Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Didn't know it?
click below
Knew it?
click below
Don't know
Remaining cards (0)
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

GIT infections

Lectures 33-38

colonization and adjustment of the gut (0-4 days) before birth-sterile; immediately after-E. coli and streptococci appear; 4 days after birth-facultative anaerobes create reducing environment, Bifidobacterium appear, possibly Bacteroides and Clostridium
GI environment due to breast feeding E. coli, streptococci, Bacteroides, and clostridium #s decrease, Bifidobacterium #s remain high; beginning of weaning-E. coli, Streptococci and Clostridium #s return to high levels, flora now similar to formula fed infants
GI environment due to formula feeding Lactobacilli are predominant, capable of metabolizing sugars in bottle milk
Mouth initial digestion by chewing food, saliva contains defenses, microbial count is high (>500 different species:anaerobes and facultatives), attach in biofilms, fungi and transient viruses present too
Stomach little absorption, parietal cells release HCl, chief cells release pepsinogen, microbial count is sterile or very low (10^5-10^7 indicates problem), H. pylori may be isolated
Liver releases bile, begins digestion of fats, replication site of hepataviruses
Pancreas pancreatic juice, sodium bicarbonate neutralizes acidity from stomach. Enzymes: amylase, lipase, zymogens (trypsin, chemotrypsin, elastase, carboxypeptidase), nuclease
Small intestine absorption of most nutrients: sugars, amino acids, fats, and 90% of salts and water
Duodenum microbial counts increase to 10^4.5 bacterial/ml, tends to be fluctuating transients (aerobic streptococci, staph, lactobacilli, yeasts, anaerobic strep and lacto). Complete absence of coliforms and Bacteroides
Jejunum-Ileum microbial counts increas to 10^5-10^7 bacteria/ml. Enterobacteria, some strep, staph, lacto, Bacteroides, Bifidobacterium, Clostridium. Start to isolate coliforms and Bacteroides here
Large intestine/colon completes absorption, microbial counts highest: 10^10-10^12, over 400 species, 95-99% anaerobic, Bacteroides, Bifidobacterium, Clostridium, Eubacterium, and Peptostrep. Minority are Enterobacteriacea.
Factors affecting the microbial composition 1. Allogenic originating from outside the GIT (diet, age, geographic location, antibiotic therapy, surgery) 2. Autogenic- originating from within the GIT (environment, activities of microorganisms)
Diet nature of meal influences gastric emptying. Western diet: increase in bacteroides, decrease in enterococci and other aerobies. Vegetarian diet: decrease in bacteroides, increase in aerobes
Age may be due to diet in terms of quantity and type of food taken in or immune status
Geographic location differences between western and eastern societies
Antobiotic therapy causes disturbance or removal of normal flora within GIT. Leads to increased susceptibility to colonization by pathogenic microbes
Surgery alteration of bacterial population at a particular location
Environment hydrogen ion concentration,peristalsis, shedding of epithelium, mucus, conjugated bile salts, immunological response
Activities of microorganisms competition for nutritional and attachment sites, production of bacterial inhibitors, toxic metabolic end products, H2S production, maintenance of low oxidation reduction potentials
Oral disease (upper GI infections) dental caries and periodontal disease are common worldwide
Dental caries infectious disease resulting in localized dissolution and destruction of calcified tissue of the teeth. S. mutans, S. sanguis, Lactobacilli, Actinomyces, Propionibacterium, Eubacterium, Fusobacterium, Capnocytophage, Veillonella.
Peridontal disease infections affecting the supporting structures of the teeth. Gingivitis: inflammation of the gums, reversible, can progress to periodontis.
