Vivi anggelia

405100154

DIARRHEAL DISEASE
CAUSED BY BACTERIAL OR
VIRAL INFECTION

 Diarrheal abnormal fecal discharge

characterized by frequent and/ or
fluid stool; usually resulting from
disease of the small intestine and
involving increased fluid and
electrolyte loss

Food

Feces, from
humans or animals
containing
pathogenic
microbes or their
toxin
Fluids

finger

(water, milk)
Ingestion of organisms and/ or toxins
Gut

Organisms multiply and

toxins produced but
infection remains
localized in
gastrointestinal tract
Diarrhe
a
Pathogens excreted in

Organisms invade or toxins

absorbed
Disseminati
on/
penyebaran
Symptoms of systemic
infection ( fever, myalgia,

BACTERIAL CAUSE
DIARRHEA

- ESCHERICHIA COLI -

- Escherichia coli The most versatile of all bacterial

pathogens.
Some strains are important members
of the normal gut flora in humans
and animals.
Whereas others possess virulence
factors that enable them to cause
infections in the intestinal tract or at
other sites, particularly the urinary
tract.

- Escherichia coli Theirs are six distinct groups of E.coli

w/ different pathogenic mechanisms.
Enteropathogenic E.coli / EPEC
Enterotoxigenic E.coli / ETEC
Enterohemorrhagic E.coli / EHEC
Enteroinvasive E.coli / EIEC
Enteroaggregative E.colli /EAEC
Diffuse-aggregative E.coli / DAEC

Enteropathogenic E.coli
Do not appears to make any toxins
They do produce bundle forming pili (Bfp),
intimin (adhesin) and an associated
protein (translocated intimin receptor, Tir)
These virulence factors allow bacterial
attachment to epithelial cells of the small
intestine, leading to disruption of the
microvillius an attaching-effacing
mechanisms

Enteropathogenic E.coli
Epidemiology
Belong to particular O serotypes
Cause sporadic cases and outbreaks of
infection in babies and young children
Importance in adults less clear

Enteropathogenic E.coli
Laboratory diagnosis
Isolate organisms from feces
Determine serotype of several colonies
w/polyvalent antisera for known EPEC
types
Adhesion to tissue culture cells can be
demonstrated by a fluorescence action
staining test
DNA-based assays for detection of
attachment (virulence) factors

Enterotoxigenic E.coli
Possess colonization factors (fimbrial
adhesins)
These organisms produce powerful
plasmid-associated enterotoxins
which are characterized as being
either heat labile (LT) or heat stable
(ST)

 ETEC
STA
ST

Inhibisi absorbsi sodium

sekresi intestinal fluid

ETEC
STB

LT

Atrofi vili parsial

# absorbsi sodium

Osmotic diarrhea

Enterotoxigenic E.coli
Heat labile enterotoxin LT-1 very similar in
structure and mode of action to cholera toxin
produce by V.cholerae, and infection w/ strains
producing LT-1 can mimic cholera, particularly in
young and malnourished children
STs have a similar but distinct mode of action to
that of LT. Sta activates guanylate cyclase activity,
causing an increase in cyclic guanosine
monophosphate, which result in increased fulid
secretion
Immunoassays are commercially available for the
identifications of ETEC

Enterotoxigenic E.coli
Epidemiology
Most important bacterial cause of
diarrhea in children in resource-poor
countries
Most common cause of traveller
diarrhea
Water contaminated by human or
animal sewage may be important is
spread

Enterotoxigenic E.coli
Laboratory diagnosis
Isolate organisms from feces
Test commercially available for
immunologic detection of toxins from
culture supernatans
Gene probes specific for LT and ST
genes available for detection of ETEC in
feces and in fppd and water sample

Enterohemorrhagic E.coli
Isolates produce a verotoxin
Verotoxin essentially identical to shigella toxin
After attachment to the mucosa of the large intestinal
by the attaching-effacing mechanisms, the produced
toxin has a direct effect on intestinal epithelium,
resulting in diarrhea
Cause hemorrhagic(HUS)
HS destruction of the mucosa and consequent
hemmorrhage
Verotoxin receptos have been identified on renal
epithelium and may account for kidney involment
Serotypes of EHEC commonest one : O157:H7

Enterohemorrhagic E.coli
Epidemiology
Serotype O157 most important EHEC in
human infections
Outbreaks and sporadic cases occur
worldwide
Food and unpasteurized milk important
in spread
May cause hemolytic uremia syndrome
(HUS)

Enterohemorrhagic E.coli
Laboratory diagnosis
Isolate organisms from feces
Proportion of EHEC in fecal sample may
be very low (often <1% of E.coli
colonies)
Usually sorbitol non fermenters
Shiga toxin producing and associated
genes detected by biological,
immunological and nucleic-acid based
assay

 EHEC
EHEC

adhesion

Shigalike toxin

vomit

Hemorragic colitis

HUS

trombositopeni Renal failure acute Anemia hemolitik

DEATH
Incubation time >14 days...auto recovery in 8 days

Enteroinvasive E.coli
Attach specifically to the mucosa of the
large intestine
They invade cells by endocytosis by
using plasmid-associated genes.
Inside the cell, they lyse the endocytic
vacuole, multiply and spread to adjacent
cells, causing tissue destruction,
inflammation, necrosis, and ulceration,
resulting in blood and mucos in stool

