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106 Cards in this Set
- Front
- Back
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Lophentrichous
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Multiple Flagella going in the same direction
Ex.) Bartonella baciliformis |
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Amphitricous
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Multiple flagella coming off of opposite ends
Ex.) Spirillum serpens |
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Peritrichous
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Multiple flagella found all over the bacterium
Ex.) Escherichia coli |
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What alternating sugars form the backbone for Peptidoglycans?
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N-acetylglucosamine & N-acetylmuramic acid
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Steps in Gram stain procedure
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1.) Stain w/ crystal violet
2.) Wash w/ iodine 3.) Decolorization w/ alcohol 4.) Stain w/ Safranin Blue = Gram + Red = Gram - |
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Stages of peptidoglycan biosynthesis
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Stage 1 - Biosynthesis of cell wall precurssors and assembly into nucleotides
Stage 2 - Transport of precursor across the cytoplasmic membrane Stage 3 - Assembly of precursor sugars and transpeptidation cross linking |
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Fosfomycin / Cycloserine
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Inhibit Stage 1 of peptidoglycan synthesis
Fosfomycin - PEP analogue that inhibits UDP-muramic acid synthesis Cycloserine - Comeptitively inhibits conversion to D-Alanine-D-Alanine Both must be taken up into cell to be effective |
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Vancomycin / Ristocetin
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Prevent Stage 2 of peptidoglycan synthesis
Bind to D-Alanine-D-alanine and prevent its transfer to the acceptor |
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Bacitracin
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Prevent Stage 2 of peptidoglycan synthesis
Inhibits dephosphorylation of lipid carrier |
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Penicillin / Cephalosporine antibiotics
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Inhibits Stage 3 of peptidoglycan synthesis
Inactivates transpeptidase, which prevents cross-linking |
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Quinolones
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Antibiotic that inhibits bacterial DNA gyrase
Nalidixic acid and Ciprofloxacin |
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Rifampin
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Antibiotic that inhibits transcription by binding to the beta subunit of bacterial RNA polymerase
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Tetracyclines / Aminoglycosides
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Antibiotic that binds to the 30S ribosomal subunit to prevent protein synthesis
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Chloramphenicol / Erythromycin / Clindmycin
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Antibiotics that inhibits binding to the 50S subunit
Erythromycin also blocks the movement |
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Trimethoprin
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Antibiotic that inhibits bacterial metabolism by inhibiting dihydrofolate reductase
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Sulfanilamide
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Sulfa drugs that inhibit folic acid biosynthesis by acting as a competitive inhibitor of p-aminobenzoic acid
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"cord factor"
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Mycobacterium tuberculosis glycolipid
Large hydrophobic mycolic acids will float around in the air and allows TB to be transmitted via coughing |
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2 genera of bacteria that can form spores
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Bacillus and Clostridium
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Calcium Dipicolinic Acid
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Gives spores their high resiliency
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Immune Deficiencies that Predispose People to Infections
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Hypo- or agammaglobulinemia - Too little or no antibody production
Job's disease - consistently high levels of IgE that leads to improper immune response Chronic granulomatous disease - Suboptimal oxidative killing by phagocytes Chediak-Higashi Syndrome - insufficient chemotaxis of Neutrophils and phagocytes Diabetes - compromised immune system |
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Staphylococcus aureus
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DOC = Beta-Lactans (Oxacillin, Cephalosporins) & Vancomycin for MRSA
Virulence Factors - 1.) Polysaccharide Intercellular Adhesin (PIA) - forms biofilms 2.)Protein A - Binds to Fc of IgG and orients the antibody in the wrong direction 3.)Clumping factor - Binds fibrinogen causing clumping of organisms (diagnostic of aureus) 4.) Coagulase - Converts fibrinogen to fibrin and blocks off Neutrophil access (diagnostic for aureus) 5.) Catalase - Breaks down neutrophil H202 (prevents oxidative killing) 6.) Superantigens - Stimulates TNF and IL-1 causing shock 7.) TSST1 - Causes toxic shock syndrome 8.) Enterotoxins - emetic toxins causing food poisoning 9.)Exfoliatin - cleaves desmosomes resulting in blistering and loss of skin Alpha toxin - leads to pneumonia PVL - Leukocidin that lyses Neutrophils via pore formation |
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Classes of Staphylococcus aureus infection
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1.) Colonization - asymptomatic, carried in nares, throat, vagina
