BackMicrobiology Study Guide: Viruses, Infectious Diseases, Immunization, and Antimicrobial Drugs
Study Guide - Smart Notes
Tailored notes based on your materials, expanded with key definitions, examples, and context.
Viruses, Viroids, and Prions
Definitions and Structure
Viruses are acellular infectious agents composed of genetic material (DNA or RNA) surrounded by a protein coat. A virion is a complete, infectious viral particle outside a host cell.
Virion Parts: Nucleic acid core, capsid (protein coat), and sometimes an envelope.
Capsid: Protects viral genome and aids in attachment to host cells.
Capsid Shapes: Helical, polyhedral (icosahedral), and complex.
Envelope: Lipid membrane derived from host cell, contains viral glycoproteins for host recognition.
Example: Influenza virus has a helical capsid and an envelope.
Host Specificity and Classification
Host Specificity: Determined by viral surface proteins and host cell receptors; viruses infect only specific cell types.
Classification: Based on nucleic acid type, presence of envelope, shape, and size.
Viral Replication Cycles
Lytic Cycle: Virus replicates rapidly, lyses host cell to release progeny.
Lysogenic Cycle: Viral genome integrates into host DNA (prophage), replicates with host, may later enter lytic cycle.
Release Mechanisms: Lysis (host cell bursts) vs. budding (enveloped viruses exit without killing cell).
Latency and Oncogenesis
Latency: Animal viruses may remain dormant in host cells, reactivating later (e.g., herpesviruses).
Neoplasia: Uncontrolled cell division; tumor is a mass of neoplastic cells.
Benign vs. Malignant: Benign tumors do not invade; malignant tumors (cancers) invade and metastasize.
Viral Oncogenesis: Some viruses (oncoviruses) disrupt cell cycle control, leading to cancer.
Viroids and Prions
Viroids: Small, circular RNA molecules infecting plants; lack protein coat.
Prions: Infectious proteins causing neurodegenerative diseases by inducing abnormal folding of normal proteins.
Prion Control: Resistant to standard sterilization; require incineration or strong chemicals.
Prion Diseases: Creutzfeldt-Jakob disease, kuru, scrapie, bovine spongiform encephalopathy (mad cow disease).
Infection, Infectious Diseases, and Epidemiology
Symbiosis and the Microbiome
Symbiosis describes close associations between different organisms. The human microbiome consists of all microorganisms living on and in the body.
Types of Symbiosis: Mutualism (both benefit), commensalism (one benefits, other unaffected), amensalism (one harmed, other unaffected), parasitism (one benefits, one harmed).
Resident Microbiota: Permanent, established microbes.
Transient Microbiota: Temporary, may be removed by competition or immune system.
Opportunistic Pathogens: Cause disease when host defenses are compromised, normal microbiota are disrupted, or introduced to unusual sites.
Reservoirs and Transmission
Reservoirs: Human (carriers), animal (zoonoses), and nonliving (soil, water, food).
Contamination vs. Infection: Contamination is presence of microbes; infection is successful invasion and multiplication.
Portals of Entry: Skin, mucous membranes, placenta, parenteral route (injection, wounds).
Adhesion Factors: Structures or molecules (fimbriae, adhesins) that help pathogens attach to host cells.
Pathogenicity and Disease
Infection: Invasion by pathogen.
Disease: Disruption of normal body function.
Morbidity: State of being diseased.
Pathogenicity: Ability to cause disease.
Virulence: Degree of pathogenicity.
Symptoms: Subjective effects (pain, fatigue).
Signs: Objective evidence (fever, rash).
Syndrome: Group of signs and symptoms.
Etiology: Study of disease cause.
Koch’s Postulates
1. Pathogen must be present in all cases of disease.
2. Pathogen must be isolated and grown in pure culture.
3. Pure culture must cause disease in healthy host.
4. Pathogen must be re-isolated from experimentally infected host.
Limitations: Some pathogens cannot be cultured; ethical issues; polymicrobial diseases.
Virulence Factors
Extracellular Enzymes: Aid invasion (e.g., hyaluronidase).
Toxins: Exotoxins (secreted), endotoxins (part of Gram-negative cell wall).
Adhesion Factors: Facilitate attachment.
Antiphagocytic Factors: Capsules, proteins that inhibit phagocytosis.
Stages and Transmission of Infectious Diseases
Stages: Incubation, prodromal, illness, decline, convalescence.
Transmission: Contact (direct, indirect, droplet), vehicle (air, water, food), vector (biological, mechanical).
