Escherichia coli
and Salmonella
Shuzo Kaneko
Andrea Tu
Vipin Sandhu
Escherichia Coli
1. Gram-negative, short rods
2. Common member of the normal flora
of the large intestine.
3. As long as these bacteria do not
acquire genetic elements encoding for
virulence factors, they remain benign
commensals.
4. Strains that acquire bacteriophage or
plasmid DNA encoding enterotoxins or
invasion factors become virulent and
can cause either a plain, watery
diarrhea or an inflammatory dysentery.
Virulence classification of E.coli
(ETEC)
EHEC: Enterohemorrhagic
EPEC: Enteropathogenic
ETEC: Enterotoxigenic
Serotype of Escherichia coli : specific Ogroup/H-antigen combinations
1. The presence or absence of specific heat-stable somatic antigens
(O antigens) composed of polysaccharide chains linked to the core
lipopolysaccharide (LPS) complex.
2. The H antigens are the flagellar antigens.
Example:
O157:H7  enterohemorrhagic (EHEC) E.coli cause the
hemolytic uremic syndrome
Enteropathgenic E. coli (EPEC)
1. Defined as those pathogenic E. coli whose pathogenic
mechanisms are not related to the production of heat-labile
enterotoxins (LT), heat-stable enterotoxins (ST), or to Shigellalike invasiveness.
2. Most EPEC strains adhere to cultured cells (Hep-2), which is
rarely observed with other strains.
3. 94-kDa outer membrane protein, EPEC adherence factor
(EAF)
Entero-Toxigenic E.coli (ETEC)
A: Heat-labile toxin (LT)
1. Related antigenically and structurally to cholera toxin.
2. Inactivated at 65oC for 30min.
3. LT1 subunits possess ADP-ribosylating activity.  cAMP 
 decreased absorption of Na+ by the tips of the intestinal villi
and increased secretion of Cl- by the crypt areas between the villi.
The net result in absorption of water into the intestine which
manifests itself as diarrhea.
B: Heat-stable toxin (ST)
1. Theses strains are designated ST. These are small polypeptide of
from 1.5 to 4.0 kDa.
2. Their small size provides them with their heat stability (100 oC for
30min) as well as their non-antigenicity.
Enterohaemorrhagic (EHEC) E.coli: O157:H7
1. Complete genome sequenced (2001)
2. Comparison with the nonpathogenic strain K-12
3. 1,387 new genes were found in this
strain.  these include candidate
virulence factors
Circular genome map
Salmonella: Structure,
Classification, and
Antigenic Types
1. Gram-negative, flagellated and
facultative anaerobic bacteria
2. The cell envelope contains a complex
lipopolysaccharide (LPS) structure.
(an outer O-polysaccharide coat, a middle
portion, the R core, and an inner lipid A
coat)
3. This LPS structure is thought as an
endotoxin, and important in determining
virulence of the organisms.
Invasion of intestinal mucosa by Salmonella
How were Salmonella’s virulence
factors acquired?
1.
Genes for the virulence factors of the Salmonella tend to
cluster together.
2.
The lower G-C content of the pathogenicity islands
(around 38%) compared to the rest of the genome (over
50%).
It is believed that these genes were acquired through
horizontal gene transfer.
Genes for Virulence factors
1. Pathogenicity Island 1 (SPI-1)
Genes necessary for bacterial entry into the cells of the
intestinal epithelium.
2. Pathogenicity Island 2 (SPI-2)
Genes necessary for intracellular bacterial replication
and the initiation of systemic infection of the host.
Both pathogenicity islands code for protein complexes,
known as Type III Secretion Systems (TTSSs), used to
deliver virulence factors to host cells.
Horizontal Gene Transfer
Definition
The movement of genetic material between bacteria
other than by descent in which information travels
through the generations as the cell divides.
Bacterial species have acquired several mechanisms
by which to exchange genetic materials.
