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61 Cards in this Set

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  • Back
what are common traits and common virulence factors of the enterobacteriae?
bacilli, gram neg, facultative. endotoxin (LPS). capsule of polysaccharide that interferes with opsonizing antibodies and prevents phagocytosis. antigenic phase variation via loss of expression (like flagella or capsule), change of gene expression (different protein made but still functions as capsule or flagella). type III secretion systems. sequestration of growth factors (like iron). resistance to serum killing. resistance to antibiotics.
what are the three true commensals of the enterobacteriae?
E. coli, klebsiella, and proteus
what is the morphology of E. coli?
gram -, bacillus, motile, facultative
are E. coli infections exogenous or endogenous?
where is the infection if you have bloody diarrhea? watery diarrhea?
large intestine. SI
what are the five E. coli pathogenic strains and tell which are bloody diarrhea (BD) or watery diarrhea (WD).
enteropathogenic (WD), enterotoxigenic (WD), enterohemorrhagic (BD), enteroinvasive (WD-BD), and Enteroaggregavative (WD)
how does E. coli 0157:H7 AKA enterohemorrhagic get transmitted to humans in developed countries? what are the symptoms?
reservoir is in dairy cattle, thus the manure contaminates the soil and can contaminate veggies, fruits, and the animals that eat around them... contaminated food is ingested, survives stomach acid, invades large intestine and thus severe cramps, no fever, watery diarrhea followed by bloody diarrhea w/i eight days of exposure
what can eneterhemorrhagic E. coli 0157. H7 progress to from gastroenteritis and what are the symptoms of this?
hemolytic uremic syndrome (HUS). anemia, damage to BV walls, renal failure (kidney damage) all due to an endotoxin. Only effects elderly and children and can be fatal
what are preventative measures to get rid of E. coli 0157?
reduce # of infected cattle by changing from grain fed to hay fed. Also make water tight manure pits
are most of the UTI's from Ecoli exogenous or endogenous?
endogenous from uropathogenic ecoli (upec) which has specefic adhesins for genitourinary epi cells
what is infected in upper UTI's and what are the symptoms? lower?
upper is pyelonephritis: fever, sweating, nausea, vomiting, back pain. Lower: cystitis (bladder): fullness and discomfort, can be hemorrhagic; urethritis: urgent and frequent urination. note sex can push the ecoli up in there but this is not an STD
how do you treat ecoli UTI's?
lower UTI-3days antibiotic, upper-10 days... use cephalexin but check susceptibility. also increase fluid intake to increase urination
why are women more susceptable to UTI?
short urethra, sexual intercourse forces bacteria into urinary tract, estrogen deficiency or antibiotics leads to reduction of normal flora lactobacillus which would lower the vag pH and inhibit other bacs.
what infections do ecoli cause?
gastroenteritis, UTI, neonatal meningitis (strains with K1 capsular antigen), bacteremia, intraab infections
what groups usually contain ecoli with K1 capsular antigen in their normal flora
pregnant women and newborns GI tracts
T/F ecoli that causes meningitis in babies has 8% mortality rate and survivors will have neurologic abnormalities. This almost always occurs with sepsis
what are the classic symptoms of a baby with meningitis?
fever headache, neck stiff, refusal to eat, seizures... also have systemic symptoms due to sepsis
how do you determine neonatal meningitis by ecoli?
first do blood cultures, if negative then do spinal tap
how do you treat the neonate with ecoli meningitis?
1st week of life: ampicillin + gentamycin + cefotaxime. after 1st week: ampicillin + cefotaxime + an aminoglycoside. repeat lumbar puncture at 24-48 hours, if still positive after 48 hours and/or suspect neurological complications then do cerebral ultrasound and/or computed tomography. also reassess therapy based on culture and antibiotic susceptibility results
how can ecoli cause bacteremia and what is the mortality rate?
it is endogenous it must migrate through a wound via surgery, catheter etc. High mortality in immunocompromised as well as if gets in CNS
if ecoli infection is from traveling what is the protocol?
culture with specefic media designated in refernce labs due to the fact that the strain may be different from where that person came from
what antibiotics should be used with ecoli?
