MicroBio
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Created by:
Bradster399 on March 7, 2012
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139 terms
Terms | Definitions |
|---|---|
 bubo | an enlarged lymph gland, due to the bubonic plague, usually appear in the groin, armpit or neck areas |
| Yersinia pestis | Bacterium that causes bubo |
| y. pestis causes bubonic, septicemic, and pneumonic plague while enteropathogenic Yersinia cause food borne illness | genetic elements that set Y. pestis apart from the enteropathogenic Yersinia |
| 3 | Y. pestis carries blank # of plasmids |
| 1 | enteropathogenic Yersinia carry blank # of plasmid |
| 70kb virulence plasmid | genetic element that is shared by all three pathogenic Yersinia species |
| specialized secretion system called type 3 secretion system (T3SS) | 70kb virulence plasmid that encodes |
| full length inv gene | genetic element that enteropathogenic Yersinia have that Y. pestis lost |
| invasion (inv gene) | chromosomal gene of enteropathogenic Yersinia initially identified as allowing invasion of cultured mammalian cells, involved in crossing the intestinal epithelial barrier |
| gentamicin | kills extracellular bacteria without affecting intracellular bacteria |
| used in an internalization assay | special about gentamicin |
| gentamicin | critical component of the invasion assay |
| gentamicin | aminoglycoside antibiotic |
| Yersinia outer membrane proteins (Yops) | things that the 70kb virulence plasmid encodes that enable Yersinia to survive in mammalian host |
| T3SS, mammalian, actin cytoskeleton, killing | Yops, delivered by the BLANK, are injected directly into BLANK cells, paralyzing the mammalian cell BLANK and thereby preventing the mammalian cell from taking up and BLANK the bacteria |
| needle-like multi-protein complex that is associated with transferring toxic proteins to host cells | Type 3-secretion system (T3SS) |
| secretes necessary proteins required for cell invasion and inflammation | importance of type 3-secretion system in Salmonella virulence |
| host cytoskeleton, host | proteins secreted by the T3SS can modify BLANK leading to bacterial entry into the BLANK cell. |
| bacterial chromosome regions of foreign origin that contain clustered genes for virulence | What are pathogenicity islands |
| large spans of chromosomal DNA that are present in Salmonella but not E. coli | Example of pathogenic island |
| pathogenicity islands, virulence, Salmonella | BLANK or discreet regions of DNA, encode many of the BLANK properties of BLANK |
| actin | motility of Listeria monocytogenes inside host cells is BLANK based motility |
| invasion, escape from primary vacuole, movement through cytoplasm, cell to cell spread, and escape from secondary vacuole | Steps involved in motility of Listeria monocytogenes; stages of infections include: |
| any deviation from a condition of good health and well being | Define disease |
| a disease condition caused by the presence or growth of infections microorganisms (or parasites) | define infectious disease |
| accurate determination of the etiological agent and knowing the incidence of this infectious disease in the population | Two major aspects of infectious disease control |
| the criteria for identifying a pathogen as the causative agent of a disease | In short what does Koch's postulates provide |
| organism (pathogen) is regularly found in the lesions of the disease but absent from healthy individuals. Organism can be isolated from this and grown in pure culture on artificial media. Inoculation of pure culture produces similar disease in animals. Once again the same organism must be recovered from lesions in the new diseased animals. (thus must be the same organism as before) | Koch postulates |
| science that evaluates, occurrence, determinants, distribution, and control of health and disease in a defined human population. | What is epidemiology |
| constantly present; low numbers | describe an endemic disease |
| high incidence; localized populations | describe an epidemic disease |
| worldwide epidemic disease | Describe an pandemic disease |
| occurs occasionally and at irregular intervals | sporadic disease |
| common source and propagated (host to host) | What are the two types of epidemics |
| common source has a rapid peak in the number of individuals infected and then a rapid (more gradual) decline. propagated epidemic curve has a gradual rise and then a gradual decline | Difference between common source and propagated epidemic |
