Pemicu 4

GE + Thypoid Fever
Pitri Erlina Lay
405110177
 Gastroenteritis
Inflammation of stomach or intestines
Inhibits nutrient absorption and excessive H2O and
electrolyte loss
Bacterial
Viral
Parasites
Poisoning by microbial toxins
food borne intoxication
 Signs and Symptoms:
General features: diarrhea, loss of appetite, abdominal
cramps, nausea, vomiting and possibly fever
Dysentery
Typically self Limiting

Enteric fevers
Systemic with severe headache, high fever, abscesses,
intestinal rupture, shock and death
 Epidemiology
Occurs worldwide
Oral to fecal route of transmission
Water common reservoir
Overcrowding & poor sanitation are risk factors
Animals may be source of infection
 Epidemiology
Major cause of mortality & morbidity in
children world wide.
Transmission:
person-to-person
feco-oral route
Water & food borne
 High risk groups
Young age groups
Immune deficient individuals
Measles
Malnutrition
Travel to endemic areas
Lack of breast feeding
Exposure to unsanitary conditions
Attendance to child care centers
Poor maternal education
 General approach
Clinical assessment:Historical points :
Diarrhea :
duration & severity
Stool consistency
Mucous & blood
Associated symptoms :
GI
Fever
Neurological Symptoms
Others
Risk factors
Social & family History
 Clinical assessment
Physical examination:
General appearance
Hydration Status
Mild
Moderate
severe
Systemic Examination
Extraintestinal manifestations
 Extraintestinal manifestations

Reactive arthritis :Salmonella ,shigella , Yersinia,

campylobacter C.difficile
Guillain-Barre Syndrome: campylobacter
Glomerulonephritis:Shigella , campylobacter ,Yersinia
IgA nephropathy :campylobacter
Erythema nodosum: Yersinia ,campylobacter, salmonella
Hemolytic anemia : Yersinia ,campylobacter
HUS: shigella , E. coli
 Diagnostic Methods
Stool samples :
fresh collected
Mucous,bld,white cells
parasites:
Recent travel to endemic area,stool cultures,diarrhea > 1wk
Part of an outbreak
Immunocompromised
Stool cultures:
As early as possible
Bloody diarrhea
outbreaks
 Diagnostic Methods
Stool cultures :
Routine : Salmonella, shigella,yersinia,campylobacter.
Toxin assays: C. difficle,E.coli
Special stains:Aeromonas, cryptosporidium & vibrio sp.
Duodenal aspirate & Biopsy: Giardia,
Isospora,cryptosporidium.
ELISA
E.M.
Colonoscopy & sigmoidoscopy.
Even with the application of all available
laboratory studies , 20-40 % of all acute
infectious diarrhea remain undiagnosed.
 Management
Fluids & electrolytes & refeeding:
Treating dehydration is the corner stone in
managing diarrhea.
Infants are more susceptible to dehydration
Oral rehydration therapy
Home remedies
feeding
 Specific therapy
Anti-microbial therapy :
Indications are organism-dependant.
Salmonella : Infants< 3months, typhoid fever, bacteremia ,
disseminated disease with local suppuration.
Shigella : all cases
Vibrio cholera : all cases
Aeromonas: dysentery like, prolonged diarrhea.
C. difficile: moderate to severe disease.
E.coli.
Anti diarrheal agents
 Prevention
Precautions during hospitalization
Education
Child care attendance
Health authority notification.
Vaccines ??
 Prevention
Hand washing
Proper food handling and complete cooking
Pasteurization of milk and juices
Adequate sanitation
Safe water supplies

