam (for muscle spasms).


Clostridia botulinum

gram positive, spore forming, obligate anaerobic bacilli. Produces a preformed, heat labile toxin that inhibits ACh release at the neuromuscular junction, causing botulism. In adults, disease is caused by ingestion of preformed toxin. In babies, ingestions of spores in honey causes disease (floppy baby syndrome). Treat with antitoxin


Clostridia perfringens

gram positive, spore forming, obligate anaerobic bacilli. produces alpha toxin (lecithinase, a phospholipase) that can cause myonecrosis (gas gangrene) and hemolysis. Perfringens perforates a gangrenous leg.


Clostridia difficile

gram positive, spore forming, obligate anaerobic bacilli. Produces two toxins. Toxin A, enterotoxin, binds to the brush border of the gut. Toxin B, cytotoxin, causes cytoskeletal disruption via actin depolymerization leading to pseudomembranous colitis causing diarrhea. Often secondary to antibiotics, especially clindamycin or ampicillin. Diagnosed by detection one or both toxins in stool by PCR. Treat with metronidazole or oral vancomycin. For recurrent cases, consider repeating prior regimen, fidaxomicin or fecal microbiota transplant.



caused by Bacillus anthracis, a gram positive, spore forming rod that produces anthrax toxin. The only bacterium with a polypeptide capsule (contains D glutamate).


cutaneous anthrax

painless papule surrounded by vesicles causing ulcer with black eschar (painless, necrotic) and can uncommonly progress to bacteremia and death.


pulmonary anthrax

inhalation of spore, which causes flu like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis and shock.


Bacillus cereus

Bacillus cereus is an endemic, soil-dwelling, Gram-positive, rod-shaped, motile, beta hemolytic bacterium. causes food poisoning. Spore survive cooking rice. Keeping rice warm results in germination of spores and enterotoxin formation. Emetic type usually seen with rice and pasta. Nausea and vomiting within 1-5 hr. Caused by cereulide, a preformed toxin. Diarrheal type causes watery, nonbloody diarrhea and GI pain within 8-18 hr. Reheated rice syndrome.


Listeria monocytogenes

Listeria monocytogenes is a non-spore forming beta-hemolytic, catalase-positive gram-positive bacillus. facultative intracellular microbe; acquired by ingestion of unpasteurized diary products and cold deli meats, via transplacental transmission, or by vaginal transmission during birth. Forms rocket tails (via actin polymerization) that allow intracellular movement and cell to cell spread across cell membranes, thereby avoiding antibody. Characteristic tumbling motility; is only gram positive organism to produce endotoxin. Can cause amnionitis, septicemia, and spontaneous abortion in pregnant women; granulomatosis infantiseptica; neonatal meningitis; meningitis in immunocompromised patients; mild gastroenteritis in health individuals. Treatment: gastroenteritis is usually self limited; ampicillin in infants, immunocompromised, and the elderly as empirical treatment of meningitis.



Like Nocardia, forms long, branching filaments resembling fungi. Gram positive anaerobe, not acid fast, located in normal oral flora, causes oral/facial abscesses that drain through sinus tracts, forms yellow "sulfur granules". Treat with penicillin. Treatment is a SNAP: Sulfonamides for Nocardia; Actinomyces treated with Penicillin



Like Actinomyces, forms long, branching filaments resembling fungi. Gram positive aerobe, acid fast (weak), found in soil, causes pulmonary infections in immunocompromised and cutaneous infections after trauma in immunocompetent. Treat with sulfonamides. Treatment is a SNAP: Sulfonamides for Nocardia; Actinomyces treated with Penicillin


primary tuberculosis

Due to infection with mycobacterium tuberculosis, in nonimmune host (usually a child). Causes hilar nodes and Ghon focus, usually found in lower to mid zones of the lung. There are several different potential outcomes: Ghon complex can heal by fibrosis leading to immunity, hypersensitivity, and a tuberculin positive test. It can also progress to lung disease, usually in HIV patients or those who have malnutrition; can progress to death rarely. It can also cause severe bacteremia, causing miliary tuberculosis and death. It can also result in preallergic lymphatic or hematogenous dissemination, leading to dormant tubercle bacilli in several organs, which can reactivate in adult life.


Extrapulmonary tuberculosis

can be located in CNS (parenchymal tuberculoma or meningitis), vertebral body (Pott disease), lymphadenitis, renal, GI, adrenals. Can reactivate later in lungs.


Secondary tuberculosis

Due to reactivation or reinfection with mycobacterium tuberculosis, in partially immune hypersensitized host (usually adult). Causes fibrocaseous cavitary lesion, usually in upper lobes.


PPD test

positive test shows current or past infection with mycobacterium tuberculosis. False positives with BCG vaccination. negative test if no infection or anergic (steroids, malnutrition, immunocompromise) and in sarcoidosis.


Interferon gamma release assay

positive test shows current or past infection with mycobacterium tuberculosis. fewer false positives from BCG vaccination.


caseating granuloma

has central necrosis with multinucleated Langhans giant cell. This appearance is classic for TB, but may be seen in fungal infections as well.


Mycobacterium tuberculosis

causes TB, often resistant to multiple drugs. Symptoms include fever, night sweats, weight loss, cough (nonproductive or productive), hemoptysis.



a genus of gram-positive, aerobic, acid-fast bacteria, occurring as slightly curved or straight rods. Produce cord factor in virulent strains, which inhibits macrophage maturation and induces release of TNF-alpha (causes acute phase reaction). Sulfatides (surface glycolipids) inhibit phagolysosomal fusion.


Mycobacterium avium and Mycobacterium intracellulare

causes disseminated non-TB disease in AIDS; often resistant to multiple drugs. Prophylaxis with azithromycin when CD4+ count is below 50 cells/mm3.


Mycobacterium scrofluaceum

cervical lymphadenitis in children.


Mycobacterium marinum

hand infection in aquarium handlers


Leprosy (Hasen disease)

cause by Mycobacterium leprae, an acid fast bacillus that likes cool temperatures (infects skin and superficial nerves, leading to glove and stocking loss of sensation) and cannot be grown in vitro. Reservoir in United States: armadillos. Has two forms: lepromatous and tuberculoid.


Lepromatous Hasen Disease

cause by Mycobacterium leprae, an acid fast bacillus. presents diffusely over the skin, with leonine (lion like) facies and is communicable; characterized by low cell mediated immunity with a humoral Th2 response. Treatment is dapsone, rifampin, and chlofazimine. Can be lethal.


Tuberculoid Hasen Disease

cause by Mycobacterium leprae, an acid fast bacillus. Limited to a few hypesthetic, hairless skin plaques; characterized by high cell mediated immunity with a largely Th1 type immune response. Treatment includes dapsone and rifampin.


Lactose fermeting enteric bacteria

fermentation of lactose leads to pink colonies on MacConkey agar. Examples include Citrobacter, Klebsiella, E coli, Enterobacter, and Serratia (weak fermenter). E coli produces beta-galactosidase, which breaks down lactose into glucose and galactose. On EMB agar, lactose fermenters grow as purple/black colonies. E coli grows colonies with a green sheen.



gram negative diplococci. Both gonococci and meningococci ferment glucose and produce IgA proteases. MeninGococci ferment Maltose and Glucose. Gonococci ferment Glucose.


Neisseria gonococci

gram negative diplococci. Unlike meningococci, it does not have a polysaccharide capsule, ferment maltose, and there is no vaccine due to antigenic variation of pilus proteins. It is sexually or perinatally transmitted. It can cause gonorrhea, septic arthritis, neonatal conjunctivitis, pelvic inflammatory disease (PID) and Fitz-Hugh-Curtis syndrome. Condoms decrease sexual transmission. Erthromycin ointment prevents neonatal transmission. Treatment includes ceftriaxone and either azithromycin or doxycycline for possible chlamydial coinfection.


Neisseria Meningococci

gram negative diplococci. Unlike gonococci, it does have a polysaccharide capsule, ferment maltose, and there is vaccine (type B vaccine, not widely available). It is transmitted via respiratory and oral secretions. It causes meningococcemia and meningitis, Waterhouse- Friderichsen syndrome. Prophylaxis includes rifampin, ciprofloxacin, or ceftriaxone for close contacts. Treatment includes ceftriaxone or penicillin G.


Haemophilus influenzae

Haemophilus influenzae is an encapsulated gram-negative coccobacilli. Small gram negative (coccobacillary) rod. Aerosal transmission. Nontypeable strains are the most common cause of mucosal infections (otitis media, conjuctivitis, bronchitis) as well as invasive infections since the vaccine for capsular type b was introduced. Produces IgA protease. Culture on chocolate agar, which contains factor V (NAD+) and X (hematin) for growth; can also be grown with S aureus, which provides factor V through the hemolysis of RBCs. haEMOPhilus causes Epiglottitis (cherry red in children), Meningitis, Otitis media, and Pneumonia. Treat mucosal infections with amoxicillin with or without clavulanate. Treat meningitis with ceftriaxone. Rifampin prophylaxis for close contacts. Vaccine contains type b capsular polysaccharide (polyribosylribitol phosphate) conjugated to diphtheria toxoid or other protein. Given between 2 and 18 months of age. Does not cause the flu (the influenza virus does).


Legionella pneumophila

Gram negative rod. Gram stains poorly, use silver stain. Grow on charcoal yeast extract culture with iron and cysteine. Detected by presence of antigen in urine. Labs may show hyponatremia. Aerosol transmission from environmental water source habitat (eg air conditioning systems, hot water tanks). No person to person transmission. Treat with macrolide or quinolone.


Legionnaires disease

Caused by Legionella pneumophila. Causes severe pneumonia (often unilateral and lobar), fever, GI, and CNS symptoms


Pontiac fever

Caused by Legionella pneumophila. Causes mild flu like syndrome


Pseudomonas aeruginosa

Aerobic, motile, gram-negative rod. Non-lactose fermenting, oxidase positive. Produces pyocyanin (blue-green pigment); has a grape like odor. Produces endotoxin (fever, shock) and exotoxin A (inactivates EF-2). PSEUDDOmona is associated with: Pneumonia, Sepsis, otitis Externa (swimmers ear), UTIs, Diabetes, Drug use, Osteomyelitis (eg puncture wounds). Depending on source and severity, treatment may include: extended spectrum beta lactams (eg piperacillin, ticarcillin, cefepime), carbapenems (eg imipenem, meropenem), monobactams (eg aztrenam), fluoroquinolones (eg ciprofloxacin), aminoglycosides (eg gentamicin, tobramycin), for multidrug resistant strains: colistin, polymyxin B. AERuginosa=AERobic. Pseudomonas often occurs in burn victims. Mucoid polysaccharide capsule may contribute to chronic pneumonia in cystic fibrosis patients due to biofilm formation.


Ecthyma gangrenosum

Caused by Pseudomonas aeruginosa. Rapidly progressive, necrotic cutaneous lesion caused by Pseudomonas bacteremia. Typically seen in immunocompromised patients.


E coli virulence factors

Fimbriae causes cystitis and pyelonephritis; K capsule causes pneumonia, neonatal meningitis; LPS endotoxin causes septic shock.


Enteroinvasive Escherichia coli (EIEC)

Escherichia coli is a lactose fermenting, gram-negative, facultative anaerobic bacillus. Microbe invades intestinal mucosa and causes necrosis and inflammation. Clinical manifestations similar to Shigella. Causes dysentery


Enterotoxigenic Escherichia coli (ETEC)

Escherichia coli is a lactose fermenting, gram-negative, facultative anaerobic bacillus. Produces heat labile and heat stable enteroToxins. No inflammation or invasion. Known as travelers diarrhea (watery)


Enteropathogenic Escherichia coli (EPEC)

Escherichia coli is a lactose fermenting, gram-negative, facultative anaerobic bacillus. No toxin produced. Adheres to apical surface, flattens villi, prevents absorption. Causes diarrhea, usually in children (Pediatrics).


