Salmonella

MORPHOLOGY
Gram (-) bacilli
Motile with peritrichous flagella
Facultative anaerobe
Produce H2S unlike Shigella spp.

Shigella
MORPHOLOGY
Slender, Gram (-) rods
Bacilli, coccobacilli
Non-spore forming
Facultative anaerobes

Escherichia

Campylobacter
MORPHOLOGY
Gram (-) rods w/ comma or S or GULL
WING SHAPED (bird in flight; cell
division, before separation of two
cells)
MOTILE WITH SINGLE POLAR FLAGELLUM
(rapid motility)
Non spore former
Small (0.3-0.6 um) try to filtrate

Vibrio
MORPHOLOGY
Gram (-) bacilli, curved rod /
COMMA SHAPED
0.5 x 1.5 to 3 um
Polar flagella (single)
facultative anaerobe

SPECIES
S. bongori has serotypes: (causes septicemia)
S. enterica (MC: human cases)
o
Can cause enteric fever

S. typhi septicemia in
humans only

S. paratyphi (a and b) in
humans only (can cause
enteric fever)

S. cholerasuis in humans
and animals
o
Can cause gastroenteritis

S. typhimurium - humans and

animals

S. enteriditis - humans and

animals

SPECIES
Shigella dysenteriae (Shigellosis
common in developing countries,
prototype)
S. flexneri (Shigellosis common in
developing countries)
S. boydii (Shigellosis in developed
countries / industrial world)
S. sonnei (Shigellosis in developed
countries / industrial world)

SPECIES
E. coli (part of the normal flora
and incidentally causes disease;
most important and most
common cause of diarrhea;
normal flora + virulence factor =
disease)
o BACTEROIDES - most
common anaerobic Gram
(+) bacteria in the GIT
o E. coli - Most common
cause of urinary tract
infection (both for men
and women) and
accounts for
approximately 90% of first
urinary tract infections in
young women
E. blattae (cockroaches)
E. hermanii (wound)
E. vulneris( wound)

SPECIES
There are actually 18 species, among them
are the following:
C. jejuni MOST COMMON
C. coli (also a common species)
C. fetus (opportunistic pathogen)
C. upsaliensis (from contaminated
dogs, occasionally causes diarrhea in
humans)

ANTIGENIC STRUCTURES
For identification of subspecies:
o O antigen
o H antigen
o Capsular (K) antigen
(Vi) antigen protects organisms from action of
complement
Pili for adherence to the epithelium
Endotoxin common among gram (-) bacteria
Tolerant to acid in phagocytic vesicles
Can survive in macrophages

ANTIGENIC STRUCTURES
O antigen
Endotoxin
SHIGA TOXIN (S. dysenteriae)- similar
to entero invasive property (major)
o Exotoxin that disrupts protein
synthesis causing endothelial cell
damage
May also cause HUS (like
Enterohemorrhagic E. coli)
Invasive property - can destroy
epithelial lining of the gastrointestinal
tract that can produce bloody stools
invasion plasmid Antigens - surface
antigens that promote adhesion of
the organism to the mucosa
Type 1 (exotoxin)
2 activities:
Diarrhea- ENDOTOXIN
activities

ANTIGENIC STRUCTURES
A. ADHESIONS - for adherence to
the epithelium of the GlT and
urinary mucosa
Pili
Colonization factor
antigens (ETEC)
Aggregative adherence
fimbriae
Bundle forming pili
Intimin
IpA protein
B. ENTEROTOXINS (all causes
diarrhea) presence of
enterotoxins depends on the
serotype
Heat stable toxin
Heat labile toxin
Verotoxins (shiga toxins)
Hemolysins

ANTIGENIC STRUCTURES
Lipopolysaccharides (LPS) (lahat gram
(-) so lahat may LPS) (sino ang
nagpoproduce ng bloody stool:
enteroinvasive and
enterohemorrhagic, shigella and
campylobacter)
Flagellar antigens (the H antigen)
Enterotoxin, ADHESINS, cytotoxic
enzymes (roles are poorly defined),
motility

SPECIES
V. cholera most medically
important because it causes
Cholera
1. V. cholera O1
(endemic/pandemic)
causes cholera
2 biotypes:
a. EI Tor
(milder form
of cholera)
name was
taken from
the camp
that first
isolated
cholera
b. Classical
2. V. cholera 0139
similar to EI Tor but they do
not produce
polysaccharide 01
V. parahaemolyticus based on O
and K antigens; also causes
diarrhea, from eating infected
shellfish (seafood), gastroenteritis
V. vulnificus also causes diarrhea
& infection of open wounds; from
infected oyster
ANTIGENIC STRUCTURES
FLAGELLA
O lipopolysaccharides
CHOLERA TOXIN like ETEC with
subunit A and B; causes
hypersecretion of electrolytes and
H2O (thereby responsible for the
diarrhea), non bloody diarrhea
COREGULATED PILUS adherence to
mucosal cells
HEMAGGLUTINATION PROTEASE
includes intestinal inflammation
Siderophores iron sequestration
Neuraminidase increases toxin
receptor

