Pemicu 3

Vicky
405100042
Diarrhea
An increase in the frequency of bowel movements / a
decrease in the form of stool (greater looseness of
stool)

Caused by increased secretion of fluid into the

intestine, reduced absorption of fluid from the
intestine / rapid passage of stool through the
intestine

Adults + typical western diet: stool weight

>200g/d considered diarrheal
 Duration

acute if < 2 weeks, persistent if 2-4 weeks, chronic if > 4

weeks in duration

Mechanisms
Osmotic diarrhea: nonabsorbed solutes increase
intraluminal oncotic pressure, causing outpouring of water.
Secretory diarrhea: active ion secretion cause obligatory
water loss.
Diarrhea Exudative: inflammation, necrosis, and sloughing of
colonic mucosa.
Altered intestinal motility: alteration of coordinated
control of intestinal propulsion.
Decreased absorptive surface: arise from surgical
manipulation.

Etiology

Infection:
Bacteria
Parasite
Viral
Non-infection: anatomic defects, neoplasms, etc
Non-infection
 Agents that commonly cause toxin-induced
gastroenteritis and gastrointestinal infection
Organism Pathogenic Mechanism Clinical Features
Escherichia coli
ETEC In the gut produces heat-labile (HL) Travelers diarrhea, including watery
or heat-stable (HS) enterotoxin diarrhea
STEC Shiga toxin, no invasion Hemorrhagic colitis, hemolyticuremic
syndrome
EPEC Attaches to mucosal epithelial cell Watery diarrhea, infants, and toddlers
and produces cytoskeletal changes
EIEC Inflammatory invasion of the Fever, pain, diarrhea, dysentery
colonic mucosa
EHEC Produces vero toxin (Shiga-like Watery, bloody diarrhea
toxin)
Salmonella spp. Superficial infection of gut, little Fever, pain, diarrhea or dysentery,
invasion bacteremia, extra-intestinal infection,
common source of outbreaks
Shigella spp. Invade epithelial cells Diarrhea, can have blood and pus iin
stool, dysentery
Campylobacter Toxin, invasion Fever, pain, diarrhea, dysentery, fresh
jejuni blood in stool
Yersinia Invasion, translocation, Fever, pain, diarrhea, mesenteric
enterocolitica lymphoid inflammation, lymphadenitis, extra-intestinal infection,
dissemination food sources
Vibrio cholerae Toxin cause hypersecretion Watery diarrhea, cholera
in small intestine
Clostridium difficile Cytotoxin, enterotoxin, local Fever, pain, bloody diarrhea, after
invasion epithelial cell antibiotic use, nosocomial acquistion
necrosis
Clostridium Enterotoxin produced during Watery diarrhea, food sources
perfringens sporulation in gut
hypersecretion
Bacillus cereus Enterotoxin formed in food Vomiting and diarrhea
or in gut from growth of B
cereus
Vibrio Toxin cause hypersecretion Watery diarrhea, stol may be bloody
parahaemolyticus vibrios invade epithelium
Shigella dysentriae Produces cytotoxin and Dysentery, bloody diarrhea
type 1 neurotoxin

Rotavirus Induces histopathologic Watery diarrhea, fever, vomiting

changes in intestinal
mucosal cells
Giardia lamblia Complex and poorly Watery diarrhea
understood interaction of
parasite with mucosal cells

Entamoeba Invades colonic mucosa and Diarrhea, dysentery, abdominal pain,

histolytica lyses cells weight loss, fever

Yersinia Gastroenteritis or mesenteric Diarrhea, fever, PMNs and blood in stool

enterocolitica adenitis, toxin produced
occasionally

Adenovirus serotype Diarrhea

40 and 41

Norwalk Diarrhea

Caliciviruses and Vomiting and watery diarrhea

astroviruses
 Nemathelminthes
Site in host Portal Source of Most common clinical Lab
of entry infection symptoms diagnosis

Trichuris Caecum, Mouth Eggs from soil Abdominal discomfort, Eggs in

trichiura largeintestine, or vegetables anemia, bloody stool stool
ileum

Strongyloide In wall small skin Larva in soil Abdominal discomfort, Larvae in

s stercoralis intestine bloody stool stool

Platyhelminthes
Site in host Portal Source of Most common clinical Lab
of entry infection symptoms diagnosis

