Chapter 13: Viruses, Viroids, & Prions

General Properties of Viruses

Viruses are acellular infectious agents that require a host cell for replication. They are much smaller than bacteria and cannot be seen with a light microscope.

• Obligate intracellular parasites: Viruses cannot reproduce outside a host cell.

• Structure: Composed of genetic material (DNA or RNA) surrounded by a protein coat.

• Non-living: Do not carry out metabolic processes independently.

Parts of a Virus

• Capsid: Protein shell that encases the nucleic acid; provides protection and aids in attachment.

• Nucleic Acid: Either DNA or RNA, single or double-stranded; contains viral genetic information.

• Envelope: Lipid membrane derived from host cell; present in some viruses, not all.

• Spikes: Glycoproteins protruding from the envelope or capsid; facilitate attachment to host cells.

All viruses possess a nucleic acid and capsid. Some viruses possess an envelope and spikes.

Host Range and Specificity

Host range refers to the spectrum of host cells a virus can infect. Specificity is determined by the presence of compatible receptors on the host cell surface.

• Receptors: Viral attachment depends on specific host cell receptors.

• Example: HIV infects only cells with CD4 receptors.

Taxonomy of Viruses

• Family: Ends in -viridae (e.g., Herpesviridae).

• Genus: Ends in -virus (e.g., Herpesvirus).

• Species: Named by disease or host (e.g., Human herpesvirus 1).

• Subspecies: Designated by numbers or letters.

Bacteriophage Replication: Lytic Cycle

Bacteriophages infect bacteria and replicate via the lytic cycle, resulting in cell lysis.

1. Attachment: Phage binds to bacterial surface.

2. Penetration: Phage injects DNA into host.

3. Biosynthesis: Viral components are synthesized.

4. Maturation: Assembly of new phage particles.

5. Release: Host cell lyses, releasing new phages.

Lysogenic Cycle

Phage DNA integrates into the host genome as a prophage, remaining dormant until triggered to enter the lytic cycle.

• Prophage: Phage DNA incorporated into bacterial chromosome.

• Provirus: Viral DNA integrated into animal host genome.

Animal Virus Replication

1. Attachment: Virus binds to host cell receptors.

2. Penetration: Entry via endocytosis or fusion.

3. Uncoating: Viral capsid removed, releasing nucleic acid.

4. Biosynthesis: Viral genome replicated and proteins synthesized.

5. Maturation: Assembly of viral particles.

6. Release: Viruses exit via budding (enveloped) or lysis (non-enveloped).

Comparison: Animal Virus vs. Bacteriophage Replication

Types of Viral Infections

• Acute: Rapid onset, short duration (e.g., influenza).

• Persistent: Virus remains in host for long periods (e.g., hepatitis B).

• Latent: Virus remains dormant, can reactivate (e.g., herpes simplex).

Oncogenic Viruses (Oncoviruses)

Viruses that can cause cancer by transforming host cells (e.g., HPV).

Cytopathic Effects

• Cell lysis

• Inclusion bodies

• Syncytia formation

• Cell transformation

Prions

Prions are infectious proteins causing spongiform encephalopathies, characterized by sponge-like degeneration of brain tissue.

• Diseases: Spongiform encephalopathies (e.g., Mad Cow Disease).

Chapter 7: Controlling Microbial Growth

Key Terms in Microbial Control

• Sterilization: Complete destruction of all microbial life, including spores.

• Bactericidal (biocide/germicide): Kills bacteria.

• Microbiostatic/bacteriostatic: Inhibits growth, does not kill.

• Disinfection: Destroys pathogens on inanimate objects.

• Decontamination: Reduces microbial load to safe levels.

• Sanitization: Cleans and reduces microbes to acceptable levels.

• Degermation: Removal of microbes from living tissue.

Actions of Antimicrobial Agents

• Alteration of membrane permeability: Disrupts cell membrane, causing leakage.

• Damage to nucleic acids: Prevents replication and transcription.

• Damage to proteins: Denatures enzymes and structural proteins.

