Micro Exam 1 Block 1

Front 1

phenotypic bacteriology classification schemes

Back 1

colony and cellular morphology
-biotyping
-serotyping
-antibiotic susceptibilities
-phage typing

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difference b/w pili and fimbriae

Back 2

pili are longer and used during conjugation and may have phage receptors
-fimbriae are used for adhesion to host cell.

Front 3

benefit to having capulse

Back 3

-aid in adhesion to surfaces
-aid in phagocytosis resistance

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gram positive cell wall

Back 4

1. plasma membrane
2. peptidoglycan

-has periplasmic space

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gram negative cell wall

Back 5

1.outer membrane
2. peptidoglycan
3. plasma membrane

-has periplasmic space

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gram-staining procedure

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1.crystal violet for 30 seconds, water rinse 2 seconds
2. gram's iodide 1 minute, rinse w/ water
3. wash with 95% ethanol or acetone for 10-30 sec, water rinse
4. safranin 30-60 seconds, water rinse and blot

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koch's postulates

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1. the suspected pathogenic organism should be present in all cases of the disease and absent from healthy animals
2. suspected organism should be grown in pure culture
3. cells from the pure culture of the suspected organism should cause disease in a healthy animal
4. the organism should be reisolated and shown to be the same as the original

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laboratory diagnosis of bacterial agents of disease

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1. staining techniques
2. biochemical tests
3. types of hemolysis
4. antibiotic susceptibilities
5. serological tests
6. nucleic acid-base testing

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9 serological methods of classification/identification

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Ouchterlony immunodouble diffusion
Immunofluorescence
Enzyme immunoassay
Immunofluorescence Flow Cytometry
Western blot
Radioimmunoassay
Complement Fixation
Hemagglutination inhibition
Latex agglutination

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6 molecular methods of classification/id

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Guanine plus Cytosine ratio
Nucleic Acids Hybridization
Nucleic Acids Sequence Analysis
Plasmid Analysis
Ribotyping (rRNA RFLP analysis)
Chromosomal DNA fragment analysis

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3 ways to measure cell growth

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1. plate count
2. optical density
3. direct microscopic counts

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toxic forms of oxygen

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superoxide
hydrogen peroxide
hydroxyl radical
-often formed near nucleic acids in DNA and cause mutations

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3 ways new genetic material gets horizontally transferred in to bacterial cells

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1. transformation: uptake of "naked" DNA directly from environment
2. transduction: phage-mediated transfer of DNA
3. conjugation: transfer via cell-cell contact; pilus mediated

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antibacterial agents

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1. antiseptics: can be used on living tissue
2. disinfectants: used on inanimate objects
3. sterilants: strong disinfcectants
4. antibacterial chemotherapeutic agents: used inside the body to inhibit growth

Front 15

growth factor analogs

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Compounds that resemble molecules that are vital for bacterial growth. These are things that we can make (ex: in chemistry lab). Looks like another molecule but doesn’t work quite like it.

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antibiotics

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Molecules produced by microorganisms (bacteria, molds, yeasts) that kill other microorganisms. These natural products may be chemically modified to increase their efficacy (semisynthetic antibiotics)

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antibiotic spectrum

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the range of species for which an antibiotic is effective

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bacteriocidal

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antibiotic quality indicating that the affected bacteria are killed

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bacteriostatic

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antibiotic quality in which bacterial growth is reversibly inhibited

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antibiotic synergism

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effect of a combination of antibiotics is greater than the sum of either antibiotic separately

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antibiotic antagonism

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interference of efficacy of one antibiotic when coupled with a second antibiotic

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benefits of normal flora to host

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Compete (normal bacteria present) with pathogenic inhabitants for real estate and nutrients within the host.

Help with metabolism to provide nutrients to the host

Produce anti-microbial products that inhibit pathogen growth

Alter the local environment to prevent growth of pathogens

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microbial inhabitants of upper respiratory tract

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staphylococci (both coagulase-plus and -minus), streptococci, and diptheriods (club-shaped, considered a rod). Also, Haemophilus, Neisseria, and Moraxella. Anaerobes outnumber aerobes, mainly due to gingival and plaque organisms like Fusobacterium and Actinomyces.
Staph arius is the one to worry about: virulent

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microbial inhabitants of ears

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(outer) Mostly coagulase-negative staphylococci (e.g., S. epidermidis). Also, potentially pathogenic organisms including S. pneumoniae and Pseudomonas aeruginosa.

