5 organisms that can cross the placenta

rubella, cytomegalo virus, HIV, Treponema pallidum, listeria


encounter, entry, spread, multiply, damage, outcome

Exogenously acquired diseases

From outside the body. Exogenously acquired diseases are those that result from an encounter with a microbe in the environment. (EX: common cold, gonorrhoea, surgical infection, malaria, typhoid fever, coccidoidomycosis)

Endogenously acquired diseases

acquired diseases from agents present in or on the body (normal flora)
EX: cut can lead to the production of pus caused by the staphylococci that inhibit healthy skin


the presence of microorganisms in a site of the body that may or may not lead to tissue damage and signs and symptoms of disease


condition whereby colonisation within a human host progresses to cause disease

What is the most common infection?

Respiratory infection


Entry w/o penetration through tissues (w/o crossing epithelial barriers)
EX: cholera, whooping cough, bladder infections


Entry into tissues after crossing epithelial barriers
EX: insect bites, cuts and wounds, organ transplants, blood transfusions, and inoculum size

Inoculum size

the # of invading organisms

Bacteria from body sites

skin: e. coli, staphylococcus epidermidis, s. aureus
vagina: streptococci, staphylococci, bacteroides, fusobacterium

Resident biota

a large array of microorganisms that favourably inhabit the human body in abundance

Transient microbiota

colonises the superficial layers of the skin; amendable to removal by routine hand hygiene.

transient v. resident microbiota

transient microbiota are present for a relatively short time


cause disease when given opportunity

5 roles of normal flora

- Microbial antagonism: the most significant (competitive exclusion)
- Stimulate the immune system and provide antigens to train IS
- Provide vitamins B12 and K
- Can be a common source of infection
- Help digestion


The relationship btwn normal microbiota and the host
commensalism, mutualism, parasitism


one organism benefits and the other is unaffected


both organisms benefit


One organism benefits at the expense of the other

What kind of symbiotic relationship exists btwn humans and members of their normal microbiota?


Why is skin a hostile place for bacteria?

- Crowded conditions (keep out invaders)
- Dry skin
- High salt
- Sloughing off of dead cells

Microbiota can grow back to near-normal numbers within

approx. one day

Losing a large area of the skin (burn victims) most probable cause of death

Psuedomembranous colitis

Pseudomembranous colotis

antibiotic associated diarrhoea caused by Clostridium difficile

Harmful effects of normal biota

- use vitamins
- chemical conversions

Helpful effects of normal biota

- Microbial antagonism
- Stimulate the immune system
- Provide supplemental vitamins (B12 and K)

The three challenges

nutrition, occupancy, and resistance

Nutrition as a challenge

intermittent availability of food

Occupancy as a challenge

need to remain in a certain habitat - avoid being washed away by liquid

Occupancy as a challenge


Resistance as a challenge

resistance to damaging agents such as antibiotics

Feast and famine

Bacteria feast for a given time then go through famine stage. This increases bacterial population growth rate but decreases total population size.


Bacteria must be able to remain in a given place and avoid being washed away by liquid contents

T/F: All bacteria are smaller than eukaryotic cells?

FALSE, there are always exceptions

Small size promotes metabolic efficiency

Surface area grows slower than volume
- High SA: V increases as size of cell decreases

Issues in bacterial colonisation

- Sweep away by liquid currents: adhere to epithelial cells
- Kill microbes w/ host phagocytes
- Starve microbes for lack of needed nutrients
- Inhibit growth by secreting antimicrobial factors such as cationic peptides

Avoid being taken up

Slimy capsules

Kill the phagocyte

Toxin punches hole in neutrophil membrane

Derive needed nutrients from host cells

Lyse RBCs and use the iron

Structure of Gram (+) peptidoglycan layer

Thick multilayer peptidoglycan murein (cell wall)


sugars (glycan) chains that are cross-linked to one another via peptides; critical component in maintaining rigidity of both G+ and G-; larger role in G+

Structure of Gram (-) peptidoglycan layer

Use an outer membrane outside the murein cell wall made of Lipid A, the core, and O-antigen.

Outer membrane (G-)

- Made of Lipid A, the core, and O-antigen.
- Functions as an endotoxin.
- Protects against antibiotics and disinfects

Disadvantage of outer membrane (G-)

some bacteriophages use outer membrane proteins as attachment sites for infecting their host bacteria

Which one has Teichoic acid and Lipoteichoic acid in their cell wall?


What biological roles are played by peptides that contain D- amino acids?

- Structural function in cell wall
- Growth fitness
- Biofilm development
- Spore germination
- Signaling

How does gram staining work?

What kind of cell wall
G+ - crystal violet - no cell wall
G- - pink - cell wall

Cytoplasmic membrane

Contains the enzymes and equipment that carry out photosynthesis and respiration as well as transporting molecules in and out of the cell.

