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198 Cards in this Set
- Front
- Back
What is the difference between dysentery and typhoid fever?
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Dysentery has fever, abdominal cramps, and bloody, mucopurulent diarrhea that is produced by invasive organisms that target the colon.
Typhoid fever is a systemic febrile illness of prolonged (3 to 5 weeks) with fever, persistent bactermia, and metastatic spread BUT NO DIARRHEA. |
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What is the causative agent of typhoid fever?
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Salmonella typhi
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What is the most common agent of acute infectious diarrhea in the US?
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Campylobacter
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How does Yersina enterocolitica cause dysentery?
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Y. Entercolitica organisms penetrate the surface epithelium of the distal small bowel and quickly make their way to deep tissues, including regional lymphatics
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Why does Yersina enterocolitica infection mimic acute appendicitis?
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Y. enterocolitica can penetrate their way through the distal small bowel to the regional lymphatics.
clinical features include diarrhea and prominent right lower quadrant abdominal pain. the Clinical spectrum of these organisms includes mesenteric adenitis mimicking acute appendicitis. |
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Where is the common location for Yersinia enterocolitica infections?
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certain European countries and Canada
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Which of the infectious enteric bacteria can be transmitted from person to person?
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Shigella , this is unique among the enteric pathogens
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What layers of the bowel are affected in invasive bacteria?
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The initial lesions caused by these inflammatory pathogens are confined to the epithelial layer; however, as the disease progresses, the lamina propria becomes involved extensively with an inflammatory response --> crypt abscesses are common
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What are some common causes of protozoan diarrhea?
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The most common protozoa are Giardia, Cryptosporidium, and Cyclospora
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Enterotoxic E.Coli causes _________ but Enterohemorrhagic E.Coli causes ________.
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Traveler's diarrhea
Acute hemorrhagic colitis |
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What is the most common cause of viral cause of diarrhea?
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Rotavirus
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Rotavirus mainly affects ______ and Norovirus mainly affects ______
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pediatric populations
adult populations |
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What is the mechanism for bacterial secretory diarrhea?
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These organisms colonize the proximal small bowel and stimulate fluid and electrolyte secretion resulting in watery diarrhea.
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Why are fecal leukocytes not usually not seen in amebic colitis?
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The amebae engulf the white cells and RBCs for food.
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What is the causative agent of the amebic colitis?
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Entamoeba histolytica is a common invasive protozoan that causes dysentery (amebic colitis) with complications (liver abscess)
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Which types of hepatitis can lead to liver cancer?
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Hepatitis B and C
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What are the risk factors for hepatitis A?
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eating contaminated seafood or imported berries
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What does the presence of leukocytes indicate in diarrhea?
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Inflammatory diarrhea
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What does the presence of frank or occult blood or mucus indicate in the diarrhea?
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Dysentery syndrome
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Describe Campylobacter.
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Bacteria in the genus Campylobacter are motile, Gram- negative curved rods ( comma or seagull shaped organisms)
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What is the difference in the virulence factors of Campylobacter fetus and Campylobacter jejuni?
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A major virulence factor of Campylobacter fetus a proteinaceous capsule- like structure. The virulence factor of C. jejuni is its flagella
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How is Campylobacter cultured?
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Growth of Campylobacter strains requires selective media, microareophilic conditions (5% oxygen, 5% to 10% CO2) and incubation at 42 C
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How do we differentiate between the species of Campylobacter?
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Differentiation of Campylobacter species is based on biochemical reactions
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How are most cases of Campylobacter transmitted?
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Most cases are associated with improper food handling and preparation of poultry
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What is the infectious dose of Campylobacter jejuni?
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Ingestion of only 500 organisms
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How does Campylobacter damage intestinal mucosa?
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A cytolethal distending toxin and an endotoxin likely contribute to tissue injury
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What is the incubation period of Campylobacter?
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2 to 5 days
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How does Campylobacter penetrate the intestinal mucosa?
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The microaerophilic organisms are adapted for survival in the GI mucosa layer and they colonize the intestinal mucosal layer , mediated by flagella and putative adhesins
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What type of tissue damage is seen with Campylobacter infection?
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An acute, nonspecific neutrophilic and monocytic inflammatory reaction causing tissue damage in lamina propria and jejunal epithelium is seen
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What is the role of antibiotics in Campylobacter infection?
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It is generally self-limited infection but if antibiotics are indicated, they should be given early in the course for maximum benefit.
