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257 Cards in this Set
- Front
- Back
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Where do the ingested food encounter immune exposure in the gut?
A. Stomach B. Duodemum C. Jejunum D. Ileum E. Colon |
D.
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Give one flora of the stomach.
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Helicobacter pylori
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Most cases of type B gastritis and peptic ulcers are caused by____.
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Helicobacter pylori
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List some normal flora of the small intestine.
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1. Streptococci
2. Lactobacilli 3. yeasts (candida albican) |
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What are the main bacteria of the colon?
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1. Bacteroides
2. Bifidobacterium 3. Eubacterium 4. Coliforms 5. Streptococcus 6. Lactobacillus 7. Clostridium |
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Where is vitamin K produced in the GI tract?
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large intestine.
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Flora of the small intestine are mainly found in ____.
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the terminal ileum.
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What are the four pathogenic mechanisms in the GI tract?
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1. ingestion of preformed toxins.
2. production of enterotoxin in the GI tract lumen. 3. mucosal invasion with cellular destruction. 4. adherence to mucosal surface. |
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Which of the following mechanism is associated with common diarrhea:
A. ingestion of preformed toxins. B. production of enterotoxin in the GI tract lumen. C. mucosal invasion with cellular destruction. D. adherence to mucosal surface. |
B.
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1. What is this symptom called?
Small volumes, blood and pus, cramping and abdominal pain and tenesmus. 2. This symptom is due to ___. |
1. Dysentery
2. invasion of intestinal wall |
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Describe dysentery.
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Small volume of stool, blood and pus, cramping, abdominal pain, and tenesmus. (invasion of intestinal wall)
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1. What is this symptom called?
Nonpainful, profuse water diarrhea. 2. This symptom is due to __. |
1. Cholera
2. enterotoxin |
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What is a sign of noninvasive diarrhea in infants?
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vomiting, fussiness
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What is a sign of noninvasive diarrhea in young children and adults?
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vomiting, nausea, and cramps
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What is the duration of acute diarrhea?
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<14 days
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What is the duraton of chronic diarrhea?
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>30 days.
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What is the duration of persistent diarrhea? What is the main causative organism of this kind of diarrhea?
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1. between 14 to 30 days.
2. parasites (Giardia) |
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What is a sign of invasive diarrhea in infants?
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fever, bloody stools.
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What is a sign of invasive diarrhea in adults?
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fever, bloody stools, tenesmus.
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T/F: Adults tend to have much larger volume than infants and kids in diarrhea.
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T.
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How does normal flora defend us against diarrhea?
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1. competition for resources.
2. produce inhibitory compounds. |
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List some defense of the gut against GI infections.
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1. Acidic pH of the stomach
2. peristalsis 3. normal flora: competition for resourcea, and produce inhobotory compounds. |
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Which of the following is the major defense against GI infections:
A. Stomach B. Intestine C. Normal flora of gut |
A. Kills 90% of the bacteria in the ingested food.
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How do some bacteria escape stomach acidity?
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Protein in the food help organisms avoid low acid (ex egg salad, perfringens).
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How do some pathogens fight against our body's defense?
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1. Acid resistance.
2. specific adherence mechanism and motility. 3. enterotoxin production. |
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What are some pathogenicity of noninvasive diarrhea?
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1. enterotoxin production
2. adherence, translocation of bacteria 3. destruction of villus cells by virus 4. adherence by parasites. |
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Invasive diarrhea are caused by _____.
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Production of cytotoxins and direct invasion of large intestine.
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How do some bacteria cause noninvasive diarrhea?
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1. produce enterotoxin.
2. adherence and translocation |
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How do some virus cause noninvasive diarrhea?
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Destruction of villus cells
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How do some parasites cause noninvasive diarrhea?
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Adherence to epithelium
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This kind of diarrhea could be stopped when no food is ingested.
1. What kind of diarrhea is this? 2. What are some possible causative organisms? |
1. osmotic
2. Giardia, crytosporidium, post viral |
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What kind of diarrhea will cause continuing watery stool even when food is no longer ingested?
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Secretory diarrhea. (ex. enterotoxin producing cholera)
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How does GI pathogens transmit?
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1. fecal oral (majority)
2. aerosol of vomit (person to person). 3. contaiminated water (outbreak). 4. food borne (outbreak). |
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Which of the following is resistant to chlorination?
A. Helicobacter pylori B. Vibrio cholerae C. Giardia D. Cryptosporidium |
D.
*C is moderately resistant |
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What is the #1 waterborne-disease associated with drinking water?
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Legionella
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Which subgroup of E.coli infect duodenum? Which subgroup of E.coli infect colon?
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1. Enterotoxigenic and Enteropathogenic
2. Enterohemorrhagic and Enteroinvasive. |
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Which organism infect the stomach?
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Helicobacter pylori
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What are some organisms that infect the proximal small intestine?
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1. Vibrio cholerae
2. E.coli (enterotoxigenic and enteropathogenic) 3. Giardia lamblia 4. Cryptosporidiun parvum 5. virus (rotavirus, caliciviruses, adenovirus) |
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What are some organisms that infect the distal small intestine?
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1. Salmonella spp.
2. Campylobacter jejuni 3. Yersinia spp. |
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What are some organisms that infect the colon?
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1. Shigella spp
2. E.coli(enterohemorrhagic and enteroinvasive) 3. entammoeba histolytica 4. clostridium difficile and perforingens 5. Bacillus cereus |
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Vibrio cholerae cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Enterotoxigenic E.coli cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Enteropathogenic E.coli cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Giardia lamblia cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Cryptosporidium parvum cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Rotavirus cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Calicivirus cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Adenovirus cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
A.
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Salmonella cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
B.
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Campylobacter jejuni cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
B.
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Yersinia spp cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
B.
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Shigella spp cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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Enterohemorrhagic E.coli cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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Enterinvasive E.coli cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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Clostrisium difficile cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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Clostridium perforingen cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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Entameoba histolytica cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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Bacillus cereus cause infection in ____.