Abscess in mouth, leading to deep tissue (alveolar bone, lung, brain, or extremities)
Most common bacterial pathogens associated with food ingestion 1. Campylobacter jejuni 2. Salmonella 3. Shigella 4. E. Coli 5. Yersinia enterolytica 6. S. aureus 7. C. perfringens 8. Vibrio parahaemolyticus 9. Listeria monocytogenes
Food poisoning toxemia, arises from the ingestion of food containing toxins, only from C. botulinum, S. aureus, and B. cereus, and mushroom and marine sources
Food associated infections arise from the ingestion of food containing the causative organism, once ingested the organism relases a toxin
enteritis inflammation of the intestinal mucosa
gastroenteritis inflammation of stomach and intestinal lining
colitis inflammation of large intestine
enterocolitis inflammation of small and large intestine
dystentry inflammation of GIT with blood and pus in feces
diarrhea frequent and/or fluid stool (>3 loose stools)
exotoxin protein toxin secreted by living microorganisms into the surrounding environment
enterotoxin toxin specific for cells of the intestine, causing inflammation, typically cause excessive secretion of fluids and electrolytes
cytotoxin substances that inhibit or prevent functions or cause destruction of cells or both
enteroadherent organisms that adhere to microvilli
enteroinvasive organisms that invade the intestinal mucosa
Gastroenteritis (overview) food poisoning, due to S. aureus, B. cereus, C. botulinum, wild mushrooms, aflatoxin, ciguatera, scromboid, neurological and paralytic poisonings. Ingestion of preformed toxins, not a result of microbial growth in GIT. Rapid, no fever/fecal leukocytes
Staph aureus gram + cocci, in singles pairs and clusters, aerobic or facultative, coagulase +, catalase +, human and animal pathogen, found on skin and nares of nose in 50% of people
S. aureus pathogenesis makes 1 of 8 exotoxins, A&D most implicated in food outbreaks. Exotoxin: chromosomal encoded ST enterotoxin, water soluble, low weight protein, infective dose=1 microg (100,000 bacteria), mode of action unknown, may act on gut receptors
S. aureus clinical symptoms incubation 1-6 hr, vomiting, self limiting with duration of 24 hr, may also have nausea, abdominal cramps, diarrhea (watery), headaches, muscular cramps, and/or prostration
S. aureus incriminating foods cooked meat, fish, poultry, bakery foods (cream filled), dairy produce, fruit, vegetables, and salads. Outbreaks due to poor handling of foods. Use selective differential media, confirmation=coagulase + test
Bacillus cereus gram + rods, arranged in chains, facultative or aerobic, spore forming, cause emetic and diarrheal gastroenteritis, in the air, soil, water, and dust, easy cross contamination with food
B. cereus pathogenesis produces a ST neurotoxin, infective dose unknown, mode of action unknown
B. cereus clinical symptoms closely resembles S. aureus food poisoning, incubation 1-5 hr, duration 6-24 hr
B. cereus incriminating foods Rice and pulses, boiled rice stored at inappropriate holding temp before quick frying (allows spores to germinate and multiply in rice). Implicated food has >10^5 org/g, use non-selective medium (blood agar w/ polymyxin to suppress gram-)
Clostridium botulinum gram + rods, anaerobic, ferments many CH2Om spore forming, produced exotoxins, susceptible to penicillin, found in soil and lower GIT in human and animals, causes descending symmetrical paralysis, associated with home canning, infant botulism most common
C. botulinum pathogenesis makes 1 of 8 exotoxins, human infection due to A, B, E and rarely F, animal infection with C and D. Exotoxin: protein neurotoxin, 10^-8 of A can kill, causes food poisoning, wound and infant botulism
food poisoning botulism toxin in contaminated food is ingested with food, incubation 12-36 hr, small % absorbed in intestinal mucosa, rest eliminated in feces
food poisoning botulism clinical symptoms illness varies, GI disturbances in 1/1 of patients with A or B and almost all with E, also nausea, vomiting, abdominal pain, diarrhea, constipation. Toxemia afterGI symptoms, no fever in absence of complicating infections
Diagnosis (food poisoning botulism) reportable disease, fatal food toxemia. Presumptive=rapidly descending paralysis and history of ingestion of home canned food. Confirmative=demonstration of toxin in serum/feces or incriminating food (mouse toxin-neutralization test)
