Bacterial Classification and Characteristics Quiz

Introduction to Antimicrobial Treatment

• The use of antimicrobial agents, such as antibiotics, aims to eliminate the infecting microorganism from the body.
• However, the agents may also harm the host, necessitating careful consideration of potential side effects and interactions.
• Different types of microorganisms, including bacteria, fungi, viruses, and parasites, can cause infections.
• Infections can cause harm depending on the microbe and the severity of infection (e.g. local or systemic).

Topic Objectives

• Students will be able to define an infection and list the common microorganisms that infect humans.
• Students will be able to describe the infection process.
• Students will be able to list the modes of transmission of various infections.
• Students will be able to define common terminologies used when discussing infections.

What is an Infection?

• An infection occurs when microorganisms (bacteria, fungi, viruses, or parasites) enter the human body and multiply.
• If the infection causes harmful effects on the body, it's considered a disease.

What Happens in an Infection?

• Infections may or may not produce noticeable signs or symptoms.
• Infections confined to a specific area of the body are called local infections.
• Infections spreading throughout the body are called systemic infections.

Patterns of Infection

• Mixed infection- several microbes simultaneously infect the location.
• Primary infection- an infection that develops in a healthy individual.
• Secondary infection- an infection that develops in an existing infection.
• Acute infection- rapid-onset, short-duration effects
• Chronic infection- prolonged, persistent effects

Infectious Disease Process

• Infectious agents, susceptible hosts, reservoirs, modes of transmission, portals of entry and exit are critical elements of infectious disease.

CHAIN of INFECTION

• Infectious agent or pathogen
• Reservoir
• Portal of exit
• Mode of transmission
• Portal of entry
• Susceptible host

Infectious Agent/Pathogen

• Microorganisms (bacteria, viruses, fungi, protozoa, parasites) that can cause diseases.

Reservior

• Animate sources (humans, animals, insects)
• Inanimate sources (soil, water, food, medical equipment)
• Pathogens need appropriate environmental conditions to survive (food, oxygen, water, temperature, pH, light).

Living Reservoirs

• Carrier - a person who shelters a pathogen and unknowingly spreads it to others (may or may not be affected by the microbe).
• Asymptomatic carrier - an individual who carries the agent but does not exhibit symptoms (e.g. incubation carriers, convalescent carriers, chronic carriers).
• Passive carrier- contaminated healthcare provider transfers the pathogen to patients.

Living Reservoirs (continued)

• Individuals at risk for carrying microbes without showing symptoms.

Portal of Exit/Entry

• Skin and mucous membranes
• Respiratory tract
• Urinary tract
• Gastrointestinal tract
• Reproductive tract
• Blood

Modes of Transmission

• Contact (direct & indirect)
• Droplet
• Airborne
• Vehicles
• Vectors

Susceptible Host

• Susceptibility- the degree of resistance to infection.
• Factors influencing susceptibility include: age, nutritional status, chronic disease history, immunity, genetics, and personal hygiene.

The Infection Process

• Infection has four key stages:
  • Incubation period- from initial exposure to first symptom. The infection agent is multiplying but the damage is not significant enough to produce symptoms.
  • Prodromal stage- vague feelings of discomfort.
  • Invasion period- multiplication at higher levels that produce many symptoms.
  • Convalescence period- decrease in symptoms as the host responds to the infection.

Major Factors in the Development of an Infection

• True pathogens- able to cause disease in healthy individuals with normal immune defenses (e.g., influenza virus, plague bacillus, malaria).
• Opportunistic pathogens- cause disease when the host's defenses are compromised (e.g., Pseudomonas sp., Candida albicans).
• Virulence- the severity of the disease depends on this factor.

How to Break the Infection Chain?

• Identification of infectious agent and appropriate treatment
• Potential hosts and carriers practice proper hygiene, sanitation, and equipment disinfection.
• Covering mouth and nose when coughing or sneezing.
• Proper handwashing
• Use of PPE

How to Break the Infection Chain (cont)

• Handwashing, isolation of infected patients, and disinfection/sterilization
• Aseptic technique, proper catheter care/wound care
• Treatment of underlying disease and immunizations.

Antimicrobial Therapy

• Therapeutic goal- removing the infecting microorganisms from tissues.
• Chemicals destroy microbes, but can harm the host.

