Basic Concepts Of Medical Microbiology
Microbiology
Study of microscopic organisms
Medical Microbiology
Study of the characteristics of pathogens
Epidemiology
Study of health and diseases in populations
Three Major Branches: Domains
Bacteria--> Prokaryotes
Archaea
Eukaryota--> Eukaryotes
Prokaryotes
DNA: Yes--> Single Circle
Mitotic Division: No
Chromosomes: One
Membrane Bound Organelles: No
Ribosome Size: 70s (smaller)
Cell Wall w/ Peptidoglycan: Yes
Eukaryotes
DNA: Membrane-Bound Nucleus (slower)
Mitotic Division: Yes
Chromosomes: Multiple
Membrane Bound Organelles: Yes
Ribosome Size: 80s (bigger)
Cell Wall w/ Peptidoglycan: No--> No Peptidoglycan
Taxonomy
Domain
Kingdom
Phylum
Class
Order
Family
Genus
Species
Viruses
Not alive
Must infect cell to reproduce
Obligate Intracellular Parasites
Contain DNA OR RNA --> NEVER BOTH
Target bacteria the most
Obligate Intracellular Parasites
Must live inside other organisms
Prions
Infectious proteins
Ingestion of infected meat
Cause Spongiform Encephalopathy
No Treatment/Fatal
Protists
Microscopic Eukaryotes
-Algae + Slime Molds
-Protozoa + Fungi --> Cause Human Disease
Most Impressive Pathogen?
Those that cause infection in healthy people
Protozoa
Flagellates
Amebae
Sporozoa
Ciliates --> Paramecia
Trypanosoma
SOI: Blood, Lymph
Transmission: Tse Tse Fly
Causes: Sleeping Sickness
Plasmodium
SOI: Blood, Liver
Transmission: Mosquito Bite
Causes: Malaria
Entamoeba
SOI: Colon, Liver, Organs
Transmission: Fecal/Oral
Caused By: Infected Water
Giardia
SOI: Small Intestine
Transmission: Fecal/Oral
Caused By: Infected Water
Crypotsporidium
SOI: Small Intestine, Respiratory Tract
Transmission: Fecal/Oral
Caused By: Infected Water
Trichomonas
SOI: Vagina
Transmission: Sexual
Acanthamoaeba
SOI: Brain, CNS, Eye
Transmission: Nasal Membrane/ Wound
Fungi
Eukaryotic Heterotrophs
Yeasts, Dimorphic, Molds
Yeasts
Unicellular
Reproduce by Budding
Cryptococcus/Candida
Dimorphic
Endemic Fungi b/c Endemic to Certain Regions
At Room Temp--> Molds
Inhale Them--> Spread Through Body As Yeasts
Histoplasma
Molds
Multicelluar
Reproduce By Spores--> We Inhale Them
Very Hard To Treat/ Infect Sick People
Lung Transplant and Cancer Patients
Aspergillus
Size Comparison
Cells > Bacteria > Viruses > Molecules
Bacteria
Prokaryotes --> No Nucleus
Simpler
No Visible Structures
Single Chromosome Of DNA
Rigid Cell Wall (Survive Hypotonic Environment)
Cocci --> Round
Bacilli --> Rods
Spirochetes --> Spiral
Bacterial Capsule
Selectively Express or Lose
One of the ways vaccines are developed
Outermost layer
Bacterial Cell Wall
Made of Peptidoglycan
Bacterial Plasma Memebrane
Under Cell Wall
Bacterial Cytoplasm
Contains:
Chromosomes
Nucleotoids
Extra Chromosomal DNA
Free Flowing Ribosomes (In EUKARY Rib fixed on RER)
Bacterial Pilli (Fimbriae)
Help Adhere
May prevent being engulfed
Bacterial Flagellum
Whip to move
Chemotaxis
Chemotaxis
Attracted to chemicals for pathway
Gram Stain Process
1. Fixation
2. Crystal Violent
3. Iodine Treatment
4. Decolorization w Alcohol
5. Counter Stain --> Safarin
Gram (-) Cell Wall
Outer membrane
Leads to Intrinsic Resistance to Antibiotics
Porin Channels
Thin Layer of Peptidoglycan
Periplasmic Space
