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101 Cards in this Set
- Front
- Back
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Salmonella typhi 1
Metabolism/Characteristics |
Produces H2S
Does not ferment lactose |
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Salmonella typhi 2
Antigenic structure |
H-antigen (flagella --> motile)
Vi antigen (Capsule sounding O-antigen -->protects O-antigen from antibody attack, similar to K-antigen) |
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Salmonella typhi 3
Pathogenesis |
salmonella typhi results in typhoid fever (aka enteric fever).
ingestion --> small intestine --> mesenteric lymphatics (incubation period, asymptomatic, 7-14 days, are phagocytosed in lamina propria but instead of being destroyed they multiply, they are facultative intracellular parasites) --> lymph nodes --> blood (via thoracic duct, bacteremia 1st time: symptoms begin. shaking, chills, fever) --> redesposited in lymph nodes (bacteremia 2nd time, much more severe, will get into many organs resulting in ulceration, perforation, or hemmorhage) lasts 8 weeks from initial infection infective dose - dose required to get infection is 10^5-10^8 (even can be 10^3 for S. typhi) |
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Salmonella typhi 4
Clinical |
1st bacteremia --> symptoms begin. shaking, chills, fever
2nd bacteremia --> much more severe, will get into many organs resulting in ulceration, perforation, or hemmorhage mesenteric lymphatics (incubation period, asymptomatic, 7-14 days, are phagocytosed in lamina propria but instead of being destroyed they multiply, they are facultative intracellular parasites) --> lymph nodes --> blood (via thoracic duct, bacteremia 1st time: symptoms begin. shaking, chills, fever) --> redesposited in lymph nodes (bacteremia 2nd time, much more severe, will get into many organs resulting in ulceration, perforation, or hemmorhage) lasts 8 weeks from initial infection |
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Salmonella typhi 5
Diagnosis |
1. blood --> + weeks 1-4
2. stool --> + during first incubation and after weeks 2,3,4. 3. agglutinins for serology --> peak bet. weeks 3 & 6. Widal test: for following antigens: O (> or equal to 1:160), H (1:160), Vi (high in carriers) |
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Salmonella typhi 6
Epidemiology & Control |
-Always pathogenic --> never part of normal GI flora
-Lives in GI tract of animals -Infection results from contamination of food or water w/ animal feces (fecal-oral route) -Water, dairy, meat, eggs -NOT zoonotic as the disease is only carried by humans -Food, Fingers, Feces, Flies can cause disease -After healing from typhoid fever, 2-5% are carriers --> normal except that excrete salm. typhi in stool. can also grow in gallbladder. if can't eradicate w/ penicillin, do cholecystectomy. |
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Salmonella typhi 7
Treatment |
-chloramphenicol
-ampicillin -trimethoprim + sulfamethoxazole -cholecystectomy in carriers(if penicillins don't work) |
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Salmonella typhi 9
Prophylaxis |
-hygiene of water and food
-hygiene of persons dealing w/food -preventing food contact w/flies -bacteriological tests of food |
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Salmonella typhi 8
Immunity |
-some degree of immunity due to circulating Ab's to O and Vi.
-secretory IgA prevents attachment to intestinal epith. |
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Salmonella
typhoid-like fevers/paratyphoid (type of enteric fever) |
caused by the following non-typhi salmonella species:
S. para A – S. paratyphi S. para B – S. schottmiilleri S. para C – S. hirschfeldii -milder disease -shorter incubation -shorter duration (7-10 days) |
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Salmonellosis 1
Pathogenesis |
localized mainly in the GI tract
salmonellosis = food poisoning |
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Salmonellosis 2
Symptoms |
-headache
-chills -cramps -nausea -vomiting -diarrhea -last 1-4 days |
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Salmonellosis 3
Epidemiology |
-more than 1800 strains (serotypes) can cause it
-sources are animals (zoonotic): cows, sheep, pigs, etc. (unlike in typhoid fever) |
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Salmonellosis 4
Diagnostic method |
only stools are to be sent to lab
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Shigellosis 1
4 types of Shigella that cause Bacillary dysentery |
Sh. dysenteriae (group A)
Sh. flexneri (sickgut) (group B) Sh. boydi (group C) Sh. sonnei (group D) -listed in order of most to least virulent -all produce endotoxins -some produce exotoxins |
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Shigellosis 2
General characteristics |
No flagella (no H antigen)
40 serotypes due to the O antigen |
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Shigellosis 3
Epidemiology |
-very contagious.
