Download E. histolytica

Parasitic infection
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫از مجموع ‪ 53995‬نفر نمونه مورد بررسی‪ ،‬تحقيق روی ‪ 45128‬نفر که ‪ %45/8‬جنس‬
‫مذکر و ‪ %61‬مربوط به ساکنين مناطق شهری بودند‪ ،‬انجام گرفت‪.‬‬
‫آلودگی در‪ %19/ 3‬وجود داشت که در مردان‪ 19/ 7‬و در زنان‪ 19/ 1‬درصد بود‪.‬‬
‫با‪ %1/ 5‬از‬
‫در بين انواع تک ياخته‪ ،‬ژيارديا با‪ %10/ 9‬و از بين کرم ها آسکاريس‬
‫شيوع بيشتر برخوردار بودند‪.‬‬
‫آلودگی در گروه سنی کمتر از ‪ 15‬سال به ميزان‪ %25/ 5‬و در سنين باالی ‪ 70‬سال به‬
‫ميزان‪ 11/ 6‬بود‪.‬‬
‫ميزان آلودگی در ساکنين شهری‪ %16/ 4‬و در روستاييان‪ %24/ 3‬گزارش شد ‪.‬‬
‫نتيجه گيری و توصيه ها‪ :‬ميزان عفونت انگلی روده ای در ايران جای نگرانی دارد‪ .‬با توجه به‬
‫عوارض شناخته شده‪ ،‬بررسی علل آن و اجرا برنامه ها برای کاهش مشکل توصيه می شود‪.‬‬
• Parasites are divided into 2 main groups
taxonomically: protozoans, which are
unicellular, and helminths, which are
multicellular.
• Chemotherapeutic agents appropriate for 1
group may not be appropriate for the other,
and not all drugs are readily available.
Protozoan Diseases
•
•
•
•
•
•
•
•
•
•
•
Primary Amebic Meningoencephalitis
Amebiasis
Giardiasis and Balantidiasis
Cryptosporidium, Isospora, Cyclospora, and Microsporidia
Trichomoniasis (Trichomonas vaginalis)
Leishmaniasis (Leishmania)
African Trypanosomiasis (Sleeping Sickness; Trypanosoma brucei Complex)
American Trypanosomiasis (Chagas Disease; Trypanosoma cruzi)
Malaria (Plasmodium)
Babesiosis (Babesia)
Toxoplasmosis (Toxoplasma gondii)
Amebiasis
• Entamoeba histolytica infects up to 10% of the world's
population; endemic foci are particularly common in the
tropics, especially in areas with low socioeconomic and
sanitary standards.
• In most infected individuals, E. histolytica parasitizes the
lumen of the gastrointestinal tract and causes few symptoms
or sequelae.
• The 2 most common forms of disease caused by E. histolytica
are amebic colitis with parasitic invasion of the intestinal
mucosa and amebic liver abscess with dissemination of the
parasite to the liver.
Etiology
• E. histolytica, the pathogenic species, causes a
spectrum of disease and can become invasive.
• Infection is acquired through the ingestion of
parasite cysts, which measure 10-18 mm in diameter
and contain 4 nuclei.
• Cysts are resistant to harsh environmental conditions
including the concentrations of chlorine commonly
used in water purification but can be killed by
heating to 55C.
• After ingestion, cysts are resistant to gastric acidity
and digestive enzymes and germinate in the small
intestine to form trophozoites.
• These large, actively motile organisms colonize the
lumen of the large intestine and may invade the
mucosal lining.
• Infection is not transmitted by trophozoites, as these
rapidly degenerate outside the body and are unable
to survive the low pH of the stomach if swallowed.
Epidemiology
• It is estimated that infection with E. histolytica leads
to 50 million cases of symptomatic disease and
40,000-110,000 deaths annually.
• Prospective studies have shown that 4-10% of
individuals infected with E. histolytica develop
amebic colitis and that <1% of infected individuals
develop disseminated disease, including amebic liver
abscess.
Clinical Manifestations
• Clinical presentations range from asymptomatic cyst passage
to amebic colitis, amebic dysentery, ameboma, and
extraintestinal disease.
