Family Enterobacteriaceae

Opportunistic enterobacteria:
Genus Escherichia. Genera Klebsiella,
Enterobacter, Serratia. Genera Proteus,
Morganella, Providencia.

Prof. Dr. Lena Sechanova

 Thе Enterobacteriaceae is the largest
family of medically important gram-
negative rod shape bacteria.
Enterobacteriaceae are ubiquitous
organisms, found in soil, water, and
vegetation, and are part of the normal
intestinal flora of humans and most
animals.
A total of 40 genera and >150 species
have been described on the basis of
biochemical properties, antigenic
structure, and DNA hybridization and
sequencing of 16S rDNA genes.
™ Fewer than 20 species are responsible
for more than 95% of the infections.

™ They cause a variety of human

diseases, including 30% to 35% of all
septicemias, more than 70% of urinary
tract infections (UTIs), and many
intestinal infections:
Group Genus, spp. Diseases
Obligatory Salmonella Typhoid fever (S. typhi), gastroenteritis (S. enteritidis, S.
pathogenic: typhimurium etc.)
Shigella Shigellosis – enterocolitis caused by S. dysenteriae, S. flexneri,
S. boydii, and S. sonnei.

Yersinia Plague – (Y. pestis);

Gastroenteritis, mesarteritis (mimic acute appendicitis), sepsis
(Y. enterocolitica, Y. pseudotuberculosis)

Klebsiella Granuloma inguinale (former Calymmatobacterium

granulomatis granulomatis )

Opportunistic Escherichia Opportunistic infections in immunocompromised patients:

(members of the coli, sepsis, wound infections, meningitis, pneumonia, UTI, etc.
normal commensal species of the Citrobacter freundii, Ciirobacter koseri, Enterobacter
or saprofites - genera aerogenes,. Enterobacter cloacae, Escherichia coli, Klebsiella
Serratia) Klebsiella, pneumoniae, Klebsiella oxytoca. Morganella morganii, Proteus
Enterobacter, mirabilis, Proteus vulgaris
Serratia;
Proteus,
Morganella,
Providentia;
Citrobacter
Strains that become eg. E. coli Normally commensal organisms that become pathogenic when
pathogenic when they they acquire virulence factor genes on plasmids,
acquire virulence bacteriophages, or pathogenicity islands ETEC – traveller
factor genes diarrhea - Ent plasmid is associated with,
EHEC – hemorrhagic enterocolitis - phage genes code SLT
 Infections can originate
from an animal reservoir
(e.g., most Salmonella
species, Yersinia spp.),
from a human carrier
(e.g., Shigella spp. and S.
typhi), or through the
endogenous spread of
commensal organisms in
Wound infections
a susceptible patient
Escherichia
Klebsiella, (e.g., E. coli) and can
Enterobacter,
Serratia; Proteus involve virtually all body
sites.
 STRUCTURE
‰ Gram-negative, moderately sized (0.3 to
1.0 X 1.0 to 6.0 μm), rod shaped bacteria.
Motile with peritrichous flagella (E. coli,
Salmonella, Proteus, etc.) or nonmotile
(Shigella, Klebsiella, etc.)
‰ Non spore forming. Some
Enterobacteriaceae have prominent
capsules (Klebsiella), whereas other
strains are surrounded by a loose-fitting,
diffusible slime layer or have
microcapsule. Pili are common.
 Cell wall of Enterobacteriaceae
have the structure of Gram-
negative bacteria, consisting of
¾ peptidoglycan and
¾ outer membrane:
lipopolysaccharide (LPS) and
phospholipid molecules are the
major constituents forming
asymmetric bilayer of the OM.
¾ Three types of protein are
shown: the pore proteins
(porins), OmpA and
lipoprotein. Lipoprotein is
connected to the
peptidoglycan.
They share a common antigen (enterobacterial common
antigen)
H antigen
K antigen The serologic
O antigen
classification of the
Enterobacteriaceae
is based on three
major groups of
antigens:
- somatic О LPS Ag
- capsular К Ag
(polysaccharide or
protein), and the
- flagellar Н Ag
(protein).
Specific О antigens are present in each
genus, although cross-reactions between
closely related genera are common (e.g.,
Salmonella with Citrobacter, Escherichia
with Shigella).
The antigens are detected by
agglutination with specific antibodies
(slide agglutination of Gruber).