Fasciolopsis Small mouth Water nuts and Diarrhea, edema, Eggs in

buski intestine vegetables abdominal pain stool

Clonorchis Bile duct mouth Fresh-water Indigestion, diarrhea, Eggs in

sinensis fish hepatomegaly stool
 Protozoa
Site in host Portal Source of Most common clinical Lab
of entry infection symptoms diagnosis

Entamoeba Lumen and Mouth Cyst in food Mild to severe GI Cysts &
histolytica wall large and water, distress. dysentry trophozoit
intestine from feces es in stool
Dientamoen Large Mouth Stool (trophs) Abdominal discomfort, Troph in
a fragilis intestine diarrhea stool
Balatidium Large Mouth Stool (cyst) Diarrhea, dysentry Cysts &
coli intestine troph in
stool
Giardia Upper small Mouth Cyst in food Mild GI distress Cysts &
lamblia intestine and water, &diarrhea tropozoit
from feces in stool
Mechanism of diarrhea
Patophisiology of Secretory Diarrhea
The Vibrio cholerae produces cholera toxin

Activates adenylyl cyclase,

Prolonged increase in intracellular concentration of cyclic AMP within crypt
enterocytes.

Pprolonged opening of the chloride channels

Allowing uncontrolled secretion of water

Secretion of water into the intestinal lumen increased

Diarrhea
Patophisiology of Osmotic Diarrhea
Lactose intolerance.
Ingested lactose

The intestinal epithelium is deficient in lactase,

Lactose cannot be effectively hydrolyzed into glucose and galactose

The osmotically-active lactose is retained in the intestinal lumen, where it

"holds" water.

The unabsorbed lactose passes into the large intestine

Lactose fermented by colonic bacteria

resulting excessive gas.

Patophisiology of Inflammatory
Diarrhea
Examples of pathogens :
Bacteria :Salmonella, E. coli, Campylobacter
Viruses: Cytomegalovirus (immunocompromised)
Protozoa:,Entamoeba histolitica and Balantidium coli
Helminth: Schistosoma sp. ,Trichuris trichura

Infected of pathogens

Immune responses (Inflammated)

Activation of white blood cells

Secrete inflammatory mediators and cytokines

Stimulate secretion

Inflammatory diarrhea.
 ETEC uses fimbrial adhesins (to bind enterocyte cells in the small
intestine.
ETEC can produce two proteinaceous enterotoxins:

The larger ,LT enterotoxin, is similar to cholera toxin in structure

and function.

the smaller protein, ST enterotoxin causes cGMP accumulation

in the target cells and a subsequent secretion of fluid and
electrolytes into the intestinal lumen.

the most common cause of traveler's diarrhea.

P
a
t
h
o
g
e
n
e
s
i
s
Parasites
Entamoeba histolytica
Balantidium coli
Trichuris Life Cicle
Sign and Symptoms of Diarrhea
Weepy
Anxious
Decreased appetite & weight
Frequent, loose, watery stools
Abdominal cramps
Abdominal pain
Fever
Blood in the stool
Bloating
Dehydration signs (if lost much fluid)
Nausea and vomiting
5 High Risk Groups :
1. Travelers (Enterotoxigenic E. Coli
Campylobacter, Shigella, Aeromonas,
Coronavirus and Salmonella)
2. Consumers of certain foods
3. Immunodeficient person
4. Daycare attendees and their family
members
5. Institutionalized persons
Diagnose & treatment
Complications of Diarrhea
Loss of water and electrolytes Dehydration, hypokalemia,
metabolic acidosis, seizures, metabolic alkalosis
Impaired blood circulation hypovolemic shock
Hypoglycemia Disturbance nutrition, protein energy malnutrition
Weight loss
Disturbance of renal function
 Anterior fontanelle in the 1 month
human