there are a bunch you can use, go by susceptability test, but if they have bacteremia or meningitis, must throw something at them fast
what is the basic biology of salmonella?
gram - bacilli, facultative anaerobe, susceptible to drying, survives acid environments of phagosome, and survives and grows in macrophages
describe the disease caused by salmonella enteridis and typhimurium.
both just cause gastroenteritis, they will not cause systemic disease. Note typimurium will cause typhus in mice but not humans. It causes enterocolitis which is sudden acute diarrhea and vomitting with fever, ab cramps, nausea, bloody or nonbloody stools, last about 1 week and can persist longer
what is the epidemilogy of salmonella enteridis and typhimurium?
resorvoir usually live stock and gets into contaminated food like eggs and polutry and dairy products. Is secreted in feces. Other sources include reptoles, pets, and animal feed
what is the pathogenesis of enteric salmonella?
oral ingestion of large inoculum, goes to intestinal tract and attaches to enterocytes of ileum and colon, invasins invade epi cells, persists in mesenteric lymph nodes, produces salmonella enterotoxin which is an exotoxin. infection is confined to the intestinal tract..
how do you diagnose enteric salmonella in the lab?
with serology for the presence of Ab against O and H antigens
what is the treatment for enteric salmonella? prophylaxis?
symptomatic treatment, will have spontaneous resolution, antibiotic treatment not recommended, replace fluid and electrolyte loss. prophylaxis is food hygeine
what species of salmonella cause typhoid fever?
S. typhi and S. paratyphi A, B, and C
what is the epidemiology of the typhoid salmonellas?
strict human pathogens, person to person with low infectious dose, there are chronic asymptomatic carriers that can pass to others via food and drinking water, direct contact, usually travellers get it in a country with endemic typhoid. NOTE typhoid is very rare now
what is the pathogenesis of the typhoid salmonellas?
oral- intestines-epi cells of jejunum via cystic fibrosis transmembrane conductance regulator-endocytosis-translocates-exocytosis-macs phagocytoze them-macs spread through lymph and blood (septicemia) especially liver, spleen, marrow, and skin (roseola). gall bladder colonization and reinfection of intestines in chronic carriers. JUST KNOW ITS SEPTICEMIC
what is the clinical presentation of typhoid fever?
1 to 3 wk incubation. week 1 is rising fever. weel 2 is stupor, headache, myalgias, malaise, anorexia. week 3 is diarrhea and intestinal bleeding (when your pt is in troubl). This is all an inflammatory reaction
when diagnosing salmonella what should you use?
look for local outbreaks in news, serology, selective media for growth, pt history may help but it cannot be distinguished from other diarrheal diseases
if the salmonella goes septic, what are the possible outcomes
osteomyelitis, arthritis, endocarditis, reiters
what is a common complication of salmonella?
reiter's: joint pain, irritation of the eyes, painful urination. it lasts for months or years and may lead to chronic arthritis. antibiotic treatment makes no difference. Also note that ppl have a genetic predisposition to reiters
how can one differentiate between shigella and escherichia?
must culture and do biochemical assays, not even able to tell difference on polynucleotide level with something like PCR. Both are biochemically similar and cause diarrhea or dysentary
what are the shigella virulence factors?
LPS:45 O antigen serotypes. Invasins for intracellular replication and the exotoin shiga toxin (if bac has shiga toxin you will get dysentary, if not you will have milder diarrhea)
what is the epidemiology of shigella bacs?
three important species: sonnei is most common cause in US, flexneri is in developing countries and has some outbreaks in US and is very endemic, dysenteriae is most severe and rare in US but can have epidemics elsewheere. humans only reservoir, person to person via fecal oral (last in stool for two weeks after disease, can get by contaminated hands which is most common way) asymptomatic colonization in small number of pts. usually effects peds ots and healthy male homos. it is highly communicable, only takes 10 to 200 for infection.
where do shigella bacs replicate?
in the enterocytes and note that it kills them
what is the mechanism of the shiga toxin?