Mucosal destructionCYTOTOXIC activities

EPIDEMIOLOGY
Pathogenic for humans/ animals
Widely distributed
Common source: contaminated poultry, eggs, dairy
products, food and water by contaminated food
handlers, etc.
Direct spread through the oral-fecal route
Diseases: ENTERIC FEVER (typhoid fever),
BACTEREMIA, SALMONELLOSIS / ENTEROCOLITIS,
enteritis, septicemia

EPIDEMIOLOGY
70% of cases occur in CHILDREN < 10
years old
HUMANS are the only reservoir
Transmission: spread from person-toperson through the FECAL-ORAL
ROUTE
Highly communicable: small amount
(200) of bacilli can establish an
infection
Diseases caused GASTROENTERITIS &
BACILLARY DYSENTERY
Transferred by 4F: Food, finger, fecal,
flies
Always pathogenic

LABORATORY DIAGNOSIS
Specimen: STOOL
1st wk get blood, 2nd- urine, 3rd, stool
Growth culture characteristics
o SALMONELA- SHIGELLA AGAR - black colonies
o (+) H2S
o Motile (Shigella - non motile)
o Non Lactose Fermenters (MAC & EMB)
o Enrichment broth Selenite broth, SS agar
Other tests
o Slide agglutination test
Widals test?
Serotyping

LABORATORY DIAGNOSIS
Specimen:
o Fresh stool (around an hour to
submit in lab, para di mapanis)
o Mucus flecks-(mucus part of the
stool) used to document the
diarrhea because it contains a
lot of organisms
o Rectal swab
Culture/ Growth Characteristics:
o HEAKTON ENTERIC AGAR /
SALMONELLA-SHIGELLA (SS)
AGAR contains antibiotics that
can eliminate other
Enterobacteriaceae. Can also
differentiate Shigella from
Salmonella
o Facultative anaerobes
o Non-motile (as opposed to
Salmonella)
o Convex, circular, transparent
colonies
o NON-LACTOSE FERMENTER
(except S. sonnei)
o (-) lysine decarboxylase
o (-) hydrogen sulfide
In the SS agar, colonies
would appear transparent
with a black center
o TSI: K/A without gas

C.

ENDOTOXIN it is present since

they are gr
0020ec3,am (-)
gram
organisms
D. INVASIVE CAPACITY - it is the
ability of some strains to destroy
the epithelial lining of the GIT
(eg. Intestine), thus causing
bloody diarrhea
EPIDEMIOLOGY
MOST COMMON GRAM (-)
BACILLI IN GIT (E. coli); [*most
common Gram (+) bacteria in
GIT = Bacteroides]
Most infections are
ENDOGENOUS (ones own
normal flora)
Strain causing GASTROENTERITIS
are acquired EXOGENOUSLY
(from contaminated food
and/or water)
Diseases: bacteremia, UTI,
gastroenteritis (in which diarrhea
is a symptom), meningitis, intraabdominal infections (increases
if you have rupture of the
intestine secondary to trauma or
obstruction), pneumonia,
prostatitis (in men).
BAP
EMB (Eosin Methylene Blue)
produce blue black colonies
with GREEN METALLIC SHEEN

MAC PINK COLONIES

(indicating that the organism is
LACTOSE FERMENTER)
Emb: metallic green
(+/-) motility
not a routine to isolate different
strains
A/A with gas
Indole (+)
Voges-Proskauer (-)
Methyl Red (+)
Citrate (-)
H2S (TSI) (-)
Urease (-)
Phenylalanine Deaminase (-)
Lysine Decarboxylase (+ or -)
Ornithine Decarboxylase
(variable)
Acid produced from lactose (+)

EPIDEMIOLOGY
C. jejuni and C. coli contaminated
food, unpasteurized milk, poultry,
water,
ZOONOTIC INFECTIONS (domestic
animals like dogs, cattle, sheep,
poultry (remember)
Killed by gastric juices
Diseases: GASTROENTERITIS, meningitis,
septicemia, spontaneous abortion
Worldwide distribution

EPIDEMIOLOGY
Found in Marine and water surface
worldwide
Spread thru ingestion of
contaminated food (shellfish, oyster,
etc.) and water
Diseases: cholera, wound infection,
gastroenteritis, bacteremia
Infectious dose is very high: 108 to
1010 particles

