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60 Cards in this Set

  • Front
  • Back
What is Listeriosis?
Listeriosis is caused by Listeria monocytogenes, which is a gram-positive rod isolated from soil, vegetation, and many animal reservoir.
Where does L. monocytogenes generally occurs to?
L. monocytogenes generally occurs in pregnancy and in people who are immunosuppressed due to illness and medication.
Where is L. monocytogenes attibutable to?
It is a food-borne transmission traced to sources such as contaminated milk, soft cheeses, vegetables, and meat.
What are the symptoms of L. monocytogenes?
It doesn't cause gastrointestinal illness; however, it causes invasive symptoms such as meningitis, sepsis and still-birth.
Is L. monocytogenes an intracellular pathogen?
Yes, a characteristic consistent with its predilection for causing illness in persons with deficient cell-mediated immunity
How does L. monocytogenes invade in an immunosuppressed individual?
In immunosuppressed individual, invasion, intracellular multiplication, cell-to-cell spread of the bacterium appears to be mediated by proteins called internalin, hemolysin listeriolysin O, and phospholipase C.
How does listeria move within and between cells?
Listeria uses host cell actin filaments to move within and between cells.
Why is there an increased risk of infection in pregnant women for listeria?
The increased risk of infection in pregnant women may be due to both systemic and local immunological changes due to pregnancy. Ex. local immunosuppression at the maternal-fetal-interface at the placenta may facilitate intraurine infection.
How is listeriosis diagnosed?
Diagnosis is by culture of the bacterium.
What is the treatment for listeriosis?
Treatment is intravenous administration of either penicillin or ampicillin.
What is the frequently known serovars from human for Salmonellosis?
Typhimurium and Enteriditis
What is salmonellae?
Salmonellae are gram-negative, non-motile, nonspore forming.
What is the initial source of salmonellae?
Initial source is from the intestinal tract of pigs and other animals.
How does human acquire salmonellae?
Human acquire the bacteria from contaminated food such as beef products, poultry products, eggs, and egg products.
What is the incubation time of Salmonellae.
Incubation time is 8 to 48 hours.
How many cases of salmonella is reported in the U.S? worldwide?
45,000 cases are reported in the U.S., but as many as 2 to 3 million cases annually worldwide.
Why is salmonellosis considered to be a true food-borne infection?
It's considered a true food-borned infection because the bacteria multiply and invade the internal mucosa, where they produce an enterotoxin and cytotoxin, which destroy the ephithelial cells.
What are the symptoms of salmonellosis? How long does it normally last?
Prominent symptoms includes abdominal pain, cramps, diarrhea, nausea, vomiting, fever, which normally last for 2-5 days, but can last up to several weeks.
Why does salmonellosis causes problems to children and elderly.
Due to losss of fluids.
How is salmonellosis get diagnosed?
Laboratory diagnosis is by isolation of bacterium from food or from patient's stools.
What is the treatment for salmonellosis?
Treatment is with fluid and electrolyte replacement.
How do we prevent salmonellosis?
Prevention depends on good food-processing practices, proper refrigeration, and adequate cooking.
What is the cause of Typhoid fever?
Salmonella enterica serovar Typhi
How do we acquire Typhoid fever?
Typhoid fever is acquired by ingestion of food and water contaminated by feces of infected human or person-to-person contact.
What is the milder form of Typhoid fever?
A milder form of tyhpoid is parathypoid fever, which is caused by Paratyphi A, B, C of Salmonella enterica subspecies enterica.
What is the incubation period of typhoid bacteria in the small intestine?
In the small intestine, incubation period is about 10-14 days.
How does Typhi works and what are its symptoms?
The bacteria colonize the small intestine, penetrate the epithelium and spread to lymphoid tissue, blood, liver and gall bladder. Symtoms include fever, headache, abdominal pain, anorexia, and malaise, which last for several weeks. Bacteria then reinfect the gastrointestinal tract, causing abdominal pain and diarrhea.
When does most individual, with Typhoid fever stop shredding the bacterium in their feces?
After approximately 3 months, most individuals should stop shredding bacteria in their feces. Although few individuals may still shed S. Typhi for extended period of times, but will show no symptoms. These carriers, the bacteria will continue to grow in the gallbladder and will reach the intestine through the bile duct.
How does typhoid fever get diagnosed?
Laboratory diagnosis of typhoid fever is by demonstration of typhoid bacilli in the blood, urine or stools and serology (Widal test)
What is the treatment for typhoid fever?
Treatment is with ceftriaxone and ciprofloxacin has reduced mortality rate to less than 1%.
What are the most prophylactic measures of typhoid fever?