Factors Influencing Effectiveness

• Number of microbes

• Environment: Presence of organic matter, temperature, pH.

• Time of exposure

• Microbial characteristics: Endospores, biofilms, etc.

Physical and Mechanical Methods of Microbial Control

• Heat: Moist heat (autoclave, boiling, pasteurization) and dry heat (incineration, hot air).

• Low temperatures: Microbiostatic, slows growth but does not kill.

• Desiccation: Removal of water inhibits growth.

• Radiation: Ionizing (sterilization) vs. non-ionizing (disinfection).

• Filtration: Mechanical removal of microbes; HEPA filters for air, membrane filters for liquids.

Effectiveness Table

Moist heat is preferred for sterilization due to shorter exposure times and greater effectiveness.

Chemical Agents for Microbial Control

• Phenol: Disrupts cell membranes and denatures proteins.

• Halogens: Oxidize cellular components (e.g., chlorine, iodine).

• Alcohols: Denature proteins and dissolve membranes.

• Surfactants: Lower surface tension, disrupt membranes.

• Peroxygens: Oxidizing agents (e.g., hydrogen peroxide).

• Organic acids: Inhibit metabolism, preserve food.

Relative Resistance of Microbes

Chapter 20: Antimicrobial Drugs

Key Terms

• Broad spectrum: Effective against many types of microbes.

• Narrow spectrum: Effective against specific microbes.

• Selective toxicity: Drug targets microbe without harming host.

• Antibiotics: Natural substances produced by microbes to inhibit others.

• Prophylaxis: Preventative use of drugs.

Selective toxicity is difficult to achieve for fungal and viral infections because their cells are similar to human cells or rely on host machinery.

Major Antibiotic-Producing Genera

• Streptomyces

• Bacillus

• Penicillium

• Cephalosporium

Five Actions of Antimicrobial Drugs

1. Inhibition of cell wall synthesis: Drugs like penicillins and cephalosporins inhibit peptidoglycan cross-linking, causing cell lysis.

2. Disruption of cell membrane: Polymixins disrupt membrane integrity, especially in Gram-negative bacteria.

3. Inhibition of protein synthesis: Aminoglycosides bind 30S ribosome, causing misreading; tetracyclines block tRNA binding; chloramphenicol inhibits peptide bond formation; erythromycin blocks 50S ribosome.

4. Inhibition of nucleic acid synthesis: Drugs interfere with DNA/RNA replication and transcription.

5. Block metabolic pathways: Sulfonamides and trimethoprim inhibit folic acid synthesis via competitive inhibition.

Drug Interactions

• Competitive inhibition: Drug mimics substrate, blocks enzyme (e.g., sulfa drugs).

• Synergism: Combined drugs enhance effect.

• Antagonism: Drugs interfere with each other's action.

Drug Resistance Mechanisms

1. Enzymatic destruction of drug

2. Alteration of drug target

3. Decreased permeability

4. Efflux pumps

5. Bypass of metabolic pathway

Side Effects and Superinfection

• Side effects: Unintended reactions to drugs.

• Normal flora: Beneficial microbes; disruption can lead to superinfection.

Drug Susceptibility Testing

• Kirby-Bauer disk diffusion test: Measures zone of inhibition.

• Dilution tests: Determine minimum inhibitory concentration (MIC).

• E-test®: Gradient diffusion for MIC.

• Therapeutic index: Ratio of toxic dose to effective dose; higher is safer.

Survey of Major Antimicrobial Drug Groups

• Cell wall inhibitors: Beta-lactams (penicillins, cephalosporins); non-beta-lactams (vancomycin, bacitracin).

• Cell membrane disruptors: Polymixins for Gram-negative infections.

• Protein synthesis inhibitors: Aminoglycosides, tetracyclines, oxazolidinones, chloramphenicol, erythromycin.

• Metabolic pathway blockers: Sulfonamides, trimethoprim block folic acid synthesis.

• Antifungal agents: Amphotericin B, nystatin disrupt fungal membranes; toxicity due to similarity to human cells.

