The role of radiological imaging in the identification of abdominal parasitoses

Full article

https://doi.org/10.53453/ms.2023.11.8

The role of radiological imaging in the identification of abdominal
parasitoses
Milda Sondaitė
1
, Miglė Viliušytė
1
, Algidas Basevičius
2
1
Lithuanian University of Health Sciences, Faculty of medicine, Kaunas, Lithuania
2
Lithuanian University of Health Sciences, Department of Radiology, Kaunas, Lithuania
Abstract
Background. Various parasites are found in the human body. Some of them infect the human body and form a
symbiotic relationship with it. Other parasites cause serious and even fatal complications. The most frequent
abdominal parasites include Echinococcus spp., liver flukes, and Entamoeba histolytica.
Aim: to review information on current radiological imaging possibilities to identificate abdominal parasitoses as
reported in the literature.
Methods. Literature sources were selected from PubMed medical database using these keywords: radiological
imaging, abdominal parasitosis, echinococcus granulosus, echinococcus alveolaris, liver flukes, entamoeba
hystolitica.
Results. Ultrasonography, computed tomography, and magnetic resonance imaging (MRI) are the most often
utilized imaging technologies in diagnosis. Furthermore, in the majority of instances, serological testing is
required to confirm the diagnosis.
Conclusions. Parasitic diseases are highly prevalent worldwide and cause severe infections or death. Radiological
diagnostic tests and accessible serological testing are crucial in the identification of parasitic diseases.
Keywords: radiological imaging, abdominal parasitosis, echinococcus granulosus, echinococcus alveolaris, liver
flukes, entamoeba hystolitica.
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
Medical Sciences 2023 Vol. 11 (6), p. 61-73, https://doi.org/10.53453/ms.2023.11.8
61
1. Introduction
Parasitic diseases are among the most severe and
widespread infections in the world, causing millions
of morbidities and deaths each year. Although
parasitosis can affect practically any organ in the
human body, the majority of infections result in liver
damage. Parasites in the liver cause a wide range of
diseases and mortality by inducing recurrent
cholangitis, cirrhosis, liver failure and cancer. The
most frequent orally transmitted parasites that
invade the liver following mucosal penetration or by
portal-venous blood flow include Echinococcus
spp., liver flukes, and Entamoeba histolytica.
However, the proper identification of a hepatic
parasite is frequently delayed due to clinicians
unfamiliarity with the corresponding organi-
sms [1,2].
The liver has a unique feature of immune status, that
it can promote tolerance rather than immunity. This
function can be used by the parasites to avoid host
immunity [2]. Hepatic immune tolerance is caused
by a unique combination of anatomical and
histological properties of the liver. The liver
receives practically all of its blood supply directly
from the portal system, making it the first organ to
be exposed to gut-derived compounds such as
innocuous bacterial metabolites and nutrients [3].
The liver provides the most scavenger cells in the
body, primarily Kupffer cells (KCs), liver-resident
macrophages, and liver sinusoidal endothelial cells
(LSECs). KCs eliminate larger blood-borne
particles via phagocytosis, whereas LSECs remove
small particles (< 200 μm) and macromolecules via
receptor-mediated endocytosis. Both of these cell
types are essential for the liver's barrier effectiveness
and blood filtering ability. Many of the eliminated
elements are potential inflammatory inducers, but
their removal by liver cells is often not associated
with inflammatory immune responses. Instead,
immunological responses are frequently repressed
by multiple mechanisms, known as immune
tolerance in the liver. Although liver tolerance is
presumably an essential response to its frequent
exposure to a variety of food and microbial antigens,
it is one of the mechanisms that enable parasite
invasion in liver cells [3,4].
2. Methods
The PubMed database was used for the literature
review. Publications were collected in June and July
of 2023. Keywords used: "radiological imaging",
"abdominal parasitosis", "echinococcus
granulosus", "echinococcus alveolaris", "liver
flukes", "entamoeba hystolitica".
3. Results
3.1. Echinococcus spp.
3.1.1 Echinococcus granulosus
Cystic Echinococcosis (CE) or hydatid disease (HD)
is triggered by infestation with metacestodes (larval
phase) of Echinococcus granulosus tapeworm.
Human echinococcosis is a zoonotic secondary
illness [510]. E. granulosus is a common parasite
in certain regions of the globe, and it can be found
on every continent except Antarctica. Consequently,
CE impacts a significant number of indivi-
duals [5,10].