Modern Chemotherapy

• Paul Ehrlich introduced the concept of chemotherapy, using chemicals for treating diseases.
• Ehrlich envisioned drugs that target parasites but weren't toxic to humans.

First Antibiotic

• Penicillin G was discovered in 1929 by Alexander Fleming.
• Penicillin was clinically tested and produced in the 1940s.
• Fleming observed that Penicillium fungus made an antibiotic, Penicillin, which killed S. aureus.

Streptomycin and related agents

• In 1944, Waksman isolated streptomycin and other agents like chloramphenicol, tetracyclines, and erythromycin from soil samples.

Oxford University Group and Penicillin

• In 1939, Florey and his colleagues at Oxford University re-isolated penicillin.

Antibiotics

• Chemicals produced by microorganisms (bacteria, fungi, actinomyces) suppress or destroy other microorganisms.
• Some are created via chemical synthesis or semisynthesis.

How to Achieve Therapeutic Goal?

• Organism must be susceptible to the drug.
• Drug concentrations of the antibiotic must reach the infection site.
• Sufficient drug levels must be maintained at the infected site.
• Host defenses help clear the infection.

Types of Antimicrobial Agents

• Antibacterial agents (antibiotics)
• Antifungals
• Antivirals
• Antiprotozoans
• Antihelmintics

Clinical Uses of Antimicrobial Agents

• Empirical therapy or initial therapy. The antimicrobial should cover all likely pathogens until microorganisms are identified. May be needed in serious infections before lab results come.
• Definitive therapy or pathogen-directed therapy. Once the causative microbe is identified, this method utilizes definitive antimicrobial therapy with a narrow-spectrum, low-toxicity agent to complete the course.
• Prophylactic or preventive therapy (e.g., surgery, recurrent infections)

Antimicrobial Regimen Selection

• Confirming the presence of infection
• Identifying the pathogen
• Selecting rational antimicrobial therapy
• Monitoring therapeutic response

Classification of Antibacterials

• Antibiotics can be categorized based on structure and mechanism of action to help understand how antibiotics work on microorganism.

Bacterial Classification, Shape & Oxygen Requirements

• Bacteria are single-celled organisms in various shapes.
• Classified by cell wall (Gram-positive/Gram-negative).
• Classified by shape (cocci, bacilli, spirilli).
• Classified by oxygen requirements (aerobic/anaerobic).

How Bacteria Cause Disease

• Many bacteria act as opportunistic pathogens, harming the host when conditions allow their growth.
• Some bacteria release toxins that harm the host cells.
• Bacteria can release toxins that damage host cells and disrupt cell membranes. Some gram-negative bacteria produce toxic components in the cell walls.

Principles of Antibacterial Action

• Must kill harmful bacteria without damaging the host cells.
• Must target bacterial cell structures different from eukaryotic human cells (selective toxicity).

Bacteriostatic vs. Bactericidal

• Bacteriostatic- inhibits bacterial growth. Host defenses kill the bacteria.
• Bactericidal- kills bacteria. Bacteria cannot replicate once the antibiotic is removed.

Bacteriostatic and Bactericidal agents

• List of bacteriostatic and bactericidal agents.

Concentration Dependent Vs Time-Dependent Killing

• Concentration-dependent killing: the rate and extent of killing increase with rising drug concentration (e.g. aminoglycosides, fluoroquinolones, metronidazole).
• Time-dependent killing: bactericidal activity continues as long as the plasma concentration is above the minimum bactericidal concentration (MIC) (e.g., beta-lactams, vancomycin, macrolides, tetracyclines).

Selective Toxicity and Spectrum of Activity

• Selective toxicity- drugs toxic to microorganisms but not to human cells.
• Narrow spectrum: effective against limited microorganisms
• Broad spectrum: effective against many microorganisms

Principles of Antimicrobial Selection

• Match drug to the bug
• Consider the spectrum of the drug
• Consider combination therapy
• Consider infection site/administration

Principles of Antimicrobial Selection and Administration: Maintain Adequate Blood Levels

• Many antibiotics need regular dosing to maintain sufficient blood levels.
• Oral doses often require an empty stomach.

Principles of Antimicrobial Selection and Administration: Antibiotic Combinations

• Combinations of antibiotics which act via different mechanisms may be synergistic (e.g., enhance antibiotic effectiveness) or antagonistic (oppose each other's effects).
• Necessary in treating mixed infections (more than one bacterial species).
• Combinations can discourage antibiotic resistance.
• Combine only when indicated.