-lowest infective dose of all enteric bacilli (10^3) -FFFF (food, feces, flies, fingers) -ONLY human host -prevention by eliminating bacterium from water, food, milk, fly control, sewage. |
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Shigellosis 4
Shigellosis dysenteriae (group A) 2 types of toxins |
Type 1: produces an exotoxin (called Shiga toxin) which acts as an enterotoxin (causing diarrhea) as well as a neurotoxin), heat labile
Type 2: similar to type 1 |
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Shigellosis 5
Diagnosis |
Shigella is limited to GI tract, thus can only be isolated from feces --> stool sample
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Shigellosis 6
Pathogenesis |
enter GI tract --> invade mucosa --> cause microabscesses in wall of large intestine --> cause necrosis, superficial ulceration, bleeding and formation of ‘pseudomembrane’
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Shigellosis 7
Symptoms |
-very leaky diarrhea
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Shigellosis 8
Endotoxin |
-upon autolysis release LPS --> irritation of the bowel
-Endotoxin is NOT the virulence factor. |
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Shigellosis 9
Treatment |
-chloramphenicol
-ampicillin -tetracycline -trimethoprins + sulfamethoxazole |
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Vibrio cholera 1
Epidemiology |
-endemic in India, South Asia
-carried by shipping, pilgrims -occurs in places where people are crowded - ingest 10^8 - 10^10 in order to produce disease -worldwide epidemics 1800, 1900, 1961 (El-Tor) -Vibrios survive in water for 3 weeks -Patients should be isolated, their excreta, etc. |
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Vibrio cholera 2
Pathogenesis |
-not invasive (doesn't go to other places) --> localized in GI
-multiply in GI --> produce toxin (called choleragen) --> toxin is absorbed by GI epith. --> hypersecretion --> outpouring of fluid and electrolytes --> causes diarrhea dehydration, acidosis, shock, death |
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Vibrio cholera 4
Clinical presentation |
1-4 days incubation
sudden onset of: -nausea -vomiting -profuse diarrhea -abdominal cramps -high mortality rate of 25-50% w/out treatment ("El Tor" is a biotype of Vibrio cholera which causes milder disease than the classical type). -stool looks like "rice water" |
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Vibrio cholera 5
Diagonsis |
lab culture of stools
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Vibrio cholera 6
Treatment |
water + electrolytes + antibiotics (tetracyclines)
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Vibrio cholera 7
Immunity |
IgA lumen of intestine (but lasts only a few months)
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Vibrio cholera 3
Enterotoxin (exotoxin) |
exotoxin binds to GI epith --> activates adenylyl cyclase --> causes ATP to form cAMP --> causes ion channels in GI epith cells to open and electrolytes and liquids flow into GI lumen
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Vibrio cholera 8
Vaccine |
-there is a vaccine for travelers
-only lasts 1/2 year -if the vaccinated person contracts Vibrio cholera, he will not get sick but will spread it to others. |
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Vibrio parahemolyticus 1
Epidemiology |
-causes milder disease than Vibrio cholera
-halophilic ("salt-loving") --> grow in ocean -can be contracted through eating contaminated sea food, raw fish, shellfish |
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Vibrio parahemolyticus 2
Clinical presentation |
-Lasts for 12-24 hours
-diarrhea -nausea -vomiting -abdominal cramps -fever -watery stools |
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Vibrio vulnificus 1
Epidemiology |
-found only in saltwater
-can cause serious infections |
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Vibrio vulnificus 3
Infection in person w/ weakened immune system |
-can get infection by eating contaminated seafood such as raw/undercooked oysters, clams, mussels, & other shellfish
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Vibrio vulnificus 2
Infection in healthy person |
-can get infection in cuts or sores that get contaminated w/ saltwater from bay or ocean.