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microbial inhabitants of eyes

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(surface) Mostly coagulase-negative staphylococci. Tearing helps to keep populations down. Tears have lysozyme that breaks down chain of sugars that makes cell wall of most bacteria.

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microbial inhabitants of urethra and vagina

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Gram-negative, facultative organisms like E. coli, and Proteus mirabilis.

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microflora of skin

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First line of defense, the skin is a dry and acidic environment.

Hair follicles, sebaceous fluids favor growth of anaeobes (e.g., Propionibacterium acnes

It is predominated by Gram-positive cocci-due to thick cell wall to protect in dry environment; most common are coagulase-negative staphylococci, also several hardy potential pathogens.

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4 types of nonspecific resistance as a host defense

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biological barriers
chemical barriers
general barriers
physical barriers

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specific immunity (immune response) has two types of acquired immunity (natural and artificial): name the 4 types within those

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natural:
1. active-antibodies as a result of an infection
2. passive- passed from mother to fetus
artificial:
1. vaccinations
2. antibodies produced by another animal or in vitro and given to another animal

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7 non-specific humoral defense

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Lysozyme
Lactoferrin/Transferrin
Lactoperoxidase
β-lysin
Chemotaxis Response
Properdin
Defensins

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Transduction has two cycles

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lytic and (lysogenic)

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temperate cycle

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can replicate new virions (lytic cycle) or integrate its genome into the host, replicating with the bacterium (lysogenic cycle).

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specialized transduction

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All phage particles end up with some host DNA (blue) in them. These transducing particles may or may not be infectious.
-specific sequences-ones pulled out during excision. Have recognition sites where they can bind.

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gram positive cocci

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Staphylococcus
Streptococcus

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gram positive rods (8)

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Bacillus/Clostridium
Listeria
Corynebacterium
Norcardia
Mycobacterium
Actinomyces
Propionibacterium
Lactobacillus

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gram funky

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Mycoplasma Group
Mycoplasma
Ureaplasma
Rickettsia Group
Rickettsia
Ehrlichia
Coxiella
Chlamydia/Chlamydophila

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gram negative cocci

Back 37

Neisseria
Moraxella

Front 38

gram negative rods (10)

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Pseudomonas
Legionella
Brucella
Bordetella
Francisella
Campylobacter
Helicobacter
Vibrio
Pasteruella
Haemophilus

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gram negative facultative rods (9)

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Escherichia
Shigella
Salmonella
Citrobacter
Klebsiella
Enterobacter
Serratia
Proteus
Yersinia

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anaerobes (3)

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Bacteroides
Prevotella
Fusobacterium

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spirochetes (3)

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Treponema
Borrelia
Leptospira

Front 42

three clinically important staphylococci

Back 42

Staphylococcus aureus (coagulase pos: pathogen)
S. epidermidis
S. saprophyticus
these last two are both coagulase negative)

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staphylooccus

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Micrococcus, Alloiococcus, and Stomatococcus.
All are Gram-positive, aerobic or facultatively anaerobic, grow in irregular clusters
Found in soil, water, and on the skin of humans.

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Micrococcus

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two species, aerobes, can cause opportunistic infections

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Alliococcus

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one species, slow growth, chronic otitis media agent

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Stomatococcus

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opportunistic pathogen, normal flora of oropharynx, extensive capsule, known to cause meningitis, septicemia, endocarditis, and catheter-related sepsis

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S. aureus

Back 47

Catalase-positive
Coagulase-positive

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S. epidermidis

Back 48

catalase positive
Coagulase-negative

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S. aureus Virulence Factors

Back 49

Capsule—inhibits phagocytosis
Protein A—inhibits phagocytosis, binds antibody
TSST-1—superantigen (toxic shock)
Exfoliative toxins—unknown mechanism (SSSS)
Enterotoxins
Cytotoxins
Enzymatic Factors

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Enzymatic Virulence Factors of Staphylococcus aureus