Erythromycin should be given if antimicrobial therapy is required and quinolones in complicated cases |
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What groups are likely to have bacteremia with Campylobacter jejuni?
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Elderly and patients with AIDS
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What bacterial infection had Guillain-Barre syndrome been associated with?
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Campylobacter jejuni
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What complications are likely in patients with HLA-B27 with Campylobacter infection?
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Reactive Arthritis
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What is Guillain- Barre syndrome?
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It is one of the most common cause of flaccid paralysis in the US and manifests as symmetrical ascending muscle weakness and facial diplegia
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What is treatment of choice in Campylobacter enteritis?
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Rehydration
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Describe the Salmonella bacteria.
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Gram negative rods
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How are the different strains of Salmonella differentiated?
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Antigenic analysis of strains are based on cell wall (O) and flagellar (H) antigens
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Which antigen of Salmonella undergo phase variation?
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H antigens undergo phase variation via DNA rearrangements
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Salmonella ferment _____, but not ferment______ and reduce______, they are facultative ______ organisms.
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glucose
lactose nitrates anaerobic |
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What are the main reservoir for Salmonellae?
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Animals are the main reservoir
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what is the role of antibiotics in nontyphoidal Salmonella infection?
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Antibiotics are not usually required to treat
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How is salmonella infection acquired?
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Infection is acquired by ingestion of contaminated food or water, by contact with infected animals or person to person
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What is the infective dose of Salmonella?
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10^5 organisms
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How does Salmonella cause infection?
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The organisms adhere to a distal portion of small intestinal mucosa, this is mediated by fimbriated adhesins. A localized infection in the intestinal epithelial cells are mediated by bacterial invasins
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What defines complicated enteritis of Salmonella?
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Dissemination throughout the reticuloendothelial system and bacteremia
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Salmonella typically causes ______ diarrhea.
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bloody
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How does the immune system react to Salmonella?
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There is an overwhelming influx of neutrophils to the intestines
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What causes complicated enteritis of Salmonella?
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Phagocytosis of macrophages
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How does Salmonella typhi differ from other salmonella?
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S. typhi is an encapsulated organism but all the others are non- encapsulated
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How are clinical isolates of Salmonella typhi identified?
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S. typhi is identified by biochemical reactions and by agglutination with O, H, and Vi antibodies
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The incubation period for S. typhi is _____ but the incubation period for nontyphoidal Salmonella is ______
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3 days to 3 months
6 to 48 hours |
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How does Salmonella typhi reach the submucosal lymph nodes of the intestine?
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The typhoidal salmonellae bind to intestinal M cells by an unknown adhesin. After invasion, the M cells die and deliver the salmonellae into the Peyer patch.They then migrate through the intestinal mucosa of the terminal ileum into the submucosal lymph nodes
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What is the preferred antibiotic empirical therapy?
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Ciprofloxacin
|
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What group of people are susceptible to chronic infection of Salmonella typhi?
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Those individuals with biliary obstruction or gallstones are particularly prone to becoming long term carriers
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What is the skin manifestations of S. typhi?
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Rose spots
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What are rose spots?
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They are erythematous maculopapular lesions caused by thrombocytopenia and vascular capillary leakage caused by S. typhi
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What are the intestinal changes with an infection of S. typhi?
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An infiltration of mononuclear cells into the colonic mucosa
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How does Salmonella typhi survive and multiply?
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It survives and multiplies within macrophages by inhibiting the oxidative burst
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How does S. typhi cause hepatomegaly and splenomegaly?
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They are carried inside the monocytes and delivered to the RES.
|
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What is the causative agent of enteric fever?
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The signs and symptoms of enteric fever including abdominal pain are caused by the secretion of cytokines and pyrogens by macrophages
|
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How does one vaccinate against S. typhi ?
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There is a live vaccine that is taken orally and consists of the attenuated mutant of S. typhi
There is also an IM vaccine based on the Vi capsular polysaccharide antigen |
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Why can S. typhi cause chronic infection in those with biliary obstruction or with those that have gallstones?
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The typhoidal salmonellae are resistant to bile
|
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How does S. typhi cause diarrhea days after the febrile illness?
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It reenters the intestines in bile, causing diarrhea
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How does the body eventually overcome a Salmonella typhoidal infection?
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Humoral antibody and activated macrophages
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How long does it take to overcome a Salmonella typhoidal infection?
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3 weeks
|
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What is the causative agent for bacillary dysentery?