2.)Local Invasion - MCC of non-spreading pyogenic skin infections 3.) Dissemination - Gains access to bloodstream causing bacteremia (proteases, nucleases, TSST-1 causes spesis) 4.) Metastatic infections - invade, transverse, or persist in endothelial cells or tissues 5.) Toxinosis - caused only by toxin without bacterial invasion (Toxic Shock Syndrome) |
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Staphylococcus aureus is the most common cause of:
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1.) Non-spreading Pyogenic skin infections (Folliculitis, furuncles, carbuncles)
2.) Osteomyelitis & Septic Arthritis 3.) Endocarditis in IV drug abusers / Acute Endocarditis 4.) Epidural abscess 5.) Pyomyositis (muscular disease) 6.) Food poisoning |
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Staphylococcus aureus Toxinoses
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1.) Toxic Shock Syndrome - Caused by TSST-1 gaining access to the blood through the vagina or nose during gauge packing. Massive induction of TNF and IL-1. Causes hypotension, sunburn-like rash, peeling of palms and soles, and fever
2.) Scalded Skin Syndrome - Exfoliatin causes entire skin layer to peel off or causes blisters 3.) Food Poisoning - S. aureus is salt tolerant and the toxin is heat stable. Causes vomiting and acts quickly |
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Staphylococcus epidermidis
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Most common cause of infections of IV catheters, heart valves, and artificial joints
Often resistant to multiple antibiotics Virulence Factor - PIA forms Biofilms that allows them to adhere to foreign bodies Only cause infection in association with a foreign device |
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Staphylococcus saprophyticus
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Second to E. coli as the most common cause of UTI's
Identified by the fact that they are Novobiocin resistant |
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Tests to Identify different Staphylococcal strains
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All are Catalase positive (distinguishes from Strept.)
1.) Only S. aureus has a positive clumping and Coagulase test 2.) S. aureus is a Mannitol fermentor and S. epidermidis is not 3.) S. saprophyticus is the only strain resistant to Novobiocin |
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Streptococcus hemolysis on blood agar
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Hemolysis caused by Streptolysis O & S
Alpha - "Al"most hemolytic (Viridans Strept. and S. pneumoniae) Beta - "B"est (S. pyogenes) Gamma - No hemolysis (Enterococci and some Viridans strept.) |
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Differentiation of different strains of Streptococcus
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Group A (S. pyogenes) - Sensitive to bacitracin
Group B (S. agalactiae) - positive cAMP test (enlarges the zone of hemolysis produced by Staph. aureus), Hydrolizes Hippurate Strept. pneumoniae - Lysed in bile, Optochin antibiotic sensitive, Quellung test, typically dicocci (not in long beads) Enterococci - Turns bile esculin black, No hemolysis (Gamma) |
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Streptococcus Pyogenes
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DOC = Penicillin
Virulence Factors: 1.) M protein - Major virulence factor that blocks phagocytosis by binding fibrinogen to form a protective coating. Becomes a highly variable target for opsonization by antibodies 2.) Hemolysins - (Diagnostic) Streptolysin O is "O"xygen labile. Streptolysin S is oxygen "S"table 3.) Exotoxins - antigen specific (SPEA, SPEB, etc.) and activate TNF IL-1, T and B cells. Cause Scarlet Fever 4.) Tissue degrading enzymes - makes Strept more invasive than Staph. |
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Streptococcus Pyogenes is the most common cause of:
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1.) Cellulitis - skin infection that spreads tissue
2.) Erysipelas - rapidly spreading cellulitis 3.) Necrotizing fascitis - severe infection involving skin, fascia, and muscle. High mortality rate 4.) Impetigo - localized clusters of pustular lesions. No severe infections or Scarlet fever, but highly contageous 5.) Pharyngitis - Most common infection caused by Group A Strept. Common prelude to Scarlet fever and ARF 6.) Scarlet Fever - only cause of this. Pyrogenic exotoxin causes sunburn-like rash 7.) Strept Toxic Shock Syndrome - Exotoxin causes severe disease. Often after cellulitis and high mortality rate. 8.) Puerperal fever - Sepsis after childbirth |
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Post-streptococcal syndromes
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Acute Rheumatic fever (ARF) - following pharyngitis, causes inflammation in joints, heart, skin, and CNS (chorea) caused by autimmune cross-reaction w/ M protein
Acute post-streptococcal glomerulonephritis - inflammation of glomerulus caused by immune response to deposits on the kidney |
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Stretptococcus agalactiae
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DOC = Penicillin
Virulence Factors: 1.) capsular polysaccharide is the major virulence factor Most Common Cause of neonatal meningitis. Acquired as newborns transverse the birth canal of colonized mother. |
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Viridans Streptococci
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DOC = Penicillin, Vancomycin
Low virulence and commonly found in oral cavity Most common cause of chronic endocarditis (acute = S. aureus) Also causes dental caries Not lancefield typable b/c don't possess group specific carbohydrate antigen |
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Enterococcal Streptococci
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DOC = Combo therapy of Ampicillin / Penicillin + Aminoglycoside b/c antibiotic resistant
Cause infective endocarditis, UTIs, and wound infections |
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Streptococcus bovis
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Nonenterococcal Group D strept.