Periplasmic Space
B/w Peptidoglycan and Cytoplasmic Membrane
Separates Cytoplasm from Cell Wall
Gram (+) Cell Wall
Peptidoglycan
-Outermost layer, very thick
-Antibiotic has to diffuse through it
Gram (+) Table
Outer Membrane: No
Peptidoglycan: Thick, Outermost
Teichoic Acids: Yes
Endotoxin: No
Porin Channel: No
Gram (-) Table
Outer Membrane: Yes
Peptidoglycan: Thin, Covered by Outer Mem
Teichoic Acids: No
Endotoxin: Yes --> What Body Responds To
Porin Channel: Yes --> Antibiotic has to diffuse through peptidoglycan
Porin Channels
Proteins through outer mem that allow nutrients ( and antibiotics) to diffuse
Antibiotics have to be relatively polar and hydrophilic to get through
Selectively Expressed --> Can evolve to stop expressing porin channels therefore antibiotics can't get in
Endotoxin: Lipopolysaccharide (LPS)
Structural Component of Outer Mem
Responsible for Clinical Sepsis--> Promotes Pro Inflammatory cytokines in immune cells
Bacterial Peptidoglycan
Series of Cross Linked Sugars In Cell Wall:
3 Steps:
- Production of monomers in cytoplasm
- Brought over to cell wall where they're lined up against each other to make chains
- Push chains together through "Cross Linking"
*Cant stretch out, must take apart and add
Bacteria break it down w autolysins and replace it to grow
Bacterial Cytoplasmic Membrance
Separates cytoplasm from cell wall
Phospholipid bilayer
Secretes Cellular Material, transports molecules in
Daptomycin targets this
Bacterial Capsule
Gelatinous Polysaccharide Layer covering bacterium --> Sugar Layer
Limits Phagocytosis
Antigentic--> Target for vaccine
Bacterial Glycocalyx (Slime Layer)
Promotes Adherence
Biofilms--> slow growing, talkative bacteria
Promotes Drug Resistance
Protein Synthesis
Proteins--> how organisms express their genetic info
In Bacteria, Fast (happening at same time)
In Humans, Slow (Happen step by step)
DNA
Where its stored
Stores Genetic Info
RNA
Where it goes to tell cell how to make proteins
Express Genetic Info
Protein Syn--> Ribosomes
In cytoplasm, translate mRNA generated from transcription of DNA in genome
Two Types of DNA of Bacteria
Chromosomal & Extrachromosomal
Chromosomal
Like eukaryotes
Fixed --> There all the time
Nucleoid
Nucleoid
"Naked" In cytoplasm
DNA Supercoils
Encodes for intrinsic antibiotic resistance
Extrachromosomal
Found outside of the cell
Plasmids
Transposons
Plasmids
** #1 GENETIC CAUSE OF ACQUIRED ANTIBIOTIC RESISTANCE **
Contains DNA outside of chromosome
Transmitted By Conjugation ---> transmit antibiotic resistance gene
Encode for virulence factors and antibiotic resistance
Transposons
mobile genetic elements "jump" in other DNA
transmit antibiotic resistance
less common than plasmids
Prokaryote Nucleiod
Looks like nucleus
no membrane bounding it in
Eukaryote Nucleus
Membrane Bound Nucleus w/ Nucleolus
-Transcription occurs in nucleus to create mRNA that goes through pores to get to RER where the ribosomes are translated to proteins
Nucleolus
Most DNA rich area
Endospores
Dormant and highly resistance structures
no metabolic activity
Form when nutrients are poor
--> germinate into bacteria when nutrients available
difficult to eradicate
When Bacteria Not Growing...