Horizontal Gene Transfer (Examples)
1. Transformation
The uptake of naked DNA
Common mode of horizontal gene transfer
Mediate the exchange of any part of a chromosome
2. Conjugation
The transfer of DNA mediated by conjugal plasmids or
conjugal transposons. Requires cell to cell contact.
3. Transduction
The transfer of DNA by phage
Requires that the donor and recipient share cell surface
receptors for phage binding
Usually limited to closely related bacteria.
The type III secretion
system (TTSS)
1.
2.
This system is made up of 20 proteins,
and ensure controlled secretion and
delivery of virulence factors to the host
cells.
The base of the complex assembles in
step wise order. The PrgI needle
structure is secreted by the incomplete
TTSS already in place.
PrgI
SPI-1 TTSS is necessary for
Salmonella’s initial interaction with
host intestinal epithelial cells
1. Salmonella contains genes encoding two forms of TTSS,
one located on SPI-1 and the other located on SPI-2.
(Mutants lacking working copies of these genes are no longer
virulent.)
2. SPI-1 TTSS probably mediates the entry of Salmonella into
host cells, by a process termed bacteria-mediated endocytosis.
3. Entry into the host cell then activates the expression of the
Salmonella Pathogenicity Island-2 Type III Secretion System
(SPI-2 TTSS).
Bacterial effector proteins trigger
cytoskeleton rearrangements in host cell
1. Cytoskeleton-associated proteins relocate to the site of bacterial
entry when Salmonella contact with the host cell.
2. The apical cell surface itself undergoes structural changes,
causing its brush border to resemble the membrane ruffles.
3. These changes trigger the endocytosis of the bacteria in
membrane-bound vesicles.
Bacterial effector proteins trigger
cytoskeleton rearrangements in host cell
(continue)
4. This process is different from the route of receptor-mediated
endocytosis followed by most pathogens into the host cell.
5. After internalization some of these vesicles translocate to the
basolateral surface of the cell, allowing the apical membrane to
reassume its normal, non-ruffled structure.
SipA and SipC : SPI-1 effector protein
for host invasion
SipA:
Binds actin and stabilizes actin filaments, thus decreasing the
minimum cellular concentration required for actin polymerization.
Therefore, SipA maximizes the efficiency of Salmonella invasion of
the host cell.
SipC:
Aids the entry of other SPI-1 effector proteins.
It is believed to activate actin monomers to polymerize and
stimulate actin filament bundling, indicating a role in Salmonellainduced host cytoskeleton rearrangements.
SopB : the primary virulence factor
1. Two domains homologous to eukaryotic inositol
polyphosphate 4-phosphatases.
2. SopB as a enterotoxin is associated with the SPI-1 TTSS.
3. SopB induce an increase the concentration of cellular
inositol polyphosphate.
SopB : the primary virulence factor
(continue)
1. Increased concentration of inositol polyphosphate causes an
increase in chloride secretion from the intestinal epithelium
into the lumen.
2. This efflux of chloride ions and influx of sodium ions alters
the charge equilibrium across the epithelium, leading to a
massive fluid secretion designed to restore equilibrium.
3. The secreted fluid causes the watery stool.
Dam (DNA adenine methylase) mutants
are unable to colonize deep tissues and
are avirulent
1. The Dam enzyme methylates adenine residues in the genome.
2. Regulate the timing of biological processes including DNA
replication, mismatch repair, and transposition.
3. Dam regulates the expression of at least 20 genes encoding
virulence factors, such as various pili operons and the Pag
genes.
Types of E. coli
Commensal Strains
Extraintestinal Pathogenic Strains
(ExPEC)
Intestinal Pathogenic Strains
Urinary Tract Infection
Entrotoxigenic E. coli
(ETEC)
Abdominal Infection
Entropathogenic E. coli
(EPEC)
Meningitis
Entroinvasive E. coli
(EIEC)
Pneumonia
Entroaggregative E. coli
(EAggEC)
Cellulitis/Musculoskeletal Infection
Diffusely Adherent E. coli
(DAEC)
Endovascular Infection
Entrohemorrhagic E. coli
(EHEC)
Bacteremia
Miscellaneous Infection
Commensal Strains
• Facultative fecal flora.