Enteroinvasive E.coli
Epidemiology
Impotant cause of diarrhea in area of
poors hygiene
Infections usually food-borne; no
evidence of animal or environmental
resevoir

Enteroinvasive E.coli
Laboratory diagnosis
Isolate organisms from feces
Test for enteroinvasive potential in
tissue culture cell or nucleic-acid based
assays for invasion-associated cells

 EIEC
endocytosis
EIEC

invasion

Enterocyte colon

multiplication
Invasion the other cell

nekrosis
Blood
and
mucous

Intestinal ulceration

Enteroaggragative E.coli
Derive their name from their characteristic
attachment pattern to tissue culture cells
The pattern is an aggreagtive or stacked brick
formation.
These organisms act in the small intestine to cause
persistent diarrhea especially in children in resource
poor countries
Their aggregative adherence ability is due to
plasmid-associated fimbriae
Produce heat labile toxins ( an enterotoxin and a
toxin related to E.coli hemolysin) but their role in
diarrheal disease is uncertian

Enteroaggragative E.coli
Epidemiology
Characteristic attachment to tissue
culture cells
Cause diarrhea in children in
resource poor countries
Role of toxin uncertain

Enteroaggragative E.coli
Laboratory diagnosis
Tissue culture assay for aggregative or
difuse adherence

Diffuse aggregative E.coli

Produce an alpha hemolysin and cytotoxic
necrotizing factor 1
They are aslo known ad diffuse adherent or
cell deatching E.cli
Theirs role in diarrheal disease, especially
in young children, is incompletly
understood and somewhat controverisal,
with some studies reporting ni association
Epidemiology and laboratory diagnosis=
idem EAEC

Pathogenesis

Interaction of various pathogenic E.coli with the epithelial cells of the gut. A.ETEC bind loosely
via fimbriae, secrete toxins (like Cholera toxins) into the gut that then gain entry into the cell without
disruption of cytoskeleton. B. EPEC destroys the brush border microvilli, and becomes firmly attached
through a pedestal consisting of actin and actin binding proteins. C. EIEC, gains entry into the cell,
escaping from the immune system by digesting the phagolyosome. EIEC can grow and divide in the
cell cytoplasm and gain entry to neighbouring cells by bursting through and digesting membranes. D.
EHEC, operates like EPEC, but in addition Shiga toxins are liberated that the epithelial cells take up in
coated pits and taken to the Golgi. The toxins then travel from Golgi to the E.R. where they destroy
ribosomes by the removal of a single adenine residue from the 28SrRNA. This results in the death of
the cell.

EPEC and ETEC

Re the most important contribulators to global
incidence of diarrhea, while EHEC is more important
is resource rich countries
ETEC diarrhea in children in resource poor
countries may be clinically indistinguishable from
cholera
EIEC and EHEC cause bloody diarrhea
EHEC infection, HUS is characterized by acute renal
failure, anemia and thrombocytopneia, may be
neurologic complications
HUS most common cause of acute renal failure in
children in the UK and USA

Spesific test are needed to indentify

strains of pathogenic E.coli
Routine stool culture are required to
identify spesific diarrhea associated
E.coli types
EHEC has led most labratorues in
resource rich countries to screen for
E.clo O157:H7

Antibacterial therapy is not

indicated for E.coli diarrhea
Specific antibacterial therapy is not indicated
Fluid replacement may be necessary young
children
Treatment HUS urgent and may involve
dialysis
Provision of a clear water supply ad adequate
systems for sewage disposal are fundamental
to preventions of the diarrheal disease
EIEC and EHEC food and unpasteurized milk
can be important vehicle of infection

Pathog
ens

Incubat Duratio Sympto

ion
n
ms
Vomitin Abdomin
period
al
Diarrhe g
cramps
a

fever

EPEC

1-2 days Weeks

Watery

ETEC

1-7 days 2-6 days Watery

EHEC

3-4 days 5-10

days

Bloody

EIEC

1-3 days 7-10

days

Bloofy

SHIGELLA

Vibrio Cholerae
The diarrhea can be extremely severe, with
characteristic rice water stools, which can lead to
rapid dehydration, circulatory collapse, and death.
Vibrio cholerae secretes cholera toxin (CT) binds to
enterocytes The A subunit catalyzes the ADPribosylation of the GTP binding protein activation of
adenylate cyclase accumulation of cAMP in
enterocytes increase in secretion of chloride and
water secretory diarrhea.

SALMONELLA

Salmonella
Are the most common cause of food associated
diarrheal in many resource-rich countries
More than 2000 serotypes defined on the basis
of differences in the wall (O) and flagellar (H)
antigens.
All salmonella except for salmonella typi and
paratypi are found in animal as well as humans.
Transmitted: food, especially poultry and dairy
products, person to person.
Water borne infection is less common.

Salmonella
Animal feed

Domestic
food animals

Human food

Human

effluent

sewage

Human

Wild
animals

Salmonella
Are almost acquired orally in food
and drink that is contaminated.
Diarrhea is produce as a result of
invasion by the salmonella of
epithelial cell in the terminal portion
of the small intestine.
Initial entry is probably through
uptake by M cell (antigen samplers of
the bowel) w/ subsequent spread to
epithelial cells.

