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MCRO 251
| Question | Answer |
|---|---|
| Bacteria Ribosomes | 70S size w/ 50S and 30S subunit 16s rRNA |
| Eukaryotic Ribosomes | 80S size w/ 60s and 40S subunit 18s rRNA |
| Bacteria | Prokaryotic (unicellular) HAS PEPTIDOGLYCAN (Eukarya does not) Has circular chromosomes & plasmids (small extra structure that replicates independently of chromosomes |
| Archaea | Prokaryotic (unicellular) Specific ribosomal RNA |
| Eukarya | Eukaryotic (multi/unicellular) Largest Cell type (think YOU-karyotic, you are bigger than bacteria) |
| Microbiome | The normal collection of microorganisms that live in and on the human body |
| Microbiome (what it does) | - Protect against infections - Oral tolerance - Aids digestions - Producing by-products - Takes up space |
| Hygiene Hypothesis | Early childhood exposure to microorganisms help develop the immune system and protect against allergies |
| Viruses | NON-LIVING - are obligate intracellular parasites meaning they must be inside cell to replicate and do damage 2 primary components: a protein coat and genetic into (DNA or RNA) |
| ID50 | The amount of pathogens it takes to get more than 50% people sick (how infectious the disease is) Low ID50 (bad, easier to get infected) & High ID50 (better, harder to get infected) |
| Ro (R naught) | An estimation of how many people an infected individual will ALSO infect for a particular disease - How contagious it is (must be over 1 ) Higher Ro = more infectious |
| Bacteremia | Presence of bacteria in blood |
| Septicemia | Presence of actively multiplying bacteria in blood |
| Viremia | Presence of viruses in blood |
| Toxemia | Presence of toxins in blood |
| Localized | Infection in 1 specific place |
| Systemic | Infection that has spread throughout the body |
| Focal | Infection that starts local but travels elsewhere in the body |
| Primary pathogen | The pathogen that causes disease in healthy host |
| Secondary pathogen | Pathogen that otherwise wouldn't cause disease but takes advantage of sickness (opportunistic) |
| Colonization | Presence of pathogen with no disease (aka asymptomatic infection) |
| Zoonosis | Disease predominate in animals that accidentally infect humans (ex. rabies) |
| Reservoir | Where it replicates |
| Symptoms | Things that the disease causes that can be felt (ex. headache) |
| Signs | Things that the disease causes that can be seen or measures (ex. fever) |
| Incubation (1) | Time between introduction of organism to onset of symptoms |
| Prodromal Period (2) | Initial feelings of malaise |
| Acute Period (3) | Individual experiences with classic signs and symptoms of disease |
| Convalescence (4) | Period of recuperation and recovery |
| Latency (5) | Infection doesn't "leave" |
| Koch's Postulates (what) | Used to determine the cause of an infectious disease by culturing the agent and reproducing the disease |
| Koch's Postulates (steps) | 1. Pathogenic strains present in disease 2. Microorganism must be grown in culture from diseased hosts 3. Disease must be produced when pure culture of the micro. is introduced into susceptible hosts 4. Micro. must be recovered from infected hosts |
| Koch's Postulates (problems) | - If the microbe can't be cultures - If the microbe has to grow in a community and can't isolated - If the microbe doesn't cause the same disease every time - If the microbe has a human reservoir (unethical) |
| Prevalence | Total number of cases (old and new) in a given population at a specific point of time |
| Incidence | Rate of new cases in a given population within a specific time |
| Duration | Time the disease lasts |
| Morbidity | Incidence of specific disease/ illness (causes of infection) |
| Mortality | Death rate of specific disease/population |
| Immunocompromised | People who have weak immune systems - Can be elderly (65+), chronic illness, babies (<1yr), extremely stressed, pregnant women, malnourished, transplant recipients |
| Sporadic | Disease that happens infrequently and irregularly |
| Endemic | Disease that is constantly maintained at a baseline level in a specific area |
| Outbreak | Sudden increase in disease casa in a relatively small region at a specific point of time |
| Epidemic | Widespread disease in a large area at a specific point of time |
| Pandemic | Disease thats prevalent in every country |
| Virulence factors | ANYTHING that makes an organism more infectious |
| Modes of Transmission: Direct | Reservoir to host - Horizontal - Vertical |
| Modes of Transmission: Direct Indirect | Reservoir to someone else to host - Droplet Nuclei - Vectors (Mechanical vs Biological) - Formites |
| Peptidoglycan | Contains sugar and amino acids that form mesh like layer outside cytoplasmic membrane |
| NAG-NAM sugars | Linked by glycosidic bonds - NAM only has peptide chains on them |
| Tetra peptide chain | Proteins attached to NAM sugar - NAG always nagging NAM - Gram (+) linked together by interbridge - Gram (-) directly linked together |
| Autolysin | Enzyme that breaks down glycosidic bonds - for reproduction |
| Bactoprenol | Molecule that transfers monomer across cell membrane - bacitracin inhibits this |
| Transpeptidase | Makes inter bridges for multiple layers of NAG and NAM |
| Transglycosidase | Makes glycosidic bonds (NAG to NAM) |
| Gram Positive Cell Wall | Lipotechoic acid: Anchors peptidoglycan to plasma membrane Techoic acid: Gives peptidoglycan a neg. charge Have thicker peptidoglycan = more susceptible to antibiotics Purple Gram Stain |
| Gram Negative Cell Wall | Thinner peptidoglycan * LPS = Endotoxin = Gram (-) -> same meaning LPS: sugar on OUTER cell membrane *endotoxin* - Lipid A: Same in all G(-), causes issues in people - O antigen: differs between species & strains Pink Gram Stain |