Enterohaemorrhagic Escherichia coli (EHEC)

Escherichia coli is a lactose fermenting, gram-negative, facultative anaerobic bacillus. also called STEC (shiga toxin producing E coli). O157:H7 is most common serotype in US. Shiga-like toxin causes hemolytic-uremic syndrome. Causes dysentery (toxin alone causes necrosis and inflammation). Does not ferment sorbitol (distinguishes EHEC from other E coli).


hemolytic-uremic syndrome

caused by shiga like toxin, secreted by EHEC. triad of anemia, thrombocytopenia, and acute renal failure due to microthrombi forming on damaged endothelium leading to mechanical hemolysis (with schistocytes on peripheral blood smear), platelet consumption, and decrease renal blood flow.



Klebsiella pneumoniae is an encapsulated, urease-positive, gram-negative, facultative anaerobic bacillus. An intestinal flora that causes lobar pneumonia in alcoholics and diabetics when aspirated. Very mucoid colonies caused by abundant polysaccharide capsules. Dark red currant jelly sputum (blood/mucus). Also causes nosocomial UTIs. The four A's of KlebsiellA: Aspiration pneumonia, Abscess in lungs and liver, Alcoholics, di-A-betics.


Campylobacter jejuni

Campylobacter jejuni is a microaerophilic, comma-shaped, urease-negative, oxidase positive, motile, gram-negative bacillus. Major cause of bloody diarrhea, especially in children. Fecal-oral transmission through person-to-person contact or via ingestion of poultry, meat, unpasteurized milk. Contact with infected animals (dogs, cats, and pigs) is also a risk factor. Comma or S-shaped, oxidase positive, grows at 42 degrees Celsius. Common antecedent to Guillain-Barre syndrome and reactive arthritis.


Salmonella typhi

Both Salmonella and Shigella are gram negative bacilli that are non lactose fermenters and oxidase positive. S. typhi only exists in humans. It can disseminate hematogenously, produces H2S, contains flagella (salmon swim). Contain endotoxin and Vi capsule. A large inoculum is required because organism is inactivated by gastric acids. Antibiotics prolong duration on fecal excretion. Immune response is primarily monocytes. Manifests as GI constipation, followed by diarrhea. There is oral vaccine contains live attenuated S typhi IM vaccine contains Vi capsular polysaccharide. Causes typhoid fever (rose spots on abdomen, constipation abdominal pain, and fever); treat with ceftriaxone or fluoroquinolone. Carrier state with gallbladder colonization.


Salmonella spp. (except typhi)

Both Salmonella and Shigella are gram negative bacilli that are non lactose fermenters and oxidase positive. salmonella can exist in humans and animals. It can disseminate hematogenously, produces H2S, contains flagella (salmon swim). Contain endotoxin. A large inoculum is required because organism is inactivated by gastric acids. Antibiotics prolong duration on fecal excretion. Immune response is PMNs in disseminated disease. GI manifestation is bloody diarrhea/ There is no vaccine. Poultry, eggs, pets, and turtles are common sources. Gastroenteritis is usually caused by non-typhoidal Salmonella.



Both Salmonella and Shigella are gram negative bacilli that are non lactose fermenters and oxidase positive. Reserved in humans only. Spreads from cell to cell; no hematologenous spread. They do not produce H2S or contain flagella. Contain endotoxin and shiga toxin (enterotoxin). A very small inoculum is required for infection; resistant to gastric acids. Antibiotics shorten duration of fecal excretion. Immune response consists of primarily PMN infiltration. Causes bloody diarrhea (bacillary dysntery). No vaccine. Four F's: fingers, flies, food, feces are the principal factors in transmission. In order of decreasing severity (less toxin produced): S dysenteriae, S flexneri, S boydii, S sonnei. Invasion is the key to pathogenicity: organisms that produce little toxin can cause disease due to invasion.


Vibrio cholerae

Vibrio cholerae is a comma-shaped gram-negative bacillus. Produces profuse rice water diarrhea via enterotoxin that permanently activates Gs, increases cAMP. Comma shaped, oxidase positive, grows in alkaline media. Endemic to developing countries. Prompt oral rehydration is necessary.


Yersinia enterocolitica

Yersinia enterocolitica is a facultative anaerobic, non lactose-fermenting gram-negative coccobacillus. usually transmitted from pet feces (eg puppies), contaminated milk or pork. Causes acute diarrhea or pseudoappendicitis (right lower abdominal pain due to mesenteric adenitis and/or terminal iletis).


Helicobacter pylori

Causes gastritis and peptic ulcers (especially in the duodendal). Risk factor for gastric adenocarcinoma and MALT lymphoma. Curved gram negative rod that is catalase, oxidase, and urease positive (can use breath test or fecal antigen test for diagnosis). Creates alkaline environment. Most common initial treatment is triple therapy: proton pump inhibitor plus clarithromycin plus amoxicillin (or metronidazole if penicillin allergy).



Spiral shaped bacteria with axial filaments. Includes Borrelia (big size), Leptospira, and Treponema (BLT). Only Borrelia can be visualized using aniline dyes (Wright or Giemsa stain) in light microscopy due to size. Treponema is visualized by dark field microscopy. Borrelia is Big


Leptospira interrogans

Leptospira interrogans is an aerobic, motile spirochete and is described as having “ice tong” ends. found in water contaminated with animal urine, causes leptospirosis- flu like symptoms, myalgias (classically of calves), jaundice, photophobia with conjunctival suffusion (erythema without exudate). Prevalent among surfers and in tropics (ie Hawaii).


Weil disease (icterohemorrhagic leptospirosis)

severe form of leptospirosis with jaundice and azotemia from liver and kidney dysfunction, fever, hemorrhage, and anemia. Caused by Leptospira interrogans.


Borrelia burgdorferi

spiral gram negative bacteria. Borrelia burgdorferi is a microaerophilic spirochete. causes lyme disease, which is transmitted by the Ixodes deer tick. Mice are important to tick life cycle. Borrelia can be visualized using aniline dyes (Wright or Giemsa stain) in light microscopy


Ixodes deer tick

a vector for Borrelia burgdorferi (lyme disease), Anaplasma supp., and the protozoa Babesia.


Lyme disease

caused by Borrelia burgdorferi, spiral gram negative bacteria. Common in northeaster US. Initial symptoms include erythema chronicum migrans, flu like symptoms, with or without facial nerve palsy. Later symptoms include monoarthritis (large joints) and migratory polyarthritis, cardiac (AV nodal block), neurologic (meningitis, facial nerve palsy, polyneuropathy). Treatment includes doxycycline or ceftriaxone.



caused by spirochete Treponema pallidum, best visualized by dark field microscopy.


Primary syphilis

localized disease presenting with painless chancre (a painless ulcer, particularly one developing on the genitals as a result of venereal disease). If available use dark field microscopy to visualize treponemes in fluid from chancre VDRL is positive in 80%.


Secondary syphilis

Disseminated disease with constitutional symptoms, maculopapular rash (including palms and soles), chondylomata lata (smooth, moist, painless, wart like white lesions on genitals); also confirmable with dark field microscopy. Secondary syphilis=Systemic. Latent syphilis (positive serology without symptoms) follows.


Serologic testing for syphilis

VDLR/RPR is nonspecific, confirm diagnosis with FTA-ABS.


Tertiary syphilis

Gummas (chronic granulomas, aortitis (vasa vasorum destruction), neurosyphilis (tabes dorsalis, general paresis), Argyll Robertson pupil (constricts with accommodation but is not reactive to light; prostitutes pupil, since it accommodates but does not react). Signs include broad based ataxia, positive Romberg sign, Charcot joint, stroke without hypertension. For neurosyphilis, test spinal fluid with VDRL and PCR.


Congenital syphilis

Present with facial abnormalities such as rhagades (linear scars at angle of mouth) snuffles (nasal discharge), saddle nose, notched (Hutchinson) teeth., mulberry molars, short maxilla; saber shins (a sharp anterior bowing of the tibia); CN VIII deafness. to prevent, treat mother early in pregnancy, as placental transmission typically occurs after first trimester.


VDRL false positives

VDRL detects nonspecific antibody that reacts with beef cardiolipin. Inexpensive, widely available test for syphilis, quantitative, sensitive but not specific. False positive results can occur due to: Viral infection (mono, hepatitis), Drugs, Rheumatic fever, Lupus and Leprosy.


Jarisch- Herxheimer reaction

Flu like syndrome (fever, chills, headache, myalgia) after antibiotics are started; due to killed bacteria (usually spirochetes) releasing endotoxins.



caused by anaplasma spp., transmitted by Ixodes ticks (live on deer and mice). The microorganism is gram-negative and occurs in the red blood cells. Anaemia may be severe and result in cardiovascular changes such as an increase in heart rate. Haematuria may occur due to the lysis of red blood cells. General systemic signs such as diarrhea, anorexia and weight loss may also be present. A blood smear stained with Giemsa should be observed for identification of infected red blood cells and will allow definitive diagnosis. Treatment is doxycycline


Cat scratch disease, bacillary angiomatosis

caused by Bartonella spp, an facultative intracellular, pleomorphic, gram-negative bacillus, transmitted by cat scratch. BA is characterised by the proliferation of blood vessels, resulting in them forming tumour-like masses in the skin and other organs.


Relapsing fever

Causes Borrelia recurrentis, spiral gram negative bacteria. Transmitted by louse (recurrent due to variable surface antigens). Most people who are infected develop sickness between five and 15 days after they are bitten. The symptoms may include a sudden fever, chills, headaches, muscle or joint aches, and nausea. A rash may also occur. These symptoms usually continue for two to 9 days, then disappear. This cycle may continue for several weeks if the person is not treated.


Brucellosis (undulant fever)

Brucella spp. are small, gram-negative, nonmotile, nonspore-forming, rod-shaped (coccobacilli) bacteria. They function as facultative intracellular parasites. Transmitted by unpasteurized dairy. The symptoms are like those associated with many other febrile diseases, but with emphasis on muscular pain and sweating. The duration of the disease can vary from a few weeks to many months or even years.



Causes Clamydophila psittaci. Transmitted by Parrots, other birds. Diagnosis can be suspected in case of respiratory infection associated with splenomegaly and/or epistaxis.


Q fever

caused by Coxiella burnetii. transmitted by aerosols of cattle/ sheep amniotic fluid, no arthropod vector. Presents as pneumonia. Cost common cause of culture negative endocarditis. Q fever is queer because it has no rash or vector and its causative organism can survive outside in its endospore form. Not in the Rickettsia genus, but closely related. Treatment is doxycycline



Caused by Ehrilichia caffeensis. Transmitted by the Lone star tick (Ambylomma). Monocytes with morulae (berry-like inclusions) in cytoplasm. The most common symptoms include headache, muscle aches, and fatigue. A rash may occur, but is uncommon. Ehrlichiosis can also blunt the immune system by suppressing production of TNF-alpha, which may lead to opportunistic infections such as candidiasis. Treatment is doxycycline



caused by Francisella tularensis, a rod (bacillus) gram negative zoonotic intracellular bacteria. It is also sometimes described as coccobacilus. Transmitted by ticks, rabbits, and deer fly. characterized by ulcers at the site of infection with a black base, fever, and loss of weight.



Leptoperia spp., transmitted but animal urine. Signs and symptoms can range from none to mild such as headaches, muscle pains, and fevers; to severe with bleeding from the lungs or meningitis


Pasteurella multocida

rod (bacillus) gram negative zoonotic bacteria. causes cellulitis and osteomyelitis. Transmitted by animal bite from cats or dogs


Epidemic typhus

caused by Rickettsia prowazekii. Transmitted by louse. Symptoms of typhus include an incubation of 8-16 days. The onset of illness is usually relatively abrupt, usually presenting with a sudden onset of: Chills, High fever, Headache, Maculopapular rash appearing on the trunk and spreading to extremities, usually sparing the face, palms, and soles.



Yersinia pestis. transmitted by fleas from rats and prairie dogs.


Gardnerella vaginalis

a pleomorphic, gram variable rod involved in bacterial vaginosis. Presents as a gray vaginal discharge with a fishy smell; nonpainful (vs vaginitis). Associated with sexual activity, but not sexually transmitted. Bacterial vaginosis is also characterized by overgrowth of certain anaerobic bacteria in the vagina. Clue cells, or vaginal epithelial cells covered with Gardnerella bacteria (stippled appearance along outer margins), are visible under the microscope. Amine whiff test- mixing discharge with 10% KOH enhances fishy odor.


