Intro to Bacteria 8/15/25

Vocabulary flashcards covering key concepts from growth, genetics, virulence factors, transmission, culture, and antibiotic resistance topics in the lecture notes.

Binary fission

Asexual bacterial reproduction where a cell divides into two genetically identical ‘daughter cells’, with complete genome replication and envelope synthesis. Can replicate in 20 minutes! (doubling time)

4 phases of growth curve

Lag – initial

• Bacteria making and turning on enzymes etc. to start eating • No actual replication yet Log/exponential

• Rapid replication, using nutrients • Generation time determined here

Stationary

• Nutrients all used up • Build up of toxic substances, not good for growth • # new cells = # dying cells

Death

• Cells dying, not replicating

Bacterial protein synthesis

codons are the same as euks

bacterial ribosome units are different from eukaryotes (30s+50s=70s) and are targeted by abx aminoglycosides

Bacterial diversity

1.Genotypic and phenotypic diversity • E.g. oxygen requirements

2. Ability to cause disease • Some bacteria weren’t pathogens until they acquired a

new piece of DNA … virulence factors later this talk

3. Ability to develop resistance to antibiotics •

”Simple” genetic material • Haploid - 1 chromosome

point mutations

A type of gene mutation where a single nucleotide base is replaced, inserted, or deleted in the DNA sequence.

inhibitors of bacterial transcription

Rifamycin group (e.g., Rifampin)

• Binds to the RNA polymerase and prevents it from

reading the DNA to make mRNA • Bactericidal • Point mutations in RNA polymerase = resistance • Often given with with other antibiotics

vertical transmission

genetic info from mother to 2 daughter cells

Bacterial genome replication

each DNA strand acts as template for new complementary strand. Made by DNA polymerases. requires bacterial enzymes (primase, helicase, ligase, topoisomerase, gyrase) and polymerase

Generation time

The doubling time; the time required for a bacterial population to double in number; varies by species.

Chromosome

The main circular, haploid bacterial DNA molecule that carries essential genes. 5’ → 3’ orientation, same base pairing as euks. 2 circular strands.

No introns, no splicing

Inhibitors of bacterial DNA synthesis

Sulfonamides and Trimethoprim (bactrim)

• Binds to enzymes and inhibits folate synthesis • If you can’t make bases, you can’t make DNA • Together … bactericidal (death)

Fluoroquinolones

• If you can’t safely keep DNA untangled • Bactericidal (death)

Metronidazole

• DNA breaks • Bactericidal (death)

Plasmid

Extrachromosomal, double‑stranded circular DNA that replicates independently of the chromosome and often carries accessory genes that can carry traits like antibiotic resistance, new toxins/enzymes/adhesins/etc.

Transmissible plasmids

Plasmids capable of transferring between bacteria via conjugation, spreading traits such as resistance.

Contain genes responsible for synthesis of the sex pilus and for the enzymes required for transfer

Non-transmissible plasmids

Plasmids that cannot transfer by conjugation and may remain within the original cell. Mother to daughter cells (vertical transmission)

Recombination

DNA from 2 different sources are combined to produce a new nucleotide sequence by homologous or nonhomologous methods.

Enterococcus got DNA to be vancomycin resistant

Conjugation

DNA transfer between bacteria through direct cell contact, mediated by a sex pilus; often involves transfer of a plasmid.

F plasmid

Fertility plasmid in F+ cell that carries genes for the sex pilus and conjugation tube for transfer to F- cell

Sex pilus

A pili used to connect donor and recipient cells during conjugation to transfer DNA.

Transduction

DNA transfer/movement between bacteria mediated by bacteriophages (phages=transport truck); can move virulence or resistance genes.

Virulent phage

A lytic bacteriophage that immediately kills the bacterial host and can spread bacterial DNA. Kills bacteria

Temperate phage

A phage that can integrate into the bacterial genome and later transfer DNA via transduction. Transfers bacteria DNA from one bacteria cell to another - it may lead to a new pathogen arising (cholera, diptheria)

Transformation

Uptake of free, naked DNA from the environment by competent bacteria, followed by recombination and integration.

