Term
Name the 4 groups of shigella. Which is most common in the US? |
|
Definition
| A: shigella dysenariae, B. Shigella flexneri, C: shigella boydii, and D. Shigella sonnei (the most common.) |
|
|
Term
|
Definition
| Bacterial dysentery, fever, chills, convulsions, abdominal cramps, bloody stools |
|
|
Term
| Which groups most commonly get shigellosis? |
|
Definition
| Children, aged, malnourished |
|
|
Term
| What makes shigella so easy to spread around? |
|
Definition
| Low infectious dose due to it being acid resistant |
|
|
Term
| What does the protein IpaBC do for shigella? |
|
Definition
| Helps it get into the cell, and then helps it escape from the vacuole. |
|
|
Term
| Which type of cell does shigella like to attach to when it attacks the intestine? |
|
Definition
| M cells, whatever those are. |
|
|
Term
| What does the protein IcsA do for shigella? |
|
Definition
| Allows it to polymerize actin at one pole and make actin tails to propel itself around the cell. |
|
|
Term
| What does shiga toxin do? |
|
Definition
| It is a shigella toxin is an A:B toxin. It cleaves the 28s rRNA. It is not involved in diarrhea, but it is thought to contribute to HUS (renal railure.) |
|
|
Term
How does shigella cause diarrhea? How does it spread from the intestine? |
|
Definition
| By killing epithelial cells and thereby blocking fluid absorption. However it doesn't spread much at all because it doesn't survive in macrophages. |
|
|
Term
| What makes shigella diarrhea special? |
|
Definition
| Blood, pus, and lots of culturable shigella. |
|
|
Term
| How can you differentiate shigella from salmonella in culture? |
|
Definition
| Shigella is H2S negative in culture (hektoen plate will grow black salmonella colonies but shigella won't.) and nonmotile. |
|
|
Term
| Are shigella urease positive? Are they indole positive? What does indole positive mean anyway? |
|
Definition
| Urease negative, indole positive half the time. Indole positive means they can convert tryptophan into indole. Why it would want to do this, I have no earthly idea. |
|
|
Term
| What is appropriate therapy for shigella? |
|
Definition
Fluid and electrolyte replacement.
Possibly antibiotics (quinolones, due to rampant resistance to other things carried by a plasmid) |
|
|
Term
Which vibrio are oxidase positive? |
|
Definition
|
|
Term
| What does a gram stain of vibrio look like? |
|
Definition
| Small curved gram neg rods |
|
|
Term
| How can you differentiate vibrio from enterics? |
|
Definition
Unlike enterics, they are oxidase positive and grow at pH9. |
|
|
Term
| What is special about the vibrio cholera genome? |
|
Definition
|
|
Term
| Which serotype of vibrio cholerae causes cholera? |
|
Definition
|
|
Term
| What is special about cholera diarrhea? |
|
Definition
| Large volume (10-15 L per day) and rice water consistency. Contains mucous, epithelial cells, oodles of vibrios. |
|
|
Term
| Where is cholera endemic? |
|
Definition
| India, Bangladesh, Africa, Phillipines |
|
|
Term
| What's one way to know how much fluid to give a cholera patient? |
|
Definition
| Measure the amoutn of diarrhea, and put that much fluid back in. |
|
|
Term
| What is the infectious dose of vibrio cholera normally? What accounts for this? |
|
Definition
| 1 billion. They are sensitive to stomach acid. |
|
|
Term
| What factors make a person particularly succeptible to cholera? |
|
Definition
| Immune deficiency, proton inhibitors, malnutrition. |
|
|
Term
| What organism has a TcpA pilus and what does it do and why is it called that? |
|
Definition
| vibrio cholerae. It adheres to intestinal cells. It's Toxin Coregulated, which means it is regulated by the same thing that regulates cholera toxin expression. |
|
|
Term
| Describe cholera toxin's activity. |
|
Definition
| It is an A:B toxin with 5 A subunits and 1 B subunit. The A subunit gets it in via a lipid raft and then hijacks the machinery for retrotranslocation of misfolded proteins and gets into the golgi, the ER, and then the cytoplasm. The toxin then continually activates adenylate cyclase by ADP ribosylating its stimulatory G protein and making it always-on. Level of cAMP rises. CFTR channel is activated, leading to an ionic imbalance that makes water move out of the cell. |
|
|
Term
|
Definition
| It is a virulence factor produced by vibrio cholerae that makes diarrhea worse because it increases the number of GM1 binding sites for cholera toxin. |
|
|
Term
| How can you tell vibrio cholerae apart from vibrio parahemolyticus in culture? |
|
Definition
| Plate on thiosulfate-citrate-bile sucrose. It has a pH of 8.6 and bile. Both will grow on it, but cholerae will tunrn it yellow and parahemolyticus will turn it light blue. (The plate starts out green) |
|
|
Term
| What is the appropriate therapy for cholera? |
|
Definition
Fluid and electrolyte replacement
Tetracycline in severe cases. |
|
|
Term
| What type of disease to vibrio parahemolyticus cause? |
|
Definition
|
|
Term
| How does one get infected with vibrio parahemolyticus? |
|
Definition
|
|
Term
| What is the appropriate treatment for vibrio parahemolyticus infection? |
|
Definition
| tetracycline if it is severe. |
|
|
Term
| What are the two ways you can get a vibrio vulnificus infection? |
|
Definition
| Wound infections or eating raw oysters (the latter if you have liver kidney or immune dysfunction or are taking acid inhibitors.) |
|
|
Term
| What is it that makes vibrio vulnificus infections so lethal once established? |
|
Definition
| -once in bloodstream, it has a 10 min generation time. |
|
|
Term
| Which type of vibrio may be responsible for a fever of unknown origin (all the usual suspects are ruled out.)? |
|
Definition
|
|
Term
| What is the most common bacterial cause of diarrhea? The most common viral cause? |
|
Definition
| Campylobacter and rotavirus |
|
|
Term
| What does campylobacter look like on a gram stain? |
|
Definition
