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Kuliah Typhoid Fever Blok 7 0612
Kuliah Typhoid Fever Blok 7 0612
Epidemiology
Incidence
– US, Western Europe, Japan: 0.2 – 0.7 /
100.000
– Southern Europe: 4.3 – 14.5 / 100.000
– Developing country: 10 – 540 / 100.000
– Indonesia: 350 – 810 / 100.000 =
600.000 – 1.5 million cases/yr
Epidemiology
Transmission
– Contaminated drinking water or food.
– Large epidemics: most often related to fecal
contamination of water supplies or street
vended foods.
– A chronic carrier stateexcretion of the
organism for more than 1 yearoccurs in
approximately 5% of infected persons.
Etiology
– Others: S.paratyphi
using a Flagellar
stain technique
(1979)
Salmonellae:
– gram-negative bacilli, Enterobacteriaceae
family, non-spore-forming, nonencapsulated,
flagella.
Etiology
– Killed by heating to 130°F (54.4°C) for
1 hr or 140°F (60°C) for 15 min.
– Remain viable at ambient or reduced
temperatures for days, survive for weeks in
sewage, dried foodstuffs, pharmaceutical
agents, and fecal material.
Pathogenesis
Clinical Manifestation
1st week:
– Fever “step ladder temperature chart”,
Insidious increase, unremitting, highest: end
of 1st week
– Systemic symptoms: headache, lethargy,
malaise, myalgia, nausea, vomiting,
abdominal pain
Clinical Manifestation
2nd week:
– Hepatosplenomegaly, rose spot,
headache stupor
– Relative bradicardia: rare in
children
Clinical Manifestation
Clinical Features
– Clinically mild, can be asymptomatic
– Obviously:
Fever
GIT distubance
– Change of level of consciousness
Diagnosis
Laboratory
– Culturing Salmonella
Blood (40 – 54%),
bone marrow (80 – 90%),
urine (7%),
stool (35 – 37%),
duodenal fluid (58%), rose spot (63%)
Laboratory
Diagnosis:
Laboratory
– Serology
Widal: four fold rise in O agglutinin or a titer
of ≥ 1/160 not recommended by WHO
IgM and IgG for Salmonella, Tubex, Typhi dot
– DNA probe
– PCR
Diagnosis:
Laboratory
– Peripheral blood exam:
Lekopenia, relative lymphocytosis,
aneosinophilia
Not spesific
Complication
Others:
– Typhoid hepatitis, typhoid
encephalopathy, cholecystitis,
pneumonia, septic shock, pyelonephritis,
endocarditis, osteomyelitis, meningitis,
cerebral thrombosis, ataxia, aphasia, etc
Therapy
– Blood transfusion
Intestinal haemorrhage and perforation
Therapy
ANTIBIOTIC
Empiric therapy
– Narrow spectrum AB, good penetration, easy
to give, resistency <, minimal side effect,
clinical effication evidence
Treatment successfull parameter: time of
defervescence
– Min. 36 hours of therapy for fever
Therapy
ANTIBIOTIC
1st Line
– Chloramphenicol (1st drug of choice)
– Ampicillin / amoxicillin
– Cotrimoxazole
Therapy
ANTIBIOTIC
2nd Line
– Ceftriaxon
– Cefixim
– Fluoroquinolon not recommended for
children
– Azythromycine
– Aztreonam
Therapy
ANTIBIOTIC
1st Line
– Chloramphenicol
75 – 100 mg/kgBW/day IV or PO in 2 divided
dose for 10 – 14 days
Max. dose 2 gr/day
CI: leukopenia (< 2000/ul)
Terapi
ANTIBIOTIC
1st Line
– Ampicillin
200 mg/kgBW/day PO or IV in 4 divided dose
for 10 – 14 days or,
– Cotrimoxazole
10 mg/kgBW/day (TMP) in 2 divided dose for
14 days
Terapi
ANTIBIOTIC
2nd Line
– Ceftriaxon
50 – 80 mg/kgBW/day, single dose for 10
days
Cure rate up to 90% in 3 – 5 days duration of
therapy
Therapy
ANTIBIOTIC
2nd Line
– Cefixim
10 – 15 mg/kgBW/day PO in 2 divided dose
for 10 - 14 days
Cure rate in IKA RSCM 1999 – 2000: 84%
Therapy
ANTIBIOTIC
2nd line
– Fluoroquinolone
Superior than cephalosporin, cure rate ≈
100%, child controversion
– Ciprofloxacine, 10 mg/kgBW/day in 2 divided dose,
– Ofloxacine 10 -15 mg/kgBW/day in 2 divided dose
– Duration: 2 – 5 day
– MDR typhoid
Therapy
Dexamethasone
Severe case with altered mental status
Initial dose 3 mg/kgBW 1 mg/kgBW
every 6 hr for 48 hr mortality from 35-
55% to 10%
Prognosis