When carnivores consume the entrails of
contaminated intermediate hosts, such as pigs or
sheep, they frequently become infected with
Echinococcus granulosus. The gravid proglottids,
which are eventually eliminated in the infected
animal's feces, are released by the parasite once it
has entered the small intestine and adheres rigidly to
the mucosa. Each proglottid contains a number of
eggs that can be consumed by intermediate hosts. As
seen in sheep that become infected after grazing on
grass contaminated with dog excrement containing
the eggs, the eggs develop into cysts and offspring
cysts in these hosts. Handling or eating infected
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
62
sheep's meat or organs carries no risk of human
infection [5]. Humans are accidental intermediate
hosts who become infected either by direct contact
with a dog contaminated with egg-bearing
excrement or through ingestion of contaminated
water, food, or soil [5]. The asymptomatic
incubation phase, during which ingested eggs
release oncospheres that are capable of penetrating
the human intestinal wall, is the first stage of
infection. These oncospheres can access the liver,
lungs, and other organs by penetrating the portal
venous system. Then the oncospheres start to
develop cysts, which can have a diameter between
one and fifteen centimeters. Cysts are most
commonly found in the liver (70 %) or lungs (20 %),
10 % of cysts, however, can be discovered anywhere
in the body, including the spleen (6 %), heart (2 %),
kidney (2 %), and brain (2 %) [5,7,8,11] - with the
exception of hair, teeth, and fingernails, it can affect
nearly any organ in the body [8].
Hydatid cysts may be unintentionally found during
radiologic workup. Because of the gradual growth
and development of cysts, as well as the immune
system's reaction, CE might go undiagnosed for a
long period of time [5,10], because the majority of
cases are asymptomatic for years [11]. In the early
stages of the disease, patients may either be
completely asymptomatic or exhibit vague signs and
symptoms [13]. The symptoms of cystic
echinococcosis differ depending on where the cyst
is located.
The liver is the most affected organ in the body
because it acts as the first filter for portal venous
blood and obstructs roughly 75 % of ingested
embryonated eggs. While hydatid cysts of the liver
are often asymptomatic and found incidentally on
medical imaging, they might cause symptoms due to
cyst expansion, which can cause hepatomegaly or
the host's inflammatory reactions. Hydatid cyst
infection, biliary duct fistula, and rupture into the
peritoneum or chest are the most common
consequences [10].
Patients with intra-abdominal CE present with
symptoms late in the course of the illness [10].
Depending on their size and location, cysts may
eventually put pressure on surrounding tissues,
causing stomach pain and discomfort [5,9,10].
Despite being a non-malignant ailment, the
manifestation of hydatid disease can result in
elevated morbidity and mortality rates [7]. Cyst
rupture or leakage can cause immunologic
symptoms because it triggers an immunoglobulin
(Ig)E response, which can cause allergic reactions
characterized by hives, flushing, and swelling of the
mucous membranes. Anaphylactic shock can be
lethal if there is a major rupture [5]. As per the
research conducted by the World Health
Organization in 2010, the fatality rate for human
echinococcosis is 4 %, where the majority of deaths
are caused by anaphylactic shock induced by cyst
rupture [7]. Prompt diagnosis and therapy are
required to avoid potentially fatal complications
such as anaphylactic shock or pressure effects on
essential organs [10,11].
Imaging and serologic testing is used to diagnose
CE. Simple serum studies typically have low
sensitivity associated with undetected
immunological responses, making diagnosis
challenging. About 3040 % of patients have no
antibodies at all, even in those with circulating
parasite antigens. Low sensitivities of serum liver
enzyme assays make them typically unreliable in
determining the underlying severity of the
infection [5]. Complete blood count tests might be
helpful for these patients because they can have
eosinophilia [5,10,12].
The field of medical imaging holds great
significance in both the identification of a hydatid
disease and determining the extent of its progression
[12]. Depending on the cyst's stage, different
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
63
imaging results are obtained. In up to 30 % of CE
cases, calcification may be seen on radiographs.
During the CE process, calcification can happen at
any point. The pericyst is where calcifications are
typically deposited. Once a cyst has fully calcified,
the pathogen is considered to be dormant or
dead [5].While chest radiography is widely used as
the main diagnostic tool, it is insufficient for
evaluating the complications and progression of
hydatid disease [8].
The detection of CE is now commonly done through
ultrasound. The precision of ultrasound diagnostics
can go up to 90 %, contingent upon the proficiency
and skill of the user. This method is presently the
preferred choice for screening due to the
convenience and availability of the device, even in
small, remote medical centers. Because of its lack of
radiation, exceptional precision for identification,
distinguishing between ailments, categorization, and
screening to evaluate the pervasiveness of hydatid
cysts in the abdomen, ultrasound scanning is the
preferred option [10]. Ultrasound is not only
valuable for diagnosis but also for tracking post-
treatment progress [5,10]. Due to its potential to
provide comprehensive information about the mass,
including a more accurate assessment of its
dimensions, exterior characteristics, the presence of
a secondary cyst, and other pertinent anomalies in
the area, ultrasound is particularly responsive [12].
Inside the hydatid cyst, an ultrasound can clearly
show the hydatid sand, membranes, daughter cysts,
and vesicles. It has 96 % sensitivity and 98 %
specificity in distinguishing hydatid cyst of the liver
from simple liver cysts [10]. Its inability to
differentiate between hydatid disease and other
conditions is one of its weaknesses [12]. While
ultrasound is a superb means of preliminary
diagnosis, sonography can sometimes fall short due
to various factors such as obesity, excessive
intestinal gas, and past surgical procedures [5].
