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71 Cards in this Set

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Components of MAC agar
-crystal violet and bile salts (inhibit growth of Gram positive organisms)
-neutral red (pH indicator)
-lactose
Red colony on MAC agar means?
bacteria ferments lactose
Components of EMB
-lactose
-Eosin
-methylene blue
Positive/negative result on EMB = ?
Lactose fermenters precipitate dyes
purple centers OR
green metallic sheen
Lactose non fermenter:
Light pink, translucent
Components of HEK agar
lactose, sucrose, salicin
bromthymol blue
pH indicator
bile salts
Result on HEK
fermentation causes yellow, salmon or orange color otherwise translucent green
ferric ammonium citrate
black ppt if H2S producer
Component of Triple sugar iron agar
Sugars
-glucose (1 part)
-lactose (10 parts)
-sucrose (10 parts)
Phenol red
-pH indicator

acid fermentation
-red to yellow
Ferrous sulfate
-turns black in presence of H2S
Proteins: Beef and yeast extract
Enterotoxigenic E. coli Physiology and structure
Gram negative rod
lactose fermentation
Enterotoxigenic E. coli Virulence factors
heat labile toxin (LT)
-structure-mechanism (cholera)
heat stable toxin (ST)
-stimulation of guanylate cyclase
attachment pili
-Able to attach to epithelium
Enterotoxigenic E. coli entry?
ingestion of contaminated food or water
Enterotoxigenic E. coli Establishment
& Mechanism of disease
attachment to small intestinal epithelial cells
-bacteria do not invade
secretion and uptake of toxin
-heat labile
-heat stable
Enterohemorrhagic E. coli antigens
O & H
Enterohemorrhagic E. coli Virulence factors
Shiga like toxin
-phage encoded
Enterohemorrhagic E. coli agar speciality?
Grows on sorbitol plate
E. coli O157:H7 Epidemiology
undercooked meats
Fecally contaminated water
foods (coleslaw, cheese, unpasteurized apple juice)
Very few organisms needed for infection
E.coli O157:H7 Clinical syndromes
Secretory diarrhea
-inucubation period of 2-3 days
-Non-bloody
-Most patients will not get other symptoms
severe abdominal pain, bloody diarrhea
-If bacteria get to colon only
-Can be accompanied by fever
hemorrhagic colitis
hemolytic uremic syndrome (HUS)
-Triad of acute renal failure, thrombocytopenia & hemolytic anemia
-10% of patients who get bloody diarrhea will get this
Salmonella enterica Physiology and structure
Gram negative rod
motile
does not ferment lactose
Salmonella enterica Epidemiology
food contamination
fecal oral spread
antacids increase susceptibility to Salmonella enterica True or False?
True
Salmonella enterica Pathogenesis
attachment to epithelial cells
uptake by epithelial cell
replication in endosome
penetration to subepithelial tissue
inflammatory response
Salmonella typhi Clinical syndromes
incubation period 7-21 days
can start out as diarrhea
fever, malaise, anorexia, headache, myalgia
long term fever 3-4 week course without treatment (typhoidal)
complications: infection of bone, heart valves, brain
Salmonella typhi Virulence factors
Vi polysaccharide - capsule
endotoxin
Salmonella typhi Mechanism of disease
invasion of M cells in Peyer’s patches in terminal ilieum
Replication and transport to subepithelial
survival in macrophages
entry into blood and lymphatics
replicate in liver and spleen
prolonged release of endotoxin
gall bladder colonization- shed in bile
Shigella Physiology and structure
Gram negative rod
non motile
classified by “O” antigens
no “H” antigens
does not ferment lactose
Relatively biochemically inactive
Shigella Virulence factors
Shigatoxin
virulence plasmid
Shigella Establishment
attachment to “M” cells
bacterial directed endocytosis
-virulence plasmid
escape from endosome
replication in cell
lysis and spread to adjacent cells (basal and lateral)
Dysentery symptoms
blood and pus
fever, abdominal pain, cramps
acute and self limiting 2-7 days
Dysentery causative agents
EIEC
EHEC - O157:H7
Salmonella enterica (typhimurium)
Shigella sp.
Campylobacter jejuni
Clostridium difficile
Yersinia entercolitica
Yersinia entercolitica Physiology and structure
Gram negative bacillus
motile (conditional on temperature)
Non-motile @ body temperature, but motile @ cold T
flagella produced at 22C not 37C
Growth at 4C
Yersinia entercolitica Epidemiology
fecal oral spread
transmission through milk, food and water
Common in Scandinavia and cold areas of North America
increased metabolic activity at lowered temp
Yersinia entercolitica Clinical syndromes
diarrhea, fever, abdominal pain in right lower quadrant Due to necrosis of the lymph nodes
Yersinia entercolitica post infective sequelae
reactive arthritis
Yersinia entercolitica Pathogenesis and immunity
invasive
heat stable enterotoxin similar to E.coli ST
Campylobacter jejuni Physiology and structure
Gram negative rod
small - 0.3 u
S or comma shaped
motile
single polar flagella
darting corkscrew motility
Campylobacter jejuni special growth requirements
reduced oxygen
increased CO2
elevated temperature
most common cause of bacterial gastroenteritis?