Droplet vs. Airborne: Droplet is short-range; airborne is long-range, suspended particles.
Mechanical vs. Biological Vectors: Mechanical (passive carriers), biological (pathogen develops in vector).
Classification and Epidemiology
Classification: By body system, taxonomic group, longevity (acute, subacute, chronic, latent), communicability (communicable, contagious, noncommunicable).
Epidemiology: Study of disease distribution and determinants.
Incidence: New cases in a time period.
Prevalence: Total cases at a given time.
Endemic: Constantly present.
Sporadic: Occasional cases.
Epidemic: Sudden increase.
Pandemic: Worldwide epidemic.
Healthcare-Associated Infections (HAIs)
HAIs: Acquired in healthcare settings; influenced by patient susceptibility, invasive procedures, and hospital environment.
Types: Exogenous (from environment), endogenous (from patient’s own flora), iatrogenic (from medical procedures).
Immunization and Immune Testing
Types of Vaccines
Attenuated (live): Weakened pathogens; strong, long-lasting immunity; risk for immunocompromised.
Inactivated (killed): Safer, weaker response; may require boosters.
Toxoid: Inactivated toxins; require boosters.
Subunit: Purified antigens; fewer side effects.
Conjugate: Linked antigens for better response in children.
Immunization Strategies
Routine Immunization: Protects individuals and populations (herd immunity); contact immunity can protect unvaccinated.
Risks: Rare adverse reactions; benefits outweigh risks for most populations.
Passive Immunotherapy: Antibodies from humans or animals; immediate, short-term protection.
Active Immunization: Stimulates immune memory; slower onset, longer duration.
Antimicrobial Drugs
Principles and Mechanisms
Selective Toxicity: Drugs target microbial structures/functions not found in host.
Mechanisms:
Inhibit cell wall synthesis (e.g., penicillins, cephalosporins).
Inhibit protein synthesis (e.g., tetracyclines, aminoglycosides).
Disrupt cytoplasmic membranes (e.g., polymyxins, amphotericin B).
Inhibit metabolic pathways (e.g., sulfonamides).
Inhibit nucleic acid synthesis (e.g., quinolones, nucleotide analogs, reverse transcriptase inhibitors).
Block attachment/entry (e.g., attachment antagonists, fusion inhibitors).
Drug Spectrum and Efficacy
Narrow-spectrum: Target specific microbes; fewer side effects.
Broad-spectrum: Affect many types; risk of superinfection.
Therapeutic Index: Ratio of toxic dose to effective dose:
Therapeutic Window: Range of doses that are effective without being toxic.
Antimicrobial Resistance
Resistance Development: Arises via mutation or acquisition of resistance genes (e.g., R plasmids).
Mechanisms:
Enzymatic drug inactivation
Altered drug targets
Decreased permeability
Efflux pumps
Bypass metabolic pathways
Target overproduction
Biofilm formation
Gene Transfer: Conjugation, transformation, transduction.
Cross Resistance: Resistance to similar drugs; Multiple Resistance: Resistance to unrelated drugs.
Retarding Resistance: Use drugs only when necessary, complete courses, use combination therapy, limit agricultural use.
Ideal Antimicrobial Drug Characteristics
Selective toxicity
Nonallergenic
Stable in body fluids
Low resistance development
Inexpensive
Broad tissue distribution
Table: Comparison of Vaccine Types
Vaccine Type | Example | Advantages | Disadvantages |
|---|---|---|---|
Attenuated (Live) | MMR | Strong, long-lasting immunity | Risk for immunocompromised |
Inactivated (Killed) | Polio (Salk) | Safe, stable | Weaker response, boosters needed |
Toxoid | Tetanus | Targets toxins | Requires boosters |
Subunit | Hepatitis B | Fewer side effects | Weaker response |
Conjugate | Hib | Effective in children | Complex production |
Table: Mechanisms of Antimicrobial Resistance
Mechanism | Description |
|---|---|
Enzymatic Inactivation | Drug destroyed by microbial enzymes (e.g., beta-lactamases) |
Altered Target | Drug target modified to prevent binding |
Decreased Permeability | Reduced drug entry into cell |
Efflux Pumps | Active removal of drug from cell |
Bypass Pathways | Alternative metabolic pathways used |
Target Overproduction | Excess target molecules produced |
Biofilm Formation | Protects microbes from drugs |
Additional info: Some explanations and examples were expanded for clarity and completeness based on standard microbiology textbooks.