Salmonella
The bacterial migrate to lamina
propria layer of the iliocecal region
multiplication stimulates
inflammatory response which both
confines the infection of the GIT and
mediate the release PG turn
activate cyclic adenosine
monophosphate and fluid secretion
diarrheal

Salmonella
Species salmonella that normally cause
diarrheal S. enteritidis, S.choleraesuis
may become invasive to patients w/
particular predispositions ( children,
immunocompromised, sickle cell anemia).
The organisms are not contained within the
GIT, but invade the body to cause septicemia;
consequently , many organs become seeded
w/ salmonella, sometime leading to :
osteomyelitis, pneumonia or meningitis.

Salmonella
In the vast majority of cases,
samonella spp. Cause an acute but
self-limiting diarrhea, though in the
young and the elderly the symptoms
may be more serve.
Vomiting is also common w/
enterocolitis, while fever is usually a
sign of invasive disease.
S.typi and paratypi systemic
illness.

salmonella
Culturing fecal specimens on selective
media are summarized in the Appendix.
The organisms are not fastidious and can
usually be isolated within 24h although
small number may requires enrichment
in selenite broth before culture.
Preliminary identification can be made
rapidly, but the complete result, including
serotype, take at least 48h

salmonella
Fluid and electrolyte may be
required young and the elderly
Unless there is evidence of invasion
and septicemia, antibiotic should be
positively discouraged because they
do not reduce the symptoms or
shorten the illness, and may prolog
excretion of salmonellae in the feces.

Salmonella
May be excreted in the feces for
serveral weeks after a salmonella
infection.
pathog
ens

Incubati
on
period

Durati Diarrhe Vomitin Abdomin fever

on
a
g
al
cramps

Salmon
ella

6h-2days

48h7days

Watery

CAMPYLOBACTER

Campylobacter

Are among the commonest causes of diarrhea

Curved or S shaped gram-negative rod.
Growing well at 42 C
They do not therefore grow on the media used for isolating E.coli
and salmonella.
Several species of the genus campylobacyer are assiociated w/
human disease, bit campylobacter jejuni is by far the most
common.
As w/ salmonella, there is a large animal resevoir of
campylobacter : cattle, sheep, rodents, poultry and wild birds.
Infection are acquired by consumption of contaminated food,
especially poultry, milk and water.
Person to persn spread by fecal-oral route is rare, as is
transmission from food handlers.

campylobacter
Diarrhea is clinically similar to that caused by
other bacteria such as salmonella and shigella.
The gross pathology and histologic apperances
of ulcer action and inflamed bleeding mucosal
surfaces in the jejenum, ileum and colon are
compatible w/ inavion of the bacteria, but the
production of cytotoxins by C.jejuni has also
been deminstrated.
Invasion and bacteremia are not common,
particulary in neonatus and debilitated adults.
Long incubation period and a longer duration

campylobactere
Erythromycin is used for severe
campylobacter diarrhea.
Invasive infections, may required
treatment w/ an additional antibiotic
such as a quinolone or an
aminoglycoside.
Preventive screening food handlers
because contamination of food by
this route is very uncommon.

campylobacter
Pathog
en

Incubat Duratio Diarrhe Vomitin Abdomi Fever

ion
n
a
g
nal
period
cramps

Campyl
obacter

2-11
days

3 days3 weeks

Bloody

CHOLERA

Cholera
An acute infection of the GIT caused
by the comma-shaped gram-negative
bacterium V.cholera.
The disease have a long history
characterized by epidemics and
pandemics.

Cholera
Cholera flourishes in communities w/ inadequate
clean drinking water and sewage disposal.
Is a free living inhabitant of fresh water, but only
in humans.
The disease Is spread via contaminated food;
shellfish grown in fresh and estuarine water have
also been implicated
Direct person to person spread is though to be
uncommon.

Cholera
Serotypes are based on somatic (O)
antigens)
Serotype O1 most important and is
futher divides into 2 biotypes
:classical and EI tor.

Cholerat
He symptoms of cholera are caused by an
enterotoxin
The organisms requires additional virulence factors
to enable it to survive the host defences and adhere
to the intestinal mucosa.
The severe watery non bloddy diarrgea is known as
rice water stool, and can be result in the loss of 11
of fluid every hours.
Fluid loss electrolyte imbalance dehydration,
metabolic acidosis (loss bicarbonate), hypokalemia
(potassium loss), hypovelemic shock resulting in
cardiac failure.

Cholera
Culture is necessary to diagnose sporadic or
imported cases of cholera and carries.
Oral or intravenous rehydration may be used
Antibiotics are not necessary, but tetracycline
may be given, as some evidence indicates that
this reduces the time of excretion of V. Cholera
thereby reducing the risk of transmission
Clean drinking water supply and adequate
sewage disposal are fundamental to
preventions of Cholera.

Cholera
A killed whole cell vaccine is
available and is given parenterally,
but is effective in only about 50% of
those vaccinated, w/ protection
lasting for only 3-6 months.