Empiric Therapy

• Administration of antibiotics based on the practitioner's best guess of the infecting pathogens to avoid treatment delay.

Definitive Therapy

• Antibiotics given based on results from culture and sensitivity tests.
• A narrow-spectrum drug with minimal toxicity is utilized.

Prophylactic Antibiotic Therapy

• Antibiotic use to prevent infection before anticipated exposure, such as pre-operative surgery.

Superinfection

• Secondary infection that arises during the treatment of another infection.
• Occurs when the antibiotic destroys normal flora, creating conditions for another infection to flourish.

Examples of Superinfections

• Yeasts and fungal infections
• Diarrhea due to disruption of normal intestinal bacteria.

Organism Sensitivity

• A laboratory test confirms the drug's toxicity to the specific microorganism causing the infection.

Culture and Sensitivity Testing of Bacteria

• Isolate bacteria from infection site and culture them.
• Apply antibiotic-soaked discs to the plate.
• Clear area around the disc indicates sensitivity.
• The clear area's size reflects the antibiotic's effectiveness against that specific bacteria.

Classification of Antibacterials (continued)

• Classification of antibiotics typically based on chemical structure and mechanism of action (examples).

Chemical Classification of Antibacterials

• List of antibiotics categorized by chemical agents (examples).

Mechanisms of Action of Antibiotics

• Inhibition of cell wall synthesis
• Inhibition of protein synthesis
• Inhibition of nucleic acid synthesis
• Injury to plasma membrane
• Inhibition of essential metabolite synthesis

Modes of Antimicrobial Action

• Visual representation demonstrating the impact of antibiotics on bacterial processes (cell wall, nucleic acids, protein synthesis, etc.).

Inhibition of Cell Wall Synthesis

• Most bacteria have cell walls for protection against osmotic pressure.
• Peptidoglycans are linked by transpeptidase to form a rigid structure.
• Inhibiting this process prevents bacteria from creating new walls, leading to cell rupture and death.
• Examples of drugs include penicillins, cephalosporins, and vancomycin.

Inhibition of Protein Synthesis

• Antibiotics target bacterial ribosomes to prevent protein production, necessary for growth and cell division.
• Examples of drugs include tetracyclines, aminoglycosides, and macrolides.

Inhibition of Nucleic Acid Synthesis

• Drugs disrupt the enzymes involved in DNA replication and transcription.
• Examples of drugs include rifampicin and fluoroquinolones.

Inhibition of Essential Metabolite Synthesis

• Bacteria synthesize essential molecules like folic acid.
• Antibiotic drugs block the synthesis of these molecules needed for bacterial growth.
• Examples of drugs include sulfonamides and trimethoprim.

Injury to Cell Membrane

• Antibiotics can dissolve bacterial membranes, increasing permeability.
• Cell contents leak out, leading to microbial death.
• Example: Polymyxin B.

Inhibitors of Cell Wall Synthesis (beta-lactams)

• Penicillins, cephalosporins, and carbapenems belong to this group.
• The β-lactam ring is crucial for their antibacterial activity.

Penicillins

• Inhibit bacterial enzymes that crosslink peptidoglycans.
• Bactericidal.
• Effective against dividing cells only.
• High therapeutic index (safe for humans).

Examples of Penicillins

• Benzylpenicillin, phenoxymethylpenicillin, ampicillin, amoxicillin, bacampicillin, and cloxacillin are examples of penicillins.
• Oral penicillins are generally best taken with an empty stomach to avoid reduced absorption due to food.

Pharmacokinetics of Penicillins

• Some penicillins are destroyed by gastric acid — not suitable for oral use.
• Bound to plasma proteins, not efficiently crossing the blood-brain barrier but can reach CNS if meninges are inflamed.
• Excreted by kidneys; probenecid may delay excretion to prolong effect.

Penicillin Allergy

• Allergic response to penicillin may range from mild skin rash to severe anaphylaxis. May also be allergic to other beta-lactam drugs like cephalosporins.
• Allergic reaction possibility increases with repeated exposure.

Adverse Effects of Penicillins

• Common adverse effect- allergic reactions.
• Other adverse effects- diarrhea and neutropenia, neurologic problems with overdose.