7/27/2017 40
Treatment of
Dehydration
Typhoid fever
Defenition
Typhoid fever, also known as enteric fever, is a systemic bacterial
disease contracted by consuming food or water that has been
contaminated with the bacterium Salmonella typhi.
EPIDEMIOLOGY
Typhoid fever occurs worldwide, primarily in developing nations
whose sanitary conditions are poor
Typhoid fever is endemic in Asia, Africa, Latin America, the Caribbean,
and Oceania, but 80% of cases come from Bangladesh, China, India,
Indonesia, Laos, Nepal, Pakistan, or Vietnam
Within those countries, typhoid fever is most common in
underdeveloped areas
Typhoid fever infects roughly 21.6 million people (incidence of 3.6 per
1,000 population) and kills an estimated 200,000 people every year
Etiology of Typhoid fever
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.
Bacteriology
The enteric bacili have 3 common
antigens:
- H antigen on the flagellae

- O antigen (body or somatic)

- Vi antigen (virulence antigen)

The bacteria may also have different

phage types which number over 70, and

are only recognize by the use of

different bacteriophages.
Bacteriology
The H antigens differ from one another.
The O antigens are group specific.
The Vi antigen is used in detection of carriers.
Enterobactericeae
Table. Clinical Diseases Induced by Salmonellae.

Enteric Fevers Septicemias Enterocolitis

Incubation period 720 days Variable 848 hours
Onset Insidious Abrupt Abrupt
Fever Gradual, then high Rapid rise, then Usually low
plateau, with spiking "septic"
"typhoidal" state temperature
Duration of disease Several weeks Variable 25 days
Gastrointestinal Often early Often none Nausea, vomiting,
symptoms constipation; later, diarrhea at onset
bloody diarrhea
Blood cultures Positive in first to Positive during high Negative
second weeks of fever
disease
Stool cultures Positive from 2nd Infrequently positive Positive soon after
week on; negative onset
earlier in disease
Risk Factors
Worldwide, children are at greatest risk of getting the disease,
although they generally have milder symptoms than adults do.
If you live in a country where typhoid fever is rare, you're at increased
risk if you:
- 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 MANIFESTATIONS
After incubation period (3 21 days) fever is the most prominent
symptom.
Additional nonspecific symptoms include:
Chills, headache, sweating, cough, malaise, and arthralgia
GI symptoms are variable and can include:
Anorexia, nausea, vomiting, diarrhea, constipation (less often)
Abdominal pain (30 40 %)
Physical findings include:
Rash (rose spots), hepatosplenomegaly, epistaxis, bradycardia
SYMPTOMS BY WEEK
First week of illness Second week of illness
Once signs and symptoms do If you don't receive treatment for
appear, you're likely to typhoid fever, you may enter a
experience: second stage during which you
become very ill and experience:
Fever,
Continuing high fever
Headache and dizziness
Relative bradycardia
Weakness and fatigue
Coated tongue
Sore throat
Either diarrhea that has the
Abdominal pain color and consistency of pea
Diarrhea (children) or soup, or severe constipation
constipation (adult) Considerable weight loss
Rash: Extremely distended abdomen
a rash of small, flat, rose-
colored spots on your lower
chest or upper abdomen.
The rash is temporary, usually
disappearing in two to five days.
SYMPTOMS BY WEEK
Third week of illness
Become delirious
Lie motionless and exhausted
with your eyes half-closed in
what's known as the typhoid
state
Life-threatening complications
often develop at this time.
Fourth week of illness
Improvement may come slowly
Your fever is likely to decrease
gradually until your temperature
returns to normal in another
week to 10 days.
But signs and symptoms can
return up to two weeks after
your fever has subsided
Sign and Symptom
Characteristic Typhoid fever
PATHOGENESIS
Salmonella cause infection when 103-106 organisms are ingested.
Conditions that reduce gastric acidity or decrease intestinal integrity
increase susceptibility to infection.
Organisms penetrate the small intestinal mucosa and traverse the
intestinal layer through cells within Peyers patches.
S. typhi and S. paratyphi survive within macrophages, then
disseminate throughout the body via lymphatics, and ultimately
colonize reticuloendothelial tissues.
Pathogenesis Endotoxins

Salmonella Typhi
Fever

Food and
Mouth Small intestine
Beverage

Bloodstream lymphatic
(Transient bacteremia) vessels

Organs Bloodstream
(Liver, spleen) (Secondary bacteremia)

