Typhoid Fever,

(Salmonella)

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 Overview

• Salmonella is a rod-
shaped, gram-
negative,
facultative/mndiri
anaerobe in the
family
Enterobacteriaceae
Rod togkat

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 Typhoid Fever
• Typhoid fever is a systemic infection with the bacterium
Salmonella enterica serotype typhi.
• A subset of Salmonella serotypes that includes S. typhi and S.
paratyphi causes enteric (typhoid) fever and is restricted to
growth in human hosts.
• Clinically S. typhi > S. paratyphi

Restrc batsi
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 Classification
• Enterobacteria
• Gram-negative
• Facultative anaerobes
• Glucose-fermenting/pnguraian
• Straight, rod
• 2-3 µm in length
• Flagellated
• Many serovars
• Typhi
• Typhimurium
• Enteriditis

Fermn mmuaijky
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A general picture of a salmonella bacterium.Notice the flagella
S. Typhi has an outer-capsule, while most other serovars have
the lipopolysaccharide coat.
•

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This is a membrane of S.
typhi. Other serovars do
not have the outer capsule.
Notice parts of
LPS/Lipopolysaccharide.
Lipid A (conserved)/p
nympnan. Polysaccharide
part is variable, especially O
polysaccharide (what
antibodies bind to) 7
 Infection

• Ingestion of contaminated
food or water
• Passes through mucosa of
intestine to epithelial cells
• Causes membrane
ruffling/mngerut
• Releases effector proteins
through Type III Secretion
system
• Endocytosis/mem fagosit bnd
asing
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 Salmonella
• Salmonella can be further
divided into serovars based
on the detection of three
major antigenic
determinants:
• the somatic O antigen
[lipopolysaccharide
(LPS) cell-wall
components]
• the surface Vi antigen
(restricted/mbtasidfy to
S. typhi and S.
paratyphi C),
• the flagellar H antigen.

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 Epidemiology
• Endemic in developing contries
• Incubation period : 3 d – 3 m (1-3 wk)
• Transmission :
– most cases of disease result from
ingestion of contaminated food or water
– anal-oral transmission
– health care workers

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(grm(-)

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 Pathogenesis
 Disebabkan ok S.typhi dan endotoksinnya merangsang
sintese.Penularan S.thypi terjadi melalui mulut,oleh makanan yg
tercemar.Sbgn akan dimusnahkan melalui lambung oleh asam
lambung,sgbn masuk ke usus halus,mencapai jaringan limfoid/m
nyrpai limfosit,lalu berkembang biak.Kuman masuk aliran
darah,mencapai sel-sel retikuloendotelial hati,limpa,organ
lain.Proses ini terjadi pada masa tunas,yg berkhir saat sel-sel
retikulo endotelial melepaskan kuman kedalam peredaran darah
dan menimbulkan bakteriemi yg kedua kalinya.Masuk
limpa,usus,kandung empedu.Penelitian dahulu mengira demam ok
endotoksin.

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 PATOLOGI
 Kelainan patologi utama terjadi di usus halus,di ileum
distal.
 Pada minggu pertama penyakit,terjadi hiperplasi plaks
Peyer ,disusul minggu kedua terjadi nekrosis,dalam
minggu ketiga terjadi ulserasi plak Peyer,minggu
keempat terjadi penyembuhan ulkus,meninggalkan
sikatriks.Ulkus dpt menyebabkan perdarahan,sampai
perforasi usus.
 Hepar mebesar dg infiltrasi limfosit,sel plasma dan sel
mono nukler,serta nekrosis fokal.
 SRE menunjukkan hiperplasi dan kelenjar mesenterika
dan limfe membesar.
 Kelaian patologik juga
 dpat dijumpai
 pd ginjal,paru,jantung,
 selaput otak,otot,tulang.
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 Pathogenesis
 Once phagocytosed, the bacteria are
protected from PMNs the complement
system, and antibodies.
 After phagocytosis, salmonellae
disseminate throughout the body in
macrophages via the lymphatics and
colonize reticuloendothelial tissues (liver,
spleen, lymph nodes, and bone marrow).
 Signs and symptoms, including fever and
abdominal pain, probably result from
secretion of cytokines by macrophages
when a critical number of organisms have
replicated. . 14
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Patofisiologi

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 GAMBARAN KLINIS
• Masa tunas 10-14 hari.
• Gejala amat bervariasi,dari yg ringan,tdk terdiagnosis sp
yg khas,komplikasi sp kematian.Seorang yg ahli pun dpt
mengalami kesulitan untk mendiagnosis.

