TUTORIAL 6

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You are a forth year medical student in ER department. Alba, a 45-year old man came with
right abdominal pain since 4 days ago. This complain was accompanied with fever in nights
and days, anorexia, nausea, and vomit.
The pain increased according the position of the body, therefore he preferred lying down to
the left position.
Last week before the pain, he had a diarrhea accompanied with blood, mucus, abdominal
cramp, and tenesmus.
Alba is man from low sosioeconomic situation, had poor hygiene and sanitation.

Questions :
1. Identify the problems!
2. Generate a list of hypothesis!

TUTOR GUIDE

1. Identify the patient’s problem

The problems are:
- right abdominal pain
Fever
Anorexia, nausea, vomit
- Bloody diarrhea with mucus
Tenesmus , abdominal cramp

Review:
Problem 1 : Bloody and mucus-laden diarrhea
The students should be guided (reminded) about dysentery-form diarrhea.

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Guiding questions for tutor to focus on dysenteri-form diarrhea (refer to GI system):

- What is the term or characteristics of dysentery-form diarrhea?

A dysenteri-form diarrhea is a term for diarrhea that characterizied by bloody and
mucus stooling, usually is accompanied by abdominal pain and tenesmus. It also can
be accompanied by fever.

- What is the most common cause of dysentery-form diarrhea?

Dysenteri-form diarrhea can be caused by:
1. Bacterial infection: Shigella dysentriae, Salmonella spp., Campylobacter
jejuni, Yersinia enterocolica, enteroinvasive E. coli (EIEC) or
enterohemorhagic E coli (EHEC)
2. Protozoal infection : Entamoeba histolytica, Balantidium coli
3. Inflammatory bowel disease: particularly if chronic feature

Main Discussion
‘Problem 2 and 3 : Right abdominal pain and fever.
The student should be asked (guided), whether abdominal pain and fever are
1. concomitant symptoms (signs) or some complication according to the
dysentry form diarrhea?

2. Different Diagnosis with same complain Such as hepatoma, acute

cholecystitis,paracytic cyst, pyogenic abcess, pulmonary and subphrenic
absesses e.c bacteria.

3. Hepatic ambiasis
The most common symptom is abdominal pain, which is sharp pain increasing
with the position of the body.
There is a high fever continuously in 90% pf this patient.
Right lobe abcess will result pain that radiating to the neck, back, right shoulder.

Patogenesis
Parasit ability to produce proteolytic enzime made the trophozoit virulent, strated to
invade the intestinal mucosa. It can then established extra intestinal infection though the
portal vein, and most commonly at liver. Depression to the mucus blanket,trophozoites
attach to the cell of interglandular epithelium, with the help of the proteolytic enzymes
that degrades elastin,collagen, fibronectin, especially cyctein proteinase, phospolipase,
and hemolysin, they invade the colonic eptheliumby disruption of extra celullar matrix.
. The trophozoites invade the submucosa and spread out laterally, creating the classic
flask-shaped amebic ulcer.
Histopathology shows necrotic areas and vascular congestion. There is little
inflammation in contrast with the extension of the lesion. The amoebas may be found in
the surface layer of the ulcers or in adjacent sites [14]. Invading the small vessels of
submucosa, the trophozoites gain access to the superior mesentery, and disseminating

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 throughout the blood stream, they reach the portal system to cause microembolus and
infarction of small vascular branches. Resisting complementmediated lysis, the
trophozoites pass to the liver, causing areas of focal necrosis.

Amebic lysis of neutrophils at the edge of the lesion, releases mediators, and this leads
to hepatocyte death, extending the damage to distant hepatic cells and increasing the
number of small lesions that coalesce to develop a larger hepatic lesion, which is
unsuitably named the amebic abscess. The content of its central cavity is a thick, clotty
exudate. This is generally homogeneous, and varies in color, ranging from creamywhite
to dirty brown and pink, similar to “anchovy sauce”.

Clinical manifestasion

Some days or months after the onset of classic dysentery, or as usually happens, without
any symptoms or a history of intestinal amebiasis, the clinical features begin to appear.
Despite the size and the site of the hepatic lesion, the most common symptoms are
fever, pain and hepatomegaly.
In patients with acute onset, the fever is generally present in more than 90% of the
cases. It is often very high, continuous or intermittent and accompanied by chills,
weakness and profuse perspiration. In chronic forms the fever is low and develops more
gradually, without chills or sweating. Abdominal pain is the earliest and most frequent
complaint, present in almost 100% of the patients. It starts as a feeling of heaviness, and
then becomes a sharp pain that increases according to the position of the body,
compelling the patient to find relief in bed by turning to the opposite side of the lesion.
In abscesses of the right lobe the pain is felt in the right hypochondria, in the right
subcostal area or in the cystic point, and may radiate to the shoulder, right side of the
neck
Besides these prevailing symptoms, patients may also complain of malaise, nausea,
vomiting, anorexia and weight loss. Diarrhea may be present in about 2% of the cases,
with 4 to 5 episodes per day of a watery stool, with mucus and blood, tenesmus,
abdominal cramping and distension due to potassium loss.

Clinical Syndromes

Intestinal Amebiasis

The most common type of amebic infection is asymptomatic cyst passage. Even in highly
endemic areas, most patients harbor E. dispar.

Symptomatic amebic colitis develops 2–6 weeks after the ingestion of infectious cysts. A
gradual onset of lower abdominal pain and mild diarrhea is followed by malaise, weight
loss, and diffuse lower abdominal or back pain. Cecal involvement may mimic acute
appendicitis. Patients with full-blown dysentery may pass 10–12 stools per day. The stools
contain little fecal material and consist mainly of blood and mucus. In contrast to those

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with bacterial diarrhea, fewer than 40% of patients with amebic dysentery are febrile.
Virtually all patients have heme-positive stools.

More fulminant intestinal infection, with severe abdominal pain, high fever, and profuse
diarrhea, is rare and occurs predominantly in children. Patients may develop toxic
megacolon, in which there is severe bowel dilation with intramural air. Patients receiving
glucocorticoids are at risk for severe amebiasis. Uncommonly, patients develop a chronic
form of amebic colitis, which can be confused with inflammatory bowel disease. The
association between severe amebiasis complications and glucocorticoid therapy
emphasizes the importance of excluding amebiasis when inflammatory bowel disease is
suspected. An occasional patient presents with only an asymptomatic or tender abdominal
mass caused by an ameboma, which is easily confused with cancer on barium studies. A
positive serologic test or biopsy can prevent unnecessary surgery in this setting. The
syndrome of postamebic colitis—persistent diarrhea following documented cure of amebic
colitis—is controversial; no evidence of recurrent amebic infection can be found, and re-
treatment usually has no effect.

Amebic Liver Abscess

Extraintestinal infection by E. histolytica most often involves the liver. Of travelers who
develop an amebic liver abscess after leaving an endemic area, 95% do so within 5
months. Young patients with an amebic liver abscess are more likely than older patients to
present in the acute phase with prominent symptoms of <10 days' duration. Most patients
are febrile and have right-upper-quadrant pain, which may be dull or pleuritic in nature
and may radiate to the shoulder. Point tenderness over the liver and right-sided pleural
effusion are common. Jaundice is rare. Although the initial site of infection is the colon,
fewer than one-third of patients with an amebic abscess have active diarrhea. Older
patients from endemic areas are more likely to have a subacute course lasting 6 months,
with weight loss and hepatomegaly. About one-third of patients with chronic presentations
are febrile. Thus, the clinical diagnosis of an amebic liver abscess may be difficult to
establish because the symptoms and signs are often nonspecific. Since 10–15% of patients
present only with fever, amebic liver abscess must be considered in the differential
diagnosis of fever of unknown origin (Chap. 19).

Complications of Amebic Liver Abscess

Pleuropulmonary involvement, which is reported in 20–30% of patients, is the most

frequent complication of amebic liver abscess. Manifestations include sterile effusions,
contiguous spread from the liver, and rupture into the pleural space. Sterile effusions and
contiguous spread usually resolve with medical therapy, but frank rupture into the pleural
space requires drainage. A hepatobronchial fistula may cause cough productive of large
amounts of necrotic material that may contain amebas. This dramatic complication carries
a good prognosis. Abscesses that rupture into the peritoneum may present as an indolent
leak or an acute abdomen and require both percutaneous catheter drainage and medical
therapy. Rupture into the pericardium, usually from abscesses of the left lobe of the liver,

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carries the gravest prognosis; it can occur during medical therapy and requires surgical
drainage.

Other Extraintestinal Sites

The genitourinary tract may become involved by direct extension of amebiasis from the
colon or by hematogenous spread of the infection. Painful genital ulcers, characterized by
a punched-out appearance and profuse discharge, may develop secondary to extension
from either the intestine or the liver. Both these conditions respond well to medical
therapy. Cerebral involvement has been reported in fewer than 0.1% of patients in large
clinical series. Symptoms and prognosis depend on the size and location of the lesion.

Referensi : Principles of Internal Medicine - Harrison's

4. What is your opinion about his family condition?

We must know the family condition, because it is important for guiding us to diagnosis
particularly for infectious disease. Most of contagious diseases usually occur in the
crowded and poor sanitation condition. The socioeconomic status and the number of
family member also important as risk factor or predispositon for infectious diseases
directly and also can influence the disease through nutritional status.

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Page 2

Physical examination
revealed severely ill
Composmentis BW 60 kg
VS : BP 120/80 mmHg PR: 110/mnt RR: 24/mnt T: 38.7˚C
Head : Conjungtiva slightly anemic,
Thorax : within normal limit
Abdomen : Distension, pain in upper right quadran
Liver : Palpable 2 cm bac, 1 cm bpx , smooth edge, with tenderness

Lab finding :

Blood : Hb 10 g/dl; WBC: 16.100/mm3; Platelet: 180.000/mm3; Ht: 45%

Total bilirubin: 0,6 mg%;
ALT: 50 IU/L; AST: 41 IU/L;
Urine : Within normal limit

1. Does this information change your hypothesis?

2. What further examination do you need?

Physical examination on hepatic amebiasis

thropozoit can invade the small vessel in submucosa and reach the superior mesentery
artery, and disseminating through the blod stream, enter the portal circulation and invade
the liver causing focal necrosis.

Hepatomegaly is very important sign, according the size of the abcsess.

The hepatic lesion is usually solitary, and most frequently is located in the right lobe,
situated contiguously with the liver capsule. Variable in size, in some cases it may occupy
more than 80% of the whole liver surface
This may be explained by the larger volume of the right lobe, which receives most of the
venous drainage from the right colon, a segment of the bowel frequently affected by
intestinal amebiasis

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Diagnosis

the non-invasive imaging procedures, including ultrasonography, computerized

tomography, magnetic resonance imaging and, principally serology, have dramatically
improved the clinician’s ability to promptly diagnosis hepatic amebiasis and quickly start
treatment.

Diagnostic Tests

Laboratory Diagnosis

Stool examinations, serologic tests, and noninvasive imaging of the liver are the most
important procedures in the diagnosis of amebiasis. Fecal findings suggestive of amebic
colitis include a positive test for heme, a paucity of neutrophils, and amebic cysts or
trophozoites. The definitive diagnosis of amebic colitis is made by the demonstration of
hematophagous trophozoites of E. histolytica (Fig. 202-1). Because trophozoites are killed
rapidly by water, drying, or barium, it is important to examine at least three fresh stool
specimens. Examination of a combination of wet mounts, iodine-stained concentrates, and
trichrome-stained preparations of fresh stool and concentrates for cysts (Fig. 202-2) or
trophozoites (Fig. 202-1) confirms the diagnosis in 75–95% of cases. Cultures of amebas
are more sensitive but are not routinely available. If stool examinations are negative,
sigmoidoscopy with biopsy of the edge of ulcers may increase the yield, but this procedure
is dangerous during fulminant colitis because of the risk of perforation. Trophozoites in a
biopsy specimen from a colonic mass confirm the diagnosis of ameboma, but trophozoites
are rare in liver aspirates because they are found in the abscess capsule and not in the
readily aspirated necrotic center. Accurate diagnosis requires experience, since the
trophozoites may be confused with neutrophils and the cysts must be differentiated
morphologically from Entamoeba hartmanni, Entamoeba coli, and Endolimax nana,
which do not cause clinical disease and do not warrant therapy. Unfortunately, the cysts of
E. histolytica cannot be distinguished microscopically from those of E. dispar. Therefore,
the microscopic diagnosis of E. histolytica can be made only by the detection of
Entamoeba trophozoites that have ingested erythrocytes. In terms of sensitivity, stool
diagnostic tests based on the detection of the Gal/GalNAc lectin of E. histolytica compare
favorably with the polymerase chain reaction and with isolation in culture followed by
isoenzyme analysis.

Serology is an important addition to the methods used for parasitologic diagnosis of

invasive amebiasis. Enzyme-linked immunosorbent assays (ELISAs) and agar gel
diffusion assays are positive in more than 90% of patients with colitis, amebomas, or liver
abscess. Positive results in conjunction with the appropriate clinical syndrome suggest
active disease because serologic findings usually revert to negative within 6–12 months.
Even in highly endemic areas such as South Africa, fewer than 10% of asymptomatic
individuals have a positive amebic serology. The interpretation of the indirect
hemagglutination test is more difficult because titers may remain positive for as long as 10
years.

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Up to 10% of patients with acute amebic liver abscess may have negative serologic
findings; in suspected cases with an initially negative result, testing should be repeated in
a week. In contrast to carriers of E. dispar, most asymptomatic carriers of E. histolytica
develop antibodies. Thus, serologic tests are helpful in assessing the risk of invasive
amebiasis in asymptomatic, cyst-passing individuals in nonendemic areas. Serologic tests
also should be performed in patients with ulcerative colitis before the institution of
glucocorticoid therapy to prevent the development of severe colitis or toxic megacolon
owing to unsuspected amebiasis.

Routine hematology and chemistry tests usually are not very helpful in the diagnosis of
invasive amebiasis. About three-fourths of patients with an amebic liver abscess have

leukocytosis (>10,000 cells/ L); this condition is particularly likely if symptoms are
acute or complications have developed. Invasive amebiasis does not elicit eosinophilia.
Anemia, if present, is usually multifactorial. Even with large liver abscesses, liver enzyme
levels are normal or minimally elevated. The alkaline phosphatase level is most often
elevated and may remain so for months. Aminotransferase elevations suggest acute
disease or a complication.

Radiographic Studies

Radiographic barium studies are potentially dangerous in acute amebic colitis. Amebomas
are usually identified first by a barium enema, but biopsy is necessary for differentiation
from carcinoma.

Radiographic techniques such as ultrasonography, CT, and MRI are all useful for detection
of the round or oval hypoechoic cyst. More than 80% of patients who have had symptoms
for >10 days have a single abscess of the right lobe of the liver (Fig. 202-4).
Approximately 50% of patients who have had symptoms for <10 days have multiple
abscesses. Findings associated with complications include large abscesses (>10 cm) in the
superior part of the right lobe, which may rupture into the pleural space; multiple lesions,
which must be differentiated from pyogenic abscesses; and lesions of the left lobe, which
may rupture into the pericardium. Because abscesses resolve slowly and may increase in
size in patients who are responding clinically to therapy, frequent follow-up
ultrasonography may prove confusing. Complete resolution of a liver abscess within 6
months can be anticipated in two-thirds of patients, but 10% may have persistent
abnormalities for a year.

Referensi : Principles of Internal Medicine - Harrison's

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Page 3

Fresh stool examination revealed bloody stool, some mucus, fully bad odor, no bacteria, a few
of fecal leukocytes, and some trophozoites as shown in figure below.

SLIDES FROM PARASITOLOGY DEPARTMENT

(figure of trophozoite of E histolytica)

Questions :
1. What is your diagnosis now?
2. What is the etiology of amebiasis?
3. Can you describe about the epidemiology of amebiasis?
4. What is the pathophysiology of amebiasis?
5. What is the properly management?
6. What is your opinion about his younger sibling and his mother?
7. What is the course or prognosis of amebiasis?

1. What is your diagnosis now?

Hepatic Amebiasis

1. What is the etiology of this disease?

2. Can you describe about the epidemiology of this disease?
3. What is the pathogenesis/pathophysiology of this disease?
4. What is the properly management?
5. What is the other complication?
6. How the course or prognosis of amebiasis?
7. How to prevent or control this disease?

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 2. What is the etiology of amebiasis?
Amebiasis is a parasitic infection caused by the protozoon Entamoeba histolytica. It is
the third leading parasitic cause of death worldwide, surpassed only by malaria and
schistosomiasis. The parasite exists in 2 forms: a motile form, called the trophozoite, and a
cyst form, responsible for the person-to-person transmission of infection. The trophozoite
of E histolytica inhabits the large intestine to produce lesions of amebic colitis. Invasion of
the colonic mucosa leads to dissemination of the organism to extracolonic sites,
predominantly the liver. Faced with an adverse colonic environment, the trophozoite
changes to the cystic form, better adapted to survival.

3. Can you describe about the epidemiology of amebiasis?

Approximately 10% of the world's population is infected by either E histolytica or E
dispar. Amebiasis affects about 50 million persons each year, resulting in approximately
100,000 deaths, all of which are due to E histolytica. Incidence of amebiasis is higher in
developing countries. Areas of high prevalence include the Indian subcontinent, southern
and western Africa, the Far East, South America, and Central America.
In endemic areas, as many as 25% of patients may be carrying antibodies to E
histolytica due to prior infections, which may be largely asymptomatic. A variety of
factors, such as poor education, poverty, overcrowding, contaminated water supply, and
unsanitary conditions, contribute to the fecal-oral transmission.
Travel to endemic areas can predispose individuals to amebiasis. However, amebiasis
is an uncommon cause of traveler's diarrhea. The disease usually occurs after a longer stay
in endemic areas (eg, >1 month).

About 10% of the world's population is infected with Entamoeba, the majority
with noninvasive Entamoeba dispar. Amebiasis results from infection with E. histolytica
and is the third most common cause of death from parasitic disease (after schistosomiasis
and malaria). The wide spectrum of clinical disease caused by Entamoeba is due in part to
the differences between these two infecting species. Cysts of E. histolytica and E. dispar
are morphologically identical, but E. histolytica has unique isoenzymes, surface antigens,
DNA markers, and virulence properties (Table 202-1). Most asymptomatic carriers,
including homosexual men and patients with AIDS, harbor E. dispar and have self-limited
infections. These observations indicate that E. dispar is incapable of causing invasive
disease, since Cryptosporidium and Isospora belli, which also cause only self-limited
illnesses in immunocompetent people, cause devastating diarrhea in patients with AIDS.
However, host factors play a role as well. In one study, 10% of asymptomatic patients who
were colonized with E. histolytica went on to develop amebic colitis, while the rest
remained asymptomatic and cleared the infection within 1 year.
Referensi : Principles of Internal Medicine - Harrison's

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Epidemiologi ( Buku ajar ilmu penyakit dalam)
o Di negara dengan iklim tropis lebih sering ditemukan dibanding di negara-
negara sub-tropis yang beriklim sedang.
o Di USA, prevalensi amebiasis berkisar antara 1-5%
o Di Indonesia, laporan mengenai insidensi amebiasis masih belum dapat
dipastikan, tetapi dilihat dari gejala dan laporan mengenai abses hati
diperkirakan insidensinya cukup tinggi.
10% populasi hidup terinfeksi entamoeba, yaitu entamoeba dispar yang
bersifat non-infeksius

4. What is the pathophysiology of amebiasis?

The ingestion of cysts of E histolytica is followed by excystation in the small bowel
and invasion of the colon by the trophozoites. The incubation period varies from 2 days to
4 months. Invasive disease begins with the adherence of E histolytica to colonic mucins,
epithelial cells, and leukocytes. Adherence of the trophozoite is mediated by a galactose-
inhibitable adherence lectin. This lectin is a 260-kd surface protein containing a 170-kd
subunit and a 35-kd subunit. The heavier subunit has galactose-binding activity and at
least 6 distinct epitopes. These epitopes are different in E dispar.

After adherence, trophozoites invade the colonic epithelium to produce the ulcerative
lesions typical of intestinal amebiasis. The trophozoites of E histolytica lyse the target
cells by using lectin to bind to the target cells' membranes and using the parasite's
ionophorelike protein to induce a leak of ions (ie, Na+, K+, Ca+) from the target cell
cytoplasm. A number of hemolysins, encoded by plasmid (ribosomal deoxyribonucleic
acid [rDNA]) and cytotoxic to the intestinal mucosal cells, have been described in E
histolytica. An extracellular cysteine kinase causes proteolytic destruction of the tissue,
producing flask-shaped ulcers. Phorbol esters and protein kinase C activators augment the
cytolytic activity of the parasite.

Spread of amebiasis to the liver occurs via the portal blood. The pathogenic strains evade
the complement-mediated lysis in the bloodstream. Trophozoites ascend the portal veins to
produce liver abscesses filled with acellular proteinaceous debris. This material has the
appearance of anchovy paste. The trophozoites of E histolytica lyse the hepatocytes and
the neutrophils. This explains the paucity of inflammatory cells within the liver abscesses.
The neutrophil toxins may contribute to hepatocyte necrosis. Triangular areas of hepatic
necrosis also may occur due to ischemia caused by portal venous obstruction. The
trophozoites of E histolytica may be present along the periphery of these hepatic lesions.

Serum antibodies in patients with amebic liver abscess develop in 7 days and persist for up
to 10 years. E dispar infections do not elicit antibody response, unlike asymptomatic E
histolytica infections. Mucosal immunoglobulin A (IgA) response to E histolytica occurs
during invasive amebiasis. However, no evidence exists that invasive amebiasis is
increased in incidence or severity in patients with IgA deficiency.

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Cell-mediated immunity is important in limiting the disease and preventing recurrences.
Antigen-specific blastogenic responses occur, leading to production of lymphokines,
including interferon-d (IFN-d), which activates the killing of E histolytica trophozoites by
the macrophages. This killing depends on contact, oxidative pathways, nonoxidative
pathways, and nitric oxide (NO). Lymphokines, such as tumor necrosis factor-alpha (TNF-
a), are capable of activating the amebicidal activity of neutrophils. Incubation of CD8 +
lymphocytes with E histolytica antigens in vitro elicits cytotoxic T-cell activity against the
trophozoites. During acute invasive amebiasis, T-lymphocyte response to E histolytica
antigens is depressed by a parasite-induced serum factor.

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Referensi : https://wwwnc.cdc.gov/travel/yellowbook/2016/infectious-diseases-related-
to-travel/amebiasis

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Entamoeba hystolitica

Two form :
1.Trophozoit
Size 10-60 u, active motion with pseudopodia.
Clear, finger-like, ectoplasmic, pseudopodia extended rapidly.
Wide clear, refractile, ectoplasm will sharply separated forming endoplasm.
Finely granular endoplasm and find erythrocyte

2.Cyst

5. What is the properly management?

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 The principles of management include:
- Activity against anaerobic bacteria and protozoa is exhibited by several
agents. Metronidazole is considered the drug of choice for symptomatic,
invasive diseases. Metronidazole can be administered orally or
intravenously, 30-50 mg/kg/day divided in 3 doses for 7 - 10 days...
Paromomycin is the drug of choice for noninvasive disease. Because
parasites persist in the intestine of 40-60% of patients treated with
metronidazole, follow it with Paromomycin to cure luminal infection.
- Supportive: blood transfusion (fresh whole blood), fluid and electrolyte
balance and dietetic treatment.
- Health education for his parents particularly about disease transmission and
prevention, early sign and symptoms and should be seeked the health care
personnel immediately.

In critically ill patients, with large and multiple abscesses, metronidazole is used at 500
mg by IV infusion every 8 hours, for five or ten days. By oral route the metronidazole
dose must be 750 to 800 mg, three times daily for 10 days for adults and 50 mg/kg/ day
for children. Most patients treated with metronidazole improve after 3 or 4 days and cure
has been reported in more than 90% of the cases. This drug is available in capsules of 250
and 500 mg, and 500 mg for IV infusions. Common side effects of

Intestinal Disease

(Table 202-2) The drugs used to treat amebiasis can be classified according to their
primary site of action. Luminal amebicides are poorly absorbed and reach high
concentrations in the bowel, but their activity is limited to cysts and trophozoites close to
the mucosa. Only two luminal drugs are available in the United States: iodoquinol and
paromomycin. Indications for the use of luminal agents include eradication of cysts in
patients with colitis or a liver abscess and treatment of asymptomatic carriers. The
majority of asymptomatic individuals who pass cysts are colonized with E. dispar, which
does not warrant specific therapy. However, it is prudent to treat asymptomatic individuals
who pass cysts unless E. dispar colonization can be definitively demonstrated by specific
antigen-detection tests

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Tissue amebicides reach high concentrations in the blood and tissue after oral or parenteral
administration. The development of nitroimidazole compounds, especially metronidazole,
was a major advance in the treatment of invasive amebiasis. Patients with amebic colitis
should be treated with intravenous or oral metronidazole. Side effects include nausea,
vomiting, abdominal discomfort, and a disulfiram-like reaction. Another longer-acting
imidazole compound, tinidazole, is also effective and was recently approved in the United
States. All patients should also receive a full course of therapy with a luminal agent, since
metronidazole does not eradicate cysts. Resistance to metronidazole has been selected in
the laboratory but has not been found in clinical isolates. Relapses are not uncommon and
probably represent reinfection or failure to eradicate amebas from the bowel because of an
inadequate dosage or duration of therapy

Amebic Liver Abscess

Metronidazole is the drug of choice for amebic liver abscess. Longer-acting

nitroimidazoles (tinidazole and ornidazole) have been effective as single-dose therapy in
developing countries. With early diagnosis and therapy, mortality rates from
uncomplicated amebic liver abscess are <1%. The second-line therapeutic agents emetine
and chloroquine should be avoided if possible because of the potential cardiovascular and
gastrointestinal side effects of the former and the higher relapse rates with the latter. There
is no evidence that combined therapy with two drugs is more effective than the single-
drug regimen. Studies of South Africans with liver abscesses demonstrated that 72% of
patients without intestinal symptoms had bowel infection with E. histolytica; thus, all
treatment regimens should include a luminal agent to eradicate cysts and prevent further
transmission. Amebic liver abscess recurs rarely.

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Aspiration of Liver Abscesses

More than 90% of patients respond dramatically to metronidazole therapy with decreases
in both pain and fever within 72 h. Indications for aspiration of liver abscesses are (1) the
need to rule out a pyogenic abscess, particularly in patients with multiple lesions; (2) the
lack of a clinical response in 3–5 days; (3) the threat of imminent rupture; and (4) the need
to prevent rupture of left-lobe abscesses into the pericardium. There is no evidence that
aspiration, even of large abscesses (up to 10 cm), accelerates healing. Percutaneous
drainage may be successful even if the liver abscess has already ruptured. Surgery should
be reserved for instances of bowel perforation and rupture into the pericardium.

Referensi : Principles of Internal Medicine - Harrison's

7. What is the course or prognosis of hepatic amebiasis?

 Intestinal infections due to amebiasis generally respond well to appropriate
therapy. The severity of amebiasis is increased in the following individuals:
o Children, especially neonates
o Pregnant and postpartum women
o Those using corticosteroids
o Those with malignancies
o Malnourished individuals
 Mortality rate in patients with uncomplicated amebic liver abscess is less than 1%.

 Fulminant amebic colitis has a mortality rate of more than 50%.

 Pleuropulmonary amebiasis has a 15-20% mortality rate.
 Amebic pericarditis has a case fatality rate of 40%.
 Cerebral amebiasis is highly fatal with a 90% death rate.

8. Differential Diagnosis
Despite a similarity with several diseases such as hepatoma, acute cholecystitis, parasitic
cysts, subphrenic and pulmonary abscesses provoked by bacteria, the differential
diagnosis of hepatic amebiasis must be established principally against.

The differential diagnosis of intestinal amebiasis includes bacterial diarrheas (Chap. 122)
caused by Campylobacter (Chap. 148); enteroinvasive Escherichia coli (Chap. 143); and
species of Shigella (Chap. 147), Salmonella (Chap. 146), and Vibrio (Chap. 149).
Although the typical patient with amebic colitis has less prominent fever than in these
other conditions as well as heme-positive stools with few neutrophils, correct diagnosis
requires bacterial cultures, microscopic examination of stools, and amebic serologic
testing. As has already been mentioned, amebiasis must be ruled out in any patient thought
to have inflammatory bowel disease.

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Because of the variety of presenting signs and symptoms, amebic liver abscess can easily
be confused with pulmonary or gallbladder disease or with any febrile illness with few
localizing signs, such as malaria (Chap. 203) or typhoid fever (Chap. 146). The diagnosis
should be considered in members of high-risk groups who have recently traveled outside
the United States (Chap. 117) and in inmates of institutions. Once radiographic studies
have identified an abscess in the liver, the most important differential diagnosis is between
amebic and pyogenic abscess. Patients with pyogenic abscess typically are older and have
a history of underlying bowel disease or recent surgery. Amebic serology is helpful, but
aspiration of the abscess, with Gram's staining and culture of the material, may be required
for differentiation of the two diseases.

Referensi : Principles of Internal Medicine - Harrison's

9. Complication

The spreading of the amebic lesion to adjoining structures, involving a contiguous

mechanism, is a frequently reported complication. The close vicinity of the diaphragm to
the superior surface of the hepatic lesion may lead to inflammatory reactions of the
diaphragm itself, subphrenic space, pleura, lungs and pericardium

Clinically this can result in atelectasis, pleuritis, empyema and pulmonary condensation.
These are frequently detected at the right hemithorax, corresponding to lesions of the right
lobe of the liver, reported in most cases

10. What is prevention of amebiasis?

 Improved sanitation and clean water supply decrease incidence of amebiasis. The
amount of chlorine normally used to purify water is inadequate in killing the cysts.
Drinking water can be rendered safe by boiling, 0.22 µm filtration, or iodination
with tetraglycine hydroperiodide. Bottled water may be used for drinking when
traveling to endemic areas.
 Eating only cooked food or self-peeled fruits in endemic areas minimize risk.
Avoid eating raw fruits and salads, which are difficult to sterilize.
 Disease transmission can be reduced by early treatment of carriers in nonendemic
areas.

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 Tutorial Day 2
Epilogue

Alba had treated with metronidazole 10 mg/kg body weight intravenously three times in a
day. He also had Liver puncture procedure and the other supportive treatment. He was
discharged with improvement

CASE END

19
Tambahan dari buku ajar Ilmu Penyakit Dalam PAPDI

 Definisi
Amebiasis atau biasa disebut disentri ameba, enteritis ameba, atau kolitis ameba
merupakan penyakit infeksi usus besar yang disebabkan oleh parasit usus
Entamoeba histolytica.

 Epidemiologi
o Di negara dengan iklim tropis lebih sering ditemukan dibanding di negara-
negara sub-tropis yang beriklim sedang.
o Di USA, prevalensi amebiasis berkisar antara 1-5%
o Di Indonesia, laporan mengenai insidensi amebiasis masih belum dapat
dipastikan, tetapi dilihat dari gejala dan laporan mengenai abses hati
diperkirakan insidensinya cukup tinggi.
10% populasi hidup terinfeksi entamoeba, yaitu entamoeba dispar yang
bersifat non-infeksius

 Etiologi
o Infeksi melalui fecal-oral
o E. histolytica merupakan protozoa usus, sering hidup sebagai
mikroorganisme komensal (apatogen) di usus besar manusia.
o Apabila suatu kondisi memungkinkan maka dapat menyebabkan kolonisasi
di usus besar sehingga menimbulkan luka di bagian usus.
o Terdapat dua bentuk siklus hidup yaitu tropozoit dan kista.
o Tropozoit terbagi menjadi dua yaitu komensal dan patogen, tropozoit
patogen dapat dijumpai di intraintestinal dan ekstraintestinal yang dapat
menghasilkan gejala berupa disentri, diameternya lebih besar
dibandingkan dengan trofozoit komensal dan sering menelan eritrosit
(haematophagous trophozoite).
o Kista terbagi menjadi dua yaitu kista muda dan kista dewasa, dan hanya
ditemukan di dalam lumen usus (Intraluminal) memiliki peran untuk
penularan penyakit, dan dapat hidup lama diluar tubuh manusia
o Kista dapat tumbuh dan hidup di dalam asam lambung, dan kadar klor
didalam sistem air minum.

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 Patogenesis

 Klasifikasi
o Berdasarkan berat ringannya gejala, maka dapat dibedakan
menjadi:
 Carrier (Cyst passer)
 Amebiasis intestinal ringan (disentri ameba ringan)
 Amebiasis intestinal sedang (disentri ameba sedang)
 Amebiasis intestinal berat
 Disentri ameba kronik.

 Manifestasi Klinik
o Carrier (Cyst Passer)
Pasien tidak menunjukan gejala klinis sama sekali, hal tersebut
dikarenakan ameba yang berada di dalam lumen usus besar, tidak
menginvasi ke dinding lumen.
o Amebiasis Intestinal Ringan
Adanya keluhan perut kembung
Timbul diare ringan 4-5 kali dalam satu hari
Tinja berbau busuk
Bercampur darah dan lendir
Terkadang adanya hepatomegali yang bersifat ringan
o Amebiasis Intestinal Sedang
 Keluhan dan gejala pasien biasanya lebih berat dari gejala
disentri ringan, tetapi pasien masih mampu untuk
melakukan aktivitas sehari-hari
 Tinja disertai darah dan lendir
 Pasien mengeluh adanya perut kram
 Demam dan lemah badan
 Hepatomegali dengan nyeri yang ringan
o Disentri Ameba Berat

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 
Keluhan dan gejala klinis lebih hebat lagi

Penderita mengalami diare disertai darah yang sangat
banyak >15 kali per hari.
 Demam tinggi, 40-40,5oC
 Mual dan gejala anemia sangat khas
o Disentri Ameba Kronik
 Gejala menyerupai disentri ameba ringan, serangan diare
diselingi dengan periode normal atau tanpa gejala.
 Keadaan tersebut terjadi selama berbulan-bulan
 Terdapat gejala khas berupa neurastenia

 Diagnosis
 Biasanya sangat sulit dibedakan dengan irritable bowel syndrome
(IBS)
 Melalui Anamnesis yang menunjang dan mengarah ke gejala
Amebiasis
 Melalui pemeriksaan fisik berupa (Inspeksi, palpasi, dan auskultasi)
di bagian abdomen.
 Pemeriksaan Tinja (Gold standard) yang harus dilakukan untuk
melihat temuan trofozoit.
 Pemeriksaan penunjang berupa USG Abdomen dapat dilakukan
untuk melihat kemungkinan gejala hepatic amebiasis.

 Komplikasi

Komplikasi Intestinal
 Perdarahan usus, terjadi apabila ameba mengadakan invasi ke
dinding usus besar dan merusak pembuluh darah.
 Perforasi usus, terjadi apabila abses menembus lapisan muskular
dinding usus besar, sering mengakibatkan peritonitis yang
mortalitasnya cukup tinggi
 Ameboma, terjadi akibat infeksi kronik yang mengakibatkan reaksi
terbentuknya massa jaringan granulasi, biasa terjadi di daerah
caecum dan sering menyebabkan ileus obstruktif/penyempitan
usus.
 Intususepsi, banyak terjadi di daerah caecum
 Penyempitan usus (Striktura) dapat terjadi pada disentri kronik,
akibat terbentuknya jaringan ikat

Komplikasi ekstra intestinal

• Amebiasis hati, merupakan salah satu penyulit yang paling sering
terjadi, insidensinya berkisar 5-40%
• Lebih sering terjadi pada laki-laki dibandingkan wanita dan tersering
pada usia 30-40 tahun

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 • Abses dapat timbul beberapa minggu, bulan, ataupun tahun setelah
terinfeksi ameba
• Infeksi ini terjadi akibat embolisasi ameba dan dinding usus melalui
vena porta yang selanjutnya mengalami hepatitis ameba yang
merupakan stadium awal dari abses hati, kemudian timbul nekrosis
fokal kecil (mikroabses) yang saling bersatu dan membentuk abses
tunggal yang cukup besar dan menimbulkan nanah yang berwarna
kecoklatan yang merupakan akumulasi dari jaringan sel hati yang rusak
dan bercampur darah.
• Pasien sering mengeluh adanya nyeri spontan di perut bagian kanan
atas.

 Pengobatan
o Ameba dapat ditemukan di dalam lumen usus, di dalam dinding
usus maupun di luar usus. Hampir semua obat amebisid tidak
dapat bekerja secara efektif di semua tempat tersebut, terutama
bila diberikan obat tunggal. Oleh karena itu sering digunakan
kombinasi obat untuk meningkatkan hasil pengobatan.
o Amebiasis asimptomatik (Carrier atau Cyst passer)
 Diloksanit furoat (diloxanite furoate) 3 x 500mg sehari
selama 10 hari. Saat ini obat ini merupakan amebisid
luminal pilihan, karena efektifitasnya yang cukup tinggi (80-
85%), efek samping sangat minimal yaitu hanya adanya
mual dan kembung.
 Diyodohidroksikin (Diiodohydroxyquin) 3 x 600mg sehari
selama 10 hari.
 Yodoklorohidroksikin (lodochlorohydroxyquin) atau
Kliokinol (clioquinol) 3 x 250mg sehari, selama 10 hari,
efektifitasnya 60-70%.
o Disentri Ameba Ringan-Sedang
 Pada pasien disentri ameba ringan sedang sering
ditemukan trofozoit di dalam lumen dan di dinding usus
maka obat pilihan yang dapat diberikan adalah
metronidazol dengan dosis 3x750 mg sehari selama 5-10
hari.
 Tinidazol atau ornidazol juga dapat diberikan dengan
jumlah yang sama seperti metronidazole.
o Disentri Ameba Berat
 Biasanya pasien tidak hanya memerlukan obat amebisid
saja, tetapi juga memerlukan infus cairan elektrolit ataupun
transfusi darah.
 Obat biasanya diberikan melalui suntikan IM atau subkutan
yang dalam

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  Dosis emetin 1mg/kg berat badan sehari (maksimum 60
mg sehari) selama 3-5 hari
 Penderita sebaiknya dirawat di rumah sakit dan tirah baring
selama pengobatan. Hal ini disebabkan karena bahaya efek
samping emetin terhadap jantung.
 Pemberian dosis tinggi dapat mengakibatkan nekrosis otot
jantung dan penderita meninggal mendadak.
 Maka penderita perlu diobservasi dengan teliti memeriksa
tekanan darah, denyut nadi, dan EKG.
o Amebiasis Ekstra Intestinal dan Ameboma
 Penderita abses hati ameba dapat diberi metronidazole
atau obat lain golongan nitroimidazol dengan dosis seperti
obat yang telah disebutkan sebelumnya.
 Dapat pula diberi klorokindifosfat dengan dosis 1 gram
sehari selama 1-2 hari, dilanjutkan dengan 600mg sehari
selama 4 minggu. Masing-masing obat tersebut perlu
ditambah dehidroemetin atau emetin dengan dosis yang
sama seperti obat sebelumnya selama 10 hari
 Apabila terdapat abses hati yang besar (> 5 cm) biasanya
akan sukar sembuh, sehingga perlu dipertimbangkan
tindakan pungsi abses untuk mempercepat penyembuhan.

 Pencegahan
o Makanan, minuman, dan keadaan lingkungan hidup yang
memenuhi syarat kesehatan merupakan sarana pencegahan
penyakit yang sangat penting.
o Air minum sebaiknya dimasak terlebih dahulu, karena kista akan
hilang bila air dipanaskan 50 derajat celcius selama 5 menit.
o Jamban keluarga, isolasi, dan pengobatan pasien carrier
 Prognosis
o Prognosis ditentukan berdasarkan berat-ringannya
penyakit.
o Pada umumnya prognosis amebiasis adalah baik terutama
yang tanpa komplikasi.
o Prognosis yang kurang baik apabila terdapat penyulit
seperti abses otak ameba.

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