A. proximal small intestine B. distal small intestine C. colon |
C.
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What are the two mechanisms that cause systemic manifestations(eg paralysis) of GI infection?
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1. absorption of toxins ingested with the pathogens.
2. pathogens localize, multiply, invade, and disseminate. (Typhoid fever by Salmonella) |
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What are the three possible route to cause GI disease after organism has localized and multilplied? Give an example for each route.
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1. invade and disseminate to cause systemic manifestations. Ex. salmonella enterica that cause typhoid fever.
2. invade locally and cause dysentery. Ex. campylobacter jejuni 3. produce toxins and cause diarrhea. Ex. Cholera. |
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What are some diagnostic techniques for GI infections?
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1. fecal exam: fecal lactoferrin, microscopic exam for fecal leukocytes, parasite exam(wet-mount, iodine stain, trichome, acid-fast stain), antigen detection or DNA probe.
2. Culture: gold standard. 3. Serology: not useful for acute infections. 4. PCR |
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What are some examples of fecal exams?
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1. fecal lactoferrin (leukocyte level)
2. microscopic exam for fecal leukocyte 3. ova and parasite exam: wet-mount, iodine stain, trichome stain, acid-fast stain 4. antigen detection/DNA probe |
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List some routinely cultured organisms from feces.
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SSCYE
1. Salmonella 2. Shigella 3. Campylobacter 4. Yersinia 5. E.coli O157:H7 |
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What is the treatment for gastroenteritis?
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Usually self-limiting
1. oral rehydration therapy(ORT), Bismus sulfate to reduce enterotoxin action, antimotility agents. 2. Antibiotics indicated for very young, very old, immunocompromised. It shortens duration and lower communicability. |
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Describe helicobacter pylori:
1. gram stain morphology 2. mucosal penetration? 3. site of localization |
1. GN, small, curved, with sheathed flagellae.
2. No 3. stomach |
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How does helicobacter pylori survive the acidic environment of the stomache?
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Produce potent urease that result in increasing ammonia level which in turn raises the pH.
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Stomach has a thick layer of mucus to protect the epithelium lining. How does helicobacter pylori colonize in this thick layer?
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1. produce mucus degrading protease.
2. flagella |
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T/F: Type A gastritis is associated with cancer.
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T.
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What factors are necessary for helicobacter pylori to colonize?
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1. urease
2. mucus degrading protease |
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What does colonization of helicobacter pylori cause?
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inflammation (leukocyte infiltrate)which lead to chronic active gastritis.
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What are some enzymes produced by helicobacter pylori?
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Many!
1. urease 2. mucinase 3. superoxide dimutase 4. catalse 5. hsp 6. cytotoxin |
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What is the flagella in helicobacter pylori different from that of campylobacter spp?
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Helicobacter pylori: several sheathed flagella.
Campylobacter spp: single unsheathed flagella. |
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T/F: Helicobacter pylori colonization may have protective effect that diminish the risk of esophageal reflux and its consequences.
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T.
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What are the virulence factors of helicobacter pylori?
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1. cagA: enter epithelial cell and interact with human proteins. Cause more severe inflammation, higher risk for ulcers and cancer. Part of type IV secretion system (pathogenicity islands).
2. vacA: present in every strain. Compromise WBC, diminish immune response. Vaculation in cultured cells. 3. urease: raise pH |
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What are some risk factors for stomach cancer?
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smoking and certain diet.
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Which stain is associated with highest risk of stomach cancer?
A. stains contain cagA B. strains contain vacA C. strains contain both cagA and vacA |
C.
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A patient complains about gnawing, dull, aching of the stomach, nausea and loss of appetite. He mentioned this kinds of symptom comes and goes for quite a while.
1. These symptoms are indicative of what kind of disease? be specific 2. What is the causative agent? |
1. ulceration of the stomach
2. helicobacter pylori |
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A patient complains about heartburn, stomach pain and a burning feeling at the back of his throat. This usually happens around 4 hours after meals. He also noticed gradual weight gain.
1. What kind of disease is this? be specific 2. What is the causative agent? |
1. ulceration of the duodenum.
2. helicobacter pylori |
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An young adult present with vomiting, burping, and fever. He mentioned that this has been happening for more than a week.
1. What does he have? 2. acute or chronic? |
1. helicobacter pylori
2. acute |
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You decide to do an endoscopy to confirm the suspision of helicobacter pylori. What are you actually looking for?
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Inflammation, ulcers.
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What are some diagnostic tests for helicobacter pylori?
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1. endoscopy with rapid urease determination from biopsy specimen.
2. urea breathe test 3. stool antigen determination: definitive test 4. PCR |
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How to treat for helicobacter pylori infection?
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Combination therapy of two antibiotics, colloidal bismuth compounds, gastric acid blockers(H2 antagonists) for 2-3 wks.
May develop antibiotic resistence. Disease may return when therapy discontinued. |
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How to prevent exposure to H. pylori and enteric campylobacters?
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Proper preparation of food and potable water supplies.
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What is the observation over the years about H. pylori suggesting not to treat asympomatic patients?
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With controlled H. pylori infection, incidents of acid reflux, esophageal cancer rise.
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Describe vibrio cholerae:
1. gram stain morphology 2. oxidase + or - 3. site of localization 4. fementative or not |
1. GN, comma shaped, single flagella(nonsheathed).
2. oxidase + 3. jejunum 4. fementative |
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Which serovars, biotypes, and serotypes of vibrio cholera are epidemic associated?
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Serovars O1 and O139
biotypes El Tor serotypes Ianbam Ogawa, Hikpjima. |
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T/F: There are 20 times more symptomatic cholera patients than asymptomatic patients.
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F. More asymptomatic patients.
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Is virbrio cholerae invasive?
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No. It's enterotoxin based noninvasive.