• Minggu pertama,spt flu like syndrome,demam,nyeri

kepala,pusing,nyeri
otot,anoraksi,mual,muntah,obstipasi,diare dll.
• Px suhu meningkat

• Minggu kedua gejala lebih jelas,demam,relatif bradi

kardi,lidah kotor(kotor ditengah,tepi dan ujung
merah,tremor),hepatomegali,splenomegali,meteorismus,
ggn mental,stupor,koma,delirium.
• Roseolae di Indonesia jarang dtemukan.
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Rose spot

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Relative bradicardia

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Widal Test

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Widal Test
 Adalah reaksi aglutinasi antara antigen anti
bodi(aglutinin).
 Aglutinin yg spesifik thd salmonela tdpt pd serum
penderita tyfoid,juga pd yg pernah ketularan
salmonela.atau yg pernah divaksinasi.thd tifoid.
 Antigen yg digunakan pd reaksi Widal adalah suspensi
salmonella yg sdh dimatikan dan diolah di lab.
 Maksud reaksi Widal dalah untk menetukan adanya
aglutinin dlmserum penderita yg diduga menderita
typhoid.

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Widal Test

 Pada infeksi yg aktif,titer Widal akan meningkat

pd pemeriksaan ulang yg dilakukan selang 5
hari.
 Kenaikan titer empat kali lipat pd pemeriksaan
ulang dpt memastikan diagnosis.
 Pada pndrta yg sembuh,aglutinin akan berada
dlam darah dl wkt lama,mk reaksi Widal bukan
menrupakan para meter kesembuhan
penderita.
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Treatment

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 Complications
• Complications occur in 10 to 15 percent of patients
• Gastrointestinal bleeding, intestinal perforation, and
typhoid encephalopathy are the most important.
• Gastrointestinal bleeding is the most common,
occurring in up to 10 percent of patients. It results
from erosion of a necrotic Peyer’s patch through the
wall of an enteric vessel.

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Acute Pancreatitis

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Associated Structures of the
Gall Bladder and Pancreas

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Definition
• Acute inflammation of the pancreas
• Varying degree of regional tissue
involvement and remote/jauh organ
systems
• Classified as acute unless there is
evidence of chronic pancreatitis,
otherwise considered as
exacerbation of inflammation
superimposed on chronic
pancreatitis

remtejauhsdy 35
Acute Pancreatitis Epidemiology
• Second most common principal inpatient
GI diagnosis after cholelithiasis and acute
cholecystitis
• Unreliable data due to misdiagnosis
• Estimated yearly incidence of 5-40/100,000
• 1998 data from the U.S. about “pancreatic
diseases”
• 327,000 inpatient stays
• 78,000 outpatient hospital visits
• 195,000 visits
• 531,000 office visits
• >2800 deaths due to acute pancreatitis in
2000
• Estimated annual cost in 2000 was
$2,500,000,000 36
Natural History
• 80% of cases are mild
• 20% are severe with organ failure and
local complications
• Estimated 25-33% mortality
• Overall mortality estimates range from 2%
to 10%
• Half of death occur within the first week,
perhaps 25% to 33% of deaths occur within
the first 48 hours
• Obese patients have higher rates of local
complications, respiratory failure, severe
acute pancreatitis and death from sterile
necrosis than non-obese patients
• Older and multi-morbid patients have 37
higher mortality rates
Pathology
• Initial injury to peripheral acinar
cells, fat necrosis and autodigestion
• Interstitial (edematous) pancreatitis:
• Interstitial edema associated with
inflammatory cells in the parenchyma
• Parenchymal necrosis is microscopic
• Necrotizing pancreatitis
• Focal macroscopic or diffuse necrosis
• Hemorrhage, vascular thrombosis
• Involvement of the main pancreatic duct
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Pathogenesis of Acute
Pancreatitis
• Trypsinogen to trypsin conversion in acinar
cells overwhelms neutralization
mechanisms
• Proenzymes (trypsinogen, elastase,
phospholipase A2 (PLA2) and
carboxypeptidase) are activated by trypsin
• Activation of complement and kinin
systems
• Pancreatic autodigestion with self-
sustaining cycle of proteolytic, etc.
enzyme activation
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Etiologies of Acute
Pancreatitis
• Obstructive
• Toxic
• Metabolic
• Infectious
• Vascular
• Trauma
• Iatrogenic
• Hereditary
• Controversial etiologies
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Obstructive causes
of Acute Pancreatitis