differential diagnosis (food poisoning botulism) Guillan-Barre: ascending paralysis, elevated CSF protein. Myasthenia gravis: descending paralysis, accentuation of muscle fatigability during exercise and + response to endrophomium. Other food poisonings: no CN involvement, faster symptoms
Infant botulism 2wks-6mo, ingestion of spores, germination in GIT, vegetative cells replicate, release toxin in intestines (A and B). May be due to incomplete flora, no constant link to particular food type
Infant botulism clinical symptoms initial illness and constipation, lethargy, suck and gag reflexes diminshed, dysphagia with drooling, head control lost, flaccid, respiratory arrest
Infant botulism diagnosis and treatment differential=neurological and GI, toxin demonstration in feces, reportable disease. Treatment=large doses horse C. botulinum antitoxin and supportive measures, maintain respiration. Botulism immune globulin intravenous (human)
Mushroom (fungal) toxins short acting: variety of toxins (museinol, muscarine, psilocybin, coprius, artemetarius, ibotenic acid), quick onset, acute symptoms (nausea,vomiting, diarrhea. Long acting: amantia, 4-8hr incubation, diarrhea, abdominal cramps, can be fatal
Mycotoxogenic fungi Mycotoxins: secondary metabolites that develop on/in food during poor storage (aspergillus, fusarium, penecillium). Aflatoxins: fungal growth on tree nuts, peanuts, oilseed, acute necrosis, cirrhosis, and carcinoma (Aspergillus flavus and parasiticus)
Marine toxins ciguatera and scromboid poisoning
Ciguatera poisoning pathogenesis predatory reef fish eat dinoflagellate algae Gambierdiscus toxicus. Dinoflagellates release Ciguatoxin in fish. Bioaccumulation of toxin in fish liver and viscera, cooking does not denature or remove toxin
Ciguatera poisoning clinical symptoms incubation mins-30 hrs (typically 3-6), duration 1-2 weeks, watery diarrhea, nausea, abdominal cramps after 12 hr, muscle aches, burning sensation. Neurologic: circumoral and extremity paresthesia, severe pruritis, hot/cold temp reversal
Scromboid poisoning pathogenesis (non-allergic histamine fish poisoning) histidine normally present in fish, bacteria in/on fish convert histidine to histamine, results in histamine accumulation in fish. Cannot be eliminated by cooking, freezing, salting, etc
Scromboid poisoning clinical symptoms incubation mins-3hrs (usually 1 hr), durations 3 hr-several days, watery diarrhea, nausea, vomiting, burning sensation in mouth (metallic taste), urticaria, facial flushing, pruritis, paresthesia
Neurolytic and paralytic shellfish poisonings ingestion of comtaminated shellfish, often harvested in algal blooms (red and brown tides)
Neurolytic poisoning pathogenesis dinoflagellate algae (Gymnodimium breve) produces brevotoxin
Neurolytic poisoning clincal symptoms incubation <1-3 hours, duration 24-73 hours, paresthesia, mouth numbness, tingling sensation of moth and extremities, GI upset
Paralytic poisoning pathogenesis Dinoflagellate algae (Alexandrium, Gymnodinum catenatum, Pyrodinium bahamense, Gonyaulux) produce saxitoxins
Paralytic poisoning clincal symptoms incubation 15 min-10hr (usually <2), duration 3 days, tingling/numbness of mouth spreading to extremities, GI symptoms less common, ataxia, severe=muscular paralysis, respiratory paralysis
Non-inflammatory diarrhea food borne infection(E. coli (EPEC&ETEC), V. cholerae, C. perfringens, B. cereus, rotavirus, noroviruses, adenoviruses, C. difficile (not foodborne))Production of toxins after intestinal colonization. Watery diarrhea without fever/dysentry, no SI invasion
E. coli normal intestinal flora, gram- bacilli, facultative anaerobe, complex antigenic structure, produces many toxins, major opportunistic pathogen, 6 strains: ETEC, EPEC, EAEC, EHEC, EIEC
Enterotoxogenic E. Coli (ETEC) transmitted in contaminated food and water, infective dose: 100 million-10 billion cells, #1 cause of travellers diarrhea
ETEC pathogenesis 1. following ingestion, colonization of SI with CFA's 2.once colonized release of 1 or 2 plasmid encoded enterotoxins (both AB). Heat labile (LT) activated adenylate cyclase. Heat stabile (ST) activate guanylate cyclase
ETEC clinical symptoms incubation 10hr-3 days, duration 3-5 days, self limiting, rapid onset of watery diarrhea, nausea, and vomiting. Manage with ORT.
