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100 Cards in this Set
- Front
- Back
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Bacteria that cause disease w/o colonizing the intestine
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1. Staphylococcus Aureus
2. Clostridium Botulinum- Botulism 3. Bacillus Cereus- Food Poisoning 4. Clostridium Perfringens |
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Staphylococcus Aureus
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gram + coccus both anaerobic and aerobic few nutritional requirements. Coagulase-positive. Part of the nasopharynx resident microbiota. Causes disease through enterotoxins.
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Where does S. Aureus grow?
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food that is allowed to stand at room temp.
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When does S. Aureus produce enterotoxin?
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During active growth. The enterotoxin is then ingested along with the food.
The enterotoxin is heat stable resistant to acid and proteolytic degradation in the stomach and intestine.Once ingested the bacteria no longer add to the illness the enterotoxin that was produced prior to ingestion does all the work |
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What are the known immunological types of S.Aureus and which is most common in the US
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Types A, B, C, D, E, And G
Type A is most common in the US. |
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Symptoms of S. Aureus infection
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nausea, acute vomiting, severe abdominal pain, and diarrhea. Rapid onset and rapid resolution. symptoms begin about 1-6hrs after ingestion and last <24hrs.
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What type of enterotoxin is that of staphylococcal infections
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Superantigen
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Clostridium Botulinum- Botulism
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gram +, spore-forming, anaerobe ubiquitous to soil.
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What serotypes of botulinum toxin are most often associated with human disease in the US?
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Serotypes A & B
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Why does ingesting botulinum spores not cause disease?
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The bacteria can not compete with normal flora for nutrients so the spores never colonize to produce toxin. There what makes C.botulinum dangerous is the exotoxin it produces prior to ingestion.
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Why don't you feed babies honey?
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Honey contains botulism spores and while the spore don't cause disease in the adult, an infant has not developed the resident flora that will compete with botulinum and it will colonize the colon and cause infant botulism.
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How does BoTox kill you?
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1. Toxin is absorbed from intestine into blood stream
2. Binding portion binds to specific sialic acid containing glycoproteins and glycolipids found in neurons 3. the active portion is internalized and acts on neuronal vesicles to prevent acetylcholine release. 4 the active portion proteolytically nicks neuronal vesicle proteins called Synaptobrevins or SNARE proteins 5 the net effect is to stop nerve transmission in peripheral nerves causing a flaccid paralysis that affects the ability to breath and acts on essential organs like the heart. |
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What are the symptoms of botulism?
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Nausea, vomiting, headache, double vision, and slurred speech. Death is caused by the collapse of the respiratory system and heart failure.
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How are botulism spores killed?
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They are not killed by boiling. So you must use autoclave conditions (extream pressures) to attain temps high enough to kill the spores. Cases of botulism are usually associated with canned foods. Unlike S. Aureus C. botulinum toxin is NOT heat stable and boiling will inactivate it- so boil your canned foods before eating them!
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What is the treatment for botulism?
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Antibiotics are useless unless it is infant botulism because the bacteria isn't what is making you sick its the toxin produced prior to ingestion. So you need to administer an antitoxin to neutralize the toxin in the blood stream, and focus on maintaining respiratory and cardiac functions.
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Bacillus cereus
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1. Gram+
2.aerobic 3. Spore-forming rod found in soil |
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What are Bacillus spores resistant to?
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1. Heat and germinate if cooked food is left unrefrigerated.
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what food is most commonly involved with infection of B.cereus?
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Rice- bacteria growing in the cooked rice produce heat stable toxin.
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What are the symptoms of B.cereus?
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Vomiting but NOT diarrhea. The onset of symptoms is rapid and sumptoms disappear w/i 24h.
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B. cereus can cause another type of toxin- this second less common type is associated with what food?
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contaminated meat vegetables or sauces. In this case the bacteria are ingested and produce a diarrheal toxin in the intestinal tract. colonization is NOT involved. The diarrheal toxin is very similar to cholera toxin which prevents the absorption of water.
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Clostridium perfringens
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1. Spore forming
2. anaerobe- relatively oxygen tolerant 3. Bacteria germinate and grow in food.- But produce little or no toxin |
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When does C. perfringens start to grow spores?
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When it enters the stressful situation of the stomach.
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How do the spores of C. perfringens cause disease?