Drug Interactions of Penicillins

• Synergistic with aminoglycoside antibiotics.
• May reduce effectiveness of oral contraceptives.

Bacterial Resistance to Penicillins

• Bacteria produce β-lactamases to break open the β-lactam ring in penicillins, rendering them inactive.
• Bacteria can also modify penicillin-binding proteins (PBPs).
• Reduced permeability of the cell membrane can also reduce antibiotic action on bacterial cells and their subsequent lysis.

Beta-Lactamases

• Enzymes that break the β-lactam ring of penicillin, making it ineffective.
• Some bacteria produce these beta-lactamases resulting in resistance to beta-lactam type antibiotics.

Beta-Lactamase Inhibitors

• Drugs that bind to beta-lactamases and prevent them from destroying the β-lactams.
• Examples: Clavulanic acid, sulbactam, tazobactam

Penicillin/Cephalosporin-Beta-Lactamase Combinations

• Drug preparations combine a β-lactam with a beta-lactamase inhibitor (examples and trade names).

Cephalosporins

• Derived from fungi.
• Similar structure and mechanism of action to penicillins (inhibit cell wall synthesis).
• First-generation drugs do not reach therapeutic levels in cerebrospinal fluid (CSF). Important for treating meningitis.

Mechanism of Action of Cephalosporins

• Inhibit cell wall synthesis via binding to penicillin-binding proteins (PBP).
• Bactericidal.
• Time-dependent killing – Maintain drug levels above MIC.

Pharmacokinetics of Cephalosporins

• Widely absorbed and distributed in most body fluids, including placenta and breast milk.
• Excreted in urine; dose adjustments needed in renal impairment.
• First-generation do not reach good levels in CSF; 2nd- and 3rd-generation drugs reach good levels and are especially important in treating meningitis

Classification of Cephalosporins

• Categorized based on spectrum of activity; newer generations have wider Gram-negative antibacterial activity with some less Gram-positive activity.

Examples of Cephalosporins

• A table of 1st, 2nd, 3rd, and 4th generation cephalosporins, showing their routes and dosage information.

Major Differences between Cephalosporin Generations

• Table summarizing the activities against Gram-negative bacteria, resistance to beta-lactamases, and distribution to CSF.

Clinical Uses of Cephalosporins

• Broad spectrum and safety profile for infections.
• Earlier generations are common in community-acquired infections.
• Later generations help treat Gram-negative bacteria infections, such as hospital-acquired or complicated infections.

Adverse Effects of Cephalosporins

• Common adverse effects- allergic reactions (cross-allergy with penicillin).
• Prolonged high doses can cause blood disorders in some patients, such as diarrhea, pain at injection sites, and nephrotoxicity.

Mechanisms of Bacterial Resistance

• Mechanisms by which bacteria develop resistance to cephalosporins:
• Destruction of the β-lactam ring by β-lactamases.
• Altered affinity of cephalosporins for their target site.
• Decreased penetration of cephalosporins to its target site.

Carbapenems

• Another beta-lactam group.
• Broad-spectrum, resistant to beta-lactamases.
• Often a last resort in treating infections (e.g., septicemia, intra-abdominal infections).
• Examples: Imipenem, meropenem.

Vancomycin

• Glycopeptide antibiotic used for serious gram-positive bacterial infections when other choices fail.
• Treatment of choice for methicillin-resistant Staphylococcus aureus (MRSA).
• MOA- Inhibit cell wall synthesis at a site different from beta-lactams.

Pharmacokinetics of Vancomycin

• Poorly absorbed from the gastrointestinal tract (oral).
• Widely distributed in tissues; excreted by kidneys.
• Time-dependent killing, therapeutic drug monitoring (TDM) required in renal failure.

Adverse Effects of Vancomycin

• Serious adverse effects- ototoxicity (tinnitus, deafness), nephrotoxicity (at high plasma levels).
• Rapid IV administration may cause vasodilation and hypotension (red man syndrome).
• Other side effects: fever, rash, injection site pain.

Inhibition of Protein Synthesis

• Antibiotic list example of drugs that inhibit protein synthesis.

Aminoglycosides

• Inhibit protein synthesis in ribosomes by binding to 30S ribosomes.
• Bactericidal, concentration-dependent killing.
• Used for specific bacterial infections.

