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65 Cards in this Set
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enterobacteriaceae general characteristics |
gram negative rods, facultative (can grow either with or without oxygen), non sporulating (really the only spore formers are gram positive rods) |
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what are the indigenous flora of the GI tract |
anaerobic bacteria (10^10 to 10^11 per gram); facultative/aerobic bacteria (10^8 to 10^9 per gram); so there are way more anaerobics but we are talking about the facultatives today; pathogenic potential |
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antigenicity factors of enteric gram negative rods |
O antigen= outer membrane of cell wall, lipopolysaccharide (so the lipid A which has all of the endotoxic activity), the core (common between all of the enterobacteriacea and can also be called the R antigen), and the O specific chain); K antigen= capsular antigen, polysaccharide, anti phagocytic (in salmonella it is called Vi antigen); H-antigen= flagella, protein; pili/fimbriae |
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infections produced by endogenous enteric bacteria |
abscess, UTI, wound infection, septicemia, pneumonia, meningitis, endocarditis |
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common virulence factors- endotoxin |
the lipid A component of the LPS; it is a pyrogen becuase when a phagocyte attacks the bac cell the lipid A releases a substance that goes to the hypothalamus and causes fever; blood changes (leukopenia, leukocytosis, thrombocytopenia); capillary permeability increase; shock |
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other common virulence factors |
capsule, antigenic phase variation (K and H ags) (a bac can change their antigens to escape detection), type III secretion systems (bac using hypodermic needle to insert chemotoxin into a host cell), sequestration of growth factors (like iron), resistance to serum killing |
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escherichia coli: characteristics |
exclusive colonization of mammalian intestinal tract (some strains are normal flora (and only cause disease when they get out of the intestines) and some strains that are enteric pathogens (causes disease wherever they are)); antigenically diverse |
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escherichia coli: antigenic designation |
example O55:K9:H6 means somatic O55, capsular K9, and flagella H6; many different serotypes |
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escherichia coli: clinical diseases |
septicemia, UTI, neonatal meningitis, intraabdominal infections, gastroenteritis |
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Klebsiella- 2 species we are concerned with |
klebsiella pneumoniae (forms thick mucoid capsule that makes the pneumoniae bad and also makes it difficult for the immune system and antibiotics to kill it) and klebsiella oxytoca; this is a normal part of the intestinal flora that only causes infections when it is out of the intestinal tract |
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klebsiella clinical disease |
pneumonia, wound and soft tissue infections, UTI |
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klebsiella granulomatis formerly known as |
donovania granulomatis or calymmatobacterium inguinale; this is a normal part of the intestinal flora that only causes infections when it is out of the intestinal tract |
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klebsiella granulomatis- clinical diseases |
this is an STD; ganulomatis disease of genitalia and inguinale area; forms lesion that is very similar to siphilus; under microscope it has PMNs that are full of these bac |
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proteus mirabilis- clinical diseases |
this is a normal part of the intestinal flora that only causes infections when it is out of the intestinal tract; UTI; it causes the hydrolysis of urea |
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action of urease |
breaks apart urea; part of the breakdown product is bicarbonate buffer that causes an increase in the pH of urine which causes Ca and Mg to precipitate out and form kidney stones and it also damages the epithelial cells of the urinary tract |
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enterobacteri, citrobacteri, morganella, serratia- clinical diseases |
hospital acquired infections; citrobacter koseri- meningitis and brain abscess in neonates |
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3 types of intestinal infections caused by pathogenic enteric bacteria |
watery diarrhea, dysentery, and systemic involvement |
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watery diarrhea- site infection and examples of bac that can cause this |
proximal small bowel; vibrio cholerae and e coli (ETEC); this is due to enterotoxin production |
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dysentery- site of infection and examples of bac that can cause this |
distal small bowel or colon; shigella spp., EPEC, EIEC, EHEC, EAEC, DAEC, and V. parahaemolyticus; this is due to superficial ulceration |
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systemic involvement- site of infections and examples of bac that can cause this |
distal small bowel or colon; salmonella, campylobacter, yersinia, helicobacter, plesiomonas; this is due to penetration (systemic) |
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enterotoxigenic E coli (ETEC): disease process |
ingestion of fecally contaminated food or water (takes a large dose to become infected); multiplication in small intestine; attachment to epithelial cells (colonization factor antigens (CFA/I, CFA/II, CFA/IV)(so it needs to have a plasmid that carries these), adhesins); enterotoxin production; do not infect the intestinal cells just sit on top and make toxin |
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E. coli enterotoxins produced |
heat labile enterotoxin (LT-I, LT-II) (mechanism of action like cholera toxin), heat stable enterotoxin (STa, STb) (stimulates guanylate cyclase); plasmid mediated; some only make LT, some only make ST, and some make both |
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mechanism of action of escherichia coli enterotoxin |
