Study of microscopic organisms

Study of the characteristics of pathogens

Study of health and diseases in populations

Bacteria--> Prokaryotes

Archaea

Eukaryota--> Eukaryotes

DNA: Yes--> Single Circle

Mitotic Division: No

Chromosomes: One

Membrane Bound Organelles: No

Ribosome Size: 70s (smaller)

Cell Wall w/ Peptidoglycan: Yes

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

Domain

Kingdom

Phylum

Class

Order

Family

Genus

Species

Not alive

Must infect cell to reproduce

Obligate Intracellular Parasites

Contain DNA OR RNA --> NEVER BOTH

Target bacteria the most

Must live inside other organisms

Infectious proteins

Ingestion of infected meat

Cause Spongiform Encephalopathy

No Treatment/Fatal

Microscopic Eukaryotes

-Algae + Slime Molds

-Protozoa + Fungi --> Cause Human Disease

Those that cause infection in healthy people

Flagellates

Amebae

Sporozoa

Ciliates --> Paramecia

SOI: Blood, Lymph

Transmission: Tse Tse Fly

Causes: Sleeping Sickness

SOI: Blood, Liver

Transmission: Mosquito Bite

Causes: Malaria

SOI: Colon, Liver, Organs

Transmission: Fecal/Oral

Caused By: Infected Water

SOI: Small Intestine

Transmission: Fecal/Oral

Caused By: Infected Water

SOI: Small Intestine, Respiratory Tract

Transmission: Fecal/Oral

Caused By: Infected Water

SOI: Vagina

Transmission: Sexual

SOI: Brain, CNS, Eye

Transmission: Nasal Membrane/ Wound

Eukaryotic Heterotrophs

Yeasts, Dimorphic, Molds

Unicellular

Reproduce by Budding

Cryptococcus/Candida

Endemic Fungi b/c Endemic to Certain Regions

At Room Temp--> Molds

Inhale Them--> Spread Through Body As Yeasts

Histoplasma

Multicelluar

Reproduce By Spores--> We Inhale Them

Very Hard To Treat/ Infect Sick People

Lung Transplant and Cancer Patients

Aspergillus

Cells > Bacteria > Viruses > Molecules

Prokaryotes --> No Nucleus

Simpler

No Visible Structures

Single Chromosome Of DNA

Rigid Cell Wall (Survive Hypotonic Environment)

Cocci --> Round

Bacilli --> Rods

Spirochetes --> Spiral

Selectively Express or Lose

One of the ways vaccines are developed

Outermost layer

Made of Peptidoglycan

Under Cell Wall

Contains:

Chromosomes

Nucleotoids

Extra Chromosomal DNA

Free Flowing Ribosomes (In EUKARY Rib fixed on RER)

Help Adhere

May prevent being engulfed

Whip to move

Chemotaxis

Attracted to chemicals for pathway

1. Fixation

2. Crystal Violent

3. Iodine Treatment

4. Decolorization w Alcohol

5. Counter Stain --> Safarin

Outer membrane

Leads to Intrinsic Resistance to Antibiotics

Porin Channels

Thin Layer of Peptidoglycan

Periplasmic Space

B/w Peptidoglycan and Cytoplasmic Membrane

Separates Cytoplasm from Cell Wall

Peptidoglycan

-Outermost layer, very thick

-Antibiotic has to diffuse through it

Outer Membrane: No

Peptidoglycan: Thick, Outermost

Teichoic Acids: Yes

Endotoxin: No

Porin Channel: No

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

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

Structural Component of Outer Mem

Responsible for Clinical Sepsis--> Promotes Pro Inflammatory cytokines in immune cells

Series of Cross Linked Sugars In Cell Wall:

3 Steps:

1. Production of monomers in cytoplasm
2. Brought over to cell wall where they're lined up against each other to make chains
3. 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

Separates cytoplasm from cell wall

Phospholipid bilayer

Secretes Cellular Material, transports molecules in

Daptomycin targets this

Gelatinous Polysaccharide Layer covering bacterium --> Sugar Layer

Limits Phagocytosis

Antigentic--> Target for vaccine

Promotes Adherence

Biofilms--> slow growing, talkative bacteria

Promotes Drug Resistance

Proteins--> how organisms express their genetic info

In Bacteria, Fast (happening at same time)

In Humans, Slow (Happen step by step)

Where its stored

Stores Genetic Info

Where it goes to tell cell how to make proteins

Express Genetic Info

In cytoplasm, translate mRNA generated from transcription of DNA in genome

Chromosomal & Extrachromosomal

Like eukaryotes

Fixed --> There all the time

Nucleoid

"Naked" In cytoplasm

DNA Supercoils

Encodes for intrinsic antibiotic resistance

Found outside of the cell

Plasmids

Transposons

** #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

mobile genetic elements "jump" in other DNA

transmit antibiotic resistance

less common than plasmids

Looks like nucleus

no membrane bounding it in

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

Most DNA rich area

Dormant and highly resistance structures

no metabolic activity

Form when nutrients are poor

--> germinate into bacteria when nutrients available

difficult to eradicate

not affected by most antibiotics

Factors that increase pathogenicity

Endotoxins, Exotoxins, Peptidoglycan, Pilli, Capsules, Destructive Enzymes

Capacity to cause disease

Primary Pathogens

Opportunists

Amphibionts/ Commensals

Non-Pathogens

Cause disease in heathy people

Ex. Skin Infection

Require compromised host or barrier to be pathogenic

not aggressive enough on their own

Mutualists that sometimes become pathogenic

ex. E. Coli

Most microorganisms

Frequency of it in nature decreases

transcribed to/ list of directions on how to make protein

bring aa over to growing peptide chain

Structural element of ribosomes

target of many antibiotics

highly conserved---> used in bacterial identification

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

Divide by Binary Fission

Makes Clones of each other

1. Lag
2. Logarithmic
3. Stationary
4. Death

getting ramped up and ready to go

doubling over and over until run out of nutrients

Just wait

Vegetation State

Biofilms****

Free Flowing Bacteria

** 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**

Occurrence: Nutrients Plentiful

Impact of Enviro Conditions: Big Impact/ Die

Antimicrobial Resistance: Low Resistance

Growth: Rapid

Community Effects: None

Clinical Implications: Rapid Growth + Speed

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

Talking to each other

Need O2 to grow

ex. Tuberculosis, Molds (fungi) in lungs

Cannot tolerate oxygen

hard to culture

ex. Bacteroides, fusobacterium in gut

Prefer oxygen filled enviro but can grow w/o it

ex. E.coli, stapphoric, E.Faecalis

commensals

benefit from us w/o damaging us

relatively fixed

can re-establish if killed

colonize for period of time

Bacterial Interference --> prevent colonization of pathogens

Nutrient Synthesis --> Vit. K

Can prevent chronic disease

Can cause disease in compromised patients

Obligate, Spore forming anaerobe

treated w antibiotics ~30% success

treated w fecal transplant ~ 90% success

antibiotics also destroy everything there

if treatment fails, more likely to fail again

Presence of Organisms w/o Infection

1. Suspect Infection
2. Culture Suspected Sites (Begin Empiric Therapy)
3. Stain Sample
4. Identification
5. Susceptibilities (What Drugs Will Work)
6. Definitive Therapy

"best goes" treatment

Targeted for that patients exact strain