Exam 1 Study Guide PDF

Exam I study guide The following learning objectives will be on Exam I. Chapter 1 1.Describe in general terms the differences between prokaryotes (bacteria and archaea), eukaryotes, viruses, viroids, and prions. Give specific examples of each. Prokaryotes: Simple cells without a n...

Exam I study guide The following learning objectives will be on Exam I. Chapter 1 1.Describe in general terms the differences between prokaryotes (bacteria and archaea), eukaryotes, viruses, viroids, and prions. Give specific examples of each. Prokaryotes: Simple cells without a nucleus. Bacteria: E. coli – have a cell wall. Archaea: Methanogens – live in extreme environments, have different cell membranes. Eukaryotes: Complex cells with a nucleus. ▪ Protists: Paramecium – single-celled, with organelles. ▪ Fungi: Yeast – have a cell wall made of chitin. Viruses: Genetic material surrounded by protein coat. Not really alove Example: Flu virus. Viroids: Short pieces of RNA affecting plants. Example: Potato spindle tuber viroid. Prions: Misfolded proteins causing brain diseases. Example: Creutzfeldt- Jakob disease. Protozoa- Animal like protist. Be careful what water you drink. 2.Discuss one example of how microbiology was used in the ancient world. Ancient Egyptians used molds for making bread and beer, which involved yeast. 3.Discuss the contributions of Florence Nightengale, Louis Pasteur, Ignaz Semmelweiss, Joseph Lister, Edward Jenner, Robert Koch, and Alexander Flemming. [This will be a matching question on the exam.] Florence Nightingale: Tracked Soldiers deaths from different causes. Helped show that germs spread disease. Louis Pasteur: Considered the father of microbiology disproving spontaneous generation. Ignaz Semmelweis: Tried to get doctors to wash their hands before delivering babies, but wasn’t very successful. Joseph Lister: Developed chemicals to clean surgical instruments. Edward Jenner: Created the smallpox vaccine. Robert Koch: Searching for a cause of cholera, he developed the process for identifying pathogens. Alexander Fleming: Discovered penicillin. 4.Explain Koch’s postulates for showing that a microbe causes disease. 5.Discuss three of the five limitations of Koch's postulates. [Extra credit for more!] Postulate 1: Isolate infected host Postulate 2: Pure culture the specimen of infected host. Postulate 3: “Inject” a health host with results given from past culture. Postulate 4: Re-isolate the new specimen 1. Some microbes can’t grow. For example, viruses need a host cell to replicate. 2. Lack of proper animal models, some microbes can’t affect certain animals (cause of syphilis study) 3. Non-pathogenic strains. For example, 85% of people who have the HIV disease don’t have sx. 4. Asymptomatic carriers 5. Chronic carriers, they can have the microbe to infect other people, but the host doesn’t have sx. Chapter 2 1. Using specific examples, explain the difference between signs and symptoms. Signs: Observable by others (e.g., rash). Symptoms: Felt by the patient (e.g., headache). 2. Explain the difference between normal microbiota and pathogens. Normal Microbiota: Good bacteria living on or in the body (e.g., Lactobacillus). Pathogens: Harmful microorganisms that cause disease (e.g., Staphylococcus aureus). 3. Discuss three ways normal microbiota can prevent overgrowth of pathogenic bacteria (microbial antagonism). Compete for Nutrients: Outcompete pathogens for resources. Produce Antimicrobials: Create substances that kill or inhibit pathogens. Maintain pH Levels: Produce acids that make the environment less favorable for pathogens. 4. Explain how the microbiome is acquired and discuss three different factors that can determine the make up of an individual’s microbiome. Acquired: From birth, environment, and diet. Factors: ▪ Birth Method: Vaginal vs. cesarean delivery. ▪ Diet: Changes in diet can alter microbiome. ▪ Antibiotics: Can disrupt normal microbiota. 5. Define the different types of infections and give examples of each: acute, chronic, opportunistic, secondary, localized, focal, systemic, latent. Acute: Short-term, quick onset (e.g., flu). Chronic: Long-lasting (e.g., tuberculosis). Opportunistic: Affect weakened immune systems (e.g., Candida in immunocompromised individuals). Secondary: Follows a primary infection (e.g., bacterial pneumonia after flu). Localized: Limited to a specific area (e.g., boil). Focal: Originates in one area but spreads (e.g., dental abscess). Systemic: Spreads throughout the body (e.g., sepsis). Latent: Pathogen is inactive but can reactivate (e.g., herpes simplex virus). 6. Define the terms and give examples of each: communicable, non-communicable, contagious, iatrogenic, nosocomial, zoonotic. Communicable: Spread from one person to another (e.g., tuberculosis). Non-communicable: Not spread between people (e.g., tetanus). Contagious: Easily spread (e.g., chickenpox). Iatrogenic: Caused by medical treatment (e.g., infections from procedures). Nosocomial: Acquired in healthcare settings (e.g., MRSA). Zoonotic: Transmitted from animals to humans (e.g., rabies). 