| reduce or eliminate source of infection, break connection between source and individuals, and reduce number of susceptible individuals | three types of control measures of epidemics |
| maintain reservoir (place to live before and after causing infection), be transported to host, adhere to/colonize/invade host, multiply or complete life cycles on or in host while evading host defenses, damage host, leave host and return to reservoir or enter new host | steps in pathogenesis of bacterial diseases |
| normal flora (normal colonization of bacteria in human body), non-specific defenses (physical barriers/nutritional barrier), and specific defenses (immune system) | Host defenses |
| number of organisms present, virulence of pathogen, and host defenses (or degree of resistance) | 3 factors impacting outcome of host-pathogen relationships |
| determined by invasiveness, toxicity and other factors produced by a pathogen | What is virulence |
| products of the infectious organism that contribute to pathology | What are virulence factors |
| molecules that allow pathogen to colonize (adhesion molecules and enzymes), molecules that allow the organism to obtain nutrients and grow, toxins, and mechanisms to avoid host immune defense | describe some virulence factors |
| number of pathogens that will kill 50% of hosts | what is lethal dose 50 |
| number of pathogens that will infect 50% of hosts | what is infectious dose 50 |
| specific substance that damages host | what is a toxin |
| composed of two subunits, A subunit and B subunit | AB exotoxins |
| responsible for toxic effect and acts on the host cell | A subunit (AB exotoxins) |
| binds to target cell | B subunit (AB exotoxins) |
| clostridium tetani (an anaerobic, gram positive spore former) | Tetanus is caused by what |
| endospores found in soil, dust, hospital environments, and mammalian feces. produces tatanospasmin in low oxygen tension environments which cases prolonged muscle spasms. Also produces tatanolysin, a hemolysin. Skin wounds in portal of entry | Tetanus |
| binds to inhibitory interneurons, preventing release of glycine and relaxation of muscle. (normally inhibitory interneurons release glycine which stops acetylcholine release and allows for relaxation of muscle) | action of tetanus toxin |
| consists of seven related toxins that are the most potent biological toxins known. Botullinum toxin blocks release of acetylcholine, inhibiting contraction. | Botulinum toxin |
| membrane disrupting exotoxins. Pore-forming exotoxins and phospholipases | what are cytolytic toxins and give two examples |
| hemolysins. they kill erythrocytes (red blood cells), leukocytes, and many other cells | what are spore forming exotoxins called and what do they do |
| lipopolysaccharides derived from outer membrane of gram negative bacteria. release upon lysis of bacteria, and cause fever and systemic toxic effects in host. (generally less toxic than exotoxins | what are endotoxins |
| aquatic organisms, occurring in marine and fresh water habitats. They grow in synthetic media with glucose as a carbon and energy source, require salt or sea water for optimal growth, grow in 10-37C, and can tolerate alkaline media but are sensitive to acid | what are Vibrios and describe their growth factor requirements |
| gram -, facultative anaerobe, curved rod shape, motile via polar flagellum and is differentiated serologically on the basis of the O antigen of its lipopolysaccharide | Describe Vibrio cholerae |
| toxigenic, serogroups | Cholera toxin-producing (BLANK) strains of the 01 and 0139 BLANKS cause the vast majority of the disease |
| a strain that harbors the genes for toxin production (in the case of V. cholerae, these are the genes for cholera toxin) | define toxigenic |
| a group of strains sharing the same dominant antigens (in the case of V. cholerae, this is the lipopolysaccharide O antigen | what is a serogroup |
| water borne illness. transmitted by ingestion of food or water contaminated with V. cholerae. Primary site of infection is small intestine. colonize epithelium without invasion or apparent damage (does not invade host tissue). | cholera |
| endemic to india, bangladesh, regions of south america, africa, australia, and gulf coast of US. Have been 7 pandemics since 1817 | Epidemiology of Cholera |
| a protein toxin produced by V. cholerae that triggers fluid and electrolyte secretion by intestinal epithelial cells. (composed of two polypeptides, A and B subunits. B:A is 5:1 thus you have a pentamer of B that binds specific receptors on the eukaryotic cell. B subunit binds with affinity exclusively to GM1 ganglioside) | What is cholera toxin |
