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Staphylococcus aureus
- Gram (+) grape like clusters
- Catalase (+)
- b-hemolytic
- coagulase (+): fibrin formation around the bac
- Protein A: bind the Fc portion of IgG
- Leukocidins
- Penicillinase
- Proteins to Tunnel Tunnel Through Tissue
- Hyaluronidase, Staphylokinase, Lipase, Protease
- Exotoxin Assault Weaponry
- Exfoliatin (scalded skin syndrome)
- Enterotoxins
- Toxic Shock Syndrome toxin (superantigen binds to MHCII--> Tcell outpouring of cytokines)
- Enterotoxins:
- - grow in food
- - 1-6 hr onset; <24 hrs duration
- - heat stable, resistant to hydrolysis by gastric & jejunal enzyme
- - acute inflammation of gastric and SI mucosa
- - binds to neural receptors in the gut --> stimulate vomiting center
- - vomiting, diarrhea, abdominal pain and occasionally fever
MRSA- resistant to b-lactams due to altered penicillin-binding protein
Causes acute bacterial endocarditis, osteomyelitis
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Bacillus Cereus related to Bacillus Anthracis
- gram (+) facultative anaerobic spore-forming rods
- motile, non-encapsulated, penicillin resistant, b-hemolytic
- Enterotoxic: similar to ETEC and cholera
- - lay spores in food
- - germinate in the food and release their enterotoxin
- - heat-labile toxin: rice; onset >6 hr, duration: 20-36 hrs
- increase cAMP which inhibit NaCl absorption and
- increase NaCl secretion. Nausea, abdominal pain and
- watery diarrhea
- - heat stable toxin: meat, vegetables; onset <6 hrs;
- duration: 8-20hrs; Severe nausea and vomiting.
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Clostridium difficile related to botulism, tetani, perfringens
(DIfficili causes DIarrhea)
gram (+) anaerobic spore-forming rods
antibiotics (clindamycin or ampicilin) --> kill normal flora (5-10days) --> Clostridium difficule grows spontaneously --> release Toxin A and B --> diarrhea, abdominal cramping and fever --> on colonoscopy reveal red inflammed mucosa, & areas of white exudate (pseudomembranes colitis) --> detect cytotoxin and enterotoxin in feces --> Rx Metronidazole or vancomycin
- Toxin A: enterotoxin stimulate infiltration of PMN into ileum -->induce cytokine production -->disrupts tight cell
- junctions
- Toxin B: cytotoxic causes actin depolarization --> loss of
- cell cytoskeleton --> cell death
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E. coli
gram (-) faculative anaerobes rod, oxidase (-)
- EMB agar: inhibit growth of gram (+); deep purple to back colonies
- MacConkey agar: bile salt inhibit gram (+); pink-purple colonies
- Sorbitol MacConkey: all E. coli except EHEC grow
- Antigenic Classification
- O antigen: the most external component of LPS (O=Outer)
- K antigen: capsule (Kapsule) that covers the O antigen
- H antigen: subunits of the bacterial flagella
- Diarrhea
- No Cell Invasion: SI, self-limiting (3-5 days), liq
- feces....ETEC, EPEC, EAEC, V. Cholera, V.
- parahaemolyticus, C. perfringers, Giardia lambica,
- cryptosporidium spp
- Invasion of the interstinal epithelial cells: LI, blood and
- pus in feces, last longer... EIEC, Shigella, Salmonella
- enteritidis, Entamoeba histolytica
- Invasion of the lymph nodes and blood: system
- symptoms of fever, headache and white blood cell count
- elevation... Salmonella typhi, Yersinia enterocolitica,
- Campylobacter jejuni
- Diseases
- - diarrhea
- - Urinary tract infection
- - neonatal meningitis
- - sepsis in hospitalized patients
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Enteropathogenic E. coli
(P= pediatrics)
yellow colonies, affects infants worldwide at low dose and adults at high dose
- P --> P
- BfpA: Bundle forming pilus- attachment to enterocytes
- Type III secretion system of Tir
- intimin- modification of enterocyte cytoskeleton protein
binding of bacteria --> flattening of microvilli and formation of filamentous actin pedestals disrupt intestinal absorption --> malabsoption --> H20 diarrhea
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Enteroaggregative E. coli
Chronic H2O diarrhea associated w/ growth retardation in children and persistant diarrhea in AIDS patients.
