Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

62 Cards in this Set

  • Front
  • Back

what are most organs of the GI tract protected by?


organs involved in grinding food or providing digestive secretions

accessory digestive organs

which digestive structures are almost free of microbes? (3)




what helps prevent colonization of microbes in the digestive system?

peristalsis and the rapid transport of food

what is plaque?

-a biofilm composed of polysaccharide, protein, and lots of bacteria

how is plaque formed?

-begins with the colonization of tooth enamel by acidogenic bacteria

-co-aggregation of bacteria through carbohydrate-lectin interactions

what three things do you need to make plaque?

1) teeth

2) dietary sucrose

3) acidogenic bacteria

what do streptococcal enzymes do? what is a specific enzyme called?

polymerize glucose from dietary sucrose into dextran polymers. Dextransucrase

-long chains of glucose that cement bacteria to form plaque.

what are they also known as?

what is fluorine broken down into?



-gets made into organic acid

how does plaque formation lead to dental caries (cavities)? (4)

1) plaque formation

2) Streptococcus mutans, S. mitis, S. oralis, S salivarius, S. sanguis, and Lactobacillis produce acids (lactic acetic, formic, butyric) after metabolizing sugars. Plaque is not permeable to salica so acids are not diluted or washed away

3) acids demineralize the enamel and underlying dentin

4) decay progresses into pulp

how does plaque cause cavities?

saliva cant dilute the acid secreted by the plaque, resulting in acid eroding the enamel

how do you prevent the formation of plaque?

-use polymers to cover teeth blocking the binding sites of bacteria


how does fluoride prevent plaque formation?

-displaces the hydroxyl ions in hydroxyapatite

-reduces the solubility of tooth enamel because fluorapatite is more resistant to decay than hydroxyapatite

What is an example of periodontal disease?

Acute Necrotizing Ulcerative Gingivitis

causative agents of periodontal disease? (3)

-Porphyromonas gingivalis, Leptotrichia buccalis (gram negative rods)

-Treponema vinventii (gram negative spirochete)

process of periodontal disease?

1) with plaque formation bacteria colonize periodontal pockets at gum/tooth border

2) bacteria produce toxins and proteases

3) cause inflammation of gums (gingivitis) then bone destruction

4) loss of tooth possible

causative agent for Staphylococcal food intoxication?

Staphylococcus aureus (gram positive cocci)

key reservoirs for Staphylococcal food intoxication

nose and skin

transmission of Staphylococcal food intoxication (2)

-sneezing or coughing

-contact with boils or abscesses

characteristics of Staphylococcus aureus

-salt tolerant

-can grow over a broad temperature range (8-45 degrees celsius)

-found in meats (ham!), fish, dairy products

how is Staphylococcus aureus identified

grown on mannitol salt agar

difference between food infection and food intoxication

food infection: due to you eating a live bacteria. longer incubation time (1-3 days), so longer time to feel effects (Salmonella)

food intoxication: due to a bacteria making a toxin found on food. effects are almost immediate (30 minutes to 1 hour) (Staphylococcus aureus)

pathogenicity of Staphylococcal food intoxication

heat-resistant enterotoxin:

-30 to 100 degrees Celsius wont destroy it

-toxin binds to nerves in the intestine causing brain to send signals for vomiting and intestinal water secretion (diarrhea)

-toxin is tasteless

incubation time of staphylococcal food intoxication

1-6 hours

treatment and prevention of staphylococcal food intoxication

-no treatment

-prevention is proper hygiene

causative agent of cholera

vibrio cholerae (gram negative curved rod)

transmission of cholera

-water or food (raw oysters) contaminated with feces

symptoms of cholera (4)

-diarrhea (1L/hr)

-dehydration, cramps

-blood thickens, resulting in shock and eventually coma

-70% mortality

pathogenicity of cholera

-cholera toxin stimulates fluid loss

action of cholera toxin in intestine

1) cholera toxin binds to membrane of epithelial cell

2) portion of toxin enters cell

3) A1 is an enzyme that activates adenylate cyclase

4) Adenylate makes cyclic AMP (cAMP)

5) cAMP stimulates cell to secrete Cl-, Na+, and other electrolytes

6) Water follows electrolytes into lumen (diarrhea)

diagnosis of cholera

based on characteristic diarrhea

treatment of cholera (2)