Treatment
Rapid replacement of fluids and electrolytes
Anti-nausea medication
Antimicrobials may be used in severe cases
 Acute diarrhea
Normal bowel phenomena
Definition
Mechanisms of diarrhea
Acute diarrhea
Gastroenteritis
General approach to children with acute
diarrhea
 Normal phenomena
The number ,color & consistency of stools
varies with age & diet :
Meconium
Transitional stools
Milk stools
Color of stools
Presence of solid particles
 Diarrhea cont
Toddler`s diarrhea
1-3 years
Healthy child
Excessive ingestion of beverages with high
carbohydrate content.
Typically during the day
Limit sugar containing beverages, increase fat in
the diet
 Definitions
Diarrhea : excessive loss of fluids &
electrolytes in stool
More than 5g /kg /day
Increase in liquidity & frequency
Pseudodiarrhea & hyperdefecation
Encopresis
Dysentery : small volume , frequent,bloody,
tenesmus , urgency
 Diarrhea
9 liters of fluid enter the GI tract
4-5l absorbed in jejunum , 3-4 ileum, 800 ml in
colon.
Water transport follows Na & nutrient active
& passive transport .
The basis for ORS treatment
 Mechanisms of diarrhea
Disturbed intestinal solute transport, water
movement across intestinal wall.
Secratory
Osmotic
Dysmotility
Inflammatory
SECRETORY DIARRHEA
Laxative abuse (nonosmotic laxatives)
Post-cholecystectomy (from bile salts)
Congenital syndromes (chloridorrhea)
Bacterial toxins
Ileal bile acid malabsorption
Inflammatory bowel disease
Ulcerative colitis
Crohn's disease
Microscopic (lymphocytic) colitis
Collagenous colitis Diverticulitis
Vasculitis
Drugs and poisons
Disordered motility Postvagotomy
diarrhea Postsympathectomy
diarrhea Diabetic autonomic
neuropathy Hyperthyroidism
Irritable bowel syndrome
Neuroendocrine tumors
Gastrinoma
VIPoma
Somatostatinoma
Mastocytosis
Carcinoid syndrome
Medullary carcinoma of thyroid
Neoplasia
Colon carcinoma
Lymphoma
Villous adenoma
Addison's disease
Epidemic secretory (Brainerd) diarrheaI
diopathic secretory diarrhea
 Secratoy Diarrhea
Agent that binds to surface receptors , increasing
cAMP,increased secretion.
Watery , large volume , normal osmolality( 2* Na+K )
Persists during fasting,no stool leukocytes.
Examples; cholera, toxigenic E.coli,carcinoid ,VIP,
congenital chloride diarrhea,Clostridium
difficile,cryptosporidium.
OSMOTIC DIARRHEA
 Osmotic Diarrhea
Occurs after ingesting a poorly absorbed solute .
Stools are of less volume, acidic, reducing
substances, high osmolality > 2* Na + K.
Stops with fasting , increased breath hydrogen with
malabsorption,no stool leukocytes.
Examples : lactase deficiency , glucose-galactose
malabsorption,lactulose, laxative abuse.
 Motility Diarrhea
Increased motility :
decreased transit time.
Stimulated by gastro-colic reflex
Irritable bowel syndrome
Thyrotoxicosis
Post vagotomy
Infections
Decreased motility:
Stasis : bacterial overgrowth.
Pseudo-obstruction, blind loop
INFLAMMATORY DIARRHEA
Inflammatory bowel disease
Ulcerative colitis Crohn's
disease Diverticulitis
Ulcerative jejunoileitis
Infectious diseases
Pseudomembranous colitis
Invasive bacterial infections
Tuberculosis,
yersinosis,
othersUlcerating viral infections
Cytomegalovirus
Herpes simplex
Amebiasis/other invasive parasites
Ischemic colitis
Radiation colitis
Neoplasia
Colon cancer
Lymphoma
 Inflammatory
Inflammation .
decreased mucosal surface area &/Or colonic
reabsorption.
Blood & increased WBC`s in stool.
Infectious gastroenteritis
dysentery
FATTY DIARRHEA

