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144 Cards in this Set
- Front
- Back
Shape of helicobacter?
Get nutrition? |
gram negative
spiral shaped Ferment amino acids, but do not ferment or oxidize carbs |
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What are the three species of helicobacter that infect humans?
|
H. Pylori
H. cinaedi H. fennelliae |
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H. Pylori pathogenesis?
|
lives in mucous gel that coats gastric mucosa and or between mucous layer and epithelium
may attach to gastric epithelium Produces large amounts of urease bacterial surface factors attract neutrophils and monocytes that contribute to epithelial cell injury Bacterial proteases and phopholipases break down mucous gel that shields gastric epithelium from acid Host inflammatory response causes additional gastric epithelial damage but doesn't resolve infection -- ulcers |
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Virulence factors of H. Pylori?
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Cag A (cytotoxin associated gene protein)
Vac A (vacuolating cytotoxin) Pic B (induces cytokine production) |
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Why does H. pylori produce urease?
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catalyzes breakdown of urea
local neutralization of acid allows survival of bacteria NH3 damages epithelial cells |
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What leads to ulcers in H. pylori?
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combo of toxins, inflammatory responses and exposure to acid
|
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What is gastritis and what causes it?
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H. Pylori
infliltreation of neutrophils and mononuclear cells into gastric mucosa acute: feeling of fullness, nausea, vomiting, decreased acid production in stomach may develop into chronic |
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What is peptic ulcer disease and what causes it?
|
H. pylori
Ulcers develop at sites of intense inflammation --> - junction between corpus and antrum - gastric ulcer - proximal duodenum - duodenal ulcer Epigastric pain randing from ill-defined sensation like hunger pain to burning, gnawing discomfort. - relieved by antacids or eating with duodenal ulcers - may be exacerbated by eating with gastric ulcers |
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What does chronic gastritis normally lead to?
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replacement of normal mucosa with fibrosis and proliferation of intestinal type epithelium
this increases risk of gastric adenocarcinoma |
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H. pylori is also associated with infiltration of what kind of tissue into gastric mucosa?
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lymphoid tissue
Monoclonal population of B cells develops in small percentage of pts may evolve into MALT lymphoma |
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Shape of salmonella?
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gram negative rod
enterobacteriaceae |
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Pathogenesis of salmonella enterica
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Attach to intestinal mucosa and invade into microfold cells (M cells) in Peyer patches
Replicate within endocytic vacuoles Can be released into blood or lymphatic circulation Invasion process regulated by genes located in two pathogenicity islands Inflammatory response confines most infections to GI tract Inflammatory response also: - mediates release of prostaglandins - stimulates cAMP production and fluid secretion into lumen (diarrhea) |
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What is gastroenteritis? Caused by?
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Salmonella enterica
Incubation period: 6-48 hrs Nausea, vommiting, diarrhea (loose, non-bloody) Low grade Fever, abdominal cramps, headache, and myalgias also common Usually self-limiting (resolving in 3-7 days) Neonates, elderly and IC pts susceptible to dehydration, disseminated infections |
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What are some of the localized infections that result from bacteremia as a result of salmonella?
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Endovascular infections (arteritis, endocarditis)
Intraabdominal infections (rare) Meningitis (mostly in infants) Pulmonary infections Bone and joint infections Reiter's syndrome |
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What are the different types of salmonella?
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Salmonella enterica - gastroenteritis
S. Typhi - typhoid fever S. paratyphi - paratyphoid fever others. |
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Pathogenesis of S. typhi and paratyphi?
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Pass through cells lining intesting and engulfed by macrophages
Replicate after being transported to bone marrow, speen, liver Colonize gall bladder and re-infect intestines |
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Transmission of S. typhi and paratyphi?
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food contaminated by infected food handler or water contaminated with fecal material
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Enteric fever? Caused by?
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S. typhi and paratyphi
also called typhoid fever, paratyphoid fever Incubation: 10-14 days Most prominent symptom: prolonged fever which may last for 4 weeks if not treated Headache, myalgias, malaise, anorexia common Rash is an early finding (rose spots) Hepatosplenomegaly |
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Symptoms of severe enteric fever? Caused by?
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S. typhi, paratyphoid fever
Gastrointestinal bleeding and intestinal perforation can develop in 3rd or 4th week Possible neurologic manifestations: meningitis, GB syndrome, neuritis |
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Shape of shigella?