Enteropathogenic E. Coli (EPEC) causes childhood diarrhea (<5yrs) in developing countries (50% mortality rate), minor cause of traveller's diarrhea.
EPEC pathogenesis not fully understood, no ST or LT production, no CFA. Do have plasmid borne bundle forming pilus (BFP) which attaches to epithelial cells of SI and causes effacement of microvilli. Leads to an osmotic imbalance-> watery diarrhea. Use rehydration therapy
Vibrio cholerae gram- rods, motile, non-spore forming, oxidase+,O&H antigens, classic strains O1 serotype, ferment sucrose and mannose, not arabinose, acid sensitive, halotolerant. Found in sea water
Vibrio cholerae pathogenesis infective dose 10^8-10^10, colonization of SI, release of bacteriophage encoded cholera toxin (AB enterotoxin), A activates adenylate cyclase
vibrio cholerae clinical symptoms incubation 2-3 days, duration up to 1 week. Extensive watery diarrhea (rice water stool), dehydration due to loss of water and electrolytes, hypovolemic shock, hypokalemia, metabolic acidosis, death from uremia
Cholera management Primary: replace ionic loss, oral and/or IV administration of glucose with normal NaCl, greater K and HCO3. Tetracycline (reduce duration of diarrhea.
Prevention of Cholera parentally administered vaccine, not recommended by FDA, only 50% effective, lasts 3-6 months only. Must make clean and sanitary living conditions. Diagnose with stool oxidative activity, use TCBS agar (sucrose differentiating agent)
Clostridium perfringens necrotic enteritis is rare, common in Papua New Guinea (strain C). Type A=food borne infection, major cause of food borne infection in US
C. perfringens pathogenesis ingestion of 10^6-10^7 orgs in meat or gravy, spore forming, generation time=10 minutes, ingestion of bacterium in cooled meat, produces C.perfringens enterotoxin (CPE) beta toxin active on GIT.
C. perfringens clinical symptoms incubation 8-24 hrs, duration 24 hrs, self limitin, watery diarrhea, severe abdominal pain, no fever, no nausea, no vomiting. Mortality=0, but monitor elderly/immunocompromised. Diagnose by large # in stool and vegetative cells in food
Bacillus cereus pathogenesis LT enterotoxin activates adenylate cyclase, produced and released during vegetative growth in SI
B. cereus clinical symptoms incubation 8-16 hrs, duration 12-24 hrs, watery diarrhea and abdominal pain. implicated foods=meat and vegetable dishes, sauces, pasta, desserts, dairy products
Viral causes of non-inflammatory diarrhea rotaviruses, noroviruses, adenoviruses, astroviruses, torovirus, Hep A and E. Probably #1 cause of GIT infections
Rotavirus #1 viral cause of diarrhea, wheel shaped, double layered capsid, dsRNA, serotypes G1-4; G1 worldwide, G2 in china
Rotavirus: factors for high incidence/mortality unsafe water, inadequate sanitation, asymptomatic infants <6 mo and children >5yrs. May be seasonal
Rotavirus pathogenesis fecal oral trans(also water and air borne), incubation 1-3 days,duration 4-6 days, multiplies in SI epithelial cells, shedding may persist for 10 days or more (peak 8 d), shortening and blunting of villi, patchy, irregular, intact mucosa, lose absorp area
Rotavirus clinical symptoms sudden onset watery diarrhea +/- vomiting, duration up to 6 days, may have dehydration which can be life threatening, use rehydration therapy, detect with ELISA, latex agglut, microscopy. Vaccine available
Norwalk virus small, non-enveloped, ss+RNA, single structural protein, causes 50% of outbreaks of actue, non-bacterial gastroenteritis. Older children/adults: camps, schools, nursing homes. #1 cause in this age group. Fatalities rare, winter seasonality
Norwalk pathogenesis fecal oral trans (also water/food borne), multiplies in SI, produces transient lesions of intestinal mucosa, spares LI, shed in feces
Norwalk clinical symptoms incubation 1-2 days, duration 1-2 days, abdominal cramps, myalgia, malaise, nausea, low grade fever, 1-2 days diarrhea
Norwalk like viruses considerable genetic homology with Norwalk and shared virological characteristics. Transmission: food, water, easy person to person, most outbreaks from restaurants
Adenovirus small, isocahedral dsDNA, 2 serotypes (40 and 41)
Adenovirus pathogenesis infect epithelial cells of pharynx, conjunctiva, SI, and others. Replicates in intestine, present in stool, watery diarrhea +/- vomiting, 5-15% of cases of childhood diarrhea (second to rotavirus)
Astroviruses non-enveloped, star shaped, ss+RNA, 7 serotypes, 2-8% sporadic cases in infants, peak in winter
Small round structured viruses (SRSV) have been isolated as causes of diarrhea, status uncertain
Toroviruses emerging GI pathogen, increased bloody diarrhea, decreased vomiting, aged, immunosuppressed, and hospitalized at risk.