Susceptible to beta-lactams like penicillin Can cause bacteremia - an indicator of colon cancer |
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VRE / VREF
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Enterococci that are resistant to all available antimicrobial chemotherapy (beta-lactams, vancomycin, and aminoglycosides)
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Streptococcus pneumoniae
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DOC = Penicillin G & Vancomycin for Penicillin resistant
Virulence Factors: 1.) Capsular polysaccharide is the major virulence factor. Capsule is anti-phagocytic Most Common Cause of: 1.) Community-acquired pneumonia 2.) Adult bacterial meningitis (following pneumonia) Prominent cause of otitis media Vaccine is available |
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Forms of Bacillus anthracis
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1.) Cutaneous - most common, least fatal. Papule followed by necrotic eschar
2.) Inhalation - Most fatal. Spores incubate in lymph nodes and then cause hemorrhagic necrosis. Can lead to meningitis. Diagnosed by widened mediastinum on x-ray 3.) GI - Rare, but fatal. After consuming contaminated meat products. Invasion through intestine - inflammation, vomiting, diarrhea |
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Bacillus anthracis
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DOC = IV Ciprofloxacin
Virulence factors: 1.) poly-D-glutamyl capsule 2.) 2 AB toxins that produce lethal edema and share binding subunit (PA). EF activates Adenylate cyclase = increased cAMP. LF cleaves MAPKK causing necrosis |
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Bacillus cereus
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DOC = none needed
Causes 2 types of food intoxication: 1.) Short incubation emetic form - heat-stable enterotoxin causes vomiting, nausea and cramps(1-6 hrs.) 2.) Long-incubation diarrheal form - caused by HBL that activates adenyl cyclase in intestine (8-16 hrs.) Also causes explosive intraocular virulence via swarming bacterial motility following penetrating injury |
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Listeria monocytogenes
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DOC = Ampicillin or penicillin
Resistant to temp. extremes and dessication. Often food-borne Virulence Factors: 1.) Internalins - promote uptake by non-phagocytic cells 2.) Listeriolysin - cholesterol-dependent hemolysin used to escape from phagocytic vacuoles 3.) ActA - hijacks host cytoskeleton for intracellular motility 4.) Membrane phospholipases - PlcA and PlcB synergize w/ Listerolysin to allow escape of secondary vacuole caused by entering second cell |
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Corynebacterium diphtheriae
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DOC = Penicillin G or Erythromycin w/ diphtheria antitoxin
non-spore forming, gram (+), "Chinese letters". Highly contageous Virulence factors: 1.) Diptheria toxin - AB exotoxin that causes ADP-ribosylation of EF-2 that inhibits translation 2.) Toxin regulated by DtxR that represses it in high levels of iron 3.) Phospholipase - increases vascular permeability and allows spread through nasopharyngeal tissue Disease manifestation - Infects mucus membrane and can form adherent membrane over throat and tonsils. Toxin causes most symptoms such as labored breathing, palor, sweating, tachycardia. Complications can lead to paralysis or respiratory system, and kidney damage |
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Forms of Diphtheria vaccines
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1.) DTP - also tetanus and pertussis. 40s-50s
2.) DTaP - Less reactive. Recommended for Peds 3.) DT - when pertussis vaccine is contraindicated 4.) Tdap - For adolescents and adults 5.) Td - every 10 years after Tdap |
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Bordetella pertussis
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DOC = Supportive measures. Erythromycin, azithromycin - prevents transmission, but doesn't shorten duration
Gram (-), aerobic, fastidious spread via respiratory tract droplets 1.) Catarrhal stage - incubation followed by non-productive cough (most contagious here) 2.) Paroxysmal stage - frequent, intense coughing that can cause vomiting or hernia (lower transmissibility) 3.) Convalescent stage - prolonged complications such as development of pneumonia Virulence Factors: 1.) Pertussis toxin - AB toxin. Adhesion to ciliated respiratory tissue, blocks Gi leading to increased cAMP, which kills cells 2.) Filamentous hemagglutinin (FHA) - binds to host receptor and PMNs. Allows organism to disseminate. 3.) Invasive Adenylate cyclase toxin - inhibits chemotaxis and phagocytosis (requires Calmodulin) 4.) Lethal toxin - local tissue damage (diff. from anthrax LF) 5.) Tracheal cytotoxin - prevents clearance of organism by inhibiting DNA replication in ciliary cells 6.) Pertactin - afimbrial adhesin |