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Vibrio vulnificus 4
Symptoms following infected cut/sore |
-can be fatal
-can cause necrosis of parts of body that will need to be amputated -red, pain, swelling around cut that spreads quickly -cuts or sores that get larger, deeper, and blister |
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Vibrio vulnificus 5
Symtpoms following ingestion of raw/undercooked seafood |
-nausea
-vomiting -diarrhea -stomach pain |
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Vibrio vulnificus 6
Risk factors for infection |
-chronic liver disease (liver is responsible for detox)
-alcoholism (prevents antibody prod.) -weakened immune system (due to medication, AIDS, HIV, etc.) |
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Escherichia coli 1
4 main diseases E. coli causes |
(E. coli is a normal flora of GI, but some strains cause disease)
-UTI (90% of the infections) -Traveler's diarrhea -Sepsis (esp. in absence of IgM, in absence of normal host defense) -Meningitis in infants (40% of neonatal meningitis) |
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Escherichia coli 3
5 different groups of E. coli that cause Traveler's Diarrhea |
EPEC - entero pathogenic E. coli
ETEC - entero toxigenic E. coli EIEC - entero invasive E. coli EHEC - entero hemorrhagic E. coli EAEC - entero aggregative E. coli |
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Escherichia coli 4
EPEC (entero pathogenic E. coli) |
can attach to brush boarder, enter in after they destroy the brush border and cause diarrhea
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Escherichia coli 5
ETEC |
-some strains make the LT (heat-labile toxin --> heat can destroy it)
-some strain make the ST (heat-stable toxin --> heating will not destroy it) -some strains make both toxins -cause diarrhea like cholera |
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Escherichia coli 2
Traveler's Diarrhea |
-acute gastroenteritis
-similar to shigellosis -caused by 5 different groups of E.coli which are not the normal flora of the GI (note: today Traveler's diarrhea includes E.coli, Campylobacter, Yersinia, etc.) |
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Escherichia coli 6
EIEC (entero invasive E. coli) |
strains that can invade tissue and cause diarrhea etc.
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Escherichia coli 7
EHEC (entero hemorrhagic E. coli) |
cause hemorrhage like shigella
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Escherichia coli 8
LT (heat-labile toxin) mechanism of action |
-under control of transmissible plasmid
-AB toxin -subunit B attaches to GM1 ganglioside at brush border of epith cells --> subunit A enters cell and activates adenylyl cyclase which increases concentration of cAMP --> prolonged hypersecretion of water and chloride --> inhibits reabsorption of Na+ |
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Escherichia coli 9
ST (heat-stable toxin) mechanism of action |
-under control of transmissible plasmid
-AB toxin -subunit B attaches to GM1 ganglioside at brush border of epith cells --> subunit A enters cell and activates activates guanylyl cyclase --> cGMP increases --> prolonged hypersecretion of water and chloride --> inhibits reabsorption of Na+ |
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Campylobacter jejuni
Epidemiology 1 |
-infection by oral route (food, milk, drink, anal-genital-oral sexual activity)
-low infective dose = 10^4 -easily spread |
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Campylobacter jejuni
Pathogenesis 2 |
multiply in small intestine --> invade epith and cause inflammation --> RBCs in stool
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Campylobacter jejuni 4
Diagnosis |
-very selective media are needed for isolation
-incubation of plates at 42-43 degrees celcius will result in growth (most bacteria grow at 37 degrees, so grow one plate at 37 and one at 42 to identify if it's Campylobacter) |
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Campylobacter jejuni 3
Clinical presentation |
-enteritis
-RBCs in stool |
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Campylobacter jejuni 5
Treatment |
erythromycin (can be resolved w/out treatment)
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Yersinia enterocolitica
General facts |
-belongs to group of Pasteurella
-can cause diarrheal diseases -more widespread among children -symptoms like in Salmonellosis and Shigellosis |
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Aeromonas
General Facts |
-diarrhea
-vomiting -found in fresh or brackish (salt content in bet. fresh and saltwater) water |
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Helicobacter pylori 1
Epidemiology |
-As populations achieve better living conditions, incidence of H. pylori decreases --> it is a submerging pathogen (rather than emerging)
-U.S. has lower incidence rates and the higher rates are in Africa, Mexico, Eastern Europe -main cause in >95% of stomach ulcers -spread from fingers, food, orosexula/orofecal way -sole reservoir is man --> can be spread from one person to another -very "exotic" bacterium -spiral, curved shape and flagellae |
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Helicobacter pylori 8
Proposed mechanism of Pathogenesis |
H. pylori uses flagella to swim through mucous layer of stomach, adheres to epith cells, bacterium releases toxins that cause excessive prod. of cytokines and chemokines, results in massive inflammatory response, leukocytes leave capillaries, accummulate in area of infection, discharge their lysosomes, this kills the bacteria but also the mucous-secreting mucous membranes of the stomach, w/out protective layer gastric acids are able to cause ulceration.