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Shigella flexneri
|
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What is the most virulent species of Shigella?
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S. dysenteriae
It belongs in serogroup A |
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What is the most predominant form of shigella in the United States?
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Shigella sonnei
|
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Which type of Shigella secretes the Shiga toxin?
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S. dysenteriae type 1
|
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How does Shiga toxin work?
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Stx is an inhibitor of protein synthesis, targeting the 23S ribosomal RNA. It kills intestinal epithelial cells and endothelial cells
|
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Which Shigella strain produces watery and less severe diarrhea?
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S. sonnei
|
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How is Shigella cultured?
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On Hektoen agar
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Shigella is a _______ anaerobe
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facultative
|
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How does the Shigella bacteria cause local spread?
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Infected intestinal epithelial cells produce attractants for neutrophils, which migrate between the epithelial cells, causing a breakdown of the tight junctions and facilitating the local spread of the bacteria
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Which host protein is essential for the spread of Shigella?
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cadherin L-CAM
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How does the Shigella bacteria move from infected intestinal cell to uninfected intestinal cell?
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Passage of the bacteria into adjacent epithelial cells occurs through finger-like projections from the surface of an infected cell to the surface of the an uninfected cell
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What are the systemic complications of S. dysenteriae type 1?
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Hemolytic-uremic syndrome and TTP are the systemic complications
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What is the antimicrobial of choice in the treatment of Shigella?
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TMP/SMX
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What antimicrobial is recommended for the treatment of Bactrim resistant Shigella?
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quinolones
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Where does the Shigella bacteria initially invade the colonic mucosa?
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In the COLONIC mucosa, the invasive bacteria penetrate the M cells and are taken up by the macrophages in the lamina propria
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What happens the Shigella bacteria ingested inside the dead macrophages?
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the bacteria released from the dead macrophages also invade the intestinal epithelial cells via their basolateral membrane
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All Shigella bacteria do not ferment lactose except _______
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S. sonnei
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What is the most common pathogen that is isolated from bloody diarrhea?
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E. coli O157:H7
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How is E. coli O157:H7 cultured?
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On sorbitol - MacConkey agar medium
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How is the diagnosis of E. coli O157:H7 made?
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Identification of E. coli O157:H7 is made on the basis of an indole-positive, lactose positive, sorbitol- nonfermenting isolate that is positive for agglutination of O157- specific antibodies
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Describe the course of hemorrhagic colitis.
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It is characterized by abdominal cramps and watery diarrhea that after a few days became streaked with blood or grrossly bloody
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What are the major vehicles of infection for E. coli O157:H7?
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Ground beef and unpasteurized milk
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Which E. coli infection is like mild cholera and which is like mild shigellosis?
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Enterotoxigenic E. Coli is like mild cholera and Enteroinvasive E. coli is like mild shigellosis
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Which form of E. coli infection has the complications of hemolytic-uremic syndrome and TTP?
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E. coli O157:H7, EHEC
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What other form of E.coli invades the colonic mucosa like the Enterohemorrhagic E.coli?
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Enteroinvasive E.coli
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What is the serotype of Enteropathogenic E.coli?
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O26:H111
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How does Enterohemorrhagic E. coli invade colonic mucosa?
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EHEC strains produce virulence factors that allow them to attach and efface the brush border of the intestinal epithelium
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What happens to the enterocyte after Enterohemorrhagic E.coli attaches to it?
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The affected enterocytes show a dramatic loss of microvilli and rearrangement of cytoskeleton elements, with a proliferation of filamentous actin under the areas of attachment
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How does E. coli O157:H7 ( EHEC) kill enterocytes?
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With Shiga toxin -1 and Stx-2
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Why does hemolytic uremic syndrome occur in EHEC?
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The Stx-1 or Stx-2 binds to a glycolipid receptor molecule on the surface of endothelial cells in the kidney
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Shiga toxins are cytotoxic to colonic and _______ cells
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renal endothelial
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How does enterotoxigenic E.coli kills colonic endothelial cells
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With enterotoxins
The heat labile LT stimulates adenyl cyclase and this increases cAMP |
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If a colonoscopy was done in a patient with E.coli, and it showed a necrotic mucosa what should we suspect?
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Enteroinvasive E.coli
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If a colonoscopy was done in a patient with E.coli, and it showed a necrotic mucosa what should we suspect?