Pato
gens

Shige
lla

incu
batio
n
perio
s

Dura
tion

2Up to
3days 7
days

Diarr Vomi
hea
ting

Abdo Feve
mina r
l
cram
ps

water +
y

SHIGELLOSIS

Shigellosis
Bacillary disentery because in its more severe
form its characterized by an invasive infection
of the mucosa of the large intestine causing
inflammation and resulting in the presence of
pus and blood in the diarrheal stool.
There is 4 species:
S. sonnei most infections at the mild end of the
spectrum
S.flexneri and Boydii usually produce more
severe disease
S.dysenteriae the most serious

Shigellosis
Is primarily a pediatric disease. When
associated w/ severe malnutrition it may
precipitate complications such as protein
deficiency syndrome (kwashiokor).
Animal pathogen w/o animal resevoir, they are
not founs in environment, being spread from
person to person by fecal-oral routes and less
frequently by contaminated food and water.
10-100 organisms be able to initiate
infections

Shigellosis
Attach to and invade, the mucosal epithelium of the
distal ileum and colon, causing inflammations and
ulceration.
They rarely invade through the gut wall to the
bloodstream.
S. dysenteriae produce a (Shiga) toxin similar to that
associated w/ EHEC cause damage intestinal
epithelium and glomerular ndothelial cells kidney
failure
Diarrhe usually watery initially, but later contains mucus
and bloodlower abdominal cramps can be occur,
especialy in young n elderly
Complication malnutrition.

Shigellosis
Regyration may be indicated.
Antibiotic decrease intestinal motility,
sholud not be given except in severe cases.
Plamsid mediated resistance is common,
and antibiotic susceptibility test should be
preformed on shigella isolates if treatment
is required.
Education in peronal hygiene and proper
sewage disposal are important.

ROTAVIRUSES

rotaviruses
Replicating rotavirus causes diarrhea by damaging transport
mechanisms in the gut
Incubation periods is 102 days
After replication in the intestinal epithelial cells there is an acute
onset of vomiting, which is sometime projectile, and diarrhea
which lasts from 4 to 7 days.
Replicating virus damages transport mechanisms in gut, and loss
of water, salt and glucose cause diarrhea
Infected cells in the intestine are destroyed, resulting in villous
atrophy.
The villi, long fingers-like projections, become flattened resulting in
the loss of both the surface area absorption and the digestive
enzymes, and raise the osmotic pressure in the lumen gut cause
diarrhea
There is no inflammation or loss of blood

rotaviruses
Infections is commonest under 2
years of age, and has a seasonal
pattern, being most frequent in the
cooler months of the years in
temperature climates.
Rotavirus are well adapted intestinal
infectious agent, as few as 10
ingested particles can cause
infection

rotaviruses
Particles can be seen in fecal sample
by electron microscopy show cubic
symmetry and an outer capsid coat
arranged like spokes of a wheel viral
RNA or antigen van be detected in
feces: PCR and ELISA

rotaviruses
Fluid and salt replacement can be life
saving in rotavirus diarrhea

PARASITE AND THE GIT

Parasite and the GIT

protozoa
Small intestine
Girdia lamblia
Cryptosporidium
parvum
Isospora belli

Large intestine
Entamoeba histolytica
Dientemoeba histolytica
Balantidium coli

worms
Small intestine

Ascaris lumbricoides
Ancylostoma duodenale
Necator americanus
Strongyloides
stercolariis
Taenia saginata

Large intestine
Enterobius vermicularis
Trichuris trichura

ENTAMOEBA HISTOLYTICA

Entamoeba histolytica
Is the most found in subtropical and tropical countries.
The trophozoite stage of the amebae live in the large
intestine on the musocal surface
Reproduction of these stages is by simple binary fission
and there is periodic formation of resistant encysted
forms, which pass out the body
The cyst can survive in the external environment and act
as a infective stages
Infection occurs: food n drink contaminated either by
infected food handlers or as a result of inadequate
sanitation.
Transmission cam also take place as a result of anal
sexual activity

Entamoeba histolytica
The cyst can pass intact trough the
stomach when swallowed and excyst
in the small intestine adhere to
epithelial cell n damage them by
phagocytosis and cytolysis invade
the mucosal n feed on host tissue
including red blood cells amebic
colitis

Entamoeba histolytica
May produce small localised superficial ulcers or
involve colonic muocsa with the formation of deep
confluent ulcers.
The former causes a mild diarrhea , whereas most
severe invasion lead to amebic dysentery
Amebic dysentery: mucus and blood in stool
Complication: perforation of the intestinal, leading t
peritonitis and extra intestinal invasion trophozoites
can spread via blood to the lover with the formation
of an abscess, and may secondarily extend to the
lung and other organs, rarely abscesses spread
directly and involve the overlying skin.

Entamoeba histolytica
Trophozoites can be found in cases of
dysentery (when the stool are loose and
wet), but they are fragile and deteriorate
rapidly
ELISA test are available as is a triage panel
assay that can distinguish between
E.histolytia/dispar, cryptosporidium parvum
and gardia lamblia.
Differentiation of histolytica and dispar
requires immunological tests or PCR

Entamoeba histolytica
Metronidazole is useful against both
the intestinal and extraintestinal
sites of infection, but if the latter
become secondarily infected either
bacteria, additional antibiotics and
drainage are necessary
Prevention: approaches to hygiene
and sanitation as those adopted for
bacterial infections of the intestine

TYPHOID FEVER

Definition of Typhoid
Fever
Typhoid fever is a systemic disease
characterized by fever and abdominal pain
and caused by dissemination of S. Typhi or
S. Paratyphi.
Typhoid
fever
was
clearly
defined
pathologically as a unique illness on the
basis of its association with enlarged
Peyer's patches and mesenteric lymph
nodes.

