microbiology final studying

• invasiveness
• infectivity
• toxigenicity

motility, flagella

• adherence (adhesion proteins and pilli)
• capsules

secretion of toxins

• number of organisms present
• degree of virulence
• host defenses or degree of resistance

• Primary - usually causes disease
• Opportunistic - isn't in the right place, or over grows, if considerations are right.

the transfer of disease between species

• 1) maintain a reservoir
• 2) transport to host
• 3) adhere to, colonize, and/or invade host
• 4) evasion of host defenses
• 5) multiple or complete the life cycles on or in host
• 6) damage host

humans, animals, and environment

direct and indirect contact

• Indirect: vehicles (soil, food, and water),
• arthropods, and fomites

pilli, fimbrae, capsule and slim layer, and s layer

also charged molecules hanging outside of the cell, help it adhere

• prevention of fusion process
• secretion of pore forming proteins (to colaspe lysome)
• evading the complement system (moditification of proteins)
• antigen variation, a race to out modify the immune system

active - secretion of an enzyme tobreak down host's barrier. 

passive - through a scrap or puncture by an arthropod.

genes that cause pathology

genes that encode the virulence factors

endotoxins -  usually gram negative, toxins are in cell wall

Exotoxins - secreted proteins ofter gram postive, some of the most potent toxins.

• 1) AB exotoxins (B binds) (Not all AB are type 2)
• 2) Specific host site bonding (many are AB)
• 3) membrane disrupting exotoxins (pore forming or degrade membrane)
• 4) superantigens (overactivates the immune system)

• 1) neurotoxins (neurvous system, Botulism, tetanus)
• 2) enterotoxins, (vibrocholerae cholera)
• 3) cytotoxins (cell death, diphtheria, AB, no ribosomal created protein)

• 1) pore forming exotoxins
•      hemolysins from streptococcus and s. Aureus.

• 2) Phospholipases
•      causes necrosis of tissues
•      Gangrene is caused by clostridium profrengenes

the over reaction of the immune system

a toxins triggers the t-cell response without the antigen presenting cell (APC)

toxic shock syndrome (icky tampon!)

lipopolysaccharides (LPS) - lipid A portion of the LPS causes the disease

• t-cell binds to the lipid A portion
• not as potent as exotoxins, yes.

they are used to treat disease.  They are selectively toxic to 16S Ribosomal DNA in prokaryotes, we have 18S rDNA

Gram positive in the log phase.

Turbcurlosis (TB), kills more microbes.  Targets SS ribosomes.

thick mycolic acid, stains g(+), but more like gram (-)

• selective toxicity
• therapeutic index

(toxic dose)/(therapeutic does) = TI

• 1) minimal inhibitory concentration (MIC)
•      where no growth was seen
•     
• 2) minimal lethal concentration (MLC)
•      Where subculture does not grow

• 1) Dilution susceptibility test
•        Different concentrations of the drug in the media, differentiates the MIC from the MLC

• 2) Disk diffusion test (Zone of inhibition)
•           Cannot compare Zone of inhibition directly across different antibiotics)

• 3) Kirby-Bauer method
•            Standardized method that compares disk diffusion to the degree of microbial resistance.

• 4) Epsilemeter test
•             intersection of elliptical zone of inhibition with strips that indicate MIC (tear shape of inhibition, the microbes are sad and crying) 

"Death to the Microbes!!" Andrea, otherwise a cheerful person, but not to bad microbes.

• 1)  Inhibitors of cell wall synthesis
• 2)  Nucleic acid synthesis
• 3)  Metabolic antagonists
• 4)  Protein synthesis inhibitor

• Penicillin
•      inhibits transpeptidase
•      competitive inhibitor
• Semisynthetic Penicillin
•      broader spectrum
•      different side groups
• Cephalosporins
•      used by most patients that are allergic to penicillin, structually and functionally similar
• Vancomycin
•       Targets tetrapeptide linkages by physically binding to aminoacids and sterically blocking the glycosidic linkage and the peptidase.

• aminoglycoside antibiotics
•      cause misreading of mRNA by binding to the 30s ribosomal subunit, this is bacteriosidal
• Tetracyclines
•      reversibly binds to the 30s ribsomal subunit.  Inhibits binding of the aminoacyl-tRNA, bacteriostatic
• Macrolide
•      inhibits translocation of tRNA by binding to the 23s rRNA of the 50s ribosomal subunit, somewhat bacteriostaic
• chloramphenicol
•       inhibits peptidyl transferase reaction on 50s ribosomal subunit, bacteriostatic

bind to essential enzymes for metabolic processes by competively inhibiting use of metabolites by key enzymes

• 1) Sulfonamides
•          sulfur drugs, an analog for PABA (p-aminobenzoic acid) precurser to make folic acid
• 2) Trimethoprim
•          Interferes with folic acid as well, it is a synthetic antibiotic

higher side effects, blocks either DNA replication or DNA transcription

• Quinolones
•           bacteriosidal, targets gyrase, which is a topoisomerase

• Susceptibilty of pathogen to drug
• abiltiy of drug to reach:
•      the site of infection
•      Concentration in body that exceed pathogen MIC

Where + how + frequency of admin = speed of metabolism

• resistance can be transmitted
• mechanism is not confined to a single drug class
• resistant mutants arise spontaneously and are selected for
• Superbugs are resistant to multiple antibiotics

• 1) altered antibiotic target - mutation
• 2) antibiotic resistant genes (pick up plasmids)
• 3) antibiotic degrading enzyme
• 4) Antibiotic altering enzyme
• 5) Make pump to get out of cell

• 1) bacterial chromosomes
• 2) plasmids
• 3) transposons/integrons

• Monitor public health data
• Respond to disease outbreak
• Investigate emerging and reemerging diseases

MMWR-Morbidity mortality weekly report

• Sporadic-occurs occasionally at irregular intervals
• Endemic-steady low level frequency at moderately regular intercal maintained
• Epidemic-sudden increase in frequency above expected number
• Pandemic-increase in disease occurrence within large population over wide region (usually worldwide)

#new vs #new+ongoing

#infected vs # deaths

Objective vs subjective changes

• 1) incubation period
• 2) prodromal stage
• 3) Illness
• 4) Convalescence

• Review of death certificates
• field investigation of epidemics
• investigation of actual cases

• RS-gathering of digital images of Earth's surface
• GIS-data management systen organizes/displays digital map data

• Tries to determine:
•     Causative agent
•     source and or reservoir of agent
•     mechanism of transmission
•     host/environmental factors facilitating development of disease
•     best control methods
• Correlation with single causative agent

• Common source epidemic (food/water)
• Propagated epidemic (like strep throat)

Resistance of population to infection/spread based on immunizations ~70% optimal

• 1) Pathogen
•          Koch's Postulates
• 2) Source/Reservoir
•          S-Source of transmission to host
•           R-Normal location of pathogen
• 3) Transmission to host
•          Airborne, contact, vehicle, vector-borne
• 4) Susceptibility of host
• 5) Exit from host

• Airborne-Indirect (>1 meter) Direct (<1 meter)
• Contact-Direct (physical interaction), Indirect (intermediate usually inanimate-fomites), Droplet(large particles)
• Vehicle-Inanimate objects sometimes single vehicle pathogen to multiple hosts
• Vector-External (mechanical transmission-passive carriage of pathogen  on body of vector and no growth of pathogen during transmission), Internal (carried within vector 1-harborage transmission: pathogen does not undergo changes within vector, 2-Biological transmission: pathogen undergoes changes within vector)