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112 Cards in this Set
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- Back
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What is unique about Bacteroides fragilis? |
One of the few Gram -- that does not contain lipid A; therefore, LPS is not toxic. 99% of the GI flora belongs to the family of Bacteroides, and they make vitamin K.
The mouth (rarely) and vagina are as part of the normal flora. |
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Diagnosis of UTI is based on?
What is leukocyte esterase used for? |
Presence of host inflammatory cells in urine--pyuria.
Surrogate marker for the presence of WBCs using urine dipstick test. |
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Bacteroides fragilis is only problematic when?
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A laceration of the intestine (car wreck, surgery) causing peritonitis and pelvic abscess (resulting in shock, minus DIC since B. fragilis lacks the gram -- endotoxin, lipid A)
Abscesses may arise in PTs with septic abortion, PID, or with an IUD. |
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Other than UTI (cystitis and pyelonephritis) and enteritis, what else can E. coli cause?
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pneumonia, neonatal meningitis, septic shock, and hemolytic uremic syndrome.
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What is required for Bacteroides fragilis to cause an abscess? What is a further complication?
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Synergistic presence of a facultative anaerobe, such as Klebsiella pneumoniae in the peritoneal fluid. It uses up the oxygen, thereby lowering the redox potential for B. fragilis to grow.
Abscess serves as reservoir for organisms, which can cause shock but not DIC (B. fragilis lacks Gram negative endotoxin) |
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E. coli are?
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Facultatively anaerobic, all ferment glucose, are oxidase negative. They are either nonmotile or motile by flagella.
They appear as large, gray colonies on blood agar. |
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How do you treat B. fragilis?
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drain abscess + repair lesions + antibiotics (e.g., metronidazole, clindamycin)
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Which bacteria are lactose fermenter?
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Escherichia coli and Klebsiella pneumoniae
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Why is B. fragilis suited to cause an abscess? How does intercellular adhesion molecule 1 (ICAM-1) play a role?
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Its capsule promotes pyogenic inflammation and is resistant to phagocytosis.
TNF up-regulates the expression of ICAM-1. When PMNs are unable to eradicate the unwanted bacteria, they adhere to ICAM-1 expressing cells and an abscess develops, thus "walling off" the infection. |
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What is the main contributor to UTIs in men over the age of 50?
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Prostatic hyperplasia that causes compression of the urethra with partial obstruction of the urinary flow.
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Enterics are what kind of bacteria?
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Gram-negative and part of the normal intestinal flora
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E. coli are equipped with what that allows them to colonize the urinary tract and stimulate local inflammatory responses?
What allows E. coli to travel up against the urinary flow? |
P-fimbriae and type-1 fimbriae.
Flagella, the H-antigen. |
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Hospitalized PTs and alcoholics (debilitated PTs) are prone to?
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Kebsiella pneumoniae--impaired host defenses in alcoholics.
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What of E. coli resists phagocytosis and killing?
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The capsular polysaccharide (K antigen).
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Which bacteria are not lactose fermenter?
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Salmonella, Shigella, Pseudomonas aeruginosa, Proteus mirabilis, Yersinia enterolitica (and Yersinia petis, which isn't an enteric)
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What does urease from Proteus promote?
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Formation of struvite kidney stones by increasing the alkalinity of urine.
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What is the characteristic of pneumonia caused by K. pneumoniae?
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Violent, with 50% of PTs with bloody sputum, cavities in the lungs, with a high mortality rate despite antibiotic therapy.
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What is aerobactin?
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A siderophore that increases iron uptake by bacteria.
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Ability to produce H2S does?
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hydrolyze urea, liquefy gelatin, and decarboxylate specific a.a.
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IL-1 and TNF mounts?
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High fever, 39d > C, shaking chills, localized flank or low back pain.
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What does the sputum from a PT with K. pneumoniae may look like?
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Red currant jelly.
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What does white cell casts represent urine?
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Likely represents pyelonephritis (complicated UTI)
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EMB (eosine methylene blue) inhibits gram-positve bacteria, and colonies lactose fermenters to become deep purple to black. What color does E. coli turn?
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Green sheen
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Pregnant women are at a high risk of colonization with the K1 antigen (encapsulated strain of E. coli. Complications?
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E. coli accounts up to 30% of cases of neonatal meningitis.
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What else can K. pneumoniae cause?
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Nosocomial UTI. They are also among the most drug-resistant microbes causing nosocomial infections.
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MacConkey agar, the bile salts inhibit gram-positive, and lactose fermenters develop what color?
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Pink-purple coloration.
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How do you treat Klebsiella pneumoniae?
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3rd generation cephalosporin with aminoglycosides.
Extended-spectrum penicillins (e.g., piperacillin and ticarcillin), aminoglycosides, quinolones. |
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How do you diagnosis K. pneumoniae?
