뒤로Comprehensive Study Guide: Microbiology Final Exam Review
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Bacteria
Cell Structure and Function of Bacteria
Bacteria are prokaryotic microorganisms with diverse structures and functions. Their cell structures contribute to their survival, pathogenicity, and interaction with hosts.
Flagella as Virulence Factor: Flagella are whip-like appendages that provide motility. Some pathogenic bacteria use flagella to move toward host tissues, aiding in colonization and invasion. Example: Escherichia coli (certain strains), Salmonella.
Capsule as Virulence Factor: The capsule is a polysaccharide layer outside the cell wall that protects bacteria from phagocytosis and desiccation. Example: Streptococcus pneumoniae, Klebsiella pneumoniae.
Fimbriae as Virulence Factor: Fimbriae are hair-like structures that help bacteria adhere to surfaces and host cells. Example: Uropathogenic E. coli (UPEC).
Gram-Positive vs. Gram-Negative Bacteria
Bacteria are classified based on their cell wall structure, which affects their staining properties and pathogenicity.
Gram-Positive (G+): Thick peptidoglycan layer, stains purple. Example: Staphylococcus aureus, Streptococcus pyogenes.
Gram-Negative (G-): Thin peptidoglycan layer, outer membrane with lipopolysaccharide (LPS), stains pink. Example: Escherichia coli, Pseudomonas aeruginosa.
Acid-Fast Bacteria
Acid-Fast Positive: Have mycolic acid in cell wall, resist decolorization by acid-alcohol. Example: Mycobacterium tuberculosis.
Acid-Fast Negative: Lack mycolic acid, do not retain stain after acid-alcohol wash.
Antibiotics: Spectrum and Mechanisms
Antibiotics target specific bacterial structures or functions. Their spectrum refers to the range of bacteria they affect.
Penicillin, Cephalosporin: Inhibit cell wall synthesis.
Tetracycline: Inhibits protein synthesis (binds 30S ribosomal subunit).
Sulfonamides: Inhibit folic acid synthesis.
Isoniazid: Inhibits mycolic acid synthesis (effective against Mycobacterium).
Horizontal Gene Transfer and Antibiotic Resistance
Horizontal Gene Transfer (HGT): Movement of genetic material between bacteria, leading to rapid evolution of antibiotic resistance.
Mechanisms: Transformation, transduction, conjugation.
Exotoxins vs. Endotoxins
Exotoxins: Proteins secreted by bacteria, often highly toxic. Examples: Neurotoxins (e.g., Clostridium botulinum), cytotoxins, enterotoxins.
Endotoxins: Lipopolysaccharide (LPS) component of G- outer membrane, released upon cell lysis. Example: Escherichia coli LPS.
Toxin Type | Produced By | Mode of Action | Example |
|---|---|---|---|
Neurotoxin | Clostridium botulinum | Blocks nerve function | Botulinum toxin |
Cytotoxin | Corynebacterium diphtheriae | Kills host cells | Diphtheria toxin |
Enterotoxin | Vibrio cholerae | Disrupts intestinal cells | Cholera toxin |
Viruses
Basic Structure of Viruses
Viruses are acellular infectious agents with a nucleic acid core and a protein coat (capsid). Some have a lipid envelope.
Nucleic Acid: DNA or RNA, single- or double-stranded.
Envelope: Present in some viruses, derived from host membrane.
Host Specificity: Viruses infect specific hosts or cell types.
Pathogenic DNA and RNA Viruses
DNA Viruses: Herpes simplex virus, Varicella-zoster virus, Hepatitis B virus.
RNA Viruses: Influenza virus, HIV, Hepatitis C virus, Rabies virus.
Lytic vs. Lysogenic Cycles (Bacteriophage)
Lytic Cycle: Virus replicates and lyses host cell.
Lysogenic Cycle: Viral genome integrates into host DNA (prophage), replicates with host.
Reverse Transcriptase: Enzyme that synthesizes DNA from RNA (e.g., HIV).
Integrase: Enzyme that integrates viral DNA into host genome.
Virus Life Cycle and Pathogenicity
Life cycle stage affects disease severity and persistence.
Types of Viral Infections
Acute: Rapid onset, short duration (e.g., influenza).
Chronic: Persistent infection with ongoing virus production (e.g., hepatitis B).
Latent: Virus remains dormant, can reactivate (e.g., herpesviruses).