LABORATORY DIAGNOSIS
Specimen: stool
Growth characteristics:
o MICROAEROPHILES require only
small amounts of oxygen
o Incubation temp: 42C
o Selective media is needed
(reduced oxygen with added
carbon dioxide): SKIRROWS
MEDIUM (Vancomycin, Polymixin
B, Trimethoprim that can
eliminate other organism)
o CAPNOPHILIC - 5 - 10% CO2
needed for growth
o slow growing ( 2 3 days)
Biochemical Tests:
o ( + ) UREASE
o ( + ) CATALASE
o ( + ) COAGULASE
Hipurate:? deep blue color

LABORATORY DIAGNOSIS
Specimen: mucus flecks (where the
bacteria stay) from stool
Growth characteristics
o ( + ) OXIDASE: for primary
identification
o ( + ) sucrose
o TSI: ( - ) H2S and gas
o Non-lactose fermenter
Grown in peptone agar, blood agar,
TCBS (Thiosulfate Citrate Bile Sucrose agar
on which it produces YELLOW
COLONIES; board exam question) (grow
in high ph9)
o
o

Halophilic: salt-loving
STRING TEST: differentiate
Vibrio cholera(+) from other
species that causes cholera;
colonies from 24hr culture +
sodium deoxycholate (mixture
will create a viscous material
= parang sipon na hinila na
may string-like appearance)
Slide agglutination test to
differentiate the serotypes

TREATMENT
Fluid and Electrolyte Replacement
Antimicrobial therapy (in severe cases)
o Danger of prolonging symptoms and
excretion of bacteria so it depends on the
assessment of the doctor
o Neonates, chronic disease
o Invasive infections: ampicillin, trimethoprin
sulfamethoxazole, 3rd gen cephalosporin

Typhoid: give atb

Enterocollitis: no atb, it is self limiting

With vaccine

TREATMENT
Fluid replacement
Antibiotics: Ciprofloxacin, Ampicillin,
Tetracycline, Chloramphenicol
o antibiotics should be given only
to those with severe cases so as
to lessen the days of infection

TREATMENT
ORAL REHYDRATION SOLUTION
(ORS) (1L h2o, tsp nacl, 6tsp
sugar)
If patient cannot tolerate
hydride (ORS), give Gatorade
instead.
Antispasmodics: supportive
Case-to-case basis (antibiotics):
Trimethoprim-sulfamethoxazole /
ampicillin / cephalosporins
(antibiotics are given for severe
cases only to prevent
development of resistant strains)

TREATMENT
Fluid and electrolyte replacement
Antibiotics: ERYTHROMYCIN (only in
severe cases) is DOC, Azithromycin,
Clarithromycin;
RESISTANT in penicillin and
cephalosporin

PREVENTION AND CONTROL

Sanitary control of food, water and
milk
Proper sewage disposal
Isolation of patients because they
are highly contagious and
disinfection of excreta
Screening of food handlers (usually in
restaurants wherein you try to test for
fecalysis and urinalysis)
Fly control

PREVENTION AND CONTROL

Proper food handling and
cooking of beef products
Avoid unpurified water
Restrict use of antibiotics
Proper hygiene

PREVENTION AND CONTROL

Proper sanitation
Avoid ingestion of unpasteurized milk

same as E.coli

PREVENTION AND CONTROL

Good sanitation
Proper Hand washing
Carriers must not be allowed to work as food
handlers
Food must be thoroughly cooked

WATER AND ELECTROLYTE

REPLACEMENT
Immediate fluid replacement
double IV ( sometimes even 4)
MANDATORY ANTIBIOTIC THERAPY:
Tetracycline (DOC); Doxycycline

same as Salmonella

S.enteritidis (6-8 hrs. Incubation)

Ingestion

Absorbed by the epithelial cells in the terminal portion of the small intestine
Bacteria penetrate and migrate to the lamina propia in the ileo-cecal region
Mutiply in the lymphoid follicles, which would cause reticuloendothelial
hyperplasia and hypertrophy

Inflammatory response causes the release of prostaglandins

Stimulate cAMP

Active fluid secretion

(after 6-48 hours) Nausea, non-bloody diarrhea, fever, abdominal cramps,

hemolytic anemia (HA)
Spontaneous resolution (disease is self limiting a week)

From the oral-fecal route

Colonize in the small intestine

Invade and replicate in the

colonic mucosa

Would cause lower abdominal

cramps, profuse watery diarrhea,
tenesmus (painful straining), pus/
mucus/ bloody stools = INTESTINAL
DYSENTERY
(disease is self limiting =
rehydration)