| catalyzes an ADP-ribosylation reaction. CTX binds to surface sugar on the intestinal cells via B subunits. After binding A subunit which has ADP-ribosylating enzymatic activity is transported into host cell. Inside the cell, the A subunit ADP ribosylates (attaches an ADP-ribose) a G protein (largest family of mammalian cell-surface receptors, they mediate cellular response to signaling molecules) -G protein regulates activity of adenylate cyclase ADPribosylation leads to increased adenylate cyclase activity - ADP ribosylation leads to increased adenylate cyclase activity - Increased cAMP levels within intestinal epitelial - Activities of sodium and chloride transporters altered--Massive fluid and electrolyte loss - Osmotic imbalance causes water flow into the intestinal lumen---DIARRHEA | What is cholera toxin's mode of action |
| adherence. use of filamentous pili (toxin-coregulated pilus) TCP that forms bundles on bacterial surface is essential for colonization. Lacking TCP leaves to avirulence. Genes necessary for production of TCP are in an operon that contains 15 genes. This operon is part of the Vibrio pathogeniciy island (VPI) and codes for major pilin subunit, assembly, and secretion | Virulence Factors for V. cholerae |
| Toxin-coregulated pilis (TCP), and CTX toxin | Major virulence factors for V. cholerae |
| CT genes are encoded on a lysogenic filamentous bacteriophage and this phage can infect strains missing the toxin genes via the receptor for the phage, the toxin co-regulated pilus (TCP). Transfer occurs in gastrointestinal tract and aquatic environment | Cholera toxin (CTX) genetic element |
| low cell density, then hapR mRNA degraded, then aphA expressed, then toxT produced which forms toxboxes giving rise to both CTX and TCP | pathway regulating expression of CT and TCP virulence factors |
| bacteriophage species that infect V. cholerae and are known as vibriophages. | V. cholerae bacteriophages |
| filamentous, lysogenic CTX0 vibriophag. Control natural populations of V. cholerae | bacteriophage that carries the genes that encode cholera toxin and what lytic vibriophages do |
| 1959 De and Chatterjee, injected V. cholerae into lumen of ligated rabbit ileal loop and observed large amount fluid accumulation. In 1969 Finkelstein et al. purified and characterized the toxin. 1983, Levin et al. administered purified CT to patients and demonstrated that the toxin is the major mediator of the cholera syndrome. | discovery of cholera toxin |
| single exposure to V. cholerae O1 confers protective immunity. Live attenuated strain as a vaccine have ben unsuccessful. Rehydration therapy remains essential in cholera treatment. | vaccine for V. cholerae |
| gram -, aerobe, rod shaped, motile with single polar flagellum. Need complex nutritional requirements | describe Legionella pneumophila |
| identified as the culprit in a massive outbreak of pneumonia (legionnaires disease) that struck individuals attending an American Legion convention. flourishes in freshwater as a parasite of amoebae but and also replicate within alveolar macrophages | what was Legionella pneumophila responsible for and where does this bacterium flourish |
| significant cause of morbidity and mortality. Infection after inhaling aerosols of contaminated water droplets thus transmission is achieved through this airborne environmental reservoir to human host. Linked to poorly maintained artificial water systems. Accounts for 2-5% of all pneumonias that require hospitalization | Epidemiology of Legionella pneumophila |
| reproduction of bacterium in alveolar macrophages that causes localized tissue destruction. Treatment includes isolation of bacteria and immunodiagnostics, symptomatic therapy and antibiotic therapy, and identification and elimination of environmental source | Legionnaires disease |
| protozoa are susceptible to L. pneumophila infection and studies link water contaminated with both present result in outbreaks of legionellosis. In this way amoebae have acted as an incubator for the emergence of L. pneumophila as an opportunistic pathogen of alveolar macrophages | Protozoa and L. pneumophila |
| coiling phagocytosis, phagosome does not acidify and does not fuse with lysosome, phagosome surrounded by ER studded with ribosomes, multiply in phagosomes, phagosome rupture, and host cell lyses which allows bacteria to escape | Legionella infection cycle |
