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Micro lecture 14
| Question | Answer |
|---|---|
| Disease | An interaction between microbe and host that leads to damage to the host; a pathologic process |
| normal flora | microorganisms that do not cause disease in healthy individuals. Commensalists or mutualists to the host. |
| resident flora | flora occurring in or on an organ over a protracted period |
| transient flora | microbial flora only temporarily associated with a particular niche |
| colonization | establishment of colonies or growth within a region; transient or permanent |
| strict pathogen | organisms always associated with disease |
| opportunistic pathogens | organism that is pathogenic only under certain conditions; often a member of the normal flora |
| nosocomial pathogen | pathogen found in a hospital setting |
| nosocomial infection | infection acquired in hospital |
| commensal | 1 of 2 partners that lives in permanent close association, which gains a slight benefit from the association without causing serious disadvantage to the other |
| What does normal commensal microbial population provide? | Aids in food metabolism; provides essential growth factors; protects against infections with virulent microbes; stimulates immune system; needed for full development of GI tract and immune system |
| Germ-free organisms have an impaired __ _____. | GI tract |
| How is the GI tract impaired in germ-free organisms? | It compromises the ability to process nutrients, impairs the immune system, reduces the turnover of cells that line the intestine. |
| Where do normal flora come from? | Originally, the mother's birth canal. Skin is first to be colonized, followed by mucosal surfaces. |
| Normal flora is partly _____________ determined. | environmentally |
| The body works to keep normal flora beyond the skin surface and mucous membranes. What parts of the body are considered sterile? | brain, muscle, kidneys, liver, heart, blood stream, urinary bladder, and lungs |
| Name some skin normal flora | corynebacteria (diptheroids), coagulase negative staphylococci, Propionibacterium acnes, staphylococcus aureus, staphylococcus epidermidis, streptococci, pseudomonas aeruginosa, anaerobes (in hair follicles); fungi: candida, malasezzia |
| How is the eye kept healthy and free of organisms? | Lacrimal glands secrete fluid containing lysozyme and sIgA; also by blinking |
| Name some eye normal flora | staphylococcus aureus, s. epidermidis, corynebacteria |
| Name some bacterial diseases found in the eye | S. pneumoniae, S. aureus, H. influenzae, N. gonorrhoeae, Chlamydia trachomatis, Pseudomonas aeruginosa, and Bacillus spp. |
| Why do microorganisms colonize the upper respiratory tract? | There is a high water quantity, plentiful nutrients, and a constant temperature. |
| How is the epithelium protected? | The goblet cells form a mucus layer that covers the surface of the epithelium; the mucus contains secretory IgA |
| What are some normal nose flora? | S. aureus, S. epidermidis, deptheroids, streptococci |
| Name some throat bacteria | Viridans streptococci, S. pyogenes, S. pneumoniae, Neisseria spp., Staphylococcus epidermidis, Haemophilius influenzae |
| Name some anaerobes of the respiratory tract | Peptostreptococcus, Veillonella, actinomyces, fusobacterium spp. |
| How is the middle ear connected to the respiratory tract? | Auditory (Eustachian) tube allows communication between middle ear and nasopharynx, permitting equal pressures on either side of the tympanic membrane |
| Why do kids get more ear infections than adults? | Children have a more horizontal auditory canal which allows for nose crap to get into the ear. |
| Why are there fewer microorganisms (usually empty!) in the lower respiratory tract? | The mucociliary escalator lines the trachea, and there are alveolar macrophages keeping the alveoli clean. Mucus traps inhaled bacteria and cilia sweep them to be swallowed. |
| Name some routes pathogens take to get into the CNS (which is normally sterile) | Olfactory nerve pathway, Peripheral nerve pathway, Hematogenous pathway |
| Name some mouth flora | Bacteria: Streptococcus mitis and other streptococci; Protozoa: Trichomonas tenax Fungi: Candida |
| Name some teeth bacteria | Streptococcus mutans and other streptococci, Bacteroides (anaerobes), fusobacterium (anaerobes), actinmyces (also anaerobes) |
| Mucus, acid pH, and pepsinogen limits stomach microbes to those that are ____ ______. | acid tolerant |
| If you reduce your stomach acidity (antacids or heartburn meds), you increase the chances of getting | salmonella |
| The small intestine has a ton of flora, mostly in the _____. Most are ______. | ileum; anaerobes |
| Mucosal immunity in the small intestine | Paneth cells of the small intestine secrete lysozyme and defensins; enterocytes transport sIgA into lumen. Bile also has sIgA. |
| There is a LOT OF BACTERIA in the _____ intestine. Are there more aerobes or anaerobes? | large; anaerobes |
| POOP HAS A LOT OF BACTERIA. How much? | 10^11 |
| Name some large intestine bacteria | Bifidobacterum, Eubacterium, Bacteroides (B. fragilis), Enterococcus, Enterobacteriaceae (E. coli). |
| What does Bacteroides theta-iota-o-micron do? | Lots in GI tract, liberates simple sugars from complex sugar polymers. |
| Why can antibiotic treatment be bad for you? | Growth of Clostridium difficile is kept in check by the normal flora; the antibiotic gets rid of normal flora and then C. difficile can cause GI disease. |
| Why is the male urinary tract less susceptible to infection than the female urinary tract? | The male's urethra is longer and has little risk of pathogenic entry; the female has a shorter urethra located closer to the rectum. |
| Name some urethra bacteria | S. epidermidis, diptheroids, streptococci. Very lightly colonized. |