| Sporulation | Bacteria sporulate when they sense environment is becoming less favorable for survival (ONLY IN GRAM (+) ) |
| Antigenic Drift | Genome changes making harder to treat In all RNA viruses because they are fragile except for Rabies |
| Eukaryotic Flagella is made up of... | ACTIN |
| Prokaryotic Flagella is made up of... | FLAGELLIN |
| Standard Growth Curve: Lag phase | Organism not growing, but getting ready to |
| Standard Growth Curve: Log phase | Bacteria are reproducing exponentially - Primary metabolites generate amino acids, cell wall, etc. - Endospores start being made |
| Standard Growth Curve: Stationary Phase | Nutrients are gone - Dying bacteria rate = growing bacteria rate (steady) - Main phase for endospore formation - Produce secondary metabolites |
| Standard Growth Curve: Death Phase | Dying exponentially |
| Standard Growth Curve | When bacteria enters a new growth CONDITION, lag stage will occur while bacteria prepare for growth in new conditions |
| Microbial Growth | Do not die just dont grow - Mesophiles love human body |
| Superoxide dismutase | Turns radical oxygen (O2-) into water and H2O2 |
| Catalase | Turns hydrogen peroxide (H2O2) into water and O2 (important bc without them oxygen are reactive and damage cells) |
| Aerotolerant anaerobes | Obligate fermenters make superoxide dismutase but NOT cats (are indifferent to the presence of O2) |
| Aerobic organisms must have BOTH... | Superoxide dismutase & Catalase |
| T4 phage | ONLY LYTIC conversion; cell lyses every time |
| Lambda phage | Lytic or Lysogenic conversion |
| RNA Viruses (Polymerases) | All RNA Viruses only use RDRP cannot be RDDP; will always depend on RNA to make more RNA |
| What type of conditions might be revealed from a stool sample? | Can confirm digestive system infections of the presence of parasites. Abnormal absorption of nutrients or the presence of blood may reveal other conditions that affect the digestive tract and related organs like the liver and pancreas |
| What happens to ingested cysts of Giardia lambda? | Are surrounded by tough outer wall that protect them from acidity of stomach secretions - Cysts pass through stomach and release active form of parasite (trophozoites) in small intestine -> attach and multiply causing diarrhea and cramping |
| How can a stool sample confirm the vet's suspicions that Dudley was infected with Glardia? | Microscopic examination of Dudley's fecal smear that may reveal trophozoite form of parasite - Reveal the presence of cysts -> feces mixed w/ test solution denser that cysts , cysts float up able to de examined - ELISA test can also determine parasite |
| Why would the prescriptions for metronidazole (commonly used to treat infections caused by anaerobic organisms) be used for treating giardiasis? | - Gl. lack mitochondria -> no aerobic cellular respiration - Produces an enzyme similar to one made my anaerobic bacteria resulting in production of chemical that can transfer electron to metronadizole -> activates medication which bind s & damages DNA |
| Endotoxin | Toxin specific to an organism; protein |
| (Endo.) A-B toxin | A = Attack (active enzyme) B = Binding Can be made by both Gram (+) & Gram (-) ; made into toxoid vaccines |
| (Endo.) Superantigen | Make T cells recognize things that they otherwise wouldn't recognize; overrides T cell specificity -> cytokine storms Can be made by both Gram (+) & Gram (-) ; made into toxoid vaccines |
| (Endo.) Membrane damaging toxins: Cytotoxins | Damage plasma membrane and causes leakiness/cell lysis Can be made by both Gram (+) & Gram (-) ; made into toxoid vaccines |
| (Endo.) Membrane damaging toxins: Other toxins | Exfoliation -> Staph aureus toxin for SSSS (Scalded skin) Can be made by both Gram (+) & Gram (-) ; made into toxoid vaccines |
| Why would it be beneficial to Bordetella pertussis to cause coughing? | Coughing propels bacterial cells into air where it can be infectious (high Ro) |
| The bacterium colonizes the ciliated cells of the upper respiratory tract. How might it avoid being swept away by the mucociliary escalator? | Bacterium produced multiple adhesions that allow it to colonize ciliated cells - Attachment structures include protein FHA (filamentous hemagglutinin) for its ability to agglutinate RBC and fimbriae |
| The bacteria do not invade the epithelial cells, yet they damage those cells. What might cause the damage? | - Tracheal cytotoxin which is toxic to ciliated epithelial cells ( a fragment of peptidoglycan from pertussis growth phase) - Pertussis toxin (A-B toxin) -> modifies reg. protein in respiratory cells causing accumulation of mucus (unable to exit lungs) |
| Why would the physician be concerned about a secondary infection? | Bc ciliated respiratory cells are important for first-line defenses, if damaged the mucociliary escalator does not function normally -> more likely other pathogens will colonize respiratory tract |
| Why is labeled CO, produced if H. pylori is present? | Uses enzyme urease to break down urea into ammonia and CO2 & bc urea is labeled with a carbon isotope, the CO2 that is produced also has the label |
| How do flagella and the enzyme urease function as bacterial virulence factors in the development of peptic ulcers? | - Flagella propel bacterial cells though mucous layer removing them from acidic environ. - Urease breaks down urea in stomach to produce ammonia which is alkaline compound that neutralizes gastric fluids around cell |
| It took a long time for doctors to accept that peptic ulcers were caused by infection. Why? | Scientists thought no organism could survive stomach acidity and enzymes hence not believing when Barry Marshall claimed that a bacterium caused stomach and duodenal ulcers |
Created by:
Ajmt245