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56 Cards in this Set
- Front
- Back
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Physical findings of cholera?
Cause of death? |
findings such as diminished pulse, sunken eyes, and poor skin turgor will develop with severe dehydration.
death will be due to dehydration |
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Action of the A subunit of choleragen?
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the A subunit
activates G-protein, which in turn stimulates the activ- ity of a membrane-bound adenylate cyclase, resulting in the production of cAMP. Intracellular cAMP results in active secretion of Na and Cl as well as the inhibition of Na and Cl reabsorption. Fluid, bicarbonate, and potas- sium are lost with the osmotic pull of the NaCl as it trav- els down the intestine. |
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bacterium causing gastroenteritis from sushi?
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Vibrio parahaemolyticus
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3 most common causes of diarrhea in the world?
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Campylobacter jejuni, ETEC, and the Ro-
tavirus are the three most common causes of diarrhea in the world. |
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which of the main bacteria are zoonotic ?
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???
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This organism can also be acquired by
drinking unpasteurized milk. |
c. jejuni
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describe the course of c. jejuni infection
does this bacterium have cytotoxic activity? |
The illness begins with a prodrome of fever and
headache, followed after half a day by abdominal cramps and a bloody, loose diarrhea. This organism invades the lining of the small intestine and spreads systemically as do Salmonella typhi and Yersinia enterocolitica. Campy- lobacterjejuni also secretes an LT toxin similar to that of Escherichia coli and an unknown cytotoxin that de- stroys mucosal cells. |
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what is the relationship between h.pylori and aspirin?
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H. pylori is the most common cause of duo-
denal ulcers and chronic gastritis (inflamed stomach). ( Aspirin products rank second.) It is the second leading cause of gastric (stomach) ulcers, behind aspirin prod- ucts. Helicobacter pylori causes duodenal and gastric ulcers and gastritis. Visualize a Helicopter- bacteria lifting the cap off a duodenal and gastric ulcer crater. If you have a more violent disposition, visualize an Apache helicopter-bacteria shooting hellfire mis- siles at the stomach. |
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how would you treat gastric and duodenal ulcers due to h.pylori?
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Multiple recent studies have shown that treat-
ment with combinations of bismuth salts, Metronida- zole, ampicillin, and/or tetracycline, clears Helicobacter pylori and results in a dramatic decrease in both duo- denal and gastric ulcer recurrence (Veldhuyzen van Zanten, 1994; Ransohoff, 1994; Sung, 1995). |
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how do you identify p.aeruginosa?
is this bacterium fond of cytotoxic activity? |
Pseudomonas aeruginosa is an obligate aerobic (non-
lactose fermenter), gram-negative rod. It produces a green fluorescent pigment (fluorescein) and a blue pig- ment (pyocyanin), which gives colonies and infected wound dressings a greenish-blue coloration. It also pro- duces a sweet grape-like scent, so wound dressings and agar plates are often sniffed for organism identification. this bug has a weak invasive ability, but once it is inside the bloodstream, the story changes. It elaborates numerous exotoxins including exotoxin A, which has the same mechanism of action as diphtheria toxin (stops protein synthesis) but is not antigenically identical. Some strains also possess a cap- sule that is antiphagocytic and aids in adhesion to tar- get cells (in the lungs for example). imagine a hydra trying to get inside the castle walls of heroes 3 to wreak havoc! |
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Name some important pseudomonas aeruginosa infections!
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1) Pneumonia (see Fig. 16-5)
a) Most cystic fibrosis patients have their lungs colonized with Pseudomonas aeruginosa. These pa- tients develop a chronic pneumonia, which progres- sively destroys their lungs. b) Immunocompromised patients (cancer pa- tients and intensive care unit patients) are highly susceptible to pneumonia caused by Pseudomonas aeruginosa. 2) Osteomyelitis a) Diabetic patients have an increased risk of de- veloping foot ulcers infected with Pseudomonas aeruginosa. The infection can penetrate into the bone resulting in osteomyelitis. b) Intravenous (IV) drug abusers have an in- creased risk of osteomyelitis of the vertebrae or clavicle. c) Children develop osteomyelitis secondary to puncture wounds to the foot. 3) Burn-wound infections: This organism sets up significant infections of burn wounds, which eventually lead to a fatal sepsis. 4) Sepsis: Pseudomonas sepsis carries an extremely high mortality rate. 5) Urinary tract infections, pyelonephritis: This occurs in debilitated patients in nursing homes and in hospitals. They often have urethral Foley catheters, which serve as a source of infection. 6) Endocarditis: Staphylococcus aureus and Pseudo- monas aeruginosa are frequent causes of right heart valve endocarditis in IV drug abusers. 7) Malignant external otitis: A Pseudomonas ex- ternal ear canal infection burrows into the mastoid bone, primarily in elderly diabetic patients. 8) Corneal infections: This can occur in contact l ens wearers. BSU po EMC! BSU slaveriet etter EMC service |
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treatment of p.aeruginosa?