| It looks like a gram negative rod that's a little more pliomorphic (curvy) than a vibrio |
|
|
Term
Where do campylobacter infections come from? |
|
Definition
| Household pets, unpasteurized milk, poultry, eggs. Mainly eggs. Campylobacter are almost normal flora in chickens. |
|
|
Term
What type of illness can campylobacter jejuni cause? What is the prognosis? |
|
Definition
| Abdominal pain that mimics appenicitis and diarrhea with blood and pus. It will generally resolve within a week and is not life threatening. |
|
|
Term
| What toxins does campylobacter jejuni have and what do they do? |
|
Definition
| heat labile toxin and cytotoxin which causes IL-8 release, stimulating inflammation. |
|
|
Term
| How are campylobacter grown in culture to distinguish them from the usual enteric bacteria? |
|
Definition
| They are grown on CAMPY BAP (blood agar with an assortment of antibiotics that don't bother them) with reduced O2 at 42 degrees. |
|
|
Term
| are campylobacter oxidase positive or oxidase negative? |
|
Definition
|
|
Term
| What is the usual treatment for diarrhea caused by campylobacter? |
|
Definition
| Quinolones are the drug of choice. Erythromycin and tetracycline are also options. |
|
|
Term
| What bacteria are associated with guillain Barre? Why? |
|
Definition
| Campylobacter jejuni and campylobacter upsalinenis. THeir LPS bears some resemblance to the structure of nerve cell carbohydrates. |
|
|
Term
| Why is amputation often necessary with vibrio vulnificus infections? |
|
Definition
| Often this is the only way to prevent it from spreading to the blood. Septicemia is extremely dangerous due to 10 min generation time of the bacteria. |
|
|
Term
| Where are the 2 places where h. pylori tends to cause ulcers? |
|
Definition
| In the antrum of the stomach (at the bottom near the exit) and in the top of the duodenum. |
|
|
Term
| What percent of people are colonized by h. pylori? |
|
Definition
|
|
Term
| What makes H. pylori so acid resistant? |
|
Definition
| urease. It can convert urea to ammonia and co2, which neutralizes the acid around it and enables it to survive high pH |
|
|
Term
What type of bacteria are associated with gastric cancer? |
|
Definition
| H. pylori. (cause and effect unclear, tho.) |
|
|
Term
| What 2 genes are associated with H. pylori's induction of ulcers? |
|
Definition
|
|
Term
| What cytokine do gastric epithelial cells secrete in response to H pylori infection and what does it do? |
|
Definition
| IL-8, causing recruitment of neutrophils and inflammation. |
|
|
Term
| Name three diagnostic options for helicobacter pylori. |
|
Definition
| 1. Endoscopy and biopsy of ulcer, 2. Urea breath test, where the patient swallows radioactive urea. If helicobacter are in there, they will then breathe out radioactive CO2. 3. Blood test for helicobacter antigens. |
|
|
Term
| What is the proper treatment for H. pylori infections? |
|
Definition
| Omeprazole (proton pump inhibitor), metranidazole, tetracycline, amoxacillin, and clarithromycin for a month. |
|
|
Term
| How are pseudomonas aeruginosa infections usually acquired? |
|
Definition
| they are poorly invasive, but present all over the place in the environment. They may be introduced by damage. Eg. lumbar puncture, catheter. May also be in whirlpools, ventillators, or on contact lenses. |
|
|
Term
| What does pseudomonas aeruginosa ferment? |
|
Definition
|
|
Term
| Why is pseudomonas aeruginosa so dangerous to people with cystic fibrosis? |
|
Definition
| It will further gum up the mucus elevator due to its mucoid nature. |
|
|
Term
| Who is particularly vulnerable to pseudomonas aeruginosa infections? |
|
Definition
| Burn patients, people with cystic fibrosis, hospitalized and immunocompromised people. |
|
|
Term
| What does pseudomonas aeruginosa look like in a gram stain or on a plate? Oxidase pos or neg? |
|
Definition
| In a gram stain it is a gram negative rod. On a plate it has big mucoid colonies that may appear blueish or greenish due to pyocyanin or fluorescin pigments. Oxidase positive. |
|
|
Term
| Which kind of bacteria smells like grapes? |
|
Definition
|
|
Term
| How to pseudomonas aeruginosa get around? |
|
Definition
| By means of their nifty polar tufted flagella |
|
|
Term
| Why would an alcoholic be more succeptible than your average person to vibrio vulnificus infection? |
|
Definition
| It makes you immune compromised. |
|
|
Term
| What does pseudomonas aeruginosa exotoxin A do? What other bacteria has a toxin that targets the same thing? |
|
Definition
| It ADP-ribosylates EF2, which is also done by diptheria toxin |
|
|
Term
| What are the X factor and V factor that H. influenzae needs to grow in culture? |
|
Definition
|
|
Term
| Is H influenzae aerobic or anaerobic? What does it look like if you plate it on blood agar? |
|
Definition
|
|
Term
Is H. influenzae oxidase pos or neg? |
|
Definition
|
|
Term
| What is the most common pathogenic type of H. influenzae? What makes them typable, anyway? |
|
Definition
| Hib. The capsule makes it typeable. |
|
|
Term
| What kind of capsule does H. influenzae have? |
|
Definition
| a polyribotol phosphate capsule. |
|
|
Term
| What part of H. influenzae does the vaccine target? |
|
Definition
|
|
Term
| What diseases can be caused by haemophilus aegyptius? |
|
Definition
| Conjunctivitis and Purpuric fever, which is an often fatal pediatric disease involving oozing pus around eyeballs. |
|
|
Term
| What is an appropriate treatment for pink eye caused by haemophilus aegyptius? |
|
Definition
| Topical antibiotics such as gentamycin or quinolones |
|
|
Term
| What disease can be caused by Haemophilus ducreyi? |
|
Definition
| genital chancroid (papule and ulcers of genitals and lymph nodes) that is more painful than syphilis chancre. |
|
|
Term
| How common are haemophilus ducreyi infections and how are they acquired? |
|
Definition
| 200-500 cases/yr in US. Sexually transmitted. |
|
|
Term
