Enterobacteriaceae Lecture 16

Question 1

Enterobacteriaceae

Answer 1

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

Question 2

Lactose fermentation by enterobacteriaceae

Answer 2

fermentation occurs: kelbsiella, escherichia, enterobacter

does not occur: shigella, salmonella, yersinia, proteus, pseudomonas

occurs slowly: serratia, vibrio

Question 3

Virulence facotrs enterobacteriacaea

Answer 3

endotoxin, capsule, antigenic phase variation, Type III secretion, sequestration of growth factor, resistance to serum killing, antimicrobial resistance

Bacteremia associated with enterobacteriaceae

Question 4

diseases caused by E. Coli

Answer 4

gastroenteritis

hemolytic uremic syndrome

UTI

neonatal meningitis

septicemia

Question 5

E coli gastroenteritis

Answer 5

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

Question 6

Enterotoxigenic E. Coli (ETEC)

Answer 6

Plasmid mediated

noninvasive

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

Question 7

Enteropathogenic e coli (EPEC)

Answer 7

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

Question 8

Enterhemorrhagic E. Coli (EHEC)

Answer 8

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

O157:H7

Question 9

Enteroinvasive E. Coli (EIEC) like shigella

Answer 9

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)

Question 10

Enteroaggregative E Coli (EAGGEC)

Answer 10

adhesins not characterized (GVVPQ fimbriae)

noninvasive

produce ST like toxin and a hemolysin

persistent diarrhea in young children without immunization, no fever

Question 11

Virulence factors of uropathogenic e. coli

Answer 11

P fimbria- lyelonephritis- associated pili which binds specifically to the P blood group antigen that contains a d galactose d galactose residue

Question 12

treatment and control of E. Coli

Answer 12

Enteric pathogens are treated symptomatically unless disseminations occur

antibiotic therapy is guided by invitro antibiotic susceptibility tests

infection- control in hospital

high hygienic standards

Question 13

Salmonella

Answer 13

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

Question 14

Diseases caused by salmonella Spp.

Answer 14

gastroenteriti: the most common cause of food borne infections, indicating its hard to develop immunity

typhoid (enteric) fever (S. typhi)

bacteremia

localized infections in other site (osteomyelitis, meningitis)

Question 15

Typhoid (enteric) fever

Answer 15

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.

Question 16

Enterocolitis (salmonella)

Answer 16

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.

Question 17

Septicemia (salmonella)

Answer 17

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

Question 18

spread and multiplication (salmonella)

Answer 18

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

Question 19

treatment and preventions of salmonella

Answer 19

symptomatic relief

unrestricted use of antibiotics: selection for resistant bacteria

poultry industry

vaccine against S. typhi 50-70% effective and short term protection

education

Question 20

Shigella

Answer 20

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.

Question 21

Shigella 2

Answer 21

shigella is very similar to invasive E. Coli

non lactose fermenting, gram negative rods
they do not produce H2S

nonmotile

produce no gas when fermenting glucose

shiga toxin (shigella dysenteriae)

no animal reservoir

Question 22

Virulence mechanisms of Shigella

Answer 22

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.

Question 23

Reiter’s syndrome shigella

Answer 23

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)

Question 24

Clinical diagnosis shigella

Answer 24

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

Question 25

Clinical manifestation of shigella

Answer 25

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)

Question 26

transmission of shigella

Answer 26

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

Question 27

treatment and prevention of shigella

Answer 27

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

Question 28

Other enterobacteriaceae

Answer 28

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.