Microbiology notes for November 30 and December 2nd

Microbiology, November 30, 2009
RNA not Retro viruses use RNA replicase to replicate.
Host-pathogen interactions
Questions to consider:
• How do pathogens and hosts influence each others’ evolution?
• How does ecology contribute to the ability of pathogens to cause disease?
• Do pathogens inevitably evolve to become less virulent to their hosts?
• Why do bacteria make “toxins”?
• What is the difference between a pathogen and normal flora
I. Terminology
a. Incidence vs. Prevalence
Incidence – Number of new cases of disease/total number of people in population
Prevalence – Total number of a disease in a population/Total number of people in population
b. Epidemic – The increase in the incidence of a disease
c. Reservoir – Where microbe {that  disease}(the disease causing organism) (habitually) exists in nature, usually. (ex. HIV  in humans) (C. perfringens  in soil) (V. fischeri  in squids or seawater) Over time, most microbes become less virulent in reservoir. (Most microbes tend to be less virulent in their reservoir.)
d. Vector – organisms that transmits infectious disease (that carries a microbe) from host to host (not all microbes have vectors) (ex. Y. pestis (plague) vector is a flea
e. Virulent – Microbe that causes symptoms
Virulence – ability to cause symptoms.
f. Virulence Factor – Any chemical made by a pathogenic microbe that contributes to that microbe’s ability to cause symptoms
g. Invasive disease – Infectious disease where symptoms because of microbes growing in what, in a healthy host, is a sterile site(heart blood and deep muscle tissues)
- i. Invasion factors – chemicals produced by microbes that cause disease (pathogen) that allow those pathogens to get into normally sterile tissue
h. Toxigenic Disease – infectious disease where the symptoms are caused by a toxin that is secreted by the bacteria growing in a normally not sterile site. (microbes growing in normally not sterile site, producing “toxin” that  symptoms in host) (ex. Toxic shock syndrome (exotoxin) – S. aureus can produce TSST-1 in an aerobic environment. )
- i. Exotoxin – Protien that is expressed by activily growing bacteria  symptoms
- ii. Endotoxin = Lipid A of LPS is expressed by dead bacteria because Lipid is in cell wall. Not secreted by activily growing bacteria but is secreted by dying bacteria which can cause septic shock or other diseases.
II. Two Examples of toxigenic bacterial diseases
a. Botulism
i. Clostridium botulinum – secrete botox and are anaerobic spore forming bacteria. (like other clostridia sp., they are strict anaerobes, spore-forming) Spores very durable suspended-animation state of bacteria. Reservoir: soil.
ii. Botulism toxin – actively growing C. botulinum expresses this (ex. Of exotoxin) Deadly dose: 1ng/kg weight of person. Death from suffocation – BoTox disables motor neurons, including those that control diaphragm  can’t breath
iii. Botulism food poisoning – Anaerobic environment created canning  germination of C. botulnim spores  expression of botox gene  lots of botox in jar
iv. Infant botulism and normal flora – human gut is non-sterile, anaerobic, C. botulinum spores in soil, elsewhere – Gut a good place for C. botulinum to grow. – EXCEPT that, in heathly adult, normal flora fills spots for C. botulinum to grow. – human gut is non-sterile, anaerobic in infants, little normal flora displace C. botulinum bacteria  “Floppy Baby Syndrome” (Don’t Feed babies Honey)