it is cytotoxic via disruption of protein synth leads to microvascular damage andd hemorrhage. Also neurotoxic with fever and ab cramping. and enterotoxic by blocking adsorption of electrolytes glucose and amino acids, it contributes to more severe infection and systemic signs and symptoms
what is a big clue that your pt may have shigella dysenteriae?
tennemus (non productive straining) and blood in diarrhea
how must you isolate shigella?
stool samples with selective media
what is the treatment for shigella?
it is usually self limiting with rehydration but may take a while for BM's to be normal. Do not need antibiotics but can use empiric theory of ampicillin or trimethoprim/sulfamethoxazole, may need to follow in vitro susceptability tests if this does not work
what shigella species is associated with reiters?
s. flexneri
what are the shigella complications?
reiters, reactive arthritis, and hemolytic uremic syndrome
what is the basic biology of yersenia?
gram neg rod, facultative, LPS, capsule, mac killers via disrupting actin filaments, subject to drying
what is one characteristic of all yersenia infections?
zoonotic infections (primary means of infection is from animals to humans, note non zoonotic infections can be from animal to ppl and zoonotic can also go from ppl to ppl, zoonosis just means the main way of catching it is through animal to person)
how is yersenia pestis chiefly transmitted?
through the rat flea bite or through direct contact with an infected animal
how does yersenia pestis invade the human?
penetrates from flea bite and regurgitation from blood meal, loses capsule and thus is phagocytized by PMN or mac, spreads to nodes, then grows in the mac and kills it. proliferates in that lymph node and makes the node hot, tender, and hemorrhagic
-> bubonic plague. then if untreated, pt becomes bacteremic and it can go to lungs shifting to the pneumonic form in which the pt can cough up contaminated droplets and infect other ppl.
what are the symptoms of bubonic plague? pneumonic plague?
high fever and pain at regional lymph nodes. hemorrhagic changes in skin plus cyanosis from necrotzing pneumonia producing dark skin, if left untreated will have 100% mortality.
how do you diagnose y. pestis?
aspirates from blood and bubo can be seen under microscope and geimsa stained to reveal bipolar or safety pin appearance. or it can be cultured
treatment for y. pestis?
streptomycin 1st and tetracycline if not. isolate pts, do not incise the buboes
T/F: there is no vaccine for yersenia pestis.
how would one contract yersenia enterocolitica or pseudotuberculosis?
via contact with the wild animals and livestock or ingestion of contaminated water or food that penetrates the mucosa layer of the lower intestine
what are the disease symptoms in yersenia entereocolitica and pseudotuberculosis?
pseudotuberculosis is not pathogenic in ppl. gastroenteritis with fever, abdominal pain, diarrhea, sometimes confused with appendicitis, sometimes it can go extraintestinal in an opportunistic infection (transfusion related) to cause sepsis, can lead to complications and immunopathologies in adults like arthritis and erythema nodosum. it can cause reiter's syndrome.
how can yersenia enterocolitica and oseudotuberculosis be ID-ed in the lab?
stool sample and growth on most non selective mediums or do an antibody titer
what is the treatment for y enterocolitica and y pseudotuberculosis?
uncomplicated cases usually resolve, but can do streptomycin, tetracyclines, or chloramphenicol
what are the safe food practices for y entericolitical and pseudotuberculosis?
no eating raw or undercooked pork, eat only pasteurized milk, wash hands, watch out for raw chitterlings.
what enterobacteriaceae is a pulmonary commensal seen in community primary lobar pneumonia or 10% f nosocomial infections and is a problem in alcoholics and diabetics?
Klebsiella pneumonia
aside from Klebsiella pneumoniae, where are other species of klebsiella found? how would you treat them?
in wounds after surgery leading to bacteremia, in the soft tissue of the nose, forming inguinal granulomas, nosocomial UTI in catheters. They are resistant to many antibiotics and thus need susceptability tests
where are proteus mirablis infections usually found? how do you ID them? How do you treat them?
commensal UTI's, can be nosocomial in catheter (note they form biofilms), complications can lead to SIDS, ID via antibodies to O antigens, generally treated with quinolones