Epidemiology
Nontyphoidal Salmonellosis :
The actual number of cases 15
million/yr
Rates of morbidity and mortality
associated with NTS are highest among
the elderly, infants, and
immunocompromised individuals
Transmission : animal food products,
especially eggs, poultry, undercooked
ground meat, and dairy products and
fresh produce contaminated with animal

Epidemiology
Enteric (Thypoid) Fever :
In 2002 : 22 million cases, with 200.000
deaths
More common in urban than rural areas
and among young children and
adolescents
Transmission : food-borne or waterborne
results from fecal contamination by ill or
asymptomatic chronic carriers

Sources of Infection
Water
Contamination with feces often results in explosive epidemics.
Milk and Other Dairy Products (Ice Cream, Cheese, Custard)
Contamination with feces and inadequate pasteurization or improper handling. Some outbreaks
are traceable to the source of supply.
Shellfish
From contaminated water.
Dried or Frozen Eggs
From infected fowl or contaminated during processing.
Meats and Meat Products
From infected animals (poultry) or contamination with feces by rodents or humans.
"Recreational" Drugs
Marijuana and other drugs.
Animal Dyes
Dyes (e.g, carmine) used in drugs, foods, and cosmetics.
Household Pets
Turtles, dogs, cats, etc.

Salmonellosis
Salmonella infection in man is caused
by the enteric fever group which
includes:
- Salmonella typhi Typhoid fever
- Salmonella paratyphi A paratyphoid
fever
- Salmonella paratyphi B paratyphoid
fever
- Salmonella paratyphi C has different
symptomatology.

Etiolog
Salmonella
y

Morphology

Bacillus shaped
Gram negative
Non spore
Anaerob fakultatif
Size : 1-3.5m x 0,5-0,8m
Have flagel peritrich for movement

Risk factors
Work in or travel to areas where typhoid
fever is endemic
Work as a clinical microbiologist
handling Salmonella typhi bacteria
Have close contact with someone who
is infected or has recently been infected
with typhoid fever
Have an immune system weakened by
medications such as corticosteroids or
diseases such as HIV/AIDS
Drink water contaminated by sewage
that contains S. typhi

Clinical Manifestation
Salmonell
a thypi
infection
per oral
patients went to the
doctor yet

week 1:
prodormal
symptoms:
fever
anorexia
nausea, vomiting
constipation
myalgia

second week
and next:
relative
bradikardi
thypoid tongue
oeganomegali
delirium

patient went to the doctor

Incubation period 10-14

Week
days
1
No
Symptom
symptom
s begin
s

second week
and next

Pathophysiology
salmonella typhi

Survives the acidity of the stomach

Invades the Peyers Patches of the intestinal wall

Macrophages (Peyers Patches)

The bacteria is within the macrophages and survives

Bacterias spread via the lymphatics while inside the

macrophages

Access to reticuloendothelial system, liver,

spleen,gallbladder and bone marrow

First week : elevation of the body temperature

Second week : abdominal pain, spleen

enlargement , and rose spots

Third week : necrosis of the Peyers Patches

Leads to perforation, bleeding

And if left untreated, death is imminent

Pathogenesis
Salmonella thypoid
digestion
Absorbed by the intestine
Bacteria enter the systemic blood flow
Intestinal lymphoid glands
ulcer

heart

hepatomega
ly

Bleeding and perforation

spleen

endotoxin

splenomegaly

Palpability pain

nausea

malnutrition
Less risk of fluid volume

fever

Signs & Symptoms

Symptoms
Abdominal pain

Signs

Fever

Abdominal tenderness

Chills

Hepatosplenomegaly

Diarrhea

Sustained fever

Constipation

Relative Bradycardia

Nausea

Rash (rose spots)

Neuropsychiatric
symptoms

Intestinal hemorrhage

Cough

Visceral Abscess

Myalgia

Septic Shock

Arthralgia

Altered Mental Status

Pneumonia
Febrile Seizure

Intestinal perforation

Characteristic Typhoid fever

PREVALENCE TYPOID FEVER

SIGN & SYMPTOM FIRST

WEEK

SIGN & SYMPTOM SECOND

WEEK

SIGN & SYMPTOM THIRD

WEEK

SIGN & SYMPTOM FOURTH

WEEK

LAB EXAMINATION

Culture of bacteria

Laboratory examination
Routine Inspection
complete peripheral blood examination found:
Leukopenia
Mild anemia and thrombocytopenia

Widal test
for detection of antibodies against S. typhi
bacteria. Widal test intention was to
determine whether there aglutinin in serum of
patients with suspected typhoid fever:
a. Aglutinin O (from the body of germs)
b. Aglutinin H (flagella germs)
c.Aglutinin Vi (hoop germs)

Widal Test
Aglutinin O & H used for the
diagnosis of typhoid fever
acute phase first arise aglutinin O
followed by H aglutinin
People who have recovered remains
were found aglutinin O 4-6 months,
whereas a longer stay aglutinin H 912 months.