• Colonize the intestines of virtually all warm blooded animals
shortly after birth.
• Does not cause disease within the intestinal tract.
• Does not usually cause disease outside of the intestinal tract
except in presence of other factors.
• Strains lack virulence traits.
ExPEC Strains
• Also present in normal human fecal flora, but possess special
genes that code for virulence factors.
• Entry into the extraintestinal site, and not acquisition, is the
limiting factor for infection.
• ExPEC infections can occur in nearly every organ and site, and
in all age groups and host types, regardless of human or
animal.
• Coincidental disease and abnormalities in host defenses result
in more adverse outcomes.
• Primarily community-acquired, but is also the most frequently
isolated gram neg. bacteria in nosocomial environments.
ExPEC: Urinary Tract Infection (UTI)
• The urinary tract is the most common site of ExPEC infection
(90% of ambulatory UTIs; 25-30% long-term care and hospital
UTIs).
• Serotype O4:H5 is commonly associated with UTI.
• UTI is the second most common infection responsible for
hospitalization.
• 7 epidemiological groups:
1) children under 1 years old
2) school-age girls
3) premenopausal women
4) men with prostatic or other causes of urinary tract
obstruction
5) postmenopausal women
6) individuals with neurogenic bladders
7) patients with indwelling catheters
ExPEC: Urinary Tract Infection (UTI)
• Inflammation of urethra and bladder common, with symptoms of
painful urination, frequency and pain in the suprapubic region.
• Complications include kidney infection, characterized by fever
and/or back pains.
• Prolonged or increasing fever may indicate intrarenal abscess
and/or obstruction, which may led to renal cell damage or renal
failure.
• Prostate infection is also a complication in men.
• UTI inducing ExPEC is sometimes referred to as Uropathogenic
E. coli (UPEC).
ExPEC:Abdominal Infection
• The abdomen is the second most frequent site of ExPEC
infections.
• Events resulting in a distruption in the bowel mucosa can lead
to an acute peritoneal infection.
• Peritoneal abscess formation may also occur following acute
peritonitis or as a consequence of subclinical fecal spillage.
• Acute peritonitis and intraperitoneal abscesses often involve
multiple organisms - both aerobes and anaerobes, with E. coli
as the commonest organisms.
ExPEC:Meningitis
• Most cases of E. coli meningitis occurs in newborn infants.
• ExPEC is the primary cause of meningitis in the first month of
life (25%-33% of cases), and almost all are caused by the K-1
strain (75% of E. coli possess the Capsular K-1 antigen).
• Premature or low-birth weight babies are at higher risk.
• Even with treatment, morbidity rate is 20%, and survivors may
suffer permanent brain damage.
• Infection may occur during delivery.
• Otherwise, E. coli meningitis is rare (2% of all meningitis
cases), and occurs comorbid to cirrhosis or as a result of a
disruption of the meninges.
• Neonatal meningitis causing ExPEC is sometimes referred to
as Neonatal Meningitis E. coli (NMEC).
ExPEC:Pneumonia
• Only 2%-5% of community-acquired pneumonia are caused by
enteric gram-negative bacteria (GNB) such as ExPEC.
• Enteric gram-negative bacteria such as ExPEC are a common
cause of pneumonia acquired long-term care homes, and the
primary cause of pneumonia acquired in a hospital setting.
• GNB caused pneumonia will result in severe illness and
mortality rates of 20%-60%.
ExPEC:Cellulitis/Musculoskeletal
Infection
• ExPEC often causes infection of decubitus ulcers and some
lower-extremities infections in diabetic patients.
• Cellulitis, burn site or surgical infections can also be caused by
ExPEC, especially if near the perineum.
• Inflammation of the bone as a result of ExPEC acquired
through the blood can also occur.
• Though rare, E. coli may also cause orthopedic deviceassociated infections and hematogenously acquired
inflammation of voluntary muscles.
