LO 1

 Able to know and explain about Gastroenteritis

Diarrhea
• Rapid movement of fecal matter through the
intestines resulting in poor absorption of
water, nutritive elements, and electrolytes and
producing abnormally frequent watery bowel
movements. (dorland)
• Increased stooling, with stool consistency less
solid than normal, constitutes a satisfactory, if
somewhat imprecise (clevelandclinic)
Types of diarrhea
Acute, persistent, &
chronic diarrhea
• Acute diarrhea is defined as a greater number
of stools of decreased form from the normal
lasting for less than 14 days.
• If the illness persists for more than 14 days, it
is called persistent.
• If the duration of symptoms is longer than 1
month, it is considered chronic diarrhea.
Osmotic diarrhea

• osmotic force that acts in the lumen to drive

water into the gut (caused by hyperosmotic
drugs (MgSO4, Mg(OH)2), malabsorption,
defect in mucosal absorption (disacharide
deficiency, glucose/galactose malabsorption)
Secretory diarrhea
• increase in the active secretion
• inhibition of absorption.
• The most common cause of this type of
diarrhea is a cholera toxin that stimulates the
secretion of anions, especially chloride ions.
Inflammatory diarrhea
• Damage to the mucosal lining or brush
borderpassive loss of protein-rich fluids, and a
decreased ability to absorb these lost fluids.
• Features of all three of the other types of diarrhea
can be found in this type of diarrhea.
• It can be caused by bacterial infections, viral
infections, parasitic infections, or autoimmune
problems such as inflammatory bowel diseases.
• It can also be caused by tuberculosis, colon cancer,
and enteritis.
Exudative diarrhea
• Exudative diarrhea occurs with the presence
of blood and pus in the stool. This occurs with
inflammatory bowel diseases, such as Crohn's
disease or ulcerative colitis, and other severe
infections
 Ethiology (infectious)
Host Cause

E. coli and viruses such as rotavirus, Minimal to moderate mucosal inflammation

Norwalk agent, and HIV

Shigella, enteroinvasive E. coli Bacteria that destroy entherocytes

Entamoeba Histolytica, Salmonella, that penetrate the mucosa, result in

Campylobacter jejuni, and Yersinia moderate to severe inflammation with or
enterocolitica without ulceration.
B. cereus, S. aureus, and Clostridium Ingestion of preformed toxin produced by
perfringens bacteria can result in acute jejunitis.

Aeromonas, Shigella, and Vibrio spp. (e.g., produce enterotoxins and also invade the
V. parahaemolyticus) intestinal mucosa.

Clostridium difficile and hemorrhagic E. coli produce inflammation from cytotoxins

0157:H7
ESCHERICHIA COLI
• Five classes of e. coli
– Enterotoxigenic E. coli (ETEC)
– Enteroinvasive E. coli (EIEC)
– Enteropathogenic E. coli (EPEC)
– Enterohemorrhagic E. coli (EHEC)
– Enteroaggregative E. coli (EAEC)
Ethiology (noninfectious)
• Inflammatory bowel disease
• Irritable bowel syndrome
• Ischemic bowel disease
• Partial small bowel obstruction
• Pelvic abscess in the rectosigmoid area
• Fecal impaction
• The ingestion of poorly absorbable sugars, such as
lactulose and acute alcohol ingestion.
Ethiology (noninfection)
 Bacteri Shigella, Salmonella, E.Coli, Gol. Vibrio, Bacillus cereus
E Clostridium perfringens, Stafilokokus aureus, Campylobacter aeromonas
T
H Infection Viral Rotavirus, Norwalk/Norwalk like agent, Adenovirus
Protozoa, Entamoeba histolytica, Giardia lamblia, Balantidum coli
I
O Cacing perut, Ascaris, Trichiuris, Strongyloides
Parasite
L Jamur, Candida

O
G
Carbohydrate Disakarida (laktosa, maltosa, sukrosa)
Y Monosakarida ( glucosa, fructosa, galactosa)
Malabsorpsi Fat Especially Long Chain trigyceride
O
F Asam amino, B lactoglobulin
Protein

D Food : spoiled food

I
A Poisoned : poisounous food (bacteri : Clostridium botulinum, Stafilokokus)
R mixture food poison (chemical)
R Konstitution : Kwashiorkor, Marasmus
H Allergic : milk allergy, food allergy, cow’s milk protein sensitive enterophaty (CMPSE)
E
Imunodeficiency
A
Other reason (psikis)
Mechanism of Diarrhea
Pathogenesis of
infectious diarrhea
Pathogenesis diarrhea-
antibiotic cause
DIARRHEA – ANATOMIC
CLASSIFICATION
 Pathophysiology
•Viruses injure the absorptive surface of mature
villous cells,resulting in decreased fluid absorption
and dissacharidase deficiency.
•Bacteria produce intestinal injury by directly
invading the mucosa,damaging the villous surface or
releasing toxin.
 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.
Bacterial infection
 Entamoeba histolytica
• Although many species of amoeba exist, only E. histolytica is
clearly pathogenic. Transmission occurs by fecal contamination
of food or water. Infection is endemic throughout the world,
especially where poor sanitation exists.
• Clinical manifestations :
– Diarrhea (with blood & mucus)
– Abdominal pain / acute colitis with abdominal cramps,
• Diagnosis is usually made by identification of cysts or
trophozoites in stool. Serology also may be helpful,particularly
with diagnosis of extraintestinal amebiasis and
liverinvolvement.
 Strongyloides stercoralis
• This roundworm,2.5 mm in length, is endemic in southern U.S.
and common in tropicsand Asia.
• Clinical manifestation:
– Skin becomes red and pruritic after penetration by larvae, which usually
occurs on feet.
– Diarrhea,
– Vomiting
– Abdominal pain
– Cough and pneumonia after migration of larvae through lung scan
– Peripheral eosinophilia may occur.
• Identification of larvae in stool isdiagnostic.
 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 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.
 Clinical Features of Diarrheal Diseases
Location of Infection
Small Bowel Large Bowel
V. cholerae Shigella
ETEC, EPEC, EAggEC EIEC, EHEC
Rotavirus Campylobacter
Norwalk virus E. histolytica
Pathogens Giardia

Location of pain Midabdomen Lower abdomen, rectum

Volume of stool Large Small

Type of stool Watery Mucoid

Blood in stool Rare Common

Common (except in
Leukocytes in stool Rare amebiasis)
Mucosal ulcers;
Protoscopy Normal hemorrhage; friable mucos
 How is the cause of
diarrhea diagnosed?
Diagnostic tests to find the cause of diarrhea may include
the following:
• 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 diarrhea responds to a
change in diet.
• 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.
Treatment and therapy
acute diarrhea
• Antidiarrheal medication are ineffective (kaolin-
pectin combination) or even dangerous (Loperamid,
tincture of opium, diphenoxylate with atropin)
• Bismuth subsalycilate preparation may reduce stool
volume but are not critical to recovery.
• Oral immunoglobulin or specific antiviral agents have
occasionally been useful in limiting duration of
disease in immunocompromised patients.
Therapy
Therapy
Complication of
Diarrhea
• Hypernatremia
• Hyponatremia
• Fever
• Oedem/overhydration
• Asidosis
• Hypokalemia
• Paralyticus ileus
• Cramp
• Lactose Intolerance
• Glucose Malabsorption
• Renal failure
Prevention of Diarrhea
• Breastfeeding
• Improved feeding practices
• Use of safe water
• Handwashing
• Food safety
• Use of latrines and safe disposal of stools
• Measles immunization
 Dehydration
• The body needs the correct amount of water and
electrolytes (salts) to function properly.
• Diarrhea causes excess loss of fluids and essential
electrolytes from the body. When fluid lost in the
stools is not replaced, diarrhea can lead to
dehydration (abnormally low water content in the
body).
• Dehydration can be a life-threatening complication of
diarrhea for some individuals, especially infants,
small children and elderly people
Assessment of
Dehydration
Treatment of
Dehydration
 LO 2
 Able to know and explain about Typhoid Fever
 Definition
“also known as enteric fever, is a potentially
fatal multisystemic illness caused primarily by
Salmonella typhi. The protean manifestations
of typhoid fever make this disease a true
diagnostic challenge”

-Medscape
Typhoid epidemiology
• 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 long-term 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
Etiology
 Structure and Physiology
• Gram-negative, non–spore-forming bacilli.
• Ferment glucose, maltose, and mannitol but not
lactose or sucrose. (TSIA test: -/+)
• Reduce nitrates and do not produce cytochrome
oxidase.
• Does not produce gas (Almost all salmonellae
produce gas with fermentation).
• Motile by means of peritrichous flagella
• Resistant to sodium deoxycholate, brilliant green,
sodium tetrathionate (all can reduce other enteric
bacteria growth)
 Antigen
• Salmonella typhi has 3 kind of antigen:
– Flagella antigen (H): survive up to 60⁰C, to alcohol
and acid. IgG is the antibody against this antigen
– Somatic antigen (O): located in outer membrane,
survive up to 100⁰C, to alcohol and acid. IgM is the
antibody against this antigen
– Vi antigen: located on O antigen, prevent
phagocytosis, survive up to 60⁰C, not resistant to
alcohol and acid
 A schematic diagram of a single Salmonella typhi cell
showing the locations of the H (flagellar), 0 (somatic), and Vi
(K envelope) antigens.
 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)3
 Risk factor
• 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
 Sign and symptoms
First week of illness
Once signs and symptoms do appear, you're likely to experience:
• Fever, often as high as 103 or 104 F (39.4 or 40 C)
• Headache
• Weakness and fatigue
• Sore throat
• Abdominal pain
• Diarrhea or constipation
• Rash
• Children are more likely to have diarrhea, whereas adults may become
severely constipated
• During the second week, you may develop 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
• Either diarrhea that has the color and consistency of pea soup, or severe
constipation
• Considerable weight loss
• Extremely distended abdomen

Third week of illness

By the third week, you may:
• Become delirious
• Lie motionless and exhausted with your eyes half-closed in what's known
as the typhoid state
• Life-threatening complications often develop at this time

Fourth week of illness

Improvement may come slowly during the fourth week. Your fever is likely
to decrease gradually until your temperature returns to normal in another
week to 10 days. But signs and symptoms can return up to two weeks
after your fever has subsided
 Incidence and Timing of Various Manifestations of Untreated
Typhoid Fever
Incubation Week 1 Week 2 Week 3 Week 4 Post

Systemic Recovery 10%-20%

phase or relapse; 3%-
Stepladder Very Very common death (15% 4% chronic
fever pattern common of untreated carriers;
or insidious cases) long-term
onset fever neurologic
sequelae
(extremely
Acute high Very rare rare);
fever gallbladder
cancer
Chills Almost all
(RR=167;
carriers)
Rigors Uncommon

Anorexia Almost all

Diaphoresis Very common

 Incubation Week 1 Week 2 Week 3 Week 4 Post

Neurologic
Malaise Almost all Almost all Typhoid state
Insomnia Very (common)
common
Confusion/de Common Very
lirium common
Psychosis Very rare Common
Catatonia Very rare

Frontal Very
headache common
(usually mild)

Meningeal Rare Rare

signs
Parkinsonism Very rare

Ear, nose, and throat

Coated Very
tongue common
Sore throatf
 Incubation Week 1 Week 2 Week 3 Week 4 Post

Pulmonary

Mild cough Common

Bronchitic Common
cough
Rales Common

Pneumonia Rare (lobar) Rare Common

(basal)
Cardiovascular

Dicrotic pulse Rare Common

Myocarditis Rare

Pericarditis Extremely
rareg
Thrombophleb Very rare
itis
 Incubation Week 1 Week 2 Week 3 Week 4 Post

Gastrointestinal

Constipation Very common Common

Diarrhea Rare Common (pea soup)

Bloating with Very common

tympany (84%)

Diffuse mild Very common

abdominal pain

Sharp right lower Rare

quadrant pain

Gastrointestinal Very rare; Very common

hemorrhage usually trace

intestinal Rare
perforation
Hepatosplenome Common
galy
Jaundice Common

Gallbladder pain Very rare

 Incubation Week 1 Week 2 Week 3 Week 4 Post

Urogenital

Urinary Common
retention

Hematuria Rare

Renal pain Rare

Musculoskeletal

Myalgias Very rare

Arthralgias Very rare

Rheumatologic

Arthritis (large Extremely rare

joint)

Dermatologic

Rose spots Rare

Miscellaneous

Abscess Extremely Extremely Extremely rare

(anywhere) rare rare
 Pathophysiology
intestine
IgA immune response is less
well
Salmonella breed

DIE
macrofag
Penetrate the epithelial
cells and proliferate in Plaque peyeri
the lamina propia Survive

KGB
mecenterica

Organ
RE
Leaving
the
phagocyt
e cells Torasikus
bacteremia duct
 Pathophysiology
Systemic Bakteriremi Breed in the
phagocyt
symptom a II extracellular es cell
organ

gall
Liver bladder

hypera Macrofag
already Penetrate more Intestinal
ctive
and reactions as
activated lumen
previously

hypersensitivity
Releasing cytokines Symptoms reactions
feces
Reaction hiperplasi plaque Hyperplasia or
peyeri necrosis

Erosion of blood vessels Accumulation in

GI bleeding inflammatory bowel
mononuclear

Penetrate the mucosa and

The process continues Perforation
muscle layer
 Laboratory Examination
1. Routine examination
• Complete Perifer Blood test
– mostly leucopenia (possibly normal leukocytes or
leukocytosis)
• Mild anemia and trombositopenia
• Leukocytes count : aneosinofilia and limfopenia
• LED : increased
• SGOT,SGPT : increased
2. Widal test  used to determine the existency of
aglutinin in the patient’s serum
- Aglutinin O (from bacteria’s body)
- Aglutinin H ( bacteria’s flagela ) To diagnose
- Aglutinin Vi (simpai kuman )

Factors that affect Widal test:

- Premature treatment of antibiotic
- Disability of develop antibodies and corticosteroid
treatment
- Time of blood taking
- History of vaccination
- Anamnestic reaction ( caused by past typhoid infection)
- Examination tecnic of the laboratorium
3. Blood culture
• Positif (+) result  typhoid fever +
• Negative (-) result  possibility of typhoid
fever, because of :
- Early antibiotic treatmentinhibits growth of
bacteria.
- Lackness of blood volume (± 5cc of blood)
- Vaccination history
 Laboratory Studies
• Culture
– The criterion standard for diagnosis of typhoid fever has long been
culture isolation of the organism. Cultures are widely considered 100%
specific.
– Culture of bone marrow aspirate is 90% sensitive until at least 5 days
after commencement of antibiotics
– Blood, intestinal secretions (vomitus or duodenal aspirate), and stool
culture results are positive for S typhi in approximately 85%-90% of
patients with typhoid fever who present within the first week of onset
– Multiple blood cultures (>3) yield a sensitivity of 73%-97%
– Stool culture alone yields a sensitivity of less than 50%, and urine
culture alone is even less sensitive
 Incubation Week Week Week Week
1 2 3 4
Bone marrow aspirate 90% (may decrease after 5 d of antibiotics)
(0.5-1 mL)
Blood (10-30 mL), stool, 40%-80% ~20% Variable (20%-60%)
or duodenal aspirate
culture
Urine 25%-30%, timing unpredictable
• Specific serologic tests
– Assays that identify Salmonella antibodies or antigens support the diagnosis
of typhoid fever, but these results should be confirmed with cultures or DNA
evidence.
– The Widal test was the mainstay of typhoid fever diagnosis for decades. It is
used to measure agglutinating antibodies against H and O antigens of S typhi
– Indirect hemagglutination, indirect fluorescent Vi antibody, and indirect
enzyme-linked immunosorbent assay (ELISA) for immunoglobulin M (IgM)
and IgG antibodies to S typhi polysaccharide, as well as monoclonal
antibodies against S typhi flagellin,37 are promising, but the success rates of
these assays vary greatly in the literature.
• Other nonspecific laboratory studies
– erythrocyte sedimentation rate (ESR), thrombocytopenia, and relative
lymphopenia
– elevated prothrombin time (PT) and activated partial thromboplastin time
(aPTT) and decreased fibrinogen levels
– Mild hyponatremia and hypokalemia are common
LAB EXAMINATION
TUBEX Test
To detect antibody anti-S.typhi O9 in patient’s
serum
The interpretation based on the color of the
solution (redness – bluish)

Lab test
• IgM Dipstick Test
– To detect the IgM antibodies specific to S.typhi in
serum specimen or whole blood

Lab test
 Culture of S.Tyhpi
• Selected media : EMB , McConkey , SS
(salmonella-shigella) , XLD and TSIA (triple
sugar iron agar)
• Result :
– Colorless colony in McConkey
– TSIA, result : -/+ (H2S without gas)
McConkey (left) XLD

SS TSIA
 Imaging Studies
• Radiography: Radiography of the kidneys, ureters, and
bladder (KUB) is useful if bowel perforation (symptomatic
or asymptomatic) is suspected.
• CT scanning and MRI: These studies may be warranted to
investigate for abscesses in the liver or bones, among
other sites.
 Histologic Findings
• Infiltration of tissues by macrophages (typhoid cells) that contain
bacteria, erythrocytes, and degenerated lymphocytes
• In the mesenteric lymph nodes, the sinusoids are enlarged and
distended by large collections of macrophages and
reticuloendothelial cells
• The spleen is enlarged, red, soft, and congested; its serosal surface
may have a fibrinous exudate. Microscopically, the red pulp is
congested and contains typhoid nodules
• The gallbladder is hyperemic and may show evidence of cholecystitis
• Liver biopsy specimens from patients with typhoid fever often show
cloudy swelling, balloon degeneration with vacuolation of
hepatocytes, moderate fatty change, and focal typhoid nodules
 Management
Non pharmacology
• Bed rest and treatment to prevention complication and make more
faster for healing
– Bed rest like having meal, drink, take a bath, stools
– Once in care need in taking care of cleanliness of the bed, clothes, and
equipment in use
• Diet and suporting therapy
– Some researcher show that solved food (rice with side dish low
cellose) safe for patien
• Surgical Care
– Surgery is usually indicated in cases of intestinal perforation.
– Most surgeons prefer simple closure of the perforation with drainage
of the peritoneum.
– Small-bowel resection is indicated for patients with multiple
perforations.
 Antibiotic Recommendations by Origin and Severity
Location Severity First-Line Antibiotics Second-Line Antibiotics
South Asia, East Asia 45 Uncomplicated Cefixime PO Azithromycin PO
48, 40
Complicated Ceftriaxone IV or Aztreonam IV or
Cefotaxime IV Imipenem IV
Eastern Europe, Middle Uncomplicated Ciprofloxacin PO or Cefixime PO or
East, sub-Saharan Africa, Ofloxacin PO Amoxicillin PO or
South America 46, 49 TMP-SMZ PO
or Azithromycin PO
Complicated Ciprofloxacin IV or Ceftriaxone IV or
Ofloxacin IV Cefotaxime IV or
Ampicillin IV
or
TMP-SMZ IV
Unknown geographic Uncomplicated Cefixime PO plus Azithromycin PO*
origin or Southeast Ciprofloxacin PO or
Asia 50, 45 Ofloxacin PO
48, 40, 46, 49
Complicated Ceftriaxone IV or Aztreonam IV or
Cefotaxime IV, plus Imipenem IV, plus
Ciprofloxacin IV or Ciprofloxacin IV
Ofloxacin IV or
Ofloxacin IV
 Prevention and Control
• Two typhoid vaccines are commercially available:
1. Ty21a
– An oral live attenuated S. Typhi vaccine
– Given on days 1, 3, 5, and 7, with a booster every 5
years
– Minimal age for vaccination is 6 years old
2. Vi CPS
– A parenteral vaccine consisting of purified Vi
polysaccharide from the bacterial capsule
– Given in 1 dose, with a booster every 2-3 years
– Minimal age for vaccination is 2 years old
• There is no licensed vaccine for paratyphoid fever.
Prevention and Control
Contraindication vaccination
– Ty21a:
• Allergic
• Pregnant
• ↓ immunity
Side effects
– Vaccination Ty21a
• Fever (0-5%)
• Headache (0-5%)