Treatment for all rickettsial disease and vector borne illness



Rocky Mountain spotted fever

Rickettsie rickettsii, vector is a tick. Despite the name, it occurs primarily in the south atlantic states, especially North Carolina. Rash typically starts at wrists and ankles and then spreads to trunk, palms, and soles. Classic triad of headache, fever, and rash (vasculitis). Palms and soles rash is seen in Coxsackievirus A infection (hand, foot, and mouth disease), Rocky Mountain spotted fever and secondary syphilis: you can drive CARS using your palms and soles. Treatment is doxycycline



endemic fleas, Rickettsie typhi. Epidemic human body louse- R. prowazekii. Rash starts centrally and spreads out, sparing the palms and soles. Typhus on the Trunk. Treatment is doxycycline



Chlamydiae cannot make their own ATP. They are obligate intracellular organisms that cause mucosal infections. 2 forms: Elementary body (small, dense) is Enfectious and Enters cell via Endocytosis; transforms into reticulate body. Refticulate body Replicates in cell by fission; Reorganizes into elementary bodies. Chlamys=cloak (intracellular). Lab diagnosis: cytoplasmic inclusions seen on Giemsa or fluorescent antibody-stained smear. The chlamydial cell wall lacks classic peptidoglycan (due to reduced muremic acid), rendering, beta-lactam antibiotics less effective.


Chlamydia trachomatis

causes reactive arthritis (Reiter syndrome), follicular conjunctivits, nongonococcal urethritis, and PID


Chlamydia pneumoniae and C psittaci

cause atypical pneumonia, transmitted by aerosol. Treatment azithromycin (one time treatment) or doxycycline. Chlamydophila psittaci have an avian reservoir.


Chlamydia trachomatis types A, B, and C

Chronic infection, cause blindness due to follicular conjunctivitis in Africa. ABC= Africa, Blindness, Chronic disease


Chlamydia trachomatis types D-K

Urethritis/PID, ectopic pregnancy, neonatal pneumonia (staccato cough) with eosinophilia, neonatal conjunctivitis. Neonatal disease can be acquired during passage through infected birth canal.


Lymphogranuloma venereum

Chlamydia trachomatis types L1, L2, and L3. Small paibless ulcers on genitals, swollen, painful inguinal lymph nodes that ulcerate (buboes). Treatment with doxycycline


Mycoplasma pneumoniae

Classic cause of atypical walking pneumonia (insidious onset, headache, nonproductive cough, patchy or diffuse interstitial infiltrate). X-ray look worse than patient. High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs.Grown on Eaton agar. Treatment: macrolides, doxycycline, or fluoroquinolone (penicillin ineffective since mycoplasma have no cell wall). Not seen on Gram stain. Pleomorphic. Bacterial membrane contains sterols for stability. Mycoplasmal pneumonia is more common in patients under 30. Frequent outbreaks in military recruits and prisons.


Systemic mycoses

Includes histoplasmosis, blastomycosis, coccidioidomycosis, paracoccidioidomycosis. All can cause pneumonia and can disseminate. Except for coccidioidomycosis, all are caused by dimorphic fungi: cold (20 degrees Celsius)=mold; heat (37 degrees Celsius)=yeast. Coccidioidomycosis is a spherule (not a yeast) in tissue. Treatment includes fluconazole or itraconzole for local infection; amphotericin B for systemic infection. Systemic mycoses can mimic TB (granuloma formation), except, unlike TB, have no person to person transmission



Located in Mississippi and Ohio River valleys. Causes pneumonia. Macrophage filled with Histoplasma (smaller than RBC). Histo Hides within macrophages. Bird or bat droppings.



States east of Mississippi River and Central America. Causes inflammatory lung disease and can disseminate to skin and bone. Forms granulomatous nodules. Broad-based budding (same size as RBC). Blasto Buds Broadly



Located in southwestern US, California. Causes pneumonia and meningitis; can disseminate to bone and skin. Case rate increases after earthquakes (spores in dust thrown into air and are inhaled, causing spherules in lungs). Spherule (much larger than RBC) filled with endospores. Coccidio Crowds. San Joaquin Valley fever, Desert bumps=erythema nodosum, Desert rheumatism=arthralgias.



Located Latin America. Budding yeast with captain's wheel formation (much larger than RBC). Paracocidio PARAsails with the captains wheel all the way to Latin America.


Tinea (dermatophytes)

A type of cutaneous mycoses. Tinea is the clinical name given to dermatophyte (cutaneous fungal) infections. Dermatophytes include Microsporum, Trichophyton, and Epidermaphyton. Branching septate hyphae visible on KOH preparation with blue fungal stain.


Tinea capitis

A type of cutaneous mycoses, a dermatophyte. Occurs on scalp. Associated with lymphadenopathy, alopecia, scaling.


Tinea corporis

A type of cutaneous mycoses, a dermatophyte. Occurs on body. Characterized by erythematous scaling rings (ringworm) and central clearing. Can be acquired from contact with an infected cat or dog.


Tinea cruris

A type of cutaneous mycoses, a dermatophyte. Occurs in inguinal area. Often does not show the central clearing seen in tinea corporis.


Tinea pedis

A type of cutaneous mycoses, a dermatophyte. There are three varieties: interdigital (most common), moccasin distribution, vesicular type


Tinea unguim

A type of cutaneous mycoses, a dermatophyte. Onychomycosis, occurs on nails.


Tinea versicolor

A type of cutaneous mycoses. caused by Malassezia spp., (Pityrosporum spp.), a yeast like fungus (not a dermatophyte despite being called tinea). Degradation of lipids produces acids that damage melanocytes and cause hypopigmented and/or pink patches. Can occur any time of year but common in summer (hot, humid weather). Spaghetti and meatballs appearance on microscopy. Treatment includes topical and/or oral antifungal medications, selenium sulfide.


Antimicrobial prophylaxis for high risk for endocarditis and undergoing surgical or dental procedures



Antimicrobial prophylaxis for exposure to gonorrhea



Antimicrobial prophylaxis for history of recurrent UTIs



Antimicrobial prophylaxis for exposure to meningococcal infection

Ceftriaxone, ciprofloxacin, or rifampin


Antimicrobial prophylaxis for pregnant women carrying group B strep

Penicillin G


Antimicrobial prophylaxis for prevention of gonococcal conjunctivitis in newborn

erythromycin ointment


Antimicrobial prophylaxis for prevention of postsurgical infection due to S. aureus



Antimicrobial prophylaxis for prophylaxis of strep pharyngitis in child with prior rheumatic fever

Benzathine penicillin G or oral penicillin V


Antimicrobial prophylaxis for exposure to syphilis

Benzathine penicillin G


Prophylaxis in HIV patients for cell count under 200 cells/mm3

prophylaxis includes TMP-SMX for Pneumocystis pneumonia.


Prophylaxis in HIV patients for cell count under 100 cells/mm3

prophylaxis includes TMP-SMX for Pneumocystis pneumonia and toxoplasmosis.


Prophylaxis in HIV patients for cell count under 50 cells/mm3

prophylaxis includes Azithromycin or clarithromycin for Mycobacterium avium complex.


Treatment of MRSA

vancomycin, daptomycin, linezolid, tigecycline, ceftaroline


Treatment of VRE

linezolid and streptogramins (quinupristin, dalforistin)


Treatment of multidrug resistant P. aeruginosa, multidrug-resistant Acinetobacter baumanii

polymyxins B and E (colistin)


Amphotericin B mechanism

Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes. AmphoTERicin TEARs holes in the fungal membrane by forming pores.


Amphotericin B clinical use

Serious, systemic mycoses. Cryptococcus (amphotericin B with/without flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor. Intrathecally for fungal meningitis. Supplemental K and Mg because of altered renal tubule permeability.


Amphotericin B toxicity

Fever/chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (amphoterrible). Hydration decreases nephrotoxicity. Liposomal amphotericin decreases toxicity.


Nystatin mechanism

Same as amphotericin B. Topical use only as too toxic for systemic.


Nystatin clinical use

Swish and swallow for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.


Flucytosine mechanism

inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase.


Flucytosine clinical use

Systemic fungal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B.


Flucytosine toxicity

Bone marrow suppression.



Clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, voriconazole


Azoles (clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, voriconazole) mechanism

inhibits fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.


Azoles (clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, voriconazole) clinical use

Local and less serious systemic mycoses. Flucanzole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for tropical fungal infections.


Azoles (clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, voriconazole) toxicity

Testosterone synthesis inhibition (gynecomastia, especially with ketoconazole), liver dysfunction (inhibits P450).


Terbinafine mechanism

Inhibits fungal enzyme squalene epoxidase


Terbinafine clinical use

Dermatophytoses (especially onychomycosis- fungal infection of finger or toe nails).


Terbinafine toxicity

GI upset, headaches, hepatotoxicity, taste disturbance



Anidulafungin, caspofungin, micafungin


Echinocandins (anidulafungin, caspofungin, micafungin) mechanism

Inhibit cell wall synthesis by inhibiting synthesis of beta-glucan.


Echinocandins (anidulafungin, caspofungin, micafungin) clinical use

Invasive aspergillosis, Candida


Echinocandins (anidulafungin, caspofungin, micafungin) toxicity

GI upset, flushing (by histamine release)


Griseofulvin mechanism

Interferes with microtubule function, disrupts mitosis. Deposits in keratin-containing tissues (eg nails)


Griseofulvin clinical use

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm)


Griseofulvin toxicity

Teratogenic, carcinogenic, confusion, headaches, an increase in P450 and warfarin metabolism


Antiprotozoan therapy

Pyrimethamine (toxoplasmosis), suramin and melarsoprol (Trypanosoma brucei), nifurtimox (T. cruzi), sodium stibogluconate (leishmaniasis)


Anti-mite/louse therapy

Permethrin (blocks Na channels, which can cause neurotoxicity), malathion (acetylcholinesterase inhibitor), lindane (blocks GABA channels, which can cause neurotoxicity). Used to treat scabies (Sarcoptes scabiei) and lice (Pediculus and Pthirus).


Chloroquine mechanism

blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.


Chloroquine clinical use

Treatment of plasmodial species other than P. falciparum (frequency of resistance in P. falciparum is too high). Resistance due to membrane pump that decreases intracellular concentration of drug. Treat P. falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria, use quinidine in US (quinine elsewhere) or artesunate.


Chloroquine toxicity

Retinopathy; pruritus (especially in dark skinned individuals)


Antihelminthic therapy

Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel.


Oseltamivis, zanamivir mechanism

Inhibit influenza neuraminidase leading to decrease release of progeny virus


Oseltamivis, zanamivir clinical use

Treatment and prevention of both influenza A and B


Acyclovir, famciclovir, valacyclovir mechanism

Guanosine analogs. Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, which means fewer adverse effects. Triphosphate formed by cellular enzymes. Preferentially inhibit viral DNA polymerase by chain termination.


Acyclovir, famciclovir, valacyclovir clinical use

HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV- induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability. For herpes zoster, use famciclovir.


Acyclovir, famciclovir, valacyclovir toxicity

obstructive crystalline nephropathy and acute renal failure if not adequately hydrated.


Acyclovir, famciclovir, valacyclovir mechanism of resistance

mutated viral thymidine kinase


Ganciclovir mechanism

5'-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. Preferentially inhibit viral polymerase by cain termination.


Ganciclovir clinical use

CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better bioavailability.


Ganciclovir toxicity

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.


Ganciclovir mechanism of resistance

mutated viral kinase.


Foscarnet mechanism

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor. Binds to pyrophosphate binding site of enzyme. Does not require activation by viral kinase. Foscarnet=pyroFOSphate analog.


Foscarnet clinical use

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistanct HSV.


Foscarnet toxicity

Nephrotoxicity, electrolyte abnormalities (hypo- or hypercalcemia, hypo- or hyperphosphatemia, hypokalemia, hypomagnesemia) can lead to seizures.


Foscarnet mechanism of resistance

mutated DNA polymerase.


Cidofovir mechanism

preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.


Cidofovir clinical use

CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life.


Cidofovir toxicity

Nephrotoxicity (coadminister with probenecid and IV saline to decrease toxicity).