May change something in the bacteria that causes immune system to no longer recognize it (surface capsule, etc)

Homologous recombination

DNA exchange requiring long stretches of sequence identity between similar sequences. Requires large segments of sequence identity

Non‑homologous recombination

DNA exchange not requiring extensive sequence identity; can insert DNA at non‑homologous sites. DNA doesn’t have to be complementary

Horizontal gene transfer

Movement of genetic material between organisms other than parent-offspring (transformation, transduction, conjugation).

Mutation

Heritable change in DNA sequence that can alter phenotype; arises during replication or due to damage.

Culturing

isolate single colonies (genetically identical cell mass that has grown to be visible with naked eye)

Bacterial growth requirements

temperature, oxygen, nutrients, specific others

Temperature requirements

Mesophiles prefer 37 celsius (mesophiles)

Some are specific:

4oC – Listeria monocytogenes

42oC – Campylobacter jejuni

31oC – Mycobacterium leprae

obligate anaerobe

Bacteria that can’t grow in the presence of any oxygen • Lack 1 and/or 2 enzymes that help neutralize reactive oxygen species

clostridium perfringens

facultative anarobe

Bacteria that can respire to make ATP when oxygen is present, but can ferment at least 1 type of sugar when oxygen is not available

e. coli

aerotolerant anaerobe

use fermentation to produce ATP • Do not use oxygen, but can protect themselves from reactive oxygen molecules

strep pyogenes

microaerophilic

Bacteria that require oxygen for growth but only at concentrations lower than that of the atmosphere

campylobacter jejuni

Key stages to infection establishment

Entry – Neisseria meningitidis

• Direct contact with respiratory droplets:

oropharynx

Adherence • Surface pili (oropharynx epithelial cells etc.)

Invasion and colonization

• Colonization, growth

• Invasion into blood unknown

Evasion of host immune response

• Capsule is antiphagocytic, allowing survival and

entrance into BBB

Damage to host (disease

symptoms/production)

• Immune response … other bacteria have toxins etc

bacterial virulence factors

• Any molecule or structure produced by a pathogen that enhances its ability to cause disease • Help bacteria colonize a host, evade or suppress the host's immune response, obtain nutrients from the host, and inflict damage on host tissues

Groups: adhesion factors, movement, invasion factors, evasion of host immune response, toxins, endospores

surface structures

adhesins, pili, fimbriae

provide tissue tropism

biofilms

surface can be living or inert. very sticky. matrix made of proteins, polysaccharide, eDNA, protect against immune system and abx

flagella

gram +or -. must be rod shaped (never cocci). can have 1 or multiple present. move towards nutrients and away from toxins. they reach target tissues (spread) and cross barriers (burrowing, etc).

also does adhesion

spirochetes have internal flagella and do corkscrew movement to move thru viscous tissues and penetrate various body systems

invasion factors

usually enzymes (spreading factors).

Clostridium perfringens (gram+ rod anaerobe that causes gas gangrene) has lecithinase to break down cell membranes.

collagenase (degrades collagen), hyaluronidase (breaks down hyaluronic acid), streptokinase/staphylokinase (activates plasinogen to plasmin and breaks fibrin clots → bacteria escape and spread

flagella can be included here.

capsules

Most bacteria have polysaccharide capsules (Some are unique, helps as a clue)

Outside the cell wall

Hides surface antigens e.g., peptidoglycan

(Hide from Toll-like receptors, antibodies)

Some vaccines (e.g., Meningococcus) tell the body to make antibodies against the capsule! (Negates their ”protection”)

“Negative stain” to reveal capsule on microscopy

coagulase

On staphylococcus.