| List 3 diseases typically caused by type B H. influenzae. |
|
Definition
| Meningitis, epiglottitis, bacteremia |
|
|
Term
| What rare but serious disease caused by Hib could lead to respiratory arrest? |
|
Definition
|
|
Term
| Name 4 diseases that could be caused by nontypable H. influenzae |
|
Definition
| pneumonia, tracheobronchitis, sinusitis, and otitis media |
|
|
Term
| Prior to the Hib vaccine, what was the most common illness caused by Hib? |
|
Definition
|
|
Term
| how many Hib infctions are diagnosed per yr in the US? |
|
Definition
|
|
Term
| what 2 organisms account for the highest percentages of bacterial bronchitis? |
|
Definition
H. influenzae (28%) and strep. pneumoniae (21%) |
|
|
Term
| Name 2 virulence factors of H. influenzae. |
|
Definition
capsule
IgA protease which destroys IgA on mucous membranes. |
|
|
Term
| How does H. influenzae get iron while in a human? |
|
Definition
| It has receptors for lactoferrin and transferrin. It can take it up and wrestle the iron out of it. It can also get iron out of hemoglobin and heme systems like cytochromes. |
|
|
Term
| How might one diagnose meningitis caused by H. influenzae? |
|
Definition
Gram stain it directly in CSF or culture it on chocolate agar.
For type B, it is also possible to detect the PRP antigen in CSF or urine.
It may also be detected by PCR.
Show that it can only be cultured on blood agar in the presence of factors X and V. |
|
|
Term
| How would you treat meningitis caused by H. influenzae? What would you give to the patient's close contacts? |
|
Definition
| Cephalosporins. Contacts get rifampin. |
|
|
Term
| Why is the Hib vaccine given along with the DTaP series? |
|
Definition
| The B antigen is poorly immunogenic, but when given along with DTaP (containing tetanus and diptheria toxoids) it gets a better response. |
|
|
Term
| What diseases can be caused by Haemophilus Parainfluenzae? |
|
Definition
| pneumonia and endocarditis. |
|
|
Term
| Why is whooping cough called whooping cough? |
|
Definition
| Whoop during inspiration during coughing. |
|
|
Term
| What organism causes whooping cough? |
|
Definition
|
|
Term
| How do bordatella pertussis infections spread? |
|
Definition
|
|
Term
| What are some symptoms of whooping cough? |
|
Definition
| Thick mucus buildup in lungs, violent coughing spells, inspiratory gasp (whoop) and possible fever, convulsions, brain damage, and death. |
|
|
Term
What is the trend in the number of cases of whooping cough reported to the CDC per year? |
|
Definition
|
|
Term
| Describe the 3 stages of whooping cough. |
|
Definition
| 1- Catarrhal stage (bacteria attach to the trachea and cause cold like symptoms. Contagious. 1-2 wks) 2- paroxysmal stage (begins making toxin. Attacks of coughing, vomiting. 1-6 wks.) 3- convalescent stage (recovery. Organisms are gone, but coughing persists. succeptible to secondary infection) |
|
|
Term
| At what stage of whooping cough are antibiotics most helpful? |
|
Definition
|
|
Term
| At what stage is whooping cough most contagious? |
|
Definition
|
|
Term
| At what point might bordatella pertussis cause septicemia |
|
Definition
| After establishing an infection in the lungs. |
|
|
Term
bordatella pertussis: Aerobic or anaerobic? Oxidase pos or neg? Motile or nonmotile? |
|
Definition
|
|
Term
| What type of cells does B. pertussis adhere to? What function does their adherence interfere with? |
|
Definition
| Ciliated respiratory cells. Interferes with ciliary movement. |
|
|
Term
| What does filamentous hemagglutinin do for B. pertussis? |
|
Definition
binds galactose on glycolipids or complementr eceptors and can get it taken up into the cell. (It's a facultative intracellular bacterium) |
|
|
Term
| what does pertussis toxin do? |
|
Definition
| it is an A:B toxin. The B part gets it in via surface receptors on host cell. Once in, it ADP ribosylates and thereby inactivates the Gi protein that normally negatively regulates adenylate cyclase. This increases respiratory secretions and mucus production. |
|
|
Term
Why does the adenylate cyclase made by B. pertussis affect only the host cells? |
|
Definition
| It requires calmodulin for activity, and the bacteria don't have calmodulin. |
|
|
Term
| What is targeted by the TCT toxin of B. pertussis? |
|
Definition
| The cilia. It helps destroy them. |
|
|
Term
What animals can be reservoirs of Bordatella pertussis? |
|
Definition
|
|
Term
| What is the best treatment for B. pertussis infections? |
|
Definition
| Erythromycin given at the catarrhal stage. |
|
|
Term
| Why wouldn't mom's antibodies protect babies from B. pertussis much? |
|
Definition
| By the time people are grown up, the protection imparted by childhood vaccines has mostly worn off. |
|
|
Term
| What kind of animals is brucella abortis associated with? How about brucella suis? Brucella melitensis? |
|
Definition
| Abortus: cattle, suis: pigs, melitensis: sheep and goats |
|
|
Term
| What type of bacteria are responsible for undulant fever? |
|
Definition
|
|
Term
| Are brucella aerobic or anaerobic? motile or nonmotile? oxidase pos or neg? |
|
Definition
| Aerobic, nonmotile, ox. pos |
|
|
Term
| Are brucella urease positive or negative? |
|
Definition
|
|
Term
| Why does brucella cause spontaneous abortion in animals but not humans? |
|
Definition
| It tends to accumulate on fetal membranes and in placentas of farm animals, but not humans. |
|
|
Term
| What happens to brucella once they are phagocytized? |
|
Definition
| They convert their vacuole to a paracytopherous vacuole where they can replicate. They prevent fusion of the phagosome with a lysosome. |
|
|
Term
| What immune system mechanism is most useful for fighting a Brucella infection? |
|
Definition
| CD8 cytotoxic t-cells kill the host and the bacteria inside |
|
|
Term
| What are he initial symptoms of a brucella infection? |
|
Definition