ribosylates adenylate cyclase making a lot of cAMP (can not longer stop making cAMP) which leads to secretion of Cl- out of the cell into the intestine and prevents the uptake of Cl and Na into the cell; the osmolarity of the cell then causes the outpouring of water into the intestine=diarrhea |
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ETEC: symptoms and treatment |
watery diarrhea in adults and infants; traveler's diarrhea; treatment is fluid replacement |
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enteric pathogens that invade colon tissue but do not get into the blood stream |
shigella species, enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC), enterohemmorhagic E. coli (EHEC), and enteroaggregative E. coli (EAEC) |
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shigella species that we are interested in |
shigella sonnei, shigella flexneri, shigella dysenteriae, shigella boydii |
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shigella- what or who does it infect |
humans and other primates are the only reservoir; primarily a pediatric disease |
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shigella: transmission |
contaminated hands, food, or water (contaminated with fecal matter); doesn't require a huge dose to cause infection |
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shigella: institutional outbreaks |
daycare centers, mental hospitals, nursing homes, prisons, indian reservations |
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shigella: disease process |
multiplication in small intestine (toxin production); penetration of large intestine epithelial cells (plasmid mediated) anf then production of enterotoxins (so looks like enterotoxigenic infection at first); PMN inflammatory response; when it gets to the colon the M (mucus) cells take them up and then the bac multiply and can spread through hijacking the host cell's actin filaments to push itself from cell to cell; this dividing causes the death of the host cells and this causes sloughing and blood loss = bloody diarrhea |
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shiga toxin: produced by what species and what are its characteritics |
produced by shigella dysenteriae, protein (70,000 daltons), consists of A and B subunits (inactivates protein synthesis leading to cell death), damage to intestinal epi and glomerular endothelial cells (renal failure) (the bac DOES NOT get into the blood stream but the toxin does which is why there is renal failure) |
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shigella: treatment |
antibiotic therapy, fluid replacement |
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enteropathogenic E. coli (EPEC) causes what disease and what is the disease process |
infantile diarrhea; adherence to enterocytes in small bowel, type III secretion of cytotoxin into cells (so bloody diarrhea again like shigella) |
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enteroinvasive E. coli (EIEC)- what disease and what is the disease process |
shigella like disease (invasion of colonic epithelial cells); plasmid mediated invasion; bloody diarrhea (inflammation, ulceration, dysentery) |
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enterohemorrhagic E. coli (EHEC): serotype and disease that it causes |
E. coli serotype O157:H7 (hemorrhagic colitis); reservoirs cows (beef)(so don't eat undercooked beef) (can also be found in produce that is grown near farms) |
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the H antigens of Escherichia coli consist of: a. cell wall lipopolysaccharide b. fimbriae proteins c. flagella proteins d. pili proteins e. capsular polysaccharide |
c. flagella proteins |
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enterohemorrhagic E. coli: disease process |
ingestion of fecally contaminated food (small dose); multiplication in large intestine; shiga like cytotoxins (disrupts protein synthesis, hemorrhages in the colon); hemolytic uremic syndrome (HUS) (anemia, thrombocytopenia, acute renal failure) |
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enteroaggregative E. coli (EAEC): where is it found, what does it do |
developing countries; aggregates with itself; autoagglutination; small intestine epithelial cell damage (diarrhea); chronic diarrhea rather than the acute diarrhea from everything else described so far |
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all of the following statements regarding enterotoxigenic Escherichia coli enterotoxin are true except: a. increases intracellular concentration of cyclic AMP (cAMP) b. prevents sodium and chloride absorption into intestinal epithelial cells c. ribocylates the adenylate cyclase complex d. causes and death and sloughing of the epithelial cells e. can cause the pt to have 'rice water' diarrheal stools |
D. causes death and sloughing of the epi cells |
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shigella dysenteriae can be transmitted to humans through ingestion of food and water contaminated with the intestinal contents of infected domesticated animals: a. true b. false |
false (only in humans and primates) |
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salmonella: antigenic structure |
somatic (O) antigens, flagella (H) antigens, and capsular (Vi) antigens |
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salmonella classification |
don't worry about this slide just know what he calls the different bac; kauffman-white scheme (serotypes given species designation); CDC scheme= S. typhi (typhoid fever, human acquired), S. choleraesuis (septicemia, animal acquired), and S. enteritidis (gastroenteritis, animal acquired); correct nomenclature= salmonella enterica, serovar Typhi (salmonella typhi) |
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salmonella transmission |
ingestion of contaminated food and water (needs large dose); human reservoirs= human carriers (feces and urine) for salmonella Typhi and salmonella paratyphi; animal reservoirs= wild animals (poultry, reptiles, rodents, birds), domestic animals, eggs for all of the other species |
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diseases produced by salmonella species |
gastroenteritis= salmonella typhimerium; enteric fever (typhoid fever)= salmonella typhi; septicemia= salmonella choleraesuis |