| they do not acidify or fuse with lysosomes | how do the vacuoles that harbor L. pneumophila differ from conventional phagosomes |
| type 4 secretion system which allows for substrates from the bacterial cytoplasm directly to be inserted into the cytoplasm of infected host cells. | L. pneumophila uses what kind of secretion system for virulence |
| when amino acids become scarce, bacteria express several traits that facilitate escape from the depleted cell and transmission to a new host | explain the stringent response model for virulence regulation |
| autophagy is an essential, homeostatic process by which cells break down their own components, as to liberate molecules needed for vital cellular activities. The replication vacuoles used by L. pneumophila resemble that of autophagosomes and elevated rates of autophagy facilitate replication vacuole formation and thereby enhance bacterial growth. | what is autophagy and how is it important to L. pneumophila replication |
| when ingested by amoebae or macrophages, L. pneumophila exports factors via the Dot/Icm secretion system to modify the nascent phagosome and separate it completely from endosomal pathway. | Model for the L. pneumophila life cycle |
| the legionella pneumophila Dot/Icm (defect in organelle trafficking/intracellular multiplication) T4SS is an essential virulence determinant that translocated effector proteins into eukaryotic cells. | what is the Dot/Icm system and what does it do |
| delay endocytic maturation of the vacuole in which the bacterium resides and promote remodeling of the L. pneumophila containing vacuole. Does this by eliminating late stage proteins (lysosomal-associated membrane proteins LAMP-1 and LAMP-2) from the membrane of the phagosome that indicate maturation of the phagosome | what do the effector proteins translocated by the Dot/Icm system function to do |
| post exponential phase bacteria establish a vacuole that does not acidify or interact with the endosomal pathway, but is surrounded by ER. Inside this protected vacuole, bacteria convert to an acid tolerant replicative form and no longer express virulence factors such as Dot/Icm. Then vacuoles merge with the lysosomal compartment, an acidic, nutrient rich replication niche and once the local amino acid supply is depleted, the progeny convert to virulent form, expressing factors to escape the spent host, and survive and disperse in the environment. | what happens after L. pneumophila is engulfed within phagosomes |
| ppGpp, phagocyte | once bacterial progeny have depleted the local amino acid supply, the intracellular second messenger BLANK accumulates, triggering expression of traits important for transmission of L. pneumophila to a new BLANK |
| type 2 and type 4 secretion system and effectors and motility | What are the major virulence factors of L. pneumophila |
| the distinct microbial community occurring on skin and mucosal surfaces in every healthy human | what is normal microbiota |
| mutualistic, both partners benefit | the relationship between human host and normal microbiota is usually what? |
| exist in host in a non disease inducing manner or cause chronic infection or cause acute infection of host | what are the 3 types of host-microbe interaction |
| normally harmless organisms that can cause infection when the host immune system is compromised | what are opportunist pathogens |
| transient microbiota | what are microbiota that do not establish long term residency in humans |
| microorganisms that occasionally enter a human and cause disease. Including normal microbiota that can be opportunistic pathogens | describe accidental pathogens |
| skin, oral cavity, respiratory tract, gastrointestinal tract, and genitourinary tract (intestinal tract is colonized within 24 hr of birth!) | Where do microbes establish themselves on human infants during and soon after birth |
| 10^13 or 10 trillion | about how many estimated bacteria live in or on an adult human |
| because human health depends on maintenance of the normal microbiota and use of an anti-biotic would alter normal microbiota | Why does prolonged antibiotic therapy that alters or suppresses the normal microbiota lead to serious health problems |
| normal human microbiota | what organisms are not pathogenic on skin or mucous membranes |
| sebaceous (assoc. w/ hair follicles, secrete lipids sebum) and sweat glands (secrete water, urea, amino acids, lactic acid, and salts) | name some nutrient sources of skin microbiota |
| staphylococcus, Micrococcus, Corynebacterium, and propionobacterium | name some skin gram + normal microbiota |