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Gram negative rode, capsule, mucoid appearing colonies, and lactose fermenting, urease-positive, and indole-negative. They are nonmotile and nonflagellated.
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Enterics have three major surface antigens (slightly different between bugs)
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O antigen (LPS of gram-neg.), K antigen (Kapsule that covers the O antigen), and H antigen (antigenic determinant that makes up the subunits of the bacterial flagella).
Note: the lipid A component of LPS causes septic shock |
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What effect does the capsular polysaccharide on Klebsiella pneumoniae provide?
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Inhibition of formation of membrane attack complex (C5b - C9).
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What happens in the lungs from Klebsiella pneumoniae?
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Inflammatory infiltrates from bronchioles into adjacent alveoli cause bronchopneumonia (patchy opacity on x-ray). Lung abscess.
Cavity formation and blood-tinged sputum due to endothelium damage. |
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What does Pseudomonas aeruginosa usually inhabit?
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In the hospital, found in aqueous solutions, disinfectants, ointments, dialysis fluids, etc. Transmission: ingestion or water or ice; aerosolization, or ingestion of Pseudomonas-laden foods (eg., tomatoes).
Soil, water, large intestine. Many environmental areas. They might be found in a biofilm, attached to a surface. |
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What produces diarrhea with invasion of the intestinal epithelial cells resulting in systemic immune response with leukocytes in the stool, blood in the stool (from cell death), and fever?
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Shigella dysenteriae, Salmonella enteritidis, and Enteroinvasive Escherichia coli (EIEC)
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Cystic fibrosis PTs, hospitalized PTs, IV drug users, diabetics, and those using a hot tub, may present with Pseudomonas aeruginosa as?
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CF (pneumonia); hospitalized PTs (UTIs); IV drug users (endocarditis, osteomyelitis); diabetics (osteomyelitis, malignant external otitis); and hot tub users (folliculitis). P. aeruginosa can also occur with burn wound infection, cause septicemia, and corneal infections.
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What produces diarrhea with no cell invasion? This includes without a systemic symptoms, such as fever.
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Enterotoxigenic Escherichia coli (ETEC) and Vibrio cholera
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Who does Pseudomonas aeruginosa usually infect?
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Sick, immunocompromised hospitalized PTs. Healthy people do not get infected with this bacteria.
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Why is P. aeruginosa a problem?
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It is resistant to almost every antibiotic.
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What produces diarrhea with invasion of the lymph nodes and blood stream, with RBC and WBC in the stool, with fever and headache.
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Yersinia enterocolitica and Campylobacter jejuni both cause bloody diarrhea. However, Salmonella typhi does not cause blood diarrhea per-say (diarrhea is either watery, or contains less commonly contains mucous and trace blood.
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How can you diagnose P. aeruginosa?
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Gram -- rod, with blue/green colonies (pyocyanin pigment--blue pus) with fruity odor. They are motile with single polar flagellum.
They are strictly aerobic, and also nonfermentative and oxidase positive. |
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What are the toxins associated with P aeruginosa?
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Exotoxin A: causes ADP-ribosylation of EF-2, resulting in inhibition of protein synthesis and ultimate cell death.
Phospholipase C: hydrolyze phospholipids of eukaryotic mm. Elastase: hydrolyzes elastin and collagen Endotoxin |
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How do you treat P. aeruginosa?
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Extended spectrum penicillin (e.g., piperacillin/ticarcillin) + aminoglycoside (e.g., gentamicin/tobramycin).
Cephalosporin (ceftazidime) or carbapenem (e.g., imipenem) have been used as well. Fluoroquinolones have antipseudomonas activity. |
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What does the alginate capsule provide for Pseudomonas aeruginosa?
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It develops into a biofilm, which protects the colonizing bacteria from phagocytosis, ciliary action, ABs, and complement.
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What is the major cause of morbidity in cystic fibrosis?
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The LPS from Pseudomonas aeruginosa stimulates neutrophilic responses that interferes with pulmonary function.
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What can Pseudomonas aeruginosa cause?
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PSEUDOmonas
With wound and burn infection Pneumonia (in CF), Sepsis (black lesion on skin), External otitis (swimmer's ear), UTI, Drug use and Diabetic Osteomyelitis, and hot tube folliculitis. Malignant otitis externa in diabetics. |
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What is the appearance of Pseudomonas aeruginosa from respiratory secretions from cystic fibrosis PTs?
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Mucoid appearance, due to its production of alginate capsule.
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What are the toxins of E. coli? And what are they similar to?
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Heat labile toxin (LT; osmotic loss of water; similar to cholera toxin); heat stabile toxin (ST; water remains in stool; similar to Y. enterocolitica toxin); and Shiga-like toxin (SLT; blocks protein synthesis, similar to Shigella toxin)
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Toxins LT and ST look similar to?
