(Please Let me Pass) BIOL 251 Final Exam

Propage

viral DNA that has been inserted into the chromosome of a bacterial cell during the lysogenic cycle

Viral envelope

• lipid membrane that surrounds the capsid

• stolen from the host cell during viral exit (usually through budding)

• Helps virus attach to host cells

• Assists in fusion with host membranes

• Helps evade the immune system

Lysogenic cycle

• The virus injects its DNA, but instead of replicating, the viral DNA integrates into the host chromosome.

• The viral DNA is now called a prophage.

• It replicates along with the host cell every time it divides.

• The host is not destroyed, and can live for a long time with the prophage inside.

📌 Key Feature: Virus “hides” in the host genome.

Lytic cycle

• The virus injects its DNA into the host.

• The host’s machinery is hijacked to make viral parts.

• New viruses are assembled.

• The host cell bursts (lyses), releasing viruses to infect new cells.

📌 Key Feature: Host is killed.

Basic staining

positive, stains cell

Acidic staining

negative, stains background

How is a virus observed

• can’t be seen with light microscopes, they need electron microscopes

Who created the compound microscope

Robert Hooke

Gram positive

thicker, more porous cell wall that retains the crystal violet stain.

Gram negative

thinner cell wall, has LPS and a more complex structure.

Species

• Genetically similar

• Share key characteristics

• Usually can reproduce (in sexually reproducing organisms)

Strain

• a genetic variant or subtype

• A few mutations

• Added plasmids

• Gained/lost virulence genes

Bacteria cell structure

• prokaryotic

• Lack a nucleus

• Lack membrane-bound organelles

• 70S ribosomes (50S and 30S subunits)

ribosome

• made up of RNA and proteins

• assemble amino acids to make proteins

• read genetic code

• release protein when complete (process is called translation)

• 30S small subunits = the decoder (read the genetic message on mRNA)

• 50S large subunits = the builder (links amino acids into a protein chain)

Prokaryotic cells

• no nucleus (DNA is in nucleoid)

• single, circular chromosomes

• may contain plasmids

• no membrane bound organelles (no mitochondria, ER, etc)

• Smaller 70S

• binary fission

• Ex: Bacteria and Archaea

*like a studio apartment everything in one room

Eukaryotic cells

• has a nucleus

• linear chromosomes

• has membrane bound organelles

• larger 80S

• mitosis or meiosis

• Ex: animals, plants, fungi, protists

*like a house there are multiple rooms

Structure of a virus

• Either DNA or RNA (never both)

• Capsid (protein coat)

• envelope (some)

• spikes (glycoproteins) - help attach and enter host cells

Virus

• Can’t reproduce on its own

• Must infect a host cell to replicate

• Is not made of cells — it’s simpler than even bacteria

• non-living

Plasmids

• circular, double stranded DNA

• in cytoplasm (not part of the chromosome)

• self replicating

• small

• can carry non essential genes (antibiotic resistance, toxins, metabolic enzymes fertility (conjugation) genes)

*bacterias keep these because they give an advantage (resistance and aid in adhesion/invasion)

*can be transferred through conjugation and sometimes transformation but never through transduction!!!

how are plasmids transferred

Horizontal gene transfer

1. Conjugation (most famous) – one bacterium donates a plasmid to another through a pilus (like a bridge)

2. Transformation – bacteria pick up free plasmid DNA from the environment

3. Transduction – a virus accidentally moves plasmid DNA from one bacterium to another

*Cool, Trashy, Delivery

Endospores

• produced by certain gram positive bacteria produce these (ex: clostridium and bacillus)

• dormant (inactivated)

• highly resistant structures (high heat, radiation, drying, chemicals, and disinfectants)

• become active through germination (which cause serious disease in host)

Transformation

• getting genes from the outside world

*Trashy

Transduction

• transfer of genes from bacteriophage to bacteria 

*Delivery (remember B and D go together)

Conjugation

• swapping of plasmids through a physical connection called a pilus (DNA handshake)

• requires cell to cell contact

*Cool

Obligate aerobe

• Require oxygen to survive.