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Enteroinvasive E.coli
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What are the different types of E.coli that can result in bloody diarrhea?
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Enteroinvasive E. coli
Enterohemorrhagic E. coli |
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What is the antimicrobial therapy for E.coli?
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Most cases do not require antimicrobial therapy.
|
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Describe Vibrio bacteria.
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The bacteria inthe genus Vibrio are curved, Gram negative rods with a single flagellum
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Vibrio are nonspore forming, oxidase-_______ and facultative ________.
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positive
anaerobes |
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How is Vibrio cultured?
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On Thiosulfate-citrate-bile agar--> this supports Vibrio growth but inhibits the commensal colonic bacteria
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What type of cholera cause epidemics?
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Organisms that agglutinate in 0:1 antiserum.
|
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What type of cholera causes pandemics?
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Organisms that agglutinate in 0:1 antiserum.
|
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Where is the current pandemic of cholera located?
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The seventh global pandemic is in Asia, Africa and Latin America and it began in Sulawesi, Indonesia
|
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What is the causative agent in the current pandemic of cholera?
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El Tor 0:1
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What medication would predispose a person to cholera?
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Antacids or any drug that would reduce stomach acidity
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What are the risk factors for developing cholera in the United States?
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Ingestion of contaminated raw seafood
|
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Where would we expect to see cases of cholera in the United States?
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Along the Gulf Coast, mainly in Texas and Louisiana
|
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How does reduced stomach acidity give Vibrio cholera an advantage to infection?
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V. cholorae lacks a mechanism for acid resistance so they need a very large inoculum size for infection EXCEPT for patients with reduced gastric acidity
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Where does V.cholerae colonize in the body?
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In the small intestine
|
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How does V. cholerae colonize the GI tract?
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V. cholerae colonizes the small intestine via long filamentous pili
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Describe the cholera toxin.
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CTX is an A-B type ADP-ribosylating enterotoxin
|
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How does CTX enter an intestinal cell?
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The B pentamer binds to Gm1 ganglioside, a glycolipid on the surface of jejunal epithelial cells that serve as the toxin receptor and facilitates the delivery of the A subunit to its target
|
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What is the toxin receptor for the Cholera toxin?
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Gm1 ganglioside on the jejunal epithelial cell
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How does the cholera toxin cause the secretory diarrhea?
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Via the functional A subunit.
It activates the adenyl cyclase cascade system by irreversible transfer of an ADP- ribose subunit from NAD to membrane Gs protein --> raising intracellular concentrations of cAMP --> activates excretory chloride transport system in the crypt cells--> NaCl accumulates in the lumen |
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Describe the diarrhea caused by the cholera toxin
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Rice water diarrhea
|
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How much fluid loss can occur with cholera in an hour?
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1 L/hr
|
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What is the antibiotic of choice with cholera?
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Doxycycline
|
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Why is cholera vaccine NO LONGER recommended for travelers?
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Killed cholera vaccine has limited value --> protects only 50% of those vaccinated of short duration (3-6 months)
|
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In the current pandemic of cholera, virulence is ____ but carrier rate is _____.
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low
high |
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What is the most common cause of watery diarrhea in travelers?
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Enterotoxigenic E. coli
|
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Why does food poisoning due to S.aureus and B.cereus have a rapid onset of 1- 6 hours?
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They have a pre- formed toxin
|
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How can you identify Staphylococci on blood agar?
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They are yellowish colonies that are identified based on a coagulase- positive reaction.
|
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What mechanism allows S aureus to cause food poisoning via a meat dish despite reheating the dish to a high temp before serving?
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If the dish was left out at a warm temp for hours, the heat stable enterotoxin would have already formed
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What would be the source of S. aureus food poisoning?
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S. aureus is of human origin, from a purulent discharge of an infected finger or eye, abscesses, acneiform facial eruptions, or nasopharyngeal secretions of food preparers
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What is the antibiotic of choice for S. aureus infection ?
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There is none
The syndrome is self-limiting |
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How long does the upper GI symptoms caused by the enterotoxin of S. aureus last?
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12 to 24 hours
|
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What are the common food sources of S. aureus enterotoxin?
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Ham (meats), mayonnaise, custard
|
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What are the common food sources that cause Bacillus cereus food poisoning between 1-6 hours
|
Reheated fried rice
|
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What are the common food sources that cause Bacillus cereus food poisoning between 8-24 hours
|
Cream sauce
|
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The heat-stable enterotoxin of Bacillus cereus causes _______but the heat- labile enterotoxin causes _______
|
Acute upper GI symptoms
Watery Diarrhea |
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What types of toxin does Bacillus cereus produce?