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Cholera, stool looks like rice water.
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Enterotoxigenic Escherichia coli (ETEC) causes what by which toxins?
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Traveler's diarrhea, through both LT and ST toxins.
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Enterohemorrhagic Escherichia coli (EHEC) causes what by which toxins?
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Hemorrhagic colitis via the Shiga-like toxin, which may spread to the blood stream to produce hemolytic uremic syndrome. Accompanied by severe abdominal cramps. Does not invade!
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Enteroinvasive Escherichia coli (EIEC) causes what by which toxins?
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Dysentery with WBC and RBC in stool, via Shiga-like toxin,
Does invade! |
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E. coli is the most common cause of?
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UTI (usually in women and hospitalized PTs with catheters), and Gram -- spesis.
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EHEC (0157:H7) results in and from what?
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Hemolytic uremic syndrome caused from poorly cooked hamburger meat.
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How mobile is Proteus mirabilis?
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Very motile. When smeared on a plate, the colonies will not be round, but rather confluence as a result of its excessive motility.
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What can Proteus mirabilis perform? What is the result?
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Split urea from urease. This increases the pH, precipitating ammonium magnesium phosphate that leads to struvite calculi formation. This will back log urine causing damage to kidneys and persistent UTI.
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Proteus vulgaris antigens can diagnosis what and how?
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Can diagnosis Rickettsia, since the antigens cross-react with the PT's serum ABs against Rickettsia
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P. mirabilis can cause?
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Struvite stones, UTI, and nosocmial infections.
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How do you treat P. mirabilis?
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TMP-SMX or ampicillin
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How do you treat E. coli?
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Rehydration for diarrhea; TMP-SMX, penicillin for UTI; 3rd generation cephalosporin for meningitis and sepsis
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Is Shigella motile?
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No
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Who does Shigella usually infected?
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Usually strikes preschool age children, and populations in nursing homes.
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How is Shigella spread?
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Fecal-to-oral route.
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Shigella part of the normal intestinal flora?
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No
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Shigella is similar to?
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Enteroinvasive Escherichia coli (EIEC) and enterohemorrhagic E. coli (EHEC)
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What are characteristics of Shigella dysenteriae?
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WBC respond, causes mucosal ulcers and bleeding that prevents intestine to absorb fluid. There are flecks of bright red blood and pus in stool.
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What is the mechanism of the Shiga toxin?
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inactivates 60S ribosome, causing further damage to mucosa.
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How do you treat S. dysenteriae?
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Oral rehydration for moderate cases, and fluoroquinolones for severe cases.
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How can you diagnosis S. dysenteriae?
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Non-motile (vs. motile Salmonella), doesn't produce H2S (vs. Salmonella), and doesn't ferment lactose (vs. E.coli) , and gram negative rod in stool
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How do you diagnosis P. mirabilis?
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Gram --, "swarming growth", and urease +, and alkaline urine
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How do you diagnosis E. coli?
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Gram -- rod, ferments lactose (green metallic sheen on EMB, light purple on MacConkey), and serology for O and H antigen
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How do you diagnosis Salmonella?
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Gram -- rod in blood (typi) or stool/urine (enteritidis); motile by flagella (vs. non-motile Shigella); H2S producing (vs. Shigella); and does not ferment lactose (vs. E. coli)
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What antigen in Salmonella is similar to the K antigen, and what is special about it?
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Vi angiten, allows survival in phagocytes in Peyer's patches.
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How is Salmonella similar to Shigella?
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Both are never considered normal flora of GI
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Salmonella enteritidis is carried only by? What is the clinical presentation?
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Animals (chickens, uncooked eggs, turtles), in their GI tract and infects humans when food is contaminated by their feces. Gastroenteritis
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Salmonella typhi survives only in? What are the clinical presentations?
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Humans. Typhoid fever and osteomyelitis in sickle cell PTs
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Salmonella typhi is considered what type of parasite?
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Facultative intracellular parasite
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What is the clinical presentation of typhoid fever?
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Fever, headache, abdominal pain (mistaken for appendicitis), diarrhea, hypertrophy of spleen, rose spots on abdomen.
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In asymptomatic carriers of typhoid fever, where is S. typhi stored in? And what may be necessary?
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Gallbladder, and its removal.
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What is the treatment of Typhoid fever?
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Ceftriaxone for resistant strains; ciprofloxacin and ampicillin for carriers.
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How does the body remove Samonella?
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Salmonella is encapsulated and our body clears encaspulated bacteria by opsonizing them with AB, which the macrophages and neutrophils in the spleen remove. Therefore, those without a spleen will have difficulty removing encapsulated bacteria and are more prone to becoming infected by them.
