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405090079

Diarrhea

DEFINITION
Diarrhea is loosely defined as passage of
abnormally liquid or unformed stools at
an increased frequency.
For adults on a typical Western diet, stool
weight > 200 g/d can generally be
considered diarrheal.
Source: Harrisons ,17 th edition, vol 1,
page 247

ETIOLOGY

Viruses : Enterovirus, adenovirus, rotaviru

Enteral Infection

Infection

Bacteria : Vibrio, E. coli, Shigella,


Salmonella, Campylobactr,
Yersinia, Aeromonas
Protozoa : G. Lamblia, E.
Histolitica, Isospora belli
Parasites

Caused
of diare

Helmin : Ascaris,
Trichuris, Oxyyuris,
Strongyloides
Fungal : Candida albicans

Parenteral Infections : OMA, Tonsilofaringitis,


Bronkopneumonia, Morbilli
Malabsorption : Carbohydrate, Lipid, Protein
Food : out-of-date, poisonous
Allergic
Immunodeficiency
Phsycology : afraid,

Incub
ation

Duratio
n

Vomiting

Fever

Abdomina
l Pain

1-7 d

4-8 d

Yes

Low

No

8-10 d

5-12 d

Delayed

Low

No

Norovirus

1-2 d

2d

Yes

No

No

Astrovirus

1-2 d

4-8 d

+/-

+/-

No

Calicivirus

1-4 d

4-8 d

Yes

+/-

No

Aeromonas
species

None

0-2 wk

+/-

+/-

No

Campylobact
er species

2-4 d

5-7 d

No

Yes

Yes

Variabl
e

Variable

No

Few

Few

1d

Mild

No

Yes

Organism
Rotavirus
Adenovirus

C difficile

Minima
C perfringens
l

Incubati
on

Duratio
n

Vomitin
g

Fever

Abdomina
l Pain

Enterohemor
rhagic E coli

1-8 d

3-6 d

No

+/-

Yes

Enterotoxige
nic E coli

1-3 d

3-5 d

Yes

Low

Yes

Plesiomonas
species

None

0-2 wk

+/-

+/-

+/-

Salmonella
species

0-3 d

2-7 d

Yes

Yes

Yes

Shigella
species

0-2 d

2-5 d

No

High

Yes

Vibrio
species

0-1 d

5-7 d

Yes

No

Yes

Yenterocoliti
ca

None

1-46 d

Yes

Yes

Yes

Giardia
species

2 wk

1+ wk

No

No

Yes

5-21 d

Months

No

Low

Yes

5-7 d

1-2+ wk

No

Yes

No

Organism

Cryptosporid
ium species
Entamoeba

Vibrio cholera

Salmonella

Shigella

Campylobacter jejuni

E. coli

1. E coli Enteropatogenik
(EPEC)
Cause by baby`s,especially in
developing country
Wattery diarhea,self-limited but can
be chronic diarhea

2. E coli Enterotoksigenik
(ETEC)
Traveller`s diarhea
Strain which produces eksotoksin which
hot resistantsubunit B binds at
brushborers epitelial intestine Gangliosida
dan facilitate influx subunit A into cell,then
activated adenil cyclaseincreased Camp
consentrationwater&clhypersecretionblocked natrium
reabsroptionintestine lumen
strachinghypermotilitydiarhea

2. E coli Enterotoksigenik
(ETEC)
Strain which produces
enterotoksin,hot resistant sTa(BM
1500-4000)
sTa activate Guanil cyclase in
enteric epitel cell and stimulate fluid
secretions

3. E coli Enterohemoragik
(EHEC)
Produces verotoxin
Caused colitic ulcerative, severe
diarhea, hemolitic uremic syndrom.

4. E coli Enteroagregratif
(EACE)
Caused acute and chronic diarhea et
developing country
Transmission by foods

Enteroinvasive E.coli (EIEC)


Cause : bacillary dycentriae-like illness
Ussualy in develpment country because
bad sanitation & hygiene
Mechanism to invation :
EIEC stick & invation enterocyte colon
Multiplication cell death bacteria release
to colon invation another cell
Necrotic & duodenum ulcer bloody feces &
mucous

Receptor : plasmid 120 140 MDa

Classification
Duration:

Acute Diarrhea (<15 days)


Chronic Diarrhea (>15 days)

Patophysiology

Osmotic diarrhea
Secretory diarrhea
Inflammatory and Infectious Diarrhea
Diarrhea Associated with Deranged Motility

Infection and non-infection

Diarrhea
Pathophysiology
1.Osmotic diarrhea
2.Secretory diarrhea
3.Inflammatory and Infectious Diarrhea
4.Diarrhea Associated with Deranged
Motility

Diarrhea
1.Osmotic Diarrhea
The Osmotic Diarrhea typically results
from one of two situations:
Ingestion of a poorly absorbed
substrate
Malabsorption

Diarrhea
Ingestion of a poorly absorbed
substrate
Ingested poorly absorbed substarte
Mannitol or sorbitol, epson salt
(MgSO4) and some antacids (MgOH2)

Unabsorbed substrate in the intestinal


lumen

Diarrhea

Malabsorption:
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.