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gram negative rod
enterobacteriaceae |
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What are the four GI pathogens of Shigella?
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Dysenteriae
Flexneri Boydii Sonnei |
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Pathogenesis of shigella?
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attach to and invade M cells in Peyer Patches
lyse phagocytic vacuole and replicate in cytoplasm Invasion proceeds via cell-to-cell passage Bacteria can induce apoptosis |
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Shigella: how does the invasion of the pathogen work? (mechanism)
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cell-to-cell passage
Rearrangement of actin propels bacteria --> cytoplasm to adjacent cells (move directly from one cell to another) Allows bacteria to avoid AB related clearance |
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Shigella: how does bacteria induce apoptosis?
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release of IL-1B--> attracted of PMNs --> intestinal wall destabilization --> bacterial invasion of deeper epi cells)
|
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Which strain of shigella uses Shiga toxin?
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Dysenteriae
Similar to EHEC Cleaves 28S rRNA in 60S subunit of ribosomes; disrupts protein synthesis Primary effect: damage to intestinal epithelium In small % of pts: damage to glomerular endothelial cells --> renal failure (HUS) |
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Populations that Shigella affects?
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Peds
Homosexuals (males) |
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Transmission of Shigella?
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person to person by fecal-oral route
- primarily on contaminated hands - less often in contaminated food or water |
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What is Shigellosis?
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caused by Shigella
Incubation: 1-4 days Typical initial manifestations: transient fever, limited watery diarrhea, malaise, anorexia - range from mild discomfort to severe cramps, diarrhea, fever, vomiting, tenesmus (straining to defecate) - symptoms often more severe in children than in adults May resolve or go to dysentery stage |
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What is the dysentary stage of shigellosis?
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Acute collitis (mainly in distal colon and rectum)
Small volumes of bloody, mucopurulent stools Increased tenesmus and abdominal cramps Most cases self-limiting |
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What are the potential complications of Shigellosis?
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Toxic megacolon: severe inflammation extends to colonic smooth-muscle layer --> paralysis and dilation
Hemolytic uremic syndrome |
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Shape of Vibrio?
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gram negative curved rods
|
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What are the medically important species of vibrio?
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Cholerae (different serotypes) (water/food)
Parahaemolyticus (shellfish/seawater) Vulnificus (shellfish/seawater) |
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Virulence factors for Vibrio cholerae.
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Lysogenic bacteriophage CTXO encodes:
- Cholera toxin - accerssoy cholera enterotoxin: increases intestinal fluid secretion - zonula occludens toxin: increases intestinal permeability - chemotaxin proteins: adherence to intestional mucosa Adherence to intestional mucosa Bacteria does not invade epitheliuml just attaches to surface and excretes toxins |
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What does the V. Cholerae cholera toxin do?
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A-B exotoxin binds to intestinal epithelial cells
causes increase in levels of intracellular cAMP Hypersecretion of water and electrolyes |
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Accessory cholera enterotoxin - bacteria and what does it do?
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V. Cholerae
increases intestinal fluid secretion |
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Zonula occludens toxin - bacteria and what does it do?
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V. cholerae
increases intestinal permeability |
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Chemotaxis proteins - bacteria and what does it do?
|
v. cholerae
adherence to intestinal mucosa |
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Transmission of V.cholerae?
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contaminated food and water
|
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What is cholera?
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V. Cholerae
Incubation: 24-48 hours Sudden onset of painless watery diarrhea that soon becomes voluminous -Characteristic gray, cloudy fluid with flecks of mucous and no blood (rice-water stool) - Somewhat sweet, inoffensive odor Diarrhea often followed shortly by vomiting Rapid and dangerous dehydration without fluid and electrolyte replacement |
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Shape of clostridium? Nutrition?
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gram POSITIVE
spore forming rods Mostly stricy obligate anaerobes |
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Species of clostridium important for humans?
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Difficile
Perfringens tetani botulism |
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Virulence of C. difficile
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Enterotoxin (toxin A)
Cytotoxin (toxin B) Bacterial surface layer proteins (SLPs) |
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What does enterotoxin (toxin A) in C.difficile do?
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stimulates infiltration of ileum by PMNs and release of cytokines
Disrupts tight cell-cell junctions (increased permeability of intestinal wall --> diarrhea) |
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What does cytoxin (toxin B) in C.difficile do?