Fatty diarrhea
Malabsorption syndromes
Mucosal diseases
Short bowel syndrome
Postresection diarrhea
Small bowel bacterial
overgrowth
Mesenteric ischemia
Maldigestion
Pancreatic exocrine
insufficiency
Inadequate luminal bile
acid
 CHRONIC DIARRHEA
DEFINITION
More than 200 gms ?
Increased volume ? Hard to quantify
Increased frequency ? Some individuals have increased fecal
weight due to fiber ingestion but do not complain of diarrhea
because their stool consistency is normal. Conversely, other
patients have normal stool weights but complain of diarrhea
because their stools are loose or watery
conceptually
ratio= water-holding capacity of insoluble solids/
total water present
Consensus statement by AGA=
decrease in fecal consistency lasting for four
or more wks
ORGANIC vs FUNCTIONAL DIARRHEA

shorter duration of diarrhea (less than 3 months),

nocturnal diarrhea,
an abrupt onset of diarrhea,
weight loss of more than 11 lb (5.0 kg), and
stool weight of more than 400 g per day.

70 % SPECIFIC FOR FUNCTIONAL ETIOLOGY

 Acute diarrhea
Common Rare
Infant: Infant:
Gastroenteritis
Primary disaccharidase
Systemic infection
deficiency
Antibiotic use
Adrenogenital s.
Child:
Hirchsprung colitis
Gastroenteritis
Food poisoning Child:
Systemic infection Toxic ingestion
Adolescent: Adolescent:
Gastroenteritis thyrotoxicosis
Food poisoning
antibiotic
 Bacterial enteropathogens
Inflammatory:
Aeromonas, campylobacter jejuni,clostridium
deficile,enteroinvasive E. coli,shiga toxin
producing E. coli, salmonella, shigella, yersinia
enterocolitica.
Non- inflammatory:
Enteropathogenic E.coli,
Vibrio cholera
 Bacterial Gastroenteritis

3 groups of gram negative bacteria account for most

bacterial intestinal infections:
Vibrio cholerae (Cholera)
Enterics (Salmonella, Shigella, E. coli)
Campylobacter jejuni
 Cholera
Causative agent: Vibrio cholerae
High infectious dose
Bacteria sensitive to stomach acid
Adheres to small intestine and multiply
Bacteria dont enter cells
 Cholera toxin
Potent exotoxin
Causes intestinal cells to
rapidly pump out
electrolytes
Passive osmotic H2O loss
follows
Metabolic acidosis
Shock
 Heavy loss of fluid
rice-water stool
Up to 20L of fluids lost per day
May discharge 1 million bacteria per ml of feces

Untreated cases potentially fatal

Fluid/electrolyte replacement
Tetracycline reduces toxin production
 VACCINES
An oral cholera vaccine is available, which
gives immunity to 50-60% of those who take
the vaccine, and this immunity lasts only a few
months.
 PREVENTION
Safe drinking water and food
Boil it, cook it, peel it, or forget it. "
Hand washing
Proper sanitation
 Shigellosis
Causative Agent: Shigella sp.
S. dysenteriae, S. flexneri, S. boydii, S. sonnei
Low infecting dose
Bacteria not sensitive to stomach acid
Characterized by fever and dysentery
Infects cells of large intestine and
initiates intense inflammatory
response

Dead cells slough off

Produces areas covered with pus
and blood
 All species produce enterotoxin and type III secretion
systems
S. dysenteriae produces powerful endotoxin
shiga-toxin
Ciprofloxacin, rifampin or azithromycin may reduce
duration and infectivity
No vaccines are available against shigellosis
 COMPLICATIONS:
DYSENTERY
Electrolyte imbalances
Convulsions
Hemolytic uremic syndrome (HUS)
Leukemoid reaction
Toxic megacolon
Protein losing enteropathy
Arthritis
Perforation
 Travelers Diarrhea
Causative Agent: Escherichia coli
Multiple antigenic strains (O, H, K)
Virulent strains have fimbriae, adhesions and
multiple toxins