How do bacteria protect the cytoplasmic membrane?

G+ - peptidoglycan cell wall
G- : outer membrane
Mycobacterium - large amounts of waxes in cell walls


- Naturally lack cell wall
- Extremely tiny (pleomorphic cells)
- Cell membrane stabilised by STEROLS and resistant to lysis
- Offset turgor pressure by pumping Na+ out of cells
- Most important medical species: Mycoplasma pneumoniae

Most important medical species of Mycoplasma

Mycoplasma pneumoniae

Pleomorphic cells



- No nucleus (DNA in nucleoid)
- No membrane-bound organelles
- Cell wall contains peptidoglycan
- Less than several micrometers in size


- Nucleus
- Membrane-bound organelles
- No peptidoglycan is cell wall is even present
- May be 10x larger than prokaryotes in size

Flagella arrangement: Monotrichous

single flagellum at one pole

Flagella arrangement: Amphitrichous

single flagellum at each pole

Flagella arrangement: Lophotrichous

two of more flagella at one pole

Flagella arrangement: Peritrichous

flagella all over surface of cell

Structures ONLY in prokaryotes: Capsule

well organised layer composed of polysaccharides that surround cell wall

Structures ONLY in prokaryotes: Slime layer

like a capsule, but more loosely associated with cell wall.

Purpose of slime layer

1) make cell virulent
2) attachment
3) avoid dehydration

Structures ONLY in prokaryotes: Endospores

Bacillus, Clostridium, Sporosarcina: Sporolactobacillus, Thermoactinomycetes contain calcium - dipicolinic acid, heat resistant


Lack all traces of a cell wall (G+ rxn to lysozyme)


destroys bacterial cell walls


Lack most of cell wall (G- rxn to lysozyme)

L forms

strains of bacteria that sometimes lose their ability to make cell walls


genetic structure that can replicate independently from chromosomes. typically small and circular shaped; in cytoplasm of bacterium or protozoan

5 modes of action of antibiotics

- Inhibition of cell wall synthesis
- Inhibition of protein synthesis
- Inhibition of nucleic acid synthesis
- Inhibition of folic acid synthesis
- Disruption of cell membrane

Inhibition of cell wall synthesis

Penicillins, Cephalosporins, Vancomycin, Bacitracin

Inhibition of protein synthesis

Chloramphenicol, Tetracyclines, Streptomycin, Erythromycin

Inhibition of nucleic acid synthesis

Ciprofloxacin, Rifampin, some anti-viral agents

Inhibition of folic acid synthesis


Disruption of cell membrane

Polymyxin B, antifungal agents


Glycopeptide antibiotic antibiotic used for G+ infections (staphs, streps, and enterococci)


Affect peptidoglycan synthesis where biosynthetic target is absent in the host

Penicillin can...

cause strong allergic rxn

Bacitracin antimicrobial drugs...

affect many targets in prokaryotic cells

Fungal and protozoan infections are more difficult to treat because...

the cells are similar to human cells

Paul Ehrlich

developed the concept of chemotherapy to treat microbial disease

Magic Bullet

Paul Ehrlich; kill pathogens but not human cells

Alexander Fleming (1928)

discovered penicillin produced by Penicillium notatum

First clinical trials of Penicillin were done in...


The first antimicrobial agents used to cure infections in humans


Why do Sulfonamides kill bacteria without bothering the host?

Bacteria must synthesise their own folic acid. When sulfonamides are added, it competes with and ultimately displaces pBMA and stops folkc acid synthesis. Because humans cannot make folic acid, we are not bothered.

Sulfa drugs...

interfere with bacteria cell metabolism

General action...

is either by:
- Directly killing microorganisms (Bactericidal)
- Inhibiting their growth (Bacteriostatic)

A narrow-spectrum drug...

affects only a single microbial group

A broad-spectrum drug....

is effective against two or more groups of microbes

Attributes of an ideal antimicrobial agent
Solubility in Body Fluids

agents must dissolve in body fluids

Attributes of an ideal antimicrobial agent
Selective Toxicity

agents must be more toxic to microorganism than to host cells

Attributes of an ideal antimicrobial agent
Toxicity is not easily altered

The agents should maintain a standard toxicity and not be made more or leas toxic by foods or other drugs

Attributes of an ideal antimicrobial agent

No allergic rxns

Attributes of an ideal antimicrobial agent
Maintenance of constant therapeutic concentration in blood and tissue fluids

should be sufficiently stable and degraded and excreted slowly

Attributes of an ideal antimicrobial agent

Resistance by microorganisms not easily acquired

Attributes of an ideal antimicrobial agent
Shelf life

Shelf life should be long

Attributes of an ideal antimicrobial agent

Cost should be reasonable

Selective toxicity

Agents are more toxic to microorganisms than to host cells

What must Beta-Lactam antibiotics do?