Lymphoid Gland Perforation

Peyers patches
small intestine
Hemorrage

Gallblader Chronic Carrier Peritonitis

Pathogenesis
Entry in GIT localisation in Gut associated lymphoid tissue
Lymphatic channel thoracic duct circulation primary silent
bacteremia localisation in macrophages of RES in spleen, liver,
bone marrow (incubation period 8-14 days) secondary bacteremia.
rabiezahran@gawab.com
Life cycle of
Salmonella
typhi.
Pathological changes in typhoid fever.
1) The changes in the Payer's patches of the ileum vary from
hyperplasia and ulceration to frank ulceration and typhoid
perforation.
2) The liver may be enlarged with fatty changes.
3) The skin may show changes with collections of bacilli, which cause
the classical rose spots
 Pathological changes in typhoid
fever
4) Cholecystitis may lead to the formation of infected gall stones in the
gall bladder.
These may be asymptomatic & may be a potent source of infection in
the typhoid carrier, sometimes many years after the initial infection.
5) The spleen is enlarged and soft.
6)The mesenteric glands are enlarged.
 Pathological changes in typhoid
fever
7)The kidneys show cloudy swelling and as a result this may result in
albuminuria.
8)Bronchitis is common in typhoid fever, and diffuse rales and rhonchi
are a usual finding on clinical auscultation of the lungs in typhoid
fever.
9)In a severe case of typhoid fever the heart may be enlarged and
affected by fatty degeneration.
10)Finally thrombosis of the deep veins may occur, particularly in the
lower limb, and lead to a fatal pulmonary embolus.
Tests & Diagnostics
Medical and travel history
Your doctor is likely to suspect typhoid fever based on your symptoms
and your medical and travel history.
Routine lab tests
Body fluid or tissue culture
For the culture, a small sample of your blood, stool, urine or bone
marrow is placed on a special medium that encourages the growth of
bacteria. In 48 to 72 hours, the culture is checked under a microscope
for the presence of typhoid bacteria. A bone marrow culture often is
the most sensitive test for S. typhi.
Laboratory findings
Routine examinations:

White blood cell count is normal or decreased.

Leukocytopenia (specially eosinophilic

leukocytopenia).
 Gambaran Darah Tepi pada Demam
Tifoid

JUMLAH LEUKOSIT JUMLAH TROMBOSIT

60 40
35
50
30
40
25
30 20
15
20
10
10
5
0 0
<5 5 - 10 > 10 10 - 50 50 - 100 100 - 150 > 150

ribu/mm3 ribu/mm3
Bacteriological examinations:

Blood culture:
the most common use

80-90% positive during the first 2 weeks of illness

50% in 3rd week

not easy in 4th week

re-positive when relapse and recrudesce attention to the

use of antibiotics
Bacteriological examinations:
The bone marrow culture
the most sensitive test specially in patients
pretreated with antibiotics.
Urine and stool cultures
increase the diagnostic yield
positive less frequently
stool culture better in 3~4 weeks
Rose spots: Not use routinely
Serological tests (Widal test):
Five types of antigens:
somatic antigen(O), flagella(H) antigen, and
paratyphoid fever flagella(A, B, C) antigen.
Antibody reaction appear during first week
70% positive in 3-4 weeks and can prolong to several
months.
In some cases, antibodies appear slowly, or remain at a
low level, some(10-30%) not appear at all.
 "O" agglutinin antibody titer 1:80 and "H" 1:160 or
"O" 4x higher supports a diagnosis of typhoid fever
"O" rises alone, not "H", early of the disease.Only "H"
positive, but "O" negative, often nonspecifically elevated
by immunization or previous infections or anamnestic
reaction.
Antibody level maybe lower when have used antibiotics
early.
 Some cross reaction between group D and A.
False positive in some infectious diseases.
Some positive in blood culture ,but negative in vidal
test.
'Vi" often useful for carrier (1:40)

Molecular biological tests:

DNA probe or polymerase chain reaction (PCR)
 MANIFESTASI KLINIK
Ink Mg I Mg II Mg III Mg IV