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depolymerizes actin, causes destruction of cytoskeleton, damage to intestinal epithelium
|
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What does SLPs in C.difficile do?
|
bacterial surface layer proteins
facilitate binding to intestinal epithelium |
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what is pseudomembranous colitis and what is it caused by?
|
C. difficile
pseudomembranes develop on colonic mucosa 1-2 mm whitish-yellow plaques (contain fibrin, mucous and inflammatory cells); converge and become confluent Abdominal cramps, fever, and leukocytosis May lead to toxic megacolon etc |
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Basic characteristics of hepatitis viruses
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Hep A - infectious Hep
Hep B - serum hepatitis Hep C - Non-A, Non-B post transfusion hep Hep D - Enteric non-A, non-B hep |
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Which Heps have envelope?
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B, C,D,G
|
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Which Heps have + sense ss-RNA genomes?
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A, C,E,G
|
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Hep A and E pathogenesis
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Hit and Run
Replicate in hepatocytes and Kupffer cells (released by exocytosis) Large numbers of virions shed in stool 10 days before any obvious symptoms develop or ABs can be deteected (virions --> bile ducts --> intestines) Liver pathology probably caused primarily by immune responses |
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What is the clinical presentation of Hep A and E?
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Milder in children than adults
Incubation period 15-50 days Initial symptoms (fever, fatigue, nausea, abdominal pain, loss of appetitie) occur abruptly and intensify for 4-6 days Icteric phase: jaundice, dark urine, pale stools Complete recovery in 2-4 weeks |
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Hep B pathogenesis
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Replicates in hepatocytes with little cytopathic effect (released by exocytosis; not cytolytic)
Infection progresses slowly over relatively long time; can take 45 days or longer for symptoms to develop Cell-mediated immunity, inflammation --> symptoms, but also work to resolve infection (highly effective but with severe symptoms) Insufficient T cell response may lead to mild symptoms but inability to resolve infection and chronic disease) Infections may be acute or chronic, symptomatic or asymptomatic |
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Clinical presentation of Acute Hep B infection
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Less severe in children
Long incubation period Subtle onset of symptoms Prodormal period Icteric period Fulminant hep develops in 1% of icteric pts |
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Clinical presentation of Chronic Hep B infection
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Occurs in 5-10% of HBV infections
there is chronic active and chronic passive |
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Three types of Hep C diseases?
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Acute
Chronic Persistent infection - initial disease asymptomatic - usually progresses to chronic active disease in 10-15 yrs Severe, rapid progression to cirrhosis |
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What is Hep D?
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Delta agent
Incomplete virus that replicates and causes disease only in people with active HBV infections -uses HBV and target cells proteins to replicate Increases likelihood of fulminant hepatitis Chronic infections possible |
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Rotavirus: enveloped? genome?
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Non-enveloped
ds RNA |
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Pathogenesis of rotavirus
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Diarrhea
Replicates in columnar epi cells covering villi of small intestine Mucosal damage leads to malabsorption which leads to a net secretion of water and loss of ions = diarrhea |
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Transmission of rotavirus?
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fecal-oral
survives well on fomites |
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Diseases that rotavirus can cause
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Gastroenteritis
|
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what is cryptosporidium?
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protozoan parasite with worldwide distribute
|
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What are the species of cryptosporidium that infect humans?
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C. parvum and C. hominis
|
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Transmission of cryptosporidium?
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fecal oral
oral anal |
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cryptosporidium pathogenesis
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invasion of tissues limited to epithelium
not alot known about it |
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What is cryptosoridiosis? Caused by?
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cryptosporidium
presentation in IC hosts: Incubation period 1 week Watery diarrhea some cases have prodome Illness usually subsides in 1-2 weeks Clinically significant dehydration Biliary tract involvement can cause midepigastric or upper right quadrant pain |
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Life cycle of the pinworm
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Ingestion of embryonated eggs starts infection
Larvae hatch in small intesting, migrate to large intestine, and mature into adults. Fertilized females migrate to perianal area at night and deposit eggs in folds of skin there The eggs mature rapidly and become infectious within a few hours. |
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What is enterobiasis? Caused by?
|
Pinworm
Severe pruritus in people allergic to worm secretions Many asymptomatic |
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What are strongyloides?