Enterotoxigenic E. coli
Enterotoxins
Type III secretion system
Typically self limiting
 Enterohemorrhagic E. coli
O157:H7
Produce potent Shiga-like toxins and type III secretion
systems

Antimicrobials cause increase in toxin production

 Campylobacteriosis
Causative agent: Campylobacter jejuni
Leading cause of bacterial diarrhea in United States
Estimated 1million cases annually with ~100 deaths
Associated with poultry
Low infecting dose
 Virulent strains possess adhesions, cytotoxins and
endotoxin
Induce endocytosis in cells of intestine and initiate
inflammation and bleeding lesions
Non-motile mutants are avirulent

Severe cases treated with ciprofloxacin or

azithromycin
 Guillain-Barr Syndrome
Tingling of the feet leads to progressive paralysis of the legs,
arms and rest of the body
40% of cases preceded by campylobacteriosis
May be associated with autoimmune response
80% recover completely; 5% mortality with treatment
 Epidemology
Infect intestinal cells causing cell death
Typically self-limiting
Norovirus epidemics cause 90% of cases
Rotaviruses responsible for 50% infant cases of
serious diarrhea
600,000 worldwide annual fatalities
Oral vaccine available
 Bacterial Food Intoxication
Staphylococcus aureus
Halotolerent; grows well in foods at room temp
Associated with cafeterias and social functions
 5 heat stable enterotoxins:
1000 for up to 30 min
Stimulate muscle contractions, nausea and intense
vomiting, diarrhea and cramping
Acute and self limiting
symptoms begin 4-6 hrs after consumption and end
within 24 hrs
 Botulism
Causative agent:
Clostridium botulinum
Obligate anaerobic, Gram +, spore forming bacillus
Produce 7 different neurotoxins
One of most deadly toxins known
 Signs & Symptoms
Dizziness, dry mouth, blurred vision
Abdominal symptoms include pain, nausea,
vomiting and diarrhea or constipation
Progressive paralysis
Paralysis of respiratory muscles most common cause of
death
 3 forms of botulism:
Food-borne botulism progressive paralysis of all
voluntary muscles due to toxin production

Wound botulism similar symptoms

Infant botulism bacteria grow in the intestines,

producing non-specific symptoms
floppy baby syndrome
 Epidemiology
Food borne botulism
Commercial sterilization
Toxin destroyed by heating foods

Wound botulism
deep crushing wounds

Infant botulism
Inhalation or ingestion of spores
Commonly associated with honey or
juices
 Prevention
Proper sterilization and sealing of canned food
No honey or unpasteurized juices for infants!!

Treatment
Antitoxin
Gastric washing and surgical removal of tissues
Artificial respiration may be required
Anti-microbials given to kill bacteria in infant and wound
botulism
 Viral enteropathogens
Rotavirus
Enteric adenoviruses
Astrovirus
Norwalk agent-like virus
Calicivirus
 Viral Gastroenteritis
Common causative agents:
Rotaviruses and Noroviruses
Both naked RNA viruses

Star-like Noroviruses

A vaccine against rotavirus diarrhea has been

withdrawn recently from the market.
Wheel -like Rotaviruses
 Pathogenesis of Rotavirus enteritis
Rotaviruses attach and replicate in the mature
enterocytes at the tips of small intestinal villi