| Flu-like symptoms and undulating fever (higher in the day and lower at night. The fever also dies down after a couple weeks and goes up again when the organism changes its antigenic presentation. |
|
|
Term
| How is a brucella infection diagnosed during the chronic phase? |
|
Definition
| Careful case history and serology. At this point, blood cultures are usually negative. |
|
|
Term
| How are people normally infected with brucella? |
|
Definition
| From animals. Through a cut or drinking unpasteurized milk. Or from working in a lab and accidentally injecting themselves. Human to human transmission or inhallation is rare. |
|
|
Term
How long should you wait for a suspected Brucella culture to grow before declaring it negative? |
|
Definition
|
|
Term
| What is the best treatment for a brucella infection? |
|
Definition
| doxycycline and rifampin for 6 weeks |
|
|
Term
| What are the three ways to prevent Brucella infections? |
|
Definition
| Vaccinate cattle, pasteurize milk, and cook meat. |
|
|
Term
| What does MacConkey agar have in it? Under what conditions do the colonies turn red? |
|
Definition
| Peptone, lactose, crystal violet and bile salts to inhibit gram pos. organisms, and neutral red. If they ferment lactose, organisms form red colonies. |
|
|
Term
| What is in Hektoen agar? What makes colonies turn orange? What makes them turn black? |
|
Definition
| It contains peptone, bile salts, lactose, sucrose, Brom Thymol blue, thiosulfate and ferric ions, and acid fuchsin. Colonies turn orange if they can ferment lactose or sucrose. They turn black if they are H2S positive. |
|
|
Term
| Of e-coli, salmonella, and shigella, which one(s) is/are H2S positive? |
|
Definition
|
|
Term
| Of E. coli, salmonella, and shigella, which can ferment lactose? |
|
Definition
|
|
Term
| Of E. coli, salmonella, and shigella, which are urease positive? |
|
Definition
|
|
Term
| What disease can Salmonella typhi and Salmonella paratyphi cause? |
|
Definition
| Typhoid fever, which can include septicemia. |
|
|
Term
| What disease can a Salmonella choleraesuis infection cause? |
|
Definition
|
|
Term
| How do people normally get Typhoid fever? |
|
Definition
| Ingestion of bacteria, which penetrate intestinal mucosa and get into the bloodstream. |
|
|
Term
| What are the symptoms of typhoid fever? Incubation period? |
|
Definition
| Sumptoms: gradually rising fever, possible mild GI symptoms including constipation first then watery diarrhea, rose spots (pink papules mostly on trunk.) Incubation period is 7-20 days. |
|
|
Term
At what point would blood and stool cultures grow up some S. typhi if a person had typhoid fever? |
|
Definition
| Blood: first and second weeks, stool 2nd week on. |
|
|
Term
| What species of Salmonella causes gastroenteritis? |
|
Definition
|
|
Term
| What is the incubation period for a Salmonella Enterica infection? What are the symptoms? |
|
Definition
| 8-48 hrs. Symptoms begin abruptly and include a low grade fever and nausea, vomiting, and diarrhea for 2-5 days. |
|
|
Term
| If someone had a salmonella enterica infection and were already sick, would blood and stool cultures be positive? |
|
Definition
| Stool culture only. S. enterica does not penetrate the epithelial barrier and get into the blood. |
|
|
Term
| What are the symptoms of illness caused by Salmonella cholerasuis infection? |
|
Definition
| Abrupt onset of quickly rising fever. Metastatic infections of bones, join, meninges, lung and heart may cause a variety of symptoms. |
|
|
Term
| How does Salmonella typhi getinto the boodstream? |
|
Definition
Attaches to M cells in peyer's patch, injects bacterial proteins via type 3 secretion system, causinf cell to ruffle and accidentally engulf bacteria. They replicate in the phagosome and transcytose to basal side of the membrane. They are then engulfed by macrophages, which bring them to lymph nodes, where they enter the blood. |
|
|
Term
| What does R typhi's Vi antigen do? |
|
Definition
| Prevents phagocytosis by pmns, making strains that have it more virulent. |
|
|
Term
What's the preferred treatment for somebody who has typhoid fever? What about a carrier? |
|
Definition
| cephtriaxones. For carrier, amoxacillin or quinolones. |
|
|
Term
| How might typhoid fever be diagnosed? |
|
Definition
| rose spots, organisms in blood or stool, ELISA for antibodies, Widal test (4-fold rise in agglutination antibodies to the O antigen, |
|
|
Term
| What is the usual treatment for gastroenteritis caused by salmonella? |
|
Definition
| Fluid and electrolyte replacement. Antibiotics don't usually shorten the course of the illness and may induce a carrier state. |
|
|
Term
| What are O antigens? H antigens? K antigens? |
|
Definition
| O antigens are sugar sidechains on LPS. H antigens are flagella. K antigens are capsules. |
|
|
Term
| What does peritrichous mean? |
|
Definition
| They have flagella on all sides. |
|
|
Term
| When enterobacteriaciae are motile, how do they move? |
|
Definition
| They are peritricous: they have flagella on all sides. |
|
|
Term
| What do these abbreviations stand for? ETEC? EIEC? EHEC?EPEC? EAEC? UPEC? |
|
Definition
| Enterotoxogenic E-coli, Enteroinvasive e-coli, enterohemorragic e-coli, enteropathogenic e-coli, enteroaggregative e-coli, and uropathogenic e-coli. |
|
|
Term
| What toxin does ETEC have that can be inactivated by heat? |
|
Definition
| LT (labile toxin, because it is labile to heat treatment. It's an A/B toxin that binds GM1, enters the cell, and ADP ribosylates Gs unit that stimulates adenylate cyclase, making it more active by interfering with its intrinsic ATPase activity. |
|
|
Term
| Why do people heterozygous for cystic fibrosis CFTR get milder diarrhea when infected with ETEC? |
|
Definition
Normally, the cAMP rise would make chloride leave the cell and water would follow it, but due to the defective CFTR, chloride doesn't leave so efficiently. |
|
|
Term
| What does ETEC's heat stable toxin do? |
|
Definition
| increases cGMP, which in turn inhibits NaCl absorption |