• E. histolytica infection is asymptomatic in about 90% of
persons but has the potential to become invasive and should
be treated.
• Severe disease is more common in young children, pregnant
women, malnourished individuals, and persons taking
corticosteroids.
• Extraintestinal disease usually involves the liver, but less
common extraintestinal manifestations include amebic brain
abscess, pleuropulmonary disease, ulcerative skin, and
genitourinary lesions.
Diagnosis
• A diagnosis of amebic colitis is made in the presence of compatible
symptoms with detection of E. histolytica antigens in stool.
• This approach has a greater than 95% sensitivity and specificity and
coupled with a positive serology test is the most accurate means of
diagnosis in developed countries.
• The E. histolytica II stool antigen detection test (TechLab, Blacksburg, VA)
is able to distinguish E. histolytica from E. dispar infection.
• Microscopic examination of stool samples has a sensitivity of 60%.
• Sensitivity can be increased to 85-95% by examining 3 stools, since
excretion of cysts can be intermittent.
• However, microscopy cannot differentiate between E. histolytica and E.
dispar unless phagocytosed erythrocytes (specific for E. histolytica) are
seen.
Differential diagnosis
• The differential diagnosis for amebic colitis includes colitis
due to bacterial (Shigella, Salmonella, enteropathogenic
Escherichia coli, Campylobacter, Yersinia, Clostridium difficile),
mycobacterial (tuberculosis and atypical mycobacteria), and
viral (cytomegalovirus) pathogens, as well as noninfectious
causes such as inflammatory bowel disease (IBD).
• Pyogenic liver abscess due to bacterial infection, hepatoma,
and echinococcal cysts are in the differential for amebic liver
abscess.
• However, echinococcal cysts are rarely associated with
systemic symptoms such as fever unless there is cyst rupture
or leakage.
Treatment
• Invasive amebiasis is treated with a
nitroimidazole such as metronidazole or
tinidazole and then a luminal amebicide.
Prevention
• Control of amebiasis can be achieved by exercising
proper sanitation and avoiding fecal-oral
transmission.
• Regular examination of food handlers and thorough
investigation of diarrheal episodes may help identify
the source of infection.
• No prophylactic drug or vaccine is currently available
for amebiasis.
Giardiasis
• Giardia lamblia is a flagellated protozoan that
infects the duodenum and small intestine.
• Infection results in clinical manifestations that
range from asymptomatic colonization to
acute or chronic diarrhea and malabsorption.
• Infection is more prevalent in children than in
adults.
• Giardia is endemic in areas of the world with poor
levels of sanitation.
• It is also an important cause of morbidity in
developed countries, where it is associated with
urban child-care centers, residential institutions for
the developmentally delayed, and water-borne and
food-borne outbreaks.
• Giardia is a particularly significant pathogen in
people with malnutrition, certain
immunodeficiencies, and cystic fibrosis.
Etiology
• The life cycle of G. lamblia (also known as Giardia intestinalis
or Giardia duodenalis) is composed of 2 stages: trophozoites
and cysts.
• Giardia infects humans after ingestion of as few as 10-100
cysts (which measure 8-10 mm in diameter).
• Each ingested cyst produces 2 trophozoites in the duodenum.
• After excystation, trophozoites colonize the lumen of the
duodenum and proximal jejunum, where they attach to the
brush border of the intestinal epithelial cells and multiply by
binary fission.
Epidemiology
• Giardia occurs worldwide and is the most common intestinal
parasite identified in public health laboratories in the USA,
where it is estimated that up to 2 million cases of giardiasis
occur annually.
• The age-specific prevalence of giardiasis is high during
childhood and begins to decline after adolescence.
• The asymptomatic carrier rate of G. lamblia in the USA is as
high as 20-30% in children younger than 36 mo of age
attending child-care centers.
• Asymptomatic carriage may persist for several months.
• Transmission of Giardia is common in certain high-risk groups,
including children and employees in child-care centers,
consumers of contaminated water, travelers to certain areas
of the world, men who have sex with men, and persons
exposed to certain animals.