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Helicobacter pylori 9
Link to cancer |
-infection with H.pylori for many years causes adenocarcinoma of the stomach
-destruction of epithelium and mucous layer may be major risk factor for cancer -H. pylori are concentrated at the pylorus. When they are present for too long result in chronic superficial gastritis after weeks or months. If not eradicated after yrs or decades --> chronic atrophic gastritis --> after years leads to gastric adenocarcinoma. |
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Helicobacter pylori 5
Diagnosis |
Invasive:
Biopsy = this is best method. done by endoscopy. -Urease test of biopsy -Histology of biopsy w/Giemsa stain, -Grow culture. If bacteria are present then it is a diagnosis. High sensitivity tests. Non-Invasive: -ELISA (serology) = done by blood test. sensitivity is still high but not as diagnostic as biopsy tests (Abs last for long time thus can't diff. bet. old & new infection) -Urea breath test = patient drinks C14 labeled urea. H. pylori has urease. The urea will be split into C14 labeled CO2 and if measure high level of CO2 then test is +. |
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Helicobacter pylori 6
How the bacterium survives in the acidic environment of the stomach |
-the bacteria have enzymes that can dissolve the mucus of the stomach, resulting in a more basic pH
-they have urease which breaks down urea resulting in basic product like ammonia -duodenum is not very acidic, so some bacteria can live there w/out a problem -the bacteria are found deep in the mucous which is impermeable. grow at pH 6-7. |
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Helicobacter pylori 10
Treatment |
-beta-lactam Antibiotics for 2 weeks together with macrolides, tetracycline, clarithromycin, amoxicillin
-bismuth subsalicylate (stomach lining protector) and metranidazole (a.k.a flagellin-this is a good medicine for anearobic bacteria). -proton pump inhibitors (PPI- commercial name is omeprazole, lasopraxole, rabeprazole, esomeprazole, pantoprozole) to inhibit some of the acidity made in stomach to allow the ulcer to heal. -H2 blockers - cimetidine, ranitidine, famotidine, nizatidine |
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Helicobacter pylori 3
Virulence factors |
-catalase + (neutralizes peroxides thereby avoiding phagocytosis)
-urease (neutralizes stomach acid, creating a more supportive environment for microorganism) -protease (dissolves mucous) -flagella (can penetrate mucous layer, protecting them from acid environment) -oxidase + (redox rxn) |
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Helicobacter pylori 4
Clinical presentation |
-nausea & vomiting which can persist for yrs.
-pain upon eating acidic food (b/c stomach mucous layer has been destroyed) -achlorhydric gastritis -bad breath |
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Helicobacter pylori 2
Associated diseases |
-antral gastritis
-duodenal (peptic) ulcer -gastric ulcer -gastric carcinoma |
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Helicobacter pylori 7
Pathogenesis |
-pathogenic mechanism unknown
-produce 100X more urease than nonaffected persons -autoimmune response -toxins, active inflammatory cells -incubation is a few days |
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Enteric bacilli (Endotoxins) 4
Endotexemia |
-endotoxins in the blood
-common cause of death in hospitals, regardless of microorganism causing it. -show toxic effect in very low concentration |
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Enteric bacilli (Endotoxins) 2
Endotoxin |
-complex of LPS derived from cell walls & liberated when bacteria lyse.