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An anti-
pseudomonal penicillin is usually combined with an aminoglycoside for synergy (for example, piperacillin and gentamicin). |
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which family of enterics comprise 99% of the intestinal flora??
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Bacterioidaceae (they also live in the oral cavity and vagina)
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b.fragilis is normally peaceful... what can evoke its wrath?
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When a bullet tears into the intestine, when a
seat belt lacerates the intestine in a car wreck, when ab- dominal surgery is performed with bowel penetration, or when the intestine ruptures secondary to infection (appendicitis) or ischemia, THEN the bacteria go wild in the peritoneal cavity, forming abscesses. |
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fusobacterium causes...?
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This bacterium is just like Bacteroides melaninogeni-
cus in that it also causes periodontal disease and aspi- ration pneumonias. Fusobacterium can also cause abdominal and pelvic abscesses and otitis media. |
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b. melaninogenicus causes...?
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This organism produces a black pigment when grown
on blood agar. Hence, the name melaninogenicus. It lives in the mouth, vagina, and intestine, and is usually involved in necrotizing anaerobic pneumonias caused by aspiration of lots of sputum from the mouth (during a seizure or drunken state). It also causes periodontal disease. |
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ANAEROBIC GRAM POSITIVE COCCI
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Peptostreptococcus (strip or chain of cocci) and Pepto-
coccus (cluster of cocci) are gram-positive anaerobes that are part of the normal flora of the mouth, vagina, and intestine. They are mixed with the preceding or- ganisms in abscesses and aspiration pneumonias. Members of the Streptococcus viridans group, dis- cussed in Chapter 4, are mentioned here because they are gram-positive, microaerophilic, and are frequently isolated from abscesses (usually mixed with other anaer- obic bacteria). These oxygen-hating critters have many names (such as Streptococcus anginosus and Streptococ- cus milleri) and are a part of the normal GI flora. |
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GENERAL PROPERTIES OF ENTEROBACTERIACEAE - transmission?
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- gram negative rods
- fecal - oral - migrates up the urethra (e.g. thru catheters) - |
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E.coli - transmission?
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fecal-oral
urethral migration, catheter migration aspiration pneumonia |
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E.coli virulence factors?
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fimbriae (pili)
siderophore adhesins capsule (K) flagella (H) for motility |
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e.coli toxins?
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LT
ST Shiga-like toxin (verotoxin) inhibits 60S ribounit |
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E.coli - clinical manifestations?
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newborn meningitis
UTIs hospital acq. sepsis hospital acq. pneumonia diarrhea - normal traveller's diarrhea (ETEC), hemorrhagic colitis (EHEC) or even shigellosis-like diarrhea (EIEC) |
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which types of e-coli have we?
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ETEC, EHEC, EIEC
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treatment of e.coli?
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cephalosporins
AGs Trimet & sulfamet fluoroquinolones |
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how do you diagnose e.coli?
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1 gramstain
2 culture (urine, sputum, CSF or blood) can grow at 45.5 degrees C 3 EMB/McConkey agars |
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klebsiella can cause:
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sepsis (common, just behind e.coli)
UTIs, in pat. w/ foleys violent cavitating pneumonia red currant jelly like sputum! |
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proteus can split...?
and causes ....? |
urea
UTIs |
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is shigella always a pathogen?
what does it cause what is the target of shiga toxin? |
yes
it causes the same type of diarrhea as EIEC does - bloody with pus 60 S ribounit hates shigella! |
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how is salmonella contracted?
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Salmonella differs from the other enterics because it
lives in the gastrointestinal tracts of animals and in- fects humans when there is contamination of food or wa- ter with animal feces. Today in the U.S., Sal- monella is most commonly acquired from eating chick- ens and uncooked eggs. Salmonella typhi (the 2 other clinical ones being cholera-suis and enteridis) is an exception as it is not zoonotic |
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salmonella causes...?
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1) the famous ty-
phoid fever, 2) a carrier state, 3) sepsis, and 4) gastroenteritis (diarrhea) |
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describe typhoid fever
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Typhoid fever, caused by Salmonella typhi,
depicted by a Salmon with fever (thermometer) and rose spots on its belly. Salmonellosis starts 1-3 weeks after exposure and includes fever, headache, and abdominal pain that is either diffuse or localized to the right lower quadrant (over the terminal ilium), often mimicking ap- pendicitis. As inflammation of the involved organs oc- curs, the spleen may enlarge and the patient may develop diarrhea and rose spots on the abdomen-a transient rash consisting of small pink marks seen only on light-skinned people. |
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salmonella diagnosis and treatment?