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Somatic antigen is called ___.
Flagellar antigen is called ___. Capsular antigen is called ___. |
O antigen
H antigen Vi antigen |
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Describe the pathogenesis of vibrio cholerae.
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1. Free living organism in fresh water.
2. Attach to shell fish, may switch to dormant state under unfavorable conditions. 3. Ingestion of contaminated food (10^9 load). 4. attach to jejunum via fimbrae and colonize. 5. produce cholera toxin |
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What season does someone likely to get cholera?
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hot seasons.
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Which vibrio cholerae caused the 7th pandemic in Indonesia?
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biotype El Tor
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Which vibrio cholerae caused the 8th pandemic in Bangladash and India?
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Serovar O139
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What are the pandemic area of cholera?
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Africa and south Asia.
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For a healthy person, it takes 10^9 organisms to cause disease from H. pylori. But for someone who is hypochlorhydric (antacids), how many organism are required to cause disease?
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100
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What is the mechanism of action of cholera toxin?
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1. 5B subunits bind to GM2 ganglioside receptor of crypt enterocyte.
2. Subunit A convert ADP to cAMP. 3. cAMP stimulation of Cl that lead to osmotic loss of water and block entry of sodium into enterocytes. |
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A guy presents with vomiting, abdominal distention, and profuse diarrhea. He described his stool as "rice-water stools".
1. what does he have? 2. How to treat it? 3. What happens if left untreated? |
1. cholera: 1-3 days incubation.
2. Rehydration in 2 phases: IV first for less than 4 hours, then oral rehydration (water+sugar+salt)therapy. Tetracyclin or doxycyclin might be helpful to shorten the duration and prevent spread. 3. will die in four hours. |
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An infant presents with vomiting, diarrhea. You noticed "tenting" of the skin on the child's abdomen when you pinched the skin.
1. What does the sign tell you? 2. What does the kid have? |
1. The kid has lost 5% of body water(dehydration).
2. cholera |
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How to diagnose cholera?
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1. clinical signs: profuse diarrhea, rice-water stool, skin "tenting".
2. culture with alkaline media(TCBS): will change from green to yellow. |
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Culture with TCBS came back and the color turns from green to yellow.
1. What is this test for? 2. What does the result tell you? |
1. cholera: need alkaline condition to grow.
2. it is positive for cholera. |
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What are some preventative measures of cholera?
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1. sanitation
2. whole cell killed vaccine: not recommended by WHO. |
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Describe ETEC:
1. gram stain morphology 2. fermentive or not 3. oxidase + or - 4. Growth on macConkey agar? 5. localization |
1. facultative GNR
2. fermentive 3. oxidase negative 4. yes 5. jejunum 1-4 are characteristics of enterobacteriacea |
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Describe the pathogenesis of ETEC.
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1. fimbrae attach to jejunum epithelium.
2. produce 2 toxins: heat labile LT toxin increase intracellular cAMP and heat stable ST toxin increases intracellular cGMP. 3. toxins cause water loss. |
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ETEC cause enterotoxin based noninvasive diarrhea. What toxins are involved?
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1. LT toxin: heat labile, increases cAMP.
2. ST toxinL heat stable, increases cGMP. |
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An infant previously living in Mexico presents with watery diarrhea less profuse than cholera.
1. What is the causative agent? 2. How do you treat it? |
1. ETEC
2. supportive fluids and electrolytes. Antibiotics may shorten the duration. |
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A young man came back from India two days ago and presents with watery diarrhea less profuse than cholera.
1. What's his symptom called? 2. What is the causative organism? |
1. traveler's diarrhea
2. ETEC |
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Which one of the following don't have fimbrae?
A. vibrio cholera B. ETEC C. EPEC D. EHEC |
C.
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Describe the pathogenesis of EPEC.
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1. adheres tightly to jejunum epithelium.
2. destroys microvilli. 3. produces cytotoxin. |
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How to diagnose ETEC?
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1. clinical signs: 1-3 days of incubation, watery disrrhea less profuse.
2. ELISA for toxin. |
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A 5 month old kid presents with watery diarrhea less severe than cholera.
1. What does he have? 2. How do you treat it? |
1. EPEC
2. Supportive fluids and electrolytes. |
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What is the unique host of EPEC?
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Infants who have not aquired normal intestinal flora and they don't have specific immunity.
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Premature babies are in danger of getting___.
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EPEC. They have poorly developed homeostasis and limited water and electrolyte reserves.
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Describe vibrio parahemolyticus:
1. gram stain morphology 2. aerobe or anaerobe? 3. invasive or not? |
1. GNR
2. facultative anaerobe 3. locally invasive |
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A guy came into the hospital with mild frank dysentery-like syndrome. He mentioned he had oysters the day before.
1. What does he have? 2. How to treat it? 3. what test is associated with this organism? |
1. Vibrio parahemolyticus.
2. supportive (self-limiting within3-4 days). 3. Kanagawa test: detect thermostable direct hemolysin. |
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What does halophilic mean?
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salt requiring (vibrio parahemolytica).
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How to diagnose vibrio parahemplytica?
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1. Clinical history: contaiminated seafood.
2. few leukocyte in stool 3. fecal culture using halophilic TCBS (see green colonies) or CHROMagar. |
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What type of diarrhea does giardia lamblia cause?
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osmotic
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Describe pathogenesis of giardia lamblia.
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1. ingestion of contaminated water.
2. cysts ingested and excyst in duodenum and jejunum. 3. trophozoite adhere and multiply by binary fission 4. impaired intestinal absorption and result in inflammation. |
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Describe giardia lamblia:
1. life cycle stages 2. morphology of organism |
1. infectious environmentally resistent cysts(4 nuclei) in water and trophozoite in human body.
2. 4 pairs of flagella |
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A kid presents with bloating, flatulence, nausea, weight loss. These may be the initial signs of _____. What kind of stools are produced at this stage?