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Two
Heat stable (emetic) Heat labile (diarrheogenic) |
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What type of symptoms does a Clostridium perfringens infection cause?
|
Watery diarrhea
|
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What are the common food sources of Clostridium perfringens?
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Reheated meat dishes, gravy
|
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When would we see symptoms from a Clostridium perfringens infection?
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Within 8-12 hours
|
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Clostridium botulinum is a Gram _____, spore- forming _____ .
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positive
rod |
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Clostridium botulinum is an ______ anaerobe.
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obligate
|
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What is associated commonly with cases of wound contamination of Clostridium botulinum?
|
Skin-popping black tar heroin
|
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What is the most frequently encountered form of botulism?
|
Infant botulism
|
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What places infants at risk for contracting botulism?
|
Ingestion of honey and to a lesser extent corn syrup
|
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What is the disease causing agent in Clostridium botulinum infection?
|
A heat labile neurotoxin
|
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What are the primary sources of adult botulism?
|
Ingestion of preformed toxin in home- canned fruit, sausage, and fish products
|
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What is the action of Clostridium botulinum neurotoxin at the neurotoxin junction?
|
It cleaves the components of the neuroexocytosis apparatus, irreversibly preventing release of ACh from the neuromuscular junction
|
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What are the clinical effects of Clostridium botulinum food poisoning?
|
descending symmetrical flaccid paralysis
diarrhea vomiting blurred vision bulbar weakness dysarthria ptosis dysphagia dry mouth |
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Where should we first see the effects of Clostridium botulinum paralysis?
|
It usually beginning with the cranial nerves, that may progress rapidly
|
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How does Clostridium botulinum move the GI tract to the NMJ?
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It doesnt. The spores germinate and produce the neurotoxin, which then circulates in the bloodstream.
|
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Describe the involvement of the CNS with Clostridium botulinum neurotoxin.
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the CNS is not involved.
|
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What are the targets for the Clostridium botulinum neurotoxin.
|
Peripheral cholinergic nerve terminals, including NMJ, postganglionic parasympathetic nerve endings, and peripheral ganglia.
|
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What is the role of antibiotics in infant botulism?
|
Antibiotics are contraindicated because these drugs may increase the levels of toxin in the gut by bacterial lysis
|
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What is the treatment of adult botulism?
|
Use purgatives to expel retained food
You can use equine antitoxin serum to neutralize toxin that is not yet internalized in neurons |
|
How does the Clostridium botulinum neurotoxin enter a nerve cell?
|
It attaches specifically to peripheral cholinergic synapses and is internalized inside the nerve cell to endocytic vesicles, from where it is translocated into the cytosol.
|
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Why does Clostridium botulinum neurotoxin cause dry mouth, ptosis?
|
It affects peripheral cholinergic nerve terminals
|
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What is the role of antibiotics in wound botulism?
|
Penicillin, metronidazole with wound debridement is an effective modality for management.
|
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What effect does boiling have on food that is already contaminated with Clostridium botulinum?
|
It can inactivate the toxin but the spores are more difficult to destroy
|
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Why can adults eat honey but infants can't?
|
The spores of Clostridium botulinum are not able to germinate in older children or adults like they can in infants
|
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Clostridium difficile is a strict _______ bacterium
|
anaerobe
|
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Clostridium difficile is Gram ______ and a spore- forming ____
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positive
rod |
|
How does Clostridium difficile cause disease?
|
via either one of its two toxins: toxin A or toxin B
|
|
What is the carrier rate for Clostridium difficile in the adult population
|
4%
|
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What is the carrier rate for Clostridium difficile in the neonate population
|
50%
|
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What is the carrier rate for Clostridium difficile among hospitalized adults that have received antibiotic therapy?
|
46%
|
|
What are the commonly incriminated antibiotics involved in Clostridium difficile associated diarrhea?
|
Clindamycin,
3rd generation Cephalosporin Ampicillin |
|
Primary cases of Clostridium difficile associated diarrhea occur via________ but secondary cases occur via _______.
|
endogenous mode in precolonized patients exposed to antibiotics
exogenous transmission of spores in the hospital |
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Which is the more potent toxin of Clostridium difficile?
|
Toxin B
|
|
How do broad spectrum antibiotics encourage Clostridium difficile associated diarrhea?