• Humoral immunodeficiencies, including common variable
hypogammaglobulinemia and X-linked agammaglobulinemia,
predispose humans to chronic symptomatic Giardia infection,
suggesting the importance of humoral immunity in controlling
giardiasis.
• Selective immunoglobulin A (IgA) deficiency is also associated
with Giardia infection.
Clinical Manifestations
• The incubation period of Giardia infection usually is
1-2 wk but may be longer.
• A broad spectrum of clinical manifestations occurs,
depending on the interaction between G. lamblia
and the host.
• Children who are exposed to G. lamblia may
experience asymptomatic excretion of the organism,
acute infectious diarrhea, or chronic diarrhea with
persistent gastrointestinal tract signs and symptoms,
including failure to thrive and abdominal pain or
cramping.
• Symptomatic infections occur more frequently in
children than in adults.
• Most symptomatic patients usually have a limited
period of acute diarrheal disease with or without
low-grade fever, nausea, and anorexia; in a small
proportion of patients, an intermittent or more
protracted course characterized by diarrhea,
abdominal distention and cramps, bloating, malaise,
flatulence, nausea, anorexia, and weight loss
develops.
Diagnosis
• Giardiasis should be considered in children who have acute nondysenteric
diarrhea, persistent diarrhea, intermittent diarrhea and constipation,
malabsorption, chronic crampy abdominal pain and bloating, failure to
thrive, or weight loss.
• It should be particularly high in the differential diagnosis of children in
child care, children in contact with an index case, children with a history of
recent travel to an endemic area, and children with humoral
immunodeficiencies.
• Testing for giardiasis should be standard for internationally adopted
children from Giardia-endemic areas, and screening for iron deficiency
should be considered in internationally adopted children with giardiasis.
• Stool enzyme immunoassay (EIA) or direct fluorescent antibody tests for
Giardia antigens are now the tests of choice for giardiasis in most
situations. EIA is less reader dependent and more sensitive for detection
of Giardia than microscopy.
• Traditionally, a diagnosis of giardiasis has been established by microscopy
documentation of trophozoites or cysts in stool specimens, but 3 stool
specimens are required to achieve a sensitivity of >90%.
• In patients with chronic symptoms in whom giardiasis is suspected but in
whom testing of stool specimens for Giardia yields a negative result,
aspiration or biopsy of the duodenum or upper jejunum should be
considered.
• In a fresh specimen, trophozoites usually can be visualized by direct wet
mount.
Treatment
• Children with acute diarrhea in whom Giardia organisms are
identified should receive therapy.
• In addition, children who manifest failure to thrive or exhibit
malabsorption or gastrointestinal tract symptoms such as
chronic diarrhea should be treated.
• Asymptomatic excreters generally are not treated except in
specific instances such as in outbreak control, for prevention
of household transmission by toddlers to pregnant women
and patients with hypogammaglobulinemia or cystic fibrosis,
and in situations requiring oral antibiotic treatment where
Giardia may have produced malabsorption of the antibiotic.
Prevention
• Infected persons and persons at risk should
practice strict handwashing after any contact
with feces.
• This point is especially important for
caregivers of diapered infants in child-care
centers, where diarrhea is common and
Giardia organism carriage rates are high.
Leishmaniasis (Leishmania)
• The leishmaniases are a diverse group of diseases caused by
intracellular protozoan parasites of the genus Leishmania,
which are transmitted by phlebotomine sandflies.
• Multiple species of Leishmania are known to cause human
disease involving the skin and mucosal surfaces and the
visceral reticuloendothelial organs.
• Cutaneous disease is generally mild but may cause cosmetic
disfigurement.
• Mucosal and visceral leishmaniasis is associated with
significant morbidity and mortality.
Visceral Leishmaniasis
• VL (kala-azar) typically affects children <5 yr of age in
the New World and Mediterranean region (L.
infantum/chagasi) and older children and young
adults in Africa and Asia (L. donovani).
• After inoculation of the organism into the skin by the
sandfly, the child may have a completely
asymptomatic infection or an oligosymptomatic
illness that either resolves spontaneously or evolves
into active kala-azar.