• Use aerobic respiration (O₂ is the final electron acceptor).

• Die without O₂.

🧪 Example: Mycobacterium tuberculosis
🧫 Growth pattern in broth: Grows only at the top

Facultative anaerobe

• Prefer to use oxygen (aerobic respiration) because it makes more ATP.

• But can switch to fermentation or anaerobic respiration if no O₂ is present.

• Very adaptable.

🧪 Example: Escherichia coli
🧫 Growth pattern in broth: Grows throughout, but densest at the top

Obligate anaerobe

• Cannot tolerate oxygen — it’s toxic to them.

• Use anaerobic respiration or fermentation.

• Lack enzymes like catalase or superoxide dismutase (SOD) to detoxify O₂.

🧪 Example: Clostridium botulinum
🧫 Growth pattern in broth: Grows only at the bottom

Microaerophile

• Require small amounts of oxygen — too much is toxic.

• Have limited ability to detoxify oxygen radicals.

• Grow best in low-oxygen environments (around 2–10% O₂, lower than atmospheric 21%).

🧪 Example: Helicobacter pylori
🧫 Growth pattern in broth: Grows just below the surface of the medium.

Aerotolerant anaerobe

• Don’t use oxygen, but can survive in its presence.

• Only use fermentation for energy.

• Have enzymes like SOD to detoxify oxygen radicals.

🧪 Example: Streptococcus pyogenes
🧫 Growth pattern in broth: Grows evenly throughout the tube.

What is a bacterial growth curve

Lag → Log (Exponential) → Stationary → Death

Lag Phase

• No increase in cell number, but cells are metabolically active.

• Bacteria are:

  • Sensing their new environment

  • Making enzymes

  • Repairing damage

  • Synthesizing proteins

Think: “Warming up” — like stretching before a workout.

Log Phase (Exponential Phase)

• Rapid cell division — the population doubles at a constant rate.

• Cells are healthy and growing at their fastest.

• This is when bacteria are most:

  • Susceptible to antibiotics (because they’re actively replicating)

  • Useful for lab experiments

Think: "Full speed ahead!"

Stationary Phase

• Growth rate = death rate → Total population stays constant.

• Nutrients are running out, and waste is building up.

• Cells may slow metabolism, make endospores, or express stress genes.

Think: "Running out of gas, holding steady."

Death Phase (Decline Phase)

• More cells die than divide → Population declines.

• Causes:

  • No nutrients left

  • Too much toxic waste

  • pH change, overcrowding

Think: "Toxic environment — collapse begins."

when are bacteria are most sensitive to antibiotics

log phase (they are actively growing)

What Is Sterilization?

complete destruction or removal of all forms of microbial life, including:

• Bacteria

• Viruses

• Fungi

• Bacterial endospores (the toughest to kill!)

Moist Heat (Autoclaving)

• 121°C for 15–20 min at 15 psi

• Kills everything, including endospores

• Uses steam under pressure

• Most common in hospitals and labs

🧫 Used for: Surgical tools, lab media, biohazard waste

Dry Heat

• 160–170°C for 2+ hours

• Kills by oxidation of cell components

• Takes longer than moist heat

🧫 Used for: Glassware, metal instruments

Filtration

• Physically removes microbes from liquids or air using a filter with small pores

• Does not kill, but removes bacteria and even viruses (with small-pore filters)

🧫 Used for: Heat-sensitive liquids (like antibiotic solutions, vaccines)

Radiation

• Damages DNA → causes death

• Can penetrate through packaging

🧫 Used for: Disposable medical supplies (syringes, catheters)

Chemical Sterilants

• High-level disinfectants used for items that can't be autoclaved

• Must be used properly (right concentration, time)

🧪 Examples:

• Ethylene oxide gas – used for delicate instruments

• Glutaraldehyde – used for respiratory therapy equipment

• Hydrogen peroxide vapor

🧫 Used for: Heat-sensitive medical devices (scopes, plastic tools)

Ethylene Oxide

Used for:

• Heat-sensitive materials like:

  • Catheters

  • Syringes

  • Pacemakers

  • Surgical instruments with plastics, electronics, or optics

Glutaraldehyde

Used for:

• Delicate medical equipment that can't be heat-sterilized:

  • Endoscopes

  • Respiratory therapy tools

  • Dialysis equipment

  • Soaking or immersion method

Cell Wall Synthesis Inhibitors

• Target peptidoglycan, which is unique to bacterial cell walls.

• Without a cell wall, bacteria burst from osmotic pressure.

🧪 Examples:

• Penicillins

• Cephalosporins

• Vancomycin

📌 Only work on growing bacteria (actively making new cell walls).

Protein Synthesis Inhibitors

• Bind to 70S ribosomes (prokaryotic only — not 80S ribosomes in humans).

• Prevent bacteria from making essential proteins.

🧪 Examples:

• Tetracyclines

• Aminoglycosides (like streptomycin)

• Macrolides (like erythromycin)

📌 Different antibiotics bind to either the 30S or 50S ribosomal subunit.

DNA/RNA Synthesis Inhibitors

• Interfere with nucleic acid replication or transcription.

• Block enzymes like DNA gyrase or RNA polymerase.

🧪 Examples:

• Fluoroquinolones (DNA gyrase inhibitors)

• Rifampin (RNA polymerase inhibitor)

📌 Often used to treat serious infections like tuberculosis.

Metabolic Pathway Inhibitors

• Mimic enzymes or substrates to block key bacterial metabolic reactions.

• Often target folic acid synthesis, which bacteria must make themselves (humans get it from food).

🧪 Examples:

• Sulfonamides (sulfa drugs)

• Trimethoprim

📌 These drugs are often used together for synergistic effect (TMP-SMX combo).

Plasma Membrane Inhibitors

• Disrupt the bacterial membrane, causing leakage and cell death.

• Less selective → can be toxic to human cells, so used carefully.

🧪 Examples:

• Polymyxins

• Daptomycin

📌 Usually used for topical or last-resort treatments (e.g., drug-resistant Gram-negatives).

Features of Effective Antibiotics

• Kills bacteria, not host cells

• Broad = many types; Narrow = specific targets

• must reach infection site intact

• minimal side effects

• slower to become ineffective

• oral or IV, not complex or expensive

Vertical Gene Transfer

Parent → offspring (traditional inheritance)

Horizontal Gene Transfer

One organism → another (same generation), not via reproduction

Why Antibiotics Are NOT Effective Against Viruses

1. Viruses aren’t cells: (Antibiotics attack structures in prokaryotic cells (like bacterial cell walls, ribosomes, or DNA enzymes). Viruses have none of these)

2. No metabolism: (Antibiotics interfere with metabolic processes — viruses don’t metabolize. They’re dormant outside a host.)

3. No ribosomes: (Many antibiotics stop protein synthesis — viruses don’t have ribosomes, so there’s nothing to target)

4. Viruses replicate inside human cells: (Antibiotics can’t get inside host cells to reach the virus without also harming you)

Nosocomial Infection

• An infection you get while in a hospital or healthcare facility, after admission.

• It was not present or incubating at the time of admission.

• Caused by:

  • Contaminated equipment

  • Poor hand hygiene

  • Airborne spread

  • Other patients

🧪 Examples:

• MRSA from a hospital bed

• Clostridium difficile (C. diff) after antibiotic use in a nursing home

📌 Keyword: Hospital environment

Iatrogenic Infection

• An infection that results from a medical procedure or treatment.

• Not necessarily in a hospital — can be in a clinic, surgery center, etc.