| Name some vaginal bacteria (pre-puberty) | staphylococci, streptococci, diptheroids, E. coli |
| Name some vaginal bacteria (post-puberty) | Lactobacilli aerophilus, Trichomonas vaginalis |
| What does Lactobacilli aerophilus do? | In vagina, metabolizes glycogen to lactic acid and maintains an acid pH in vagina. |
| What is a negative effect of antibiotic treatment in the vagina? | The fungus Candida albicans is held in check by the acid environment created by lactobacilli; antibiotics kill lactobacilli and can result in an overgrowth of C. albicans |
| What do microbes need to do in order to survive? | 1. Enter the body, 2. Adhere/colonize, 3. Get foodstuffs, 4. Avoid host immune system. |
| How can skin flora be pathogenic? | S. epidermidis in the bloodstream can colonize heart valves and cause bacterial endocarditis. |
| How can gut flora be pathogenic? | E. coli can cause UTIs, Bacteriodes fragilis causes intra-abdominal abscesses. |
| True pathogens | Can cause disease in most host organisms |
| Carrier state | When a true pathogen is carried by a healthy individual and it can be transmitted to others where it causes disease. |
| Opportunistic bacteria | take advantage of pre-existing lowered host defenses |
| Virulent bacteria | Promote growth at the expense of host's tissue/organ function. |
| Virulence factors | Genetic traits that enhance ability of bacterium to cause disease. Facilitate entry, adherence to host cells, invasiveness, creation of toxins. |
| How is virulence measured? | ID50s (how many organisms needed to cause disease in 50% of exposed) or LD50s (how many to kill 50% of test animals) |
| How do bacteria evade phagocytosis? | If they have an outer polysaccharide capsule (i.e. S. pneumoniae, H. influenzae, N. meningitidis) |
| What natural defenses do enteric Gram-negative bacteria evade? | Lysozyme, Low pH, bile |
| What natural defenses are weakened in cystic fibrosis patients? | Mucociliary escalator, thickened mucosal secretions, unable to clear respiratory pathways leading to colonization of lungs with s. aureus and p. aeruginosa |
| What are the different ways bacteria adhere? | fimbriae, nonfimbrial adhesion, hydrophobic adhesion |
| What bacteria need fibriae/pili to colonize? | E. coli in the urinary tract, N. gonorrhoeae |
| How does afimbrial adhesion work on Streptococcus? | the F protein binds to fibronectin, a protein secreted by many mammal cells |
| Hydrophobic adhesion | P. aeruginosa can adhere to both hydrophobic and hydrophilic contact lenses and the binding is more tenacious than hydrophilic S. aureus |
| Why is adhesion important? | If a bacterium can adhere to epithelial or endothelial surfaces they cannot be washed away. |
| Biofilms | can protect bacteria from host defenses |
| Quorum sensing | ability of bacteria to communicate and coordinate behavior via signaling molecules |
| What can't most bacteria cross? | intact skin |
| What is type III secretion machinery? | Bacteria inject proteins directly into host cell and induce cell to take in the bacteria |
| Pathogenicity islands | large chromosomal regions containing sets of genes encoding several virulence factors; virulent processes that require coordinated expression of several genes are found in pathogenicity islands. Can be turned on by a single stimulus. |
| Name some ways tissues can be destroyed | from bacterial growth byproducts or degradative enzymes. |
| Exotoxins | produced inside mostly gram-positive bacteria as part of growth/metabolism; then released into surrounding medium. |
| Endotoxins | part of outer portion of gram-negative cell wall; freed when bacteria die and cell wall breaks apart |
| Endotoxins are PAMPs T/F | True. Activate TLRs on myeloid cells and stimulate inflammatory cytokine production |
| Name the gram-positive endotoxins and what they activate | peptidoglycan, teichoic and lipoteichoic acids; TLR1 and TLR2 |
| Name the gram-negative endotoxin and what it activates | LPS (lipid A) activates TLR4 |
| Why can antibiotic treatment sometimes exacerbate symptoms | gram-negative cell death and sudden massive release of endotoxin into the circulation can initially increase symptoms |
| Exotoxins are proteins produced by both gram positive and negative bacteria T/F | True. |
| What do the parts of the A B Exotoxins do? | A = active enzyme B = binding portion; needed to provide entry of A into the cell |
| How does the Diptheria toxin affect a cell? | blocks protein synthesis on 80S ribosome by modifying eEF-2 |
| How does the Cholera toxin affect a cell? | modifies cell signaling mechanism (a G protein) in intestinal absorptive cells |
| How do Clostridial exotoxins affect cells? | Cleave proteins needed to release neurotransmitter substances. |
| How does the Shiga toxin affect cells? | Cleaves a specific adenine from host 28S rRNA of 80S ribosome resulting in protein synthesis inhibition |
| Superantigens | Toxins that activate T cells by binding to both TCR and MHCII simultaneously without requiring antigen. |
| What do superantigens do? | Nonspecifically activate groups of T cells and can trigger lots of interleukin release and lead to death of T cells. |
| Name some superantigens | S. aureus TSS toxin, staphylococcal enterotoxins and the erythrogenic toxins of Streptococcus pyogenes |
| Immunopathogenesis | excessive immune and inflammatory responses triggered by an infection |
| Name some examples of immunopathogenesis | Sepsis, Meningitis, M. tuberculosis |
| What are some mechanisms to evade host defenses? | Capsules, Antigenic mimicry, Antigenic masking, Antigenic variation, Phase variation, Antigenic shift... |
| Antigenic variation | expression of various alternative forms of antigen on cell surface |
| Phase variation | On-Off expression of surface features |
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