Converts fibrinogen to fibrin • Coats bacteria in a fibrin layer • Shield from recognition, phagocytosis and other immune defenses • Why Staphylococci are so good at causing abscesses!

intracellular survival

Hiding from immune system recognition (Pick a cell type, probably a microbe that can live inside, Immune or non-immune cell)

Escapes lysosome

Inhibit phagosome-lysosome fusion

Resists low pH of lysosome

Form protective vacuoles in cytoplasm

Enzymes to destroy ROS

Antigenic variation

Not just bacteria! Viruses, parasites too

• Alteration of surface proteins (e.g., pili, LPS) during infection

• Avoid recognition by antibodies or T cells that recognized the previous

version

• Persistent infections (Lyme disease)

• Reinfection (e.g., gonorrhea)

anti-complement mediated strategies

Capsule – prevents C3b deposition

Molecular mimicry – cover self with host antigens

• M-protein (Streptococcus pyogenes) binds Factor H

• Not only “self” antigen, but Factor H tells complement not to attack

Interfere with complement components

• M-protein interferes with formation of C3 convertase = no MAC formation

• Secrete complement-degrading enzymes (e.g., degrade C3 and C5)

• Inhibit MAC deposition (some O-antigens in LPS)

• Protein A (Staphylococcus aureus) binds antibodies at their Fc, preventing antibody-mediated activation of complement

Biofilms

endospores

Gram + rods bacillus and clostridium species only!

Dried out, hibernating bacteria form

Can survive for decades through heat, cold, desiccation, etc

Infectious (direct contact thru broken skin, inhalation, ingestion)

schaeffer-fulton method

spore staining using malachite green and safranin

endotoxin

LPS (lipopolysaccharide)

• Gram-negative outer membrane (lipid A toxic)

• NOT secreted, but can be detached when cell dies

exotoxin

made inside, secreted!

• Gram-neg OR Gram-pos

• Proteins

exotoxin classes

AB toxin • A – active (EFFECT on host cell) • B – binds to specific host cell

Superantigen • Non-specific immune system activation

Cytolytic (membrane disrupting) • Punches holes in cell membranes • Can be cell-type specific

Proteases

AB toxins

B – Binding (cell receptor)

A – Active • Different activities, different outcomes • Protein synthesis inhibition (Leads to cell death) • ↑ cAMP via ADP ribosylation of Gs (Watery diarrhea (cholera)) • Blocks neurotransmitter release (Tetanus, botulism)

superantigens

Non-specifically activate T cells by linking MHC II and TCR (No antigen presentation required)

Massive cytokine storm (Unregulated)

• Scarlet fever • Toxic shock syndrome

membrane disrupting toxins

“Hole-punchers” = kill cells

• Can target different cell types

• MOST have “lysin O” at the end of the name

panton-valentine leukocidin (PVL)

Some S. aureus strains express

• Specifically target neutrophils = death

• Extreme necrosis, pyrogenic infections

proteases

Enzymes that cleave or inactivate host proteins

• Botulism and Tetanus cleave SNARE proteins, preventing neurotransmitter release (technically also AB toxin)

escherichia coli

Uropathogenic (urinary infections) • Fimbriae and pili specific for bladder and kidney cells • No toxins

Enterotoxigenic (traveler's diarrhea, watery diarrhea) • AB toxin that causes fluid loss into small intestine

Enterohemorrhagic (bloody diarrhea) • AB toxin that prevents host cell protein synthesis (killing cell)

K1 (neonatal meningitis) • Capsule that allows survival in blood; reaches blood brain barrier = meningies

antibiotic resistance

Bacteria evolve the ability to survive antibiotics that were designed to kill them

• Infections become harder to treat • Some are now resistant to all :(

• Higher risk of complications, hospital stays, and death

• Threatens the effectiveness of modern medicine

Nonbacterial factors contributing to resistance

Overuse of antibiotics in humans and animals • Agriculture = bacteria in animal intestine become resistant, can spread to human bacteria … remember gene transfer events?

Misuse • Treating viral infections • Not finishing prescriptions

Poor infection control in healthcare settings • Hospital-acquired infections

Global spread via travel, trade, and agriculture

Environmental factors, waste disposal, antibiotic residue

How do bacteria acquire resistance mechanisms?