- Associate with the bacteria
- In G-, must penetrate OM and periplasmic space
- Interact with penicillin-binding proteins of the cytoplasmic membrane
- Activate an autolysin that degrades the cell wall

What are the 2 classes of Beta-Lactamases?

1) Penicillinases
2) Cephalosporinases

Resistance is now...

widespread because of plasmids and jumping genes (TRANSPOSONS)


- Methicillin
- Resistant S. aureus
- Can be treated with VANCOMYCIN


Partial resistance, bacteriostatic but not bactericidal b/c the lack of sufficient levels of the suicidal autolysin


Penicillin + Streptomycin
- Penetration of streptomycin often enhanced


Chloramp + Penicillin
- Blocks per syn and prevents cell growth required for penicillin to function


Each drug works no better or no worse alone or in combination

What are supergerms?

Bacteria resistant to 15 or More antibiotics (e.g. Enterococci)

Most common resistance to antibacterial agents
Penicillins, cephalosporins, carbapenems

Modification of the drug
- Hydrolysis of beta-lactam ring by beta-lactamase

Most common resistance to antibacterial agents
Methicillin (MRSA)

Target modification: acquisition of a resistant penicillin-binding protein (NOT in b-lactamase)

Most common resistance to antibacterial agents

Efflux pump transports the drug out of the cell

Most common resistance to antibacterial agents
Aminoglycosides (gentamicin, tobramycin, amikacin, streptomycin, etc.)

Modification of the drug by R-Plasmid encoded enzyme; reduced affinity for the ribosome and reduced transport into the cell

Most common resistance to antibacterial agents

Target modification: sulfanilamide-resistant dihydropteroate synthase

Most common resistance to antibacterial agents

Target modification: trimethoprim-resistant dihydrofolate reductase

Most common resistance to antibacterial agents

Target modification: methylation of 23S ribosomal RNA

Most common resistance to antibacterial agents

Modification of the drug: acetylation of hydroxyl groups by chloramphenicol transacetylase; interference w/ transport into cell

Most common resistance to antibacterial agents
Oxazolidinones (linezolid)

Target modification: mutations in 23S ribosomal RNA

Most common resistance to antibacterial agents
Quinolones (nalidixic acid, ciprofloxacin, etc.)

Target modification: mutations in genes encoding DNA gyrase and topoisomerase IV

Most common resistance to antibacterial agents

- Target modification: change in binding site in the peptidoglycan target
- Restricted access to drug target

Most common resistance to antibacterial agents

Restricted access to drug target

Why does resistance spread so fast?

Plasmids and jumping genes (TRANSPOSONS)


Enzymes produced by bacteria that provide multi-resistance to B-lactam antibiotics (penicillins, cephalosporins, cephamycins, and carbapenems)

List 4 schemes that bacteria have evolved to gain resistance to antibiotics

1) Inactivation of antibiotics
2) Efflux pumping of the antibiotics
3) Modification of the antibiotic target
4) Alteration of the pathway

All of the following are mechanisms of resistance except:

activation of antibiotic

The best way to deal with antibiotic resistance is to use

all of the prescribed antibiotic

Resistance to antibiotics seen at the level of a ribosome is caused by

changes in the shape of the ribosome (changes in proteins around ribosomes make it impossible for antibiotic to find it)

What will allow you to classify the organism as belonging to bacteria but not archaea or eukarya?

cell walls are made primarily of peptidoglycan

Which of the following is NOT a typical characteristic of most bacterial plasma membranes?

Contains cholesterol

Do plasmids exist in other (not bacterial) cells?

YES; fungi and chloroplasts of plants

Bacteria use 3 strategies to protect their cytoplasmic membranes

1) G+ use thick multilayer peptidoglycan murein (cell wall)
2) G- use an OM, outside murein cell wall, made of Lipid A, the core, and O-antigen
3) Acid-fast bacteria, such as Mycrobacterium tuberculosis, contain large amount of waxes in their cell walls

Big 4 typical bacteria

- G+ cocci
- G+ rods
- G- cocci
- G- rods


- Treponema
- Leptospira
- Borrelia

G+ Rods

- Bacillus anthracis
- Clostridium tertani
- C. botulinum
- C. perfringens
- C. difficile

G- Rods

- Enterobacteriaceae
- Escherichia
- Enterobacter
- Salmonella
- Shigella
- Klebsiella
- Proteus
- Citrobacter
- Serratia
- Yersenia


- Vibrio cholerae
- Campylobacter jenuni
- Helicobacter pylori

Fastidious small G- Rods

- Haemophilus
- Bordetella
- Brucella
- Francisella tularemia
- Bartonella
- Legionella pneumophila


- Mycobacterium: M. tuberculosis, M. leprae


strict parasites