|
|
Term
| What organism causes traveller's diarrhea and what are the symptoms? |
|
Definition
| watery stools, ofter with no fever. no blood or pus in stool. |
|
|
Term
| In what ways is EiEc similar to shigella? |
|
Definition
| -actin tails to move between cells, invade intestinal epithelia using plasmid-encoded invasion genes. |
|
|
Term
| What are the symptoms of an eiec infection? |
|
Definition
| blood and pus in stool, fever. |
|
|
Term
| Of Rickettsia, Orientia, Erlichia, Anaplasma Coxiella, and Bartonella, which one is not an obligate intracellular? |
|
Definition
|
|
Term
| How big are rickettsia, generally? |
|
Definition
|
|
Term
| What organism causes rickettsial pox and what is its vector? Reservoir? |
|
Definition
| R. akari, mite. reservoir: mites and wild rodents. |
|
|
Term
| What organism causes rocky mountain spotted fever and what is its vector and reservoir? |
|
Definition
Rickettsia rickettsii, tick, ticks and wild rodents |
|
|
Term
| Why should you be afraid of Rocky, the flying squirrel? |
|
Definition
| Rocky could be a reservoir for Rickettsia prowazekii, the causative agent of epidemic typhus! |
|
|
Term
| What insect vector spreads epidemic typhus? |
|
Definition
|
|
Term
| What is the causative agent of murine typhus? Vector? Reservoir? |
|
Definition
| Rickettsia typhi, flea, wild rodents. |
|
|
Term
| What is the most common Rickettsial disease in the US? |
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Definition
| Rocky Mountain Spotted Fever. |
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Term
Where and when in the US is a person most likely to get rocky mountain spotted fever? |
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Definition
| Southeast atlantic and south central states (tick belt) in April-October. |
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Term
| How do Rickettsia rickettsii escape host cells? |
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Definition
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Term
| What are the symptoms of Rocky Mountain Spotted Fever? |
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Definition
| Fever, chills, headache, myalgia(muscle pain). Rash after 3 days on extremities then trunk. Note: rash may be cone before doctor visit. Complications may include gi symptoms, respiratory failure, encephalitis (brain inflammation), renal failure |
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Term
| How is a person typically infected with R. prowazekii? |
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Definition
| Bitten by a louse, then scratch the infected louse's feces (containing sloughed of intestinal epithelial cells full of rickettsia) into their skin. |
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Term
| Why are lice not considered a reservoir for Rickettsia prowazekii? |
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Definition
| No transovarian transmission, and the infected lice die off in 2-3 weeks. |
|
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Term
| What are the drugs of choice for all rickettsial infections? |
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Definition
| Doxycycline, tetracycline, and chloramphenicol |
|
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Term
| Describe the 2 phases of the biphasic Rickettsia akari infection. |
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Definition
1. papule at bite for about a week becomes an eschar, and a papulovesicular rash that looks like pox develops.
2. Headache, chills, photophobia |
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Term
| What is Brill Zinsser disease? |
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Definition
| It's a less severe form of R. prowazekii infection that occurs in people who had typhoid fever but recovered without fully resolving the infection. Something triggers it to crop up again. A louse that bites a person with Brill Zinsser can then infect a naive host and cause full-blown epidemic typhus. |
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Term
| How is it thought that squirrels could transmit R. prowazekii to humans? |
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Definition
| Although the human body louse only bites humans, the squirrel fleas may be more promiscuous. |
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|
Term
| What are the symptoms of an R. prowazekii infection? |
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Definition
| Fever, chills, headache, myalgia and occasionally rash. Symptoms begin 8 days post infection on average. |
|
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Term
| Where in the US do cases of murine (endemic) typhus occur? |
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Definition
| Texas and southern california |
|
|
Term
| What organism is responsible for Q fever? |
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Definition
|
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Term
| What event is necessary to allow Coxiella burnetti to begin replicating inside the cell? |
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Definition
| phagolysosomal fusion acidifies the vacuole. |
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Term
| How can Coxiella burnetti be spread? |
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Definition
| Airborne exposure to dried organism (from exposure to placenta or animal hides etc..) or tick-vectored (not so important in human spread, but important in spread throughout animal population). |
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Term
| Explain phase variation in Coxiella burnetti. Which phases are associated with chronic vs acute infections? |
|
Definition
The cell wall LPS antigen caries. Phase 1 is highly infectious and blocks antibody binding, while phase 2 is less infectious and antibodies can bind it more easily.
