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Bacterial Growth Curve Phases

- Lag: initial phase after inoculation, when the bacteria are gearing up to grow (making more enzymes for growth, etc.)

- Exponential (Log): when bacteria are growing at a steady rate (“doubling time”)

- Stationary: bacteria use up nutrients and produce waste products, growth starts to slow
o Before: Total = Viable (almost all bacteria in culture are alive)
o After: Total > Viable


How pathogens can overcome host irons equestration

The body uses iron-binding proteins (lactoferrin and transferrin) to restrict the availability of iron for pathogens

Pathogens fight back:

1) By producing their own iron-binding molecules (e.g. siderophores)

2) Some bacteria (e.g. the pathogenic Neisseria spp.) can bind human transferrin and lactoferrin to their surface and then use that bound iron



Grow only in the presence of O2

Ex. Pseudomonas aeruginosa)



A special group of aerobes requiring O2, but at lower concentrations than found in normal air

Ex. Campylobacter spp.


Facultative anaerobes

Grow in either the presence or absence of O2 (e.g. E. coli)

Grow by fermentations in the absence of O2, but shift their metabolism to respiration in the presence of O2

More ATP is produced during respiration than fermentation, so growth is faster here

Ex. E. coli



Grow in presence or absence of O2, but metabolism always uses fermentation

Ex. most Streptococcus spp.


Strict anaerobes

Grow only in the absence of O2

Ex. Clostridium spp.


Why some bacteria are anaerobic / Why anaerobes are sensitive to oxygen

Anaerobes often lack catalase (which breaks down toxic H2O2 formed after cells are exposed to air).

Anaerobes often lack superoxide dismutase (which detoxifies free radical forms of O2 that form after cells are exposed to air).

Anaerobes may have very sensitive enzymes that require a reduced environment.

Bottom line: anaerobes must be in a low redox (reduced environment) and O2
raises the redox potential.

The redox potential of healthy tissue is too high for anaerobes to grow.

Medical conditions that can lower tissue redox potential:
- Circulatory problems
- Tight orthopedic casts
- Co-presence of facultative anaerobes (which can consume oxygen) during an infection


Body locations where anaerobes are normally found & Examples

Skin: Propionibacterium spp.

Mouth: Porphyromonas gingivalis

Vagina: Lactobacillus spp.; Prevotella bivia

Colon: Bacteroides fragilis


Gram+ Anaerobes:
Sporeforming rods (1)

Clostridium spp.


Gram+ Anaerobes:
Non-sporeforming rods (1)

Actinomyces spp.


Gram+ Anaerobes:
Cocci (2)

Peptococcus spp.
Peptostreptococcus spp.


Gram- Anaerobes:
Non-sporeforming rods (2)

Bacteriods-like group
Fusobacterium spp.


Gram- Anaerobes:
Cocci (1)

Veillonella spp.


Predisposing factors / medical conditions that can lead to anaerobic infections

Low tissue redox conditions from circulatory problems

Antibiotic therapy: can lead to Clostridium difficile infection

Bite wounds

Aspiration of mouth flora into the lungs

Spillage of intestinal contents into the peritoneal cavity due to perforation of the
GI tract


Bacteriodes-like Bacteria:
Characteristics & Entry

Gram- anaerobic rods

Found as normal flora in colon, vagina, & mouth

Cause endogenous infections (breeching epithelium via surgery, wounds, ruptures, etc.)

Need low tissue redox for growth

Not contagious


Bacteriodes-like Bacteria:
Virulence Factors

LPS is not endotoxic

Makes a capsule (antiphagocytic)

Some make an enterotoxin but not exotoxins

Not all are equally pathogenic (B. fragilis is most likely to cause disease)


Bacteriodes-like Bacteria:
Diseases & Treatment

Disease near their normal flora colonization body site:

- Bacteroides fragilis: colon, abdominal infections that involve two stages: peritonitis and then (if untreated) abscess formation.

- Prevotella bivia: female genital tract, pelvic inflammatory disease and infertility.

- Prevotella melaninogenica and Porphyromonas gingivalis: mouth, respiratory tract infections (e.g., dental, chronic sinusitis, pulmonary infections).

Inflammation and abscess formation.

Can enter the bloodstream and cause bacteremia. Can be rapidly fatal.

Treatment for abscesses: surgical drainage and use of antibiotics effective against anaerobes (e.g., metronidazole).


Histotoxic Clostridia:
Species & Characteristics

C. perfringens: most important

C. septicum: infections in pts w/ cancer of GI tract

Gram+ anaerobic spore-forming rods

Some normal GI flora, some in soil, some in both


Histotoxic Clostridia:
Virulence Factors

Exotoxins: protein toxins made and secreted outside the cell.

α toxin: most important single toxin for C. perfringens, a lecithinase (phospholipase C) that disrupts mammalian plasma membranes.


Histotoxic Clostridia:

Both endogenous & exogenous infections

1) Entry of cells or spores into wounds, ruptures, tumors, etc.

2) Need low tissue redox for growth


Histotoxic Clostridia:

1. Wound infections

- Gas gangrene (clostridial myonecrosis): bacteria are present in muscle (low redox condition); toxins kill cells to form necrotic tissue (low redox), allowing progressive spread of infection. Toxins also enter circulation and damage distant organs. Rapidly fatal w/o treatment (if possible).

- Anaerobic cellulitis: somewhat less serious, involves only cutaneous and subcutaneous tissue.

- Simple wound infections: least serious, only involves cutaneous tissue.

2. Organ infections: e.g., uterine infections

3. Septicemia/bacteremias

4. C. perfringens type A food poisoning: 3rd most common food poisoning; not usually life-threatening, an enterotoxin causes diarrhea and abdominal cramps.


Histotoxic Clostridia:

Very difficult for gas gangrene

i) Removal of affected tissue by surgery (must be performed early in infection), often involves amputation. Antibiotics are in a supportive role.

ii) Hyperbaric O2 (?)

iii) Prevention: keep wounds clean.


Bacterial Endospores:

Formed by...


Resistant to...


Why resistant

Bacillus (aerobic or facultative anaerobic) and Clostridium (anaerobic)

Survival response to a poor environment, not a reproductive strategy

- Heat
- Radiation
- Chemicals (some disinfectants)
- Drying

Aimed at killing bacterial endospores to kill all other life forms

- Low internal water
- Rich in DNA stabilizing proteins
- Lack metabolism ("suspended animation")


Diseases that can be transmitted by bacterial endospores

Anthrax: Bacillus anthracis

Tetanus: Clostridium tetani

Infections caused by the histotoxic clostridia (C. perfringens)

Clostridium difficile


Tetanus (C. tetani):


Virulence Factors


Gram+ spore-forming anaerobic rod found in soils

Tetanus neurotoxin inhibits release of inhibitory NTs --> uncontrolled muscle contractions --> lethal

- Implantation of spores at a wound or during childbirth
- Spore germinates into a new cell & makes tetanus toxin
- Long incubation time while waiting for proper conditions to grow & germinate


Tetanus (C. tetani):




1) Toxin produced in wound and then migrates along nerves into CNS

2) Toxin blocks inhibitory neurotransmitter release; muscles are constantly stimulated.

3) Convulsive muscle contractions of voluntary muscles of the jaw (trismus, lockjaw), back, extremities.

4) Death results from respiratory failure.

Treatment: very difficult, give tetanus antitoxin, muscle relaxants and assisted ventilation.

Prevention: The disease itself does not confer immunity but immunization can be induced using tetanus toxoid.