• Children with asymptomatic infection are
transiently seropositive but show no clinical
evidence of disease.
• Children who are oligosymptomatic have mild constitutional
symptoms (malaise, intermittent diarrhea, poor activity
tolerance) and intermittent fever; most will have a mildly
enlarged liver.
• In most of these children the illness will resolve without
therapy, but in approximately 25% it will evolve to active kalaazar within 2-8 mo.
• Extreme incubation periods of several years have rarely been
described.
• During the 1st few weeks to months of disease evolution the
fever is intermittent, there is weakness and loss of energy, and
the spleen begins to enlarge.
• The classic clinical features of high fever, marked
splenomegaly, hepatomegaly, and severe cachexia
typically develop approximately 6 mo after the onset
of the illness, but a rapid clinical course over 1 mo has been
•
•
•
•
noted in up to 20% of patients in some series.
At the terminal stages of kala-azar the hepatosplenomegaly is
massive, there is gross wasting, the pancytopenia is profound,
and jaundice, edema, and ascites may be present.
Anemia may be severe enough to precipitate heart failure.
Bleeding episodes, especially epistaxis, are frequent.
The late stage of the illness is often complicated by secondary
bacterial infections, which frequently are a cause of death.
• A younger age at the time of infection and
underlying malnutrition may be risk factors for
the development and more rapid evolution of
active VL.
• Death occurs in >90% of patients without
specific antileishmanial treatment.
Laboratory Findings
• Laboratory findings associated with classic
kala-azar include anemia (hemoglobin 58 mg/dL), thrombocytopenia, leukopenia
(2,000-3,000 cells/micL), elevated hepatic
transaminase levels, and hyperglobulinemia
(>5 g/dL) that is mostly immunoglobulin G
(IgG).
Differential Diagnosis
• VL should be strongly suspected in the patient with
prolonged fever, weakness, cachexia, marked
splenomegaly, hepatomegaly, cytopenias, and
hypergammaglobulinemia who has had potential
exposure in an endemic area.
• The clinical picture may also be consistent with that
of malaria, typhoid fever, miliary tuberculosis,
schistosomiasis, brucellosis, amebic liver abscess,
infectious mononucleosis, lymphoma, and leukemia.
Diagnosis
• Serologic testing by enzyme immunoassay, indirect
fluorescence assay, or direct agglutination is very useful in VL
because of the very high level of antileishmanial antibodies.
• An enzyme-linked immunosorbent assay using a recombinant
antigen (K39) has a sensitivity and specificity for VL that is
close to 100%.
• A negative serologic test result in an immunocompetent
individual is strong evidence against a diagnosis of VL.
• Serodiagnostic tests have positive findings in only about half
of the patients who are co-infected with HIV.
• In patients with VL, smears or cultures of
material from splenic, bone marrow, or lymph
node aspirations are usually diagnostic.
• In experienced hands, splenic aspiration has a
higher diagnostic sensitivity, but it is rarely
performed in the USA because of the risk for
bleeding complications.
Treatment
• All patients with VL or ML should receive
therapy.
• Glucantime
• Amphotericin B
Malaria (Plasmodium)
• Malaria is an acute and chronic illness characterized by
paroxysms of fever, chills, sweats, fatigue, anemia, and
splenomegaly.
• It has played a major role in human history, causing harm to
more people than perhaps any other infectious disease.
• Malaria is of overwhelming importance in the developing
world today, with an estimated 300 to 500 million cases and
more than 1 million deaths each year.
• Most malarial deaths occur among infants and young children.
Etiology
• Malaria is caused by intracellular Plasmodium
protozoa transmitted to humans by female
Anopheles mosquitoes.
• Prior to 2004, only 4 species of Plasmodium were
known to cause malaria in humans: P. falciparum, P.
malariae, P. ovale, and P. vivax.
• In 2004 P. knowlesi (a primate malaria species) was
also shown to cause human malaria, and cases of P.
knowlesi infection have been documented in
Malaysia, Indonesia, Singapore, and the Philippines.