If you find antibodies to just phase 2, it's probably an acute infection. If you find antibodies to phases 1 and 2, it's probably a chronic infection. |
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Term
| With Coxiella burnetti, what are the symptoms of an accute vs. chronic infection? |
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Definition
Acute: severe headache, fever, chills, myalgia. (Due to phase 2 antigen being more immune-provoking.)
Chronic: subacute endocarditis (esp. with a prosthetic heart valve). |
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Term
| What lab tests can be used to diagnose a C. burnetti infection? |
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Definition
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|
Term
| What is the accepted treatment for Coxiella burnetti infections? |
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Definition
| If they are acute, doxycycline or tetracycline. If they are chronic, rifampin and doxycycline/TMX. |
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|
Term
| What is the problem with Q-fever vaccine? |
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Definition
| It can cause a bad hypersensitivity response in someone or something who's been infected with C. burnetti before, so always do a skin test first. |
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Term
| How do erlichia and anaplasma like to grow inside the cell? |
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Definition
| They prevent phagolysosomal fusion and they grow in membrane enclosed masses called morulae. |
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Term
| What species is group A strep? And what does "group A" refer to anyway? |
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Definition
| S. pyogenes. Group A refers to the Lancefield classification, which organizes B hemolytic strep based on an antigen that is part of their peptidoglycan. |
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|
Term
What is the M protein of Strep pyogenes? |
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Definition
It's a surface protein that is anti-phagocytic because it interferes with the complement cascade by binding factor H, which in turn prevents C3 cleavage and makes it hard to deposit complement on its surface. |
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|
Term
| Some kinds of group A strep have a capsule. What's it made of? |
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Definition
|
|
Term
| What is protein G of strep pyogenes? |
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Definition
| It is a lot like protein A: it binds the Fc portion of antibodies, helping it hide from them for a while. |
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|
Term
| What is protein F of strep pyogenes? What other substance does it make that does the same thing? |
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Definition
| It binds to fibronectin, which is a common protein in the respiratory tract. Its lipoteichoic acid can also do that. |
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|
Term
Describe the 2 hemolysins of strep pyogenes? |
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Definition
| Streptolysin O is oxygen labile and it hemolyzes blood, but only anaerobically. You can stab a plate with it to get some inside the agar. You can also do anti streptolysin O titers in a patient. (ASO). Streptolysin S is oxygen stable and responsible for surface hemolysis. It isn't so antigenic. |
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Term
| Strep pyogenes secretes these 3 toxinsStreptokinase, streptodornase, and hyaluronidase. What do they do? |
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Definition
Streptokinase activates plasminogen to form plasmin and degrades fibrin to prevent fibrin from forming around it. Streptodornase is a DNAse that reduces the viscosity of pus for ease of spreading. Hyaluronidase attacks connective tissue and aids in spread. |
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Term
| How many horrible substances does S. pyogenes make? |
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Definition
|
|
Term
| What organism is responsible for flesh eating disease? |
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Definition
|
|
Term
| What does staph aureus alpha toxin do? |
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Definition
| It lyses red blood cells and produces clearing in blood agar. It is also called alpha hemolysin, but causes beta hemolysis. |
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|
Term
| Which toxin is responsible for staph. aureus food poisoning? |
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Definition
|
|
Term
| What does protein A of Staphylococcus do? |
|
Definition
It binds the Fc portion of Ig, preventing Fab binding. |
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|
Term
| What is "scalded baby syndrome" aka "SSSS" |
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Definition
It's one possible gross thing Staph. aureus can do. The skin peels (just the top layer), and blisters and turns red and generally looks like the person was scalded. The epidermolytic toxin does this. |
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|
Term
| What is impetigo and what causes it? |
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Definition
| Impetigo is a superficial skin infection that mostly happens to children and mostly on the face. A small red pustule appears, bursts, and crusts. Often there's more than one. 80% of the time it's caused by Staph aureus, but 20% of the time it is caused by streptococci. |
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|
Term
What does staph aureus TSST do? |
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Definition
| This is the toxin that causes toxic schock syndrome. It binds to class II MHC receptors and crosslinks them with the variable part of the T-cell receptor. This causes the release of lots of IL1 and 2, which in turn cause fever and hypotension leading to shock. Causes a diffuse red rash. |
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Term
| Which staphylococcus species is most likely to cause a UTI in a woman? |
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Definition
|
|
Term
| What might you treat MRSA with? |
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Definition
| Vancomycin, or possibly Zyvox as a last resort. |
|
|
Term
| What is the most common cause of osteomyelitis? |
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Definition
| Staph aureus spreads to the bones via the blood. |
|
|
Term
| Which strain(s) of Staph is/are sensitive to novobiocin? |
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Definition
| Aureus and epidermidis. (Not saprophyticus) |
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Term
| When people get food poisoning from staph, how does that work? |
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Definition
| Food gets contaminated by a human carrier. Bacterial toxin in food (enterotoxin) interacts with the vagus nerve and causes nausea and vomiting and diarrhea. It comes within 4 hrs and usually goes within 24 without the person ever being colonized by the staph. |
