Microbiology Flashcards
antimicrobials targeting folic acid synthesis (DNA methylation)
Sulfonamides (sulfadiazine, sulfamethoxazole, sulfisoxazole) and trimethoprim
antimicrobials targeting DNA topoisomerases
fluroquinolones (ciprofloxazin and levofloxacin)
antimicrobials damaging DNA
metronidazole
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)
rifampin
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).
carbapenems
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
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.
aminoglycosides
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
macrolides
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.
fluoroquinolones
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
Isoniazid
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
rifamycins
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
legionella
Sabouraud agar
fungi
aerobes
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.
anaerobes
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
actinomyces
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.
Exotoxin
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.
Endotoxin
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.
tetanospasmin
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.
transformation
takes up naked DNA from environment.
Conjugation
plasmid becomes incorporated into host.
transposition
Segment of DNA that can jump from one location to another. Can transfer from plasmid to chromosome or vice versa.
Transduction
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).
Clostridia
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.
anthrax
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.
Actinomyces
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
Nocardia
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.
Mycobacterium
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.
Neisseria
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
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.
Shigella
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).
Spirochetes
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.
Syphilis
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.
Anaplasmosis
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.
Psittacosis
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
Ehrlichiosis
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
Tularemia
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.
Leptospirosis
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.
plague
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
doxycycline
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
Typhus
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
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.