CT has a sensitivity rate close to 94 % and is
essential for detection [5]. Particular signs include
wall calcification, detached inner layer, and
daughter cysts (a defining characteristic). A CT scan
is still a more accurate examination because it can
confirm the size and location of the lesion as well as
any relation or involvement with neighboring tissue.
If surgical intervention is intended to be used to
ascertain the parenchymal involvement of the cyst
within the tissue, this can be especially helpful
during the preoperative planning stage. CT imaging
is important because it allows for a clear view of
cystic lesions and calcification, which might appear
as a thick, unilocular or multilocular heterogeneous
cyst or the presence of low-density daughter cysts
[12]. Calcifications, daughter cysts, and detached
membranes are all uncommon hydatid cyst features
[7,8]. Observations made through imaging in cases
of cystic echinococcosis vary from cystic formations
to formations that seem to be solid. The cyst may
show up as a fluid collection that is clearly defined.
Often, the endocyst may detach from the pericyst,
leading to the appearance of a membrane that
appears to be floating [9].
Although MRI plays a role in identification, the
main limitation of using this technology is its
exorbitant cost, especially when there is a chance of
reaching the diagnosis using less expensive
ultrasound or CT imaging [12]. While it isn't always
necessary, MRI may offer additional information
not visible on CT [5] - it is more effective at
exhibiting the correlation with neighboring flexible
tissues and contents of the cyst and daughter
cysts [8].
Depending on the growth stage, a hydatid cyst can
manifest in various dimensions and configurations,
resembling both benign and malignant tumors,
thereby presenting diagnostic complexities on
certain occasions. When making a differential
diagnosis for any cystic lesion, keep a hydatid cyst
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
64
in mind [7,8]. Hydatid liver cysts must be
considered as part of the differential diagnosis as
they can mimic a variety of liver lesions, such as
choledochal cysts, Caroli's disease, heman-
gioendotheliomas, mesenchymal hamartomas,
teratomas. The imaging features of hydatid cysts are
different and critical for diagnosis. Hydatid cysts
that are discovered in unexpected places could be
misdiagnosed, leading to ineffective treatment and
potentially fatal complications [11]. Radiological
imaging can thus only be used to differentiate
hydatid cysts from other infected or malignant
tumors. Hydatid cysts are infrequent, although they
might produce unexpected effects and symptoms in
rare cases [7].
Radiology is critical in both getting an accurate
diagnosis and offering assistance during the
treatment planning phase [8,12].
Figure 1. Echinococcus granulosus (Hydatid disease) cystic lesions viewed in ultrasonogram [13].
Figure 2. Contrast-enhanced computed tomography of the abdomen show unenhanced hypodense mass with well-
defined borders and no internal architecture without septa (a). Contrast-enhanced computed tomography of
abdomen (b) shows liver hydatids with multiple daughter cysts (arrows). Contrast-enhanced computed
tomography of the abdomen shows splenic hydatid cysts (c) well-defined lesions with peripheral wall calcification
and membranes appear as lamellated calcification (arrow head). Complex fluid collection with curvilinear
densities (blue arrow), consistent with detachment of the laminated membranes of the endocyst from the pericyst
of a hepatic hydatid cyst (d) [14]. [13]. The CT scan (e) reveals a patient from Kaunas Clinics with echinococcus
granulosus cysts in the liver.
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
65
3.2 Echinococcus alveolaris
Echinococcus multilocularis life cycle involves two
separate mammalian organisms, the definitive host
and the natural intermediate host. In the life cycle of
E. multilocularis, foxes are the definitive hosts while
rodents serve as intermediate hosts. The fox releases
the eggs that the adult parasite produces into the
environment, and the cycle is then completed when
the intermediate host digests tainted food. Humans
are either unintentional or atypical intermediate
hosts. The invasion of different organs by
metacestodes, primarily the liver and lungs, causes
severe problems. Alveolar echinococcosis is caused
by cestodes of Echinococcus multilocularis. AE is a
manifestation that can only be observed in the
northern hemisphere [15,16]. Echinococcus
multilocularis metacestodes have the ability to infect
multiple organs in people and exhibit neoplastic-like
growth and infiltration patterns. AE is also referred
to as "worm cancer” - it is easily mistaken for cancer
because it can metastasize to distant organs or
invade nearby ones [16]. Furthermore, because the
condition is uncommon, particularly in non-endemic
locations, diagnosing it can be difficult [15,16].
The illness typically progresses with an
asymptomatic incubation period lasting 5-15 years,
followed by a chronic phase. In more than 33 % of
cases, the condition is identified by chance. The
clinical symptoms displayed depend on the
individual organ affected and the amount of the
invasion. Other abdominal organs are damaged by
the direct invasion or metastatic spread. There have
been reports of invasions of the diaphragm, perirenal
region, abdominal lymph nodes, peritoneum,
mesenteric tissues, spleen, pancreas, adrenal glands,
kidneys, gallbladder, retroperitoneum, abdominal
wall, and stomach. Primary organ involvement
outside of the liver is extremely rare. The lungs are
the organs that are most frequently involved in
secondary AE [15].