Campylobacter jejuni
Campylobacter jejuni Transmission
animal reservoirs
chickens #1
cattle
swine
dogs and cats
contaminated foods
chicken, turkey, beef, pork, fish, milk, raw seafood, mushrooms
contaminated water
fecal contamination from animals
rare complication of Campylobacter jejuni?
Guillain-Barre syndrome
Campylobacter jejuni Virulence factors
flagella
adhesin (attachment)
endotoxin
enterotoxin
cytopathic toxin
Helicobacter pylori Physiology and structure
Gram negative spiral shaped rod
corkscrew motility
hard to grow
Helicobacter pylori Virulence factors
urease
motility and mucinase
adherence factors
endotoxin
cytotoxin
General Properties of Anaerobic Bacteria
growth inhibited or killed by oxygen
reduced levels of catalase and superoxide dismutases
considerable variation in oxygen sensitivity
pH and redox potentials (Eh) are important factors too
Obligate anaerobe
bacteria that fail to grow in the presence of any oxygen. Often lack superoxide dismutase, catalse and cytochrome systems
Facultative
bacteria that grow in the presence or absence of oxygen; these are the predominant pathogens
Microaerophilic
aerortolerant bacteria that tolerate small amounts of air
fecal anaerobes are typically resistant to penicillins while oral anaerobes respond to penicillins... True or False?
True
Bacteroides fragilis Physiology and Structure
pleomorphic, gram(-) rod, capsulate, no spores, weak LPS endotoxin
Bacteroides fragilis Establishment
agglutinins, IgA protease; IgM mediates phagocytosis by neutrophils
Clostridium perfringens Physiology and Structure
Gram(+)rod ; spores; aerotolerant
Clostridium perfringens Clinical Syndromes
Bacteremia, myonecrosis (gas gangrene)
Cellulitis, fasciitis
Food poisoning
Enteritis necroticans (Type C linked to rare and lethal food poisoning in malnourished children).
aseptic Meningitis is due to?
viruses, TB, fungi
septic or purulent Meningitis is due to?
Bacteria
Meningitis is an Inflammatory disease characterized by?
infiltration of neutrophils (and mononuclear cells)
-obstruction
-block reabsorption of CSF
-increased intracranial pressure
-herniation of temporal lobe or cerebellum
-compression of midbrain
-respiratory arrest
Common clinical symptoms of Meningitis
fever, headache, stiff neck, vomiting, photophobia, lethargy, confusion, coma
Infants - jaundice, diarrhea, irritability, convulsions
Causative Agents of Meningitis -bacteria
Neisseria meningitidis
Haemophilus influenzae
Streptococcus pneumoniae
Staphylococci
Escherichia coli
Group B Streptococcus
Listeria monocytogenes
Causes of Meningitis in neonates?
Group B Streptococcus
-Streptococcus agalactiae
Gram negative rods
-E. coli
Listeria monocytogenes
Causes of Meningitis in children?
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae
Causes of Meningitis in adults?
Streptococcus pneumoniae
Neisseria meningitidis
Staphylococci
-S. aureus
-S. epidermidis
Listeria monocytogenes
Neisseria meningiditis (Gram negative diplococcus) Virulence factors
capsule
endotoxin
IgA protease
attachment pili
Haemophilus influenzae Virulence factors
capsule
endotoxin
IgA protease
attachment pili
Haemophilus influenzae media requirements
X and V factors
Streptococcus pneumoniae (Gram positive, Alpha hemolytic, Catalase negative, Lancet shaped diplococci)
Virulence factors
polysaccharide capsule
IgA protease
Staphylococcus Virulence factors
toxins, coagulase, capsule (some), protein A (binds Fc), others
Escherichia coli Virulence factors
K1 surface polysaccharide capsule + endotoxin
Listeria monocytogenes (Gram positive rod, Growth at low temperatures) Virulence factors
internalin
listeriolysin O
UTI: Escheria Coli virulence factor
P pili (fimbriae)
-Binds galactose-containing receptors on uroepithelial cells
Capsular K antigens (pyelonephritis)
Human serum resistence
Hemolysins (cytotoxins)
LPS
UTI: Proteus Mirabilis
Produces urease (Urea Ammonia)
Raises urine pH (Toxic to renal cells) causes massive renal cell destruction
Promotes renal stones (Nidus for infections)
Treponema - Virulence Factors
Outer Membrane Proteins - adherence to host cell
Hyaluronidase - facilitates perivascular invasion
Fibronectin - from the host cell. Protection against phagocytosis
Can survive in phagocytic cell
Vibrio vulnificus is associated with?
raw shellfish
95% of all seafood related deaths
seawater infections of wounds
Watery Diarrhea is associated with which organisms?
Vibrio cholerae
Escherichia coli
-ETEC
-EPEC
-EAggEC
Clostridium perfringens
Clostridium difficile
Staphylococcus aureus
Bacillus cereus
M. pneumoniae Virulence factors
terminal adhesion protein (P1, base of cilia), stimulation of cytokine release