ExPEC:Endovascular Infection
• Infections primarily occur in in relation to intravascular devices,
and rarely in native heart valves.
• ExPEC is a rare cause of prosthetic valve endocarditis,
aneurysm infections, and vascular graft infections.
ExPEC:Bacteremia
• E. coli bacteremia can be a complication of an ExPEC infection
of any site; can result in death in the immunocompromised.
• E. coli is one of the most common blood isolates (16%-37%),
with about equal cases of community-acquired and nosocomial
bacteremia.
• Approximately 15% of bacteremias are complicated by septic
shock.
• 60% of bacteremias arise from the urinary tract.
• The second most common source of bacteremias is the
abdomen, accounting for 25% of all cases.
• Soft tissue, bone, and pulmonary infection are the third most
frequent sources for bacteremia.
• ExPEC strains are among the most common causes of sepsis
in neonates
ExPEC:Miscellaneous Infection
•
•
•
•
ExPEC infections can occur in nearly every organ and site.
Can cause a significant number of surgical site infections
Also known to cause complicated cases of sinusitis.
ExPEC may be a cause of Sudden Infant Death Syndrome
(SIDs) (Possible toxin mediated).
Diagnosis of ExPEC
• ExPEC is easily identified by a clinical microbiology lab using
standard biochemical criteria.
• Grows aerobically and anaerobically.
• Grows within 24 hrs.
• More than 90% are rapid lactose fermenters.
Intestinal Pathogenic Strains
•
•
•
•
•
Rarely encountered in human fecal flora.
Obligate pathogens.
Cause gastroenteritis or colitis when ingested. Contamination
via fecal-oral route.
Incapable of causing disease outside the intestinal tract.
Can be divided into 6 virotypes based on the following
criteria:
• Clinical characteristics
• Attachment to host cells
• Effects of attachment
• Toxins
• Invasiveness
Entrotoxigenic E. coli (ETEC)
• Incubation period: 1-7 days; Duration of Illness: 2-6 days.
• Inoculum: ID50 = 106 to 1010 colony-forming units(CFU)
• Transmission occurs via contaminated food and water; humans
are the major reservoir.
• Mediated by Heat-Labile Toxins (LT) and Heat-Stable
Toxins (STa); stimulate fluid secretion.
• Mild symptoms, including cramps, nausea, vomiting, watery
diarrhea. However, can also cause death, especially when
health care is poor.
• Children: causes death in developing countries.
• Adults: Partial immunity; Most common cause of traveler's
diarrhea (25%-75% of cases).
• ETEC uncommon in the U.S. and other developed countries.
• Serotype O148:H28 is a common ETEC.
Entropathogenic E. coli (EPEC)
• Incubation period: 1-2 days; Duration of Illness: weeks.
• Inoculum: unknown, is suspected to be low.
• Transmission occurs via rapid person-to-person spread;
humans are the major reservoir.
• Adheres to enterocyte plasma membrane and destroy microvilli;
exhibits patchy adherence; process called attaching-effacing.
• Not toxin mediated, symptoms result from invasive damages to
intestinal walls; involves the entire intestines.
• Symptoms: watery diarrhea with mucus but no blood,
deformation/destruction of microvilli.
• Primarily causes infant/neonatal diarrhea in developing
countries; breast-feeding diminishes risk of infection. May also
cause some cases of traveler's diarrhea.
• EPEC is uncommon in the U.S. and other developed countries
• Serotype O126:H11 is a common EPEC.
Entroinvasive E. coli (EIEC)
• Incubation period: 1-3 days; Duration of Illness: 7-10 days.
• Inoculum: ID50 = 108 to 1010 CFU.
• Transmission occurs via contaminated food and water; humans
are the major reservoir.
• Not toxin mediated; Invades the epithelial cells and proliferate,
resulting in death of cells and ulceration of the mucosa.
• EIEC is fairly uncommon as a cause of diarrhea; In
underdeveloped countries, sporadic EIEC induced diarrhea is
identified in children and travelers.