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Bordetella parapertussis
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Causes milder illness than Bordetella pertusis
Not as fastidious |
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Haemophilus influenzae
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DOC = Cefotaxime or Chloramphenicol (for rapid entry to CNS)
Gram (-), aerobic, pleomorphic Type B strain causes pediatric meningitis or epiglottitis (rapid blockage of airway) Non-typable strains cause ottitis media and resp. infections Virulence Factors: 1.) Produce protective capsule (Type B made from PRP is the most virulent) 2.) DNA binding protein that recognizes 11 bp DNA sequence allows easy uptake from heterologous bacteria |
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Prophylactic treatment of those that may be exposed to Meningitis causing bacteria
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Rifampin
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Haemophilus ducreyi
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DOC = Azithromycin or ceftriaxone
Cause Chancroid STD very deep, Painful lesion (syphilis lesions not painful) |
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Neisseria meningitidis
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Gram (-), Diplococci, oxidase positive, infects humans exclusively, airborne droplets transmission
Cause endemic and epidemic meningitis (only cause of this) Virulence Factors: 1.) Capsular polysaccharide - determines serogroup and blocks phagocytosis. Group B exhibits molecular mimicry and seen as self-antigen (no vaccine to this serogroup) 2.)LOS - Endotoxin similar to LPS responsible for the most damage - leads to shock (cells don't have to lyse to secrete this) 3.)Pili - mediate initial attachment to epithelial cells 4.) Opacity proteins (Opa) - tight adherence to specific tissue after pili attachment. Can induce cell to internalize bacteria 5.)OMPs - Porins such as PorB that can activate apoptosis via Ca2+ influx 6.) fH binding protein - blocks complement 7.) IgA1 protease - cleaves IgA 8.) Receptors that help steal iron from the host |
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Differences b/w Neisseria meningitidis and Neisseria gonorrhoeae
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Gonorrhoeae metabolize Glucose only.
Meningitidis metabolize Maltose and Glucose Meningitidis has a capsule that prevents dessication. Gonorrhoeae does not have a capsule so needs to be transmitted by intimate contact Meningitidis is carried as a commensal organism. Gonorrhoeae is not and is always pathogenic |
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Bacteria that commonly cause Meningitis
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Neisseria meningitidis (infants & young adults)
Streptococcus pneumoniae (infants and elderly) Streptococcus agalactiae (neonates) Haemophilus influenzae (children) |
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Seroroups of N. meningitidis that are associated with specific diseases (A, B&C, Y)
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Group A - Epidemic meningitis
Groups B&C - Endemic meningitis Group Y - pneumonia |
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Local Neisseria meningitidis infections
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All have purulent discharge
1.) Pharyngitis 2.) Pneumonia (Serogroup Y) 3.) Urethritis (purulent discharge after oral sex) |
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Klebsiella granulomatis
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DOC = Trimethoprim or Doxycycline
Pleomorphic, Gram (-) bacillus, obligate intracellular organism (lives in Monocytes, not PMNs) Causes Donovanosis or Granuloma Inguinale (GI) - prolonged incubation period, subcutaneous nodules form, breakdown to granulomatous lesions that bleed easily. Can lead to lymph node involvement (resembles LGV) Diagnosis - Staining with Giemsa or Wright's stain reveals dark staining Donovan bodies inside MONOCYTES (Not PMNs) Can relapse after treatment |
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Gardnerella vaginalis
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DOC = Clindamycin, but recurrence is common due to biofilm
Gram (+), facultative anaerobe, un-encapsulated, forms biofilms, causes Bacterial Vaginosis |
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Atopobium vaginae
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DOC = Clindamycin
Gram (+) anaerobe that produce large amounts of lactic acid and lead to Bacterial vaginosis resistant to metronidazole |