HIV therapy

Highly active antiretroviral therapy (HAART): often initiated at the time of HIV diagnosis. Strongest indication for patients presenting with AIDS-defining illness, low CD+ cell counts (less than 500 cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance: 2 NRTIs and 1 of the following: NNRTI or protease inhibitor or integrase inhibitor.


Protease inhibitors

Atazanavir, Darunavir, Fosamprenavir, Indinavir, Lopinavir, Ritonavir, Saquinavir


Protease inhibitors mechanism

Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses. Ritonavir can boost other drug concentrations by inhibiting P450. All protease inhibitors end in -navir. Navir (never) tease a protease.


Protease inhibitors toxicity

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy. Nephropathy, hematuria (indinavir). Rifampin (a potent CYP/UGT inducer) contraindicated with protease inhibitor concentration.


Nucleoside Reverse Transcriptase Inhibitors (NRTIs)

Abacavir, Didanosine, Emtricitabine, Lamivudine, Stavudine, Tenofovir, Zidovudine


Nucleoside Reverse Transcriptase Inhibitors (NRTIs)mechanism

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3' OH group). Tenofovir is a nucleoTide; the others are nucleosides and need to be phosphorylated to be active. Zidovudine is used for general prophylaxis and during pregnancy to decrease the risk of fetal transmission.


Nucleoside Reverse Transcriptase Inhibitors (NRTIs) toxicity

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), anemia (zidovudine), pancreatitis (didanosine).


Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)

Delavirdine, Efavirenz, Nevirapine


Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) mechanism

Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.


Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) toxicity

Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy.


Raltegravir mechanism

An integrase inhibitor. Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase.


Raltegravir toxicity

increases creatine kinase.


Fusion inhibitors

includes Enfuvirtide and Maraviroc


Fusion inhibitors (Enfuvirtide and Maraviroc) mechanism

Binds gp41, inhibiting viral entry


Fusion inhibitors (Enfuvirtide and Maraviroc) toxicity

Skin reaction at injection sites.


Interferon mechanism

Glycoproteins normally synthesized by virus- infected cells, exhibiting a wide range of antiviral and antitumoral properties.


clinical use of IFN-alpha

chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma.


clinical use of IFN-beta

multiple sclerosis


clinical use of IFN-gamma

chronic gramulomatous disease


Interferon toxicity

Neutropenia, myopathy


Hepatitis C therapy

includes ribavirin, simeprevir, sofosbuvir


Ribavirin mechanism

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase.


Ribavirin clinical use

Chronic HCV, also used in RSV (palivizumab preferred in children).


Ribavirin toxicity

hemolytic anemia; severe teratogen.


Simeprevir mechanism

HCV protease inhibitor; prevents viral replication.


Simeprevir clinical use

chronic HCV in combination with ribavirin and peginterferon alfa. Do not use as monotherapy


Simeprevir toxicity

photosensitivity reactions, rash


Sofosbuvir mechanism

Inhibits HCV RNA-dependent RNA polymerase acting as a chain terminator.


Sofosbuvir clinical use

Chronic HCV in combination with ribavirin, with or without peginterferon alfa. Do not use as monotherapy.


Sofosbuvir toxicity

Fatigue, headache, nausea.


Hydrogen peroxide for infection control

Free radical oxidation. Sporicidal.


Iodine and iodophors for infection control

Halogenation of DNA, RNA, and proteins. May be sporicidal.


Chlorhexidine for infection control

Denatures proteins and disrupts cell membranes. Not sporicidal.


Teratogenic effect of sulfonamides



Teratogenic effect of aminoglycosides



Teratogenic effect of fluoroquinolones

cartilage damage


Teratogenic effect of clarithromycin



Teratogenic effect of tetracyclines

Discolored teeth, inhibition of bone growth


Teratogenic effect of ribavirin

skeleton damage


Teratogenic effect of griseofulvin

Effects on growth and differentiation


Teratogenic effect of chloramphenicol

gray baby syndrome


Candida albicans

alba=white. Systemic or superficial fungal infection. Oral and esophageal thrush in immunocompromised (neonates, steroids, diabetes, AIDs), vulvovaginitis (diabetes, use of antibiotics), diaper rash, endocarditis in IV drug users, disseminated candidiasis (to any organ), chronic mucocutaneous candidiasis. Histologically, there are pseudohyphae and budding yeasts at 20 degrees Celsius.


Candida albicans treatment

tropical azole for vaginal; nystatin, fluconazole, orcaspofungin, or amphotericin B for systemic.


Aspergillus fumigatus

Invasive aspergillosis, especially in immunocompromised and those with chronic granulomatous disease. Allergic bronchopulmonary aspergillosis (ABPA) is associated with asthma and cystic fibrosis; may cause bronchiectasis and eosinophilia. Aspergillomas in lung cavities, especially after TB infection. Some species produce aflatoxins, which are associated with hepatocellular carcinoma. Histologicallym septate hyphae branch at 45 degree angles and there are conidiophore with radiating chains of spores. Think A for Acute Angles in Aspergillus; not dimorphic.


Cryptococcus neoformans

Cryptococcal meningitis, cryptococosis. Heavily encapsulated yeast. Not dimorphic. Found in soil, pigeon droppings. Acquired through inhalation with hematogenous dissemination to meninges. Culture on Sabouraud agar. Stains with india ink and mucicarmine. Latex agglutination test detects polysaccharide capsular antigen and is more specific. Soup bubble lesions in brain. Histology shows 5-10 micrometer yeast with wide capsular halos and unequal budding in india ink stain.


Mucor and Rhizopus spp.

Mucormycosis. Disease mostly in ketoacidotic diabetic and/ or neutropenic patients (eg leukemia). Fungi proliferate in blood vessel walls, penetrate cribriform plate, and enter brain. Rhinocerebral, frontal lobe abscess; cavernous sinus thrombosis. Headache, facial pain, black necrotic eschar on face; may have cranial nerve involvement. Treatment includes surgical debridement and amphotericin B. Histology shows irregular, broad, nonseptate hypae branching at wide angles.


Pneumocystis jirovecii

Causes Pneumocystic pneumonia (PCP), a diffuse interstitial pnuemonia. Yeast like fungus (originally classified as protozoan). Inhaled. Most infections are asymptomatic. Immunosuppression (eg AIDS) predisposes to disease. Diffuse, bilateral ground-glass opacities on CXR/CT. Diagnosed by lung biopsy or lavage. Disc shaped yeast forms on methenamine silver stain of lung tissue.


Treatment/ prophylaxis of Pneumocystis jirovecii

TMP-SMX, pentamidine, dapsone (prophylaxis only), atovaquone (prophylaxis only). Start prophylaxis when CD4+ count drops below 200 cells/mm3 in HIV patients.


Sporothrix schenckii

Sporotrichosis. Dimorphic, cigar shaped budding yeast that lives on vegetation. When spores are traumatically introduced into the skin, typically by a thorn (rose gardeners disease), causes local pustule or ulcer with nodules along draining lymphatics (ascending lymphangitis). Disseminated disease possible in immunocompromised host. Treatment includes itraconazole or potassium iodide. Plant a rose in the pot.



Caused by giardia lamblia, a protozoa that infects the GI. Causes bloating, flatulence, foul-smelling, fatty diarrhea (often seen campers/hikers)-- fat- rich Ghiradelli chocolates for fatty stools of Giardia. Transmitted by cysts in water. Diagnosis is based on trophozoites or cysts in stool. Treatment involves metronidazole.



Caused by Entamoeba histolytica, a protozoa that infects the GI. Causes bloody diarrhea (dysentery), liver abscess (anchovy paste exudate), RUG pain; histology shows flask-shaped ulcer. Transmission occurs through cysts in water. Diagnosis in based on serology and/or trophozoites (with RBCs in the cytoplasm) or cysts (with up to 4 nuclei) in stool. Treatment includes metronidazole; iodoquinol for asymptomatic cyst passers.



A protozoa that infects the GI. Causes severe diarrhea in AIDS. Mild disease (watery diarrhea) in immunocompetent hosts. Transmitted by oocysts in water. Diagnosis is based on oocysts seen on acid-fast stain. Treatment includes prevention (by filtering city water supplies) and nitazoxanide in immunocompetent hosts.


Toxoplasma gondii

A protozoa that infects the CNS. Causes congenital toxoplasmosis, which has the classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications; reactivation in AIDS, which leads to a brain abscess seen as ring-enhancing lesions on CT/MRI. Transmission occurs through cysts in meat (most common); oocysts in cat feces; crosses placenta (pregnant women should avoid cats). Diagnosis is based on serology and biopsy, which shows tachyzoite (crescent shaped). Treatment includes sulfadiazine and pyrimethamine.


Naegleria fowleri

A protozoa that infects the CNS. Causes rapidly fatal meningoencephalitis. It is transferred by swimming in freshwater lakes (think Nalgene bottle filled with fresh water containing Naegleria); enters via cribriform plate. Diagnosis is based on finding amoebas in spinal fluid. Treatment includes amphotericin B, but there has been few survivors.


African sleeping sickness

Caused by Trypanosoma brucei, which is a protozoa that infects the CNS. Causes enlarged lymph nodes, recurring fever (due to antigenic variation), somnolence, and coma. The two species include Trypanosoma brucei rhadesiense and Trypanosoma brucei gambiense. Transmission occurs by tsetse flies, which causes a painful bite. Diagnosis is based on blood smear. Treatment includes SURamin for blood-borne disease or MELAsoprol for CNS penetration. (It's SURE is nice to go to sleep, MELAtonin helps with sleep).



Caused by Plasmodium (P. vivax/ ovale, P. falciparum, P. malariae), a protozoa that infects the CNS. Causes fever, headache, anemia, and splenomegaly. Transmitted by Anopheles mosquito. Diagnosis is made based on blood smear, which shows trophozoite ring form within RBC, schizont containing merozoites; red granules (Schuffner stippling) throughout RBC cytoplasm seen with P. vivax/ovale.


Plamodium vivax/ ovale

Causes malaria. There are red granules (Schuffner stippling) throughout RBC cytoplasm seen with P. vivax/ovale. Incubation period is a 48 hour cycle (tertian; includes fever on first day and third day, thus fevers are actually 48 hours apart); dormant form (hypnozoite) in liver.


Plamodium falciparum

Causes malaria. There are severe; irregular fever patterns; parasitized RBCs occlude capillaries in brain (cerebral malaria), Kidneys, and lungs.


Plasmodium malariae

Causes malaria. There are 72 hour cycle fevers (quatran)


Treatment of malaria

Chloroquine (for sensitive species), which blocks Plasmodium heme polymerase. If resistant, use mefloquine or atovaquone/ proguanil. If life- threatening use intravenous quinidine or artesunate (test for G6PD deficiency). For P. vivax/ ovale add primaquine for hypnozoite (test for G6PD).



Caused by babesia, a hematologic protozoa. Causes fever and hemolytic anemia; predominantly in northeastern US; asplenia increases risk of severe disease. Transmission occurs through Ixodes tick (same as Borrelia burgdorferi of lyme disease; may often coinfect humans). Diagnosis is based on blood smear, which shows a ring form and Maltese cross, and PCR. Treatment includes Atovaquone and azithromycin.


Chagas disease

Caused by Trypanosoma cruzi, a protozoa. Causes dilated cardiomyopathy with apical atrophy, megacolon, megaesophagus; predominantly in South America. Unilateral periorbital swelling (Romana sign) characteristic of acute stage. Transmitted by Reduviid bug (kissing bug) feces, deposited in a painless bite. Diagnosis is based on flagellated trypomastigotes on blood smear in the acute form, and nonflagellated amastigotes within cells on biopsy. Treatment includes Benznidazole or nifurtimox.


Visceral leishmaniasis (kala-azar)

Caused by Leishmania donovani, a protozoa, which causes spiking fevers, hepatosplenomegaly, pancytopenia. Transmitted by the sandfly. Diagnosis is based on macrophages containing amastigotes. Treatmetn includes amphotericin B and sodium stibogluconate.


Vaginitis caused by protozoa

Caused by Trichomonas vaginalis. Causes foul-smelling, greenish discharge; itching and burning; do not confuse with Gardnerella vaginalis, a gram variable bacterium associated with bacterial vaginosis. Transmitted by sexual contact (cannot exist outside the human body because it cannot form cysts). Diagnosis is based on trophozoites (motile) on wet mount; strawberry cervix). Treatment includes metronidazole for patient and partner (prophylaxis).