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Giardia lamblia
watery initially |
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Symptoms such as diffuse abdominal pain and the passage of greasy stools that float. These are indicative of what disease? And what type of people may develop this?
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chronic giardia
immunocompromised people |
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How long is the incubation period for giardia?
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1-2 wks
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What is diagnostic of giardia lamblia?
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1. fresh fecal examination of cysts or trophozoitess:3 times in 10 days.
2. ELISA for fecal antigens and flourescent antibody test 3. string test |
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Why do you need to perform fecal exam 3 times in 10 days for giardia lamblia?
What other organism also require this type of test? |
1. Intermittent shedding. One time may not catch it.
2. Cryptosporidium and entamoeba histolytica. |
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How to treat giardia lamblia?
What are some preventative measures? |
1. metronidazole, tinidazole, nitazoxanide.
2. improved sanitation, chlorination. |
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These organisms has both sexual and asexual life cycles, and are resistant to chlorine. How to tell them apart?
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cryptosporidium parvum and cyclospora cayetanensis.
Cyclospora cayetanensis is 2x bigger and autofluorescent . *Entamoeba histolytica also has both sexual and asexual life cycles. |
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Life cycle of cryptosporidium parvum.
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1. oocysts ingested
2. sporozoites attach to duodenum/jejunum epithelium at the base of the microvilli. 3. microvilli facillitate the formation of trophozoite. 4. asexual reproduction of 8 merozoites. 5. sexual reproduction of microgametocytes and macrogametocytes that can fuse to produce oocysts. 6. cell wall excretion prior to pass out in feces. 7. sporulation immediately follows. |
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Pathogenesis of cryptosporidium parvum.
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1. sporozoites attach to the base of microvilli
2. loss of microvilli and inflammation response leads to secretory and malabsorptive diarrhea. 3. Asexual reproduction: release 8 merozoite. 4. Sexual reproduction: release microgametocyte and macrogametocyte. They fuse in the lumen to produce oocyst. Pass through feces and sporulate. |
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A patients who had a bone marrow transplant complains about watery diarrhea for 3 wks.
1. What do you suspect he has? 2. How do you make the definitive diagnosis? 3. How to treat him? |
1. cryptosporidium parvum
2. identification of oocysts in feces using concentration techniques and specialized fluorescent acid-fast stains.(monolonal fluorescent antibody test increases sensitivity) 3. paromomycin and spiramycin in immunocompromised patients like this one. |
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T/F: Giardia lamblia is susceptible to chlorination whereas cryptosporidium parvum is resistant.
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T.
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What is the incubation period for cyclospora cayetanensis?
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5 days.
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A patient has had chronic intermittent diarrhea for about 3 wks. There is no fever or vomiting and no blood in the stool. The patient travels to Latin America and Eastern Europe frequently, most recently 2wks ago. What does he have?
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parasites: Giardia (incubation 1-2 wks)or cryptosporidium(incubation unknown).
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This patient has just returned today from Latin America following a 2day business trip where he reports eating several meals of fish that he bought from street venders around his hotel. He feels very ill with profuse, watery diarrhea and vomiting. What does he have?
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vibrio cholera
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Describe rotavirus:
1. family 2. genome 3. enveloped or not 4. localization of disease |
1. reovirus
2. 11 segments dsRNA coding for VP(viral proteins). 3. nonenveloped 4. proximal intestine |
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T/F: Enveloped viruses survive better than nonenveloped viruses.
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F. Nonenveloped virus survives better.
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What are the functions of VP4 and VP7?
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capsid proteins of rotavirus: target for vaccines.
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This pathogens appear as spokes arround a hub on EM. What is it?
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Rotavirus
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What is the function of VP6?
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code for rotavirus groups A-E.
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What type of diarrhea does rotavirus cause? Cell infection to cell lyse takes ___.
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osmotic diarrhea.
10-12 hours. |
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A 1 yr old kid presents with projectile vomit, watery diarrhea, no fecal leukocyte or blood, pyrexia(fever) in January.
1. What do you suspect the kid has? 2. What other symptoms might be present? |
1. rotavirus: the winter diarrhea disease, shorter incubation(1-4 days). adenovirus: longer incubation period(8-12 days)
2. respiratory tract inflammation associated with rotavirus. |
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Symptom: watery diarrhea, vomit, no fecal leuckocyte, no blood in the stool, fever. What do these suggest?
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rotavirus
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How to diagnose rotavirus?
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1. agglutination test
2. ELISA 3. EM 4. clinical signs: winter, <2 yrs, vomit, fever, watery diarrhea, no leukocyte or blood in the stool. |
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How to treat rotavirus infection?
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1. ORT
2. no antiviral agents |
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Is there a vaccine for rotavirus?
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Yes. RotaTec: live, oral vaccine, has 5 reassortant viruses. 3 doses to infants between 6-32 weeks.
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Why is RotaTec not used for children >2 yrs old?
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Rotavirus not very dangerous to older kids anymore, only to infants.
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A young man presents with nausea, vomiting, cramps, diarrhea, and low grade fever. He was on a cruise ship two days ago and probably had some shell fish.
1. What is suspect pathogen? 2. Where is the localization of infection? |
1. Norovirus
2. jejunum |
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What pathogen cause the intestinal epithelial cells to become vacuolated and cuboidal but remain intact?
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norovirus.
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How to test for norovirus?
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1. antigen detection (EIA)
2. PCR 3. EM 4. epidemeology: occur in clusters(family, institutions). |
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Which is the #2 important cause of epidemic infantile diarrhea?
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Adenovirus.
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How many serotypes are there for adenovirus? Which ones are associated with diarrhea in young children?
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1. 7 genera(A-G), 41 serotypes.
2. serotypes 2,3,5,31,40,41. |
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Several members of a single family are ill with abdominal cramps and watery diarrhea. They just returned from visiting friends on the East Coast of the US where they consumed raw oysters 48 hours ago. What are some possible cause?