The heat-labile К antigens may interfere

with detection of the О antigens. This
problem is circumvented by boiling of the
organism to remove the К antigens.
 O-antigen chains of some strains are
much longer, ensuring high virulence
(serum resistance)

O-antigen chains are highly

heterogeneous in the sugar monomers
expressing hundreds of different
antigens.
Most species are represented by more
than one serotype – e.g. more than
2000 in Salmonella.

Core Ag is common to all

Enterobacteriaceae. It is represented
by only 6 chemotypes
Lipid A is the endotoxin of Gram-
negative bacteria.
 PHYSIOLOGY
™ All members are facultative anaerobes
(grow rapidly aerobically and
anaerobically).

™ They are nonfastidiuos and are cultured

on simple culture media.

™ The colonies of different species

Enterobacteriaceae on meat-pepton agar
medium look similar: E. coli and most of the
other enteric bacteria form circular, convex, smooth
colonies with distinct edges.
• Enterobacter colonies are similar but
somewhat more mucoid.

• Klebsiella colonies are large and very

mucoid and tend to coalesce with
prolonged incubation.

• The salmonellae and shigellae produce

colonies similar to E. coli but do not
ferment lactose.
• Some strains of Е. coli produce
hemolysis on blood agar.

• In diagnostic labs differential (e.g.

MacConkey agar) and selective (e.g.
deoxycholate agar - DOC, Salmonella-
Shigella agar, SS-agar) media are used.
.

Colonies of E. coli and Mucoid colonies of

majority of capsulated Klebsiella and
enterobacteria: round some strain of Enterobacter
convex and smooth and E. coli (tick
surface – S-form. polysaccharide capsule)
.

H2S colonies (black

S – R form colonies center) of Salmonella
on SS agar

β-hemolysis of Е. coli
Swarming motility (creeping growth) of on blood agar.
Proteus mirabilis and P. vulgaris.
 PURPOSE of using differential media and
selective media:

¾ To isolate and differentiate between

various members of the family
Enterobacteriaceae in the feces.
PRINCIPLE:

¾ Both media contain aniline dies and

citrate which inhibit Gram-positive
commensal organisms of the gut flora.
™ Contrary to differential media,
selective media (DOC and SS-agar)
contains sodium deoxycholate which
work to inhibit the growth of E. coli
that is presented in high amount in the
gut and it’s colonies prevail when
plated on agar medium.
™ The media also contains the sugar
lactose, which serves to differentiate
among enterics that ferment and do
not ferment lactose.

™ Fermentation of lactose appears as

a red color due to the pH indicator
neutral red, which is included in the
medium.
 Differential and
Selective media

Growth on DOC or SS agar plate:

Heavy (A) and light (D) lactose
fermentation.
(B) no lactose fermentation.
(C) reduced growth of a Gram-positive
organism.

E. coli

Lac+ Escherichia, Klebsiella, Enterobacter, Citrobacter, and Serratia species

Lac- Proteus, Salmonella, Shigella, and Yersinia species
• The Enterobacteriaceae ferment
glucose aerobically and anaerobically,
reduce nitrate, and are catalase-
positive and oxidase-negative.
• The absence of cytochrome oxidase
activity is an important characteristic,
because it can be measured rapidly with
a simple test and is used to distinguish
the Enterobacteriaceae from many
other fermentative and
nonfermentative gram-neg. bacteria.
.

Different biochemical reactions of

some Enterobacteriaceae species
 VIRULENCE FACTORS
¾ Numerous virulence factors have been
identified.
¾ Some are common, and others are
unique to specific virulent strains.
Common Virulence Factors Associated
with Enterobacteriaceae
¾ Endotoxin
¾ Capsule
¾ Antigenic phase variation
¾ Sequestration of growth factors
¾ Resistance to serum killing
¾ Antimicrobial resistance
 Endotoxin (lipopolysaccharide, LPS) is a
virulence factor of gram-negative
bacteria. The activity of this toxin
depends on the lipid A component of LPS,
which is released at cell lysis.
Many of the systemic manifestations of
gram-negative bacterial infections are
initiated by endotoxin, including the
following:
¾ Activation of complement
¾ Release of proinflammatory cytokines:
IL-1, IL-6, TNF-α, IFN-γ, etc.
Systemic manifestations of endotoxin:

¾ Leukocytosis
¾ Thrombocytopenia
¾ Disseminated intravascular
coagulation
¾ Fever
¾ Decreased peripheral circulation
¾ Shock
¾ Death
 Capsule
¾ Encapsulated Enterobacteriaceae are
protected from phagocytosis by the
hydrophilic capsular antigens, which repel
the hydrophobic phagocytic cell surface.
These antigens interfere with the binding
of antibodies to the bacteria and are poor
immunogens or activators of complement.
¾ Anticapsular antibodies developed during
infection or obtained as therapy are
protective – they act as opsonins.
• Antigenic Phase Variation. Each of capsular К
and flagellar Н antigens can be alternatively
expressed or not expressed (phase variation), a
feature that protects the bacteria from
antibody-mediated cell death.
• Type III Secretion Systems. A variety of distinct
bacteria (e.g., Yersinia, Salmonella, Shigella,
Escherichia, Pseudomonas, Chlamydia) have a
common effector system for delivering their
virulence factors into targeted eukaryotic cells.
• This system, referred to as the type III
secretion system, consists of approximately 20
proteins that facilitate secretion of bacterial
virulence factor into host cells. In the absence
of the type III secretion system, the bacteria
lose their virulence.
. Sequestration of Growth Factors
• Nutrients are provided to the organisms in
enriched culture media, but the bacteria must
become nutritional scavengers when growing in
vivo.
• Iron is an important growth factor required by
bacteria, but it is bound in heme proteins (e.g.,
hemoglobin, myoglobin) or in iron-chelating
proteins (e.g., transferrin, lactoferrin). The
bacteria counteract the binding by producing
their own competitive iron-chelating compounds
(e.g., siderophores: enterobactin and aerobactin)
• Iron can also be released from host cells by
hemolysins produced by the bacteria.
• Resistance to Serum Killing. Whereas many
bacteria can be rapidly cleared from blood,
virulent organisms capable of producing
systemic infections are frequently resistant to
serum killing. Although the bacterial capsule
can protect the organism from serum killing,
other factors (long-O-chain LPS) prevent
binding of complement components to the
bacteria and subsequent complement-mediated
clearance.
• Antimicrobial Resistance. As rapidly as new
antibiotics are introduced, organisms can
develop resistance to them. This resistance can
be encoded on transferable plasmids (R
plasmids) and exchanged among species,
genera, and even families of bacteria.
 RESISTANCE
E. coli and all Enterobacteriaceae are very
resistant in the environment. They survive in
weeks and months in the water, soil, food,
objects.
This explain the fecal-oral spread of
opportunistic and pathogenic enterobacterial
species. The most useful disinfectants are the
halogens (chlorine compounds) which are used
for disinfection of lavatories, drinking water, etc.
Finding of E. coli in water, food, on the objects
show fecal contamination and danger of
spreading of pathogenic bacteria and viruses by
fecal-oral mechanism.
 DISEASES CAUSED BY OPPORTUNISTIC
Enterobacteriaceae
(other than Salmonella, Shigella and Yersinia)
Е.coli is a member of the normal intestinal flora.
In some individuals the enteric bacteria may
replace the normal flora of upper respiratory and
genital mucosa where gram-positive bacteria
prevail. This is risk factor for gram-negative lung
infections.
In general, they contribute to normal function
and nutrition.
Some strains of Е. coli posses virulence factors
and may cause gastrointestinal infections
(diarrhogenic strains).
™ The opportunistic Enterobacteriaceae
become pathogenic only when they reach
tissues outside of their normal intestinal
or other less common normal flora sites
and in immunocompromised subjects.
™ Particularly in infancy or old age, in the
terminal stages of other diseases, after
immunosuppression, or with indwelling
venous or urethral catheters).
™ The most frequent sites of clinically
important infection are the urinary tract,
biliary tract, and other sites in the
abdominal cavity, but any anatomic site
(e.g., bacteraemia and sepsis, prostate
gland, lung, bone, meninges) can be the
site of disease.
™ Some of the enteric bacteria are
saprophytic opportunistic pathogens
(Serratia marcescens, Enterobacter
aerogenes).
.

Escherichia coli
™ The genus Escherichia consists of
five species, of which E. coli is the
most common and clinically most
important.

™ This organism is associated with a

variety of diseases, including sepsis,
UTIs, meningitis, and gastroenteritis.
 As expected, the multitude of strains
capable of causing disease is reflected in
the antigenic diversity of the bacteria.
Many O (190), H (75), and К (103)
antigens have been described, and they
are used to classify the isolates for
epidemiologic purposes.
Specific antigenic serogroups are also
associated with greater virulence and
organ specificity.
 E. coli possesses a range of virulence
factors.
Adhesins E. coli is able to remain in the
urinary tract or gastrointestinal tract
because the organisms are able to adhere
to the cells at these sites and avoid being
eliminated by the flushing action of
voided urine or intestinal motility.