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Criteria used to diagnose bacterial vaginosis
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Requires 3 of the following:
1.) thin, white discharge 2.) Presence of "clue cells" (bearded cells) 3.) "Fishy" odor after 10% KOH added (whiff test) 4.) pH of vaginal fluid > 4.5 Gram stain to analyze morphology of localized bacteria is the gold standard |
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Complications due to STDs
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particularly in women
1.) Pelvic Inflammatory Disease (PID) - ascending infection of uterus and fallopian tubes 2.) Infertility 3.) Chronic pelvic pain 4.) Ectopic pregnancy 2-4 associated w/ PID 5.) Cervical cancer (HPV) 6.) Premature labor / abortion 7.) Congenital infections during labor(Chlamydia, etc.) 8.) Increased risk of HIV |
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Stain for Mycoplasma and Ureaplasma
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Giemsa stain ("a gem of a stain")
Do not react w/ Gram stain b/c do not have cell well containing peptidoglycan (cell membrane contains sterols for support) |
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Mycoplasma pneumoniae
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DOC = Tetracyclines, erythromycin (Mycoplasmas immune to penicillin, etc. b/c no peptidoglycan)
Causes "walking pneumonia" or pharyngitis. Secondary complications: Neurological abnormalities, arthritis Strictly infects humans and spread through resp. droplets Diagnose w/ PCR assay, cold agglutinin (RBCs fall out of serum when put in cold env.), or culture organism |
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Mycoplasma and Ureaplasma associated w/ STDs
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Mycoplasma genitalium - urethritis and PID
Mycoplasma hominis Ureaplasma urealyticum - cleaves urea, causes Urethritis |
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General characteristics of Spirochetes
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Highly diverse
Gram (-) Lack LPS Visualized by dark field microscopy Corscrew motion via endoflagella located b/w inner and outer membrane |
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Treponema pallidum
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DOC = Penicillin G or Chloramphenicol to treat neurosyphilis since it gets into CNS easily
Causes syphilis 1.) Primary stage - spirochetes penetrate abrasions and disseminate. Non-painful Chancres develop that are rich in spirochetes if cultured 2.) Secondary stage - infection disseminated and causes flu-like symptoms and an infectious rash (may relapse) 3.) Tertiary stage - 20-30 years after infection. Organ destruction w/ granulatomous lesions called Gumma. Spirochetes hard to detect here. Can lead to neurosyphilis or death. Virulence Factors: 1.) Hyaluronidase - facilitates invasion by breaking down tissue Diagnosis - Bacteria Cannot be cultured 1.) Dark field microscopic exam of chancre 2.) VDRL or RPR - Damage from syphilis causes an increase in Cardiolipin and these tests measure this (not good for early or late phase) 3.) Treponemal antibody test for early and late phase Natural immunity develops and lasts a few years |
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Congenital Syphilis
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High chance of transmitting syphilis to child during birth.
Causes death, multi-organ deformities Most born without symptoms, but can later develop rhinitis, rash, bony destruction, and cardiovascular syphilis Prevention by testing mother before birth |
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Yaws
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Caused by T. pallidum subspecies pertenue
Initially painless papules that enlarge and ulcerate. Ulcers heal, but infection disseminates. Painful open sores may develop on the soles of the feet (crab yaws) Mostly affects children |
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Pinta
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Caused by T. pallidum subspecies carateum
Less severe cutaneous disease Begins w/ flat, reddened areas that turn into slate blue patches Common in Indians in South America |
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Bejel
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DOC = Penicillin
Caused by T. pallidum subspecies endemicum Slimy patch on the inside of the mouth followed by blisters on the trunk, arms, and legs. Bone infection may develop |
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Treponema denticola
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Causes peridontal disease when there is a species imbalance in the oral cavity.