|
infection form of the filaiform larvae penetrate human skin, enter circulatory system and migrate to lungs
larvae coughed up from lungs and swallowed, then develop into adults in small intestine adult females burrow into mucosa of duodenum and produce eggs Eggs hatch in mucosa and release rhabditiform larvae which is passed in stool |
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Direct infection cycle of strongyloides
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Free rhabditiform larvae develop into infectious filariform larvae
invade through skin of new host |
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Indirect infection of strongyloides
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free living adult worms live in soil and produce eggs and larvae
may lead to several generations as free living organisms before invading through skin of new host |
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What two pathogens cause gastroenteritis in a very short incubation period? (2 hrs)
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Staph aureus
Bacillus Cereus (most often associated with fried rice) |
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Food poisoning on Florida's Gulf coast suggests?
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Vibrio parahemolyticus
|
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How does Vibrio parahaemolyticus get into food?
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commonly present in marine and esturaine environments
can easily contaminate shellfish and other types of seafood Filter feeders (like oysters) actually concentrate Vibrio and other bacteria in their bodies (E.Coli, Hep A, Polio etc) Disease occurs when contaminated seafood is eaten raw or undercooked |
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What is kanagawa hemolysin? What pathogen does it belong to?
|
toxin of V. Parahaemolyticus
increases intracellular Ca in GI epithelial cells increase Ca leads to Cl secretion and loss of water (different from cAMP mechanism) |
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What is indicated by the combination of fever with fecal leukocytes and RBCs?
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an inflammatory diarrhea (as opposed to toxin-related food poisoning)
|
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Shape of campylobacter jejuni?
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small, comma shaped, gram negative rod
|
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What are the species of campylobacter that affect humans?
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jejuni - poultry, cattle sheep
coli - pigs, poultry, sheep, birds upsaliensis - dogs and cats (not seen in US very often) fetus - cattle and sheep (does not cause gastroenteritis) |
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How are humans infection with C. jejuni or C. coli?
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by consuming contaminated milk, food or water
zoonotic infections poultry responsible for more than half of the infections in developed countries |
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What is the most frequent cause of bacterial gastroenteritis in the US?
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C. jejuni
|
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What are the two most frequent viral causative agents of diarrhea outbreaks?
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Rotaviruses
Noroviruses (Norwalk Virus) - more likely in adults |
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Norwalk - enveloped? genome?
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+ sense RNA
Non-enveloped |
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How are norwalk viruses transmitted?
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contaminated hands via fecal-oral route
Directly from person to person contraminted food or water by contact with contaminated surfaces (fomites) May also be transmitted via aerosolized vomitus |
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What is the leading overall cause of gastroenteritis?
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Norwalk virus
|
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how is amebiasis transmitted?
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fecal oral route
|
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What does the involuntary flexing of the legs when the neck is passively flexed indicate?
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Brudzinski Sign
Indicates inflammation of meninges |
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Brudzinski Sign
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involuntary flexing of the legs when the neck is passively flexed
|
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Neisseria: shape, nutrition?
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Aerboic
Gram negative diplococci |
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Virulence of N. meningitidis?
|
Pili
Capsule Porin Proteins (PorA and PorB) Lipooligosaccacharide (LOS): contains endotoxin |
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What are physicians looking for when they check for pailledema?
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signs of increase ICP
|
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What does the involuntary flexing of the legs when the neck is passively flexed indicate?
|
Brudzinski Sign
Indicates inflammation of meninges |
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Brudzinski Sign
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involuntary flexing of the legs when the neck is passively flexed
|
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Neisseria: shape, nutrition?
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Aerobic
Gram negative Diplococci |
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Virulence of N. meningitidis?
|
Pili
Capsule Porin Proteins (PorA and PorB) Lipooligosaccacharide (LOS): contains endotoxin |
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What are physicians looking for when they check for pailledema?
|
signs of increase ICP
|
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Empiric therapy in childhood meningitis?