| diet has been found to have little affect on skin microbiota but antibiotic therapy can certainly be effective | contrary to popular what has little measurable influence on the skin microbiota and what can actually influence these populations |
| the mouth, nasopharynx and throat have bacteria while the lower respiratory tract does not due to barrier defenses. those include trachea, bronchi and lungs | which part of the respiratory tract contain populations of bacteria and which usually do not |
| the mouth, with its nutrient rich, stable pH and stable temperature environment make it favorable | where is the most favorable environment for respiratory tract normal human microbiota |
| tooth enamel is made of crystalline calcium phosphate and is colonized by Streptococcus mutans, S. sanguis, and anaerobic Actinomyces. these form plaques on teeth | what is tooth enamel made of and what is it colonized by |
| breastfed have Bifidobacterium from the skin of the mother and the milk contains amino disaccharide that this bacterium utilizes | how is the gastrointestinal tract population of microbiota different from breast fed and bottle fed infants |
| they digest much of what we eat so that it is readily available to be absorbed by the gut. they affect weight gain and loss. (fat people have more Firicutes while lean people have more Bacteroidetes | how do the microbiota of the gastrointestinal tract contribute to human health |
| a gastrointestinal disease believed to be related to perturbation to the intestinal microbiota | what is Clostridium difficile infection (CDI) |
| involves infusing intestinal microorganisms (in suspension of healthy donor stool) into the intestine of a sick patient to restore the microbiota (highly effective, showing disease resolution in 92% of cases) | what is intestinal microbiota transplantation (IMT) |
| another treatment for CDI and used with increasing prevalence of recurrent/refractory clostridium difficile infection | what is fecal microbiota transplantation and what is it used for |
| agents that selectively expand noninflammatory gut bacteria already present | what are prebiotics |
| bacteria that have the ability to confer a health effect on the host when consumed in adequate quantity. Lactobacilli and bifidobacteria | what are probiotics and name 2 examples |
| understanding of the distal gut and its associated microbiota | what will help to further understand human biology and evolution |
| advances in sequencing technology and by the application of a variety of omic technologies | what has helped to better understand microbiota of the distal gut and furthermore assist in understanding human biology and evolution |
| culture-independent methods, inventories of 16S rRNA genes | In the initial stages of understanding what constitutes the gut, BLANK, primarily , BLANK have provided a clear view of the main taxonomic groups of Bacteria in the distal gut and we are now moving towards defining the functions |
| bacteria present in lower part of urethra but the upper part, near the bladder, is sterile. | describe microbiota in the genitourinary tract |
| study of normal versus abnormal microbiota in women | what is vaginal microbiota |
| dominated by Gardnerella vaginalis and include a number of anaerobic organisms. Normal flora is dominated by various Lactobacilli | describe bacterial vaginosis |
| HIV and STDs | bacterial vaginosis flora predisposes women to infection by what |
| they have revealed unique microbial communities not previously recognized within the older, established vaginal flora categories | using high throughput sequencing techniques what can you reveal about VMB |
| common clinical syndrome in which the protective lactic acid producing bacteria are supplanted by a diverse array of anaerobic bacteria | what is bacterial vaginosis |
| gram + bacteria, staphylococci | What are the main colonizers of human skin, and sometimes cause serious infections |
| actually, due to barrier defenses, the lower respiratory tract usually does not have bacteria | what kinds of bacteria are present in the lower respiratory tract |
| they remove oxygen in the colon, making the large intestine a fermentation vat capable of being populated by masses of anaerobic bacteria | what role do facultative aerobes play in the human gastrointestinal tract? |
| bacteroidetes and firmicutes. (B. fragilis, B. melaninogenicus, and B. oralis) and Fusobacterium. Bifidobacterium, Eubacterium, Lactobacillus, Clostridium. | list major organisms found in the stomach and intestine |