A distinguishing feature of osmotic diarrhea is that it stops after the patient is


fasted or stops consuming the poorly absorbed solute.

Diarrhea
2. Secretory Diarrhea
Large volumes of water are normally secreted into the small intestinal lumen,
but a large majority of this water is efficienty absorbed before reaching the
large intestine.
Patophysioloy :
Example : Vibrio Cholerae infection
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

Additionally, cholera toxin affects the enteric nervous system independent

Diarrhea
Exposure to toxins from several other types of bacteria
(e.g. E. coli heat-labile toxin) induce the same series of
steps and massive secretory diarrhea .
In addition to bacterial toxins, a large number of other
agents can induce secretory diarrhea by turning on
the intestinal secretory machinery, including:
Some laxatives hormones secreted by certain types of
tumors (e.g. vasoactive intestinal peptide)
A broad range of drugs (e.g. some types of asthma
medications, antidepressants, cardiac drugs)
Certain metals
Organic toxins
Plant products (e.g. arsenic, insecticides, mushroom
toxins, caffeine)

In most cases, secretory diarrheas will not resolve


during a 2-3 day.

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

Infected of pathogens

Immune responses (Inflammated)

Activation of white blood cells

Secrete inflammatory mediators and cytokines

Stimulate secretion

Inflammatory diarrhea.

Diarrhea
Disruption of the epithelium of the
intestine microbial or viral pathogens
infection exudation of serum and blood
into the lumen and associated with
widespread destruction of absorptive
epitheliumabsorption of water occurs
very inefficiently diarrhea.
Reactive oxygen species from leukocytes
damage or kill intestinal epithelial cells
replaced with immature cells deficient
in the brush border enyzmes and
transporters necessary for absorption of

Diarrhea
4. Diarrhea Associated with
Deranged Motility
In order for nutrients and water to be
efficiently absorbed, the intestinal
contents must be adequately
exposed to the mucosal epithelium
and retained long enough to allow
absorption.
Disorders in motility than accelerate
transit time decrease

D. Pathophysiology

Symptoms

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

Physical
The following may be observed:
Dehydration
Dehydration is the principal cause of morbidity and mortality.
Assess every patient with diarrhea for signs, symptoms, and
severity.
Lethargy, depressed consciousness, sunken anterior fontanel, dry
mucous membranes, sunken eyes, lack of tears, poor skin turgor,
and delayed capillary refill are obvious and important signs of
dehydration.

Failure to thrive and malnutrition


Reduced muscle and fat mass or peripheral edema may be clues to
the presence of carbohydrate, fat, and/or protein malabsorption.
Giardia organisms can cause intermittent diarrhea and fat
malabsorption.

Abdominal pain
Nonspecific nonfocal abdominal pain and cramping are common with
some organisms.
Pain usually does not increase with palpation.
With focal abdominal pain worsened by palpation, rebound
tenderness, or guarding, be alert for possible complications or for
another noninfectious diagnosis.

Borborygmi: Significant increases in peristaltic activity can


cause an audible and/or palpable increase in bowel activity.
Perianal erythema
Frequent stools can cause perianal skin breakdown, particularly in
young children.
Secondary carbohydrate malabsorption often results in acidic stools.
Secondary bile acid malabsorption can result in a severe diaper
dermatitis that is often characterized as a "burn."

Diagnose The Diarrhea


Medical history and physical examination. The doctor will
ask you about your eating habits and medication use and will
examine you for signs of illness.
Stool culture. A sample of stool is analyzed in a laboratory to
check for bacteria, parasites, or other signs of disease and
infection.
Blood tests. Blood tests can be helpful in ruling out certain
diseases.
Fasting tests. To find out if a food intolerance or allergy is
causing the diarrhea, the doctor may ask you to avoid lactose,
carbohydrates, wheat, or other foods to see whether the

Sigmoidoscopy. For this test, the doctor uses a


special instrument to look at the inside of the
rectum and lower part of the colon.
Colonoscopy. This test is similar to a
sigmoidoscopy, but it allows the doctor to view
the entire colon.
Imaging tests. These tests can rule out
structural abnormalities as the cause of diarrhea.

Diarrhea
F. Diarrhea Treat
Pharmacology
1.Opiate-like antidiarrheae agents
2.Absorbents
3.Colloidal bismuth compound
4.Bile salt binding resins
5.Hormon
6.Antibiotik

THERAPY
Absorbents
Absorbents are compounds that absorb
water. Absorbents that are taken orally
bind water in the small intestine and colon
and make diarrheal stools less watery.
They also may bind toxic chemicals
produced by bacteria that cause the small
intestine to secrete fluid; however, the
importance of toxin binding in reducing
diarrhea is unclear.
The two main absorbents are attapulgite
and polycarbophil, and they are both
available without prescriptions.