Biakan Positif 60 90%

Darah Negatif Negatif

Biakan Pos / Neg Positif 80 % Pos 50 %

Feses Negatif

Tes Widal Positif 20 % Pos 50 % Pos 80 %

Negatif
Identification of Salmonella
Sub cultures are done after overnight incubation at 370c,and
subcultures are done on Mac Conkey's agar
Subcultures are repeated upto 10 days after futher incubation.
Salmonella on Mac Conkey's agar
Salmonella on XLD agar
Treatment of complication
3. Toxic myocarditis:
bed rest
cardiac muscle protection drugs, dexamethasone, digoxin.
 Farmacology
Kloramfenikol= Obat pilihan untuk demam tifoid
Tiamfenikol= komplikasi hematologi seperti anemia
aplastik < kloramfenikol
Kotrikmoksazol
Ampisillin dan amoksisilin(kemampuan menurunkan
demam lebih< dari kloramfenikol)= boleh untuk ibu hamil
Sefalosporin generasi 3(seftriakson)= boleh untuk ibu
hamil
Golongan Florokuinolon
Azitromisin
Kortikosteroid= hanya untuk demam tifoid yg mengalami
syok septik
Therapy
Indication Agent Dosage Duration,
days
Empirical Treatment ceftriaxone 1-2 g/d (IV) 7-14
Azithromycin 1 g/d (PO) 5
Fully susceptible Ciprofloxacin 500 mg bid (PO) or 5-7
400 mg q12h (IV)
Amoxicillin 1 g tid (PO) or 2 g q6h (IV) 14
Chloramphenicol 25 mg/kg tid (PO/IV) 14-21
Trimethopim- 160/800 mg bid 14
sulfamethoxazole
Multidrug-Resistant Ciprofloxacin 500 mg bid (PO) 5-7
Ceftriaxone 2-3 g/d (IV) 7-14
Azithromycin 1 g/d (PO) 5
Nalidixic Acid Ceftriaxone 1-2 g/d (IV) 7-14
Resistant
Azithromycin 1 g/d (PO) 5
High dose 750 mg bid (PO) or 400 10-14
ciprofloxacin mg q8h
 Antibiotic Recommendations by Origin and Severity
Location Severity First-Line Second-Line
Antibiotics Antibiotics
South Asia, East Asia Uncomplicated Cefixime PO Azithromycin PO
Complicated Ceftriaxone IVor Aztreonam IV or
Cefotaxime IV Imipenem IV
Eastern Europe, Uncomplicated Ciprofloxacin Cefixime PO or
Middle East, sub- PO or Amoxicillin PO or
Saharan Africa, South Ofloxacin PO TMP-SMZ PO
America or Azithromycin PO
Complicated Ciprofloxacin IVor Ceftriaxone IV or
Ofloxacin IV Cefotaxime IV or
Ampicillin IV
or
TMP-SMZ IV
Unknown geographic Uncomplicated Cefixime POplus Azithromycin PO*
origin or Southeast Ciprofloxacin
Asia PO or
Ofloxacin PO
 Supportive therapy
- Drinking fluids. This helps prevent the dehydration
that results from a prolonged fever and diarrhea. If
you're severely dehydrated, you may need to receive
fluids through a vein in your arm (intravenously).
- Eating a healthy diet. Nonbulky, high-calorie meals
can help replace the nutrients you lose when you're
sick.
5. Explain the complications,
preventions, differential diagnosis, and
prognosis of typhoid fever
Complications
Intestinal bleeding or perforation may develop in the third week
of illness. Intestinal bleeding is often marked by a sudden drop in
blood pressure and shock, followed by the appearance of blood in
your stool.
Other, less common complications
- Inflammation of the heart muscle (myocarditis)
- Pneumonia
- Inflammation of the pancreas (pancreatitis)
- Kidney or bladder infections
- Infections of the spine (osteomyelitis)
- Infection and inflammation of the membranes and fluid
surrounding your brain and spinal cord (meningitis)
- Psychiatric problems such as delirium, hallucinations and paranoid
psychosis
Complications

Typhoid Pneumonia with Empyema

Typhoid Osteomyelitis of Femur
Typhoid Spine
Preventions
Vaccines are recommended for travelers.
Drink boiled or bottled water and eat well cooked food.
Adequate water treatment, waste disposal, and protection of food
supply from contamination are important public health measures.
Personal hygiene.
VACCINES
Routine typhoid vaccination is indicated for:
travelers to endemic areas,
persons with intimate exposure to a documented S typhi carrier (e.g,
household contact),
and microbiology laboratory personnel who frequently work with S
typhi