| lactobacilli bacteria convert glycogen produced by the vaginal epithelia to lactic acid and this maintains the pH at 4.4 to 4.6 | what is the source of acidic pH in the genitourinary tract of females |
| target some function necessary for reproduction or survival. Examples include; competitive inhibition, inhibition of nucleic acid synthesis, inhibition of cell wall synthesis, disruption of cell membrane function, and inhibition of protein synthesis | discuss mode of action of some common antibacterials |
| effectiveness is expressed by minimal inhibitory concentration MIC and minimal lethal concentration MLC. You can run dilution susceptibility tests where you inoculate with media containing different concentrations of drug and analyze or you can run a disk diffusion test where disks impregnated with different drugs are placed on agar plates and inoculated with microbe. the drug diffuses from disk to agar, establishing concentration gradient and you can observe clear zones around disks where at that concentration no microbe can grow. | how is the level of antimicrobial activity determined |
| while bacteria produce AB naturally, and therefor allow isolation and production of ABs, viruses and fungi do not produce antiviral or antifungal agents as commonly. As well, unlike bacteria, fungi and viruses have similar functions/processes to humans, as fungi are eukaryotes and viruses are made of RNA and thus anti fungal or anti viral agents that would be effective would have to have selective toxicity. the ability to kill or inhibit pathogen while damaging host as little as possible | why is it so difficult to find effective antiviral and antifungal agents while antibacterials are quite plentiful |
| producing AB during nutrient limitation could inhibit growth of competitors and allow for the use of dying microbes as an alternative food source | what advantage might bacteria and fungi gain from the synthesis of antibiotics |
| natural vs. acquired resistance. Natural, microbe lacks the structure that is inhibited by the AB or antibiotic does not reach target. Acquired, microbe produces enzyme that inactivates AB, mutations result in protein that no longer bind AB, microbe contains enzyme that modifies the target of antibiotics action, microbes produce or take up an alternate molecule that replaces the target of the AB, pump AB out of the cell | how do bacteria become resistant to antibiotics |
| give the drug in high concentrations, give two or more drugs at the same time, use drugs only when necessary, and maybe one day use bacteriophages | how can the development of antibiotic-resistant pathogens be slowed or prevented |
| chemical agents used to treat disease by destroying pathogenic microbes, inhibiting their growth. most are antibiotics | chemotherapeutic agents |
| cidal refers to killing the bacteria and static refers to inhibiting its growth | what does cidal and static primary effect mean in relation to an antibiotic |
| because no lab animals could be infected and the best model system is the human one | why did Barry Marshall use himself for the H. pylori studies |
| it fulfills postulates 1-3 always but 4 only sometimes. sometimes the H. pylori is present in healthy animals, which does not fulfill number 4 | how does H. pylori fulfill and not fulfill Kochs postulates |
| Urease: enzyme that cleaves urea into NH2 and CO2, which buffers H. pylori from stomach acid, motility: required to survive in the stomach, VacA: causes apoptosis in humans cells, Cag: encodes T4SS that delivers CagA and induces cells to proinflammatory cytokines and chemokines | what happens to an H. pylori infection if you eliminated each of the H. pylori virulence factors |
| no because 90& of people who have it do not get disease and there are even findings that support the H. pylori decreases esophogeal cancer, decreases stomach acid, and protects you from asthma. | should we treat everyone with H. pylori with antibiotics |
| for diagnostics; plate the biopsy sample to grow H. pylori, test biopsy sample for urease, test blood to see if patient is making AB to H. pylori, and the urea breath test. treatment includes combination of 2-5 ABs plus strong antacid | how is H. pylori diagnosed and treated |
| because H. pylori is observed to have increasing resistance to the combination of antibiotics and antacids used. | why do you think 80% of people are cured when treated for H. pylori infection |
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