• Symptoms: an invasive, dysenteric form of diarrhea, including
fever, cramps, tenesmus and frequent stool containing blood,
leukocytes and mucus.
• EIEC rare in the U.S. and other developed countries.
Entroaggregative E. coli (EAggEC)
• Duration of Illness: long (persistent diarrhea).
• Inoculum: high amount required for infection.
• Transmission occurs via contaminated food and water; humans
are the major reservoir.
• Noninvasive, will not alter the histology of host cells; EAggEC
forms a “stacked-brick” adherence pattern.
• Mediated by Entroaggregative Stable Toxin (EAST)
• Symptoms: may cause persistent watery diarrhea, instead of
acute diarrhea.
• Primarily causes diarrhea in developing countries, affecting
young children and immunocompromised individuals. May also
cause some cases of traveler's diarrhea.
• EAggEC is uncommon in the U.S. and other developed
countries
Diffusely Adherent E. coli (DAEC)
• Duration of Illness: long (persistent diarrhea).
• Inoculum: high amount required for infection.
• Transmission occurs via contaminated food and water; humans
are the major reservoir.
• DAEC forms a “stacked-brick” adherence pattern, but in a more
diffused pattern than EAggEC.
• Symptoms: may cause persistent watery diarrhea, instead of
acute diarrhea.
• Primarily causes diarrhea in developing countries, affecting
young children and immunocompromised individuals. May also
cause some cases of traveler's diarrhea.
• Relatively little is known about DAEC.
• DAEC is uncommon in the U.S. and other developed countries.
Entrohemorrhagic E. coli (EHEC)
• Incubation period: 3-9 days; Duration of Illness: 1-2 weeks.
• Inoculum: ID50 = less than 103 CFU.
• Transmission occurs via contaminated food and water, as well
as person to person.
• Reservoir for EHEC:
1.
Mostly in intestine of cattle
2.
Also found in chickens, deer, sheep and pigs.
3.
Does not make the carrier animal sick.
4.
Meat typically becomes contaminated during the
slaughtering process.
5.
Bacteria on cow’s udders and equipment can also
contaminate milk.
• EHEC occurs more in developed countries, both outbreaks and
sporadic, peaks in summer season.
Entrohemorrhagic E. coli (EHEC)
•
•
Mediated by Shiga-like toxin (STX). Serotype O157:H7 is the
most common EHEC; result of EPEC + Phage (STX)
Typical Symptoms of EHEC Infections
1. GI tract → Large Intestines.
2. Binds tightly via attachment-effacement; Inflammation.
3. Hemorrhagic Colitis (more than 90% of cases):
a) Sudden onset of sever cramps and abdominal pain
b) Diarrhea within 24 hrs.
c) Diarrhea becomes watery.
d) Diarrhea becomes grossly
bloody.
e) Nausea and vomiting.
f) Little or no fever.
Complications of EHEC:HUS
Hemolytic Uremic Syndrome
• First described in 1955, now most common cause of kidney
failure in childhood.
• 5% - 10% of EHEC cases will develop HUS,usually within 2-14
days after diarrhea.
• HUS more common in younger children, less so in adolescents.
• 90% of HUS is caused by strain E. coli O157:H7.
• Caused when E. coli enters the circulation through the inflamed
intestinal wall and releases SLT.
• SLT attach to receptors on the endothelial cells.
• Kidney, pancreas and brain most susceptible.
• Characteristic symptoms include hemolytic anemia,
thrombocytopenia, and renal failure.
• Neurological consequences are also possible (Thrombotic
Thrombocytopenia Purpura - TPP); blood clot in brain.
Complications of EHEC:HUS
• In the active stage of
HUS (1-2 weeks):
– 50% Require dialysis due
to kidney failure
– 25% Experience seizures
– 5% Suffer diabetes
mellitus
– Majority require blood
transfusions
Complications of EHEC:HUS
• There is no known therapy to stop disease.
• With intensive care, mortality rate is 5% in America.
• Of survivors, 5% will develop end stage renal failure, and
require dialysis or transplantation.
