Microbiology Exam 2- Lecture Questions

What are the basic shapes of prokaryotic cells?

• Bacillus

• Coccus

• Vibrio

• Spirillum

• Spirochete

• Cocobacillus

Bacillus

Rods

Coccus

Spheres

Vibrio

Curved rods

Spirillum

Rigid spiral shape

Spirochete

Flexible spiral shape

Cocobacillus

Short, plump rods

How does cell division create different types of groupings in cocci?

Cells adhere together after cell division leading to characteristic arrangements (depending on plane of division)

Diplococci

Pair of cocci

Tetrad

Four cocci

Streptococci

Chains of cocci

Staphylococci

Randome arrangement, grape-like clusters

Sarcina

Two tetrads (eight cocci)

Three types of bacilli arrangements

• Diplobacillus (pairs)

• Streptobacillus (chains)

• Coccobacillus

Differences among spiral bacteria forms

• Vibrio is comma-shaped

• Spirillum is thick and rigid

• Spirochete is thin and flexible

What other types of atypical morphologies are often included with rods?

• Palisade arrangement

• Clostridium

• Filamentous

Palisade Arrangement

Bacilli joined lengthwise, not just at ends

Clostridium

Tennis rackets w/1 swollen end

Filamentous

Mold-like

Pleomorphic Bacteria (Definition + example)

• Able to change shape in response to environmental pressures or because of their structure

• Mycoplasma (lack cell wall)

Typical components of prokaryotic cells

• DNA

• Cell membrane

• Cytoplasm

• Ribosome

• Cytoplasmic filaments

• Flagella

• Cell wall

DNA purpose

Genetic organization

Cell membrane purpose

Cell compartmentation + metabolism

Cytoplasm purpose

Metabolic organization + lipid/protein transport

Ribosome purpose

Protein synthesis

Cytoplasmic filament purpose

Cell structure + support

Flagella purpose

Cell motility

Cell wall purpose

Water balance

Advantages of having one or more plasmids

• Can be transferred between cells during genetic recombination

• May code for different proteins → genetic flexibility

Peptidoglycan (Gm-, Gm+)

• Yes, thin

• Yes, thick

Teichoic Acid (Gm-, Gm+)

• No

• Yes

Lipoteichoic Acid (Gm-, Gm+)

• No

• Yes

Outer Membrane (Gm-, Gm+)

• Yes

• No

Lipopolysaccharide (Gm-, Gm+)

• Yes

• No

Porin Proteins (Gm-, Gm+)

• Yes

• No

Periplasm (Gm-, Gm+)

• Yes

• No

Peptidoglycan Function

Prevents bacteria from lysis, maintains cell shape, and protects cells from environment

Teichoic Acid Function

Aids in flexibility by attracting cations

Lipoteichoic Acid Function

Unknown function

Outer Membrane Function

Additional stability, helps keep out toxic materials

Lipopolysaccharide Function

Found on outer membrane of Gm- cells, lipid portion acts as endotoxin upon disintegration of cells/binary fission

Porin Protein Function

Acts as channels for passage of small molecules

Periplasm Function

Metabolic region between cell and outer membranes in Gm- cells

Source (Exotoxin, Endotoxin)

• Living Gm+ and Gm- cells

• Lysed Gm- cells

Location (Exotoxin, Endotoxin)

• Released from living cells

• Part of cell wall

Chemical Composition (Exotoxin, Endotoxin)

• Protein

• Lipopolysaccharide

Heat Sensitivity (Exotoxin, Endotoxin)

• Unstable

• Stable

Immune Reaction (Exotoxin, Endotoxin)

• Strong

• Weak

Conversion to Toxoid (Exotoxin, Endotoxin)

• Possible

• No

Fever (Exotoxin, Endotoxin)

• No

• Yes

Toxicity (Exotoxin, Endotoxin)

• High

• Low

Toxic Dose (Exotoxin, Endotoxin)

• Small

• Large

How are Gm+ peptidoglycan backbones linked together?

Peptide Interbridge

How are Gm- peptidoglycan backbones linked together?

Pentaglycine cross bridge

How does transpeptidase recognize sites and achieve linkages?

Forms cross bridge when D-alanine is released

Where is lysozyme found in the human/animal body?

Bodily secretions (saliva, tears, milk)

Lysozyme Function

Cleaves peptidoglycan component of cell walls → cell death, also breaks down glycosidic bonds in chitin

What type of bacteria (Gm+ or Gm-) is more susceptible to enzymatic degradation by lysozyme?