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Diagnose this infection by culturing the blood, urine,
or stool. Ciprofloxacin or ceftriaxone are considered appropriate therapy. |
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what causes the diarrhea from salmonella enteridis?
how to treat it? |
This diarrhea is caused by a yet-uncharacter-
ized cholera-like toxin (watery diarrhea) and sometimes also by ileal inflammation (mucous diarrhea). Treatment usually involves only fluid and electrolyte replacement, as antibiotics do not shorten the course of the disease and do cause prolonged bacterial shedding i n the stool. The diarrhea only lasts a week or less. |
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yershinia enterocolitica will cause what?
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Following ingestion of contaminated foods, such as
milk from domestic farm animals or fecally contami- nated water, patients will develop fever, diarrhea, and abdominal pain. This pain is often most severe in the right lower quadrant of the abdomen, and therefore pa- tients may appear to have appendicitis. Examination of the terminal ileum (located in the right lower quadrant) will reveal mucosal ulceration. |
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yershinia infection; pathogenesis?
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The pathogenesis of this organism is twofold:
1) Invasion: Like Salmonella typhi, this organism possesses virulence factors that allow binding to the in- testinal wall and systemic invasion into regional lymph nodes and the bloodstream. Mesenteric lymph nodes swell, and sepsis can develop. 2) Enterotoxin: This organism can secrete an en- terotoxin, very similar to the heat-stable enterotoxin of Escherichia coli, that causes diarrhea. |
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Diagnosis and treatment of yershinia?
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Diagnosis can be made by isolation of this organism
from feces or blood. Treatment does not appear to alter the course of the gastroenteritis, but patients who have sepsis should be treated with antibiotics. Although re- frigeration of food can wipe out many types of bacterial pathogens, Yersinia enterocolitica can survive and grow in the cold. |
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most common cause of UTIs?
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e.coli
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how does catheters compromise the urinary tract in terms of infection susceptibility?
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in addition to being a foreign body surface, catheters bypasses the flow of urine thru the urinary tract, so that bacteria aren't as easily flushed out of it!
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function of ETEC toxins?
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LT and ST. they hit cAMP and guanylyl cyclase respectively, but the end effect is the same: watery diarrhea
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what is dysentery?
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Dysentery (formerly known as flux or the bloody flux) is an inflammatory disorder of the intestine, especially of the colon, that results in severe diarrhea containing mucus and/or blood in the feces[1] with fever, abdominal pain,[2] and rectal tenesmus (a feeling of incomplete defecation), caused by any kind of infection.
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what is HUS?
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Hemolytic-uremic syndrome (or haemolytic-uraemic syndrome), abbreviated HUS, is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia). It predominantly, but not exclusively, affects children. Most cases are preceded by an episode of infectious, sometimes bloody, diarrhea caused by E. coli O157:H7, which is acquired as a foodborne illness or from a contaminated water supply. It is a medical emergency and carries a 5–10% mortality; of the remainder, the majority recover without major consequences but a small proportion develop chronic kidney disease and become reliant on renal replacement therapy.
The typical pathophysiology involves the shiga-toxin binding to proteins on the surface of glomerular endothelium and inactivating a metalloproteinase called ADAMTS13, which is also involved in the closely related thrombotic thrombocytopenic purpura (TTP).[citation needed] Once the ADAMTS13 is disabled, multimers of von Willebrand Factor (vWF) form and initiate platelet activation and cause microthrombi formation The classic childhood case of HUS occurs after ingestion of a strain of bacteria, usually types of E. coli, that expresses verotoxin (also called shiga-like toxin). Bloody diarrhea typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, low platelet count (thrombocytopenia), and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.[ |
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how may ATB treatment against EHEC excacerbate HUS?
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extra toxin release from the lysed EHEC will worsen HUS!
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treatment for e.coli ?
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in general, we dont administer treatment for gastroenteritis. lysing the e-coli might excacerbate the situation from increased toxin release momentarily!
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transmission of klebsiella?
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endogenous typically
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pathogenesis of klebsiella infecitons?