7. Explain the difference between pathogenicity and virulence. Define the terms: infectious dose, median infectious dose, LD50, ID50. Explain why the median infectious dose is used to measure virulence and not the absolute infectious dose. Pathogenicity: Ability to cause disease. Virulence: Degree of pathogenicity (how severe the disease is).  Infectious Dose (ID50): Number of pathogens needed to infect 50% of hosts. Median Infectious Dose: Reflects virulence; a lower ID50 means higher virulence. LD50: Lethal dose for 50% of hosts. 8. Define the terms host range and tissue specificity. Explain the physiological basis for each. Host Range: Types of hosts a pathogen can infect (e.g., HIV infects humans). Tissue Specificity: Specific tissues or organs targeted by a pathogen (e.g., Legionella pneumophila targets the lungs). 9.Outline the five steps/stages of the infection process/pathogenesis, explaining what happens in each step. Discuss the role adhesins, receptors, and the EPS play in the process. Incubation: No symptoms yet. Prodromal: Early symptoms begin. Illness: Full-blown symptoms. Decline: Symptoms decrease. Convalescence: Recovery phase. Adhesion: Pathogens stick to host cells using adhesins. Invasion: Pathogens enter host tissues. Colonization: Pathogens grow and multiply. Evasion: Pathogens avoid immune system detection. Damage: Pathogens cause harm through toxins or other means. EPS (Exopolysaccharides): Protect pathogens in biofilms. 10.Summarize the five stages of illness (incubation, prodromal, etc.) and describe the number of pathogens present at each stage. Incubation: No symptoms yet. Prodromal: Early symptoms begin. Illness: Full-blown symptoms. Decline: Symptoms decrease. Convalescence: Recovery phase. 11.Distinguish between endemic, epidemic, and pandemic. Describe the characteristics of pathogens capable of causing pandemics. Endemic: Regularly found in a specific area (e.g., malaria in Africa). Epidemic: Sudden increase in cases in a specific area (e.g., flu outbreak). Pandemic: Widespread across countries or continents (e.g., COVID-19). 12.Explain what emerging and re-emerging diseases are. Discuss what might happen that causes a disease to emerge or re-emerge. Emerging Diseases: New or increasing in incidence (e.g., COVID-19). Re-emerging Diseases: Old diseases that come back (e.g., tuberculosis). Causes: Changes in environment, human behavior, or microbial evolution. Chapter 5 1.Describe the structure and function of the bacterial cell. Explain how prokaryotes (bacteria) differ from eukaryotes. Terms to know: cell wall, cell membrane, capsule. Structure: Simple cells with a cell wall, membrane, and sometimes a capsule. Prokaryotes vs. Eukaryotes: Prokaryotes lack a nucleus; eukaryotes have one. 2.Using specific examples, discuss how two differences between bacteria and eukaryotes can be exploited to selectively kill bacteria with antibiotics. Cell Wall: Antibiotics like penicillin target bacterial cell walls, which eukaryotes lack. Ribosomes: Some antibiotics target bacterial ribosomes, different from eukaryotic ones. 3.Describe the structure of bacteria cell walls. Explain the difference between Gram – positive and Gram-negative cell walls. Terms to know: peptidoglycan, LPS.  Gram-Positive: Thick peptidoglycan layer, contains teichoic acids (e.g., Streptococcus). Gram-Negative: Thin peptidoglycan layer, outer membrane with LPS (e.g., E. coli). 4.Explain why Gram-negative infections are more problematic than Gram-positive ones (two reasons). LPS (Endotoxin): Causes severe immune responses. Outer Membrane: Acts as a barrier to many antibiotics. 5.Describe how the structure of mycobacteria differ from that of other bacteria and discuss the clinical significance. (Why are mycobacteria infections so much harder to treat?) Structure: Thick, waxy cell wall (mycolic acids). Significance: Makes infections hard to treat with standard antibiotics (e.g., tuberculosis). 6. Explain what virulence factors are and give specific example Definition: Molecules produced by pathogens that enhance their ability to cause disease. Example: Exotoxins produced by Clostridium tetani causing tetanus. 7.Describe the function of pili and flagella and explain the role they play in infection/pathogenesis. Pili: Help bacteria attach to host tissues. Flagella: Enable movement, aiding in infection spread. 8.Explain the role of host cell receptors in infection. Describe how antibodies to adhesins can prevent infection. You need to know about host receptors for this exam, but the part about antibodies will be on Exam II. Receptors: Pathogens bind to host cell receptors to enter cells.  Antibodies to Adhesins: Can prevent pathogens from sticking and causing infection.