not affected by most antibiotics
Virulence Factors
Factors that increase pathogenicity
Endotoxins, Exotoxins, Peptidoglycan, Pilli, Capsules, Destructive Enzymes
Pathogenicity
Capacity to cause disease
Primary Pathogens
Opportunists
Amphibionts/ Commensals
Non-Pathogens
Primary Pathogens
Cause disease in heathy people
Ex. Skin Infection
Opportunists
Require compromised host or barrier to be pathogenic
not aggressive enough on their own
Amphibonts/ Commensals
Mutualists that sometimes become pathogenic
ex. E. Coli
Non-Pathogens
Most microorganisms
As Pathogenicity increases
Frequency of it in nature decreases
mRNA--> Messenger RNA
transcribed to/ list of directions on how to make protein
tRNA --> Transfer RNA
bring aa over to growing peptide chain
rRNA --> Ribosomal RNA
Structural element of ribosomes
target of many antibiotics
highly conserved---> used in bacterial identification
Gene Expression
Very Fast Process in Bacteria b/c happens in Cytoplasm
(Slower in Eukaryotes bc start in nucleus)
DNA --> RNA Polymerase --> TRANSCRIPTION --> mRNA --> TRANSLATION--> Protein
*lots of drugs that work by stopping translation to prevent protein synthesis
Bacterial Growth
Divide by Binary Fission
Binary Fission
Makes Clones of each other
Phases Of Growth
- Lag
- Logarithmic
- Stationary
- Death
Lag Phase
getting ramped up and ready to go
Logarithmic Phase
doubling over and over until run out of nutrients
Stationary Phase
Just wait
Growth Types
Vegetation State
Biofilms****
Vegetation State
Free Flowing Bacteria
Biofilms
** MOST COMMON **
colonies of bacteria that live in harmony
Stick to something --> IV Catheders + Prosthetics
bacteria growing rapidly on the outside + dormant on the inside
bacteria can talk to each other and express genes that can lead to antibiotic resistance
**intrinsically resistant to antibiotics**
Vegetative Chart
Occurrence: Nutrients Plentiful
Impact of Enviro Conditions: Big Impact/ Die
Antimicrobial Resistance: Low Resistance
Growth: Rapid
Community Effects: None
Clinical Implications: Rapid Growth + Speed
Biofilm Chart
Occurrence: Period of stress
Impact of Enviro Conditions: Reduced
Antimicrobial Resistance: Intrinsic
Growth: Moderate to Slow
Community Effects: Quorum Sensing
Clinical Implications: Resistance to antibiotics, adherence to prosthetic material
Quorum Sensing
Talking to each other
Obligate Aerobes
Need O2 to grow
ex. Tuberculosis, Molds (fungi) in lungs
Obligate Anaerobes
Cannot tolerate oxygen
hard to culture
ex. Bacteroides, fusobacterium in gut
Facultative Anaerobes
Prefer oxygen filled enviro but can grow w/o it
ex. E.coli, stapphoric, E.Faecalis
Normal Flora
commensals
benefit from us w/o damaging us
Resident Microbiota
relatively fixed
can re-establish if killed
Transient Microbiota
colonize for period of time
Function of Normal Flora
Bacterial Interference --> prevent colonization of pathogens
Nutrient Synthesis --> Vit. K
Can prevent chronic disease
Can cause disease in compromised patients
C. Difficile Infection
Obligate, Spore forming anaerobe
treated w antibiotics ~30% success
treated w fecal transplant ~ 90% success
When C.Diff treated w antibotics
antibiotics also destroy everything there
if treatment fails, more likely to fail again
Colonization
Presence of Organisms w/o Infection
How To Treat Patients W/ ID
- Suspect Infection
- Culture Suspected Sites (Begin Empiric Therapy)
- Stain Sample
- Identification
- Susceptibilities (What Drugs Will Work)
- Definitive Therapy
Empiric Therapy
"best goes" treatment
Definitive Therapy
Targeted for that patients exact strain