|
Broad-spectrum antibiotics suppress normal flora
|
|
How does the toxins of Clostridium difficile attack the epithelial cell of the colonic mucosa?
|
They bind to the cellular GTP -binding proteins and inactivate them by glycosylation, and dysregulate the action of the cytoskeleton in epithelial cells. This causes depolymerization of actin.
|
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What is the receptor of Clostridium difficile in an epithelial cell?
|
Both toxins exert their effects by binding to cellular GTP - binding proteins.
|
|
What is the antibiotic of choice in Clostridium difficile associated diarrhea?
|
Metronidazole
|
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What should one expect to see in a colonoscopy of a patient withClostridium difficile associated diarrhea?>
|
Multiple elevated , yellowish white plaques (pseudomembranes) within the colon
|
|
What is a potentially serious complication in a patient with psuedomembranous colitis?
|
toxic megacolon
|
|
What are the cumulative effects seen in the bowel lining that has been exposed to the toxin of Clostridium difficile?
|
the bowel lining becomes erythematous and friable, with ulceration and hemorrhagic necrosis due to the breakup of actin filaments within the cell
|
|
In the _____ months, rotavirus can be very severe and is very common.
|
winter
|
|
Describe Rotavirus nucleocapsid structure.
|
The viral nucleocapsid is composed of two concentric shells.
|
|
Rotavirus is a noneveloped ______ virus in the family of _________
|
RNA
Reoviridae |
|
Describe the Rotavirus virion structure.
|
The double shelled particles are shaped like wheels with short spokes on an outer rim are the complete infectious virions
|
|
there are ____ major subgroups of rotavirus and _______serotypes of human rotaviruses
|
three
nine |
|
Describe the genome of Rotavirus.
|
Rotaviruses have a segmented genome with 11 segments of a double- stranded RNA genome
|
|
What defines the antigenic types of rotaviruses?
|
Two structural proteins on the outermost shell defines the antigenic types of the virus.
|
|
How is Rotavirus diagnosed?
|
An assay that detects rotavirus viral antigen in stool specimens
|
|
Why was a rotavirus vaccine unsuccessful?
|
It was withdrawn due to reports of intussusception as a sideeffect
|
|
How is rotavirus transmitted?
|
through fecal- oral transmission and through fomites
|
|
What is the single most important cause of severe dehydrating diarrhea in infants and in children younger than 3 years?
|
rotavirus
|
|
What is the cellular target of a rotavirus that has been ingested?
|
The virus infects the mature villus tip cell of the small intestine.
|
|
How does Rotavirus cause osmotic diarrrhea?
|
The rotavirus invasion of the epthelial cells of the small intestine results in destruction of the mature absorptive cells.
The damaged cells on villi are replaced by immature crypt cells that cannot absorb carbohydrates or other nutrients efficiently --> osmotic diarrhea |
|
What is frequently seen with active rotavirus infection?
|
Respiratory tract symptoms but with negative chest exams and radiologic studies
|
|
What is the antiviral therapy of choice for rotavirus infection.
|
There is none
Supportive care only via IV or oral rehydration therapy |
|
What is the incubation period of Norwalk virus?
|
24 to 48 hours, but most cases occur within 12 hours of exposure
|
|
Why are Noroviruses considered highly contagious?
|
An inoculum of as few as 10 viral particles may be sufficient to infect an individual
|
|
How are Noroviruses transmitted?
|
Primarily through the fecal- oral route or by direct person- person spread
|
|
What is the structure of Noroviruses?
|
NV is a spherical, nonenveloped virus
|
|
Describe the genome of Noroviruses
|
It has a positive sense, single-stranded RNA genome
|
|
How are Noroviruses visualized?
|
Human antibodies are needed to concentrate and visualize the Noroviruses.
|
|
How can an outbreak caused by Noroviruses be distinguished from other viruses?
|
1. The incubation period is 24 to 48 hours
2. Vomiting occurs in 50% or more of the cases 3. The duration of illnesses last from 12 to 60 hours 4.Diarrheal illness rapidly spreads among many individuals |
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What morphological changes are seen in the mucosa of the small bowel in a Norovirus infection?
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The biopsy should show shortening and atrophy of the villi, crypt hyperplasia,and infiltration of the lamina propria by PMN and mononuclear cells
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What is poorly absorbed as a result of a Norovirus infection?
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There is carbohydrate malabsorption
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