• Selective pressure … survival of the fittest

• Point mutations - alter target • Vertical transfer to progeny

• Horizontal transfer

• Conjugation is #1 most common

• One or more resistance mechanisms in one

place

• Don’t rely on fitness trade-off of point

mutations

• Unrelated bacteria can share

General resistance mechanisms

Target modification

• Point mutations: where antibiotic would target – can’t bind anymore

• Bacterial enzyme that chemically alters antibiotic so it doesn’t work anymore

• Class specific

Alternative target

• Still does its job, just isn’t bound by antibiotic

• Class specific

Destroy antibiotic

• Enzyme

• Class specific

Efflux pumps

• Remove antibiotic from cell before it can do its thing

Limit entry into cell

• Gram-negatives have porins in outer membrane

IgA protease

IgA = mucosal defense, innate • Respiratory tract, gastrointestinal tract, urogenital tract, tears, saliva, breast milk • Neutralizes pathogens before they penetrate epithelial barriers • Prevents attachment to host cells, blocking invasion and colonization

• Many bacteria that colonize mucous membranes secrete:Gonorrhea, Pneumococcal pneumonia, Ear infections, Sinusitis

Frameshift mutation

Insertion or deletion that shifts the reading frame, drastically altering downstream amino acids.

Silent mutation

Nucleotide change that does not alter the encoded amino acid.

Missense mutation

Nucleotide change that substitutes a different amino acid in the protein.

Nonsense mutation

Nucleotide change that creates a premature stop codon, truncating the protein.

DNA polymerase

Enzyme that copies DNA by adding nucleotides in the 5′→3′ direction.

DNA primase

Enzyme that synthesizes RNA primers to start DNA synthesis.

DNA helicase

Enzyme that unwinds the DNA double helix to create a replication fork.

DNA ligase

Enzyme that seals nicks between Okazaki fragments on the lagging strand.

Topoisomerase/Gyrase

Enzymes that relieve DNA supercoiling during replication; targets of fluoroquinolones (cipro, levofloxacin). Keeps downstream dna from breaking

Bidirectional replication

DNA replication proceeds in two directions from the origin around the circular chromosome.

Circular chromosome

Single, circular, haploid bacterial chromosome; lacks introns and splicing.

Haploid

Single set of genetic information; bacteria typically have one chromosome.

70S ribosome

Bacterial ribosome composed of 30S and 50S subunits (70S total), a common antibiotic target.

30S subunit

Small ribosomal subunit; target of aminoglycosides and tetracyclines.

50S subunit

Large ribosomal subunit; target of macrolides and chloramphenicol.

Biofilm

Surface-attached microbial communities embedded in a matrix; protect bacteria from immune clearance and antibiotics.

Capsule

Polysaccharide exterior to the cell wall; anti‑phagocytic; capsule antigens can be vaccine targets.

Coagulase

Staphylococcus aureus enzyme converting fibrinogen to fibrin, shielding bacteria from immune detection.

IgA protease

Enzyme that cleaves IgA at mucosal surfaces, aiding colonization of mucosal tissues.

Protein A

Staphylococcus aureus protein that binds the Fc region of IgG to inhibit opsonization.

Endotoxin

Lipid A component of Gram-negative LPS; released on cell death and triggers inflammation.

Exotoxin

Protein toxins secreted by bacteria; can be AB, cytolytic, proteolytic, or superantigenic.

AB toxin

Toxin with A (active) and B (binding) subunits; diverse activities (e.g., cholera toxin).

Superantigen

Toxins that non‑specifically activate T cells by bridging MHC II and TCR, causing a cytokine storm.

Lecithinase (alpha toxin)

Phospholipase C that hydrolyzes phospholipids in membranes, causing cell lysis (e.g., C. perfringens alpha toxin).

Hylauronidase

Spreading factor that degrades hyaluronic acid to promote tissue invasion.

Collagenase

Enzyme that degrades collagen to aid tissue penetration and dissemination.

Streptokinase

Enzyme that activates plasminogen to plasmin, dissolving clots to enable spread.

Endospores

Dormant, highly resistant forms produced by some Gram‑positive bacteria (Bacillus, Clostridium).

Spore staining

Schaeffer‑Fulton method using malachite green (with heat) and safranin to visualize endospores.

Portals of entry

Sites where pathogens enter the host (e.g., respiratory, GI, genitourinary, skin, parenteral, conjunctiva, placenta).

Obligate aerobe

Bacteria that require oxygen for growth (e.g., Mycobacterium tuberculosis).

will never ferment sugars

Microaerophilic

Bacteria that grow best at reduced oxygen levels (e.g., Campylobacter).