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1. vibrio parahemolyticus: incubation 1-2 days.
2. norovirus: incubation 2 days. |
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What organisms have H and O antigens?
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Vibrio cholerae
E.coli Salmonella (also have vi antigens on the capsule) |
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Which of the following has human as its primary host?
A. Salmonella typhi B. Salmonella paratyphi C. Salmonella enteritidis D. Salmonella dublin |
A,B
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Which of the following has avians as its primary host?
A. Salmonella typhi B. Salmonella paratyphi C. Salmonella enteritidis D. Salmonella dublin |
C.
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Fever, headache, abdominal pain, relative bradycardia, spleenomegaly, and leukopenia are classic symptoms of ___.
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Enteric fever: typhoid fever.
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Describe the pathogenesis of salmonella.
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1. ingestion of infected food or water.
2. suvive gastric acidity 3. Adhesion molecules attach to mannose-containing receptors on microvilli of ileal epithelial cells. 4. microvilli destruction, cell penetration, bacteria multiplication. 5. engulfed by Peyer's patche macrohage and passed to messentery lymph nodes. 6. enter blood stream (low level bacteremia). 7. seeds many organs including bone marrow. 8. second bacteremia: see symptoms. Bacteria from gall bladder reseed ileum. 9. massive inflammatory response around Peyer's patches, result in necrosis and typhoid ulcers. |
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A patient exhibit a "step ladder" rise in body temperature. His symptoms began with dry cough, epistaxis, abdominal tenderness, headache. You noticed Rose spots on his chest and upper abdomen.
1. What is the symptoms called? 2. What is the cause? 3. What condition might he develope later? 4. What later complications may be involved? 5. How to treat him? |
1. Enteric fever/Typhoid fever.
2. Salmonella typhi 3. Spleenomegaly, herpatomegaly. 4. GI hemorrhage and perforation, myocarditis, endocarditis, meningitis, osteomyelitis. 5. Antibiotics: chloramphenicol, amicillin, cotrimoxazole, ciprofloxacin for 14 days and at least 7 days following cessation of fever. |
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What is the treatment for typhoid fever?
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Antibiotics for at least 14 days and at least 7 days following cessation of fever.
chloramphenicol, amicillin, cotrimoxazole, ciprofloxacin. Important to use antibiotics since the infection is systemic. |
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How to best diagnose typhoid fever?
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blood culture or bone marrow culture for definitive diagnosis.
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What are some preventative measures of typhoid fever?
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1. identify human carriers and not to let them prepare food.
2. imporive sanitation 3. vaccine for travelers to Africa and Asia: killed bacteria vaccine. |
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What are some differences between salmonella typhi and enteritidis?
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1. Infection with S. typhi extends beyond messentery lymph node to many organs wheres as S. enteritidis does not.
2. Diarrhea is not usually present with S. typhi but is asosciated with S. enteritidis. 3. Antibiotics is neccessary to treat S. typhi(systemic) but it is contradicted in S. enteritidis(don't want to prolong the carrier state). 4. Incubation in S. typhi is longer(3-50 days) than S.enteritidis (8-48 hours). |
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A young man presents with diarrhea, nausea, abdominal pain, fever, but not vomiting. Fecal exam showed lymphocytes and some blood. He mentioned having some bean sprouts and chicken the day before.
1. What are some possble causes? 2. How to differentiate them apart? |
1. S. enteritidis, campylobacter jejuni, shigella.
2. S. enteritidis: 8-48hr incubation. Associated with bean sprouts and chicken. Campylobacter jejuni: marked pain, also have flu like symptoms before diarrea, can use special culture at 42 degree to isolate. Shigella dysentery: use sereny test, fecal cultures. |
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Describe campylobacter jejuni:
1. gram stain morphology 2. growth condition 3. localization of disease |
1. GNB, motile, s-shaped/gull-wing shaped.
2. 42 degree, microaerophilic(7-10% CO2, 5-10% O2). 3. jejunum and ileum first,then extends to colon and rectum. |
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Describe the pathogenesis of campylobacter jejuni?
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1. ingestion of >500 organism.
2. colonize jejunum and ileum 3. extends to colon and rectum. 4. invade submucosam lamina propria, mesentery lymph nodes. Cause mucosal ulceration. 5. produce cholera-like enterotoxin, two cytotoxins. |
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What are some immune responses toward campylobacter jejuni?
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neutrophils
macrophage lymphocytes |
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Cellular damage in infection with campylobacter jejuni is caused by ____.
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1. cellular cellular invasion
2. cholera-like toxin 3. two cytotoxins produced |
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A patient complains about extreme abdominal pain(cramp), diarrhea with blood. His fever and other flu-like symptoms started 24 hours ago, and his stool was watery last night.
1. What will the fecal exame reveal? 2. What is the cause? 3. If you do an endoscopy, what might you find? 4. What later complications may result? |
1. fecal leukocyte and blood
2. campylobacter jejuni 3. mucosal ulcers 4. Patient my still shed bacteria after recovery. Interestinal hemorrhage, toxic megacolon, uremic syndrome. Reactive arthritis, peripheral polyneuropathy. |
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How to diagnose campylobacter jejuni?
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1. fecal exam: leukocytes and blood
2. Definitive: culture at 42 degree and using selective antibiotics. |
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How to treat campylobacter jejuni?
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1. supportive fluids and electrolytes.
2. antibiotics used when patient is not resolving the disease. Erythromycin is effective but of little used since the diagnose is confirmed when the patient is in recovery. |
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What are some preventative measures for campylobacter jejuni?
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1. improve poutry processing and cooking.
2. avoid cross-contamination of food. |
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Which organism grow better at 25 degree and can be stored at 4degree?
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Yersinia: small GN coccobacilli, motile at 25degree.
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What serotype is most common in US in Yersinia pseudotuberculosis and enterocolitica?