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salmonella gastroenteritis (food poisoning): disease process |
ingestion of contaminated food or water (10^6 to 10^7 organisms), adherence to epithelial cells (distal ileum and colon), migration through epithelial cells to lamina propria (PMN leukocyte response and inflammation); enterotoxin production (outpouring of fluid); symptoms= nausea, fever, abdominal pain, diarrhea; no therapy recommended besides fluids |
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enteric fever (typhoid fever): disease process |
typhi and paratyphi usually cause this; ingestion of contaminated food or water, incubation period of 1 to 2 weeks, organism invades epithelium cells of distal ileum and colon, multiply within macrophages, delivered to mesenteric lymph nodes, primary bacteremia, multiply within fixed macrophages, secondary bacteremia, localization in various organs (liver, gall bladder, spleen, bone marrow, lungs, kidneys, mesenteric lymph nodes); can then enter intestine via infected bile (if it infected the bile duct) and this is the first time that you will get the intestinal symptoms like bloody diarrhea, invade lymphoid tissue; each bacteremia will bring with it the fever (because of the LPS); can become a chronic carrier if you have infection of the bile duct because it is hard to treat it (bile inactivates antibiotics) |
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typhoid fever: symptoms |
chills, spiked fever, diarrhea, abdominal pain, cough, enlarged spleen and liver; forms necrotic lesions |
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septicemia caused by what organisms |
S. choleraesuis (same as typhi and paratyphi except it can't infect the bile duct so never get intestinal symptoms), S. typhi, and S. paratyphi |
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septicemia: seen in what pts and what is it similar to |
seen in pediatric, geriatric, and AIDS pts; similar to enteric fever but no localized infection of intestinal tissue |
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prevention of salmonellosis |
exclusion of salmonella carriers, separate surface for preparation of different food types, adequate cooking and refrigeration, proper sewage disposal, pasteurization of milk, water treatment |
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pt materials for isolating salmonella |
typhoid fever= blood, feces, urine, pus; septicemia=blood, urine, pus; gastroenteritis=feces |
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salmonella treatment |
fluid replacement, antibiotics (enteric fever and septicemia but not gastroenteritis) |
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typhoid vaccines |
oral vaccines (S. typhi, strain Ty21a); parenteral vaccines (heat phenol inactivated S. typhi, capsular polysaccharide (Vi antigen) |
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hemolytic uremia syndrome is a serious complication in young children due to infection by: a. salmonella b. enterotoxigenis E. coli c. enteropathogenic E. coli d. enterohemorrhagic E. coli e. enteroinvasive E. coli |
d. enterohemorrhagic e coli |
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yersinia pestis: found where in the world, what are its reservoirs, how is it transmitted |
southwest US (prarie dogs); reservoirs are rats and fleas in urban plague and prarie dogs, rabbits, cats, and fleas in sylvatic plague; transmission is interruption of rodent flea rodent cycle, human flea, handling infected tissue, inhalation, and lab acquired |
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yersinia pestis: virulence factors |
fraction 1 (envelope antigen)= F1 gene (antiphagocytic); endotoxin- responsible for symptoms; murine toxin (damage to peripheral vascular system leading the death); coagulase and fibrinolysin breaks down tissue; plasminogen activator (degrades complement); type III secretion system (YopH gene product (antiphagocytic), YopE gene product (disrupts actin), Yop J/P gene products (antiphagocytic)) |
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yersinia pestis: clinical manifestations |
inoculation and incubation; bubonic plague- swelling of lymph nodes; septicemic plague if it gets in the blood (lung and meninges damage); pneumonic plague if it gets in the lungs (primary (get it through droplets from someone else, secondary (get it through the blood stream)); immunity if you survive to a minor extent |
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yersinia pestis diagnosis |
clinical diagnosis; gram stain (bubo aspirates, sputum, blood) see bipolar staining of bac (dark on the ends and clear in the center) very characterisitic; isolation; ID (biochemical tests, fluorescent antibody) |
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yersinia pestis: treatment |
antimicrobial agents as soon as possible; prevention (chemoprophylaxis- pneumonic plague contacts, flea borne household contacts, prevention); vaccination |
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other yersinia species |
yersinia enterocolitica, yersinia pseudotuberculosis |
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yersinia enterocolitica: reservoirs, clinical manifestations |
rodents, rabbits, game birds etc. are reservoirs; enterocolitis (mimics appendicitis), septicemia, arthritis, intrabdominal abscess, hepatitis, osteomyelitis |
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yersinia pseudotuberculosis: reservoirs, clinical manifestations |
rodents, rabbits, game birds etc. are reservoirs; causes a scarlet fever like syndrome (high fever, rash) |
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which enteric pathogen reseeds the intestinal tract via the bile duct: a. vibrio cholerae b. salmonella typhi c. enterotoxigenic escherichia coli d. shigella dysenteriae e. enteropathogenic escherichia coli |
b. salmonella typhi |
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the diagnosis of typhoid fever one week after ingestion of salmonella typhi is best made by: a. culture of urine b. culture of feces c. culture of blood d. serologically e. culture of skin lesions |
c. culture of blood |
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plague is transmitted by the: a. louse b. chigger c. flea d. mosquito e. tick |
c. flea |