• Another 5%-10% of survivors with have neurological or
pancreatic problems.
• In children, apparent recoveries may result in hypertension,
renal insufficiencies and urinary abnormalities later on in life.
Comparison of Intestinal
Pathogenic Strains
Diagnosis of Intestinal
Pathogenic Strains
•
•
•
•
Differentiate between inflammatory (EIEC and EHEC) and
non-inflammatory (ETEC, EPEC, EAggEC and DAEC)
diarrhea.
ETEC, EPEC, EAggEC and DAEC: either rare or self-limiting
= definite diagnosis is not necessary.
EIEC: rare, self-limiting = does not require definite diagnosis.
Definite diagnosis of EHEC required:
a) Most common: does not ferment in sorbitol (sorbitolMacConkey (SMAC) agar), followed by subsequent
serotyping for O157
b) More sensitive/rapid/specific: testing for presence of STX.
Treatment of Pathogenic
E. coli Infection
• Antibacterial medication is the primary treatment for
extraintestinal pathogenic (ExPEC) strains.
• For self-limiting infection resulting from EIEC, ETEC, EPEC,
EAggEC and DAEC strains, empirical antimicrobial treatment is
also administered.
• In the case of EHEC, antibiotics should be avoided, as they
may increase the risk of complications such as HUS and TPP.
• Diarrheal symptoms require replacement of lost water and
electrolytes. Antidiarrheal agents such as Imodium should also
be avoided.
How Can An E. Coli Infection Be
Prevented?
• Eating undercook beef is the
biggest risk factor for acquiring E.
coli O157:H7. Cook all ground beef
to at least 160º F.
• Don’t eat undercooked beef patties
in restaurants.
• Prevent harmful bacteria from
spreading in the kitchen by keep
raw meat separate from ready to eat
foods.
• Wash all fruits and vegetables
thoroughly, especially those that
will be eaten raw.
• Alfalfa sprouts may also contain E.
coli. There is currently no method
available to decontaminate alfalfa
sprouts.
How Can An E. Coli Infection Be
Prevented?
• Drink only pasteurized milk, juice or cider.
• Drink municipal water that has been treated with effective disinfectants
(ie chlorine), and bottled water that has been sterilized with ozone or
reverse osmosis.
• Avoid swallow water when swimming in lakes or pools, esp. public
swimming facilities.
• Persons with diarrhea should be careful in preventing person-toperson transmission.
• Outbreaks caused by person-to-person transmission can also occur at
hospitals, nursing homes, and in particular, at day care centers.
• Contamination from farm animals and manure is also possible. Avoid
contact and wash your hands thoroughly with soap and hot water.
Children under 5 should also be extra cautious around cattle, including
in petting zoos.
• More research is also necessary to reduce the number of cattle that
carry E. coli O157:H7, and the contamination of meat during
slaughtering.
Types of Salmonella
NonTyphoidal Salmonella
Typhoidal (Enteric) Salmonella
Gastroenteritis
Typhoid Fever
Bacteremia and Endovascular Infections
Paratyphoid Fever
Localized Infections
Intraabdominal Infections
Central Nervous System Infections
Pulmonary Infections
Urinary and Genital Tract Infections
Bone, Joint and Soft Tissue Infections
Nontyphoidal Salmonellosis
• Caused by S. typhimurium and S. enteritidis.
• The elderly, infants and immunocompromised individuals more
susceptible.
• Rainy season of tropical climates; Warm season of temperate
climates.
• Nontyphoidal salmonellosis is growing rapidly in the U.S; five
fold increase between 1974-1994.
• Centralization of food processing makes nontyphoidal
salmonellosis particularly prevalent in developed countries.
• Resistance is a concern, especially with multidrug-resistant
strains such as Definitive Type 104 (DT104), such as Definitive
Type 104 (DT104).
Nontyphoidal Salmonellosis
•
•
•
•
General Incubation: 6 hrs-10 days; Duration: 2-7 days
Inoculum: ID50 = 103 CFU.