Enterobius vermicularis. Transmitted through the fecal-oral route. Causes intestinal infection causing anal pruitus (diagnosed by seeing egg via the tape test). Treatment includes bendazoles (because worms are bendy).


Giant roundworm

Ascaris lumbricoides. Transmitted through the fecal- oral route; eggs are visible in feces under microscope. Causes intestinal infection with possible obstruction at ileocecal valve. Treatment includes bendazoles (because worms are bendy).


Strongyloides stercoralis

Transmitted through larvae is soil penetrate the skin. Causes intestinal infection causing vomiting, diarrhea, epigastric pain (may feel like peptic ulcer). Treatment includes ivermectin or bendazoles.



Caused by Ancylostoma deodenale and Necator americanus. Transmitted by larvae that penetrate skin. Causes intestinal infection causing anemia by sucking blood from intestinal walls. Treated with bendazoles or pyrantel pamoate.


Trichinella spiralis

Transmitted by the fecal oral route and undercooked meat (esp. pork). Causes intestinal infection; larvae enter bloodstream and encyst in striated muscle cells, leading to inflammation of muscle. Treatment includes bendazoles (because worms are bendy).



Caused by trichinella. Symptoms include fever, comiting, nausea, periorbital edema, myalgia. Treatment includes bendazoles (because worms are bendy).


Onchocerca volvulus

Transmitted by the female blackfly bite. Causes hyperpigmented skin and river blindness (black flies, black skin nodules, black sight); allergic reaction to microfilaria possible. Treatment includes ivermectin (IVERmectin for rIVER blindness).


Loa loa

Transmitted by deer fly, horse fly, mango fly. Causes swelling in skin, worm in conjunctiva. Treatment includes diethylcarbamazine.



Caused by Wuchereria bancrofti. Transmitted by female mosquito. Causes worms block lymphatic vessels, takes 9 months to a year after the bite to become symptomatic. Treatment includes diethylcarbamazine.


Toxocara canis

Transmitted through the fecal oral route. Causes visceral larva migrans. Treatment includes bendazoles.


Taenia solium

A tapeworm. Can cause intestinal infection; transmitted through ingestion of larvae encysted in undercooked pork; treated with praziquantel. Also causes cysticercosis and neurocysticercosis; transmitted through ingestion of eggs; treat with praziquantel and albendazole (neurocysticercosis).


Diphyllobothrium latum

Transmitted through ingestion of larvae from raw freshwater fish. Causes vitamin B12 deficiency (tapeworm competes for B12 in intestine) leading to megaloblastic anemia. Treated with praziquantel.


Echinococcus granulosus

Transmitted through ingestion of eggs from dog feces. Sheep are an intermediate host. Causes hydatid cysts in liver, causing anaphylaxis if antigens released (hydatid cyst injected with ethanol or hypertonic saline to kill daughter cysts before removal). Treated with albendazole.



Snails are host; cercariae penetrate skin of humans. Causes liver and spleen enlargement (S. mansoni, egg with lateral spine), fibrosis, and inflammation. Chronic infection occurs with S. haematobium (egg with terminal spine) can lead to squamous cell carcinoma of the bladder (painless hematuria) and pulmonary hypertension. Treated with praziquantel.


Clonorchis sinensis

Transmitted through undercooked fish. Causes biliary tract inflammation, which causes pigmented gallstones. It is associated with cholangiocarcinoma. Treated with praziquantel.


Parasite infection involving vitamin B12 deficiency

Diphyllobothrium latum


Parasite infection involving portal hypertension

Schistosoma mansoni, Schistosoma japonicum


Parasite infection involving perianal pruritus



Parasite infection involving myalgias, periorbital edema

Trichinella spiralis


Parasite infection involving microcytic anemia

Ancylostoma, Necator


Parasite infection involving liver (hydatid) cysts

Echinococcus granulosus


Parasite infection involving hematuria, squamous cell bladder cancer

Schistosoma haematobium


Parasite infection involving brain cysts and seizures

Taenia solium (cysticercosis)


Parasite infection involving biliary tract disease and cholangiocarcinoma

Clonorchis sinensis


Live attenuated vaccines

Induces humoral and cell-mediated immunity but have reverted to virulence on rare occasions. Killed/inactivated vaccine induce only humoral immunity but are stable. Includes smallpox, yellow fever, rotavirus, chickenpox, Sabin polio virus, Influenza (IntraNasal). (LIVE! one night only! see SMALL YELLOW ROTAting CHICKENS get vaccinated with Sabin and MMR! Its INcredible!) No booster needed. Dangerous to give to immunocompromised patients or their close contacts. MMR= measles, mumps, rubella; live attenuated vaccine that can be given to HIV- positive patient who do not show signs of immunodeficiency.


Killed vaccines

Includes Rabies, Influenza (infected), Salk Polio, and HAV vaccines. (salK=Killed, RIP Always)


Subunit vaccines

HBV (antigens-HBsAg), HPV (types 6, 11, 16, and 18)


DNA viral genomes

All DNA viruses except the Parcoviridae are dsDNA. (All are dsDNA, like our cells, except part-of-a-virus, parvovirus is ssDNA.) Parvus=small. All are linear except papilloma-, polyoma-, hepadnaviruses (circular).


RNA viral genomes

All RNA, except Reoviridae, are ssRNA. (All are ssRNA, except REpeatO-virus, REOvirus, is dsRNA). Positive stranded RNA viruses: I went to a RETRO (retrovirus) TOGA (togavirus) party where I drank FLAVored (flavivirus) CORONA (coronavirus) and are HIPPY (hepevirus) CALIfornia (calicivirus) PICkles (picornavirus).


Naked viral genome infectivity

Infectious viruses includes purified nucleic acids of most dsDNA (except for poxvirus and HBV) and all positive ssRNA (mRNA). The naked strand of negative ssRNA and dsRNA are not infectious, since they require polymerases contained within the complete virion.


Location of viral replication for DNA viruses

They all replicate in the nucleus, except for poxvirus.


Location of viral replication for RNA viruses

All RNA viruses replicate in the cytoplasm, except for influenza and retroviruses.


Naked viruses

Naked viruses include papillomavirus, adenovirus, parvovirus, polyomavirus, calicivirus, picornavirus, reovirus and hepevirus


Enveloped viruses

Generally, viruses acquire their envelopes from the plasma membrane when the exit from the cell. An exception to this are the herpesvirus, which acquire envelopes from nuclear membrane.


DNA viruses and their characteristics

Includes hepadna, herpes, adeno, pox, parvo, papilloma, polyoma. All are double stranded, except for parvo. All are leaners, except for papilloma and polyoma, which are circular and supercoiled and hepadna, which are circular and incomplete. All are icosahedral, except for pox, which is complex. All replicate in the nucleus, except for pox, which carries its own DNA- Dependent RNA polymerase.



has an envelope, and is dsDNA, linear. Includes: HSV-1, which causes oral (and some genital lesions), spontaneous temporal lobe encephalitis, keratoconjunctivitis; HSV-2, which causes genital (and some oral) lesions; VZV (HHV-3), which causes chickpox and zoster; EBV (HHV-4), which causes mononucleosis, Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma; CMV (HHV-5), which causes infection in immunosuppressed patients (AIDS retinitis (sightomegalovirus), especially transplant recipients, and congenital defects; HHV-6, which causes roseola (exanthem subitum); HHV-7, which is a less common cause of roseola; and HHV-8, which causes Kaposi sarcoma.



It has an envelope and is partially dsDNA and circular. It causes HBV, leading to either chronic or acute hepatitis. It is not a retrovirus but it does have reverse transcriptase.



It does not have an envelope. It has linear, dsDNA. It can cause febrile pharyngitis (sore throat), acute hemorrhagic cystitis, pneumonia, and conjunctivitis (pink eye)



Parvovirus does not have an envelope, and has linear, ssDNA. It is the smallest DNA virus. it is known at the B19 virus and causes apastic crises in sickle cell disease, slapped cheeks rash in children (erythema infectiosum, or fifth disease). RBC destruction in fetus leads to hydrops fetalis and death. In adults, parvovirus causes pure RBC aplasia and rheumatoid arthritis-like symptoms.



Papillomavirus does not have an envelope and is dsDNA and is circular. Also known as HPV, it causes warts (serotypes 1,2,6,11), cervical intraepithelial neoplasia (CIN), and cervical cancer (most commonly 16 and 18)



Polyomavirus does not have an envelope and is a circular dsDNA virus. Included in this category is John Cunningham virus (JCV), which causes progressive multifocal leukoencephalopathy (PML) in HIV patients. BK virus is also a member of polyomavirus and target kidneys in transplant patients. JC: Junky Cerebrum; BK: Bad Kidney



Poxvirus has an envelope and has linear, dsDNA. It is the largest DNA virus. It causes smallpox, which has been eradicated by use of live attenuated vaccine. Eradication was achieved by the world-wide use of vaccination. Also causes cowpox (milkmaid blisters) and molluscum contagiosum, which are flesh-colored papule with central umbilication.



has an envelope, and is dsDNA, linear. Causes gingivostomatitis, keratoconjunctivitis, herpes labialis, temporal lobe encephalitis (most common cause of sporadic encephalitis, can present with altered mental status, seizures, and/or aphasia). Transmitted by respiratory secretions and saliva.



has an envelope, and is dsDNA, linear. causes herpes genitalis, neonatal herpes. It can lie latent in the sacral ganglia. It is transmitted by sexual contact, perinatally.



has an envelope, and is dsDNA, linear. Varicella-zoster (chickenpox, shingles), encephalitis, pneumonia. Lies latent in dorsal root or trigeminal ganglia. Most common complication of shingles is post herpatic neuralgia. Transmitted by respiratory secretions.



has an envelope, and is dsDNA, linear. Mononucleosis is characterized by fever, heptoslpenomegaly, pharyngitis, and lymphadenopathy (especially in posterior cervical nodes). Transmitted by respiratory secretions and saliva; also called the kissing disease since it is commonly seen in young adults and teens. Infects B cell through CD21. Atypical lymphocytes are seen on peripheral blood smear, which are not infected B cells, but rather reactive cytotoxic T cells. Detected by a positive monospot test, which have heterophile antibodies detected by agglutination of sheep or horse RBCs. It is associated with lymphoma (eg endemic Burkitt lymphoma), nasopharyngeal carcinoma.



has an envelope, and is dsDNA, linear. Causes congenital infection, mononucleosis (negative monospot), pneumonia, retinitis. Infected cells have characteristic "owl eye" inclusions. It can lie latent in mononuclear cells. It is transmitted congenitally and by transfusion, sexual contact, saliva, urine, and transplant.



has an envelope, and is dsDNA, linear. Causes roseola, which is characterized by high fevers for several days that can cause seizures, followed by a diffuse macular rash. It is transmitted by saliva.



Causes Kaposi sarcoma, a neoplasm of endothelial cells. It is seen in HIV/AIDs and transplant patients. Causes dark/violaceous plaques or nodules, which represent vascular proliferation. It can also affect the GI tract and lungs. It is transmitted by sexual contact.


HSV identification

Use viral cultures for skin/genitalia. CSF PCR for herpes encephalitis. Also use Tzank test. Intranuclear inclusions are also seen with HSV-1, HSV-2, and VZV.


Tzanck test

a smear of an opened skin vesicle to detect multinucleated giant cells are commonly seen in HSV-1, HSV-2, VZV infections. Tzanck heavens I dont have herpes!



Reoviruses do not have envelopes and are linear, dsRNA, with 10-12 segments. They also have Icosahedral (double) capsid. Included in this family are Coltivirus, which is known as Colorado tick fever and Rotavirus, the number 1 cause of fatal diarrhea in children.