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pneumonia (typically in elderly, alcoholics or people with chronic lung disease pr diabetes)
sepsis |
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manifestations of klebsiella pneumonia?
treatment? |
`sputum: thick and red (jelly like), but not foul-smelling as with anaerobic infections (which typically applies to aspiration pneumoniae)
frequently causes abcesses, difficult to treat also causes UTIs kleb-infections follows a somewhat nosocomial pattern treatment: cephalosporin with AG, or fluoroquinolones |
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does shigella use the actin jet surf trail?
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yes! once inside the enteric epithelial cells, it doesnt have to go into extracellular space again! so it is invasive, it also have the proteinsynth inhibiting toxin like EHEC!,
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pathogenesis of shigella infections?
treatment? |
neurotoxic
enterotoxic (watery diarrhea followed by bloody diarrhea) HUS! it is acid resistant! as little as one bacterium can initiate an infection! incubation = 1-4 days shigella is a disease due to poor sanitation.. we usually dont use ATBs |
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facultative intracellular bacteria?
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yes frank may brush sally list's legs
yersinia franciscella mycobacterium tb brucella salmonella listeria legionella |
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which is the most motile bacterium here?
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proteus (protoss! :) ) - loads of flagella
urease positive (UTIs may thus lead to kidney stones) clinically, lower back pain presenting together with UTI symptoms should ring a bell for proteus! non-lactose fermenting sepsis as well of course (LPS) |
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salmonella
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constipation more common than diarrhea
typhoid fever treatment: cephalosporins or fluoroquinolones it inhibits macrophage phagocytotic mechanisms, and can hide inside H2S positive, motile, nonlactose fermenter watery diarrhea progresses to bloody (salmon is invasive) the diarrhea actually results from the INFLAMMATION caused by salmonella second most common gastroenteritis after c-jej the salmonella species who gets into blood, and thus causes sepsis, will have more propensity to cause osteomyelitis we culture salmonella on HE agar (shigella will be colorless, salmonella will be black - these two infections can be confused in terms of symptoms) treatment: none for gastroenteritis (self limiting) for invasive: ampicillin, cephalosporins, fluoroquin, or TMP-SMZ PREVENTION: good handwashing routine and proper sewage and sanitation, kitchen routine on poultry and eggs |
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ABC anaerobes:
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actinomyces, bacterioides, clostridia
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bacterioides
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intestinal trauma / perforation - sepsis, peritonitis and abcesses. (often mixed infections, and foul smelling)
LPS is not that superantigenic (important, since bacterioides is the most prominent bacterium in the gut) treatment: surgical drainage of abcesses, clindamycin, this bacterium is quite resistant always use prophylactic ATBs prior to biliary tract or gastrointestinal surgeries |
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hemophilus
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choc agar (requires hemin and NAD)
satelite phenomenon ! (s.aureus is b-hemolytic, and thus yeields a satelite zone where hemophilus can grow) ducreyi: sexually transmitted influenza: meningitis, pneumonia? we do have a vaccine reservoidr: nasopharynx capsule iga protease otitis media, conjunctivitis, bronchitis/pneumonia (espec. in ppl with COPD), EPPIGLOTIDIS - drooling with head hung) meningitis - cephalosporin for treatment the vaccine is polysaccharide conjugated with protein rifampin can be used to prevent transmission under outbreaks DUCREYI: CHANCROID, very painful. got to differentiate from syphilis!, (syphilis is not painful). chancres will aid the transmission of HIV treatment: azi, ceftriaxone, ciprofloxacin bla bla |
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quellung reaction?
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The Quellung reaction is a biochemical reaction in which antibodies bind to the bacterial capsule of Streptococcus pneumoniae, Klebsiella pneumoniae, Neisseria meningitidis, Haemophilus influenzae [1], Salmonella, and group B Strep (mnemonic: Some Killers Have Nice Shiny Bodies). The antibody reaction allows these species to be visualized under a microscope. If the reaction is positive, the capsule becomes opaque and appears to enlarge.
Quellung is the German word for "swelling" and describes the microscopic appearance of pneumococcal or other bacterial capsules after their polysaccharide antigen has combined with a specific antibody. The antibody usually comes from a bit of serum taken from an immunized laboratory animal. As a result of this combination, and precipitation of the large, complex molecule formed, the capsule appears to swell, because of increased surface tension, and its outlines become clearly demarcated. |
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gardnerella
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menstruation, ATBs, stress - pH disturbance - vaginosis. typically mixed infections (e.g. lactobacillus, mobiluncus, abcterioides, peptostreptococcus) i think lactobacillus reduction is a key here, since they are normal flora, and they maintain low pH)
BV: thin gray discharge fluid and foul odor. we have to distinguish from trichomonas (same smell but different discharge) ph > 4.5 clue cells (glazed with bacteria) treatment: clinda, metro |