Blood culture
Positive blood cultures ensure
typoid fever

Antibiotic Therapy For Enteric Fever in

Adults
Indication
Empirical
Treatment

Agent

Duration
, Days

Ceftriaxone
Azithromycin

1-2 g/d (IV)

1 g/d (PO)

7-14
5

Ciprofloxacin(1st line)

500mg bid (PO) or

400mg q12h(IV)
1g tid (PO) or 2 g
q6h (IV)
25mg/kg tid
(PO/IV)

5-7

Amoxicilin (2nd line)

Fully Susceptible

Dosage (Route)

Chloramphenicol
TrimethoprimSulfamethoxazole

Source : Harrison

160/800mg bid
(PO)

14
14-21
14

Indication

MultidrugResistant

Nalidixic AcidResitant

Agent

Dosage (Route)

Ciprofloxacin

5-7

Ceftriaxone

500 mg bid (PO)

or 400 mg q12h
(IV)
2-3 g/d (IV)

Azithromycin

1 g/d (PO)

Ceftriaxone

1-2 g/d (IV)

7-14

Azithromycin

1 g/d (PO)

High-dose
ciprofloxacin

750 mg bid (PO)

or 400mg q8h
(IV)

10-14

Source : Harrison

Duration, Days

7-14

 Antimicrobial
Kloramfenikol (4x500mg/day) until 7 days
without fever
Tiamfenikol (4x500mg/day)
Kotrimoksazol (2x2tablets @ 400 mg
sulfametoksazol and 80 mg trimetroprim) 2
weeks
Ampisilin and Amoxicilin (50-150 mg/kgBB/day) 2
weeks
Cephalosporin 3rd generation (3-4 g in 100cc
dextrose hour infuse / day) 3-5 days
Florokuinolon (norfloksasin, siprofloksasin, etc)
Azitromisin (2x500mg)

Kortikosteroid
typhoid fever + shock septic
Management of typhoid
Toxic typhoid
fever

Treatment to Pregnant Woman

Kloramfenikol isnt recommended in
third trimester prematur partus, fetus
intrauterin death, grey syndrome to
neonatus, aplastic anemia
Tiamfenikol isnt recommended in 1st
trimester teratogenic
Fluorquinolon, kotrimoksasol arent
recommended
Ampisilin, amoksisilin, seftriakson
can be given
Management of typhoid
fever

Management
Non pharmacology
Bed rest and treatment to prevent complication and make healing

faster

Bed rest , having meal, drink, take a bath, stools

Once in the care need ,should taking care of cleanliness of the bed, clothes,
and equipment in use

Diet and supporting therapy

Some researchers show that solved food (rice with side dish low cellulose) is
safe for patient

Surgical Care

Surgery is usually indicated in intestinal perforation cases.

Most surgeons prefer simple closure of the perforation with drainage of the
peritoneum.

Small-bowel resection is indicated for patients with multiple perforations.

Follow-up

Further Inpatient Care

If treated with well-selected antibiotics, patients with
typhoid fever (enteric fever) should defervesce within 3-5
days. However, patients with complicated typhoid fever
should finish their course intravenously and should remain
in the hospital if unable to manage this at home.
Patients with complicated typhoid fever should be admitted
through the acute phase of the illness. Uncomplicated
cases are generally treated on an outpatient basis unless
the patient is a public health risk or cannot be fully
monitored outside the home.

Follow-up

Prevention
Travelers to endemic countries should avoid raw unpeeled
fruits or vegetables since they may have been prepared
with contaminated water; in addition, they should drink
only boiled water.
In endemic countries, the most cost-effective strategy for
reducing the incidence of typhoid fever is the institution
of public health measures to ensure safe drinking water
and sanitary disposal of excreta. The effects of these
measures are long-term and reduce the incidence of
other enteric infections, which are a major cause of
morbidity and mortality in those areas.

Prevention and
Control

Provision of safe drinking water, safe disposal

sewage, high standards of food hygiene,
identification & eradication in carrier patient,
and prompt investigation and intervention when
this safeguards are breached
Travelers to endemic areas should drink boiled
or bottled water, eat thoroughly cooked food,
and avoid ice cream and fresh vegetables or
fruit that have been peeled and washed in local
water
In hospital, patients should be nursed using
enteric precautions, and patient &
convalescents advised to wash their hands after
using toilet and before preparing food

Prevention and
Control

Two typhoid vaccines are commercially

available:
1. Ty21a
An oral live attenuated S. Typhi vaccine
Given on days 1, 3, 5, and 7, with a booster
every 5 years
Minimal age for vaccination is 6 years old
2. Vi CPS
A parenteral vaccine consisting of purified
Vi polysaccharide from the bacterial
capsule
Given in 1 dose, with a booster every 2-3
years
Minimal age for vaccination is 2 years old

Differentials

Abdominal Abscess
Amebic Hepatic Abscesses
Appendicitis
Brucellosis
Dengue Fever
Influenza
Leishmaniasis
Malaria
Rickettsial diseases
Toxoplasmosis
Tuberculosis
Tularemia
Typhus

Prognosis
Symptoms usually improve in 2 to 4
weeks with treatment. The outcome
is likely to be good with early
treatment, but becomes poor if
complications develop.
Symptoms may return if the
treatment has not completely cured
the infection.