Picornavirus does not have an envelope, it is a linear, positive ssRNA with an icosahedral capsid. Includes poliovirus, which has the polio-salk (inactivated vaccine) and the Sabin (oral poliovirus) vaccines; Echovirus, which causes aseptic meningitis; Rhinovirus, which causes the common cold; Coxsackievirus, which causes aseptic meningitis, herpangina (mouth blisters, fever), hand-foot-and mouth disease, myocarditis, and pericardiditis; HAV, which causes acute viral hepatitis. PERCH. RNA is translated into 1 large polypeptide that is cleave by protease into functional viral proteins. Can cause viral (aspetic) meningitis (except rhinovirus and HAV). All are enteroviruses (fecal-oral spread) except rhinovirus. picoRNAvirus=small RNA virus.



Hepevirus does not have an envelope and is a linear, positive ssRNA virus with an icosahedral capsid. Causes HEV



Caliciviruses are not enveloped and is a linear, positive ssRNA virus with an icosahedral capsid. Included in this family is the Norovirus, which causes viral gastroenteritis.



Flavivirus does have an envelope and is a positive, linear, ssRNA with an icosahedral capsid. It causes HCV, yellow fever (an arbovirus), Dengue (an arbovirus), St. Louis encephalitis (an arbovirus), and west nile virus (an arbovirus).



Togaviruses is enveloped and is a linear, positive ssRNA and with an icosahedral capsid. Causes Rubella, Eastern equine encephalitis (an arbovirus), Western equine encephalitis (an arborvirus).



Retroviruses is enveloped and is a positive, linear ssRNA with two copies. HTLV has an icosahedral capsid, while HIV has a conical capsid. They all have reverse transcriptase. HTLV causes T-cell leukemia. HIV causes AIDS.



Coronavirus is enveloped and is a linear, positive ssRNA with a helical capsid. Causes the common cold and SARS.(Severe Acute Respiratory Syndrome)



Orthomyxoviruses are enveloped and has a linear, negative, ssRNA of 8 segments with a helical capsid. Includes the influenza virus



Paramyxoviruses are enveloped and has a linear, negative, nonsegmented ssRNA. Includes Parainfuenza, which causes croup; RSV, which causes bronchiolitis in babies (Rx is Ribavirin); Measles; and Mumps. PaRaMyxovirus. Causes disease in children. RSV causes respiratory tract infection (bronchiolitis and pneumonia) in infants. All contain surface F (fusion) protein, which causes respiratory epithelial cells to fuse and form multinucleated cells.



Rhabdovirus is enveloped and is a negative, linear, ssRNA with a helical capsid. It causes rabies.



Filoviruses are enveloped and are negative, linear, ssRNA with a helical capsid. Causes Ebola/Marburg hemorrhagic fever, which is often fatal.



Arenaviruses are enveloped and are negative, circular, ssRNA with a helical capsid. Included in this category is lymphocytic choriomeningitis virus (LCMV) and Lassa fever encephalitis, which is spread by rodents.



Bunyaviruses are enveloped and are negative, circular ssRNA with 3 segments and with a helical capsid. Types include California encephalitis (an arbovirus), Sandfly/Rift valley fevers (an arbovirus), Crimean-Congo hemorrhagic fever (an arbovirus), and Hantavirus, which causes hemorrhagic fever, and pneumonia.


Delta virus

Delta virus is a enveloped, circular, negative ssRNA with an uncertain capsid. HDV is a defective virus that requires the presence of HBV to replicate.


Negative stranded viruses

Must transcribe negative strand to make a positive strand before it is translated into protein. Virion brings its own RNA-dependent RNA polymerase. They include Arenaviruses, Bunyaviruses, Paramyxoviruses, Orthomyxovirus, filoviruses, and Rhabdoviruses (which are also helical capsid). Always Bring Polymerase Or Fail Replication.


Segmented viruses

All are RNA viruses. They include Bunyaviruses, Orthomyxoviruses (influenza viruses), Arenaviruses, and Reoviruses. BOAR



A picovirus. It is noneveloped RNA virus and causes the common cold. There are over 100 serologic types. It is also acid labile and is therefor destroyed by acid stomach and does not infect the GI like other picornaviruses. Rhino has a runny nose.


Yellow fever virus

Yellow fever virus is a flavivirus (also an arbovirus) transmitted by Aedes mosquito. Virus has a monkey or human reservoir. Symptoms include high fever, black vomitus, and jaundice. May see councilman bodies (Liver biopsy of acute viral hepatitis typically shows panlobular lymphocytic infiltrates with ballooning hepatocytes, which are indicative of hepatocyte necrosis and hepatocyte apoptosis. Eosinophilic apoptotic globules. They are indicative viral hepatitis (acute), yellow fever, or other viral syndromes.)



Rotavirus is the most important cause of infantile gastroenteritis, is a segmented dsRNA virus (a reovirus). Major cause of acute diarrhea in the US during the winter, especially in day care centers, kindergartens. Villous destruction with atrophy leads to a decrease absorption of Na and loss of K. ROTAvirus= Right Out The Anus. CDC recommends routine vaccination of all infants.


Influenza virus

Orthomyxoviruses. They are enveloped, negative, ssRNA viruses with 8 segment genome, which contain hemagglutinin (promotes viral entry) and neuramindase (promotes progeny virion release) antigens. Patients with this virus are at risk for fetal bacterial superinfection, most commonly S aureus, S pneumoniae, and H. influnezae. Undergoes rapid genetic changes. The reformulated vaccine (the flue shot) contains viral strains most likely to appear during the flu season. Killed viral vaccines are the most common. Live attenuated vaccine contains temperature-sensitive mutant that replicates in the nose but not in the lung; administered intranasally.


Genetic shift/ antigenic shift in viruses

Causes pandemics. Reassortment of viral genome segments, such as when segments of human flu A virus reassort with swine flu A virus. Sudden Shift is more deadly than graDual Drift.


Genetic drift/ antigenic drift in viruses

Causes epidemics. Minor (antigenic drift) changes based on random mutation in hemagglutinin or neuramindase genes.


Rubella virus

A togavirus. Causes rubella, once known as German (3-day) measles. Fever, postauricular and other lymphadenopathy, arthralgias, and fine rash. Causes mild disease in children but serious congenital disease. Congenital rubella findings include blueberry muffin appearance, indicative of extramedullary hematopoiesis. The rash appears as a fine, confluent macules that start on the face and spread centrifugally to involve the trunk and extremities.



It is a monoclonal antibody against F protein that prevents pneumonia caused by REV infection in premature infants.


Croup (acute laryngo-tracheobronchitis)

Caused by parainfluenza viruses (paramyxovirus). Results in seal-like barking cough and inspiratory stridor. Narrowing of upper trachea and subglottis leads to characteristic steeple sign on X-ray. Severe croup can result in pulsus paradoxus (an abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration) secondary to upper airway obstruction.


Measles (rubeola) virus

A paramyxovirus that causes measles. Usual presentation involves prodromal fever with cough, coryza (Irritation and swelling of the mucous membrane in the nose), and conjunctivitis, then eventually Koplik spots (bright red spots with blue- white center on buccal mucosa that precede the measles rash by 1-2 days), followed by a maculopapular rash (confluent erythematous macules and papules, presents late, and includes limbs as it spreads downwards) that starts at the head/ neck and spreads downward. Lymphadenitis with Warthin-Finkeldey giant cells (fused lymphocytes) in a background of paracortical hyperplasia. SSPE (subacute sclerosing panencephalitis, occuring years later, encephalitis (1:2000), and giant cell pneumonia (rarely in immunocompromised) are possible sequelae. The 3 C's of measles: cough, coryza, conjunctivitis. Vitamin A supplementation can reduce measles mortality in malnourished or vitamin deficient children.


Mumps virus

A paramyxovirus that causes mumps, an uncommon disease due to effectiveness of MMR vaccine. Symptoms include parotitis, orchitis, and aseptic meningitis (POM). Can cause sterility (especially after puberty). Mumps makes your parotid glands and testes as big as POM-poms.


Rabies virus

Bullet-shaped virus. Negri bodies (cytoplasmic inclusions in neurons infected by rabies virus) are commonly found in Purkinje cells of the cerebellum and in the hippocampus neurons. Rabies has a long incubation period (weeks to months) before symptom onset. Post exposure prophylaxis includes wound cleaning plus immunization with killed vaccine and rabies immunoglobulin. Example of passive- active immunity. The virus travels to the CNS by migrating in a retrograde fashion up the nerve axons after binding to ACh receptors. The progression of the disease is as follows: fever and malaise to agitation, photophobia, hydrophobia, and hypersalivation leading to paralysis and coma and eventually leading to death. It is most commonly transmitted from a bat, raccoon or skunk bite than from a dog bite in the US.


Ebola virus

Ebola virus is a filovirus that targets endothelial cells, phagocytes, and hepatocyes. It presents as an abrupt onset of flu like symptoms, diarrhea/ vomiting, high fever, myalgia. It can progress to DIC, diffuse hemorrhage, and shock. High mortality rate and no definitive treatment. Treatment includes supportive care. Strict isolation of infected individuals and barrier practices for health care workers are key for preventing transmission. Transmission requires direct contact with bodily fluids or formites (including dead bodies); high incidence of nosocomial infection.


Hepatitis viruses

Signs and symptoms of all hepatitis viruses include episodes of fever, jaundice, elevated ALT and AST. One may see councilman bodies (eosinophilic apoptotic globules) on liver biopsy.



HAV is a RNA picornavirus. HAV and HEV are transmitted via the fecal oral route (the vowels hit your bowels). Naked viruses do not rely on an envelope, so they are not destroyed by the gut. There is no carrier state. Incubation period is short (weeks). There is no associated hepatocellular carcinoma risk. The disease is usually Asymptomatic, Acute, and Alone (no carriers).



HBV is a DNA hepadnavirus. It is transmitted parenterally, sexually, or perinatally (Blood, Baby-making, and Birthing). There is a carrier state and incubation is long (months). There is an associated risk of hepatocellular carcinoma. In HBV, the DNA polymerase has both DNA and RNA-dependent activities. Upon entry into the nucleus, the polymerase functions to complete the partial dsDNA. The host RNA polymerase transcribes mRNA from viral DNA to make viral proteins. The DNA polymerase then reverse transcribes viral RNA to DNA, which is genome of the progeny virus.



HCV is a RNA flavivirus. It is transmitted primarily through the blood (IVDU, post-transfusion). There is a carrier state and an associated risk of hepatocellular carcinoma. There is a long incubation period. (Chronic, Cirrhosis, Carcinoma, and Carrier)



HDV is a RNA delta virus. It is transmitted parenterally, sexually, or perinatally (like HBV). There is a carrier state. In order to be infective, it must either manifest as a superinfection (HDV after HBV), with a short incubation period, or a coinfection (HDV with HBV), with a long incubation period. Super-infections have a worse prognosis There is an associated risk with hepatocellular carcinoma. (Defective virus Dependent of HBV)



HEV is a RNA hepevirus. HAV and HEV are transmitted via the fecal oral route, especially waterborne (the vowels hit your bowels). Naked viruses do not rely on an envelope, so they are not destroyed by the gut. There is no carrier state and the incubation period is short. There is no associated risk with hepatocellular carcinoma. There is high mortality in pregnant women. (Enteric, Expectant mothers, Epidemic)


Anti HAV (IgM)

IgM antibody to HAV is the best test to detect acute hepatitis A


Anti HAV (IgG)

IgG antibody indicates prior HAV infection and/or prior vaccination; protects against reinfection.


HBs Ag

Antigen found on surface of HBV; indicates hepatitis B infection.


Anti- HBs

Antibody to HBs-Ag; indicates immunity to hepatitis B.



antigen associated with core of HBV



Antibody to HBcAg; IgM= acute/recent infection; IgG= prior exposure or chronic infection. IgM anti-HBc may be the sole positive marker of infection during window period.



A second, different antigenic determinant in the HBV core. HBeAg indicates active viral replication and therefore high transmissibility.



antibody to HBeAg; indicates low transmissibility.