Transmission occurs via contaminated food and water.
Reservoir:
a) multiple animal reservoirs
b) mostly from poultry and eggs (80% cases from eggs)
c) fresh produce and exotic pets are also a source of
contamination (more than 90% of reptile stool contain
salmonella bacterium); small turtles ban.
• Salmonella spreads in hens both vertically and horizontally.
• General Symptoms: diarrhea with fever, abdominal cramps,
nausea and sometimes vomiting.
Nontyphoidal Salmonellosis:
Gastroenteritis
• Incubation: 6-48 hrs; Duration: 3-7 days for diarrhea & 72hrs for
fever.
• Inoculum: large.
• Mediated by the SopB toxin; attaches to wall of intestines and
cause inflammation.
• Symptoms include nausea, vomiting, abdominal cramps and
fever of 100.5 – 102.2 ºF. Also accompanied by loose, nonbloody stool in moderate volume; Pseudoappendicitis (Rare).
• Stool culture will remain positive for 4-5 weeks; less than 1%
will be come carriers.
• Neonates, elderly and immunocompromised individuals most
susceptible.
Nontyphoidal Salmonellosis:
Bacteremia and Endovascular
Infections
• 5% develop bacteremia; 5%-10% of bacteremia patients develop localized
infections.
• Infants, the elderly and immunocompromised patients or those with
underlying infections are most susceptible.
• Endocarditis: Salmonella often infect vascular sites; preexisting heart valve
disease risk factor.
• Arteritis: Elderly patients with a history of
back/chest + prolonged fever or abdominal pain
proceeding gastroenteritis are particularly at risk.
• Both are rare, but can cause complications that
may led to death.
• Serotypes S. choleraesuis and S. dublin are
invasive and cause sustained bacteremia and
fever.
Nontyphoidal Salmonellosis:
Localized Infections
• INTRAABDOMINAL INFECTIONS:
1) Rare, usually manifested as liver or spleen abscesses.
2) Risk factors: hepatobiliary abnormalities, abdominal abnormalities and
sickle cell disease.
3) Treatment: surgery to correct anatomic damages and drain abscesses.
• CENTRAL NERVOUS SYSTEM INFECTIONS:
1) Usually meningitis (in neonates, present with severe symptoms e.g.
seizures, hydrocephalous, mental retardation, paralysis) or cerebral
abscesses.
• PULMONARY INFECTIONS:
1) Usually lobar pneumonia.
2) Risk factors: preexisting lung abnormalities, sickle cell disease,
glucocorticoid usage.
Nontyphoidal Salmonellosis:
Localized Infections
• URINARY AND GENITAL TRACT INFECTIONS:
1) Urinary infections usually cystitis or pyelonephritis.
2) Genital infections rare, usually ovarian and testicular abscesses,
prostatitis, or epididymitis.
3) Both can be complicated by abscess formation.
• BONE, JOINT AND SOFT TISSUE INFECTIONS:
1) Bone infections usually in the femus, tibia, humerus or lumbar vertebrae.
2) Risk factors: sickle cell disease and preexiting bone disease.
3) Treatment: prolonged antibiotic usage to prevent relapse/chronic
osteomyelitis.
4) Septic arthritis: usually in knee, hip, shoulders. (same risk factors)
5) Individuals with HLA-B27 histocompatibility antigen at risk for developing
reactive arthritis and Reiter’s syndrome (the combination of arthritis,
conjunctivitis and urethritis) following Salmonella gastroenteritis.
6) Soft tissue infections rare, usually in the immunocompromised, at sites of
local trauma.
Treatment of Nontyphoidal
Salmonellosis
• Gastroenteritis: Antibiotics are usually not recommended for
Salmonella gastroenteritis; increases rates or relapse and
prolonged carriage of bacterium.
• Diarrhea: Rehydration of lost fluids and electrolytes.
• Bacteremia: Third-generation cephalosporin or quinolones for
7-14 days.
• Endovascular Infection: IV ß-lactam antibiotics for 6 weeks.