• Gallstones/microlithiasis
• Tumors
• Parasites (those causing
obstruction, e.g. Ascaris, Clonorchis)
• Duodenal diverticula
• Celiac sprue? (chronic duodenal
inflammation causing ampullary
stenosis)

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Toxic and Metabolic
Etiologies
• Toxic
• Ethanol
• Methyl alcohol
• Scorpion venom (hyperstimulation of
pancreas)
• Organophosphate insecticides
(hyperstimulation of pancreas)
• Drugs
• Metabolic
• Hypertriglyceridemia
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• Hypercalcemia
Gallstone
/Biliary Pancreatitis

• 40% of all cases of AP

• Risk of AP due to existing gallstones is
greater in men, but overall incidence is
lower as gallstones are more common in
women
• Small stones (< 5 mm) are more likely to
cause pancreatitis

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Hypertriglyceridemia
• Third most common identifiable
cause of AP
• Serum triglycerides > 1000 mg/dL
• Mechanism?
• Possibly, release of free fatty
acids may cause pancreatic acinar
or capillary endothelial damage

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Hypertriglyceridemia

• Associated conditions in adults

• Diabetes mellitus
• Alcohol abuse (chicken or the
egg?)
• Obesity
• Hypothyroidism
• Pregnancy
• Estrogen therapy
• Types I & V hyperlipoproteinemia 45
Diagnosis of AP

• Clinical findings
• Laboratory findings
• Radiological findings

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Clinical Findings
• Usually acute onset of severe pain
• Epigastric, upper quadrants
• Radiation to back and chest (DDx
myocardial ischemia)
• Nausea, vomiting, hematemesis
• Bowel obstruction
• Fever, tachypnea, shock

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Laboratory findings

• 2-3 fold elevations of pancreatic

enzymes amylase and/or lipase
• Amylase
• Cheap, fast and widely available
• Not 100% sensitive or specific
(normal values in mild attacks, in
the setting of chronic pancreatitis
or even with fatal pancreatitis
have been reported)
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Lipase
• Sensitivity similar to amylase (85%-100%)
• Probably more specific (all pancreatic
except a small amount of gastric lipase)
• Usually remains elevated longer than
amylase
• False positive values in:
• Renal insufficiency
• Macrolipasemia
• Bowel obstruction, perforation and
enteritis (increased reabsorption)

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Differential Diagnosis

• Biliary pain and acute cholecystitis

• Epigastric distress syndrome/non-
ulcer dyspepsia
• Peptic ulcer disease and perforated
hollow viscus
• Small bowel obstruction
• Inferior myocardial infarction
• Aortic dissection
• Ruptured ectopic pregnancy 50
• Acute appendicitis
TERAPI /TAMBAHAN
atas dasar problem yg timbul pd pankreatitis
akut

• 1.Syok Cairan parenteral,albumin.

• 2.Sepsis Antibiotika,operasi
• 3.Gagal ginjal Hemodialise
• 4.Hipokalsemia Infus Kalsium
• 5.Hiperglikemia Insulin
• 6.Intoksikasi Lavase peritoneum
• 7.trobosis vena Heparin
• 8.Kesakitan Analgetika

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Range of Severity

• Mild
• Minimal or no organ dysfunction
• Full recovery without
complications
• Severe
• Local complications
• Organ failure
• … death The end

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 Terima kasih

Helai ilalang jadi pena, dan lautan jadi tinta, takkan cukup untuk menulis ilmuMU

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