• Caused by:

  • Injections

  • Catheters

  • Surgery

  • Medical devices

  • Even diagnostic procedures

🧪 Examples:

• Infection from an unsterile catheter

• Abscess from an injection

• Surgical site infection from contaminated instruments

📌 Keyword: Procedure-related

Sign

• An objective, measurable indicator of disease

• Ex: Fever, rash, high blood pressure, lab results

Symptom

• A subjective experience reported by the patient

• Ex: Pain, fatigue, nausea, dizziness

Capsule

• evades phagocytosis

Biofilms

• prevents antibiotics from attaching

Collagenase

breaks down collagen allowing deeper penetration

what are the steps in pathogenesis

• Incubation

• Prodromal

• Illness

• Decline

• Convalescence 

Incubation

• Time between infection and first symptoms

• Pathogen is multiplying, but no symptoms yet. Duration varies by disease (e.g., hours for food poisoning, weeks for TB

Prodromal

• Early, mild, non-specific symptoms

• You start to feel "off" — fatigue, low fever, body aches. Pathogen numbers are rising

Illness

• Peak of disease — most severe signs/symptoms

• Immune response is active. Obvious symptoms (fever, rash, vomiting, etc.). Risk of complications is highest here.

Decline

• Symptoms begin to improve

• Immune system is winning, or treatment is working. Pathogen numbers drop. Still vulnerable to secondary infections.

Convalescence

• Recovery phase

• Body is healing and regaining strength. Pathogen may be gone, but you may still be contagious during this stage.

Exotoxin

• made up of protein

• Made by gram + and gram -bacteria

• Needs a low dose in order to be potent

Endotoxin

• made up of the lipid A portion of the lipopolysaccharide

• in gram negative bacteria

• Needs high dose in order to be potent

How Are Antibodies Produced?

• Plasma cells — which are activated B lymphocytes (B cells)

  1. A B cell encounters an antigen that matches its receptor.

  2. It becomes activated (often with help from a helper T cell).

  3. It differentiates into a plasma cell.

  4. Plasma cells pump out antibodies specific to that antigen.

What are antibodies

• Y-shaped proteins that bind to specific antigens

• made by Plasma cells (from B cells)

• After exposure to a pathogen or vaccine

• Neutralize, tag (opsonize), agglutinate, activate complement

IgG

Most abundant in blood; crosses placenta

IgA

Found in mucous membranes (respiratory, GI, secretions like saliva, breast milk)

IgM

First antibody made in infection; strong agglutinator

IgE

Involved in allergies and parasitic infections

IgD

Role not fully understood; helps activate B cells

Leeuwenhoek

→ father of microbiology

Fleming

 → made penicillin

Florey and chain

 → purified penicillin

Hodgkins

→ made semisynthetic drugs

Carl Woese

→ 16S rRNA gene sequencing

• discovered third domain of life (archaea)

Louis Pasteur

• Disproved Spontaneous Generation

• swan neck experiment

• Pasteurization

Hooke

→ made compound microscope

Koch’s postulates

1. Animal has disease, not in healthy animals 

2. Take microbe from disease and grown pure culture (only a single species)

3. We can take the microorganism to another animal → it will cause the same symptoms 

4. We can do this again 

Griffith

→ proved transformation and horizontal gene transfer

Groups of beta lactam antibiotics

1. Penicillins (e.g., amoxicillin, penicillin G) *💡 If it ends in “-cillin,” it’s almost always a penicillin-type beta-lactam.

2. Cephalosporins (e.g., cephalexin) *💡 “Cef-” or “Ceph-” = cephalosporin = beta-lactam.

3. Carbapenems (e.g., imipenem) *💡 “-penem” is your carbapenem flag.

4. Monobactams (e.g., aztreonam) *💡 Aztreonam is the only commonly used monobactam.

HINT: Some beta-lactams are combined with beta-lactamase inhibitors. These usually look like two names:

• Amoxicillin-clavulanate (Augmentin)

• Piperacillin-tazobactam (Zosyn)

What are beta-lactams

• family of antibiotics that all have a special ring structure in them called a beta-lactam ring

• They kill bacteria by stopping them from building their cell walls

What is resistance to beta-lactams?