Ingestion of contaminated
food

Multiply in small intestine

Causes crampy abdominal

pain, profuse diarrhea,
may also get bloody
diarrhea (self limiting (58days))

Prevention and Control

improvement of sanitation
isolation of patient and disinfection
of excreta (highly infective)

Ingestion of contaminated water (1 4 days)

Invasion of intestine tract via ATTACHMENT TO MICROVILLI

of the brush border of epithelial cells

Multiplication and liberation of toxin

Production of profuse diarrhea (RICE WATER STOOLS),

profound dehydration, abdominal cramps, circulatory
collapse, nausea, vomiting, anuria

Hypovolemic shock, cardiac arrhythmia, renal failure

Death (>mortality without treatment is 60%)

**Rice Water Stoolsyung stool ay whitish [parang
pinaghugasan ng bigas]

E. COLI SEROTYPES
A. ENTEROTOXIGENIC E. COLI (ETEC)
Disease: TRAVELERS DIARRHEA (most common), infants diarrhea
Site of action: SMALL INTESTINES
Produces SECRETORY DIARRHEA that can last for 3-4days
Incubation Period: 1-2 days
Produces:
o HEAT LABILE TOXINS:
LT-1 & LT-2 (has (1) A & (5) B subunit)
o HEAT STABLE TOXINS:
STa & STb
LT-I: similar to cholera toxin and causes diarrhea
LT-1 & STa: cause secretory diarrhea (infect humans)
LT-2 & STb : do not cause diarrhea
HEAT LABILE TOXIN (LT-1, LT-II)
B SUBUNIT binds to receptor GM1 ganglioside on
epithelial cells of small intestine

A SUBUNIT enters mucosa , translocates across

membrane and activates adenylyl cyclase

increase cAMP levels

hypersecretion of water and Cl, decrease

reabsorption of Na

watery diarrhea (NON-BLOODY STOOLS),

vomiting (rare), cramps, nausea, low grade fever

B.

ENTEROPATHOGENIC E. COLI (EPEC)

Disease: Major cause of INFANT
DIARRHEA
Site of action: SMALL INTESTINE

C. ENTEROINVASIVE E. COLI (EICC)

Disease: SHIGELLA-LIKE DIARRHEA

(DYSENTERY)

Site of action: COLON

Destruction of epithelial cells = scant

bloody stool

HEAT STABLE TOXIN (STa, STb)

STa + (combines with) GUANYLATE

increase GMP

hypersecretion of fluids

Bacteria attaches to epithelial cells of small

intestine

DESTRUCTION OF MICROVILLI

Malabsorption and diarrhea (NON BLOODY

STOOLS), fever, nausea, vomiting
A series of BACTERIAL GENES ON A PLASMID
mediate invasion of colonic epithelium

Bacteria lyse phagocytic vacuole and

replicate within the cytoplasm thus destroying
epithelial cells

Dysentery with SCANT BLOODY STOOLS; may

also cause COLONIC DESTRUCTION

D.

Enterohemorrhagic E. coli (EHEC)

Disease: associated with hemorrhagic
colitis (severe diarrhea); HAEMOLYTIC
UREMIC SYNDROME
Also known as the shiga-toxin
producing E. coli
Site of action: LARGE INTESTINE
PRODUCE: verotoxin (shiga toxin)
o Shigella-like toxin 1 and 2
o Most common serotype is O157:
H7 (causes HUS) (please
remember this)
HUS (hemolytic uremic syndrome) is a
complication wherein you have
ACUTE RENAL FAILURE,
THROMBOCYTOPENIA and
HEMOLYTIC ANEMIA.
This can lead to platelet fibrin thrombi
which can cause obstruction in the
blood flow in the kidney, brain and
other organs leading to multi-organ
failure and death (3-5%)
Incubation: 3-4 days
E. ENTEROAGGREGATIVE E. COLI (EAEC)
Disease: INFANT DIARRHEA
Site of action: SMALL INTESTINE
?

F . DIFFUSELY ADHERENT E. COLI (DAEC)

Disease: INFANT DIARRHEA (1-5years
old)
Site of action: SMALL INTESTINE
Pathogenesis: self-limiting

Undercooked ground beef

Produce SHIGA TOXINS

Protein synthesis and COLONIC VILLI

DISRUPTION AND DESTRUCTION

Decrease absorption

Watery diarrhea

BLOODY DIARRHEA

Severe abdominal pain (resolution in

untreated patient: 4-10 days)

EAEC: EXCESSIVE MUCUS PRODUCTION

Traps bacteria on epithelium of small intestine

Persistent WATERY DIARRHEA

Vomiting, dehydration, low grade fever

DAEC

elongation of microvilli with bacteria

embedded in cell membrane

WATERY DIARRHEA