more common in developing countries
AAF- autoagglutination in a "stacked brick"
dec fluid absorption due to biofilm on intestinal surface
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Enteroinvasive E. coli
(invasion=dysentery)
pInv gene: invasion gene on plasmid
invade the epithelial cells-->immune mediated inflammation ( fever) --> necrosis
bloody diarrhea w / leukocytes
clinical manifestation similar to Shigella
- Rx: TMP-SMX, ciprofloxacin
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Enterohemorrhagic E. coli
(H=hemolytic uremic syndrome)
Reservoir: intestine of healthy cattle
infection: uncooked beef, P--> P, H2O
release Shiga-like toxin (lysogenic bacteriophage): inhibit protein synthesis by inhibiting 60S ribosome --> Hemolytic uremic syndrome (HUS) w/ anemia, thrombocytopena, and acute renal failure which might need dialysis <-- O157:H7
Bloody diarrhea w/out leukocytes
DOES NOT ferment sorbitol
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Enterotoxigenic E. coli
(T=traveler's diarrhea)
- Cfa (colonization factor=pili)
- LT= heat labile toxin = AB toxin...LTA binds to
- ADPribosylates protein and increase cAMP --> inc NaCl
- secretion and dec NaCl absorption
- ST= heat stabile toxin= activation of cGMP
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Shigella (dysenteriae, flexneri, boydii, sonnei)
- nonmotile green colonies, acid resistant
- require only 101 organisms
- doesn't ferment lactose and doesn't produce H2S
- HUMANS are the only hosts...ALWAYS a pathogen
- infect preschool children and nursing homes
- WASH hands
invade intestinal epithelial cells (fever, shallow ulcers) and release Shiga toxin
Enter mucosa through M cells on Peyer patches --> enter underlying macrophages --> cytokine production --> leukocyte distroy tight junctions --> bacteria invade basal surface of epithelial cells --> cell to cell spread using actin and other cytoskeleton protein
bloody diarrhea w/ leukocytes
Rx: TMP-SMX, ciprofloxacin
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Salmonella enteritidis
(salmon swim)
- motile blue green colonies w/ black centers, acid sensitive
- doesn't ferment lactose but produce H2S; Vi antigen
- lives in GI tracts of ANIMALS (turtles, chicken, and uncooked eggs)
- ALWAYS a pathogen
- 1. ruffles- plasma membrane sites w/ filamentous actin cytoskeletal --> rearrangement
- 2. invasion- bacteria are captured by dendritic cells and transported to lymph nodes. some bac escape to bloodstream --> bacteriemia
- 3. inflammation
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Salmonella typhi
(typhoid fever)
- motile blue green colonies w/ black centers, acid sensitive
- doesn't ferment lactose but produce H2S
, Vi antigen - HUMANS are the only hosts....ALWAYS a pathogen
- - after invading the intestinal epithelial cells (M cells and macrophages) it invades the regional lymph nodes --> inflammation and ulceration of payer patches
- - 1-3 weeks after exposure and includes fever, headache and abdominal pain usually localized to RLQ mimicks appendicitis, spleen may enlarge, rose spots on the abdomen, cholecystitis, septicemia
constipation more freq than diarrhea
culture blood or feces
- Carrier State: harbor typhi in their gallbladders and excrete bacteria constantly...are n't actively infected themselves
- Rx: Fluoroquinolones
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Yersinia enterocolitica
gram (-) rod, w/ bipolar staining, Zoonotic pathogen, can grow at cold temp
severe pain in RLQ mimicking appedicits
- Invasion: Yops (type III secretion system)
- -invade M cells...spread to regional lymph nodes and the bloodstream. Mesenteric LN swell and sepsis can develop
Enterotoxin: diarrhea w/ blood and pus, fever, abdominal pain
pet feces (puppies), contaminated milk or pork. common outbreak in day care centers.
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Vibrio Cholera from same family as vibrio parahaemolyticus, Campylobacter jejuni, Helicobacter pylori
gram (-) curved rods, faculitative anaerobe, oxidase (+), motile, growth on alkaline media-susceptible to stomach acid, grow on TCBS: Thiosulfate Citrate Bile Salts Sucrose agar
NO p--> p transmission
- Tcp: co-regulated pilus-bacteria attaches to the epithelial cells
- Choleragen (Ctx): released cholera toxin (AB-lysogenic phage). hypersecretion of electrolytes & H2O. same mech as ETEC.
Rice Water diarrhea
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Vibrio parahaemolyticus
gram (-) curved rods, faculitative anaerobe, oxidase (+), motile, growth on alkaline media-susceptible to stomach acid. Warm coastal marine bacteria.