Strains of E. coli possess numerous

highly specialized adhesins:
 Pili
¾ - P-pili (which also binds to Р blood
group antigens),
¾ - type I pili,
¾ - Dr fimbriae (which bind to Dr blood
group antigens),
¾ - aggregative adherence fimbriae
AAF/I and AAF/II,
¾ - bundle-forming protein (Bfp) – in
EAEC and EPEC (plasmid encoded),
¾ Colonization factor antigens
¾ Intimin (OMP)
¾ Ipa protein (invasion plasmid antigen)
• Exotoxins E. coli also produces a diverse
spectrum of exotoxins:
¾ Shiga like toxins SLT-I and II in EHEC
strains (due to phage conversion),
¾ Heat-stable and heat-labile enterotoxins,
Ent plasmid encoded, (STa and STb; LT-I
and LT-II in ETEC.
¾ Hemolysins (HlyA), Hly plasmid encoded,
are considered important in the
pathogenesis of disease caused by
uropathogenic E. coli.
 Clinical Diseases
• Sepsis. E. coli sepsis originates from infections in
the urinary or gastrointestinal tract (e.g.,
peritonitis with sepsis following intestinal
perforation).

• UTI are ascendant: from the colon - urethra -

bladder, prostate, kidney, but may be caused by
hematogenous spread to the urinary tract.
Disease is more common with certain specific
serogroups. These bacteria produce adhesins for
the cells lining the bladder and upper urinary
tract, and hemolysin, which lyses erythrocytes
and other cell types.
• Neonatal Meningitis. E. coli and group В
streptococci – the main cause in infants
younger than 1 month.
• 75% of the E. coli strains possess the K1
capsular antigen, composed of sialic acid.
• The strains originate from the
gastrointestinal tracts of pregnant
women and newborn infants.
• Similarity with antigens of the neurons
containing sialic acid may explain the
pure protective response (antigenic
mimicry)
Pili adherence
 Gastroenteritis

¾ Six groups E. coli strains cause

enteritis and gastroenteritis (diarrheal
diseases).

¾ Organism/Site of action, disease and

pathogenesis are given on the next
table.
Enterotoxigenic E. Traveler's diarrhea; infant diarrhea Plasmid-mediated heat-stable and/or heat-
coli (ETEC) in underdeveloped countries; labile enterotoxins that stimu-late
watery diarrhea, vomiting, cramps, hypersecretion of fluids and electrolytes
Small intestine nausea, low-grade fever
Enteropathogenic Infant diarrhea in underdeveloped Plasmid-mediated A/E histopathology with
(ЕРЕС) countries; fever, nausea, vomiting, disruption of normal microvillus structure
nonbloody stools resulting in malab-sorption and diarrhea
Small intestine
Enteroinvasive E. Disease in underdeveloped Plasmid-mediated invasion and destruction of
coli (EIEC) countries; fever, cramping, watery epithelial cells lining colon
diarrhea; may progress to
Large intestine dysentery with scant, bloody stools

Enterohemorrhagic Hemorrhagic colitis (HC) with
(EHEC) severe abdominal cramps, initial
watery diarrhea, followed by grossly
bloody diarrhea; little or no fever;
Large intestine may progress to hemolytic uremic
syndrome (HUS)
Mediation by cytotoxic Shiga toxins (SLT-1,
SLT-2), which disrupt protein synthesis; A/E
lesions with destruc-tion of intestinal
microvillus result-ing in decreased absorption

Enteroaggregative Infant diarrhea in underdeveloped Plasmid-mediated aggregative adherence of

(EAEC) countries; persistent watery E.coli ("stacked bricks") with shortening of
diarrhea with vomiting, dehydration, microvilli, mononuclear infiltration, and
and low-grade fever hemorrhage; decreased fluid absorption
Small intestine

Diffiise aggregative Watery diarrhea in infants 1 to 5 Stimulates elongation of microvilli

(DAEC) years of age
Small intestine
¾ Disease caused by enterotoxigenic E. coli
(ETEC) is seen most commonly in
developing countries, although almost
80,000 cases are estimated to occur
annually in the United States.