• Malaria also can be transmitted through blood
transfusion, use of contaminated needles, and
from a pregnant woman to her fetus.
• The risk for blood transmission is small and
decreasing in the USA but may occur by way
of whole blood, packed red blood cells,
platelets, leukocytes, and organ
transplantation.
Clinical Manifestations
• The classic presentation of malaria is seldom
noted with other infectious diseases and
consists of paroxysms of fever alternating
with periods of fatigue but otherwise relative
wellness.
• Febrile paroxysms are characterized by high
fever, sweats, and headache, as well as
myalgia, back pain, abdominal pain, nausea,
vomiting, diarrhea, pallor, and jaundice.
• Typical laboratory findings include anemia,
thrombocytopenia, and a normal or low
leukocyte count. The erythrocyte
sedimentation rate (ESR) is often elevated.
WORLD HEALTH ORGANIZATION CRITERIA
FOR SEVERE MALARIA, 2000
Impaired consciousness
Prostration
Respiratory distress
Multiple seizures
Jaundice
Hemoglobinuria
Abnormal bleeding
Severe anemia
Circulatory collapse
Pulmonary edema
Diagnosis
• Any child who presents with fever or unexplained systemic
illness and has traveled or resided in a malaria-endemic area
within the previous year should be assumed to have lifethreatening malaria until proven otherwise.
• Malaria should be considered regardless of the use of
chemoprophylaxis.
• Important criteria that suggest P. falciparum malaria include
symptoms occurring less than 1 mo after return from an
endemic area, more than 2% parasitemia, ring forms with
double chromatin dots, and erythrocytes infected with more
than 1 parasite.
• The diagnosis of malaria is established by
identification of organisms on Giemsa-stained
smears of peripheral blood or by rapid
immunochromatographic assay.
Differential Diagnosis
• The differential diagnosis of malaria is broad
and includes viral infections such as influenza
and hepatitis, sepsis, pneumonia, meningitis,
encephalitis, endocarditis, gastroenteritis,
pyelonephritis, babesiosis, brucellosis,
leptospirosis, tuberculosis, relapsing fever,
typhoid fever, yellow fever, amebic liver
abscess, Hodgkin disease, and collagen
vascular disease.
Treatment
• Fever without an obvious cause in any patient who
has left a P. falciparum endemic area within 30 days
and is nonimmune should be considered a medical
emergency.
• Thick and thin blood smears should be obtained
immediately, and all children with symptoms of
severe disease should be hospitalized.
• If blood films are negative, they should be repeated
every few hours.
• If the patient is severely ill, antimalarial therapy should be
initiated immediately.
• Outpatient therapy generally is not given to nonimmune
children but may be considered in immune or semi-immune
children who have low-level parasitemia (less than 1%), no
evidence of complications defined by the World Health
Organization (WHO), no vomiting, and a lack of toxic
appearance; who are able to contact the physician or
emergency department at any time; and in whom follow-up
within 24 hr is assured.
Toxoplasmosis
• Toxoplasma gondii, an obligate intracellular
protozoan, is acquired perorally,
transplacentally, or, rarely, parenterally in
laboratory accidents; by transfusion; or from a
transplanted organ.
• In immunologically normal children, acute
acquired infection may be asymptomatic,
cause lymphadenopathy, or affect almost any
organ.
Clinical Manifestations
• Manifestations of primary infection with T.
gondii are highly variable and are influenced
primarily by host immunocompetence.
• There may be no signs or symptoms or severe
disease.
• Reactivation of previously asymptomatic
congenital toxoplasmosis usually manifests as
ocular toxoplasmosis.
Helminthic Diseases
•
•
•
•
•
•
•
•
Ascariasis (Ascaris lumbricoides)
Hookworms (Necator americanus and Ancylostoma spp.)
Trichuriasis (Trichuris trichiura)
Enterobiasis (Enterobius vermicularis)
Strongyloidiasis (Strongyloides stercoralis)
Flukes (Liver, Lung, and Intestinal)
Adult Tapeworm Infections
Echinococcosis (Echinococcus granulosus and Echinococcus
multilocularis)
Ascariasis
• Ascariasis is caused by the nematode, or
roundworm, Ascaris lumbricoides.