Destroy villus tip cells, variable degrees of villus blunting

mononuclear inflammatory infiltrate in the lamina propria

Impairment of digestive functions Impairment of absorptive functions

discreasing hydrolysis of the transport of water and electrolytes
disaccharides via glucose and amino acid co-
transporters
Malabsorption of complex
carbohydrates, particularly
lactose
An imbalance in intestinal fluid
absorption to secretion
Other than digested into
monosaccharide, lactose be lysis
into organic acid, hyper-osmosis
Watery stool
 Parasitic enteropathogens
G. lamblia
Entamoeba histolytica
Strongyloides stercoralis
Cryptosporedium
Cyclospora & isospora
COMMON CAUSES OF DIARRHEA-
OTHERS
Metabolic disease
Hyperthyroidism
Diabetes mellitus
Pancreatic insufficiency
Food allergy
Lactose intolerance
Antibiotics
Irritable bowel syndrome
 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
Fig. 1. The typhoid fever surveillance
study sites
Fig. 2. Incidence of typhoid fever and
mean age of patients
 Typhoid fever is an enteric
fever
Macrophages carry bacteria
to liver, spleen, bone marrow
and gallbladder
Treated with ciprofloxacin or
ampicillin
Surgical removal of
gallbladder
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.
 Common intestinal flora
of many animals
Contaminated animal
products are reservoir
Reptiles, eggs and
undercooked poultry
 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
2. Explain the risk factors, signs and
symptoms of typhoid fever
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
Once signs and symptoms do appear,
you're likely to experience:
Fever,
Headache and dizziness
Weakness and fatigue
Sore throat
Abdominal pain
Diarrhea (children) or
constipation (adult)
Rash:
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.
Second week of illness
If you don't receive treatment for
typhoid fever, you may enter a
second stage during which you
become very ill and experience:
Continuing high fever
Relative bradycardia
Coated tongue
Either diarrhea that has the color
and consistency of pea soup, or
severe constipation
Considerable weight loss
Extremely distended abdomen
 SYMPTOMS BY WEEK
Third week of illness Fourth week of illness
Become delirious Improvement may come
Lie motionless and slowly
exhausted with your eyes Your fever is likely to
half-closed in what's decrease gradually until
known as the typhoid your temperature returns
state to normal in another
Life-threatening week to 10 days.
complications often But signs and symptoms
develop at this time. can return up to two
weeks after your fever
has subsided
Sign and Symptom
Characteristic Typhoid fever
3. Explain the pathogenesis of
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.
Virulent strains tolerate stomach
acid and pass to intestines

Toxin induces phagocytosis in

intestinal cells

Pathogen reproduces inside

phagosome killing host cell

Bacteria (Typhi) may pass

through intestinal cells into
bloodstream
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.
4. Explain the supportive examinations
and treatments of typhoid fever
 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
 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
 Prevention of Typhoid Fever
Typhoid is a serious disease that can be
prevented by scrupulous personal, food and
water hygiene and vaccination. A single dose
of Vi polysaccharide antigen vaccine can
be protective for 3 years.
 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.
 Dehydration

Excessive loss of water,

especially loss of extracellular fluid
 Degree of dehydration sign + symptom
Dehydration Mild Moderate Severe
Decrease in 3% 5 510 10 15%
body weight (50ml / kg) (50100ml / kg) (100120ml / kg)
Irritable/Restless Lethargic/coma
Mental Well, alert /thirsty
Fontanel/Eye Sunken Sunken Severely sunken
Skin turgor Normal Decrease Markedly decrease
Mouth+tongue normal sticky Dry
Tears present Decrease Absent
Urine Mild oliguria oliguria Anuria
Blood pressure Normal Hypotension
heart rate Tachycardia little Tachycardia with
Normal
Pulse weak pulse
Capillary refill 2 seconds 3 seconds
 Type of dehydration
Isotonic Hypertonic Hypotonic
(isonatremic) (hypernatremic) (hyponatremic)
Loses H2O = Na H2O > Na H2O < Na
Plasma Normal Increase Decrease
osmolality
Serum Na+ Normal Increase Decrease
>150mmol/L <130mmol/L
ECV (extra Decrease Decrease Decrease +++
cellular vol) maintained Decrease +++ Increase
ICV
Thirst ++ +++ +/-