The larval stage typically manifests in the liver,
inducing infiltrative mass lesions with numerous
vesicles that range in diameter from submillimeter
to 20 cm [16]. The most common symptoms of liver
invasion are jaundice, pain in the upper abdomen,
exhaustion and weight loss. The transition from
healthy tissue to diseased tissue is indistinct, and the
masses are further characterized by diffuse fibrosis,
calcified foci, and necrotic regions, primarily
located in central zones. The infiltration of the
biliary ducts and vessels, combined with tissue death
at the core of the injury, can result in critical issues
such as bile duct inflammation, abscesses in the
liver, portal vein hypertension, Budd-Chiari
syndrome, biliary cirrhosis, or additional infections,
all of which can increase morbidity or mortality. AE
is extremely harmful to the human body, damaging
the liver in 100 % of cases and causing substantial
damage to hepatic functioning. Lung involvement is
typically discovered by chance. The primary
symptoms include hemoptysis, dyspnea, coughing,
and chest pain [15].
AE is a chronic tumor-like condition that, if
untreated or treated insufficiently, can be fatal. More
than 90 % of patients with untreated or insufficiently
treated AE die within 10 to 15 year [15,16]. Death
can result from problems with the hepatobiliary
system and associated infections, secondary biliary
cirrhosis and related complications, issues caused by
vascular structure involvement, and invasion of
distant organs. Primary involvement beyond the
liver is exceedingly uncommon (1 % of cases), with
direct invasion of other intra-abdominal organs or
secondary spread to more distant organs such as the
brain, lungs, or bones via hematogenous or
lymphatic pathways [15,16]. Multi-organ invasion is
observed in 13 % of cases [15].
While radiologic imaging techniques are important,
the diagnosis must be validated by further support of
histopathologic verification or detection of parasite
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
66
nucleic acid in the clinical sample. For some years,
conventional imaging modalities such as x-ray,
ultrasonography (US), computed tomography (CT),
and magnetic resonance imaging (MRI) have been
used in the diagnosis, follow-up, and therapy of AE.
New investigations on the diagnosis and follow-up
of the condition using contrast-enhanced
ultrasonography (CEUS), diffusion-weighted
imaging (DWI), magnetic resonance spectroscopy
(MRS), and positron emission tomography-
computed tomography (PET-CT) have recently been
published [15].
Ultrasound is often the chosen imaging modality for
diagnosis and follow-up. It is an appropriate and
efficient imaging approach for detecting AE lesions.
When there are irregular contoured mass lesions, a
mixed heterogeneous echogenic pattern, cystic
necrotic areas, and multiple scattered calcific foci,
the liver is involved. A less typical sonographic
appearance is a hailstorm pattern with several
hyperechogenic solid lesions. This look is thought to
represent early AE lesions. Radiologists in endemic
areas must precisely identify this less common
presenting form, which might be confounded with
venous malformations and other lesions of a similar
character [15].
Figure 3. CT scan (a) reveals a single giant echinococcosis cyst in the liver. CT image (b) shows CE of the
detached inner capsule type: the inner capsule is folded into a floating band symbol after being deflated and
separated. CT image (c) reveals multi-daughter cysts are visible inside the big cyst. The CT image (d) acquired
after intravenous contrast shows two hepatic masses with unclear borders and diffuse hyperdense foci of coarse
calcification [13]. The CT scan (e) reveals a patient from Kaunas Clinics with echinococcus alveolaris cysts in
the liver.
The most effective imaging modality for
demonstrating the distinctive morphologic aspects
of AE lesions in intra-abdominal organs is CT. It is
helpful in determining how the hepatic lesions
interact with the bile ducts and vascular systems. It
is also possible to demonstrate involvement of
extrahepatic organs. AE lesions resemble tumors
and have erratic borders, diverse internal structures,
and numerous, dispersed calcific foci. The affected
liver lobe exhibits atrophy and capsular retraction as
a result of vascular and biliary involvement [15].
The best imaging technique for identifying the
different parts of a parasite lesion and showing
invasion of the vascular and biliary structures is
magnetic resonance imaging (MRI). Since MRI is so
helpful in revealing expansion to nearby organs, it
should be used in preoperative imaging. The typical
MRI finding of AE in the liver is a mass lesion with
infiltrative characteristics, uneven boundaries,
internal heterogeneity, and necrotic regions in the
center. The inner edge of the fibrous zone appears as
a slightly hyperdense signal with localized
invagination forming a peninsula sign and internal
necrosis and liquefaction forming a fluid retention
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
67
cavity. These exhibit hypo- or isointensity on T1-
weighted images and hypo-, iso-, or hyperintense
signal characteristics on T2-weighted images [15].