Bismuth compounds.
Many bismuth-containing preparations are
available around the world. Bismuth subsalicylate
(Pepto-Bismol) is available in the United States.
It contains two potentially active ingredients,
bismuth and salicylate (aspirin). It is not clear how
effective bismuth compounds are, except in
traveler's diarrhea and the treatment of H. pylori
infection of the stomach where they have been
shown to be effective.
It also is not clear how bismuth subsalicylate
might work. It is thought to have some antibioticlike properties that affect bacteria that cause
diarrhea. The salicylate is anti-inflammatory and
could reduce secretion of water by reducing
inflammation.
Bismuth also might directly reduce the secretion
of water by the intestine.

Antibiotic and antiparasitics agents


Nitazoxanide (Alinia)
Inhibits growth of C parvum sporozoites and oocysts and G lamblia
trophozoites.

Tetracycline (Sumycin)
Treats gram-positive and gram-negative organisms as well as mycoplasmal,
chlamydial, and rickettsial infections.

Vancomycin (Vancocin)
Effective treatment (when PO) for antibiotic-associated colitis due to C difficile.

Sulfamethoxazole and trimethoprim (Bactrim, Septra, Cotrim)


Folate-synthesis blocker with wide antibiotic coverage. Inhibits bacterial
growth by inhibiting synthesis of dihydrofolic acid. Effective in E coli infections.

Quinacrine (Atabrine)
Very effective antiparasitic against Giardia species.

Iodoquinol (Vytone, Yodoxin)


Antiparasitic agents with wide coverage.

Rifaximin (Xifaxan, RedActiv, Flonorm)


Nonabsorbed (< 0.4%), broad-spectrum antibiotic
specific for enteric pathogens of the gastrointestinal
tract (ie, Gram-positive, Gram-negative, aerobic and
anaerobic).

Erythromycin (E.E.S., E-Mycin, Eryc, EryTab, Erythrocin)


Bacteriostatic macrolide with activity against most
gram-positive organisms and atypical respiratory
organisms. Useful for Campylobacter species and
vibrio enteritis.

Patient with diarrhea

Non-pharmacology
Try a clear liquid diet (one that includes water,
weak tea, apple juice, peach nectar, clear broth,
popsicles, and gelatin with no solids added) as
soon as diarrhea starts or when you feel that its
going to start.
Avoid acidic drinks, such as tomato juice, citrus
juices, and fizzy soft drinks.
When the diarrhea starts to improve, try eating
small amounts of foods that are easy to digest
such as rice, bananas, applesauce, yogurt,
mashed potatoes, low-fat cottage cheese, and dry
toast. If the diarrhea keeps getting better after a
day or 2, start small regular meals.
Rotavirus vaccine: active immunization to
increase resistance to infection rotavirus

Complications
Dehydration and electrolyte
imbalance
(abnormal amounts of sodium,
potassium, and acid in the blood)

Weight loss
Seizures

Patient Education

Education is most important for


prevention and treatment. Proper
ORT prevents dehydration, and early
refeeding speeds recovery of
intestinal mucosa. With caregiver,
emphasize proper hygiene and food
preparation practices to prevent
future infections and spread.

Bacterial infection: Campylobacter


Presenting Signs and Symptoms

Fever
and general
malaise,
Clinical
Symptoms
may evolve

sometimes
without
GI symptoms
Fever
and general
malaise,
sometimes without GI symptoms
When present, GI symptoms include
bloody
diarrhea,
and
When
present,
GI abdominal
symptoms pain
include
weightdiarrhea,
loss.
bloody
abdominal pain and
weight loss.

Campylobacter: Diagnostics
Campylobacter bacilli found in stool
culture

Campylobacter

Management and Treatment


Erythromycin 500 mg bid x 5 days (1st choice)

Fluoroquinolones are also effective, but


resistance rates of 30-50% have been reported
in some developing countries

Campylobacter

Unique features, Caveats

It is clinically impossible to distinguish the


different etiological agents of bacterial
gastroenteritis without a stool culture

If empiric therapy with TMP/SMX is


not effective in patients with
bacillary dysentery, try
fluoroquinolones
If symptoms of bloody diarrhea
persist , try erythromycin

Entamoeba histolytica

Presenting Signs and Symptoms

Clinical Symptoms may evolve

Colitis
Bloody stools
Cramps
Can be asymptomatic

Entamoeba histolytica
Diagnostics

Stool for ova and parasite exam


O&P present in stool exam
No fecal WBCs

Entamoeba histolytica
Management and Treatment

metronidazole 500-700 mg po or IV tid x 5-10


days
or
paromomycin 500 mg po qid x 7 days

Entamoeba histolytica
Unique features, Caveats

E. histolytica may be common in the general


population in developing countries, but may
be recurrent or more severe in HIV patients