Antiviral Therapy
Acyclovir: Inhibits herpesvirus DNA polymerase.
Zidovudine (AZT): Inhibits HIV reverse transcriptase.
Oseltamivir (Tamiflu): Inhibits influenza neuraminidase.
Eukaryotic Microorganisms
Comparison of Eukaryotic Parasites
Eukaryotic parasites include protozoa, fungi, and helminths. They differ in structure, life cycle, and disease epidemiology.
Group | Cell Structure | Life Cycle | Example Disease |
|---|---|---|---|
Protozoa | Unicellular, no cell wall | Complex, often multiple hosts | Malaria (Plasmodium) |
Fungi | Unicellular (yeast) or multicellular (mold), chitin cell wall | Spores, budding | Candidiasis (Candida albicans) |
Helminths | Multicellular, complex organs | Egg, larva, adult stages | Schistosomiasis (Schistosoma) |
Examples of Pathogenic Eukaryotes
Protozoan: Plasmodium (malaria), Giardia lamblia (giardiasis).
Helminths: Ascaris lumbricoides (roundworm), Schistosoma (blood fluke).
Fungi: Candida albicans (yeast infection), Aspergillus (aspergillosis).
Treatment of Parasitic and Fungal Infections
Amphotericin B: Antifungal, disrupts fungal cell membrane.
Ivermectin: Antihelminthic, paralyzes worms.
Praziquantel: Antihelminthic, increases cell membrane permeability.
Metronidazole: Antiprotozoal, damages DNA.
Definitive vs. Intermediate Hosts
Definitive Host: Host in which parasite reaches maturity and reproduces sexually.
Intermediate Host: Host in which parasite undergoes development but does not reach maturity.
Innate Immunity
Host-Microorganism Interactions
Normal microbiota protect against pathogens by competing for resources and producing inhibitory substances.
First Line of Defense
Physical barriers: skin, mucous membranes.
Chemical barriers: lysozyme, acidic pH.
Second Line of Defense
Phagocytosis: Engulfment and destruction of microbes by phagocytes.
Interferon: Proteins that inhibit viral replication.
Fever: Elevated body temperature inhibits pathogens.
Inflammation: Localized response to injury or infection.
Complement Proteins: Enhance phagocytosis, lyse microbes.
Pathogen Evasion of Innate Immunity
Capsule formation, antigenic variation, inhibition of phagolysosome fusion.
Epidemiology
Reservoirs and Transmission
Reservoirs: Natural habitats of pathogens (humans, animals, environment).
Transmission: Direct contact, airborne, vector-borne, fomites.
Drug Spectrum and Selective Toxicity
Narrow Spectrum: Effective against specific bacteria.
Broad Spectrum: Effective against a wide range of bacteria.
Selective Toxicity: Drug targets pathogen with minimal harm to host.
Types of Infections
Primary: Initial infection.
Secondary: Follows primary infection.
Opportunistic: Caused by normally harmless microbes in immunocompromised hosts.
Latent: Dormant infection.
Chronic: Long-lasting infection.
Acute: Rapid onset, short duration.
Endemic: Constantly present in a population.
Epidemic: Sudden increase in cases.
Pandemic: Global epidemic.
Nosocomial: Hospital-acquired infection.
Emerging/Reemerging Diseases and Bioterrorism
New or increasing diseases (e.g., COVID-19, Ebola).
Potential use of pathogens as bioterrorist agents (e.g., Bacillus anthracis).
Microbial Diseases of Organ Systems
Key Concepts
Identify reservoirs, portals of entry/exit, cell structure, and virulence factors for each disease.
Recognize symptoms and unique characteristics of diseases affecting skin, soft tissues, eyes, urinary, reproductive, respiratory, and digestive systems.
Methods of Microbial Control
Sanitization: Reducing microbial load to safe levels.
Chlorination: Disinfection of water.
Autoclave: Sterilization using pressurized steam.
Ethanol: Alcohol-based disinfectant.
Filtration: Physical removal of microbes.
UV: Ultraviolet light damages microbial DNA.
Commercial Canning: Heat sterilization of food.
Disinfectant: Chemical agents that kill microbes on surfaces.
Vaccination: Induces adaptive immunity.
Importance of Disease Prevention and Environmental Sanitation
Prevention reduces disease incidence and spread.
Sanitizing food, water, and environment is critical for public health.