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106 Cards in this Set

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Multiple Flagella going in the same direction

Ex.) Bartonella baciliformis
Multiple flagella coming off of opposite ends

Ex.) Spirillum serpens
Multiple flagella found all over the bacterium

Ex.) Escherichia coli
What alternating sugars form the backbone for Peptidoglycans?
N-acetylglucosamine & N-acetylmuramic acid
Steps in Gram stain procedure
1.) Stain w/ crystal violet
2.) Wash w/ iodine
3.) Decolorization w/ alcohol
4.) Stain w/ Safranin

Blue = Gram +
Red = Gram -
Stages of peptidoglycan biosynthesis
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
Fosfomycin / Cycloserine
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
Vancomycin / Ristocetin
Prevent Stage 2 of peptidoglycan synthesis

Bind to D-Alanine-D-alanine and prevent its transfer to the acceptor
Prevent Stage 2 of peptidoglycan synthesis

Inhibits dephosphorylation of lipid carrier
Penicillin / Cephalosporine antibiotics
Inhibits Stage 3 of peptidoglycan synthesis

Inactivates transpeptidase, which prevents cross-linking
Antibiotic that inhibits bacterial DNA gyrase

Nalidixic acid and Ciprofloxacin
Antibiotic that inhibits transcription by binding to the beta subunit of bacterial RNA polymerase
Tetracyclines / Aminoglycosides
Antibiotic that binds to the 30S ribosomal subunit to prevent protein synthesis
Chloramphenicol / Erythromycin / Clindmycin
Antibiotics that inhibits binding to the 50S subunit

Erythromycin also blocks the movement
Antibiotic that inhibits bacterial metabolism by inhibiting dihydrofolate reductase
Sulfa drugs that inhibit folic acid biosynthesis by acting as a competitive inhibitor of p-aminobenzoic acid
"cord factor"
Mycobacterium tuberculosis glycolipid

Large hydrophobic mycolic acids will float around in the air and allows TB to be transmitted via coughing
2 genera of bacteria that can form spores
Bacillus and Clostridium
Calcium Dipicolinic Acid
Gives spores their high resiliency
Immune Deficiencies that Predispose People to Infections
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
Staphylococcus aureus
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
Classes of Staphylococcus aureus infection
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)
Staphylococcus aureus is the most common cause of:
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
Staphylococcus aureus Toxinoses
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
Staphylococcus epidermidis
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
Staphylococcus saprophyticus
Second to E. coli as the most common cause of UTI's

Identified by the fact that they are Novobiocin resistant
Tests to Identify different Staphylococcal strains
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
Streptococcus hemolysis on blood agar
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.)
Differentiation of different strains of Streptococcus
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)
Streptococcus Pyogenes
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.
Streptococcus Pyogenes is the most common cause of:
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
Post-streptococcal syndromes
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
Stretptococcus agalactiae
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.
Viridans Streptococci
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
Enterococcal Streptococci
DOC = Combo therapy of Ampicillin / Penicillin + Aminoglycoside b/c antibiotic resistant

Cause infective endocarditis, UTIs, and wound infections
Streptococcus bovis
Nonenterococcal Group D strept.

Susceptible to beta-lactams like penicillin

Can cause bacteremia - an indicator of colon cancer
Enterococci that are resistant to all available antimicrobial chemotherapy (beta-lactams, vancomycin, and aminoglycosides)
Streptococcus pneumoniae
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
Forms of Bacillus anthracis
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
Bacillus anthracis
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
Bacillus cereus
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
Listeria monocytogenes
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
Corynebacterium diphtheriae
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
Forms of Diphtheria vaccines
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
Bordetella pertussis
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
Bordetella parapertussis
Causes milder illness than Bordetella pertusis

Not as fastidious
Haemophilus influenzae
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
Prophylactic treatment of those that may be exposed to Meningitis causing bacteria
Haemophilus ducreyi
DOC = Azithromycin or ceftriaxone

Cause Chancroid STD

very deep, Painful lesion (syphilis lesions not painful)
Neisseria meningitidis
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
Differences b/w Neisseria meningitidis and Neisseria gonorrhoeae
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
Bacteria that commonly cause Meningitis
Neisseria meningitidis (infants & young adults)

Streptococcus pneumoniae (infants and elderly)

Streptococcus agalactiae (neonates)

Haemophilus influenzae (children)
Seroroups of N. meningitidis that are associated with specific diseases (A, B&C, Y)
Group A - Epidemic meningitis