ALT greater than AST

viral hepatitis


AST greater than ALT

alcoholic hepatitis


significance of positive HBsAg, HBeAg, and Anti-HBc IgM

acute HBV


significance of positive HBsAg, HBeAg, and Anti-HBc IgG

chronic HBV with high infectivity


significance of positive HBsAg, Anti-HBe, and Anti-HBc IgG

chronic HBV with low infectivity


significance of positive Anti-HBs, Anti-HBe, Anti-HBc IgG

recovery from HBV


significance of positive Anti-HBs

Immunized against HBV


Structure of HIV

Diploid genome (2 molecules of RNA). The 3 structural genes (protein coded for): env (gp 120 and gp 41), which is formed from cleavage of gp 160 to form envelope glycoproteins; gag (p24), a capsid protein; and pol, reverse transcriptase, aspartate protease, and integrase. Reverse transcriptase synthesizes dsDNA from genomic RNA; dsDNA integrates into host genome. Virus binds CD4 as well as a coreceptor, either CCR5 on macrophages (early infection) or CXCR4 on T cells (late infection). Homozygous CCR5 mutation gives immunity to HIV. A heterozygous mutation causes a slower course.


gp 120

the attachment of HIV to host CD4+ T cell


gp 41

HIV uses this for fusion and entry.


HIV diagnosis

Presumptive diagnosis made with ELISA (sensitive, high false-positive rate and low threshold, therefore it is a rule out test); positive results are then confirmed with Western blot assay (specific, low false-positive rate and high threshold, a rule in test). Viral load tests determine the amount of viral RNA in the plasma. High viral load associated with poor prognosis. Also the viral load can be used to monitor effect of drug therapy. AIDS can be diagnosed with a CD4+ is less than 200 cells/mm3. (normal is 500-1500). HIV- positive diagnoses can be made with the presence of an AIDS-defining condition (eg Pneumocystis pneumonia) or CD4+ percentage less than 14%. ELISA/Western blot tests look for antibodies to viral proteins; these tests often are falsely negative in the first 1-2 months of HIV infection and falsely positive initially in babies born to an infected mother due to anti-gp 120 crosses the placenta.


Four stages of untreated HIV infection

1. Flu-like (acute), 2. Feeling fine (latent), 3. Falling count, 4. Final crisis. During the latent phase, virus replicates in lymph nodes. As CD4+ count falls, risks of reactivation of past infections (eg TBS, HSV, shingles), dissemination of bacterial infections and fungal infections (eg coccidioidomycosis), and non Hodgkin lymphoma incidence increases.


Infections that present in HIV patients with less than 500 cells/mm3

Candida albicans, EBV, Bartonella henselae presents as Bacillary angiomatosis, HHV-8, Cryptosporidium spp., HPV.


Candida albicans in HIV patients

An infection that present in HIV patients with less than 500 cells/mm3. Candida albicans presents with oral thrush and findings include scrapable white plaque, pseudohyphae on microscopy.


EBV in HIV patients

An infection that present in HIV patients with less than 500 cells/mm3. EBV presents as oral hairy leukoplakia and findings include unscrapable white plaque on lateral tongue. In patients with less than 100, B-cell lymphoma (eg non-Hodgkin lymphoma, CNS lymphoma) occurs. CNS lymphoma presents as ring enhancing, may be solitary (vs Toxoplasma).


Bartonella henselae in HIV patients

An infection that present in HIV patients with less than 500 cells/mm3. Bartonella henselae, an facultative intracellular, pleomorphic, gram-negative bacillus, presents as Bacillary angiomatosis and findings includes a biopsy with neutrophilic inflammation.


HHV-8 in HIV patients

An infection that present in HIV patients with less than 500 cells/mm3. HHV-8 presents as Kaposi sarcoma and findings include a biopsy with lymphocytic inflammation.


Cryptosporidium spp. in HIV patients

An infection that present in HIV patients with less than 500 cells/mm3. Cryptosporidium spp. presents as chronic watery diarrhea and findings include an acid-fast test showing oocysts in stool.


HPV in HIV patients

An infection that present in HIV patients with less than 500 cells/mm3. HPV presents as squamous cell carcinoma, commonly of the anus (in men who have sex with men) or cervix (in women).


Infections that present in HIV patients with less than 200 cells/mm3

Toxoplasma gondii, Dementia, JC virus (reactivation), Pneumoxystis jirovecii.


Toxoplasma gondii in HIV patients

An infection that present in HIV patients with less than 200 cells/mm3. It presents as brain abscesses and findings show multiple ring-enhancing lesions on MRI.


Dementia in HIV patients

An infection that present in HIV patients with less than 200 cells/mm3.


JC virus in HIV patients

Occurs due to reactivation. Presents as a progressive multifocal leukoencephalopathy. Findings show non-enhancing areas of demyelination on MRI.


Pneumocystis jirovecii in HIV patients

An infection that present in HIV patients with less than 200 cells/mm3. Presents as Pneumocystis pneumonia. On CXR, ground-glass opacities can be seen.


Infections that present in HIV patients with less than 100 cells/mm3

Aspergillus fumigatus, Cryptococcus neoformans, Candida albicans, CMV, EBV,


Aspergillus fumigatus in HIV patients

An infection that present in HIV patients with less than 100 cells/mm3. Presents with hemoptysis and pleuritic pain. Findings include cavitation or infiltrates on chest imaging.


Cryptococcus neoformans in HIV patients

An infection that present in HIV patients with less than 100 cells/mm3. Presents as meningitis. Findings include thickly encapsulated yeast on India ink stain.


CMV in HIV patients

An infection that present in HIV patients with less than 100 cells/mm3. Presents as retinitis, esophagitis, colitis, pneumonitis, and encephalitis. Findings include linear ulcers on endoscopy, cotton wool spots of fundoscopy. Biopsy reveals cells with intranuclear (owl eye) inclusion bodies.


Histoplasma capsulatum in HIV patients

An infection that present in HIV patients with less than 100 cells/mm3. Presents as fever, weight loss, fatigue, cough, dyspnea, nausea, vomiting, and diarrhea. Presents as oval yeast cells within macrophages.


Mycobacterium avuim-intracellulare and Mycobacterium avium complex in HIV patients

An infection that present in HIV patients with less than 100 cells/mm3. Presents as nonspecific systemic symptoms (fever, night sweats, weight loss) or focal lymphadenitis.



prion disease are caused by the conversion of a normal (predominantly alpha helical) protein termed prion protein to a beta-pleated form, which is transmissible via CNS-related tissue (iatrogenic CJD) or food contaminated by bovine spongiform encephalopathy (BSE) infefected animal products (variant CJD). Resists protease degradation and facilitates the conversion of still more prions. Resistant to standard sterilizing procedures, including standard autoclaving. Accumulation of prions result in spongiform encephalopathy and dementia, ataxia, and death.


Creutzfeldt-Jakob disease

rapidly progressive dementia due to prion disease, typically sporadic (some familial forms)



acquired prion disease noted in tribal population practicing human cannibalism.


Normal flora on skin

Staphylococcus epidermidis


Normal flora in the nose

Staphylococcus epidermidis; colonized by S. aureus


Normal flora in the oropharynx

Viridans group streptococci


Normal flora in dental plaques

Streptococcus mutans


Normal flora in the colon

Bacteroides fragilis more than E coli


Normal flora in the vagina

Lactobacillus, colonized by E. coli and group B strep.


Food poisoning due to reheated rice

Bacillus cereus. Food poisoning due to reheated rice? Be serious?!


Food poisoning due to improperly canned foods or raw honey

Clostridium botulinum


Food poisoning due to reheated meat

Clostridium perfringens


Food poisoning due to undercooked meat

E coli O157:H&


Food poisoning due to poultry, meat, and eggs



Food poisoning due to meats, mayonnaise, custard with preformed toxin

S. aureus


Food poisoning due to contaminated seafood

Vibrio parahaemolyticus and V. vulnificus, which can also cause wound infection from contact with contaminated water or shellfish


Bloody diarrhea due to comma or S-shaped organisms

Campylobacter, growth at 42 degrees celsius.


Bloody diarrhea due to protozoa, amebic dysentery, or liver abscess

Entamoeba histolytica


Bloody diarrhea causing Hemolytic-uremic syndrome (HUS)

Enterohemorrhagic E. Coli O157:H7, makes shiga like toxin


Bloody diarrhea that invades colonic mucosa

Enterinvasive E. Coli


Bloody diarrhea due to lactose negative, flagellar motility

Salmonella has an animal reservoir, transmittable in poultry and eggs.


Bloody diarrhea due to lactose negative, bacillary dysentary

Shigella causes shiga toxin (human reservoir only); with a very low infectious concentration


Bloody diarrhea seen in day care outbreaks and causes pseudoappendicitis

Yersinia enterocolitica


Watery diarrhea due to antibiotic use

C. difficile, Pseudomembranous colitis, occasionally bloody diarrhea


Watery diarrhea due to a bacteria that also causes gas gangrene

C. perfingens


Watery diarrhea due to travelers diarrhea

Enterotoxigenic E. coli, produces heat labile (LT) and heat stable (ST) toxins.


Watery diarrhea due to a protozoa

Giardia, Cryptosporidium


Watery diarrhea due to comma-shaped organisms

V. cholerae produces rice water diarrhea; often from infected seafood.


Watery diarrhea due to viruses

Rotavirus, norovirus, adenovirus


Common causes of pneumonia in neonates

Group B stretococci, E. coli


Common causes of pneumonia in children (from 4 months to 4 years )

Mycoplasma pneumoniae, Streptococcus pneumoniae, GAS (group A strep), and RSV


Common causes of pneumonia in children (from 5 to 18 years)

Streptococcus pneumoniae, EBV (epstein barr virus), Staphylococcus aureus, Mycoplasma pneumoniae, Chlamydia pneumoniae


Common causes of pneumonia in adults (from 18 to 65 years)

Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Haemophilus influenzae, Influenza virus


Common causes of pneumonia in adults (over the age of 65)

S. pneumoniae, Ifnleunza virus, Anaerobes, H. influenzae, Gram-negative rods


Infections common in alcoholic/ IV drug user

S. pneumoniae, Klebsiella, S. aureus


Infections common due to aspiration

Anaerobes (eg Peptostreptococcus, Fusobacterium, Prevotella, Bacteroides)


Common atypical infections

Mycoplasma, Legionella, Chlamydia


Infections common in patients with cystic fibrosis

Pseudomonas, S. aureus, S. pneumoniae


Infections common in immunocompromised patients

S. aures, enteric gram negative rods, fungi, viruses, P. jirovecii (with HIV)


Common nosocomial infections

S. aureus, Pseudomonas, other enteric gram negative rods


Common postviral infections

S. aureus, H. influenzae, S. pneumoniae.


Common causes of meningitis in newborns (0-6 months)

group B streptococci, E coli, Listeria


Common causes of meningitis in children (6 months- 6 years)

S. pneumoniae, N. meningitidis, H. influenzae type B, Enteroviruses. Incidence of H. influenzae meningitis has decreased greatly with the introduction of the conjugate H. influenzae vaccine in last 10-15 years. Today cases are seen in unimmunized children.


Common causes of meningitis from 6 year olds- 60 year olds

S. pneumoniae, N. meningitidis (#1 in teens), Enteroviruses, HSV


Common causes of meningitis in those over the age of 60

S. pneumoniae, Gram negative rods, Listeria


Empiric treatment of meningitis

Give ceftriaxone and vancomycin empirically. Add ampicillin if Listeria is suspected.


Viral causes of meningitis

Enteroviruses (especially coxsackievirus), HSV-2 (HSV-1=encephalitis), HIV, west nile virus (also causes encephalitis), VZV


Cause of meningitis in those with HIV

Cryptococcus spp.


CSF findings in bacterial meningitis

Increase in opening pressure, increase in PMNs, increase in protiens, and a decrease in glucose.


CSF findings in fungal/ TB meningitis

Increase in opening pressure, an increase in lymphocytes, an increase proteins, and a decrease in glucose.


CSF findings in viral meningitis

Normal or increase in opening pressure, an increase in lymphocytes, normal or an increase in protein, and normal levels of glucose.


Infections causing brain abscesses

Most commonly due to viridans streptococci and S aureus. If dental infections or extraction precedes abscess, oral anaerobes are commonly involved. Multiple abscesses are usually seen from bacteremia. A single lesion from contiguous sites is usually due to otitis media and mastoiditis and usually is seen in the temporal lobe and cerebellum. Sinusitis or dental lead to abscess in the frontal lobe. In AIDS patients, abscess is due to Toxoplasma reactivation.