Hepatitis A virus isocahedral, non-enveloped, +RNA, fecal oral trans, person to person, poor sanitation and overcrowding, virus shed in feces, 10% of all due to infected food handler, ingestion of contaminated shellfish. Fever, nausea, vomiting, jaundice
Hepatitis E virus isocahedral, non-enveloped, +RNA, prevalent in India, sporadic outbreaks, incubation 6 weeks.
Inflammatory diarrhea food borne infection (shigella, EIEC, salmonella, campylobacter, V, parahaemolyticus and vulnificus, Yersinia, EHEC, EAEC). Colnization and invasion of intestines (except EHEC and EAEC). bloody stool and fever, enterotoxins, cytotoxins
Shigella grouped based on O antigens. Group A=shigella dysenteriae, Group B=shigella flexneri, Group C=shigella boydii, Group D=shigella sonnei.
Shigella virulence factors Exotoxin: enterotoxin that acts as neurotoxin, causes meningismus and coma, ulceration of intestines. NAD glycohydrolase: destroys NAD in human cells which shuts down metabolism, resulting in cell death
Shigellosis 1. Watery diarrhea with abdominal pain and vomiting with mild to moderate dehydration. 2. Dystentary: watery diarrhea which progresses to small volume bloody mucoid stool with tenesmus
Shigella pathogenesis fecal oral route, invades LI at M cells or junctions between cells, multiply and spread to adjacent cells, cause cell death by apoptosis, inflammation by IL-8
Bacillary dystentery caused only by Shigella dysenteriae, produce and release cytotoxin (shiga toxin), inhibits protein synthesis (inactivates 28S RNA on 60S) and acts as an enterotoxin (diarrhea, inhibits sugar and AA absorption in SI), and neurotoxin (affects CNS)
other Shigella sonnei: children <5 in day cares, most common, minor traveller's diarrhea. Flexneri: sexually active gay men. Boydii: rare
Shigella management rehydration therapy, antibiotic treatment. Isolate from stools, water, and food, MacConkey or SS agar, non-motile, gram- rod, no lactose fermentation, no citric acid util, no H2S production, No gas from glucose fermentation
Enteroinvasive E. coli (EIEC) similar to shigellosis, less severe, small infective dose, does not release Shiga toxin
EIEC pathogenesis invasion of enterocytes in LI. Manage with rehydration therapy
Salmonella ubiquitous, animal reservoir, diseases mainly caused by typhimurium and enteritidis
Salmonellosis 1. Gastroenteritis: typhimurium,enteritidis, Newport. Minor cause of traveller's diarrhea. 2. Septicemia/Bacteremia: focal infection, uncommon, cholerasuis. 3. Enteric (typhoid) fever: typhi.