¾ Infections are observed in either young

children in developing countries or
travelers to these areas. The inoculum for
disease is high >108, so infections are
acquired through consumption of fecally
contaminated food or water.
• ETEC produce two classes of enterotoxins:
heat-labile toxins (LT-I, LT-II) and heat-
stabile toxins (STa and STb).
• LT-I is functionally and structurally
similar to cholera toxin. This toxin consists of
one A subunit and five identical В subunits. The В
subunits bind to the same receptor as cholera toxin (GM
gangliosides) in the small intestine. The A subunit
translocates across the membrane by endocytosis in
vacuole. The A subunit interacts with a membrane
protein that regulates adenylate cyclase. The net effect
of this interaction is an increase in cAMP levels, with
enhanced secretion of chloride, decreased absorption of
sodium and chloride. These changes lead to lose of
water and a watery diarrhea.
 STa is associated with human
disease. STa is a small, monomeric
toxin leading to an increase in
hypersecretion of fluids. Genes for
LT-I and STa are present on a
transferable plasmid.
Secretory diarrhea caused by ETEC
develops after a 1- to 2-day
incubation period and persists for an
average of 3 to 4 days.
 The symptoms - cramps, nausea,
vomiting (rare), and watery diarrhea are
similar to those of cholera but are
milder.
Neither histologic changes of the
intestinal mucosa nor inflammation is
observed.
Disease mediated by heat-labile toxin is
indistinguishable from that mediated by
heat-stable toxin.
 Toxin production is not associated
with specific serogroups, so tissue
cultures or animal model assays for
toxin activity must be performed if
toxigenic strains are to be detected.

Nucleic acid probes have also been

used to detect the toxin genes.
.

Mechanism of action of LT-І enterotoxin

ЕРЕС. Enteropathogenic E. coli is the major cause of

infant diarrhea in impoverished countries. Disease is rare
in older children and adults, presumably because they
have developed protective immunity. Although specific О
serogroups have been associated with outbreaks of ЕРЕС
diarrhea in nurseries, the serotyping of the E. coli
isolated in random or endemic disease is discouraged
except in epidemiologic investigations.
¾ Enteroinvasive E. colt (EIEC) strains are
closely related by phenotypic and
pathogenic properties to Shigella.

¾ The bacteria are able to invade and

destroy the colonic epithelium, producing a
disease characterized initially by watery
diarrhea.

¾ A minority of patients progress to the

dysenteric form of disease, consisting of
fever, cramps, blood and leukocytes in
stool.
• Enterohemorrhagic E. colt (EHEC) strains
are the most common strains producing
disease in developed countries.
• The ingestion of fewer than 100 bacilli can
produce disease. The severity of the
disease caused by EHEC ranges from mild,
uncomplicated diarrhea to hemorrhagic
colitis with severe abdominal pain, bloody
diarrhea, and little or no fever.
• Hemolytic uremic syndrome (HUS) is a
complication in 10% of infected children
younger than 10 years.
• EHEC occur in the warm months, and in
children younger than 5 years. The
disease have been attributed to the
consumption of undercooked ground beef
or other meat products, water, milk,
uncooked vegetables, and fruits.
• EHEC strains express a Shiga like toxin.
• More than 50 serogroups have been
isolated. The majority that cause disease
are believed to be serotype O157:H7.
 Enteroaggregative E. colt (EAEC) strains
have been implicated as a cause of
persistent, watery diarrhea with
dehydration in infants in developing
countries.

EAEC stimulate secretion of mucus,

which traps the bacteria in a biofilm
overlying the epithelium of the small
intestine.
 Diffusely adherent E. coli (DAEC) have
been recognized from their
characteristic adherence to cultured
cells.

DAEC stimulate elongation of the

microvilli with the bacteria embedded in
the cell membrane.

The resulting disease is a watery

diarrhea found primarily in infants
between 1 and 5 years of age.
 OTHER OPPORTUNISTIC
Enterobacteriaceae

Klebsiella
™ Members of the genus Klebsiella have a
prominent capsule that is responsible for
the mucoid appearance of isolated
colonies and the enhanced virulence of
the organisms in vivo.
• The most commonly isolated member of this
genus is K. pneumoniae, which can cause
community-acquired primary lobar pneumonia.
Alcoholics and people with compromised
pulmonary function are at increased risk for
pneumonia because of their inability to clear
aspirated oral secretions from the lower
respiratory tract.

• Pneumonia due to Klebsiella species

frequently involves the necrotic destruction of
alveolar spaces, formation of cavities, and the
production of blood-tinged sputum.