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The spores, while in the stomach, begin to produce enterotoxin that acts on the small intestinal mucosal cells and causes them to lose water (Secretory Diarrhea). The spores are excreted so the diarrhea subsides as soon as the toxin produced during sporulation exerts its effect.
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What food is most commonly associated with C.perfringens?
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Cooked meats.
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What are the symptoms of C. perfringens?
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begin 8-12h after ingestion include diarrhea and abdominal cramping. Symptoms subside spontaneously after a day. Only in malnourished infants will a more serious case be seen in which serious damage to the mucosa is seen.
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What other diseases is C. perfringens associated with?
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they produce 11 different toxins and exoenzymes that are associated with other more serious SKIN diseases such as gas gangrene.
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Helicobacter pylori
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1. Gram -
2. spiral shapped 3.Microaerophilic and fastidious |
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What chronic side effect does infection by H.pylori cause?
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Chronic superficial gastritis
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What does H. pylori cause?
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1.gastric and duodenal ulcers
2. Chronic atrophic gastritis and gastric adenocarcinoma |
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Why are some people more likely than others to developed ulcers due to H.pylori?
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1. stress
2. Inflammatory response of the immune system- So ppls immune system will continue to try and eradicate the bacterium thus causing a prolonged inflammatory response. This prolonged response produces the ulcer. |
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What unusual ability does H. pylori have and how does it do it?
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It is able to colonize the gastric mucosa. H. pyloris is killed by acid but is able to survive the acidic environment of the stomach by producing UREASE, an enzyme that cleaves urea to produce CO2 and NH3. Ammonia is able to neutralize the acid environment immediately surrounding H. pylori. This ammonia cloud protects H.pylori until it is able to reach the protected mucus layer and use its adhesins to colonize the mucosal epithelial cells.
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What are Helicobacter's virulence factors?
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1. Toxin VacA- targets mitochondria and induces apoptosis.
2. Type IV secretion system(highly virulent strains)- Cag- directly injects bacterial proteins into host cytoplasm.This allows Helicobacter to enter the epithelium 3. its O antigen is similar to our Lewis antigens that are present in glycolipids and glycoproteins- this mimicry fools our immune system into recognizing H. pylori as self so we never actually get rid of it. |
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How is H.pylori diagnosed?
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biopsy, blood testing for antibodies, urease breath test.
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How is H.pylori treated?
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10-14 day triple therapy including:
1.proton pump inhibitor- aid healing and protect the antibiotics from acid inactivation 2. clarithromycin 3. Amoxicillin or metronidazole |
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How do you get Cholera?
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Water contaminated with feces or contaminated shellfish.
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What are the symptoms of Cholera?
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Severe abdominal pain and massive diarrhea losing 15-20 liters of water a day!! Dehydration can lead to collapse of the circulatory system and death.
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Vibrio cholerae
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1. gram -
2. comma-shaped rods 3. free living in salt water organisms- Ubiquitous in the ocean 3. Human specific pathogen |
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Where does Vibrio Cholera colonize?
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The small intestine. It is motile and has specific pilus that allows it to adhere to the small intestinal mucosa and to itself. As it grows V. cholera produces and Exotoxin (cholera toxin) that is responsible for the symptoms
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What type of toxin is Choler toxin and how does it work?
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(1)A-B(5) type toxin
B portion binds to glycolipids that contain sialic acid Gm1 on the surface of mucosal cell. The A subunit enters the cell and ADP-ribosylates a G-protein, Gs, that controls levels of host adenylate cyclase, keeping it in the ON position producing high levels of cAMP. This messes with the ion pumps and ensures that the direction of water from is from the tissues to the lumen. |
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how do you treat cholera?
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Cholera is self limiting, so all you do is rehydration therapy with a solution containing glucose and salt. The massive diarrhea will wash the bacteria out of the intestinal tract.
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What serotype of cholera has been responsible for most of the pandemics?
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O1
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what is the new V. cholerae strain that does not have the O1 serotype?
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O139- this strain can infect people who are immune to O1.
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What causes travelers diarrhea?
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Enterotoxigenic E.coli or ETEC
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what causes childhood diarrhea in developing countries?
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Enteropathogenic E.coli or EPEC
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What kind of Diarrhea does ETEC cause?
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secretory diarrhea similar to that of V. cholerea. Produce a pili that allow them to adhere to and colonize the surfaces of small intestinal mucosal cells.
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ETEC bacteria growing in the small intestine produce 2 diarrheal toxins what are they?
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1. Heat liable protein toxin- LT- same mechanism of action as V. cholerae(increase cAMP) but not as efficient
2. Heat stable peptide toxin- ST- Two types STa and STb they are short peptides and this is why they are heat stable- STa increases cGMP levels |
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What type of toxin does EPEC produce?
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TRICK QUESTION!! EPEC does NOT produce any known enterotoxins. Instead it causes MALABSORPTIVE diarrhea by adhearing to mucosal tissue and using a TYPE III secrection sustem to elicit changes in host cell cytoskeleton and physiology. This affects the mucosal cell's ability to absorb water.
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How do you treat ETEC AKA travelers diarrhea?
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Rehydration therapy, some pepto (Bismuth containing product)- But be careful with antidiarrheal medications because they can prolong the infection. Remember the diarrhea is the limiting agent it washes out the bugs.
For infants rehydration therapy is life saving! |
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What causes bacterial gastroenteritis?
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A group of gram - bacteria. that invade the mucosa and underlying tissue.
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What are the symptoms of gastroenteritis?
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diarrhea, malaise, fever, and abdominal pain that is severe enough to mimic appendicitis.
Bacterial interaction with the mucosa and mesenteric lymph nodes causes inflammatory response that is responsible for the fever and abdominal pain. |
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What is a common side effect gastroenteritis?
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Reactive Arthritis elicited by circulating baterial antigens rather than by infection of the joints. usually subsides but for some it may become permanent.
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What are the two species of Salmonella?
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Salmonella bongori(rare) and Salmonella enterica(causes gastroenteritis and typhoid fever) .
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Which subdivision of Salmonella enterica infects the ovum of a hen prior to the formation of the shell?
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Salmonella enteritidis
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Virulence Factors for S. typhimurium
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Major hallmarks: ability to invade the intestinal epithelium and the ability to survive in macrophages.
1. Uses pili to colonize the small intestine 2. Uses type III secretions to inject SPI-1- causes actin rearrangement in the eukaryotic cell and engulfment of the bacteria. 3.SP1-2- allows it to live in macrophages 4. resistance to reactive forms of O2 5. Resistance to defensins. 6. Serum resistant |
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What is the most important point of entry for S.typhimurium?
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M cells of the Peyers patches. The bacteria then grow in the Peyers patch and drain into the local mesenteric lymph nodes.
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What is important of the SPI-2 type III secretion system of S. Typhimurium?
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It is what allows S. typhimurium to reside in macrophages.
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Where does each SPI system of S. typhimurium work?
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SPI-1= only in the Peyer's patch
SPI-2= only in the macrophages. |
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S. typhimurium symptoms
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self limiting gastroenteritis: with fever nausea vomiting diarrhea and cramps.
Blood in the stool is not uncommon. Can be more severe resulting in bacteremia or death. |
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How do you treat S. typhimurium
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usually antibiotics are not needed unless you get a severe infection then it must be treated and use rehydration therapy.
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What is DT104?
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New highly virulent salmonella strain.
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What is clinically important about S.typhimurium ?
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favored for the production of live vaccines.
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Campylobacter
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1. Gram -
2. motile 3. curved rod 3. microaerophile- low O2 4. Does not ferment glucose 5. similar to H.Pylori but does NOT produce Urease. |
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How do you kill Campylobacter?
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Cook your food
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Where does Campylobacter colonize
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the small intestine mucosa.
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Symptoms of Campylobacter?
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diarrhea, vomiting, fever and abdominal pain. may have blood in stool.
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How do you treat Campylobacter?
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In severe cases erythromycin. Fluid replacement is usually sufficient.
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C. jejuni is associated with what other disease?
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Guillian- Barre syndrom- an autoimmune mediated polyneuritis with progressive muscular weakness that occurs 2-3 weeks after the diarrheal infection.
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Yersinia enterocolitica
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1. Motile
2. Gram - 3. rod |
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What do you eat that gives you Y. eterocolitica?
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contaminated milk and meat.
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Symptoms of Y. enterocolitica?
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acute abdominal pain which may or may not be accompanied by diarrhea. Mimic appendicitis.
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Y. enterocolitica virulence mechanism
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binds to integrin receptors and invade eukaryotic cells usig a paticular protein termed Invasin. Prevents phagocytosis using type III secretion system to inject phagocytes and kill them.
It can grow at refrigerated temperatures |
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Vibrio parahaemolyticus.
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found in marine environments. Similar to V. cholerae except that it requires high NaCl concentration for growth.
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V. paraheamolyticus Virulence factors
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produces a hemolysin.
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V. paraheamolyticus symptoms
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fever pain diarrhea big freaking surprise there guys. you get it from eating raw fish!
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Dysentery
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Bloody stool.Can be caused by Y. enterocolitica and S. typhi or EIEC (eteroinvasive E.coli)
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What is hemolytic uremic syndrome (HUS)
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Acute inflammation that can lead to irreversible kidney damage and kidney failure. Most common in children.
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Shigella species
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they are sub strains of E.coli. highly infectious. Resistant to dying in the stomach. Important cause of infant death and dysentery.
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Shigella infection mechanism
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enter through Peyer's patch of the lower small intestine. survive ingestion of the peyer's patch macrophages. then infect adjacent mucosal cells. Host cell receptors for Shigella invasin complex are B1 integrins found on basal surface.
Shigella uses a type III secretion system to induce uptake by normally non phagocytic epithelial cells. They replicate in the the nutritionally rich cytoplasm. they use this method to spread from cell to cell until they reach the colon. |
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Does Shigella Spp cause systemic infections
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no they are unable to survive long enough in the blood to do so.
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what toxin does Shigella dysenteriae form?
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Shiga toxin duh!
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What disease does Shiga toxin cause
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HUS- shiga toxin that is floating in the blood stream enters the kidneys and causes damage to vascular tissue in the kidneys.
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What type of toxin is Shiga toxin?
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A-B type toxin
A: cleaves an N-glycosidic bond of 28s rRNA of host cell ribosomes causing a shut down in protein synthesis. |
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E.coli O157:H7 produces what toxin?
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shiga-like toxin. E.coli that produce this strain are termed EHEC- enterohemorrhagic E. coli. Can also cause HUS
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how is EHEC different than shigella spp?
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They are non invasive. they use a type III secretion system to form pedestal like structures on the colonic epithelial cells identical to that seen in EPEC infections. But they cause dysentery rather than just malabsorptive diarrhea.
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Treatment for EHEC?
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oral rehydration and supportive care to let the infection clear itself out. DONT use antibiotics because they make HUS worse.
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How do you get and infection of C. difficile?
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You get treated with antibiotics that kill your resident flora and allow it to colonize the intestine.
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C. diff
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Spore forming anaerobe
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What exotoxins are produced by C.diff
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A and B. they act synergistically to cause the symptoms of the disease.
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Symptoms of C.diff
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diarrhea caused by toxin A acting on colonic mucosa. Damages tissue directly and by attracting phagocytes. B alone des not cause damage. But together the damage is so severe that they end up forming large mats of material called a pseudomembrane. It will cause ulcerations of the colon that lead to septic shock
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treatment of C. diff
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Vancomycin and metronidazole.
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How do you diagnose C. diff
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Latex agglutination test to detect toxin A and B in the stool.
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Listeriosis monocytogenes
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1. Gram +
2. Non spore forming 3. facultative 4. Highly motile rod 5. highly invasive. 6. Uses hemolysins to escape phagocytic cells. |
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Who are the main victims of L. monocytogenes?
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neonates, elderly and pregnant women and patients with defective cell mediated immunity.
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progression of L. monocytogenes infection
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invades intestinal mucosa then spreads to the circulation where it spreads to all parts of the body. Normally our immune system handles it but when it doesn't it causes infections of the CNS
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What is an unusual property of L. monocytogenes?
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It can cross the placenta. And pregnancy can predispose you to the infection.
And grows at refrigerated temps. |
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Typhoid Fever
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Caused by S. typhi causes a systemic infection
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S.typhi vs S. typhimurium
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systemic localized/self limiting
human specific found in animals also dont cause gastroenteritis |
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S. typhi infection process
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after multiplying in the submucosal area enters blood stream and spreads to other organs notably the liver and spleen where it continues to multiply. from the liver and spleen back to blood where LPS of S. typhi produces septic shock.
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Symptoms of typhoid fever
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fever chills anorexia and delirium. Will also spread to the gall bladder. Can shed typhi for years after recovery.
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treatment of typhoid fever
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antibiotics- chloramphenicol and ampicillin .
There is a vaccine against typhoid fever but protection rates are variable. |