• Extraintestinal Nonvascular Infections: antibiotic therapy for 2-4
weeks.
• 2-3 days of preemptive antibacterial treatment for patients
susceptible to spreading infection.
• Surgical intervention to remove damaged cells.
Typhoidal Salmonellosis
• Caused by S. typhi and S. paratyphi.
• Transmission occurs via person-to-person spread; Human are
the only known hosts/reservoir.
• Children under 1 year of age are particularly susceptible.
• Rare in developed countries; Global health problem, endemic in
India, South/Central America, Asia, and recently in eastern
Europe.
• The large number of global cases serve as a reservoir for U.S.
incidence of typhoid fever.
Typhoidal Salmonellosis
• Inoculum: ID50 = 103 to 108 CFU.
• Incubation: 3-60 days; Duration: a few days.
• Symptoms:
a) Prolonged fever (75% of cases)
b) Non-specific symptoms preceding fever
c) Variable GI symptoms, such as abdominal tenderness
(majority), abdominal pain (20%-40% of cases) and diarrhea.
d) “Rose Spots” (30% of cases); Duration: 2-5 days.
e) Enlargement of the spleen/liver, nose bleeds,
bradycardia.
f) Neuropsychiatric symptoms of
“muttering delirium” or “coma vigil”
Typhoidal Salmonellosis
• Late stage complications include intestinal perforation and
gastrointestinal hemorrhage
• Immediate care such as increase antibacterial medications or
surgical resection of bowel.
• Other rare complications include inflammation of the pancreas,
endocardium, pericardium, myocardium, testis, liver, meninges,
kidneys, joints, bone, lungs, and parotid gland and
hepatic/splenic abscesses.
• In general, symptoms for paratyphoid fever is similar to typhoid
fever, but milder with a much lower fatality rate.
• Majority clear bacteria from the stool within 8 weeks. However,
1% -5% become asymptomatic chronic carriers; the gall
bladder is the primary source of bacterium.
Treatment of Typhoidal
Salmonellosis
• Third-generation cephalosporins or quinolones is the current
treatment for typhoidal salmonellosis.
• IV or IM ceftriaxone (1g-2g) is also prescribed; usually 10-14
days (5-7 days for uncomplicated cases.)
• Multi Drug Resistant (MDR) strains of S. typhi: quinolones are
the only effective oral treatment.
• Nalidixic acid-resistant S. typhi (NARST) must be tested for
sensitivity to determine course of treatment.
• Sever typhoid fever (altered consciousness, septic shock):
dexamethasone treatment
• Chronic carriers: 6 weeks of treatment with either oral
amoxicillin, ciprofloxacin, or norfloxacin.
• Surgical intervention to remove damaged cells.
Diagnosis of Nontyphoidal and
Typhoidal Salmonella
•
Methods for identifying Salmonella bacterium:
a) Stool sample or blood sample grown on agar culture plate.
b) ELIZA; pinpoints exact serovar via antibody detection.
c) Stool sample grown on agar and
exposed to bacteriophages.
d) Rapid detection of salmonella
via PCR of stool isolate
e) Other diagnostic methods
include detecting for
leukopenia and neutropenia. Colony Color Key:
•Salmonella = pink
•Klebsiella, Enterobacter = blue/green
•Serratia = black
•E.coli, G+ = white
•
How Can Nontyphoidal
Salmonellosis
Be
Prevented?
Most commonly found in chicken eggs .
•
Cook egg until the yolk is solid; heat poultry
to 180ºF.
•
Do not store food at room temperature;
instead, store at temp above 145ºF or
below 39ºF.
•
Ensure proper hygiene during food
preparation, especially in centralized/mass
food preparation.
•
Use pasteurized eggs and poultry products,
especially in hospitals and long-term care
facilities and commercial food-service
establishments.
•
Avoid antibacterial products to prevent
emergence of new resistant strains.
•
In avoiding typhoidal Salmonella, monitor
food and water intake during travel and
consider vaccination.