Gm+, because they have much thicker peptidoglycan layer

How did the discovery of antibiotics change the outcome of infectious disease?

• Previously, getting even small cuts could be deadly

• Antibiotics thought to “end all infections in man”

What warnings were issued with the discovery of antibiotics?

“evil in self-medication” through inadequate doses → resistance rather than clearance

Antibiotic

Substance naturally produced by bacterial and fungal species that inhibit or kill other microorganisms

Semisynthetic Drug

New-generation antimicrobials, chemically-modified antibiotics

Synthetic Drug

Manufactured entirely in a pharmaceutical lab

Broad-Spectrum Drug

Targets many taxonomic groups

Narrow-Spectrum Drug

Targets a few pathogens

Transpeptidation

Linking of two peptide chains (in peptidoglycan)

How do beta-lactam antibiotics (like penicillin) work?

• Resembles peptide interbridge site

• Allows penicillin to bind transpeptidase and transglycosylase, preventing their activity in manufacturing peptidoglycan linkages

Bactericidal Drugs

Any agent that KILLS bacterial cells

Bacteriostatic Drugs

Any substance that prevents the growth of bacteria (keeps them in stationary phase → death)

Which type of bacteria are beta-lactam antibiotics more effective against? Why?

• Gram-positive

• Inhibit enzymes that form peptide bridges between adjacent glycan chains in peptidoglycan → more in Gm+

When are bacteria the most susceptible to beta-lactam antibiotics?

When cell wall actively synthesizing (i.e. binary fission)

Acid-Fast

Thick peptidoglycan layer and mycolic acids enable species to resist decolorization by acids during staining (red, all else will be blue-green)

Why are infections with acid-fast bacteria so hard to treat?

May create acids that inactivate antibiotics, difficult for them to make it through the cell envelope

Mycobacteria Cell Envelope Structure (Inside → Outside)

• Cell membrane

• LAM from cell membrane to outside

• Lipoprotein

• Peptidoglycan

• Arabinogalactan (porin proteins may extend through)

• Mycolic acid

• Glycolipids

Can Mycoplasma infections be successfully treated with beta-lactam antibiotics? Are they susceptible to lysozyme treatment?

• No, lack cell wall (no peptidoglycan)

Possible targets of antibiotics (other than cell wall)

• Nucleic acid synthesis

• Metabolic processes

• Protein synthesis

Antibiotic that interferes with nucleic acid synthesis

Quinolone

Quinolone Target

Targets microbial topoisomerase

Antibiotic that interferes with metabolic processes

Sulfanilamide

Sulfanilamide Target

Enzyme necessary for production of folic acid

Antibiotic that interferes with protein synthesis

Tetracyclines

Tetracycline Target

Blocks ribosome docking site of tRNA

Aminoglycosides

Change 30S subunit shape → misread mRNA

Macrolides

Binds to 50S subunit and prevents mRNA from moving through ribosome

Chloramphenicol

Inhibits peptide bond formation

Selective toxicity of aminoglycosides, tetracycline, macrolides, and chloramphenicol

All interfere with function of bacterial rRNA (not the same as eukaryotic rRNA)

How do sulfa drugs exhibit selective toxicity?

Humans lack the folic acid pathway, so sulfa drugs only affect bacteria

Selective Toxicity

Drugs harm pathogen but NOT the host

Chemotherapeutic Index

Toxic dose divided by therapeutic dose

Toxic Dose

Concentration causing harm to host

Therapeutic Dose

Concentration eliminating pathogens in host

Why is the chemotherapeutic index important?

A larger index means a drug is safer (less toxic, more therapeutic)

Other factors that affect effectiveness of a drug

• Growth phase of bacteria treated

• Inoculum size

• Serum effect

• Interaction w/host gut microbiota

Advantage of broad-spectrum drug

Effective against a wide range of bacteria (especially if unsure exactly what is infecting)

Disadvantage of broad-spectrum drug

May target normal flora of the host

Antagonism

One drug inhibits the effect of another when used in combination

Synergism

A combination of drugs is more effective than if either are used individually

Why are synergism/antagonism under extensive study?

As more multi-drug resistant organisms arise

Erythromycin (50S ribosome inhibitor) + Penicillin…

• Erythromycin is bacteriostatic, meaning it stops growth

• Stops cell wall synthesis

• Insensitivity to penicillin

Aminoglycoside (protein synthesis inhibitor) + Cephalosporin (beta-lactam)…

Cephalosporin may weaken the cell wall, which allows the aminoglycoside into the cell