• The reproductive potential of Ascaris is prodigious; a
gravid female worm produces 200,000 eggs/day.
• After passage in the feces, the eggs embryonate and
become infective in 5-10 days under favorable
environmental conditions.
• Adult worms can live for 12-18 mo.
Ascaris lumbricoides
Epidemiology
• Ascariasis occurs globally and is the most prevalent
human helminthiasis in the world.
• It is most common in tropical areas of the world
where environmental conditions are optimal for
maturation of ova in the soil.
• Approximately 1 billion persons are estimated to be
infected.
• Key factors linked with a higher prevalence of
infection include poor socioeconomic conditions, use
of human feces as fertilizer, and geophagia.
Clinical Manifestations
• The clinical presentation depends on the
intensity of infection and the organs involved.
• Most individuals have low to moderate worm
burdens and have no symptoms or signs.
• The most common clinical problems are due
to pulmonary disease and obstruction of the
intestinal or biliary tract.
Diagnosis
• Microscopic examination of fecal smears can be used
for diagnosis because of the high number of eggs
excreted by adult female worms.
• A high index of suspicion in the appropriate clinical
context is needed to diagnose pulmonary ascariasis
or obstruction of the gastrointestinal tract.
• Ultrasound examination of the abdomen is capable
of visualizing intraluminal adult worms.
Treatment
• Albendazole (400 mg PO once, for all ages),
• Mebendazole (100 mg bid PO for 3 days or
500 mg PO once for all ages)
• Pyrantel pamoate (11 mg/kg PO once,
maximum 1 g)
• Piperazine citrate (75 mg/kg/day for 2 days
maximum 3.5 g/day)
Enterobiasis
• The cause of enterobiasis, or pinworm
infection, is Enterobius vermicularis, which is a
small (1 cm in length), white, threadlike
nematode, or roundworm, that typically
inhabits the cecum, appendix, and adjacent
areas of the ileum and ascending colon.
• Gravid females migrate at night to the perianal
and perineal regions, where they deposit up
to 15,000 eggs.
• Eggs embryonate within 6 hr and remain
viable for 20 days.
• Human infection occurs by the fecal-oral route
typically by ingestion of embryonated eggs
that are carried on fingernails, clothing,
bedding, or house dust.
• After ingestion, the larvae mature to form
adult worms in 36-53 days.
Epidemiology
• Enterobiasis infection occurs in individuals of
all ages and socioeconomic levels.
• It infects 30% of children worldwide, and
humans are the only known host.
• The prevalence of pinworm infection is
highest in children 5-14 yr of age.
Clinical Manifestations
• Pinworm infection is innocuous and rarely causes
serious medical problems.
• The most common complaints include itching and
restless sleep secondary to nocturnal perianal or
perineal pruritus.
• Eosinophilia is not observed in most cases, because
tissue invasion does not occur.
• Aberrant migration to ectopic sites occasionally may
lead to appendicitis, chronic salpingitis, pelvic
inflammatory disease, peritonitis, hepatitis, and
ulcerative lesions in the large or small bowel.
Diagnosis
• A history of nocturnal perianal pruritus in
children strongly suggests enterobiasis.
• Definitive diagnosis is established by
identification of parasite eggs or worms.
• Microscopic examination of adhesive
cellophane tape pressed against the perianal
region early in the morning frequently
demonstrates.
• Repeated examinations increase the chance of detecting ova;
a single examination detects 50% of infections, 3
examinations 90%, and 5 examinations 99%.
• Worms seen in the perianal region should be removed and
preserved in 75% ethyl alcohol until microscopic examination
can be performed.
• Digital rectal examination may also be used to obtain samples
for a wet mount.
• Routine stool samples rarely demonstrate Enterobius ova.
Treatment
• Anthelmintic drugs should be administered to
infected individuals and their family members.
• A single oral dose of mebendazole (100 mg PO for all
ages) repeated in 2 wk results in cure rates of 90100%.