-both pathogenic and non pathogenic bacteria have endotoxins -thus no correlation between pathogenicity and endotoxin production -endotoxins from various bacteria cause same biological effect but have diff. antigen structure. -heat stable, high molecular weight -include 2 important structures: O-antigen (O-fraction) and A-antigen (Lipid A) -endotoxins show toxic effect at very low concentrations: <10^ -12 g/ml or 10^ -15 M. *LPS =endotoxin = AgO |
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Enteric bacilli (Endotoxins) 1
LPS |
outermost portion of the outer membrane of gram (-) bacteria
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Enteric bacilli (Endotoxins) 5
Sources of endotoxemia |
1. liver impairment (liver normally detoxifies endotoxins resulting even from normal flora of intestine)
2. prevention of blood to intestine (endotoxins don't leave GI as long as there's proper amount of blood in GI) 3. hemorrhage 4. burns (lead to release of vasoactive substances, changes in blood vessel permeability) 5. sepsis |
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Enteric bacilli (Endotoxins) 6
Pathophysiological effects of endotoxins/endotoxemia |
1. fever (endotoxins activate temp. center. this is to tell us something is wrong)
2. leukopenia 3. hypoglycemia 4. hypotension 5. impaired organ perfusion & acidosis 6. activation of C3 and complement cascade 7. DIC (disseminated intravascular coagulation --> formation of blood clots in vessels throughout body) 8. death (may occur as result of massive organ dysfunction, shock, and DIC) |
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Enteric bacilli (Endotoxins) 7
Limulus lysate test |
-classic test to evaluate quantities of endotoxin
-can detect levels as low as 10^ -12 g/ml (or 5 X 10^ -15 M) --> this is borderline w/endotoxemia -amoebocytes of limulus (a type of crab) jellify in presence of endotoxins |
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Enteric bacilli (Endotoxins) 3
2 important structures of the LPS/endotoxin |
A-antigen/Lipid A = phospholipid. identical in all gram(-) bacteria. toxigenic portion. the toxin from various bacteria can produce same biological effect.
O-antigen/fraction O = polysacchride. antigenic fraction. NOT important for endotoxemia. structure varies among bacteria. |
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Enteric bacilli (intro)
Characteritic of enterics |
gram (-) bacilli
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Enteric bacilli (intro)
4 main groups of enterics |
Enterobacteriaceae
Vibrionacaeae Pseudomoadaceae Bacteroidaceae |
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Enteric bacilli (intro)
TSI (triple sugar iron) test |
-Sugar fermentation: 0.1% glucose, 1% sucrose, 1% lactose
-H2S formation: ferrous sulfate for detection of H2S (FeS) black (FeS is the end product and is black) -bottom of tube, anaerobic conditions; on slant is aerobic -pH indicator (yellow, low pH; red, high pH) sugar fermentation --> acid prod. --> pH decrease --> indicator color change -gas formation -innoculation by stabbing bacteria into butt -final identification into species/strains however is by serology (antigen structure, agglutination) |
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Enteric bacilli (intro)
TSI test interpretation of results |
-bottom is yellow, top is red --> only glucose was fermented (10X less).