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Salmonella enteritidis causes?
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Gastroenteritis, causing inflammation, fever, and diarrhea
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How do you treat Salmonella enteritidis?
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Fluid and electrolytes
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How do you diagnosis Yersinia enterocolitica?
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Stool culture of gram -- rod that is motile; with colonoscopy for ulcer
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Is Yersinia enterocolitica an enteric bacterium? How is it spread.
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No, but it does cause diarrhea. It is transmitted in raw milk or fecal-oral route juxtaposed to Y. pestis via the bite of a flea.
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What are the clinical presentation of Yersinia enterocolitica?
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Enterocolitis (bloody diarrhea, with ulcerations of mucosal mm) and mesenteric adenitis
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How do you treat Yersinia enterocolitica?
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Self-limiting; gentamicin or chloramphenicol for septicemia
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Presentation of Y. enterocolitica in three age groups: less than 5 y.o., greater than 5 y.o., and adults?
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Less than 5 (blood diarrhea); greater than 5 (blood diarrhea and appendicitis-like pain); and adults (bloody diarrhea + arthritis, the most common complication).
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How do you diagnosis Vibrio cholerae?
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Comma-shaped Gram -- rod, with single flagella in stool. Flat yellow colonies on TCBS agar
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How is V. cholerae transmitted?
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Fecal contaminated water, food, shellfish.
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V. cholerae is similar to?
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ETEC, but more severe, and there is no epithelial cell invasion.
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The choleragen toxin from V. cholerae makes the stool appear?
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As rice water.
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How do PTs die from V. cholerae?
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Hypovolemic shock
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PTs with V. cholerae may appear?
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Sunken eyes, poor skin turgor, diminished pulses.
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How do you treat V. cholerae?
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Oral/IV rehydration (glucose + Na for Na-glucose co-transport), tetracycline or doxycycline to shorten illness.
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Vibrio parahaemolyticus
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Presents similar to V. cholerae, and transmitted from uncooked seafood (sushi). Leading cause of diarrhea in Japan.
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How is Campylobacter jejuni diagnosed?
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Gram -- rod, S shaped- grows best at 42d C and microaerophilic
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How is Campylobacter jejuni transmitted?
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Fecal-oral route via animals or unpasteurized milk.
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How does C. jejuni present?
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Fever, headache, abdominal pain, followed by water, ill-smelling diarrhea preceding bloody stools.
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What is the toxin of C. jejuni similar to?
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LT, cholera-like enterotoxin.
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How do you treat C. jejuni?
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Erythromycin, ciprofloxacin.
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What is the most common cause of duodenal ulcers and chronic gastritis? Also, it is the second leading cause of gastric ulcers. (Aspirin is second for duodenal ulcers and chronic gastritis, but is number one for gastric ulcers).
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Helicobacter pylori
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H. pylori colonizes?
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Gastric antrum, but doesn't invade.
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How do you test for H. pylori
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Urea breath test (labeled urea ingested, and labeled CO2 is exhaled if bacteria is present); biopsy of Gram --rods with "S" or spiral shape.
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If the gastritis is limited to the antrum from H. pylori, what results?
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Hypersecretion of acid with risk of duodenal ulcers.
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If the gastritis extends throughout stomach from H. pylori?
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Hyposecretion of acid with risk of gastric ulcers and gastric carcinoma.
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How do you treat H. pylori?
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Proton pump inhibitor + amoxicillin + clarithromycin; OR PPI + BMT (bismuth therapy, metronidazole, tetracycline)
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What is the purpose of Urease for H. pylori?
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To protect from gastric acid.
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Chronic H. pylori gastritis is associated with?
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Gastric adenocarcinoma and MALT lymphoma.
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H. pylori secretes what, and what does it cause?
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Vacuolating cytotoxin (VacA) causes cell injury characterized by vacuolization, and its expression is controlled by another gene encoding cytotoxin-associated antigen (CagA)
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What is the C^13 urea breath test used for? And what does urease provide for H. pylori
What is the morphology of H. pylori? |
PT drinks C^13 urea, and the urease produced from H. pylori splits off labeled C^13O2 (radioactive carbon dioxide) which is expired from the lungs to detect presence of H. pylori.
Urease creates a cloud of ammonia as a buffering function from stomach acid. Gram --rods with "S" or spiral shape. |
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What stains can be used for H. pylori?
What selective media with nutrient supplements for growth? |
Giemsa or Warthin-Starry stains or Silver
Skirrow agar, with microaerophilic conditions at 37d C. |
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How does H. pylori avoiding elimination?
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Bacterial flagella and mucinase allows H. pylori to pass through the mucus layer (but does not invade cells!)
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H. pylori morphology?
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Gram-negative curve rod (S-shaped)
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