• Alternative regimens include a single oral dose of
albendazole (400 mg PO for all ages) repeated in
2 wk, or a single dose of pyrantel pamoate (11 mg/kg
PO, maximum 1 g).
• Frequent changing of underclothes, bed
clothes, and bed sheets decreases
environmental egg contamination and may
decrease the risk for autoinfection.
Prevention
• Household contacts can be treated at the
same time as the infected individual.
• Repeated treatments every 3-4 mo may be
required in circumstances with repeated
exposure, such as with institutionalized
children.
• Good hand hygiene is the most effective
method of prevention.
Echinococcosis
• Echinococcosis (hydatid disease or
hydatidosis) is the most widespread, serious
human cestode infection in the world .
• Two major Echinococcus species are
responsible for distinct clinical presentations,
E. granulosus (cystic hydatid disease) and the
more malignant E. multilocularis (alveolar
hydatid disease).
Clinical Manifestations
• In the liver, many cysts never become symptomatic and
regress spontaneously or produce relatively nonspecific
symptoms.
• Symptomatic cysts can cause increased abdominal girth,
hepatomegaly, a palpable mass, vomiting, or abdominal pain.
• However, the more serious complications result from
compression of adjacent structures, spillage of cyst contents,
and location of cysts in sensitive areas, such as the
reproductive tract, brain, and bone.
• Anaphylaxis can occur with cyst rupture or
spontaneous spillage, due to trauma or
intraoperatively.
• Jaundice due to cystic hydatid disease is rare.
• In the lung, cysts produce chest pain, cough,
or hemoptysis.
• Bone cysts may cause pathologic fractures,
and cysts in the genitourinary system may
produce hematuria or infertility.
Diagnosis
• Subcutaneous nodules, hepatomegaly, or a
palpable abdominal mass may be found.
• The parasite cannot be recovered from any
easily accessible body fluid unless a lung cyst
ruptures, after which protoscolices or layers of
cyst wall may briefly be seen in sputum.
• Ultrasonography is the most valuable tool for
both the diagnosis and treatment of cystic
hydatid disease of the liver.
• The presence of internal membranes and
falling echogenic cyst material (hydatid sand)
observed in real time aid in the diagnosis.
• Alveolar disease is less cystic in appearance and
resembles a diffuse solid tumor.
• CT findings are similar to those of ultrasonography
and may at times be useful in distinguishing alveolar
from cystic hydatid disease in geographic regions
where both occur.
• CT or MRI is also important in planning a surgical
intervention.
• Lung hydatid is usually apparent on chest x-ray.
• Serologic studies may be useful in confirming
a diagnosis of cystic echinococcosis, but the
false-negative rate may be >50%.
• Most patients with alveolar hydatidosis
develop detectable antibody responses.
Treatment
• Indications for surgery are the presence of
large liver cysts with multiple daughter cysts,
single superficially situated liver cysts that
may rupture spontaneously or as the result of
a trauma, infected cysts, cysts communicating
with the biliary tree and/or exerting pressure
on adjacent vital organs, and cysts in the lung,
brain, kidney, or bones.
• For simple, accessible cysts surrounded by
tissue, ultrasound- or CT-guided Percutaneous
Aspiration, Instillation (hypertonic saline or
another scolicidal agent) and Re-aspiration
(PAIR) is the preferred therapy.
• Nonpregnant patients with cysts not
amenable to PAIR or surgery or with
contraindications can be managed with
albendazole (15 mg/kg/day divided bid PO for
1-6 mo, maximum 800 mg/day). A favorable
response occurs in 40-60% of patients.
• Adverse effects include occasional alopecia,
mild gastrointestinal disturbance, and
elevated transaminases on prolonged use.
• Because of leukopenia, the U.S. Food and
Drug Administration recommends that blood
counts be monitored at the beginning and
every 2 wk during therapy.
Prognosis
• Factors predictive of success with
chemotherapy are age of the cyst (<2 yr), low
internal complexity of the cyst, and small size.
• The site of the cyst is not important, although
cysts in bone respond poorly. For alveolar
hydatidosis, if surgical removal is unsuccessful,
the average mortality is 92% by 10 yr after
diagnosis.