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Me Enterobacteriaceae
Me Enterobacteriaceae
Me Enterobacteriaceae
Enterobacteriaceae
Classification – 44 genera, more than 170
species
Enterobacteriaceae
Escherichia
Extraintestinal infection, diarrhea
Shigella
Typhoid fever, sepsis, gastroenteritis (food poison)
Salmonella
Dysentery
Enterobacteriaceae
A B C
A. E. coli on Eosin Methylene Blue agar plate.
B. E. coli on blood agar plate.
C. E. coli on MacC agar plate.
E. coli
Antigenic structure - has O, H, and K antigens.
Pathogenic factors:
Invasiveness:
Invasive outer membrane protein
K antigen
Pili/adhesin
Endotoxin
Enterotoxin
Heat labile enterotoxin, LT
Heat stable enterotoxin, ST
Shiga-type toxin
Hemolysin
E. coli toxins
Virulence factors
Toxins
(intimin)
E. coli
Clinical significance
Is the leading cause of urinary tract infections
which can lead to acute cystitis (bladder
infection) and pyelonephritis (kidney infection).
Ascending urinary tract infection
Urinary tract infections (UTI)
New evidence in women who suffer from
recurrent UTIs suggests that this is due to the
formation of pod-like E. coli biofilms inside
bladder epithelial cells.
Bacteria living on the edges of the biofilms nay break
off leading to a round of infection.
Pod-like biofilm
E. coli infections
Neonatal meningitis – is the leading cause of neonatal
meningitis and septicemia with a high mortality rate.
Usually caused by strains with the K1 capsular antigen.
Gastroenteritis –several distinct types of E. coli are
involved in different types of gastroenteritis:
enterotoxigenic E. coli (ETEC),
enteroinvasive E. coli (EIEC),
enteropathogenic E. coli (EPEC) ,
enteroaggregative E. coli (EAEC),
enterohemorrhagic E. coli (EHEC).
ETEC
Phage typing
PFGE
Serology
Center for Food Security and Public
Health, Iowa State University, 2012
Treatment
Mainly supportive
Antibiotics
Usually avoided
Do not reduce symptoms, prevent complications, or
reduce shedding
May increase risk of HUS
Antimotility drugs
May increase risk of HUS
S. sonnei D1
Shigella
A B
A. On MacConkey agar plate. E. coli colonies show pink and ferment lactose.
S. flexncri colonies are small, colorless and transparent, non-lactose
fermanting (18h, 37°C).
B. On SS agar plate. E. coli colonies are larger and red color, while S. flexncri
colonies are small, colorless and transpatent (18-24h)
Shigella species
Antigenic structure
Differentiation into groups (A, B, C, and D) is based
on O antigen serotyping; K antigens may interfere
with serotyping, but are heat labile.
O antigen is similar to E. coli, so it is important to ID
as Shigella before doing serotyping.
Shigella species
Virulence factors
Shiga toxin ( Exotoxin ) – produced by S.
dysenteriae and in smaller amounts by S. flexneri and S.
sonnei.
Acts to inhibit protein synthesis by inactivating the 60S
ribosomal subunit by cleaving a 28S rRNA.
Plays a role in the ulceration of the intestinal mucosa.
Shigella species
cytoplasm.
From there they spread laterally (Polymerization of
Virulence factors
Endotoxin – may play a role in intracellular survival
Capsule (for S. typhi and some strains of S.
paratyphi)
Adhesions – both fimbrial and non-fimbrial
Virulence factors
Type III secretion systems and effector molecules – 2
different systems may be found:
One type is involved in promoting entry into intestinal
epithelial cells
The other type is involved in the ability of Salmonella
to survive inside macrophages
Virulence factors
Outer membrane proteins - involved in the ability of
Salmonella to survive inside macrophages
Flagella – help bacteria to move through intestinal
mucous
Enterotoxin - may be involved in gastroenteritis
Iron capturing ability
Clinical Syndrome
Causes two different kinds of disease: enteric
fevers and gastroenteritis.
Both diseases begin in the same way, but for
gastroenteritis the bacteria remains restricted to the
intestine, and for enteric fevers, the organism spreads
Transmission is via a fecal-oral route, i.e., via ingestion
of contaminated food or water.
Salmonella
The organism moves through the intestinal mucosa
and adheres to intestinal epithelium.
Effector proteins of the type III secretion system
mediate invasion of enterocytes and M cells via an
induced endocytic mechanism.
Salmonella multiplies within the endosome.
Salmonella invasion of epithelial
cells
Clinical Syndrome
The endosome moves to the basal side of the cell and
Salmonella are released and may be phagocytosed by
macrophages.
For gastroenteritis the Salmonella multiply and their presence
induces a strong inflammatory response which causes most of
the symptoms seen in gastroenteritis (mild to moderate fever
with diarrhea and abdominal cramps).
The inflammatory response prevents the spread beyond
the GI tract and eventually kills the bacteria.
Clinical Syndrome
In enteric fevers (typhoid and paratyphoid) the
Salmonella disseminate before they multiply to high
enough levels to stimulate a strong inflammatory
response, so the initial symptoms are only a low-
grade fever and constipation.
Salmonella
The bacteria move via the lymphatics and bloodstream to the liver
and spleen where phagocytosis and multiplication occurs.
They re-enter the bloodstream to disseminate throughout the body
to all organs causing fever, headaches, myalgia, and GI problems.
Rose spots (erythematous, muculopapular lesions) are seen on the
abdomen. Osteomyelitis, cystitis, and gall bladder infections may
occur.
Symptoms of paratyphoid fevers (due to S. paratyphi A, B, or C) are
similar to but less severe than those that occur with typhoid fever
(due to S. typhi)
Diagnosis of typhoid fever
Blood cultures are + during 1st week and after 2nd week.
Stool cultures and sometimes urine cultures are + after 2nd week.
The Widal test is a serological test for antibodies against Salmonella
typhi. One looks for a 4-fold rise in titer between acute and
convalescent stages.
10% of those infected become short term carriers and a smaller %
become long-term carriers due to persistence of the bacteria in the
gallbladder or urinary bladder.
Salmonella
Antimicrobial therapy
Enteric fevers – use chloramphenicol usually.
Resistant strains have emerged making antimicrobial
susceptibility testing essential.
Gastroenteritis – usually doesn’t require antimicrobic
therapy.
Replace lost fluids and electrolytes.
Comparison of Shigella versus
Salmonella invasion
Shigella Salmonella