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ceftriaxone and vancomycin
|
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Pathogenesis of Neisseria meningitidis
|
Adheres to nonciliated epithelial cells in naspharynx
internalized into phagocytic vacuoles (but can avoid phagocytosis) Replicates in epithelial cells Migrates too subepi spaces then into the bloodstream and then to CNS |
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Transmission of N. meningitidis
|
droplet infection
asymp carriage faciliatates person to person transmission |
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What is meningococcemia?
|
bacteremia (without or without meningitis) --> thrombosis of small blood vessels and multiorgan involvement
Small petechial lesions on trunk and lower extremities may coalesce --> large hemorrhagic lesions Possible overwhelming DIC and shock, with bilateral destruction of adrenal glands |
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What is Waterhous-Friderichsen syndrome?
|
possible overwhelming DIC and shock with bilateral destruction of adrenal glands brought about by meningococcemia
N. meningitidis |
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What are the 6 causative agents of bacterial meningitis?
|
Strep pneumoniae: most frequent >20 y/o
N. meningitidis: 25% of all cases; up to 60% in children and young adults Enteric Gram-negative rods: mostly in pts with chronic and debilitating diseases like diabetes, cirrhosis, alcoholism Group B Streptococcus: primarily associated with meningitis in neonates, but no reported with increasingly frequency in adults Listeria monocytogenes: important cause of meningitis in neonates Hawmophilus influanzae B |
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Clostridium: shape, nutrition?
|
Gram positive
spore forming rods Mostly strict obligate anaerobes PART OF NORMAL GI FLORA |
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Types of clostridium?
|
difficile: AB associated diarrhea, pseudomembranous colitis
perfringens: soft tissue infections (cellulitis etc) food poisoning, enteritis, necroticans, bacteremia tetani: tetanus Botulinum: botulism |
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Virulence of C. tetani
|
Tetanus toxin
|
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What is tetanus toxin?
|
C. tetani
AB toxin encoded on plasmid Binds specifically to sialic acid receptors and adjacent glycoproteins on surfaces of motor neurons Internalized and transported in axon to motor neuron soma in spinal cord Enzymatically cleaves proteins that regulate release of inhibitory NTs glycine and GABA Unregulated excitatory activity in motor neurons --> spastic paralysis of muscles toxin damage irreversible, so recovery depends on whether new axonal terminals form |
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Why do you get spastic paralysis from tetanus?
|
unregulated excitatory activity in motor neurons caused by enzymatic cleavage of regulatory proteins for inhibitory NTs
|
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Where can clostridium tetani be found? (environment?)
|
Inhabitant of soils
Vegetative form killed by O2 but spores are not Spores from soil enter through would, germinate and produce toxin Tetanus quite rare in US since use of vaccine Most cases now in elderly with waning immunity |
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What is tetanus?
|
Clostridium tetani
incubation period: days to weeks Usual presenting symptom: sardonic "smile" (risus sardonicus) from sustained contraction of masseter muscles (lockjaw) Other early signs: drooling, sweating, irritability, and persistent back spasms Severe cases can involve ANS which lead to: - cardiac arrythmias - fluctuations in blood pressure - excessive sweating - dehydration |
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What are opisthotonos?
|
persistant back spasms
|
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C. botulinum virulence?
|
Botulism toxin
|
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Botulism toxin
|
binds to specific sialic acid receptors and glycoproteins (not those targeted by tetanus toxin) on surfaces of motor neurons
Toxin internalized and stays at neuromuscular junction toxin enzymatically inactivates proteins that regulate release of AcH Neurtransmission at peripheral cholinergic synapses (required for excitation of muscle) blocked Results in flaccid paralysis of muscles controlled by affected motor neurons Recovery requires regeneration of nerve endings |
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Why does C. botulinum cause flaccid paralysis?
|
Neurotransmission at cholingeric synapses blocked - these are required for excitation of muscle
Results in flaccid paralysis of muscles controlled by affected motor neurons |
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What is the recommended first line therapy for treatment of clinical tetanus?
|
Metronidazole
It stops bacterial replication to reduce production of toxin |
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Why is penicillin no longer first line for treatment of tetanus?
|
It is structurally similar to GABA the effect would be potentiation of the effect of tetanus toxoid
|
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Where can clostridium botulinum be found?
|
common resident of soil and aquatic environments
Foodborne |
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4 types of botulism?