Some bacteria fight back by making an enzyme called beta-lactamase.
🧪 This enzyme's job is to cut open the beta-lactam ring, which destroys the antibiotic and makes it useless.

It’s like:

• The antibiotic is a key 🔑 (the beta-lactam ring)

• The bacteria use a tool 🔧 (beta-lactamase) to break the key

• Now the key no longer fits the lock (the PBPs), so the drug doesn't work

How do we fight beta-lactam resistance

We combine the antibiotic with a beta-lactamase inhibitor (a chemical that blocks the bacteria’s enzyme). For example:

• Amoxicillin + clavulanic acid = Augmentin
  → clavulanic acid protects the beta-lactam ring from being destroyed

How is S. aureus responsible for food poisoning

• contaminates food
  → This often happens through human contact (e.g., skin, nose, or hands of food handlers).

• It grows in food left at room temperature
  → Think of foods like potato salad, custards, sliced meats, or cream-filled pastries that are not refrigerated properly.

• It produces an enterotoxin (specifically Staphylococcal enterotoxin)
  → This toxin is heat-stable, so even reheating the food won’t destroy it.

• You eat the toxin → and get sick quickly

Helicobacter pylori

• spiral shaped

• gram negative

• colonizes in the stomach lining

• microaerophilic (prefers low oxygen levels)

• lives in mucous layer in stomach

• can survive in acidic stomach because of an enzyme (urease)

What does urease do

• breaks down urea into ammonia and carbon dioxide

• ammonia neutralizes stomach acid around bacteria (allows helicobacter pylori to survive in acidic stomach)

What disease are caused by Helicobacter pylori

• Gastritis – inflammation of the stomach lining

• Peptic ulcers – especially in the stomach and duodenum

• Gastric cancer – long-term infection increases risk

• MALT lymphoma – a rare stomach-associated cancer

⚠ Not everyone infected develops symptoms, but many people around the world carry it silently.

Clostridium difficile

• gram-positive

• rod shaped (bacillus)

• anaerobic (doesn’t need oxygen

• spore forming

• commonly spread in hospitals or recently antibiotic-treated patients

how does clostridium difficile cause disease

1. Normal gut bacteria help protect you.

2. When you take broad-spectrum antibiotics, they kill off good gut bacteria.

3. C. diff spores survive and then grow unchecked.

4. It produces toxins (Toxin A and Toxin B) that:

   • Damage the colon lining

   • Cause inflammation, fluid loss, and diarrhea

   • Lead to pseudomembrane formation (dead cells, mucus, and bacteria coating the colon)

How is clostridium difficile treated

• Stop the antibiotic that caused the imbalance (if possible)

• Treat with specific antibiotics that target C. diff:

  • Oral vancomycin

  • Fidaxomicin

  • Metronidazole (less preferred now)

• Fecal microbiota transplant (FMT) may be used in recurrent cases to restore healthy gut flora

  *DO NOT USE BETA LACTAMS

What is budding

• A type of asexual reproduction where a new organism grows as a small outgrowth (bud) on the parent

• receives a copy of DNA, and may detach to live independently.

Which microorganism is a classic example of budding

Saccharomyces cerevisiae (yeast)

Is the daughter cell in budding genetically identical to the parent?

Yes — it’s a clone (asexual reproduction).

How does the size of the daughter cell in budding compare to the parent

The daughter cell is usually smaller than the parent.

What type of virus exits a host cell by budding

Enveloped viruses (e.g., HIV, influenza)

in viral budding, what does the virus take as it leaves the host cell

A piece of the host cell’s membrane, which becomes the virus’s envelope.