Particularly in nonendemic areas, AE may be easily
misdiagnosed by inexperienced doctors as a
metastatic malignant tumor [15,16]. The radiologist
must be knowledgeable about the multimodality
imaging findings of this disease. Ultrasonography
can be used for scanning as well as for the initial
imaging process. Additionally, ultrasound can direct
the interventional techniques. The use of CT and
MRI is essential for making sure the right diagnosis
is made, for organizing surgical procedures, and for
monitoring patients with AE. Radiology plays a
crucial role in assisting the clinician in making an
early diagnosis and selecting the best course of
action [15].
3.3 Liver flukes
Fascioliasis is a parasitic infection of the
hepatobiliary system resulting from digenean
flatworms known as liver flukes, Fasciola hepatica
or Fasciola gigantica. Whenever parasites infiltrate
the liver, the bile ducts may become obstructed. F.
gigantica survives in tropical climates, meanwhile
F. hepatica is mostly found in temperate climate
regions. Mature Fasciola hepatica flukes are around
30 mm by 15 mm in size and are visible with the
human eye. Parasites have two suckers, including a
big one on the ventral side known as the acetabulum,
which allows the fluke to attach itself to the bile duct
wall and stay in position, while the smaller anterior
sucker feeds from the fluid inside. Fasciola
gigantica flatworms, as the name implies, can grow
to be 75 mm long but resemble smaller versions [6]
The worldwide count of Fasciola infection is
believed to be between 2.4 and 17 million, with most
cases going unreported and undiagnosed. Fasciola
hepatica is indigenous to Europe and Asia, with
infrequent occurrences appearing in Northern
Africa, Central and South America, and the Middle
East, as well as the United States and the Caribbean.
Domestic livestock in Asia, the Pacific Islands, and
areas of Northern Africa are infected with Fasciola
gigantica [6,17].
The life cycle began when humans and other fish-
eating mammals, the definitive hosts, transferred
eggs into surroundings via their feces. When the
eggs appear in freshwater, the miracidia infect their
first intermediate host, a freshwater snail, and
change into sporocysts, rediae, and cercariae.
Cercariae elude the snail and infect freshwater fish,
the second intermediate host. The cercariae encyst
as metacercariae in the muscles or under the scales
and can infect humans through the consumption of
undercooked or raw cyprinoid fish products. The
metacercariae enter the human small intestine
uninjured and move until they reach the bile ducts,
where they grow into adult worms and deposit eggs
within 4 weeks. The parasites can live in the human
liver for up to 25 years [6].
The migration of metacercariae induces
parenchymal liver damage, triggering a chain
reaction of inflammatory and immunological
responses that results in acute symptoms. Adult
flukes can clog the bile ducts either entirely or
partially, causing fibrosis, hypertrophy, and
eventually dilatation of the proximal biliary system.
The level of liver damage is often positively
associated with parasite load [17].
The fascioliasis infection has two different phases.
The acute (hepatic) stage typically begins 6 to 12
weeks after ingesting metacercariae from polluted
water. The first symptom is frequently a high
temperature, discomfort in the right upper quadrant,
hepatomegaly, and jaundice. The presence of
peripheral eosinophilia can be detected by a
complete blood count (CBC). Myalgias, urticarial
rash, nausea, anorexia, and diarrhea are common
symptoms. The above symptoms are caused by
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
68
Fasciola flatworms spreading into the liver
parenchyma and triggering inflammatory and
immune system reactions. Most acute signs
disappear after 6 weeks, and the infection expands
to a chronic stage [17]. However, extrahepatic signs
such as reactive eosinophilic pneumonitis,
vasculitis, myocarditis, cerebral vasculitis and
generalised lymphadenopathy may also be present
[17,18]. Once the flukes are located inside the bile
ducts, the chronic (biliary) phase can remain for up
to a decade. This stage is normally asymptomatic,
although it can cause chronic epigastric and right
upper quadrant pain, nausea, vomiting, diarrhea,
hepatomegaly, and jaundice. Chronic common bile
duct obstruction can cause recurrent jaundice,
cholelithiasis, pancreatitis, and, more dangerously,
ascending cholangitis. Chronic biliary cirrhosis,
sclerosing cholangitis, and even cholangio-
carcinoma can arise from long-term infection and/or
a high parasite load [17,18].
Fascioliasis is a pretty rare illness, but it should be
evaluated in any individual who has abdominal pain,
fever, pruritus, skin rashes, dyspepsia, vomiting,
nausea, transaminitis, and significant peripheral
eosinophilia. If a patient has gone to endemic
locations and their food habits include watercress
intake or eating of raw vegetables washed in
possible contaminated water, suspicion must be
raised [19].
Misdiagnosis and late diagnosis are still common
since the disease is rarely observed in nonendemic
locations and has an unclear clinical appearance.