only small amount of acid produced and fermentation products are oxidized into CO2 and H2O by oxidative decarboxylation of proteins. (turns alkaline, red, increase pH) -entire tube is yellow --> lactose, sucrose, & glucose were fermented. acidic fermentation products, decrease pH. |
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Enteric bacilli (intro)
Antigenic structure |
150 heat stable O
100 heat labile K (capsular) 50 H (flagellar) there exists overlapping antigenic structure between enterobacteriaceae. antigenic formula for ex: E. coli O55:K5:H21 |
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Enteric bacilli (intro)
O-antigens |
-located on most external part of LPS
-heat stable -consists of repeating units of polysaccharide -detection is by bacterial agglutination -antibodies to O-antigens are mostly IgM |
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Enteric bacilli (intro)
K-antigens |
-external to O-antigen (covers that O-antigen like a capsule)
-heat labile -present in some enterobacteriaceae -may interfere w/ agglutination -may be associated w/ virulence (ex: E. coli K1 --> neonatal meningitis E. coli K --> UTI) -made of proteins and polysaccharides (E. coli) |
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Enteric bacilli (intro)
H-antigens |
located on flagella (makes up the subunits of the flagella)
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Enteric bacilli (intro)
Gastroenteritis |
syndrome characterized by GI symptoms including nausea, vomiting, diarrhea, and abdominal discomfort
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Enteric bacilli (intro)
Diarrhea |
abnormal fecal discharge characterized by frequent and/or fluid stool; usually resulting from disease of the small intestine and involvoing increase fluid and electrolyte loss
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Enteric bacilli (intro)
Dysentery |
an inflammatory disorder of the GI tract often associated w/ blood and pus in the feces and accompanied by symptoms of pain, fever, abdominal cramps, usually resulting from disease of the large intestine
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Enteric bacilli (intro)
Enterocolitis |
inflammation involving the mucosa of both the small and large intestine
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Enteric bacilli
Pathogens w/ animal reservoir |
E. coli
Salmonella Campylobacter Clostridium perfringens Yersinia enterocolita |
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Enteric bacilli
Foodborne pathogens |
E. coli (ETEC)
Salmonella Campylobacter Vibrio cholera Shigella Clostridium perfringens Bacillus cereus Vibrio parahaemolyticus Yersinia enterocolita |
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Enteric bacilli
Waterborne pathogens |
E. coli (ETEC)
Salmonella Campylobacter Vibrio cholera |
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Enteric bacilli (intro)
MacConkey Plate |
-is a diagnostic media with indicator that is red in acidic pH and low concentration of gecion violet => inhibit G+ bacteria
-if lactose +, can use lactose as carbon source => get acidic end product => turn indicator red. -most disease causing bacteria in GI are lactose (-). |
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Enteric bacilli (intro)
MacConkey Plate |
-is a diagnostic media with indicator that is red in acidic pH and low concentration of gecion violet => inhibit G+ bacteria
-if lactose +, can use lactose as carbon source => get acidic end product => turn indicator red. -most disease causing bacteria in GI are lactose (-). |
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Enteric bacilli (intro)
microorganism that causes typhoid fever (a type of enteric fever) |
Salmonella typhi
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Enteric bacilli (intro)
microorganism that causes typhoid like fever/paratyphoid (a type of enteric fever) |
Salmonella paratyphi A, B, & C
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Enteric bacilli (intro)
microorganism that causes salmonellosis (food poisoning) |
most Salmonella (not typhi or paratyphi)
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Enteric bacilli (intro)
microorganisms that cause food poisoning other than salmonellosis |
Clostridium botulinum
Clostridium welchii Enterotoxin Staph. |
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Enteric bacilli (intro)
microorganism that causes bacillary dysentery |
Shigella (sonnei, flexneri, boydi, dysenteriae)
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Enteric bacilli (intro)
microorganism that causes cholera |
Vibrio cholerae (and biotype el tor)
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Enteric bacilli (intro)
microorganism that causes acute gastroenteritis (infantile) |
E. coli
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Enteric bacilli (intro)
microorganism that causes gastroenteritis |
Yersinia enterocolita
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Enteric bacilli (intro)
microorganism that causes enteritis |
Campylobacter jejuni
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Enteric bacilli (intro)
Species of normal flora which are pathogenic under special circumstances |
Coliform bacilli: E. coli, Klebsiella
Enterobacter (Aerobacter), Serratia Arizona, Edwardsiella, Citrobacter Providentia, Proteus Pseudomonas group Alcaligenes group |
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Enteric bacilli (intro)
Species which are always pathogenic |
Salmonellae group
Shigellae group Vibrio cholerae Yersiniae group Campilobacter |
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Enteric bacilli (intro)
Species which are normal flora of GI but pathogenic in other parts of body |
Str. fecalis
Bacteroides Clostridium (some species) |