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Fooborne
Infant - SPORES (not toxin) Wound botulism Inhalation |
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Foodborne botulism: incubation period
|
C. botulinum
Incubation period: 1-2 days after consuming toxin |
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Fooborne botulism: initial signs
|
blurred vision
dry mouth constipation abdominal pain no fever |
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Foodborne botulism: other signs (not initial)
|
bilateral descending weakness of peripheral muscles
Death usually from respiratory paralysis |
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Infant botulism: why do they get it?
|
infant <1 year of age lack sifficient intestinal flora to compete with C. botulinum if spores ingested
C. botulinum becomes established and produces toxin (doesnt happen in adults) |
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What are initial signs of infant botulism
|
constipation
weak cry failure to thrive |
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Signs of infant botulism (not initial)
|
progressive flaccid paralysis if not treated (floppy baby syndrome)
Low mortality rate with proper treatment |
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Typical symptoms of brain abscess
|
Dull, aching, and poorly localized headaches
Focal neurologic symptoms; specific features depend on location of lesion Fever Papilledema WBC counts: normal Blood cultures are positive only in 10% cases |
|
First step in treatment of botulism. Anything different for infants?
|
admin of anti toxin
Infants CANNOT receive antitoxin because their disease is a result of the actual bacteria/spores and not just the toxin. Treat with botulism antibody (Ig) |
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Routes of infection for brain abscess
|
Direct spread from contiguous cranial infection (otitis media, dental infection, sinusitis)
|
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Treatment options for brain abscess
|
AB therapy alone: multiple, small or deep seated anscesses or if pts general condition does not allow surgery
Abscess aspiration (often by sterotaxic surgery) Open craniotomy and evacuation of abscess cavity or excision of abscess |
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What is the most frequent cause of gas gangrene associated with a dirty wound?
|
clostridium perfringens
Gram positive spore forming rod |
|
Where is clostridium perfringens found?
|
soil and fecal matter
|
|
C perfringens virulence factors
|
at least 12 toxins and enzymes
ALPHA TOXIN Phospholipase C lyses RBCs, platelets, endothelial cells massive hemolysis, increased vascular permeability, bleeding, massive tissue destruction |
|
Pathogenesis of C. perfringens?
|
Wound infection starts as cellulitis with gas bubbles
Suppurative myositis Clostridial myonecrosis (gas gangrene) |
|
Suppurative myositis
|
first stage of gas gangrene
Systemic symptoms (fever) accumumlation of pus in muscle plains no destruction of muscle tissue |
|
Clostridial myonecrosis (gas gangrene)
|
second stage of gas gangrene
|
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What would be the first line recommended treatment C. perfringens?
If pt is allergic to pen? |
Pen G
Clindamycin (good for anaerobes) Allergic: metronidazole and clindamycin |
|
C. perfringens affects what parts of the body?
|
gangrene anywhere
GI track (food poisoning) |
|
What is suggested by acute onset of pain with warmth, erythema and pain on passive movement? (Bacterial)?
|
Infection of joints
Sinovitis |
|
What are the most likely causative agents of joint infections?
|
infections of joint replacements now fairly rare
But urgent empiric treatment required prior to ID of causative agent by lab Most of these infections acquired intraoperatively or postoperatively as a result of wound infections |
|
What is the recommended empiric treatment for a pt with a joint infection?
|
You want to think about what the bug could be: P. aeruginosa, staph, strep
Vancomycin, Clindamycin, or a 3rd gen cepahlo The pt has a high probability of being infected with staph or strep introduced into the pt during surgery Since this would be a nosocomial infection, the organism is presumed to be a resistant strain. |
|
Coagulase negative staph?
|
Staph epidermidis
Staph aureus is coag+ |
|
What is the appropriate treatment for S. epidermidis is identified as the causative agent?
|
Vancomycin or Clindamycin
|
|
What is associated with fever, chills, swelling, tender, boils on neck and chest (can be scarred and crusted)?
|
osteomyelitis
|
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What organism is isolated from more than 50% of osteomyelitis patients?
|
staph aureus
|
|
Microbes enter bones by one of three routes:
|
- hematogenous route
- direct spread from contagious focus of infection - Direct introduction by penetrating wound |
|
what are sequestra?
|
progressive ischemic necrosis of bone which leads to separation of large devascularized bone fragments - this occurs in chronic osteomyelitis
|
|
What are Involucrum?
|
elevated periosteum deposits new bone tissue
|
|
Reiter's syndrome?
|
reactive arthritis that sometimes develops following certain types of bacterial infections
Classic: asymmetric poly arthritis, balanitis, urethritis, conjunctivitis, uveitis, oral ulcers, and rash Not all pts have all symptoms; some may present only with polyarthritis Follows 1% of NGU cases Known to follow other kinds of mucosal infections (GI): - Yersinia enterocolitica - Campylobacter jejuni - Salmonella |