uncooked seafood (sushi)
Japan
self limiting
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Campylobacter jejuni from same family as vibrio parahaemolyticus, Vibrio Cholera, Helicobacter pylori
gram (-) curved/spiral (gall wing) rods, faculitative anaerobe- microaerophilic atmosphere, oxidase (+), motile,grow at as high temp as 42C, Zoonotic disease: domestic animals, unpasteurized milk and poultry,
Major cause of diarrhea in US children
colonization --> toxin production --> translocation --> cell invasion --> inflammatory response diarrhea w/ blood and pus in stool
Complications: Guillain Barre Sydrome, reactive arthritis
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Helicobacter pylori from same family as vibrio parahaemolyticus, Vib
rio Cholera, Campylobacter jejuni
gram (-) curved rods, faculitative anaerobe, oxidase (+), motile, growth on alkaline media
mucous layer invasion --> alternation of gastric acid production --> gastric inflammation --> tissue distruction
- Mucinase & phospholipase: disrupt gastric mucus penetration of mucous layer
- Flagella: penetration into gastric mucous layer
- urease (+): ammonium neutralizes gastric acid
- cytotoxins: death of gastric epithelial cells
duodenal ulcers, peptic gastric ulcer, adenocarcinoma, lymphoma
Diagnosis: biopsy, stool antigen test, urea breath test, PCR
Rx: PPI, amoxicillin, clarithromycin
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Clostridium perfringens
gram (+), spore forming, obligate anaerobic bacilli
alpha- toxin (lecithinase, a phospholipase) causes myonecrosis (gas gangrene)--> CT scan reveals pockets of gas w/in the muscles and subcutaneous tissue. as the enzymes degrade the muscles, a thin, blackish fluid exudes from the skin.
palpation reveals a moist, spongy crackling consistency to the skin = crepitus
H2O diarrhea mild and self limiting from enterotoxin produced during sporulation in the gut.
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Protozoa
free-living, single celled, eucaryotic cells w/ a cytoplasmic membrane and cellular organelles, mitochondria, food vacuoles and endoplasmic reticulum
It's the cyst form that is infective when ingested by humans. Following ingestion it converts back into the motile form, trophozoite
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Entamoeba histolytica
Protozoa, pseudopodia, asymptomatic infections, bloody (dysentery) diarrhea, may penetrate the portal blood circulation forming abscesses in the liver, followed by spread through the diaphragm into the lung. Causes pulmonary abscesses that often is deadly.
excystation in SI --> trophozoites go to LI multiply and produce cyst ( encystation)--> feces
trophozoites can convert to a precyst form (contain aggregates of ribosomes, called chromotoid bodies, food vacuoles and two nuclei)
Mature cyst contain four nuclei
Trophozoites: single nucleus w/ a central karyosome and uniform peripheral chromatin. red blood cells in the cytoplasm suggest active disease
- Rx: metronidazole, tinidazole (DNA damage through the reactive reduction metabolites occurs in anaerobes/protozoals, inhibit 450)
- Tinidazole- intestinal colonization. Invasion: metronidazole followed by iodoquinol
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Giardia lamblia
protozoa, asymptomatic infections, watery diarrhea
excystation in SI --> trophozoits attach to mucosa by ventral sucking disk (coats the SI, interfearing w/ fat absorption- HORRIBLE ODOR) --> encystation as going toward colon
do NOT invade the intestinal wall but inflammation reaction to damaged epithelial cells is present
Sewage contamination, beavers, rodents (campers, hikers)- H2Oborne outbreak
- Rx: metronidazole, tinidazole (DNA damage through the reactive reduction metabolites occurs in anaerobes/protozoals, inhibit 450), Nitrazoxanide (inhibits the pryruvate: ferredoxin oxidoreductase pathway)
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Cryptosporidium parvum and hominis
protozoa, asymptomatic infections, acid fast stain (oocysts identified), watery diarrhea
round oocyst (4 motile sporozoites). life cycle occurs w/in the intestinal epithelial cells --> paralize --> causes diarrhea and abdominal pain. Self limited in immunocompetent individuals. AIDS and immunosuppressed individuals severe diarrhea (>50 stools/day)
in water parks, community swinning pools (not killed by cholorination)
Nitrazoxanide (inhibits the pryruvate: ferredoxin oxidoreductase pathway)
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Nematodes (roundworms)
mature into adults w/in the human intestinal tract
Ascaris lumbricoides, Trichuris trichiura (whipworm), Enterobius vermicularis (pinworm) acquired by ingestion of eggs.