Most common cause of osteomyelitis

S aureus


Osteomyelitis with the risk factor of being sexually active

Neisseria gonorrhoeae (rare), septic arthritis more common


Osteomyelitis with the risk factor of sickle cell disease

Salmonella and S aureus


Osteomyelitis with the risk factor with a prosthetic joint

S aureus and S epidermidis


Osteomyelitis with vertebral involvement

S aureus, Mycobacterium tuberculosis (pott disease)


Osteomyelitis due to cat and dog bites

Pasteurella multocida


Osteomyelitis with the risk factor of IV drug abuse

Pseudomonas, Candida, S aureus are the most commoon


Diagnosis of osteomyelitis

Elevated CRP and ESR are common but non specific. MRI is best for detecting an acute infection and detailing anatomic involvement. Radiographs are insensitive early but can be useful in chronic osteomyelitis.


Urinary tract infections

Cystitis presents with dysuria, frequency, urgency, suprapubic pain and WBCs (but not casts) in urine. Primarily caused by ascension of microbes from urethra to bladder. In males, often seen in infants with congenital defects, vesicoureteral reflex. In the elderly, often due to an enlarged prostate. Ascension to kidney results in pyelonephritis, which presents with fever, chills, flank pain, costovertebral angle tenderness, hematuria, and WBC casts. Ten times more common is women ( shorter urethras colonized by fecal flora). Other predisposing factors include obstruction, kidney surgery, catheterization, GU malformation, diabetes and pregnancy.


Leading cause of UTI

E coli, colonies show green metallis sheen on EMB agar.


UTI is sexually active women

Satphylococcus saprophyticus


UTI due to a bacteria with large mucoid capsule and viscous colonies

Klebsiella pneumoniae. 3rd leading cause of UTI. Urease positive.


Serratia marcescens

Another cause of UTI. Some strains produce a red pigment; often nosocomial and drug resistant.



Another cause of UTI; often nosocomial and drug resistant.


UTI caused by a bacteria that produces urease and is associated with struvite stones

Proteus mirabilis. Motility causes swarming on agar.


UTI caused by a bacteria that produces a blue green pigment and a fruity odor

Pseudomonas aeruginosa; often nosocomial and drug resistant.


Diagnostic markers of a UTI

Leukocyte esterase is evidence of WBC activity. Nitrates are reduced by bacterial species (E coli). Urease positive tests show that there is a urease producing bug (Proteus, Klebsiella)


Bacterial vaginosis

There is no inflammation within the vagina but there is a thin white discharge with a fishy odor. Lab findings show Clue cells and a pH over 4.5. Clue cells are epithelial cells of the vagina with a distinctive stippled appearance by being covered with bacteria. Treatment is metronidazole.



There is inflammation (strawberry cervix) and frothy, grey-green, foul smelling discharge. Lab findings show motile trichomonads and a pH greater than 4.5. Treatment is metronidazole. Must also treat sexual partners.


Candida vulvovaginitis

There is inflammation and a think, white, cottage cheese discharge. Lab findings show pseudohyphae and a normal pH (4-4.5). Treat with -azoles.


congenital infections

ToRCHeS infections. Microbes that may pass from mother to fetus. Transmission is transplacental in most cases or via delivery (especially HSV-2). Nonspecific signs common to many ToRCHeS infections include hepatosplenomegaly, jaundice, thrombocytopenia, and growth retardation. Other important infections include Streptococcus agalactiae (group B streptococci), E coli, and Listeria monocytogenes- all of which cause meningitis in neonates. Parvovirus B19 causes hydrops fetalis. Toxoplasma gondii, Rubella, CMV, HIV, Herpes simplex virus-2, Symphilis.


neonate with recurrent infections and chronic diarrhea

Congenital HIV


neonate with encephalitis, herpetic (vesicular) lesions

Congenital HSV-2. Mother is often asymptomatic


neonate with with hydrops fetalis, which often results in stillbirth. If child survives, presents with facial abnormalities (eg notched teeth, saddle nose, short maxialla), saber shins, and CN VIII deafness

Congenital Syphilis. Mother presents with chancre (primary) and disseminated rash (secondary). These are the two stages most likely to result in a fetal infection.


neonate with chorioretinitis, hydrocephalus, and intracranial calcifications, with or without a blueberry muffin rash

Congenital Toxoplasma gondii. Transmitted via cat feces or ingestion of undercooked meat. Maternal manifestations is usually asymptomatic or rarely lymphadenopathy.


neonate with PDA (or pulmonary artery hypoplasia), cataracts, and deafness, with or without a blueberry muffin rash

Congenital Rubella, transmitted by respiratory droplets. In the mother it manifests as a rash, lymphadenopathy, and arthritis.


neonate with hearing loss, seizures, petechial rash, blueberry muffin rash, and a periventricular calcifications

Congenital CMV, transmitted by sexual contact, organ transplants. Maternal manifestations is usually asymptomatic or a mononucleosis like illness.


Pediatric rash of oval shaped vesicles on palms and soles; vesicles and ulcers in oral mucosa

Hand-foot-mouth disease. Coxsackievirus type A


Pediatric rash of asymptomatic rose-colored macules appear on body after several days of high fever; can present with febrile seizures; usually affects infants

Roseola (exanthem subitum). HHV-6


Pediatric rash beginning at head and moves down; rash is preceded by cough, coryza, conjunctivitis, and blue-white (Koplik) spots on buccal mucosa

Measles (rubeola). Measles virus


Pediatric "slapped cheek" rash on face

Erythema infectiosum (fifth disease). Parvovirus B19; can cause hydrops fetalis in pregnant women.


Pediatric rash of pink coalescing macules begin at head and move down to trunk of a fine desquamating truncal rash; postaurical lumphadenopathy

Rubella virus (German measles)


Pediatric erythematous, sandpaper-like rash with fever and sore throat

Scarlet fever. Streptococcus pyogens


Pediatric vesicular rash begins on trunk; spreads to face and extremities with lesions of different ages

Chickenpox. VZV


Painful genital ulcer with exudate, inguinal adenopathy

Chancroid. Haemophilus ducreyi (its so painful, you "do cry")


Urethritis, cervicitis, conjunctivitis, reactive arthritis, PID

Chlamydia trachomatis (D-K)


Genital warts, koilocytes

Condylomata acuminata. HPV-6 and -11


Painful penile, vulvar, or cervical vesicles and ulcers; can cause systemic symptoms such as fever, headache, and myalgia

Genital herpes, HSV-2, less commonly HSV-1


Urethritis, cervicitis, PID, prostatitis, epididymitis, arthritis, creamy purulent discharge

Gonorrhea. Neisseria gonorrhoeae


Infection of lymphatics; painless genital ulcers, painful lymphadenopathy (ie, buboes-swollen, inflamed lymph node in the armpit or groin)

Lymphogranuloma venereum. C. trachomatis (L1-L3)


Painless chancre (ulcer)

Treponema pallidum. Primary syphilis.


Fevery, lyphadenopathy, skin rashes, condylomata lata

Secondary syphilis


Gummas (a soft, non-cancerous growth), tabes dorsalis, general paresis, aortitis, Argyll Robertson pupil

Tertiary syphilis


Vaginitis, strawberry cervix, motile in wet prep

Trichomonas vaginalis, Trichomoniasis


Pelvic inflammatory disease

Most common causes include Chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrhoeae (acute), C. trachomatis (most common bacterial STI in the US). Cervical motion tenderness (chandelier sign), purulent cervical discharge. PID may include salpingitis (inflammation of the fallopian tubes), endometritis, hydrosalpinx (a distally blocked fallopian tube filled with serous or clear fluid), and tubo-ovarian abscess. Salpingitis is a risk factor for ectopic pregnancy, infertility, chronic pelvic pain, and adhesion.


Fitz-Hugh-Curtis syndrome

A sequele of PID. An infection of the liver capsule and "violin string" adhesions of peritoneum to liver. A perihepatitis from the ascending infection that results in right upper quadrant pain and tenderness and elevated liver-function tests.


Nosocomial infections

E. coli (UTI) and S. aureus (wound infection) are the two most common causes.


Nosocomial infections in patients with altered mental status, older age, and aspiration

Polymicrobial, gram-negative, often anaerobes. Often manifest as a right lower lobe infiltrate or right upper/ middle lobe (patient recumbent); purulent malodorous sputum.


Nosocomial infections in patients with antibiotic use

Clostridium difficile, which manifests as watery diarrhea with leukocytosis.


Nosocomial infections in patients with decubitus ulcers, surgical wounds, and drains.

S. aureus (including MRSA), gram-negative anaerobes. Manifests as erythema, tenderness, induration, drainage from surgical wound sites.


Nosocomial infections in patients with intravascular catheters

S. aureus (including MRSA), S. epidermidis (long term), Enterobacter. Manifests as erythema, induration, tenderness, drainage from access sites.


Nosocomial infections in patients with mechanical ventilation, endotracheal intubation

Late onset of P. aeruginosa, Klebsiella, Acinettobacter, S. aureus. Manifests as new infiltrate on chest xray, an increase in sputum production; and a sweet odor (Pseudomonas).


Nosocomial infections in patients with renal dialysis unit and needlesticks



Nosocomial infections in patients with urinary catheterization

E. coli, Klebsiella, Proteus spp. Manifests as dysuria, leukocytosis, flank pain or costovertebral angle tenderness.


Nosocomial infections in patients with water aerosols

Legionella. Manifests as signs of pneumonia, GI symptoms (nausea and vomiting).


Rashes affecting unimmunized children

Rubella virus, the rash begins at the head and moves down with the postauricular lymphadenopathy. Measles virus, rash begins at the head and moves down; rash preceded by cough, coryza, conjunctivitis, and blue-white (Koplik) spots on buccal mucosa.


Meningitis in unimmunized children

H. influenzae type B, showing microbe colonization in the nasopharynx.


Epiglottitis in unimmunized children

H. influenzae type B (also capable of causing epiglottitis in fully immunized children). Causes fever with dysphagia, drooling, and difficulty breathing due to edematous "cherry red" epiglottis; "thumbprint sign" on xray.


Pharyngitis in unimmunized children

Corynebacterium diphtheriae (elaborates toxin that causes necrosis in pharynx, cardiac, and CNS tissue). Grayish oropharyngeal exudate (pseudomembranes may obstruct airway); painful throat.


Infections common in asplenic patient (due to surgical splenectomy or autosplenectomy, eg chronic sickle cell disease)

Encapsulated microbes, especially SHiN (S. pneumoniae is the most common followed by H. infleunzae type B, followed by N. meningitidis).


Common infections due to branching rods in oral infection and sulfur granules

Actinomyces israelii


Common infections due to a chronic granulomatous disease

Catalase positive microbes, especially S. aureus.


Common infections with "currant jelly" sputum



Common infections due to a dog or cat bite

Pasteurella multocida


Common infections with facial nerve palsy

Borrelia burgdorferi (Lyme disease)


Common infections due to a fungal infection in diabetic or immunocompromised patient

Mucor or Rhizopus spp.


Common infections in health care providers

HBV (from needlestick)


Common infections in neutropenic patients

Candida albicans (systemic), Aspergillus.


Common infections in organ transplant recipient



Common infections with a positive periodic acid–Schiff (PAS) stain

Tropheryma whipplei (whipple disease)


Common infections in pediatric infection

Haemophilus influenzae (including epiglottis)


Common infections with pneumonia in cystic fibrosis or burn infection

Pseudomonas aeruginosa


Common infections with pus, empyema, and abscesses

S. aureus


Common infections with rash on hands and feet

Coxsackie A virus, Treponema pallidum, Rickettsia rickettsii


Common infections with sepsis/ meningitis in a newborn

Group B strep


Common infections with surgical wounds

S. aureus


Common infections with traumatic open wounds

Clostridium perfringens



First generation cephalosporin



First generation cephalosporin



Second generation cephalosporin



Second generation cephalosporin



Second generation cephalosporin



Second generation cephalosporin



Third generation cephalosporin. Neisseria gonorrhoeae coverage, excreted in bile



Third generation cephalosporin. Pseudomonas coverage



Third generation cephalosporin. Treats resistant otitis media.



Fourth generation cephalosporin. Pseudomonas coverage



Fifth generation cephalosporin. MRSA coverage