Peridontal disease may lead to endocarditis Virulenc factors: Peptidases, complement binders, and proteases that allow organism to be very destructive to create deep anaerobic pockets where it can grow |
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psittacosis
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Disease carried by birds
Caused by Chlamydia psittaci |
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Borrelial hermsii
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DOC = Tetracycline
Causes Relapsing fever Transmitted by Ornithodoros ticks (tick borne TBRF) High grade fever, stopped by immune system, antigenic variation occurs, get new fever (many relapses) Virulence Factors: 1.) 40 vmp genes, but only one is bound to the promoter region and expressed at a time 2.) FhbA - Binds FH and downregulate complement Diagnosis - Microscopic examination of early spirochete filled blood smears. Need travel history |
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Baorrelial burgdorferi
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DOC = Doxycycline
Causes Lyme disease No transovarial transmission ( new larvae born uninfected) Characteristic erythema migrans rash at site of bite that expands. Also flu-like symptoms If untreated it can progress to arthritis, neurological (bell's palsy), or cardiac problems No protective immunity developed so can get reinfected Virulence factors: Easily disseminates and binds FH to block complement Diagnosis - ELISA, Western Blot 2 tier system is the best. New test is C6 ELISA |
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Leptospirae interrogans
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DOC = Penicillin G
Causes Leptospirosis characteristic hook at end of cells, grow in any moist environment, most common zoonosis, lives freely in env. (aerobic) Enter through abrasions or conjunctiva - sudden onset of flu-like symptoms (no resp. symptoms) w/ fever - can either subside or turn into Weils disease Weils disease - develops quickly and is potentially fatal. Systemic infection, renal failure, hepatic failure Diagnosis: 1.) Darkfield microscopic examination 2.) MAT microagglutination test is the best, but only performed at a few centers Can develop immunity, but only to one serobar |
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Generation Time Equation
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n= logNt - logNo / log2
Generation time = t/n |
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4 phases of growth for bacteria
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Lag phase - adaption to new medium
Exponential phase - constant growth (get generation time here) Stationary phase - No growth (toxic accumulations) Death phase |
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4 Bacterial Nutritional groups
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1.) Phtolithotrophic - Light energy source, H20 reductang source, CO2 carbon source
2.) Photoorganotrophic - light energy source, reduced organic compunds reductant source, CO2 carbon source 3.) Chemolithotrophic - Inorganic energy source, inorganic reductant source, CO2 carbon source Chemoorganotrophic - organic compunds for energy, reductant, and carbon source (all pahtogenic bacteria) |
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Acidophile examples
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Streptococci and Lactic acid bacteria (E. coli)
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MacConkey agar
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Lactose fermenters are red
Inhibit Gram (+), selective fro Gram (-) EMB plate can also be used to determine Lac (+) or (-) |
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Oxidative phosphorylation
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Glycolysis = +2 ATPs, +2 NADH, +2 pyruvate
TCA Cycle (breakdown pyruvate)(products X2 for 2 pyruvate) = +1 ATP, +4 NADH, +1 FADH, +3CO2 for carbon skeleton ETC = +34 ATP Total ATP made = +38 ATP More energy from NADH than FADH2 and more energy from O2 as e- acceptor than others all b/c of higher P/O ratio |
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Anapleurotic reactions
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"Filling up" reactions that replace intermediates for critical pathways
ex.) TCA intermediates replaced by fixing CO2 via pyruvate carboxylase |
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Predisposing factors to Opportunistic infection
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1.) Damage to epithelium
2.) Presence of foreign body 3.) Transfer to a site outside normal niche (E.coli in urethra) 4.) Immunosuppression 5.) Damage from primary infection (pneumonia after flu) 6.) Disruption of normal flora by antibiotics (Clostridium difficile) |
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Things that transmit infection (6 "Fs")
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1.) Fomites - contaminated objects (nail)
2.) Flies - arthropod vectors 3.) Feces 4.) Fingers 5.) Fornication 6.) Food |
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Auxotrophy
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Inability to grow on a defined minimal medium without nutritional additive
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Types of mutations
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Transition - Pt. mutation that replaces purine with a purine
Transversion - Pt. mutation that replaces purine w/ pyrimidine Frame-shift mutation Silent - no change in aa sequence encoded Missense - change in aa sequence encoded Nonsense - stop codon Intragenic suppressors - Second mutation that occurs WITHIN the same gene that corrects for the effect of a previous mutation Extrageinic suppressors - Second mutation that occurs OUTSIDE of the gene that corrects for the first mutaiton (ex. - different tRNA) |
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Transposons
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genetic elements that can move b/w sites on DNA by non-homologous recombination
Results in insertion mutation Homologous recombination b/w 2 copies in the SAME orientation = deletion mutation Homologous recombination b/w 2 copies in the OPPOSITE orientation = inversion mutation (DNA still there, but pointing the other way) |