Complication
Intestinal hemorrhage (severeGI
bleeding)
Intestinal perforation
Kidney failure
Peritonitis

DYSENTERY

Definition

Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in

which the loose or watery stools contain visible red blood.
Dysentery is most often caused by Shigella species
(bacillary dysentery) or Entamoeba histolytica (amoebic
dysentery). (WHO)

Dysentery is an infection of the intestines that

causes diarrhoea containing blood or mucus.(NHS)

Bacillary Dysentery

Dysentery that is caused by Shigella bacteria (bacillary

dysentery or shigellosis)
Symptoms of bacillary dysentery usually begin one to seven
days after infection.
There is usually a lot of diarrhoea to begin with, followed by
smaller amounts that are passed frequently and sometimes
painfully.
In more severe cases, symptoms can include:
watery diarrhoea that contains blood or mucus
nausea (feeling sick)
vomiting (being sick)
severe abdominal pain
stomach cramps
a high temperature (fever) of 38C (100.4F) or over

 There are four types of shigella:

Shigella sonnei

Shigella flexneri

Shigella boydii

Shigella dysenteriae: this produces the most severe symptoms

The shigella bacteria are found in faeces and are spread through poor
hygiene; for example, by not washing your hands after having diarrhoea.
The bacteria will travel from the mouth to the bowel, invading the cells
that line the large bowel. The bacteria multiply, killing the cells and
producing the symptoms of dysentery.
Dysentery is also spread through food that has been contaminated with
human faeces (stools), particularly cold, uncooked food, such as salad.
This is more likely to happen in countries where:

there is poor sanitation

water supplies and sewage disposal are inadequate

human faeces are used as fertiliser

Severe dysentery is more common in developing countries.

The time between coming into contact with the bacteria and the symptoms
starting (the incubation period) is usually one to seven days.

Epidemiology
Both sexes are affected equally
Although infection can occur at any age, it is
most common in the 2nd and 3rd year of life
In industrialized societies :
S. sonnei is the most common cause of bacillary
dysentery, with S. flexneri second in frequency

In pre-industrial societies :
S. flexneri is most common, with S. sonnei
second in frequency
S. dysenteriae serotype 1 tends to occur in
massive epidemics, although it is also endemic
in Asia & Africa

Risk factor
A number of factors increase the risk of
developing dysentery. Not all people with risk
factors will get dysentery. Risk factors for
dysentery include:
Attendance or work in a day care setting
Close contact with an infected person or animal
Consumption of untreated water from lakes, rivers
or streams
Fecal to oral contact
Travel in countries where the infection is common
Use of public swimming pools

Pathophysiology

CLINICAL SYMPTOMS
The shoots ranged from 7 hours to 7 days.
7-day average duration symptoms in adults, but
can take up to 4 weeks.
In the early phase of patients complained of
lower abdominal pain, rectal burning
sensation, diarrhea accompanied by fever
which can reach 40 C.
Further reduced but the stool was diarrhea
containing blood and mucus, tenesmus,
and decreased apetite.
In children may get a high fever with or
without convulsions, delirium, headache,
stiff neck, and lethargy.

DIAGNOSE
Microscopic examination of feces
showed eritrocytes and PMN leukocytes.
To confirm the diagnosis made from the
material culture of fresh feces or anal
swab.
Sigmoidoscopy can confirm the diagnosis
of colitis, but the examination generally not
necessary, because it causes the patient to
feel very uncomfortable.
In the acute phase of shigella infection,
serology test are not useful.

Treatment
Antibiotic medications that are effective in the
treatment of dysentery caused by bacterial organisms
include:
Ceftriaxone (Rocephin)
Ciprofloxacin (Cipro)
Trimethoprim-sulfamethoxazole (Bactrim,Septra)
The most common treatment for amebic dysentery
caused byEntamoeba histolyticais metronidazole
(Flagyl), an antiparasitic medication.
If you have diarrhea andvomiting, fluid and
electrolyte replenishment is also a component of
successful treatment.

Prevention
Encourage prolonged breast-feeding of
infants
risk of getting the infection
lessens its severity in those infants who
are infected

Educate families and child-care center

personnel in hand-washing techniques,
especially after defecation and before
food preparation and consumption

DIFFERENTIAL DIAGNOSE
Salmonellosis
Enterotoxin diarrhea syndrome due
to E. coli
Cholera
Colitis ulserosa

Complication
You can help minimize your risk of
serious complications by following the
treatment plan you and your health
care provider design specifically for you.
Complications of dysentery include:
Liver abscess
Postinfectiousarthritis(joint pain, eye
irritation, and painful urination)
Spread of infection

Prognosis
S. dysentriae severe and long
recovery time, high rate mortality
S. flexneri low rate mortality

AMEBIASIS
Amebiasis is an infectious disease caused
by a parasitic one-called microorganism
(protozoan) called Entamoeba histolytica.
Persons with amebiasis may experience a wide
range of symptoms, including diarrhea, fever,
and cramps. The disease may also affect the
intestines, liver, or other parts of the body.

Life Cycle

The trophozoite of E
histolytica
ranging from 10-60 mm
It has a clear ectoplasm
and a somewhat granular
endoplasm that contains
several vacuoles.
The trophozoite has a
single 3-mm to 5-mm
nucleus with fine
peripheral chromatin and
a central nucleolus.
Ingested RBCs may be
present within the
trophozoite.

