Enterobacteriaceae Lecture 16 Flashcards Preview

Exam 2 > Enterobacteriaceae Lecture 16 > Flashcards

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


neonatal meningitis



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)

Plasmid mediated


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)

moderately invasive

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.

Diarrhea: perforation

cholecystitis: carrier state

fever; kidney and other organ damage.


Enterocolitis (salmonella)

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.


Septicemia (salmonella)

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

symptomatic relief

unrestricted use of antibiotics: selection for resistant bacteria

poultry industry

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 2

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


Other enterobacteriaceae

klebsiella pneumoniae produces a prominent capsule for the nehanced virulence, which can cause community acquired or hospital acquired lobra pneumonia

proteus mirabilis can cause UTI. This bacterium produces large quantities of urease which splits urea into carbon dioxide and ammonia. This process raises urine pH, precipitating magnesium and calcium, causing kidney stones.