Skin turgor ++ Not lost +++

Mental state Irritable/lethargic Very irritable Lethargy/coma

 Metabolic Acidosis
Pathogeny
lose of large amount of basic substances from
gastrointestinal tract
too much acid metabolite
Blood gas analysis
pH nomarl HCO3- CO2
pH HCO3- CO2
Degree
Mild HCO3- 18~13 mmol / L
Moderate HCO3- 13~9 mmol / L
Severe HCO3- <9 mmol / L
 hypokelemia
Pathogeny
Lake of intake
Loss of potassium from gastrointestinal
tract
Blood electrolytes analysis
K+ < 3.5 mmol/L
 Hypokelemia
Clinical manifestation
Nervous system
depressed
Muscle
inertia of limbsmuscular tension down
severely retardant paralysisrespiratory
muscle paralysis
Heart
heart rate increasing, arrhythmia, Adams
Stokes syndrome, heart rate decreasing
atrioventricular block, heart sound lowering,
Cardiogram
U wave appearingUTflattened T
wave,
 Laboratory and Imaging Studies
Initial laboratory evaluation
CBC
Stool examination: mucus, blood, and leukocytes
Gas and electrolytes analysis
BUN, Cr, and urinalysis for specific gravity
Rapid test for Rotavirus
Stool cluture
for patients with fever, profuse diarrhea, and
dehydration or if HUS is suspected
Stool evaluation for parasitic agents
identification of the organism in the stool
Blood culture
uncommom
ASSESSMENT OF DEHYDRATION
Dehydration
Mild Moderate Severe
Appearance irritable, irritable, lethargy,
thirsty very coma, or
thirsty unconscious
Anterior normal depressed markedly
Fontanelle depressed
Eyes normal sunken sunken
 ASSESSMENT OF DEHYDRATION
(contd.)
Dehydration
Mild Moderate Severe
Tongue normal dry very dry,
furred
Skin normal slow very slow
retraction retraction
Breathing normal rapid very rapid
 ASSESSMENT OF DEHYDRATION
(contd.)

Dehydration
Mild Moderate Severe
Pulse normal rapid and feeble or
low imperceptible
volume
Urine normal dark scanty
Weight < 5% 6 - 9% 10% or more
loss
Fluid Management of Dehydration
Calculate 24-hr water needs
Calculate maintenance water
Calculate deficit water
Calculate 24-hr electrolyte needs
Calculate maintenance sodium and potassium
Calculate deficit sodium and potassium
Select an appropriate fluid (based on total water and
electrolyte needs)
Administer half the calculated fluid during the first 8 hr,
first subtracting any boluses from this amount
Administer the remainder over the next 16 hr
Replace ongoing losses as they occur
 Fluid Therapy
Deficit of water and electrolytes
Water Deficit: Percent dehydration weight
Sodium Deficit:Water deficit 80 mEq/L
Potassium Deficit:Water deficit 30 mEq/L
Ongoing loss
After they occur
Sodium: 55 mEq/L
Potassium: 25 mEq/L
Bicarbonate: 15 mEq/L
Maintenance
0-10kg 100 mL/kg
11-20kg 1000 mL + 50 mL/kg for each 1 kg >10 kg
>20kg 1500 mL + 20 mL/kg for each 1 kg >20 kg*(max 2400mL)
Sodium2 - 3 mEq/kg/day
potassium1-2mEq/kg/day
 Fluid Therapy
ORT
Mild to moderate dehydration from diarrhea
Intravenous
With severe dehydration
with uncontrollable vomiting
unable to drink because of extreme fatigue, stupor,
or coma
with gastric or intestinal distention
COMPOSITION OF ORS

Ingredient Amount (g/liter)

Sodium chloride 3.5
Trisodium citrate or 2.9 or
Sodium bicarbonate 2.5
Potassium chloride 1.5
Glucose 20.0
 Type of ORS
Solution Glu Na K Cl
g/L mEq/L mEq/L mEq/L
WHO 20.0 90 20 80