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Catalase—breaks down hydrogen peroxide
Coagulase—leads to clotting
Fibrinolysin—dissolves clots
Hyaluronidase—spreading factor; breaks down connective tissue
Lipases—break down lipids
Nucleases—break down nucleic acids
Penicillinase—cleaves β-lactam rings-gives antibiotic resistance

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S. epidermidis

Back 51

Abundant microflora of skin
When introduced to the body can lead to:
Bacteremia
Endocarditis
Urinary tract infections (also common with S. saprophyticus)
Wound infections
Medical device related infections (catheters, shunts and implanted devices)

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streptococci: categorized by group-specific carbohydrates. List the five groups

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Group A—S. pyogenes, S. anginosis
Group B—S. agalactiae
Group C—S. dysgalactiae
Group D—S. bovis, Enterococci
Non-Groupable—S. pneumoniae and viridans group

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streptococci: categorized by hemolysis

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Alpha—Group D and non-groupable
Beta—Serogroups A, B, C, F, and G (usually)
Non-hemolytic (gamma)—Some group D and non-groupable

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Group A β-hemolytic Streptococci
GABHS

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Gram-positive cocci in long chains
PYR-positive
Catalase-negative
Encapsulated
Bacitracin sensitive- most of the other ones are resistant

Front 55

S. pyogenes Virulence Factors

Back 55

Capsule-Antiphagocytic
Lipoteichoic acid-Adherence
M-protein-Adhesin/antiphagocytic
M-like protein-Binds Ig (also adherence)
F-protein-Adherence
Pyrogenic exotoxins- (Spes)Immune system effects
Streptolysin S- Non-immunogenic cytolysin(lyse open blood cells)
Streptolysin O- Immunogenic cytolysin
Streptokinase- Lyses clots; facilitates spread
DNase- Degrades DNA-allows to spread
C5a peptidase- Degrades C5a-prevents from being consumed by immune system

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M proteins

Back 56

Made of two α-helical proteins

C-terminal is highly conserved and anchored in CM

A-terminus is exposed and variable, >80 serotypes

Involved in binding cell surfaces, preventing phagocytosis, and degrading complement

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S. pyogenes Diseases

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Wide variety of acute diseases, some with immunologic complications

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acute diseases of S. pygoenes

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Pharyngitis—S. pyogenes is the major bacterial cause of pharyngitis (strep throat)
Scarlet fever—disseminated rash in strains with pyrogenic exotoxins (phage encoded)-possibility from sore throat
Skin infections (similar to staph)
Streptococcal Toxic Shock Syndrome (usually more organisms in bloodstream rather than superorganism.

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non-supportive complications

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Rheumatic fever—sequelae of pharyngitis, antibodies develop to host tissue
Acute glomerulonephritis—caused by M12 type strains, immune complexes bind to glomeruli

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Group B β-hemolytic StreptococciStreptococcus agalactiae

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Group B antigen
Gram-positive cocci in chains
Catalase-negative
Bacitracin resistant
Encapsulated
CAMP-positive
Hippurate hydrolysis-positive
Causes purple color and diognostic for Group B

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S. agalactiae

Back 61

Normal flora of upper respiratory tract and female genital tract (20% of women)

Major cause of neonatal septicemia, meningitis, and pneumonia
Common cause of infections of the urinary tract, wounds, and blood

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Streptococcus pneumoniae
(pneumococcus)

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Gram-positive
Catalase negative

lancet-shaped
(diplo)cocci

Bile sensitive-most of the others are resistant

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Pneumococcal Traits

Back 63

α-Hemolytic

Encapsulated

Optochin sensitive

Quellung reaction positive-capsule puffs up

Front 64

S. pneumoniae virulence factors

Back 64

CAPSULE—important virulence factor that inhibits phagocytosis by blocking opsonization
IgA protease—enhances colonization
Teichoic acids—cell wall components involved in adherence
Pneumolysin O—hemolysin, inhibits phagocyte oxidative burst
Produces Hydrogen peroxide—reactive oxygen species. Helps in competition with other bacteria and host interactions.