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Term
| Why is food poisoning caused by staph different from enterocolitis caused by staph? |
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Definition
| With enterocolitis, the staph actually colonize the gut and show up in stool. For the former, no antibiotic is necessary; for the latter it is good to give one. |
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Term
| What puts a person at risk for an infection with staph epidermidis? |
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Definition
| If a person has stuff stuck in them. Eg. dialysis, catheters, spinal tap needles. Also being immunocompromised. It's an opportunistic infection. |
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|
Term
| Staph epidermidis... what is its virulence factor? |
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Definition
| Slime factor is a secreted mucus that can interfere with antibiotic action and can form a biofilm on surfaces. |
|
|
Term
| What does staph aureus' coagulase do? What are the 2 kinds? |
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Definition
| There are secreted and cell bound kinds, but they both do essentially the same thing: convert fibrinogen to insoluble fibrin. |
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|
Term
| What are the 4 first-line drugs used to treat tuberculosis caused by mycobacterium tuberculosis? |
|
Definition
| Isoniazid, Rifampin, pyrazinamide, ethambutol |
|
|
Term
| What defines multidrug resistant TB? (MDR-TB) |
|
Definition
| Resistance to the 2 main first line antibiotic treatments: rifampin and isoniazid |
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|
Term
| What defines extensively drug resistant TB (XDR-TB)? |
|
Definition
| Resistant to the main 2 first line antibiotics (isoniazid and rifampin) and 3 or more classes of the 2nd line antibiotics. |
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|
Term
| What is the standard treatment for a case of tuberculosis disease? |
|
Definition
| 2 months with 4 drugs (ISO, RIF, PZA, ethambutol), then 4 months with 2 drugs (Rif and Iso). If the patient has cavitary pulmonary TB and positive culture results at the end of the first 2 months, extend the second phase to 7 months. Refer HIV patients who are taking antivirals to a specialist. |
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|
Term
| What percentage of people who are infected with Mycobacterium tuberculosis will develop TB in their lifetime? If they have AIDS how does that statistic change. |
|
Definition
| 10% but with AIDS it becomes 10% per year. |
|
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Term
| What type of vaccine is available for Mycobacterium tuberculosis? What are the drawbacks? |
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Definition
| The BCG vaccine is made from M. bovis. Drawbacks include: variable effectiveness, can't be used on ppl with pos PPD, not useful in immunocompromised patients, less effective in adults, makes it more difficult to read a tuberculin skin test. |
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Term
| What determines whether leprosy is tuberculoid or lepromatous? |
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Definition
| Strength of cell mediated immune response. Strong CMI favours tuberculoid |
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Term
| What is the difference between tuberculoid and lepromatous leprosy? |
|
Definition
| Tuberculoid: hypopigmented spots with few bacteria. Lepromatous: severe damage to skin, peripheral nerves, and nasal mucosa. Many bacteria. |
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|
Term
| Name 3 acid fast bacteria. |
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Definition
| M. tuberculosis, M. leprae, and Nocardia (to some degree) |
|
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Term
| Name that weird kind of bacteria found in soil that are related to MTB, weakly acid fast, aerobic, and branch like fungi. |
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Definition
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|
Term
| What kind of disease can Nocardia cause? |
|
Definition
| opportunistic pulmonary diseases |
|
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Term
| These facultative anaerobes are related to MTB but are not acid fast. They branch like fungi and form yellow colonies. |
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Definition
|
|
Term
| What type of diseases can Actinomyces cause? |
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Definition
| pulmonary diseases and abcesses at many sites. |
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|
Term
|
Definition
A classification system for mycobacteria other than MTB, based on their rate of growth and pigment formation in light vs dark. |
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|
Term
| What is lipoarabinomannan? |
|
Definition
| It is part of a mycobacterial cell wall, consisting of a polysaccharide plus mycolate. It is an LPS-like structure that can stimulate host toll-like receptors. |
|
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Term
|
Definition
| It is a combination of trehlose and mycolate that, if mycobacterium tuberculosis have it, can make them more virulent by inducing TNF and inhibiting oxidative phosphorylation. |
|
|
Term
| What does MTB use sulfolipids for? |
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Definition
| Inhibits lysosome fusion once they have been taken up into a macrophage. |
|
|
Term
| How is tuberculosis usually diagnosed? |
|
Definition
| Sputum staining with fluorescent dye. You don't have to see a lot of organisms to make a positive diagnosis. |
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Term
| How long does it take for M. tuberculosis colonies to appear on a plate or for a culture to become turbid? |
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Definition
|
|
Term
| What is the typical route of M. tuberculosis infection? 2 other possibilities? |
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Definition
| Inhaled (very drying resistant). GI or skin are other possibilities. |
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Term
| Name 2 drugs that you might be able to use to treat leprosy. |
|
Definition
| Dapsone or, if it's resistant to that, rifampin |
|
|
Term
|
Definition
| It is a really huge fatty acid (>80 carbons) that forms half the mass of M. tuberculosis' cell wall. |
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|
Term
Name 2 species other than M. tuberculosis that could cause tuberculosis in immunocompromised patients. |
|
Definition
| M. avium-intracellulare (MAC) and M. kansasii |
|
|
Term
| What type of bacteria, when grown in rich medium, makes "chinese letter formations"? |
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Definition
| Corynebacterium diptheriae. The rods bend and snap back on themselves. |
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Term
| What does corynebacterium diptheriae look like when grown in sub-optimal Loeffler's medium? |
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Definition
| Club shaped with metachromatic granules: spots of accumulated polyphosphate that stain purple/black with methylene blue. |
