Flashcards in Enterobacteriaceae Lecture 16 Deck (28):
all gram negative rods with lipolysaccharide in the cell wall
all ferment glucose and oxidase negative
serological typing: O antigen (polysaccharide portion of LPS), K (capsular) antigen, and H (flagella) antigen
Lactose fermentation by enterobacteriaceae
fermentation occurs: kelbsiella, escherichia, enterobacter
does not occur: shigella, salmonella, yersinia, proteus, pseudomonas
occurs slowly: serratia, vibrio
Virulence facotrs enterobacteriacaea
endotoxin, capsule, antigenic phase variation, Type III secretion, sequestration of growth factor, resistance to serum killing, antimicrobial resistance
Bacteremia associated with enterobacteriaceae
diseases caused by E. Coli
hemolytic uremic syndrome
E coli gastroenteritis
The strain of e. coli that cause gastroenteritis are divided into five major groups
Enterotoxigenic E. Coli
Enteropathogenic E. Coli
Enteroinvasive E Coli
Enteroaggregative E. Coli
Enterhemorrhageic E. Coli
Enterotoxigenic E. Coli (ETEC)
fimbrial adhesins, CFA I and CFA II
produce heat labile (LT) and heat stable (ST) enterotoxins
watery diarrhea in infants and traveler's diarrhea
no inflammation and no fever
Enteropathogenic e coli (EPEC)
Non fimbrial adhesion (intimin)
does not produce LT or ST
attachment effacement (eae)
bundle forming pilus (Bfp)
destruction of microvilli.
infantile diarrhea, similar to ETEC, some inflammation, no fever
common in underdeveloped countries
Enterhemorrhagic E. Coli (EHEC)
similar to EPEC, moderately invasive.
Does not produce LT or ST, but shiga like toxin (SLT) (encoded on a phage), also called verotoxin, cytotoxic to intestinal villi and colon epithelial cells
pediatric diarrhea, copious bloody discharge hemorrhagic colitis, intense inflammation and hemolytic uremia
Enteroinvasive E. Coli (EIEC) like shigella
nonfimbrial adhesions, possibly OMP
invasive (penetrate and multiply within epithelial cells)
entry site is the M cells
does not produce shiga toxin
dysentry like diarrhea (mucous blood), severe inflammation, fever.
very large plasmind (pINV)
Enteroaggregative E Coli (EAGGEC)
adhesins not characterized (GVVPQ fimbriae)
produce ST like toxin and a hemolysin
persistent diarrhea in young children without immunization, no fever
Virulence factors of uropathogenic e. coli
P fimbria- lyelonephritis- associated pili which binds specifically to the P blood group antigen that contains a d galactose d galactose residue
treatment and control of E. Coli
Enteric pathogens are treated symptomatically unless disseminations occur
antibiotic therapy is guided by invitro antibiotic susceptibility tests
infection- control in hospital
high hygienic standards
Genus: S. Bongori and S. Enterica
common in Gi tract of animals, but not human flora
S. Choleraesuis: swine and human pathogen
S. Enterica: 6 subspecies. Subsp. Enterica has more than 2500 serotypes
do not ferment lactose but do produce H2S
antigens: O, H, and capsular Vi
facultative intracellular growth
Diseases caused by salmonella Spp.
gastroenteriti: the most common cause of food borne infections, indicating its hard to develop immunity
typhoid (enteric) fever (S. typhi)
localized infections in other site (osteomyelitis, meningitis)
Typhoid (enteric) fever
S. typhi and S. paratyphi, etiological agents
6-30 days of incubation, initial symptoms include fever, hHA, malaise, and anorexia. Some have skin rash with rose colored spots.
starts in the small intestine through peyer's patces, and then spread to the phagocytes of liver, gallbladder, and spleen bacterimia.
survival in the phagosomes in phagocytic cells-carrier state
typhoid fever is transmitted only by humans.
cholecystitis: carrier state
fever; kidney and other organ damage.
invasion of epithelia and subepithelial tissue of the small and large intestines.
PMN response limits the infection to the gut and the adjacent mesenteric lymph node.
infective dose very high (100,000 CFU)
gastric acid important host defense.
only about 5-10% of salmonella infections.
underlying chronic disease: sickle cell anemia or cancer.
bacteremia results in seeding of many organs, with osteomyelitis, pneumonia, and meningitis as the most common sequelae
spread and multiplication (salmonella)
fecal oral route (all serotypes)
the diarrhea causing salmonella multiply in the lamina propria with uncertain mechanisms
asympotomatic carriers (s. typhi)
typhoid bacilli are not killed and they steadly multiply within macorphages
treatment and preventions of salmonella
unrestricted use of antibiotics: selection for resistant bacteria
vaccine against S. typhi 50-70% effective and short term protection
Four species: S. Dysenteriae (group A), S flexneri (group B), S. Boydii (group C), S. Sonnei (group D)
all four species are pathogenic in umans and cause similar disease
most effective among enteric pathogens
there are mutliple serotypes with serogroup A, B, C. multiple colicin types with S. Sonnei
S. dysenteriae type 1 mainly in developing countries
S. sonnei causes mildest disease and accounts for 75% of all shigella infections with in the USA.
shigella is very similar to invasive E. Coli
non lactose fermenting, gram negative rods
they do not produce H2S
produce no gas when fermenting glucose
shiga toxin (shigella dysenteriae)
no animal reservoir
Virulence mechanisms of Shigella
target m Cells in peyer's patches
bacterimia is uncommon with shigella
s. dysenteriae strains produce an exotoxin, shiga toxin, similar to the toxin made by EHEC. AB5, A cleaves the 28S rRNA int he 60 S ribosomal unit.
Reiter's syndrome shigella
arthritis, conjunctivitis and urethritis appear after the intestinal infections by one of the intestinal pathogens such as shigella, yersinia enterocolitiica, salmonella, kelbsiella pneumoniae, and campylobacter
cause is unclear, may be due to an autoimmune response
most patients are male (HLA b27 positive)
Clinical diagnosis shigella
methylene blue stain of a fecal sample to determine the presence of PMN. If present, they could be an invasive organism such as shigella, salmonella, or campylobacter
Clinical manifestation of shigella
tenesmus, watery, blood diarrhea
incubation 1 to 4 days, symptoms begin with fever and abdominal cramps followed by diarrhea, first watery but later contains blood and mucus (species and age)
transmission of shigella
only to human
fecal oral route: fingers, flies, food, and feces
food borne outbreaks outnumber waterborn by 2 to 1
50% shigella positive samples come from children younger than 10 years of age
no carrier state
treatment and prevention of shigella
fluid and electrolyte replacement. in severe cases, a fluoroquinolone, eg. Ciprofloxacin, is the choice.
remember need to check the multiple drug resistance (plasmid borne)
emphasis on the personal hygiene