Rehydralyte 20.5 75 20 65

Pedialyte 20.5 45 20 35

Infanlyte 20.0 50 20 40
 ORT
Mild: ORS 50 mL/kg within 4 hours
Moderate: ORS 100 mL/kg over 4 hours to
Supplementary ORS is given to replace ongoing
losses
An additional 10 mL/kg of ORS is given for each
stool
Breastfeeding should be allowed after rehydration in
infants who are breastfed
usual formula, milk, or feeding for other patients
should be offered after rehydration
AMOUNT OF SALT LOSS DURING
DIARRHEA
Diarrhea Salt (mmol/L)
Na K Cl HCO3
Cholera 88 30 86 32
(child)
Cholera 135 15 100 45
(adult)
E. coli 53 37 24 18
Rota 37 38 22 6
virus
 Intravenous treatment
Restore intravascular volume
Normal saline: 20 mL/kg over 20 min (repeat until
intravascular volume restored)

Deficit of water and electrolytes

Solution: 5% dextrose in half NS + 20 mEq/L of potassium
chloride
Given over the first 8 hrs

Ongoing loss
Solution: 5% dextrose in normal saline + 15 mEq/L
bicarbonate + 25 mEq/L potassium chloride
Maintenance
Solution: 5% dextrose in normal saline + 20 mEq/L of
potassium chloride

Given over the next 16 hrs

 Antibiotic Therapy
Organisms Antibiotic
Campylobacter erythromycin
Jejuni azithromycin
E. Coli EPEC: Indicated for infants younger than 3
months old with
ETEC: Usually none if endemic
TMP-SMZ or ciprofloxacin for traveler's
diarrhea
EIEC: Third-generation cephalosporin
TMP-SMZ
Ampicillin
EHEC: not recommend
EAEC: TMP-SMZ
 Antibiotic Therapy
Organisms Antibiotic
Shigella Third-generation cephalosporin
species Ampicillin, TMP-SMZ,
Salmonella Usually none (if 3 months old) for non
typhoid;
ampicillin, cefotaxime for S. typhi or
S.paratyphy
Yersinia None for uncomplicated diarrhea; TMP-SMZ;
enterocolitica gentamicin or cefotaxime for extraintestinal
disease
C. difficile metronidazole,
vancomycin
 Antibiotic Therapy
Organisms Antibiotic
E. histocolytica metronidazole followed by a luminal agent,
such as iodoquinol

G. lamblia Albendazole
Metronidazole
Furazolidone
Quinacrine
Cryptospodium Non specific treatment
Prognosis

Mortality
Dehydration
Malnutrition
 Prevention
Safe drinking water and food
Boil it, cook it, peel it, or forget it. "
Hand washing
Proper sanitation
Vaccines
4. Normal stool frequency ranges from three times a week to three times a dayAcute diarrheas
are those lasting less than 2 to 3 weeks or, rarely, 6 to 8 weeks.The most common cause of acute
diarrhea is infection. Learn infectious vs. non-infectious.Chronic diarrheas are those lasting at
least 4 weeks, and more usually 6 to 8 weeks or longer.There are three categories of chronic
diarrhea:osmotic (malabsorptive) diarrheasecretory diarrhea, and inflammatory vs. non-
inflammatory diarrhea.
5. Approximately 80% of acute diarrheas are due to infections with viruses, bacteria, helminths,
and protozoa.The remainder are secondary to the ingestion of medications, poorly absorbed
sugars (fructose polymers or sorbitol), fecal impaction, pelvic inflammation.Diarrhea results
from imbalance of the intestines to handle water and electrolytes
7. Acute DiarrheaBloodyMust evaluate ALL bloody diarrhea.C & S stoolSigmoidoscopyMaybe
CTNon-bloodyMost are viralMost resolve on own without definite dxRarely further
complications unless remission of a chronic conditionIf sx progress to fever, pus, dehydration,
then needs more evaluation.
8. Big Clinical Clues to Infectious vs. NoninfectiousInfectious!Fever
PusBloodEpidemicTravelBacterial: Sx onset WHILE IN visited countryParasitic: Sx onset AFTER
RETURNNoninfectiousAFEBRILENon-pus stoolNonbloodySporadicNo travel