Necator americanus (hook worm), Strongyloides stercoralis penetrate though the skin
Trichinella spiralis acquired byt he ingestion of encysted larvae in muscle (pork meat)
Trichuris trichiura (whipworm), Enterobius vermicularis (pinworm) stay in the intestinal tract
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Ascaris lumbricoides
most common worldwide, largest nematode, asymptomatic
egg --> larvae in SI --> blood --> lungs --> coughed and swallowed --> mature to adults in SI -->eggs --> excreted in feces
invade bile ducts, gall bladder, appendix and liver
children suffer from malabsorption
Diagnosis: eggs (round/oval knobby; thick shell; external layer stained bile); adults/larve in sputum
Rx: Albendazole or mebendazole (preventing microtubule polymerization & impair glucose uptake); pyrantel pamoate (agonist of nematode Ach-NR causes contraction & paralysis of parasites)
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Necator americanus/Ancylostoma duodenale
hookworm
2nd most common nematode,
larval form lives in the soil and eats bacteria and vegetation --> transforms into a long slender filariform larvae that can penetrate skin of feet --> lung alveoli --> coughed and swallowed --> adult worm in the SI --> eggs in the feces
hookworm sucks blood from teh wall of the intestine --> causes iron deficiency anemia
diarrhea, abdominal pain and weight loss; intense itching and rash at the site of penetration through the skin
Diagnosis: non-bile stained segmented eggs; thin shell developing larva inside
Albendazole or mebendazole (preventing microtubule polymerization & impair glucose uptake); pyrantel pamoate (agonist of nematode Ach-NR causes contraction & paralysis of parasites)
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Strongyloides stercoralis
- causes chronic/recurrent infection
- larval form (rhabditiform) lives in the soil and eats bacteria and vegetation --> transforms into a long slender filariform larvae that can penetrate skin of feet --> lung alveoli --> coughed and swallowed --> adult worm in the SI --> eggs hatch in the intestine --> filariform larvae has three fates:
- 1. autoinfection: go to lung and continue the cycle
- 2. pass out in the feces and infect the next individual
- 3. pass out in the stool --> develop into male and female --> produce fertilized eggs --> hatch --> infect humans
vomiting, abdominal bloating, diarrhea, anemia and weight loss, prurititic rash
when patients given immunosuppressive medications such as prednisone --> develop severe autoinfection --> filariform larvae invade the intestine, lung and other organs causing pneumonia, ARDS, and multi-organ failure.
Diagnosis: rhabditiform larvae in feces
- Albendazole or mebendazole (preventing microtubule polymerization & impair glucose uptake); ivermectin (GABA mediated signal transduction cause worm paralysis)
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Trichuris trichiura
Whipworm
slow life cycle, eggs hatch in GI tract --> migrate to LI --> mature adult produce thousands of eggs/day for one year --> eggs must incubate in moist soil for 3-6 weeks before they become infective
appendicitis, rectal prolapse, abdominal pain and diarrhea
Diagnosis: look like barrel shaped eggs w/ bipolar plugs/ bile stained
mebendazole
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Enterobius vermicularis (Pinworm)
most common in US; infections freq in school/preschool child; humans only host; autoinfection (retroinfection)
eggs --> adult in cecum and ascending LI --> female migrates to perianal area at night to lay her eggs --> perianal itching (pruritus) --> scratch --> infect
Diagnosis: scotch tape pick up eggs (ova flattened on one side larvae inside) in the morning before defecation & washing
- mebendazole, albendazole, pyrantel pamoate (treat the whole family)
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Toxocara canis or cati
- eggs ingested from handling puppies/cats
- visceral larva migrans: larvae wander aimlessly until they die because larvae is outside of its natural host
- cause inflammation; can cause blindness if larvae endup in retina
- Rx: Mebenazole, surgery
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Cestodes (tapeworms)
- long and flat like a typewriter ribbon worms
- don't have digestive tract --> suck up nutrients that have already been digested by their host
- hermaphrodites
- consists of a chain of boxlike segments called proglottids
- Scolex the head has suckers/hooks
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Taenia solium (pork tapeworm)
uncooked pork (pigs/swine) infected w/ larvae --> tapeworm attaches to the mucosa of the intestine via hooks on its scolex --> release eggs
in the animal's muscle tissue, the larvae develop into another larval form, the cysticercus --> round fluid-filled bladder w/ the larval form w/in
cysticercosis occurs when humans play the role of the pig and ingest eggs rather than encysted larvae --> eggs hatch w/in small intestine --> larvae migrate throughout the body (brain (neurocystecercosis)and skeletal m (no symptoms) most common, causes blurry and disturbed vision in the eyes)
- Praziquantel: increase permeablity of cell membranes to Ca2+ resulting paralysis & death. Bitter taste
- use -bendazole for nurocysticercosis
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Taenia saginata (Beef tapeworm)
- same life cycle as Taenia solium whoever don't develop cysticerci when ingest eggs
- intermediate hosts (cattles)
- undercooked beef muscle
- benign
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Diphyllobothrium latum (fish tapeworm)
- ingesting larvae from raw freshwater fish....ingestion of rare/raw pickled fish containing a sparganum (plerocercoid)
- 2 intermediate: crustacean and a fish
Causes B12 deficiency anemia
Praziquentel
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Echinococcus granulosus
- Definitive host: carnivores in sheep-raising areas
- ingestion of eggs --> larvae can go almost anywhere, liver is most common site where it forms hydatid cysts
- Causes anaphylaxis if echinococcal antigens are released from cysts (surgeons inject ethanol before removal to kill daughter cysts)
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