Vaccines are not approved for use children younger than 2 years.
VACCINES
Centers for Disease Control and Preventions
DIFFERENTIAL DIAGNOSIS
Paratyphoids A, B & C The laboratory is usually required as the
final authority. The paratyphoids tend to run a milder course with
profuse rose spots.
Salmonella infection and gastroenteritis Salmonellae, the
dysentery group, and staphylococci may occasionally cause an
invasive illness resembling typhoid fever with bacteremia. Usually,
however, the gastrointestinal symptoms are more acute than the
general manifestations, and the pyrexia much lower and of shorter
duration.
DIFFERENTIAL DIAGNOSIS
Other diseases in differential diagnosis
a. Malaria This may be mistaken for typhoid in countries where
both are endemic. A history of previous attacks, the more rapid
onset in malaria, the shivering and sweating, the high early pyrexia,
the relative infrequency of abdominal symptoms and signs, and a
positive blood slide all point to a diagnosis of malaria.

b. Influenza Influenza may also be confused with typhoid, but is

usually of much more rapid onset with high temperature, severe sore
throat, cough, and the absence of a palpable spleen and rose spots.
DIFFERENTIAL DIAGNOSIS
c. Bacillary dysentery This disease seldom causes much difficulty in diagnosis.
The onset is usually acute, with severe blood diarrhoea, although in mild cases
the blood may be absent. Diarrhoea with blood is rare in early typhoid. The signs
and symptoms in dysentery are usually abdominal and remain so, the mental
state and chest being clear.

d. Typhus and other rickettsial infections These conditions should be

considered important when considering the differential diagnosis. This is
because both typhus and typhoid can cause a febrile illness with delirium, chest
signs, and abdominal discomfort. In typhus, however, the onset is acute, and the
temperature high at an early stage. Shivering attacks are common at the onset,
and prostration is rapid.
The rash is quite different (brownish red in colour, and much more profuse). It does
not fade on pressure, as does the rose spot in typhoid. There is a leucocytosis and
the Weil-Felix test becomes significantly positive at about the tenth day.
 Laboratory Studies
Culture

Polymerase chain reaction (PCR)

Specific serologic tests

Assays that identify Salmonella antibodies or antigens support the

diagnosis of typhoid fever, but these results should be confirmed with
cultures or DNA evidence.

Widal test

Indirect hemagglutination, indirect fluorescent Vi antibody, and indirect

enzyme-linked immunosorbent assay (ELISA) for immunoglobulin M (IgM)
and IgG antibodies to S typhi polysaccharide

Other nonspecific laboratory studies

Serological tests (Widal test):

Five types of antigens:

somatic antigen (O), flagella (H) antigen, and paratyphoid

fever flagella (A,B,C) antigen.

Antibody reaction appear during first week

70% positive in 3~4 weeks and can prolong to several months

In some cases, antibodies appear slowly, or remain at a low

level,

some(10~30%) not appear at all.

 Examination
Blood test:
Leukopenia Liver function:
Hb
Mild Thrombocytopenia SGOT
Leukocyte
SGPT/SGOT SGPT
trombocyte

THYPHOID
Aglutination BLOOD
Antigen Widal Test
Culture + CULTURE
Antibodi BILE CULTURE

Definitive Diagnosis
Get + 6 months-1 year
POST THYPOID
Prevention
Source of transmission is from food. Therefore, must
be good enviromental sanitation

Preventing contaminating of food or other animal

that secrete Salmonella.

Meat and eggs should be cooked properly

Carriers ar einhibited working as a chef

Vaccine can stimulate antibody for Salmonella

Vaccine
2 type of vaccine:
Capsular Vi polysaccharide:
Injection typim vi
For children > 2 years old
Repead every 3 years
Ty 21-a:
Oral, vivotif: 3 doses interval 1 day
For children > 6 years
Vaccine
Injection (capsular vi polysaccharide)

- typhim vi injection

- > 2 years old

- repeat 3 years

Oral (ty 21-a)