Giardia lamblia

Presenting Signs and Symptoms

Clinical Symptoms may evolve

Enteritis
Watery diarrhea malabsorption
Bloating
Flatulence

Giardia lamblia

Diagnostics

Stool for ova and parasites


O&P in stool exam

Giardia lamblia
Management and Treatment

Metronidazole 250 mg po tid x 10 days

Giardia lamblia
Unique features, Caveats

Common cause of diarrhea in general


population, but may be recurrent or more
severe in HIV patients

Isospora belli

Presenting Signs and Symptoms

Clinical Symptoms may evolve

Enteritis; watery diarrhea


No fever
Wasting; malabsorption
** Symptoms similar to what occurs
with Cryptosporidium

Giardia lamblia
Diagnostics

Stool x 3: unstained wet preparation

Isospora belli oocysts are relatively


big (2030 m) and can be easily
identified in unstained wet stool
preparation
No fecal WBCs

Giardia lamblia
Management and Treatment

Most cases are readily treated with


sulfamethoxazole/ trimethoprim (960 mg qid
for 10 days) followed by 1 double strength
tablet (960 mg bid for 3 weeks), then chronic
suppression with sulfamethoxazole/
trimethoprim (960mg daily)
High dose of pyrimethamine with calcium
folinate to prevent myelosuppression
Long-term maintenance therapy may be
required to prevent relapse

Isospora belli infection

Microsporidium

Presenting Signs and Symptoms

Clinical Symptoms may evolve

Profuse watery, non-bloody diarrhea


Abdominal pain and cramping
Nausea
Vomiting
Weight loss

Giardia lamblia
Diagnostics
Fresh stool microscopy with modified
trichrome stain
Spores present in stool exam

Giardia lamblia
Unique features, Caveats

Species of microsporidia have been linked


to disseminated disease, e.g., cholangitis,
keratoconjunctivitis, hepatitis, peritonitis,
and infections of the lungs, muscles, and
brain

However, the presence of microsporidia


does not always correlate with
symptomatic disease

Most microsporidial infections are not


treatable

Helminthic infection:
Strongyloides stercoralis
Presenting Signs and Symptoms
Clinical Symptoms may evolve

Serpiginous erythematous skin lesions


(larva currens)
Diarrhea
Abdominal pain
Cough
Full-blown hyper-infection syndrome has
the characteristics of a gram-negative
sepsis, with acute respiratory distress
syndrome, disseminated intravascular
coagulation, and secondary peritonitis,
cough

Strongyloides stercoralis
Diagnostics

Chest x-ray: The chest x-ray may reveal


diffuse pulmonary infiltrates.
Stool microscopy, (multiple stool samples may
be necessary)
Sputum sample
In disseminated strongyloidiasis, filariform
larvae can be found in stool, sputum, bronchoalveolar lavage fluid, pleural fluid, peritoneal
fluid and surgical drainage fluid

Strongyloides stercoralis
Management and Treatment
Ivermectin 12 mg daily for 3 days. This drug
is also the drug of choice for the treatment
of systemic strongyloidiasis
An alternative treatment is albendazole 400
mg bid x 5 days

A maintenance therapy once a month is


necessary to suppress symptomatic infection
(albendazole 400 mg or ivermectin 6 mg
once monthly)

Strongyloides stercoralis
Unique features, Caveats

In immuno-compromised patients,
strongyloides can cause overwhelming
infection.This serious complication is called
strongyloides hyper-infection syndrome
and has a high case-fatality rate
Disseminated strongyloidiasis and heavy
worm loads can occur in patients with HIV,
but the full-blown hyper-infection syndrome is
less common
The likelihood of developing the hyperinfection syndrome is also increased in
patients taking high-dose steroids

Viral infectious
ROTAVIRUS
Most common cause of viral gastroenteritis.
Usually occurs between 3 months and 3yrs of age.
Although most common during wintermonths, it may
occur year round.
Clinical manifestations:

Diarrhea
Fever and vomiting.
Blood is not usually found in stools
Usually lasts for few days and up to 1 wk.

Detection of rotavirus antigen in stoolby enzyme


immunoassay is diagnostic.

Viral infectious
ADENOVIRUS
Adenoviruses may be associated with acute gastroenteritis,
especially in children <2 yrsof age.
Illness usually occurs during summer.
Diagnosed by: stool viral culture.

NORWALK-VIRUS
Usually cause epidemics in school-aged children or adults.
Infection usually comes from contaminated wateror food.
Clinical manifestations: (usually last several days)
Cramping abdominal pain
vomiting,and low-grade fever
Diagnosed by: stool viral culture.

Ascaris lumbricoides
Clinical manifestations:

Can be asymptomatic
Mild diarrhea
Intermittent epigastric pain
Anorexia
Vomiting

Diagnosed: by identifying whitish-brown Ascaris worm,20


40 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 on feetor between toes where larvae
penetrate.
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 stool examis


diagnostic.

Fungal Infections
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.

Red Flags
Symptoms of dehydration - excessive thirst, verydry
mouth, very little or no urination
Severe abdominal pain
Severe rectal pain
Blood in the stools, the stools are black
Temperature is over 39C (102 F)
A baby has not wet the diaper in over three hours
A child/baby is very sleepy, irritable, or unresponsive
A child/baby has a sunken abdomen
A child/baby has sunken eyes and/or cheeks
The child's/baby's skin does not flatten after being pinched

Typhoid fever

Typhoid fever, also known as enteric


fever, is a potentially fatal
multisystemic illness caused
primarily by Salmonella typhi.

Transmission
S typhi has no nonhuman vectors. The
following are modes of transmission:
Oral transmission via food or beverages handled
by an individual who chronically sheds the
bacteria through stool or, less commonly, urine
Hand-to-mouth transmission after using a
contaminated toilet and neglecting hand hygiene
Oral transmission via sewage-contaminated water
or shellfish (especially in the developing world)

Epidemiology
With an estimated
1633 million cases
of annually
resulting in
216,000 deaths in
endemic areas
Its incidence is
highest in children
and young adults
between 5 and 19
years old

Incidence of typhoid
fever
Strongly endemic
Endemic
Sporadic cases

Mortality/Morbidity
With prompt and appropriate antibiotic therapy,
typhoid fever is typically a short-term febrile
illness requiring a median of 6 days of
hospitalization. Treated, it has few long-term
sequelae and a 0.2% risk of mortality.17
Untreated typhoid fever is a life-threatening
illness of several weeks' duration with longterm morbidity often involving the central
nervous system. The case fatality rate in the
United States in the pre-antibiotic era was 9%13%.20
Race
Typhoid fever has no racial predilection.
Sex
Fifty-four percent of typhoid fever cases in the
United States reported between 1999 and 2006
involved males.17

Characteristic Typhoid fever

PREVALENCE TYPOID FEVER

Pathophysiology
patogene

ingestio
n
stomach
Small
intestine
phagocytizat
ion
Intralumin
al
dendritic
cell
Macrophages
(whitin
intestinal
mucosa)

Ephitelia
M cell
Presentation to
..

Ordinary
ephitelia
cell

Macrophages
(whitin intestinal
mucosa)
Latency &
multiplication
thoraci
s
Lymph
nodes
Mesenteric
lymph nodes

splee
n
Bone
narrow

Systemic desease
Blood
stream

Target
organ

hepar
transmission
Stool
Gallblader

Urine

Incubat Week 1
ion

Week 2

Week 3

Systemic
Steplad
der
fever
pattern
or
insidiou
s onset
fever

Very
commo
na

Very common

Acute
high
fever

Very
rareb

Chills

Almost allc

Rigors

Uncommon

Anorexi
a

Almost all

Week 4

Post

Recover
y phase
or death
(15% of
untreate
d cases)

10%20%
relapse;
3%-4%
chronic
carriers;
longterm
neurolo
gic
sequela
e
(extrem
ely
rare);

gallblad
der
Diaphor
Very common
cancer
esis
Table 1. Incidence and Timing of Various Manifestations of Untreated
(RR=16
Typhoid Fever
7;

Gastrointestinal
Incubation

Week 1

Week 2

Constipation

Very
common

Common

Diarrhea

Rare

Common (pea soup)

Bloating
with
tympany

Very
common
(84%)[30]

Diffuse mild
abdominal
pain

Very
common

Sharp right
lower
quadrant
pain

Rare

Gastrointest
inal
hemorrhage

Very rare;
usually
trace

intestinal
perforation
Hepatosplen

Week 3

Very common

Rare
Common

ETIOLOGY

Salmonella
Salmonella
Salmonella
Salmonella

typhi
Paratyphi A
paratyphi B
chloreasuis

Diagnose

1. Microbiology diagnose most


specific > 90%
2. Serologic diagnose Widal test
(+) if : titer 1/200
3. Clinical diagnose
First week fever, headache,
mialgia, anoreksia, nausea, vomiting,
constipation, diarrhea.
Second week hepatomegaly,
splenomegaly, comma,
neuropsiciatry disorder

Diagnose
LAB diagnose
Rutine check

-SGOT and SGPT increase


-leukositosis (aneusinofilia and limfopenia)
- LED increase

WIDAL TEST

Aglutination reaction between S. Typhii (antigen) with


antibody (aglutinin)

TUBEX test

Detect antibody anti S.Typhi 09 in the serum of


patient

Typhidot
TEST

Antibody IGM and IG G in the outer membran of


salmonela typhi

IGM dipstick
test

Antibody IGM specific S.Typhii in the whole blood


serum

Blood culture

Positive if typhoid fever but can be negative too

Therapy
Non farmaco
Rest and therapy
Diet

farmaco
DOSIS

ES

kloramfeniko 4x500 mg /Hari (oral/IV)


l

Anemia aplastik

tiamfenikol

4x500 mg/Hari

Anemia aplastik

klotrimoksaz
ole

2x 2 tablet (sulfametoksazole 400 mg


dan 80 mg trimetroprim)

ampisilim

50-150 mg/KgBB

sefalosporin

3-4 gram dalam dekstrosa 100 cc


diberikan jam infus

Complication
Complicatio
n
-Bleeding intestinal
Intestinal
-Perforation
Non intestinal Hepatitis tifosa
Pankreatitis tifosa
Complication hematology
Miokarditis
neuropsikiatrik

PREVENTION

Choose food processed for safety


Prepare food carefully
Keep food contact surfaces clean
Eat cooked food as soon as possible
Maintain clean hands
Steam or boil shellfish at least 10 minutes
All milk and dairy products should be
pasteurized
Control fly populations

Prevention of typhoid fever


1. Avoid risky foods and drinks.
2. Get vaccinated against typhoid
fever.
Remember that you will need to
complete your vaccination at least 1
week before you travel so that the
vaccine has time to take effect!!
Taking antibiotics will not prevent
typhoid fever; they only help treat it.

Typhoid Vaccines Available in the United States


Total Time
Vaccine
Needed to Set
How Given Doses
Name
Aside For
Vaccination
Ty21a

1 capsule
per oral

0.50 mL
ViCPS Intramuscul
ar Injection

2 weeks

2 weeks

Dosing
interval

2 days

Booster
Minimum
Needed
Age
Every...

6 years

5 years

Not applicable 2 years

2 years

Treatment of complication
3. Toxic myocarditis:
bed rest
cardiac muscle protection drugs,
dexamethasone, digoxin.

Differentials

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

Malaria
Malaria, which predominantly occurs
in tropical areas, is a potentially lifethreatening disease caused by
infection with Plasmodium protozoa
transmitted by an infective female
Anopheles mosquito vector.

Causes
The 4 Plasmodium species known to
cause malaria include
P falciparum (the most deadly),
P vivax,
P ovale, and
P malariae.
A fifth species, P knowlesi, has recently
been identified in Southeast Asia as a
clinically significant pathogen in humans

Severe malaria manifests as follows:


Cerebral malaria: This feature is almost always
caused by P falciparum infection.
Severe anemia: The anemia associated with
malaria is multifactorial and is usually
associated with P falciparum infection.
Renal failure: This is a rare complication of
malarial infection.
Respiratory symptoms: Patients with malaria
may develop metabolic acidosis and
associated respiratory distress.

Table. Histologic Variations Among


Plasmodium Species
P
falciparum

P vivax

P ovale

P malariae

Yes

No

No

No

Multiplyinfected
RBCs

Often

Occasionally

Rare

Rare

Age of
infected
RBCs

RBCs of all
ages

Young RBCs

Young RBCs

Old RBCs

No

Yes

Yes

No

Findings
Only early
forms
present in
peripheral
blood

Schffner
dots
Other
features

Cells have
thin

Late
Infected
trophozoites RBCs

Bandlike
trophozoites

Malaria treatment
The following is a summary of general
recommendations for the treatment of malaria:
P falciparum malaria
Quinine-based therapy - Quinine (or quinidine) sulfate plus
doxycycline or clindamycin or pyrimethamine-sulfadoxine
Alternative therapies - Artemether-lumefantrine, atovaquoneproguanil or mefloquine

P falciparum malaria with known chloroquine susceptibility


(only a few areas in Central America and the Middle East) Chloroquine
P vivax, P ovale malaria - Chloroquine plus primaquine
P malariae malaria - Chloroquine
P knowlesi malaria Recommendations same as those for
P falciparum malaria

Dengue
Dengue is transmitted by mosquitoes
of the genus Aedes, which are widely
distributed in subtropical and tropical
areas of the world, and is classified
as a major global health threat by
the World Health Organization

Causes
Dengue infection is caused by 1 of
the 4 dengue viruses (ie, DENV-1,
DENV-2, DENV-3, DENV-4) and is
transmitted to humans by the bite of
an infected mosquito.

Physical
The PAHO has developed the
following case definitions for the
diagnosis of dengue fever and
dengue hemorrhagic fever or
dengue shock syndrome

Dengue fever
The clinical description of dengue fever is
an acute febrile illness of 2-7 days duration
associated with 2 or more of the following:
Severe headache
Retroorbital pain
Severe myalgias
Arthralgia
Characteristic rash
Hemorrhagic manifestations
Leukopenia

Laboratory criteria for diagnosis include one or more of


the following:
Isolation of the dengue virus from serum, plasma,
leukocytes, or autopsy samples
Demonstration of a 4-fold or greater change in reciprocal
immunoglobulin G (IgG) or immunoglobulin M (IgM) antibody
titers to one or more dengue virus antigens in paired serum
samples
Demonstration of dengue virus antigen in autopsy tissue via
immunohistochemistry or immunofluorescence or in serum
samples via enzyme immunoassay (EIA)
Detection of viral genomic sequences in autopsy tissue,
serum, or cerebral spinal fluid (CSF) samples via polymerase
chain reaction (PCR)

Cases are classified as probable if they are


compatible with the clinical definition and
satisfy one or more of the following
criteria:
Supportive serology (reciprocal
hemagglutination-inhibition antibody titer
greater than 1280, comparable IgG EIA titers,
or positive IgM antibody test in late acute or
convalescent-phase serum specimen)
Occurrence at the same location and time as
other confirmed cases of dengue fever

Dengue hemorrhagic fever


Criteria for the diagnosis of dengue
hemorrhagic fever include :
A positive result from the tourniquet test
Petechiae, ecchymoses, or purpura
Bleeding from the mucosa,
gastrointestinal tract, injection sites, or
other sites
Hematemesis or melena and
thrombocytopenia (< 100,000 cells/L)

Dengue shock syndrome


Dengue shock syndrome is diagnosed in cases
meeting all of the above criteria plus evidence
of circulatory failure, such as the following:
Rapid, weak pulse
Narrow pulse pressure (< 20 mm Hg), with
increased peripheral vascular resistance (PVR) and
elevated diastolic pressure
Hypotension
Cool, clammy skin
Altered mental status, although the patient may
initially remain alert

Imaging test:
Chest radiography: Right-sided pleural effusion is typical
Ultrasonography

Lab test :
Basic metabolic panel findings include : Hyponatremia,
Metabolic acidosis, Elevated BUN levels
Complete blood cell count findings include the following:
Leukopenia, often with lymphopenia, is observed near the end
of the febrile phase of illness.
A hematocrit level rise of greater than 20% is a sign of
hemoconcentration and precedes shock.
Thrombocytopenia has been demonstrated in up to 50% of
dengue fever cases.

Other Tests
Arterial blood gas should be assessed
in patients with severe cases to
assess pH, oxygenation, and
ventilation.

Medication
Aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), and
corticosteroids should be avoided.

Analgesics/antipyretics
The treatment of dengue fever is
symptomatic and supportive in nature.
Bedrest and mild analgesic-antipyretic
therapy are often helpful in relieving
lethargy, malaise, and fever associated
with the disease.
Example :
Acetaminophen (Tylenol, Feverall)
Contraindications : Hypersensitivity, Hepatitis or
hepatic/renal dysfunction, alcoholism

Volume expanders
Plasma volume expanders are used in the treatment of
intravascular volume deficits or shock to restore
intravascular volume, blood pressure, and tissue perfusion.
Example:
Dextran 40 (Macrodex, LMD) ,
Contraindications: Hypersensitivity to dextran or corn products,
Pulmonary edema, severe bleeding disorders, severe CHF, severe
oliguria/anuria d/t renal dz, significant hemostatic defects, cardiac
decompensation

Albumin (Albuminar-5, Buminate)


Contraindications: Hypersensitivity to commercially available albumin
products, Severe anemia, cardiac failure

Starch (hetastarch, 6% hydroxyethyl starch)


Contraindications: Hypersensitivity to hetastarch, Severe bleeding
disorders, severe CHF, severe renal failure

Hepatitis
Hepatitis (plural hepatitides) is the
inflammation of the liver and
characterized by the presence of
inflammatory cells in the tissue of
the organ.

Causes
Acute
Viral hepatitis: Hepatitis A, B, C, D, and E, Yellow fever, KIs-V,
adenoviruses
Non-viral infection : toxoplasma, Leptospira, Q fever, rocky
mountain spotted fever
Alcohol
Toxins : Amanita toxin in mushrooms, carbon tetrachloride,
asafetida
Drugs : Paracetamol, amoxycillin, antituberculosis medicines,
minocycline
Ischemic hepatitis
Pregnancy
Auto immune conditions, e.g., Systemic Lupus Erythematosus (SLE)
Metabolic diseases, e.g., Wilson's disease

Chronic
Alcohol
Drugs :
methyldopa
nitrofurantoin
isoniazid
ketoconazole

Symptoms

profound loss of appetite,


aversion to smoking among smokers,
dark urine,
yellowing of the eyes and skin (i.e.,
jaundice)
abdominal discomfort.

Complications
Esophageal varices (enlarged veins
in the wall of the esophagus that can
cause life-threatening bleeding)
Hepatic encephalopathy (confusion
and coma) and
Hepatorenal syndrome (kidney
dysfunction).

Shigella sp.
Group A: Shigella dysenteriae (or Shiga
bacillus, 13 serotypes) developed
country
Group B: Shigella flexneri (6 serotypes,
15 subtypes)
Group C: Shigella boydii (18 serotypes)
Group D: Shigella sonnei (1 serotype)

Epidemiology
International
Shigellosis occurs worldwide, and it tends to
occur whenever war, natural calamities (eg,
earthquakes, floods), or unhygienic living
conditions result in overcrowding and poor
sanitation.
S boydii and S dysenteriae occur more
commonly internationally.
Disease from Shigella species causes an
estimated 1 million deaths and 165 million
cases of diarrhea annually worldwide.

Invasion of the
Underlying Tissue

Intercellular dissemination facilitated by the

IpaB protein lyses the plasma membrane.


The infected host cells produce an inflammatory

(IL-8, IL-10) chemotaxis of polymorphonuclear


leukocytes disruption of the epithelial barriers
integrity disruption of epithelial absorption
the characteristic diarrhea and abdominal cramps.
Shigella may cause mucosal destruction in the

form of ulcerations of the colonic mucosa


the presence of blood in the stools.

Causes
S sonnei and S flexneri cause 90% of
the cases of shigellosis.
S dysenteriae has produced epidemic
shigellosis.

Physical

Lower abdominal tenderness


Normal or increased bowel sounds
Dehydration (occasional)
Acute bloody diarrhea[3]
Crampy abdominal pain
Tenesmus
Passage of mucus
Fever (1-3 d after exposure)
Occasionally vomiting (35% prevalence)
Self-limited course (3 d to 1 wk and rarely lasts as
long as 1 mo)

Laboratory Test
Fecal leukocytes and erythrocytes
Mildly elevated hematocrit, sodium,
and urea nitrogen are indicative of
volume depletion in cases of
shigellosis.
Leukocytosis is rare.
Positive findings on stool culture of a
fresh fecal specimen

Gastroenteritis
Gastroenteritis is a condition that causes
irritation and inflammation of the stomach
and intestines
It can be transferred by contact with
contaminated food and water.
The inflammation is caused most often by
an infection from certain viruses or less
often by bacteria, their toxins (e.g. SEB),
parasites, or an adverse reaction to
something in the diet or medication.

Epidemiology
Every year, worldwide, rotavirus in
children under 5 causes 111 million
cases of gastroenteritis and nearly
half a million deaths.
82% of these deaths occur in the
world's poorest nations

Caused
Virus : norovirus, rotavirus, adenovirus,
astrovirus, parvovirus
Bacteria : Escherichia coli, Clostridium
difficile, Salmonella, Shigella and
Campylobacter
Parasites and Protozoans :
Cryptosporidium (Crypto), giardia
Chemical toxins, most often found in
seafood, food allergies,
antibiotics

Symptoms and signs

Nausea and vomiting


Dehydration
Diarrhea
Loss of appetite
Fever
Headaches
Abnormal flatulence
Abdominal pain
Abdominal cramps
Bloody stools (dysentery - suggesting infection by amoeba,
Campylobacter, Salmonella, Shigella or some pathogenic strains
of Escherichia coli)
Fainting and Weakness
Heartburn

Diagnosis
Gastroenteritis is often self-limiting,
and the care is supportive to control
symptoms and prevent dehydration.
Tests may not be needed.
If the symptoms persist for a
prolonged period of time, the health
care practitioner may consider blood
and stool tests to determine the
cause of the vomiting and diarrhea.

Complications
Dehydration
Diarrhea
Malabsorption of lactose

Leptospirosis
Leptospirosis is a disease known to
cause heating up and causing
redness of the hands.
It is caused by infection with bacteria
of the genus Leptospira, and affects
humans as well as other mammals,
birds, amphibians, and reptiles.

Epidemiology
Annual rates of infection vary from
0.02 per 100,000 in temperate
climates to 10 to 100 per 100,000 in
tropical climates.

Etiology
Leptospirosis is caused by a
spirochaete bacterium called
Leptospira spp.
There are at least five serovars of
importance in the United States and
Canada, all of which cause disease in
dogs (Icterohaemorrhagiae, Canicola,
Pomona, Grippotyphosa, and
Bratislava).

Complications

meningitis,
extreme fatigue,
hearing loss,
respiratory distress,
azotemia, and
renal interstitial tubular necrosis,
which results in renal failure and
often liver failure

Symptoms

High fever,
Severe headache,
Chills,
Muscle aches, and
Vomiting , and
may include jaundice, red eyes,
abdominal pain, diarrhea, and rash.

Diagnosis
Enzyme-Linked Immunosorbent
Assay (ELISA) and
Polymerase chain reaction (PCR).
Serological testing, the MAT
(microscopic agglutination test), is
considered the gold standard in
diagnosing leptospirosis.

Prevention and treatment


Doxycycline may be used as a prophylaxis
200250mg once a week, to prevent infection
in adventure travelers to high risk areas.
Treatment is a relatively complicated process
comprising two main components:
suppressing the causative agent
fighting possible complications

Aetiotropic drugs are antibiotics, such as


cefotaxime, doxycycline, penicillin, ampicillin,
and amoxicillin.

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