Salmonella pathogenesis ingested species reaches SI, penetrates SI, multiplies in M cells, released into lamina propria. Septecemia/enteric fever: enter lymphatics and blood stream, multiply in lymphoid tissue, carried in blood to organs. for enteric fever: infect gall bladder
Enterocolitis (gastroenteritis) localized infection in SI, excessive fluid secretion from ileum/jejunum. S. typhimurium primary isolate
Reptile associated salmonellosis lizards, snakes, or turtles. Usually in infants or children due to direct or indirect contact
Enteric fever (S. typhi) in US only seen in travellers to Asia, Mexico, and India. 2-5% become carriers, important in transmission. (multiply in bile, reinfect SI). Use rehydration therapy, antibiotics, and 3 vaccines. (paratyphoid by paratyphi and schottmelleri)
Diagnosis and management of Salmonella isolate from stools, water, and food. MacConkey or SS agar, motile gram- rod, no lactose fermentation, H2S production, gas from glucose, serotyping. Typhi: travel to endemic area, rose colored spots on abdomen, +widal rxn, no eosinophils,anemia,leukopenia
Campylobacter initially assoicated with sheep/bovine abortion and sterility. Common cause of diarrhea in humans, spiral rods, gram-, non-sporing, motile, microaerophilic, do not ferment CH2O, catalase+, in GIT of many animals, #1 food borne disease (raw milk/poultry)
Campylobacter pathogenesis infective dose 500-10^4 orgs, invasion of LI, inflammation and bacteremia, endotoxin and enterotoxi and verotoxin production
Campylobacter clinical symptoms incubation 3-5 days, duration 2-10 days, non-distinctive symptoms, slight vomiting, profuse diarrhea, severe abdominal pain and prostration, pyrexia, differs in developing/developed countries. Self limiting, Antibiotics after ID
Campylobacter complications reactive arthritis (1%) particularly in knees, may last 6-12 months, Guillan-Barre syndrome (up to 30% of cases)
Yersinia enterocolytica common in children <7, gram- rod, psychotroph, facultative psychrophile
Yersinia pathogenesis poorly understood, invades and induces inflammation in distal ileum (GALT),adjacent tissue and mesenteric lymph nodes also infected (mimics apendicitis), ST enterotoxin increases cGMP.
Yersinia clinical symptoms incubation 3-7 days, duration 2-3 weeks, self limiting, abdominal pain and diarrhea, mild fever, vomiting rare. Manage with antibiotics. diagnose with MacConkey or Yersinia agar or by serology (rising Ab titers)
Yersinia complications post infective reactive arthritis (autoimmune) in small %. May be due to induced polyclonal T-cell stimulation.
Non-Cholera Vibrio's do not agglutinate O1 sera
Vibrio parahaemolyticus ingestion of raw/poorly cooked seafood, #1 cause in Japan(sushi). Enteroinvasive, reaches lamina propria, acute abdominal pain, vomiting, watery diarrhea. Treat with tetracycline
Vibrio vulnificus contaminated sea food and infection of cuts, intense skin lesions, virulent strain, extensively invasive, needs tetracycline. Usually have pre-existing liver condition, otherwise ate raw oysters. fatality 50%
Enteroaggregative E. coli (EAEC) no EAF, initial adherence to intestinal mucosa or mucus layer by fimbriaw, strains produce mucus-->thick biofilm encrusted within EAEC. Cytotoxin damages intestinal cells (bloody diarrhea)
Enterohemorrhagic E. coli (EHEC) also known as VTEC or STEC. Causes life threatening conditions
Hemorrhagic colitis bloody diarrhea that begins as abdominal cramps and watery diarrhea, incubation 3-8 days, mainly affects adults, life threatening in elderly, acute and self limiting
Hemolytic uremic syndrome 8-11% of cases, mainly children <5, follows bloody diarrhea, acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia
Thrombotic Thrombocytopenia purpura similar to HUS, fever and neurological symptoms, attaches to epithelial cells of LI, release verotoxin (V1 and V2: both AB toxins), A inhibits protein synthesis (causes HC), B binds to renal glomerular cells and causes HUS. Rehydration, NO antibiotics
Diagnosis of E. coli normal flora, so difficult. Use MacConkey's agar and eosin methylene blue agar, sorbitol MacConkey's for EHEC, inoculate mouse adrenal cells and stimulate adenylate cyclase by LT/ST for ETEC, ELISA for all, DNA probe for all
Clostridium difficile nosocomial, present as normal flora in <3% of people, NOT food borne, range of diseases, Antibiotic associated diarrhea (ampicillin, cephalosporin, clindamycin, and amoxicillin). Can induce psuedomembranous colitis (methotrexate)