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pneumococcal diseases

Back 65

Pneumonia—major cause of bacterial pneumonia
Meningitis—Spread to CNS can occur from invasion from other sites or following trauma.
Upper Respiratory Tract (and related) Infections
Sinusitis
Otitis Media
Bacteremia—complication of pneumonia or meningitis (what happens when spreads t bloodstream)

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bacterial pneumonia

Back 66

S. pneumoniae is the leading cause, especially in adults.
Characterized by a shaking chill, high fever, and blood-tinged “rusty” sputum.
Often follows a viral infection (influenza or measles)
Oropharyngeal populations are aspirated and circumvent normal defense mechanisms
COPD (coronary obstructive pulmonary disease) and alcoholism are common risk factors

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viridans group streptococci

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Heterogeneous group
Mostly α-hemolytic (causes green color)
Optochin resistant

Normal flora of oropharynx, genitourinary tract, and gastrointestinal tract.
Diseases:
Dental caries- Streptococcus mutans, S. sanguis
Subacute Bacterial Endocarditis- S. bovis and others
Abdominal infections-S. anginosis

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enterococci

Back 68

Originally considered Group D Streptococcus
Normal flora of colon and genital and urinary tracts. Can survive for weeks on dry surfaces.
-Gram-positive
Catalase-negative
PYR-positive
Variable hemolysis (usually gamma)
Bile Esculin Positive
Resistant to 6.5% NaCl
Keeps other conc down

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bile esculin agar

Back 69

Formation of esculetin from esculin in the presence of bile is uncommon.

Ferric citrate reacts with esculetin to form a black-brown precipitate.

Bile inhibits growth of most Gram-positives.

Sodium azide inhibits growth of Gram-negatives.

6.5% NaCl is inhibitory to the growth of most

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pathogentic enterococci

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Most important members are Enterococcus faecalis and E.faecium

Most infections are from endogenous flora but hospital acquired infections are increasing problem (VRE strains).

Bile and salt resistance allow biliary infections
Urinary tract infections
If introduced into the blood stream, enterococci can colonize damaged valves (endocarditis

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Vancomycin Resistant Enterococci (VRE) andMultiple Drug Resistant Enterococci (MDRE)

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Enterococci are inherently resistant to many antibiotics. (e.g., oxacillin, cephalosporins)

They acquire resistance readily through horizonal transfer (e.g., vancomycin, aminoglycosides)

Increasing problem in hospital- acquired infections

Consequence of indiscriminate antibiotic use

No reliably effective treatment

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2 gram positive cocci (of 6 that cause disease in humans)

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streptococcus and staphylococcus

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two of 4 gram positive rods that produce spores (of six that cause disease in humans)

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bacillus and clostridium

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two of 4 gram pos rods that don't produce spores (of six that cause disease in humans)

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corynebacterium and listeria

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gram positive that does not release exotoxins, but does release endotoxins

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listeria monocytogenes

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pyrogenic exotoxins

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stimulate the release of cytoines and can cause rash, fever, and toxic shock syndrome: staphylococcus aureus and Streptococcus pyogenes

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diff between exo and endotoxins

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endotoxin is not a protein excreted from cells, but is a normal part of the outer membrane that sort of sheds off, especially during lysis. Except listeria monocytogenes, all endotoxins are only present in gram negative bacteria

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rifampicin

Back 78

binds to RNA polymerase (not to human polymerase though due to specific enzyme)
(antimicrobial chemotherapeutic agents)

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Β-Lactams
Penicillins
Cephalosporins
Vancomycin

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antibiotics that inhibit cell wall growth
-bind to penicillin binding proteins
(antimicrobial chemotherapeutic agents)

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Trimethoprim
Sulfonamides

Back 80

look like folic acid metabolism intermediates
(antimicrobial chemotherapeutic agents)

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5 general mechanisms of resistance

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Target modification
β-subunit of RNA polymerase (rifampicin)-prevents transcription.
Antibiotic efflux*
Tetracycline efflux in enteric bacteria
Antibiotic modification*
β-lactamase (penicillinase)
chloramphenicol acetyltransferase
Resistant pathways
Circumvention of folic acid synthesis (sulfonamides)
Antibiotic impermeability
Penicillin in Pseudomonas aeruginosa
(*denotes those that can be horizontally transferred)