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Yersinia pseudotuberculosis: type1.
Yersinia pseudotuberculosis: type8. More common than pseudotuberculosis. Associated with chitterlings in the US and raw pork in Europe. |
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Describe the pathogenesis of Yersinia.
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1. ingestion of >10^6 bacteria.
2. multiply in jejunum. 3. attach to ileal mucosa. 4. cellular invasion: cell death, ulceration with pronounced inflammatory infiltrate(pyogranulomatous inflammation). 5. infect macrophage and mesenteric lymph nodes. 6. further spread to liver and spleen: develop abscesses. |
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A 70 yrs old patient presents with fever, abdominal pain, vominting, bloody diarrhea. You can palpate his mesenteric lymph nodes.
1. What is likely the cause? 2. If you did a endoscopy, what would you see? 3. What are some later manifestations? |
1. Yersinia enterocolitica.
2. ulcers with marked pyogranulomatous inflammation. 3. liver or spleen abscesses, reactive arthritis for HLA-B27 type. |
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T/F: Yersinia pseudotuberculosis generally affect young males between age 5 and 15 where as Yersinia enterocolitica usually affects the very young or the elderly.
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T.
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How to diagnose Yersina?
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Cin agar culture: bull's eye with red center, halo around the periphery.
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How to treat for Yersinia?
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Generaly self limited.
When indicated, broadspectrum cephalosporins, aminoglycosides, chloramphenicol, tetracyclins, but resistant to penicillin. |
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A patient has fever, blood in diarrhea, severe lower abdominal pain. Fecal exam shows large number of leukocytes.
1. What are these symptoms suggestive of? 2. If you did an endoscopic exam, what would you find? |
1. Shigella, campylobacter, yersinia.
2. intense leukocyte infiltrate, blood, mucus. |
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Describe the pathogenesis of shigella.
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1. ingestion of 10-100 organisms.
2. attach and endocytosed by colon epithelial cell. 3. multiplication cause cell death and rupture, spread to other cells and lamina propria. 4. capillary thrombosis lead to mucosal infarction ans sloughing. 5. shiga toxin production. |
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What is sereny test?
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Classic virulence test for shigella or EIEC. Keratoconjunctivits develops after 1-7 days when a strain is dropped into conjuctival sac.
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How to diagnose shigella?
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1. clinical signs: blood, large number of leukocytes, fever.
2. fecal cultures. |
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How to treat shigella?
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1. supportive fluid and electrolytes.
2. don't use gut motility inhibitors. 3. dialysis for patients developing hemolytic uremic syndrome. |
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What are some preventative measures for shigella?
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1. proper sanitation and food handling practices.
2. improved hygiene at day-care centers. 3. personal hygiene. |
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Describe EHEC:
1. gram stain morphology 2. lactose fermenter? 3. sorbitol fermenter? 4. toxin producer? |
1. GNB, fimbrae
2. lactose fermenter 3. sorbitol fermenter 4. Stx-1, stx-2: cytotoxic to vascular endothelial cells leading to microangiopathy,hemorrhagic colitis, and hemolytic uremic syndrome. |
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Describe the toxins produced by EHEC.
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1. Stx-1: similar to shigella toxin. Neutralized by shiga toxin antiserum.
2. Stx-2: not neutralized by shiga toxin antiserum. |
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A patient has abdominal pain, bloody and watery stool without fever or fecal leukocytes.
1. What is the cause? 2. What is the definitive diagnosis? 3. How to treat it? |
1. EHEC
2. culture using sorbitol-macConkey followed by serotyping. Shiga toxin antigen is a better marker. 3. supportive. *Don't use antibiotics! |
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How do the toxins produced by EHEC or shigella cause hemolytic uremic syndrome?
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1. shiga toxin bind to renal glomerular, mesangial, and tubular cells.
2. thrombogenesis: platelet consumption. 3. RBC shearing 4. renal insufficiency and uremia. |
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What are the primary sources of EHEC infections in human?
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1. unpasteurized milk, apple cider.
2. contaminated beef. |
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Describe EIEC:
1. gram stain morphology 2. lactose fermenter? 3. glucose fermenter? |
1. GBR, nonmotile
2. non-lactose fermenter 3. glucose fermenter serotype O124 |
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A patent has a mild form of dysentery: fever, blood in the stool.
1. What are some possible causes? 2. What is the definitive diagnosis? |
1. EIEC, shigella.
2. microbiologic isolation,, serotyping. |
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What is the third leading cause of parasitic death in developing countries?
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Entamoeba
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Describe the life cycle of entamoeba histolytica.
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1. cysts enter small intestine and release 8 trophoxzoit progeny.
2. trophozoit attach to colonic mucosa. 3a. trophozoite ingest bacteria, sexual and asexual reproduction. 3b. trophozoite invade mucosal cells, feed on erythrocytes and mucosal cells. Asexual and sexual reproduction. cause pore forming ulcerations. 4. cysts in feces. |
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A patient has gradually developed abdominal pain, tenderness, and bloody stools over 3 wks. Fecal leukocytes are present.
1. What would you see if you did a colonoscopy? 2. What is the cause? 3. How to diagnose? 4. How to treat it? 5. What later condition might the patient develop? |
1. fulminant colitis with perforation, toxic megacolon.
2. entamoeba histolytica 3. detection of cysts or trophozoite in the stool/abscess.Three times over 10 days(the ones that eat RBC).Antibody detection most useful. Antigen detection is useful to distinguish pathogenic and nonpathogenic types. 4. Metronidazole/tinidazole followed by iodoquinol,paromomyxin, or diloxanide furoate. 5. liver(anchovie paste), spleen abscesses. |
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What pathogens need at least 3 fecal exams over 10 day period?
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Ones that shed intermittently: giardia, cryptosporidium, histolytica.
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Do you need to treat the asymptomatic histolytica infection?
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Yes. Iodoquinol, paromomycin, or diloxanide furoate.