• These bacteria also cause wound, soft tissue,

and UTIs.
 Proteus
• Infection of the urinary tract with P.
mirabilis is the most common disease.
• P. mirabilis produces large quantities of
urease, which splits urea into carbon
dioxide and ammonia. This process raises
the urine pH and facilitates the formation
of renal stones.
• The increased alkalinity of the urine is also
toxic to the uroepithelium. Furthermore,
in contrast to E. coli, the pili on P. mirabilis
may decrease its virulence by enhancing
phagocytosis of the bacilli.
 Enterobacter, Citrobacter, Morganella,
Serratia
• Primary infections caused by Enterobacter,
Citrobacter, Morganella, or Serratia are rare in
immunocompetent patients. They are more
common causes of hospital-acquired
(nosocomial) infections in neonates and
immunocompromised patients.

• For example, Citrobacter koseri has been

recognized to have a predilection for causing
meningitis and brain abscesses in neonates.

• Antibiotic resistance is a particularly serious

problem with Enterobacter species.
 Laboratory Diagnosis
¾ Culture
Specimens of normally sterile material, such
as spinal fluid and tissue collected at surgery, can
be inoculated onto nonselective blood agar.
Differential media (e.g., MacConkey agar) is
used for the culture of specimens normally
contaminated with other organisms (e.g., feces or
sputum).
¾ Biochemical Identification
There are many diverse species in the
family Enterobacteriaceae. Biochemical test
systems have become increasingly sophisticated,
and now virtually all members of the family can
be identified accurately in less than 24 h with one
of several commercially available identification
systems.

Commercial identification kits

. ¾ Antigenic differentiation
Serologic testing by slide agglutination is
very useful for determining the clinical
significance of an isolate (e.g., serotyping for
specific pathogenic strains, Salmonella, Shigella spp.,
EHEC - E. coli O157:H7 or Y. enterocolitica), and for
classifying isolates for epidemiologic purposes.

¾ Antibiogram
 TREATMENT, PREVENTION, AND
CONTROL
• Antibiotic therapy for infections with
Enterobacteriaceae must be guided by in vitro
susceptibility testing and clinical experience.
• Whereas some organisms are susceptible to
many antibiotics, others can be highly resistant.
• Furthermore, susceptible organisms exposed to
subtherapeutic concentrations of antibiotics in
a hospital setting can rapidly develop
resistance.
• R-plasmid multidrug resistance are easily
transferable by conjugation.
Problematic resistance mechanisms: ESBL, HLAR
• In general, AB resistance is more common in
hospital-acquired infections than in community-
acquired infections.
• Symptomatic relief, but not antibiotic
treatment, is usually recommended for patients
with E. coli or Salmonella gastroenteritis,
because antibiotics can prolong the fecal
carriage of these organisms or increase the risk
of secondary complications.
• I.v. gamma-globulin preparations, which
contain huge variety of antibodies to different
microbes are very effective tool in the
treatment of systemic infections.
 It is difficult to prevent endogenous infections
with Enterobacteriaceae because these
organisms are a major part of the endogenous
microbial population.
However, some risk factors for the infections
should be avoided:
¾ The unrestricted use of antibiotics that can
select resistant bacteria
¾ The performance of procedures that traumatize
mucosal barriers without prophylactic antibiotic
coverage
¾ The use of urinary catheters
Unfortunately, many of these factors are
present in patients at greatest risk for infection
(immunocompromised patients confined to the
hospital for extended periods).
Exogenous infection with Enterobacteriaceae is
theoretically easier to control.
For example, the source of infections with
organisms such as Salmonella is well-defined.
However, these bacteria are ubiquitous in
poultry and eggs. Unless care is taken in the
preparation and refrigeration of such foods,
little can be done to control these infections.
Shigella organisms are predominantly
transmitted in young children by fecal-oral
route, but it is difficult to interrupt the fecal-
hand-mouth transmission responsible for
spreading the infection in this population.
 Outbreaks of these infections can be
effectively prevented and controlled
only through education and the
introduction of appropriate infection-
control procedures (e.g., hand
washing, water toilets, disinfection
(tap water in kitchen, toilets etc.)
canalization for waste water, proper
disposal of soiled diapers and linens)
in the settings where these infections
typically occur.
• Vaccination with formalin-killed Y. pestis has
proved effective for people at high risk to
plague. Chemoprophylaxis with tetracycline has
also proved useful for people in close contact
with a patient with pneumonic plague.

• Improvements in the live, attenuated S. typhi

vaccines have led to development of significant
protection in populations in which the incidence
of endemic disease of typhoid fever is high. This
protection can persist for up to 5 years.

• Inactivated whole-cell vaccines, as well as

vaccination with purified Vi antigen (the
polysaccharide capsular antigen of S. typhi
associated with virulence), are also protective.