Groups B&C - Endemic meningitis

Group Y - pneumonia
Local Neisseria meningitidis infections
All have purulent discharge

1.) Pharyngitis
2.) Pneumonia (Serogroup Y)
3.) Urethritis (purulent discharge after oral sex)
Klebsiella granulomatis
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
Gardnerella vaginalis
DOC = Clindamycin, but recurrence is common due to biofilm

Gram (+), facultative anaerobe, un-encapsulated, forms biofilms, causes Bacterial Vaginosis
Atopobium vaginae
DOC = Clindamycin

Gram (+) anaerobe that produce large amounts of lactic acid and lead to Bacterial vaginosis

resistant to metronidazole
Criteria used to diagnose bacterial vaginosis
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
Complications due to STDs
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
Stain for Mycoplasma and Ureaplasma
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)
Mycoplasma pneumoniae
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
Mycoplasma and Ureaplasma associated w/ STDs
Mycoplasma genitalium - urethritis and PID

Mycoplasma hominis

Ureaplasma urealyticum - cleaves urea, causes Urethritis
General characteristics of Spirochetes
Highly diverse
Gram (-)
Lack LPS
Visualized by dark field microscopy
Corscrew motion via endoflagella located b/w inner and outer membrane
Treponema pallidum
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
Congenital Syphilis
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
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
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
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
Treponema denticola
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
Disease carried by birds

Caused by Chlamydia psittaci
Borrelial hermsii
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
Baorrelial burgdorferi
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
Leptospirae interrogans
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

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
Generation Time Equation
n= logNt - logNo / log2

Generation time = t/n
4 phases of growth for bacteria
Lag phase - adaption to new medium
Exponential phase - constant growth (get generation time here)
Stationary phase - No growth (toxic accumulations)
Death phase
4 Bacterial Nutritional groups
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)
Acidophile examples
Streptococci and Lactic acid bacteria (E. coli)
MacConkey agar
Lactose fermenters are red

Inhibit Gram (+), selective fro Gram (-)

EMB plate can also be used to determine Lac (+) or (-)
Oxidative phosphorylation
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
Anapleurotic reactions
"Filling up" reactions that replace intermediates for critical pathways

ex.) TCA intermediates replaced by fixing CO2 via pyruvate carboxylase
Predisposing factors to Opportunistic infection
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)
Things that transmit infection (6 "Fs")
1.) Fomites - contaminated objects (nail)
2.) Flies - arthropod vectors
3.) Feces
4.) Fingers
5.) Fornication
6.) Food
Inability to grow on a defined minimal medium without nutritional additive
Types of mutations
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)
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)
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.
Morbidity rate
# new cases / # individuals in population
Case fatality rate
# deaths / # with disease
Prevalence rate
# infected at specific time t / # in population at specific time t (diseased + well)
Pulse -field gel electrophoresis (PFGE)
Digest DNA w/ restriction enzyme, separate fragments w/ electrophoresis, photograph stained gel
Multi-locus sequence typing
Amplify several housekeeping genes by PCR, determine DNA sequence of each and determine how related they are
Amplify several genes by RT-PCR, determine DNA sequence of each and compare

Blast search
Hfr cells
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+)
Lysogenic conversion
When a virus integrates into a recipient and the virus's normal genes confer new properties upon the recipient
Toxins that cause diarrhea by stimulating Gs
Cholera toxin
E. coli heat-labile toxin (LT)
Shiga toxin from Shigella dysentariae

All these cause "rice water stool" (self limiting)
Types of botulism
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
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
Physiological responses to LPS
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
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
3 functions of Ig secreted by B cells
1.) Neutralization
2.) Opsonization
3.) Complement activation
Oxidase test
Tells you that the organism has active cytochrome oxidase

Helps to distinguish Fermenters (such as Enterobacteriaceae) from nonfermenters (Pseudomonas)
Indole test
Detects bacteria that convert tryptophan to indole

Used to identify E.coli, which are (+) for this test
List the 7 Gram (+) bugs
1.) Streptococcus
2.) Staphylococcus
3.) Enterococcus
4.) Bacillus
5.) Clostridium
6.) Corynebacterium
7.) Listeria

And BV causing bugs
Gram stain for the following

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 -)
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


Obligate Intracellular

1.) Chlamydia
2.) Rickettsia
4 bacteria that produce exotoxins that increase levels of cAMP
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