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Genetic tests -
Fluctuation test Replica Plating test Ames test |
Fluctuation test - Exposure to bacteriophage selects for pre-existing cells w/ resistance so you see a fluctuation in the amount of cells that survive
Replica Plating test - Find bacteria resistant to streptomycin, go back to plate that had never been exposed to streptomycin, select that colony and can grow on streptomycin plate Ames test - Type of bacteria that requires Histidine to grow (need mutation to grow). Expose bacteria to oxidase ( a mutant) and drug being tested to determine how mutagenic drug is. |
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Morbidity rate
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# new cases / # individuals in population
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Case fatality rate
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# deaths / # with disease
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Prevalence rate
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# infected at specific time t / # in population at specific time t (diseased + well)
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Pulse -field gel electrophoresis (PFGE)
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Digest DNA w/ restriction enzyme, separate fragments w/ electrophoresis, photograph stained gel
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Multi-locus sequence typing
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Amplify several housekeeping genes by PCR, determine DNA sequence of each and determine how related they are
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RT-PCR
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Amplify several genes by RT-PCR, determine DNA sequence of each and compare
Blast search |
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Hfr cells
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Cells in which a plasmid has been integrated into the chromosome
When conjugation occurs here the entire chromosome can be passed instead of just the plasmid. tra operon is the last to be transferred so these recipients are not able to become donors and stay F- The plasmid can also get back out of the chromosome and take some new segments with it to form a new F' plasmid (Recipients CAN become donors - F+) |
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Lysogenic conversion
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When a virus integrates into a recipient and the virus's normal genes confer new properties upon the recipient
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Toxins that cause diarrhea by stimulating Gs
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Cholera toxin
E. coli heat-labile toxin (LT) Shiga toxin from Shigella dysentariae All these cause "rice water stool" (self limiting) |
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Types of botulism
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1.) Foodborne botulism - toxinoses
2.) Infant botulism - Ingestion of spores in honey. Killed by GI flora of adults 3.) Wound botulism - very rare w/ symptoms like foodborne type |
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Superantigens
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No processing required
Bind to the side of MHC Class II (not in normal spot) Induce massive T cell activation that leads to shock Adaptively, the bacteria is trying to induce all of the T cells to be used up so this is why they evolved this capability |
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Physiological responses to LPS
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After binding to LPS binding protein (LBP)
1.) fever - TNF, IL-1, IL-6 2.) Intravascular coagulation 3.) Hypotension - due to complement cascade 4.) Vascular collapse and multi organ failure |
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Complement
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C3 cleaved into C3a and C3b
C3a - inflammation C3b - opsonization C5 cleaved into C5a and C5-C9 attack complex formation C5a = inflammation C5-C9 = bacterial lysis |
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3 functions of Ig secreted by B cells
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1.) Neutralization
2.) Opsonization 3.) Complement activation |
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Oxidase test
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Tells you that the organism has active cytochrome oxidase
Helps to distinguish Fermenters (such as Enterobacteriaceae) from nonfermenters (Pseudomonas) |
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Indole test
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Detects bacteria that convert tryptophan to indole
Used to identify E.coli, which are (+) for this test |
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List the 7 Gram (+) bugs
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1.) Streptococcus
2.) Staphylococcus 3.) Enterococcus 4.) Bacillus 5.) Clostridium 6.) Corynebacterium 7.) Listeria And BV causing bugs |
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Gram stain for the following
Mycobacteria Spirochetes Mycoplasma |
Mycobacteria - weakly Gram (+), but acid fast stain better
Spirochetes - Gram (-), but need darkfield microscope to see them (have additional outer membrane for stealth) Mycoplasma - No cell wall (neither Gram + or -) |
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List the Facultative Intracellular Organisms
List the Obligate Intracellular Organisms |
Facultative Intracellular
1.) Listeria 2.) Salmonella typhi 3.) Yersinia 4.) Francisella tularenesis 5.) Brucella 6.) Mycobacterium 7.) Legionella LISTEn SALly YER FRiend BRUCE Must LEave Obligate Intracellular 1.) Chlamydia 2.) Rickettsia |
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4 bacteria that produce exotoxins that increase levels of cAMP
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c = Cholera (Vibrio cholera)
A = Anthrax (Bacillus anthracis) M = Montezuma's revenge (E. coli) P = Pertussis (Bordetella pertussis) Pertussis toxin actually causes inhibition of Gi, which stimulates cAMP |