Pharmacokinetics of Aminoglycosides

• Usually given intravenously or intramuscularly.
• Eliminated primarily in urine; regular monitoring crucial in patients with renal impairment.
• Poor penetration into cerebrospinal fluid (CSF).

Adverse Effects of Aminoglycosides

• Ototoxicity, nephrotoxicity are common side effects and increase with high dose or extended duration;
• Neuromuscular blockade.
• Other potential side effects: rash, hemolytic anemia, bleeding.

Examples of Aminoglycosides

• Gentamicin, tobramycin, streptomycin, neomycin, netilmicin, amikacin, framycetin are Aminoglycosides.

Drug Interactions of Aminoglycosides

• Penicillin interactions decrease aminoglycoside effectiveness.
• Caution is needed to avoid interactions with other nephrotoxic drugs.

Macrolides

• Broad-spectrum antibiotics targeting bacterial 50S ribosomal subunits to inhibit protein synthesis.
• Mostly bacteriostatic, but can be bactericidal at high concentrations.
• Examples: erythromycin, azithromycin, clarithromycin

Examples of Macrolides

• Erythromycin (base, stearate, ethylsuccinate, estolate)
• Azithromycin
• Clarithromycin

Pharmacokinetics of Macrolides

• Gastric acid destroys erythromycin, acid-resistant salts needed for oral absorption.
• Food typically does not impact absorption of acid-resistant macrolides.
• Excreted in bile, feces, and urine; renal impairment is rarely a contraindication

Adverse Effects of Macrolides

• Common adverse effects- gastrointestinal (GI) disturbances (nausea, vomiting, diarrhea, abdominal cramps).
• Hepatotoxicity is possible at high doses.
• Reversible effects with drug discontinuation.

Interactions of Macrolides

• Can inhibit the metabolism of other medications.
• Can reduce serum levels of other drugs, including anticoagulants, other antimicrobials, and CNS/muscle relaxant drugs.
• Antacids may decrease azithromycin levels.

Mechanism of Resistance of Macrolides

• Active efflux pumps actively export the macrolide out of bacterial cells
• Altered target sites within bacterial ribosomes, making the binding site less attractive for macrolides.

Tetracyclines

• Broad-spectrum antibiotics that bind to bacterial 30S ribosomal subunits, inhibiting protein synthesis.
• Bacteriostatic.
• Selectively taken up by bacterial transport systems.

Examples of Tetracyclines

• Tetracycline, minocycline, doxycycline.

Pharmacokinetics of Tetracyclines

• Usually given orally; IM injections are painful, IV for severe infection.
• Absorption impacted by calcium, iron, or magnesium salts, or antacids—taken on an empty stomach.
• Widely distributed, including placental transfer.
• Primarily excreted in urine.

Adverse Effects of Tetracyclines

• Gastrointestinal disturbances (nausea, vomiting, diarrhea).
• Photosensitivity (protective clothing and sunblock advised).
• Discoloration of permanent teeth (contraindicated in pregnant women and children <8 years old).
• Possible vestibular disturbances (minocycline).

Other Inhibitors of Protein Synthesis

• Drugs targeting protein synthesis via diverse mechanisms.
• Clindamycin- similar spectrum to erythromycin; commonly for joint infections, dental infections, or serious intra-abdominal infections.
• Chloramphenicol- broad spectrum, but reserved for life-threatening infections. (Serious adverse effect- "gray baby syndrome"). (eye and ear drops, systemic use can cause bone marrow damage)
• (Other inhibitors of protein synthesis discussed in detail.)

Inhibition of Nucleic Acid Synthesis

• Fluoroquinolones, sulfonamides/trimethoprim, metronidazole, nitrofurantoin are included in this class to inhibit nucleic synthesis.

Fluoroquinolones

• Inhibit DNA gyrase, an enzyme vital for bacterial DNA synthesis.
• Bactericidal, concentration-dependent killing.
• Important in treating serious infections, especially hospital-acquired infections and community-acquired infections.

Examples of Fluoroquinolones

• Ciprofloxacin, moxifloxacin, levofloxacin, ofloxacin, and norfloxacin.

Adverse Effects of Fluoroquinolones

• Gastrointestinal upset, allergic reactions, CNS effects (dizziness, headache, confusion), convulsions (especially if combined with NSAIDs), tendon rupture (in elderly or on steroids).