The cyst of E histolytica

ranging from 5-20 mm
It has 1-4 nuclei that
are morphologically
similar to the nuclei of
the trophozoite.
The cyst may have
iodine-stainable
glycogen clumps and
chromatoid bodies with
smooth rounded edges.

Gross pathology of intestinal ulcers due to

amebiasis. Courtesy of Centers for Disease
Control and Prevention.

Histopathology of typical flask-shaped ulcer of

intestinal amebiasis. Courtesy of Centers for Disease
Control and Prevention.

Entamoeba histolytica in liver aspirate,

trichrome stain. Courtesy of Centers for
Disease Control and Prevention.

Histopathology of amebiasis. Courtesy of Centers for Disease Control

and Prevention.

Symptoms
Acute: Frequent dysentery with
necrotic mucosa and abdominal pain.
Chronic: Recurrent episodes of
dysentery with blood and mucus in
the feces.

Laboratory Test
Leukocytosis and hematochezia, with
fecal leukocytes not present in all
cases
Extraintestinal amebiasis
leukocytosis and elevated liver
function

Differential Diagnosis
Bacterial diarrheas caused by
Campylobacter, enteroinvasive
Escherichia coli, and species of
Shigella, Salmonella and Vibrio
Amebic liver abscess can easily be
confused with pulmonary or
gallbladder disease
Febrile illness with few localizing
signs malaria or typhoid fever

Treatment
Indication

Therapy

Asymtomatic carriage

Luminal agent: iodoquinol (650 mg

tablets); 650 tid for 20 days; or
paromomycin (250 mg tablets),
500 mg tid for 10 days

Acute colitis

Metronidazole (250 or 500 mg

tablets), 750 mg PO or IV tid for 510 days
plus
Luminal agent as above

Amebic liver abscess

Metronidazole, 750 mg PO or IV for

5-10 days
Or
Tinidazole, 2 g PO once
Or
Omidazole 2 g PO once
Plus
Luminal agent as above

PARASIT INFECTION
Parasitic can also cause
diarrhea.symptoms may
include gas,bloating and
greasy stools.

Giardia
Lamblia

Entamo
eba
Hystoliti
ca

Entamoeba histolytica
Although many species of amoeba exist, only E.
histolytica is clearly pathogenic. Transmission
occurs by fecal contamination of food or water.
Infection is endemic throughout the world,
especially where poor sanitation exists.
Clinical manifestations :
Diarrhea (with blood & mucus)
Abdominal pain / acute colitis with abdominal
cramps,
Diagnosis is usually made by identification of cysts
or trophozoites in stool. Serology also may be
helpful,particularly with diagnosis of
extraintestinal amebiasis and liverinvolvement.

TREATMENT
Emetin hidroklorida
Klorokuin
Antibiotik
Metronidazol (nitroimidazol)

Balantidi
um coli

STRONGILOIDES
STERCOLARIS

Strongyloides stercoralis
This roundworm,2.5 mm in length, is endemic in
southern U.S. and common in tropicsand Asia.
Clinical manifestation:
Skin becomes red and pruritic after penetration
by larvae, which usually occurs on feet.
Diarrhea,
Vomiting
Abdominal pain
Cough and pneumonia after migration of
larvae through lung scan
Peripheral eosinophilia may occur.
Identification of larvae in stool isdiagnostic.

Ascaris lumbricoides
Clinical manifestations:
Can be asymptomatic
Mild diarrhea
Intermittent epigastric pain
Anorexia
Vomiting
Diagnosed: by identifying whitish-brown
Ascaris worm,2040 cm in length, or finding
Ascaris eggs on microscopic exam of stool
is diagnostic.

Hookworm Infection
Adult hookworms (N. americanus and A.
duodenale)
Clinical manifestations:
Red, pruritic lesions
Diarrhea
Vomiting
Abdominal pain
Anemia from GI blood loss
Peripheral eosinophilia.
Detecting hookworm eggs on stool smear is
diagnostic.

Trichuris trichiura
T. trichiura,4-cm long whipworm, occurs
most commonly in tropical areas but is also
found in subtropical areas (e.g., southern
U.S.).
Clinical manifestations:
Most individuals are asymptomatic
Diarrhea
Tenesmus
Weight loss
Anemia
Peripheral eosinophilia
Diagnosed: by seeing eggs on microscopic

TREATMENT
Mebendazol
Albendazol
Pirantel pamoat

Protozoal infection: Cryptosporidium

Clinical Symptoms may evolve

Recent and prolonged history of
severe diarrheausually large
volume, watery stools with a lot
of abdominal pain, bowel noise
and activity
Severe weight loss/wasting in
those with longer history

TREMATODA

Heterophyes heterophyes
Fasciolopsis buski: chronic diarrhea
Metagonimus yokogawai
Echinostoma spp

FUNGAL INFECTION
Oral candidiasis is a fungal
infection of the oral mucosa.it
is most common in newborn &
infants.

Fungal infectious
Candida sp
C. albicans is most common cause of Candida
enteritis
Characterized by watery diarrhea and abdominal
pain.
Predisposing factors :prolonged antibiotic or
immunosuppressive therapy yeast forms are
ubiquitous and occur in fecal flora of normal
persons, their presence alone is not
diagnostic.
Definitive diagnosis requires demonstration of
intestinal mucosal invasion by Candida on biopsy
or isolation of Candida from ulcerative lesions.