Hepatobiliary fascioliasis in humans is diagnosed
with direct parasitological tests, indirect
immunological tests, and imaging methods like
ultrasound, CT, and MRI. Radiological tests are
useful in differential diagnosis when liver flukes are
suspected, as is the history of recent travel to the
endemic region [19]. On CT imaging, the leading
sign of hepatic fascioliasis is groups of irregular ill-
defined darkish patches, mainly immediately under
the liver surface, which may progress to inner tissue
and areas around the bile duct. Liver parenchyma
can reveal nodular, tiny, branching, and subcapsular
lesions - migrating parasites leave these wounds.
Necrosis may be visible during intravenous contrast
scanning. It may be possible to see subcapsular
hematoma, capsular thickening, or parenchymal
calcifications as well [15,19].
MRI is preferable to CT imaging because it can
detect a greater number of lesions, also it may show
the disease's typical evolutionary pattern,
representing its life cycle during the early
parenchymal phase, even without the use of a
contrast agent. Furthermore, in fascioliasis, MRI can
provide more detailed information regarding the
development of complications such as hemorrhagic
lesions and abscess formation [9,19].
Sonographic findings in hepatic fascioliasis are
frequently nonspecific. During the parenchymal
phase, they include focal hypoechoic or anechoic
liver lesions and diffuse liver involvement
(heterogeneous echotexture). During the ductal
phase of ultrasound, ductal thickening, intrahepatic
or common bile duct dilatation, and tortuousness are
frequently seen due to intraluminal parasites or the
hemorrhage/inflammatory response they cause. It
might even show a mobile fluke in the gallbladder
or dilated bile ducts [19].
During the biliary stage, ultrasound and
cholangiogram can detect mobile, leaf-like flukes in
the biliary ducts or gallbladder, which are frequently
linked with stones. Abnormal common bile duct
wall thickening, hepatomegaly, splenomegaly,
and/or periportal lymphadenopathy are frequently
observed, particularly during the acute stage [19,20].
However, in recent years, serology has emerged as
the quickest and most efficient method of testing for
fascioliasis. Titers against Fasciola antigens become
positive during the early stages of parasite migration
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
69
and are detectable for 2 to 4 weeks after initial
immune system activation [20].
Identification of Fasciola hepatica tends to be
challenging, especially in areas where it is not
endemic, because clinical and laboratory signs are
non-specific. Cross-sectional imaging is commonly
used to evaluate probable causes of these confusing
findings. On CT/MRI scans, clusters of twisted
subcapsular lesions with exterior contrast
improvement that extends into the deeper
parenchyma and periportal regions are significant
signs that strongly suggest hepatic fascioliasis.
When relevant radiological indicators are
discovered, the potential of hepatic fascioliasis must
always be considered in a proper clinical context
[19].
Figure 4. Contrast-enhanced CT picture (a) with patchy areas of decreased attenuation migrating from the liver
capsule into deeper parenchyma and periportal regions with modest peripheral contrast enhancement (arrows).
Contrast-enhanced CT-image (b) revealing clusters of hypodense lesions extending from the liver capsule into
deeper parenchyma and periportal regions with slight peripheral contrast enhancement (arrows) [21].
3.4 Entamoeba histolytica
The most prevalent cause of liver abscess in tropical
countries is amebic liver abscess (ALA), a parasite
illness caused by the protozoan Entamoeba
histolytica. Amebic liver abscess (ALA) occurs in 3-
9 % of amebiasis patients, with complications
occurring in 20-40 % of cases and a death incidence
of 2-18 % [22]. After malaria and schistosomiasis, it
is the third leading parasite cause of mortality,
killing approximately 100,000 individuals per year
[23]. Although the number of cases has decreased in
recent years, ALAs remain a major public health
concern in endemic areas [24]. Amoebiasis is most
prevalent in tropical countries with poor sanitation
and lower socio-economic status. This parasite has
been detected to infect around 20 % of the Indian
population. Homosexual men, people with acquired
immunodeficiency syndrome or HIV, cirrhotic
patients, and people living in group homes or mental
health facilities are all at high risk of getting
amoebiasis [24]. Malnutrition and alcohol use are
also risk factors. The majority of ALAs appear with
mild to moderate symptoms and respond to
antiamebic medication within three days. However,
reports from endemic areas show that the disease can
be severe in up to 40% of patients and is not
controllable with the medicine alone. These
abscesses frequently appear rapidly with rupture,
organ failure, and abnormal laboratory results -
additional percutaneous drainage is required.
Amebic liver abscesses have a 1% fatality rate [21].
Infection begins with the intake of E. histolytica
cysts found in water or food that is contaminated.
The vast majority of infected people (90 %) are
asymptomatic carriers, meaning the parasite lives
securely inside the lumen of the colon and excretes
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
70
cysts in feces to complete the entire life cycle. E.
histolytica breaks the intestinal mucosa and invades
the underlying lamina propria, where it contacts
with host immune cells, producing a raging
proinflammatory cytokine response that causes
tissue damage in 10 % of infected individuals
(symptomatic). It is unknown why a high number of
E. histolytica-colonized people do not develop
invasive illness. The complicated pathogenesis is
thought to be driven by a combination of parasite
virulence factors, host genetics, microbiome, and
immunological responses [21].