Drug Interactions of Fluoroquinolones

• Potent inhibitors of liver enzymes, increasing effects of other medications.
• Antacids decrease absorption.

Mechanisms of Resistance of Fluoroquinolones

• Efflux pumps decrease intracellular quinolone concentration.
• Plasmid-mediated resistance genes produce proteins that bind to DNA gyrase; protecting the target.
• Mutations in DNA gyrase or topoisomerase IV reduce binding affinity.

Sulfonamides

• Inhibit folic acid synthesis, crucial for bacterial nucleic acid synthesis. Not effective against organisms able to acquire folic acid from diet.
• Bacteriostatic.
• Similar structure to PABA, thus acting as a competitive inhibitor.

Sulfonamide-Trimethoprim Combinations

• Combination of drugs provides a synergistic effect.
• Inhibit different steps in folate synthesis, thus more effective against susceptible bacteria, although resistance is common.

Examples of Sulfonamides

• Sulfamethoxazole/Trimethoprim (Bactrim), sulfamethazoline, sulfadizine, silver sulfadiazine.
• Silver sulfadiazine- topical treatment for infected burns.

Pharmacokinetics of Sulfonamides

• Rapid oral absorption; widespread distribution, including brain.
• Primarily metabolized in liver, excreted by the kidneys.
• Can cause crystalluria due to low water solubility.

Adverse Effects of Sulfonamides

• Skin rash, Stevens-Johnson syndrome, blood disorders (hemolytic anemia, aplastic anemia), photosensitivity, crystalluria.

Contraindications for Sulfonamides

• Drug allergy (sulfa drugs)
• Pregnancy
• Infants younger than 2 months of age (increased risk of kernicterus).

Metronidazole

• Bactericidal against anaerobic bacteria and protozoans.
• Well absorbed orally; penetrates tissues and CSF.
• Potentially hepatotoxic; may interact with alcohol.

Nitrofurantoin

• Bactericidal against specific Gram-positive/Gram-negative bacteria causing lower UTIs.
• Rapid renal excretion; contraindicated in renal failure (high plasma levels cause toxicity).
• Limited antibacterial activity to the bladder only, because of low plasma concentrations.
• Common side effects- GI irritation, nausea, vomiting, diarrhea, neuropathy, and hemolytic anemia (G6PD patients).

Antimicrobial Resistance

• Microorganisms develop resistance to particular antibiotics.
• Resistance determined through culture and sensitivity testing.
• Resistance is a significant issue impacting treatments.

Bacterial Resistance

• Some bacteria possess inherent resistance.
• Bacteria may develop acquired resistance via mutations and gene transfers.
• Common mechanisms include inactivation, decreased permeability, modification of target, and use of alternative pathways.

What Causes Resistance?

• Widespread use of antibiotics.
• Globalized travel spreading resistant bacteria.
• Interrupted or inadequate antibiotic treatments.

Mechanisms for Acquiring Resistance

• Inactivation of antibiotic molecules
• Efflux pumping of antibiotic molecules out from bacterial cells
• Reduced permeability to antibiotics
• Modification of antibiotic targets
• Use of alternative metabolic pathways

Inactivation of Antibiotic Molecules (e.g. beta-lactamases)

• Enzymes break down the antibiotic molecule.
• Example- beta-lactamases open beta-lactam rings and inactivate drugs.

Efflux Pumping

• Active transport mechanisms pump antibiotics out of microbial cells.

Reduced Permeability

• Bacteria reduce membrane permeability, preventing antibiotic entry.

Modification of Antibiotic Targets

• Bacteria modify targets to prevent drugs from binding.

Alteration of Pathways

• Bacteria utilize modified pathways to overcome drug resistance.

Combination Antimicrobial Therapy (overview)

• Broadens spectrum of coverage in initial therapy
• Prevents resistance
• Enables potentiation/synergy
• Allows reduction of individual component toxicity.

Adverse Effects of Antibiotic Therapy

• Normal gut flora killed, leading to diarrhea or colonization with pathogenic bacteria.
• Superinfection may arise (secondary infection with antibiotic-resistant organisms).
• Common side effect- allergic reactions (most commonly penicillin).

Test your knowledge on the differences between Gram-positive and Gram-negative bacteria, including their cell wall structure and oxygen requirements. Explore key features that influence antibiotic resistance and pathogenicity in bacteria. This quiz is perfect for biology students and enthusiasts alike.