• Antiparasitic agents: Side effects common due to similarity to host cells.

• Antiviral agents: Difficult to achieve selective toxicity; mechanisms include blocking entry, preventing maturation, inhibiting nucleic acid synthesis.

Antiviral Drug Mechanisms Table

Chapters 14 & 15: Principles of Disease & Epidemiology

Key Definitions

• Infection: Invasion and multiplication of microbes in host.

• Virulence: Degree of pathogenicity.

• Endogenous infection: Caused by normal flora.

• Exogenous agents: Originating outside the body.

• Opportunistic infection: Occurs when normal flora cause disease in compromised host.

• Toxemia: Toxins in blood.

• Bacteremia: Bacteria in blood.

• Viremia: Viruses in blood.

Normal Flora (Microbiota)

• Positive impacts: Prevent pathogen colonization, aid digestion, stimulate immunity.

• Absence: Increased susceptibility to infection.

• Colonization: Begins at birth; newborns acquire flora from environment.

• Resident flora: Permanent, stable population.

• Transient flora: Temporary, may be removed.

• Sites: Skin, GI tract, respiratory tract.

• Sterile sites: Blood, cerebrospinal fluid, internal organs.

Pathogens

• Opportunistic pathogens: Cause disease in compromised hosts.

• Strict pathogens: Cause disease in healthy hosts.

Infectious Dose (ID)

Minimum number of microbes required to cause infection. Lower ID = higher virulence.

Requirements for Infection

1. Entry via portal (skin, GI, respiratory, urogenital)

2. Attachment to host (spikes, capsule, fimbriae)

3. Survival and multiplication

4. Causing damage (exoenzymes, toxins)

5. Exit via portal (respiratory, GI, skin, etc.)

Exoenzymes and Toxins

• Exoenzymes: Secreted enzymes that damage host (e.g., hyaluronidase).

• Exotoxins: Secreted proteins, specific effects (e.g., botulinum toxin).

• Endotoxins: Lipid A of Gram-negative bacteria, general effects.

Exotoxin vs. Endotoxin Table

Stages of Infectious Disease

1. Incubation period: Time between exposure and symptoms.

2. Prodromal period: Early, mild symptoms.

3. Period of illness: Severe symptoms.

4. Period of decline: Symptoms subside.

5. Period of convalescence: Recovery.

Signs vs. Symptoms

• Signs: Objective, measurable (e.g., fever).

• Symptoms: Subjective, felt by patient (e.g., pain).

Types of Infection

• Local: Confined to one area.

• Systemic: Spread throughout body.

• Focal: Starts local, spreads to another site.

• Primary: Initial infection.

• Secondary: Subsequent infection.

• Subclinical: No noticeable symptoms.

Communicable vs. Non-Communicable Diseases

• Communicable: Transmitted from person to person.

• Non-communicable: Not transmitted between people.

Epidemiology Terms

• Epidemiology: Study of disease distribution.

• Epidemic: Sudden increase in cases.

• Pandemic: Worldwide epidemic.

• Endemic: Constant presence in population.

• Sporadic: Occasional cases.

Centers for Disease Control and Prevention (CDC)

Main purpose: Monitor, prevent, and control disease.

Transmission Terms

• Vector: Living organism transmitting disease (biological: supports pathogen life cycle; mechanical: passive transport).

• Carrier: Infected individual who can transmit disease.

• Reservoir: Source of pathogen.

• Zoonotic: Disease transmitted from animals to humans.

• Fomite: Inanimate object transmitting disease.

Nosocomial Infections

Hospital-acquired infections; most common type is urinary tract infection.

Old Material: Prokaryotic and Eukaryotic Microbes

Major Groups of Prokaryotes

• Bacteria

• Archaea

Major Groups of Eukaryotic Microbes

• Fungi

• Algae

• Protozoa

• Helminths

Note: Animals and plants are not considered microbes.

Additional info: Academic context and explanations were added to ensure completeness and clarity for exam preparation. Tables were recreated and expanded based on standard microbiology knowledge.