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|
Term
| What conditions induce the production of the diptheria toxin and what benefit does this have for the bacteria? |
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Definition
| The human body is an iron poor environment, which triggers the toxin. The toxin kills eukaryotic cells, releasing iron. |
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|
Term
| Explain the mechanics of the diptheria toxin. |
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Definition
| It is an A: B toxin. The B subunit gets the toxin endoytosed and then releases A subunit into the cytoplasm when the vacuole acidifies. The A fragment ADP-ribosylates EF2, which prevents protein synthesis. |
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Term
How can you do an in-vitro toxin toes to find out whether a strain of C. diptheriae makes the diptheria toxin? |
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Definition
| Put a filter paper strip infused with antitoxin on the plate perpendicular to streaks of bacteria. the antitoxin will diffuse out of the paper and if it's present, the toxin will diffuse out of the bacteria. There will then be a zone of precipitation. |
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Term
| What grows on a tellurite plate? What is special about colony appearance? |
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Definition
| Corynebacterium diptheriae. Tellurite inhibits the growth of most other upper respiratory tract bacteria. C. diptheriae colonies make black stuff (tellurium) |
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Term
| What is the proper way to treat diptheria? |
|
Definition
| Give antitoxin and either penicillin G or Erythromycin. |
|
|
Term
| What is special about the motility of listeria monocytogenes? |
|
Definition
| At 20 degrees it has tumbling motility but at 37, it is nonmotile. |
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|
Term
| How do people usually get listeria and who is vulnerable? |
|
Definition
| Usually by eating unpasteurized dairy products or other improperly prepared foods. Usually a disease of the very young, old, and immunocompromised. |
|
|
Term
| Which type of bacteria causes food poisoning and grows fine at 4 degrees? |
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Definition
|
|
Term
| How does lysteria penetrate the intestinal epithelial barrier? |
|
Definition
| It uses internalin to bind to e-cadherin on cell surface and subverts host cell signaling to get taken up into a vacuole and then it uses lysteriolysin O to escape before fusion with the lysosome. Then it zips around and spreads by means of actin tails. It can invade macrophages and spread. |
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Term
| Which feature of the immune system is most important for fighting listeria? |
|
Definition
| Cell mediated immunity because it can spread directly from cell to cell. |
|
|
Term
| What are the symptoms of listeriosis in adults? |
|
Definition
usually mild flu-like symptoms (fever diarrhea, and muscle aches) that clear up before you ever know what happened. Can also cause meningitis and bacteremia. Usually patients have an underlying disorder. |
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|
Term
| Describe early onset listeriosis in neonates |
|
Definition
| Mother is infected and infant is infected transplacentally and exhibits symptoms at birth. Sepsis and lung involvement. Granules in liver and spleen. Stillbirth is possible. |
|
|
Term
| Describe late onset listeriosis disease in neonates. |
|
Definition
Caused by baby eating or drinking contaminated stuff. Symptoms appear after birth. Appears as meningitis. |
|
|
Term
| What is used to treat listeriosis? |
|
Definition
| Ampicillin or if they're allergic, trimethoprim sulfamethoxazole |
|
|
Term
| What's the latest in listeriosis prevention? |
|
Definition
| Safe food handling. Vaccines are being tested. Eliminating animal reservoirs is impossible. |
|
|
Term
When does listeria monocytogenes form sproes. |
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Definition
|
|
Term
| What does L. monocytogenes look like on blood agar and how can you increase their numbers relative to other organisms? |
|
Definition
| It's beta hemolytic and grows colonies that may look like group B strep. If you grow it at 4 degrees, it'll grow more than other stuff. |
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|
Term
| How can people get anthrax? |
|
Definition
| Inhallation, ingestion, or through abrasions. People who are in agriculture or who handle animal hides are most at risk because anthrax is generally a disease of animals and humans are accidental hosts. |
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|
Term
| How can you distinguish Bacillus anthracis from bacilus cereus (bacteria that can cause gastroenteritis that's not super serious)? |
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Definition
| The anthracus is not motile, but cereus is. |
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|
Term
Give 2 interesting facts about B. anthracis' capsule. |
|
Definition
| Made only in vivo. It's a peptide capsule made of d-glutamic acid. |
|
|
Term
Name the 3 forms of anthrax and tell which is most common. |
|
Definition
| Cutaneous anthrax (most common), wool sorter's disease, and intestinal anthrax |
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|
Term
| What is the typical course of a cutaneous anthrax infection? |
|
Definition
| 2-5 days post infection, a papule forms on the hand, forearm, or head. The vesicle forms with black fluid. If it spreads to regional lymph nodes then bloodstream, it has a 20% chance of killing the host. |
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Term
| What is the typical course of wool sorters' disease? |
|
Definition
| People handling animal hides and wool disturb and inhale anthrax spores. They develop pulmonary infection with fever, malaise and cough and septicemia. Death within 24 hrs. Often diagnosis occurs post-mortem because people don't worry much about early symptoms. |
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|
Term
| Describe the typical case of intestinal anthrax. |
|
Definition
| Organism enters the blood through the intestine and the host dies. |
|
|
Term
| Name the 2 virulence factors of Bacillus anthracis. Which is encoded by a plasmid? |
|
Definition
| polypeptide capsule (plasmid) and anthrax toxin |
|
|
Term
| What is the usual treatment for anthrax? |
|
Definition
|
|
Term
| Describe the 3 components of anthrax toxin and their functions. |
|
Definition
Protective antigen (PA) gets LF and EF into cells (acts as a B subunit)
Edema factor (EF) is an adenylate cyclase that is activated by calmodulin in the host cell.
Lethal factor (LF) cleaves a MAP kinase causing macrophages to release cytokines leading to lethal shock. |
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|
Term
| How do you diagnose a Bacillus anthracis infection? |
|
Definition
Look at smears from cutaneous lesions or grow up a blood culture if the person is septicemic. PCR techniques may also be used for diagnosis. |
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