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Describe clostridium difficile:
1. gram stain morphology 2. aerobe or anaerobe? 3. motile? 4. produce toxins? |
1. GPB with oval spores.
2. anaerobe 3. motile 4. enterotoxin(toxinA), cytotoxin(toxinB), bowel motility inhibitor. |
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A patient presents with watery diarrhea with fecal leukocytes, cramps, fever. He was in ICU last week.
1. What is the cause? 2. What would you see if you did a colonoscopy? 3. How to diagnose? 4. How to treat? |
1. Clostridium difficile
2. pseudomembranous colitis. 3. Endoscopy, ELISA for toxinB detection. 4. discontinue offending antibiotics. Oral metronidazole or vancomycin in severe cases. |
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Which of the following food borne disease is NOT due to intoxication of preformed toxins?
A. Staph aureus B. Clostridium perfringens C. Bacillus D. Clostrudium botulism |
B: toxin production in vivo.
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Describe the pathogenesis of clostridium perfringens.
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1. spores survive cooking of meat.
2. spores germinate in meat and multiply in meat. 3. meat ingested and bacteria protected from stomach acidity by proteins. 4. bacteria sporulate 5. produce enterotoxin 6. abdominal cramps 8-12 hours followed by watery diarrhea. |
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A couple and their parents complains about intense abdominal cramps, diarrhea. She has no pain nor vomit. Their last meal was 12 hours ago at a mexican restaurant.
1. What is likely the cause?Be specific. 2. What is the worst serotype? 3. How to diagnose? 4. How to treat it? |
1. C. perfringens type A. B-E don't suvive in soil, but colonize human intestine.
2. TypeC(big-bel) 3. epidemiologic investigation and isolation of specific strains. 4. usullay not necessary, fluids and eletrclytes. |
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Describe bacillus cereus:
1. gram stain morphology. 2. spore forming or not? 3. aerobe or anaerobe? |
1. GPR, motile.
2. spore forming. 3. aerobe |
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Describe the pathogenesis of bacillus cereus.
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1a. heat and acid resistant toxin in improperly handled rice and legumes cause rapid onset of emtitic(vomit).
1b. ingested live organisms produce enterotoxins during sporulation. Cause watery diarrhea 8-24 hours later. |
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List some heat stable toxin and what organism produces them.
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1. cholera toxin
2. ETEC produce ST toxin. 3. Vibrio parahemolyticus produces heat stable hemolysin. 4. Bacillus cereus produces heat and acid resistant toxin 5. Staph aureus produce enterotoxin. |
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What organism produce toxin that is both heat and acid resistant?
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Bacillus cereus.
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Refrigeration would prevent toxin production in what organism?
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Staph aureus.
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What organism cause "true intoxication"?
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Staph aureus: 2-6 hour incubation. Vomiting, diarrhea, no fever, no blood in the stool.
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A patient presents with diarrhea and vomit, no fever, no blood in the stool. He told you that 3 hours ago he had some egg salad in a restautant.
1. What is likely the cause? |
Staph aureus.
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What is ptomaine?
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Any of various toxic nitrogenous organic compounds produced by bacterial decomposition of protein, especially in dead animal tissue. Ptomaines are bases and are formed by removing the carboxyl group (COOH) from amino acids. Ex. Staph aureus.
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Describe Clostridium botulinus:
1. gram stain morphology 2. toxin producer? 3. aerobe or anaerobe? 4. spore forming? |
1. GPB, saphrophyte
2. yes. heat labile toxin A-H. A,B,E mostly. 3. strict anaerobe. 4. spore forming. |
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List different forms of botulism.
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1. food-born from ingetion of toxin: non-acid food.
2. intant botulism from colonization and absorption of toxin: honey 3. wound botulism secondary to bacterial growth in wound and toxin absorption. |
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What is the distinct symptom of botulism? What is the cause? How to treat it?
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1. Descendin motor loss(symetric): occular muscles, drooping eyelids, vertigo, blurred vision. Then speech problem and swallowing, progress to flaccid paralysis.
2. toxin blocks Ach. 3. polyvalent antitoxin right away and supportive. |
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What are some preventative measures of botulism?
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1. proper preparation of canned food: boiling 80degree for 30min.
2. prophylactic polyvalent antitoxin for potentially infected. 3. active immunity from toxoid injections. |
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Describe listeria:
1. gram stain morphology 2. aerobe or anaerobe? 3. motile or not? |
1. GP coccobacillus, beta-hemolytic, grow at 4 degree.
2. aerobe 3. motile |
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What are the target population for listeria?
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1. pregnant women/fetus
2. immunocompromised 3. cancer patients 4. elderly |
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Which disease has the highest case-fatality ratio of all the foodborne diseases?
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Listeria
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A baby is born with meningocephalitis.
1. What is the likely cause? 2. What are the symptoms in adult form? 3. How to treat it? |
1. Listeria that is passed from the mom.
2. flu-like symptoms, may cause meningoencephalitis in immunocompromised patients. 3. penicillin or ampicillin |
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Describe the pathogenesis of listeria?
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Intracelluar pathogen: localize in macrophages.
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Which intestinal parasite may cause pneumonitis, pain, nausea, and biliary blockage leading to cholangitis?
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Ascaris lubricoides(roundworms)
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What is a special diagnostic finding with intestinal parasites?
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pronounced eosinophilia
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List three hookworms and compare them.
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Ancylostoma duodenale: prevalent in Europe, North Africa, western Asia.
Necator amercanus: prevalent in Africa, India, South America, Central America, Southern US. Both:1)one life cycle(larva-cutaneous penetration-mulmonary migration-adults in small intestine). 2) cause iron-deficient anemia, melena, chronic diarrhea, growth retadation. Strongyloides stercaralis: two life cycles:1) free living(male&female produced) 2) parasitic(flareform larva stage which is infectious). Cause profuse diarrhea, malabsorption, autoinfection in immunocompromised patients. All: feed on mucosa and blood. |
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Which organism cause iron-deficient anemia, melena, chronic diarrhea, growth retardation?