- vivotif : 3 doses

- > 6 years old

Laboratory Test
LAB EXAMINATION
 Anemia normokrom normositer
- Lekopenia (seldom <3000 / mm3, often occurs at week 2 and at
week-1 can occur lekositosis)
- Calculate the type: aneosinofilia limfosito-sis with relative (week 2)
- Thrombocytopenia light
- LED slightly rises
 Bone marrow:
-hyperactive RES system
- macrophage cells typical of typhoid fever
- hemapoetik system depression
Serum transaminase rises slightly
Urine: proteinuria light heat
Serological:
-Widal test
-Test Typhidot
-Test Tubex
-IgM Dipstick test
- Gaal culture (identification )
Widal Test
The Widal reaction measures titres of serum agglutinins
against somatic (O) and flagellar (H) antigens; which
appear during the 2nd week.
In acute infection, O antibody appears first & become
(-) after several months, signifies active infection.
H antibody appears a little later but persists for a long
time, helps to identify the type of enteric infection.

Positive O titres of 1/80 in non-immunized people living

in non-endemic areas & titres of 1/160 in people in
endemic areas significant.
Widal test false positives are common.
 Widal Felix test: known as the Widal test

Basics: antigen - antibody reaction

Antigen from Salmonella typhii:

O Antigen
H Antigen
Antigen Vi
 Widal test
- sensitivity and specificity that is not too good - too
often a false negative (30%) and false positives
- The state can affect the results:
Giving antibiotics before blood is drawn
O and H antigens in common with other Salmo-
Nella
epitopes in common with other Enterobacteri-
ceae (false positive)
 Widal Test
In endemic areas, the normal population can have low
titer antibodies
- Jakarta: normal person: sero-tive S. tifi O (55.7%), S.
tifi H (78%) and O titer: 1 / 160 (1.3%) and the titer of
H 1/320 (7.7%)
- Determination of cut-off for positive results need to
be in an area
- Cut off the best for diagnosing fever typhoid and
paratyphoid in Jakarta: O: 1 / 160 and H 1 / 320
 LABORATORIUM

Uji Widal

Titer O (+) Titer H (+) - Titer Vi (+) -

- 1/160 - 1/320 1/5 -
titer naik 4x Carrier
capai puncak pd
fase
penyembuhan
 H titer <1 / 320
- cross reaction with strains of Salmonella, Rickettsia
(Weil Felix)

- Immunizations natural

- Post-immunization

- E coli Infection in the intestines

- Neonates (antibodies obtained from the mothe

 Tubex test
- easy to do (less than 5 minutes)
- used only nine O antigen terdpt PD Salmonella
serogroup D (S. tifi)
- Test Tubex (+): infection of S. tifi, while infection
with S. paratifi: (-)
- antigens O 9 are imunodominan stimulate
apparent on the immune response independently of
the thymus in infants and stimulate mitotic B cells
without T cell help allows for the formation of anti-O
9 can be more early (4th-5th day) of primary infection
and day 2-3) of secondary infection
 Tubex Test
- only able to detect IgM and IgG detection can not can not be
used for detection of past infection
- high sensitivity (75-80%) and species-fitas (75-90%)
 Typhidot-M test
- using 50 kD weigh antigen for detection of IgM and IgG antibodies
against S. tifi
- This test is more sensitive (100%)
- There was a bond between the antigen with the specific IgM in
serum of patients
 IgM Dipstick test
- To detect specific IgM antibodies against S. tifi on
specimens of serum or whole blood
- This test consists of
strip: containing a lipopolisacarida antigen (LPS) of
S. tifi
anti-IgM (as control)
detection reagent containing anti-IgM antibody
who glued latex dyes
fluid to wet the strip
 IgM Dipstick test
- At the start by incubation strip that has been
moistened with a liquid solution mixture of detection
reagent and serum for 3 hours at room temperature
- strip rinsed with running water and dry it
- As semikuantitatif, assessed against the test line
compare with Stip reference
- control line should be well coloured
- 65-77% sensitivity and specificity of 95-100%
 Culture
Specimens:
- blood
- faeces
-urine
- bone marrow
- cerebrospinal fluid
Seed with blood media bile (Gall culture)
Gall culture (+) if found Salmonella tifi
 Gaal culture
Blood specimens: (+) in the first week of illness (50-80%)

Bone marrow specimen (+): not influenced when taking or giving

antibiotics

Other specimens: (+) at week 2 - to-3 pain (50%)