Purification of drinking water, prevention of food handling by carriers, and complete isolation of patients.
How many cases of typhoid fever occur annually in U.S.
300 to 400 cases annually.
What is shigella?
Shigella is a gram-negative, non-motile, nonspore forming, facultative rods.
What is shigellosis?
Shigellosis or bacillary dysentery is a diarrheal illness due to acute inflammatory reaction of the intestinal tract caused by the four species of the genus Shigella.
How many cases are reported in the U.S? How many deaths are reported worldwide?
About 20,000 to 25,000 cases are reported in the U.S, around 600,000 deaths a year worldwide.
What are the usual pathogen for shigellosis?
Shigella is restricted to human host. S. sonnei and S flexneri are the most common.
How does the organism shigella get transmitted?
Shigella is transmitted by fecal-oral route. The 4Fs - Food, Fingers, Feces, Flies
What age group is shigellosis most prevalent?
Most prevalent in children 1-4 years old
What is the infectious dose of shigella?
Infectious does is around 10-100 bacteria.
Where is shigellosis a problem in the U.S.?
Shigellosis is a problem in daycare centers and custodial institutions in the U.S, where there is overcrowding.
How does shigella works?
Shigella are facultatively anaerobic, intracellular parasites that multiply within the vilus cells of the colon ephithelium. The bacteria induce the Peyer's patch cells to phagocytose them. After being ingested, the bacteria disrupt the phagosome membrane and are release into the cytoplams, wherey they reproduced. They invade adjacent mucosal cells. Shigella initiate an inflammatory reaction in the mucosa - both endotoxins and enterotoxins may participate, but the bacteria do not usually spread beyond the colonic epithelium.
What are signs and symptoms of shigella?
Watery stools often contain blood, mucus, and pus. In severe cases, colon can be ulcerated.
How does shigella works?
Shigella are facultatively anaerobic, intracellular parasites that multiply within the vilus cells of the colon ephithelium. The bacteria induce the Peyer's patch cells to phagocytose them. After being ingested, the bacteria disrupt the phagosome membrane and are release into the cytoplams, wherey they reproduced. They invade adjacent mucosal cells. Shigella initiate an inflammatory reaction in the mucosa - both endotoxins and enterotoxins may participate, but the bacteria do not usually spread beyond the colonic epithelium.
What does virulent Shigella produce?
Virulent shigella produce a heat-labile AB enterotoxin known as shiga-toxin (Sxt) - formerly verotoxin.
What are signs and symptoms of shigella?
Watery stools often contain blood, mucus, and pus. In severe cases, colon can be ulcerated.
What does virulent Shigella produce?
Virulent shigella produce a heat-labile AB enterotoxin known as shiga-toxin (Sxt) - formerly verotoxin.
What is a complete toxin of shigella molecule composed of?
The complete toxin molecule is composed of one A protein and surrounded by five B proteins.
What does the B proteins for shigella do?
The B proteins attach to the host vascular cells, stimulating the internalization of the whole toxin.
What is a complete toxin of shigella molecule composed of?
The complete toxin molecule is composed of one A protein and surrounded by five B proteins.
What does the subunit protein do?
A subunit protein is subsequently released from B protein units and binds to the host ribosomes, inhibiting protein synthesis.
What does the B proteins for shigella do?
The B proteins attach to the host vascular cells, stimulating the internalization of the whole toxin.
What does the subunit protein do?
A subunit protein is subsequently released from B protein units and binds to the host ribosomes, inhibiting protein synthesis.
What is the specific target for B proteins?
The specific target for B proteins is the glomerular endothelium. Toxin actions on these cells causes kidney failure.
What does pathogenic shigellae use to deliver virulence factors to target epithelial cells?
Pathogenic shigellae uses type III secretion system to deliver virulence fact to target epithelial cells.
What is the specific target for B proteins?
The specific target for B proteins is the glomerular endothelium. Toxin actions on these cells causes kidney failure.
What does pathogenic shigellae use to deliver virulence factors to target epithelial cells?
Pathogenic shigellae uses type III secretion system to deliver virulence fact to target epithelial cells.
What is type III secretion machinery in pathogenic shigellae?
It is responsible for delivering to host cells the specific protein components required for its invasion
What is type III secretion machinery in pathogenic shigellae?
It is responsible for delivering to host cells the specific protein components required for its invasion
What does type III bacterial secretion system in pathogenic shigellae do?
Type III bacterial secretions system is specialized for the direct export of virulence factors into target host cells.
What does type III bacterial secretion system in pathogenic shigellae do?
Type III bacterial secretions system is specialized for the direct export of virulence factors into target host cells.