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Ancylostoma duodenale and Necator americanus.
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What is hyperinfection? What organism may cause this?
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1. the ability of specific helminths, to establish a life cycle within the host, eliminating the need for an intermediate stage, and secondary hosts.
2. Strongyloides stercoralis and Hymenolepis nana: in immunocompromised patients. |
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Name a whipworm. What does it cause? How?
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1. Trichuris trichuria.
2. Chronic diarrhea, intestinal discomfort, rectal prolapse. 3. Induce epithelium syncytium formation, adult parasite embed anterior portion into colonic epithelium, posterior portion in the lumen. |
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What is a common pinworm of children? How to treat it?
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1. Enterobius vermicularis: hand-oral contamination, gravid females exit anus ans lay eggs on perianal region causing itching.
2. pyrantel pamoate, laundering, check family members. |
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1. Name the beef tapeworm.
2. Name the pork tapeworm. 3. How to treat them? |
1. tinea saginata
2. tinea solium: human as intermediate hosts. 3. praziquantel. |
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How to diagnose tinea saginata and solium?
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Identification of proglottids or ova in feces.
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What is cysticercosis?
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In fection in both human and pigs with the larval stage cestode tinea solium.
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What is cysticercosis?
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Infection of both the pig and human with larval stage of tinea solium.
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Which parasite has multiple intermediate hosts and human often get ill by eating undercooked fish?
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Diphyllobothrium latum: may compete with host for vitamin B12.
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Which parasite may compete with host for vitamin B12?
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Diphyllobothrium latum
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Name the dog tapeworm. What is its intermediate host?
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Dipylidium caninum.
Flea. |
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What is a cysticercoid?
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teania solium
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What are the causes of dysentery?
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1. shigella
2. EHEC 3. camyplobacter jejuni 4. salmonella enterica 5. vibrio parahemolyticus 6. entamoeba histolytica. |
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A patient calls and state that he and several family members are ill with severe vomiting. They ate at a church picnic 4 hours earlier. What is likely the cause?
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Staph aureus.
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A 18 month child is brought to your office with fever, bloody diarrhea, and some vomiting. She has been drinking unpasteurized milk in the last 48 hrs. No other family members are ill. What organisms may cause this?
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1. salmonella
2. shigella 3. campylobacter jejuni |
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List some motile organisms that cause GI infection.
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Flagellated bacteria:
1. helicobacter pylori(sheathed) 2. vibrio cholera(comma shaped) 3. E.coli(except EIEC) 4. Salmonella motile bacteria: 1. Yersinia 2. campylobacter(gull wing shaped) 3. clostridium difficile 4. bacillus cereus 5. listeria(tumbling motility) Protozoas 1. giardia 2. cryptosporidium 3. entamoeba histolyticus |
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Organisms that cause profuse diarreha.
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1. vibrio cholera
2. ETEC (less than cholera) 3. EPEC (less than cholera) 4. strongyloides |
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Organisms that produces enterotoxins.
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1. vibrio cholera: cholera toxin.
2. ETEC: LT and ST 3. vibrio parahymolyticus: TDH 4. campylobacter jejuni: cholera like toxin. 5. shigella, EIEC: shiga toxin 6. EHEC: stx1 and stx2. 7. clostridium difficile: toxinA 8. clostridium perfringens: lecithinase 9. bacillus cereus: heat and acid resistant toxin. 10. clostridium botulinum: heat labile. |
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Organisms that produce cytotoxins.
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1. helicobacter pylori
2. EPEC 3. campylobacter jejuni: 2 4. clostridium difficile: toxinB |
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What organisms are associated with unpasteurized milk?
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1. EHEC
2. campylobacter 3. listeria 4. Salmonella(contaminated milk products) 5. staph aureus(dairy products) |
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Which organisms destroy microvilli?
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1. EPEC
2. cryptosporidium 3. rotavirus 4. salmonella typhi |
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What organisms are associated with seafood/fish/shell fish?
|
1. vibrio parahemolyticus
2. norovirus 3. diphylobothrium latum |
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What causes secretery diarrhea?
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1. vibrio cholera
2. ETEC 3. EPEC 4. cryptosporidium cyclospora |
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What organisms we learned during this block involves both sexual and asexual life cycles?
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1. cryptosporidium
2. entamoeba histolyticus |
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What are some chlorine resistant organisms?
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1. Cryptosporidium
2. norovirus 3. giardia (moderately reistant) |
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What organisms produce heat labile toxins?
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1. ETEC: LT
2. Clostridium botulinum |
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What organism produces both heat and acid resistant toxin?
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bacillus cereus
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What are some acid fast organisms?
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crytoporidium and cyclospora
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What organisms cause ulceration of the intestine?
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1. salmonella typhi
2. campylobacter 3. yersina |
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What organisms invade macrophages?
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1. salmonella
2. yersinia 3. listeria |
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What organism can cause disease with low innoculum size?
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1. rotacirus
2. shigella 3. campylobacter(500-1000) |
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What organisms cause direct cellular invasion?
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1. salmonella typhi
2. campylobacter jejuni 3. yersinia 4. shigella(rupture cells) 5. entamoeba histolytica(kills on contact) |
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What are some members of the enteriobacteriacea?
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1. E.coli
2. salmonella 3. yersinia 4. shigella |
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What organisms cause swollen messenteric lymph nodes?
|
1. yersinia
2. campylobacter jejuni |
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What organisms cause liver and spleen abscesses?
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1. yersinia
2. entamoeba histolyticus |
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What organims cause hemorrhagic uremic syndrome?
|
1. shigella
2. EHEC |
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What organisms present risks to travelers?
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1. ETEC
2. Norovirus 3. Entemoeba histolyticus 4. salmonella |