-Oral Rehydration Solution: electrolytes and glucose

prevention of cholera

sewage and water treatment

is salmonella a food infection or intoxication?

food infection

examples of Salmonella? (2)

-Salmonellla enterica serotype Typhimurium

-Salmonella enterica serotype Enteritidis

transmission of Salmonella (3)

-poultry products, eggs (in ovaries of hens)

-cutting boards (fomites)

-live animals (Easter chicks and iguanas)

something that is inanimate that can transmit pathogenic organisms (not living)


symptoms of salmonella (salmonellosis)



-diarrhea (possible dehydration)

-abdominal cramps

-possible intestinal ulceration

what is the incubation period of salmonella (salmonellosis)

6-48 hours

pathogenicity/virulence factors of salmonella (salmonellosis) (4)

-inflammatory response to the bacterial infection increases fluid secretion

-type III secretion systems introduce toxins into host cells by pushing own membrane out and forming a point and then they stick in the human cell

-toxins disrupt mitochondria, inhibit phagocytosis (capsules), rearrange the cytoskeletons of eukaryotic cells or induce apoptosis

-flagella help them move well

-fimbriae let them stick to surfaces

transmission of E. coli diarrheas (2)

-improperly cooked ground meats (cold cuts, hamburgers)

-inadequately washed fruits and vegetables

pathogenicity of E. coli diarrheas

-low infectious dose, lots of toxins produced

-more than 100 serotypes

treatment of E. coli diarrheas

-antibiotics and rehydration

types of pathogenic E. coli (2)

-Enterotoxigenic (ETEC)

-Enterohemorrhagic (EHEC)

enterotoxigenic pathogenic E. coli characteristics

-bacteria penetrate intestinal epithelial

-makes enterotoxin which causes gastroenteritis, which results in traveler's diarrhea

enterohemorrhagic pathogenic E. coli characteristics and example

-O157:H7 strains cause bloody diarrhea, which results in hemorrhagic colitis

-can result in hemolytic uremic syndrome (HUS), kidney failure, coma, seizure, and heart attack

causative agent of antimicrobial-associated diarrhea

-Clostridium difficile

-gram postitive anaerobic spore-forming

symptoms of antimicrobial -associated diarrhea

-range from mild diarrhea to severe pseudomembranous colitis

more than 10 bloody stools a day

-lesions composed of connective tissue, dying leukocytes, dead colon cells

pseudomembranous colitis

pathogenicity of antimicrobial-associated diarrhea

-Toxin A: breaks down connectors between cells that are lining intestines( breaks down junctions holding cells of mucous membranes together), which leads to colitis and diarrhea

-Toxin B: kills the cells that have been loosened (intestinal cells) and those cells will induce the formation of dead cell fibrous material, which induces formation of pseudomembrane

treatment of antimicrobial-associated diarrhea

wiping out entire bacteria population and then doing a fecal implant (with good bacteria). this is stuffed into another person to repopulate the normal flora

causative agent of peptic ulcer disease

-Helicobacter pylori

- gram negative curved rod, microaerophilic

bacteria that can survive in the stomach


which scientist said that ulcers come from bacteria and not from what you eat?

Barry Marshall

transmission of Peptic ulcer disease

contaminated food and water

how many people are infected with peptic ulcer disease?

-affects 50% of the population

-2% are affected with ulcers

-1% are associated with stomach cancer

pathogenicity of peptic ulcer disease (3)

1) gets through mucus of stomach lining and attaches to stomach wall

2) Helicobacter pylori secretes urease

3) bacteria produce toxins and in combination with gastric acid causes ulcers

what does urease do? (3)

-digests urea

-makes ammonia

-neutralizes stomach acid (make it hospitable for the bacteria)

diagnosis for peptic ulcer disease (Heliobacter pylori)

-demonstrated by a positive urease test (biochemical test)

-urea breath test: ingest isotopically/radioactively labeled urea (carbon-13)

treatment of peptic ulcer disease (Heliobacter pylori)

-biaxin (clarithromycin)

-prilosec (omeprazole)

prevention of peptic ulcer disease (Heliobacter pylori)

-good hygiene

-adequate sewage treatment

-proper food handling

measures radioactive activity (if they breathe out samples that contain C-13, indication that the carbon dioxide is labeled with it and something in the stomach broke down urea)

Scintilation counter