Amebic liver abscesses are characterized by right
upper quadrant (RUQ) discomfort and fever.
Symptoms commonly appear subacutely. Less than
one-third of patients had diarrhea, while some may
have had dysentery in the previous months. Jaundice
affects less than 10 % of the affected ones. Patients
returning from an endemic location usually get the
condition within 8-20 weeks, with a 12-week
average. Typically, there is a leukocytosis without
eosinophilia and an increased alkaline phosphatase
that is out of proportion to any increase in
aminotransferases [20,21].
Figure 5. CT scan (a) shows the abscess's non-
enhancing and ragged edge in the absence of a
defined wall (arrows). Pay attention to the dilated
intrahepatic biliary ducts (arrowheads) due to the
mass effect. CT image (b) of an abscess showing a
double-target sign with an inner enhancing ring
(white arrowhead) and an outer hypodense ring
(black arrowhead). CT scan (c) of an abscess. Take
note of the abscess's rim-enhancing wall and the
perilesional halo-like hypodensity, as well as the
focal nodularity in the wall (arrow) reflecting
partially resorbed septa. The CT image (d) displays
a well-defined smooth wall (arrow), although there
is no contrast enhancement. The abscess wall is
surrounded by an ill-defined hypodensity (asterisk).
Take note of the huge cavity formed by the fusion of
several abscesses, as well as the intervening wall
that mimics internal septations [20].
The diagnosis of an amebic liver abscess is obtained
using a combination of imaging features and
serologic testing. A cystic intrahepatic cavity is
visible on imaging, which is usually
indistinguishable from other types of liver
abscesses. Most amoebic liver abscesses are single
lesions, however multiple lesions may occur on
occasion, and they are more commonly detected in
the right lobe than the left. On ultrasound, the lesion
shows as a spherical, well-defined hypoechoic mass.
After healing, the margin of the abscess may calcify
and form a round, thin rim [20,21,23].
ALAs have a non-specific CT appearance that has
been described as a round or oval hypodense lesion
with a thick enhancing wall and peripheral edema.
Although these characteristics are considered
classical, they are suggestive of resolving ALAs.
Wall creation and rim enhancement are late results
discovered as the healing process progresses - this
appearance is likely to suggest modest drug-
responsive illness. These characteristics are rarely
seen in acute abscesses - they are clinically
accompanied with significant symptoms or a
distorted test profile. As a result, it is critical to
distinguish aggressive abscesses from ones with
modest manifestations [22].
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
71
The typical radiographic features are insufficient to
determine a diagnosis and must be evaluated in
conjunction with serological or serum antigenic
evidence. Although the test may be negative in the
first seven days of illness, most of the patients with
amebic liver abscesses will produce detectable
antibodies to E. histolytica. Antibodies are detected
in 92- 97 % of patients with amebic liver abscesses.
The aspiration of amebic liver abscesses is not
required for diagnosis - trophozoites are only found
in a small percentage of aspirates. Furthermore,
when patients arrive with amebic liver abscesses,
stool microscopy for E. histolytica is commonly
negative, demonstrating that stool microscopy
cannot be relied on to make the correct
diagnosis[21,23].
4. Conclusion
The most common parasitosis that affects abdominal
organs are mainly caused by Echinococcus spp.,
liver flukes and Entamoeba histolytica. Orally
transmitted parasitic infections frequently cause
liver damage, due to the liver's role as the primary
organ to filter portal venous blood. Additionally, it
has the potential to spread to other organs like the
lungs, kidneys, and pancreas via blood flow or
mucosal penetration. Parasitic infections are
typically asymptomatic and diagnosis is often made
by chance. However radiological imaging plays a
crucial role in diagnostics - the most frequently used
imaging methods include ultrasonography,
computed tomography, and MRI. Moreover, in the
vast majority of cases, the diagnosis must be
clarified by serological tests.
References
1. Peters L, Burkert S, Grüner B. Parasites of the
liver epidemiology, diagnosis and clinical
management in the European context. J Hepatol.
2021 Jul 1;75(1):20218.
2. Deslyper G, Doherty DG, Carolan JC, Holland C
V. The role of the liver in the migration of parasites
of global significance. Parasit Vectors [Internet].
2019 Nov 8 ;12(1).
3. Brandl K, Kumar V, Eckmann L. Gut-liver axis at
the frontier of host-microbial interactions. Am J
Physiol Gastrointest Liver Physiol [Internet]. 2017
May 1 [cited 2023 Sep 6];312(5):G4139.
4. Gottwick C, Carambia A, Herkel J. Harnessing
the liver to induce antigen-specific immune
tolerance. Seminars in Immunopathology 2022 44:4
[Internet]. 2022 May 5 ;44(4):47584.
5. Pakala T, Molina M, Wu GY. Hepatic
Echinococcal Cysts: A Review. J Clin Transl
Hepatol [Internet]. 2016;4(1):3946.
6. Alshoabi SA, Alkalady AH, Almas KM, Magram
AO, Algaberi AK, Alareqi AA, et al. Hydatid
Disease: A Radiological Pictorial Review of a Great
Neoplasms Mimicker. Diagnostics [Internet]. 2023
Mar 1 ;13(6).
7. Şimşek S, Özmen CA. Unusual imaging
characteristics of thoracic hydatid disease. Radiol
Bras [Internet]. 2022;55(2):12833.
8. Durhan G, Tan AA, Düzgün SA, Akkaya S,
Arıyürek OM. Radiological manifestations of
thoracic hydatid cysts: pulmonary and
extrapulmonary findings. Insights Imaging
[Internet]. 2020 Dec 1;11(1).
9. Good R, Scherbak D. Fascioliasis. StatPearls
[Internet]. 2023 May 1;
10. Bulakçı M, Kartal MG, Yılmaz S, Yılmaz E,
Yılmaz R, Şahin D, et al. Multimodality imaging in
diagnosis and management of alveolar
echinococcosis: an update. Diagn Interv Radiol
[Internet]. 2016 May 1 ;22(3):24756.
11. Khalili N, Iranpour P, Khalili N, Haseli S.
Hydatid Disease: A Pictorial Review of Uncommon
Locations. Iran J Med Sci [Internet]. 2023 Mar
1;48(2):11829.
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
72
12. Hamed Al Taei T, Ali Al Mail S, Hajjaj Al
Thinayyan A, Alsetrawi A. Renal hydatid cyst: A
case report. Radiol Case Rep [Internet]. 2022 Jun
1;17(6):20636.
13. Piccoli L, Tamarozzi F, Cattaneo F, Mariconti
M, Filice C, Bruno A, et al. Long-term Sonographic
and Serological Follow-up of Inactive Echinococcal
Cysts of the Liver: Hints for a “Watch-and-Wait”
Approach. PLoS Negl Trop Dis. 2014;8(8).
14. Mehta P, Prakash M, Khandelwal N.
Radiological manifestations of hydatid disease and
its complications. Trop Parasitol [Internet]. 2016 Jul
1;6(2):103.
15. Mas-Coma S. Epidemiology of fascioliasis in
human endemic areas. J Helminthol [Internet]. 2005
Sep;79(3):20716.
16. Bayhan Gİ, Batur A, Taylan-Özkan A,
Demirören K, Beyhan YE. A pediatric case of
Fascioliasis with eosinophilic pneumonia. Turk J
Pediatr [Internet]. 2016;58(1):10912.
17. Govindasamy A, Bhattarai PR, John J. Liver
cystic echinococcosis: a parasitic review. Ther Adv
Infect Dis [Internet]. 2023 Jan 1;10.
18. Šimeková K, Rosoľanka R, Szilágyová M,
Antolová D, Nováková E, Novák M, et al. Alveolar
Echinococcosis of the Liver with a Rare Infiltration
of the Adrenal Gland. Helminthologia [Internet].
2021 Feb 10 ;58(1):100.
19. Preza O, Klapa I, Tsiakalos A, Cokkinos DD,
Chatziioannou A. Fascioliasis: A challenging
differential diagnosis for radiologists. J Radiol Case
Rep [Internet]. 2019 Jan 1;13(1):11.
20. Priyadarshi RN, Sherin L, Kumar R, Anand U,
Kumar P. CT of amebic liver abscess: different
morphological types with different clinical features.
Abdom Radiol (NY) [Internet]. 2021 Sep
1;46(9):4148.
21. Usuda D, Tsuge S, Sakurai R, Kawai K,
Matsubara S, Tanaka R, et al. Amebic liver abscess
by Entamoeba histolytica. World J Clin Cases
[Internet]. 2022 Dec 12 ;10(36):13157.
22. Bansal Y, Maurya V, Tak V, Bohra GK, Kumar
D, Goel AD, et al. Clinical and laboratory profile of
patients with amoebic liver abscess. Trop Parasitol
[Internet]. 2022 Jul 1;12(2):113.
23. Singh A, Banerjee T, Kumar R, Shukla SK.
Prevalence of cases of amebic liver abscess in a
tertiary care centre in India: A study on risk factors,
associated microflora and strain variation of
Entamoeba histolytica. PLoS One [Internet]. 2019
Apr 1;14(4).
24. Salahshour F, Tajmalzai A. Imaging findings of
human hepatic fascioliasis: a case report and review
of the literature. J Med Case Rep [Internet]. 2021
Dec 1;15(1).
Journal of Medical Sciences. 23 Nov, 2023 - Volume 11 | Issue 6. Electronic - ISSN: 2345-0592
73

Comments are closed.