C. difficile pathogenesis only involves colon, antibiotic therapy disrupts normal flora and leaves attachment sites open for C. difficile. Produces 2 toxins: A (enterotoxin)=fluid accumulation in bowel. B (cytotoxin)=decreases protein synth and disrupts microfillament system
C. difficile clinical symptoms vary, excess mucus/pus in diarrhea, watery, non-bloody, hypoalbunemia and leukocytosis common. Diagnosis difficult, sigmoid scopic examination and isolation of C. difficile from stool. Discontinue antibiotic give vancomycin or metronidazole if severe
Helicobacter pylori gram-, non spore forming, motile, mircoaerophilic, catalase +, urease +, causes gastritis, duodenal ulcers, and stomach cancer. present in gastic mucosa,increases with age. Higher in developing countries
H. pylori pathogenesis gastic colonization, route of infection unclear, urease: allows survival at pH 2, able to split ammonia from urea=alkaline environment. Detect by biopsy, urease breath test, serology
H. pylori treatment 1. 1st effective: triple regimen (bismuth salt, metronidazole, tetracylcine/amoxicillin) 2. acid suppressing drugs: omerprazole (inhibits acid pump)m amoxicillin 3. Triple therapy: imidazole, clarithromycin, omeprazole, and tinidazole (resistance)
Chron's disease affects mouth to anus, full thickness, may be caused by M. paratuberculosis. obligate intracellular pathogen, acid fast, rod
Chron's clinical symptoms fever, abdominal pain, severe anorectal complications (fistulas, fissures, abscesses), diarrhea, fatigue. Similar to Bovine Johne's disease
Chron's treatment no universally effective antimicrobial. Goals:control inflammation,correct nutritional deficiencies,releave abdominal symptoms. Diagnoses with colonoscopy (longituninal fissures/ulcers), culture(herrold's egg yolk agar+myobactin, 12-16 wk incu) PCR biopsy
Gastrointestinal abscess peritonitis, appendicitis and diverticulitis, intra-abdominal abscess, liver abscess, pancreas abscess.
GI abscess pathogenesis reduced O2 tension& oxidation-reduction potential, impaired blood supply, necrosis of tissue, growth of facultative anaerobes. Associated with vascular disease, trauma, surgery, foreign bodies, malignancy, radiation, shock, cold, edema. Bacteroides common
Peritonitis pain, abdominal distention, diffuse muscle spasm, tenderness and rebound tenderness, decrease/absent peristalsis, rigidity of abdominal wall, tender rectal/vaginal exam, fever, leukocytosis
Appendicitic/diverticulitis abdominal pain, peritoneal irritation, fever, leukocytosis
Pylephlebitis and liver abscess chills, fever, epigastric or right upper quadrant pain, nausea, vomiting, enlargement and tenderness of liver
Pelvic abscess pain, deep tenderness in 1 or both lower quadrants, fever, urinary frequency, dysuria and diarrhea with mucus in first stools, rectal/vaginal exam tenderness
Pancreatic abscess severe epigastric pain, recent history of excessive ingestion of food and alcohol. nausea and vomiting common.
Diagnosis of lesions based on type and location of pain, WBC count, biochemistries, imaging, CT, PET, ultrasound. Treat by improving vascular perfusion, eliminate primary source of infection, aspirate, treat local/distant complications
Management of diarrheal disease oral rehydration (first line), intravenous rehydration (shock, exhaustion), antiemetics (reduce fluid loss), antidiarrheal (rarely successful)
Prevention of infections safe food production, food manufacture processes, domestic and commercial food hygiene
Created by: kamarsh



Use these flashcards to help memorize information. Look at the large card and try to recall what is on the other side. Then click the card to flip it. If you knew the answer, click the green Know box. Otherwise, click the red Don't know box.

When you've placed seven or more cards in the Don't know box, click "retry" to try those cards again.

If you've accidentally put the card in the wrong box, just click on the card to take it out of the box.

You can also use your keyboard to move the cards as follows:

If you are logged in to your account, this website will remember which cards you know and don't know so that they are in the same box the next time you log in.

When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards