Download Case No. 26 - Caangay.com

Case No. 26
LIM, YOONTAEK
Clark
Case
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EF, a fresh college graduate, is
applying for a job at a pharmaceutical
company.
Routine laboratory examinations were
requested.
Fecalysis revealed: (+) E. histolitica
 Asymptomatic
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Entamoeba histolytica
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Protozoan parasite, cause of diarrhea, dysentery,
liver abscess and other syndromes
Occurs primarily in developing countries, but
immigrants, travelers, diagnosed with infection in U.S.
Must be distinguished clinically from Entamoeba
dispar, a morphologically identical parasite that is
non-invasive and does not cause disease
Onset of colitis usually gradual with symptoms > 1 wk,
distinguishing it from bacterial dysentery
Infective stage : mature tetranucleated cyst
Transmission
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Polluted water supply
Unclean handling by injected individuals
Droppings of flies and other insects
Use of human excrement an vegetable
gardens
Gross carelessness in personal hygiene
In homosexual acquired through sexual,
anal intercourse
SITES OF INFECTION
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Colon: dysentery, ameboma (tumor-like lesion of
colonic lumen; can be confused radiographically with
cecal cancer), toxic megacolon
Liver: abscess, can rupture causing peritonitis
Lung: empyema (right sided- direct extension from
liver)
Heart: pericarditis (direct extension from liver)
Brain: abscess (hematogenous spread, rare)
Skin: usually perineal, genital
GU: recto-vaginal fistula
Diagnosis of amebic colitis
1.
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6.
Observation of red cell-containing motile trophozoites on fresh
stool smear (insensitive); always heme + stool
Colonoscopy: biopsy or scraping at margin of colonic mucosal
ulcer: parasite may be seen; H&E shows necrosis, classic flaskshaped ulcer
Stool antigen test that distinguishes Eh from E. dispar is
available, more sensitive than microscopy of stool
Serology 99% sens. for amebic liver abscess; 88% sens. for
colitis, but Abs may be present yrs. later so that serology may
not be useful in immigrants from Eh-endemic regions
Ultrasound of liver: cannot distinguish amebic from pyogenic
abscess, but can guide aspiration if necessary
Liver abscess aspiration--yields anchovy paste-like material,
lack of WBCs (due to lysis by parasite) clue to diagnosis,
parasites usually not seen
Laboratory Diagnosis
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Microscopy
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Microscopic identification of cysts and
trophozoites in the stool is the common method
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Fresh stool: wet mounts and permanently stained
preparations (e.g., trichrome).
Concentrates from fresh stool: wet mounts, with or
without iodine stain, and permanently stained
preparations (e.g., trichrome).
E. histolytica trophozoites can also be identified in
aspirates or biopsy samples obtained during
colonoscopy or surgery
Trophozoites of Entamoeba histolytica
Line drawing
Trichrome stain
Trophozoites of Entamoeba histolytica with ingested erythrocytes (trichrome stain)
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Invasive form
Active, progressive, indirectional
Found in liquid stool
Eccenteric karyosome, “bulls eyes”
1 nucleus
Presence of ingested RBC
Killed by exposure to air or stomack
acid -> cannot cause infection
Cysts of Entamoeba histolytica
Line drawing
Stained with trichrome
Wet mounts stained with iodine
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Infective stage
Found in formed stool
4 nuclei
Cigar-shape chromatoidal body
With glycogen mass
Diagnosis
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Immunodiagnosis
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Antibody Detection; Enzyme immunoassay (EIA)
kits for Entomoeba histolytica
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95% of patients with extraintestinal amebiasis
70% of patients with active intestinal infection
10% of asymptomatic persons who are passing cysts
Detectable E. histolytica-specific antibodies may persist
for years after successful treatment, so the presence of
antibodies does not necessarily indicate acute or current
infection
Antigen Detection
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Useful as an adjunct to microscopic diagnosis in
detecting parasites and to distinguish between
pathogenic and nonpathogenic infections
Diagnosis
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Molecular methods
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PCR is the method of choice for
discriminating between the pathogenic
species (E. histolytica) from the
nonpathogenic species (E. dispar)
Treatment of amoebiasis
by Rang
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Acute invasive intestinal amoebiasis resulting in acute
severe amoebic dysentery : metronidazole (or
tindazole) followed by diloxanide
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Chronic intestinal amoebiasis : diloxanide
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Hepatic amoebiasis : metronidazole followed by
diloxanide
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Carrier state : diloxanide
Treatment of amoebiasis
by katzung
Clinical setting
DOC (adult dosage)
Alternative drugs (adult)
Asymptomatic intestinal
infection
Luminal agent :
Mild to moderate intestinal
infection
Metronidazole, 750mg tid or 500mg IV
every 6hours 10days
+
Luminal agent
Luminal agent
+
Tetracyclin, 250mg tid 10days or
Erythromycin, 500mg qid 10days
Severe intestinal infection
Same as mild to moderate infection
Luminal agent
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Tetracyclin, 250mg tid 10days or
Dehydroemetine or emetine, 1mg/kg SC
or IM 3~5days
Hepatic abscess,
ameboma and other
detraintestinal disease
Same as mild to moderate infection
Dehydroemetine or emetine, 1mg/kg SC
or IM 8~10days followed by (in abscess
only) chloroquine, 500mg bid 2days then
500mg qd 21days
+
Luminal agent
*Diloxanide
furoate : not available in U.S.
Diloxanide furoate, 500mg tid 10days
Iodoquinol, 650mg tid for 21days
Paromomycin, 10mg/kg tid for 7days
Treatment for asymptomatic
patient
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Luminal agents alone should be used
(not absorbed)
Iodoquinol: 650 mg tid x 20 days
Paromomycin: 25-35 mg/kg/d in 3
divided doses x 7 days
Metronidazole (nitroimidazole)
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DOC for treatment of extraluminal amoebiasis
Kills trophozoites but has no effect on the cysts
Most effective drug available for invasive amoebiasis involving
the intestine or the liver, but less against in the lumen of the gut
MOA : damage to the DNA of the trophozoite by toxic oxygen
products generated from the drug
Pharmacokinetics
 Given orally
 Rapidly and completely absorbed.
 Peak conc : 1~3 hours
 T1/2 : 7 hours
 Excreted in urine
Also used in Giardiasis (DOC), Trichomoniasis (DOC)
Metronidazole (nitroimidazole)
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S/E
 Frequent: GI intolerance, metallic taste, headache, dark urine
(harmless)
 Occasional: peripheral neuropathy (with prolonged use,
usually reversible), phlebitis at injection sites, disulfiram-like
reaction with alcohol, insomnia, stomatitis.
Drug interaction
 Disulfiram and ethanol : avoid co-administration
 Barbiturates may decrease metronidazole levels
Iodoquinol
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Lumninal agent
90% not absorbed
Unknown mechanism
Effective for trophozoite in lumen but not in
bowel wall or tissue
S/E
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GIT
Increase protein bound iodine
Dermatitis, urticaria
Neurotoxin
Nephrotoxin
Diloxanide furoate
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Luminal agent
Inactive against tissue trophozoite
Unknown mechanism
Direct amoebicidal action, affecting the amoebae
before encystment
DOC for asymptomatic infection
No serious side effects
Contraindicated in pregnancy
S/E
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Itchy rash (urticaria)
Itching (pruritus)
Excess gas in the stomach and intestines (flatulence)
Vomiting
Paromomycin sulfate
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An aminoglycoside
Luminal only
S/E
GIT
 Renal toxicity
 Caution with GIT ulceration since drug can
be absorbed with more toxicity
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Emetine & Dehydroemetine
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For tissue trophozoite
Oral unreliable
IM or SC is preferred; never IV – toxic
Only for 3~5 days not more than 10days
Dehydroemetine is preferred (less tosic)
For severe amoebiasis where metronidazole cannot be used
Combine with luminal agent
S/E
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Pain at injection site : sterile abscess
Arrythmia, CHF, hypotension
Contraindication
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Cardiac disease
Renal disease ( cannot be excreted & may accumulated )
Young children & pregnancy
Thank you!