Echinococcosis/hydatidosis is a zoonotic parasitic disease caused by the dog d’Echinococcus granulosus – Ciclo biológico de Echinococcus granulosus. Sep 25, English: Echinococcosis, Hydatid disease or echinococcal disease; العربية Ciclo biológico Echinococcus × ; 96 KB. Feb 27, Español: Representación gráfica del ciclo biológico del parásito cestodo Echinococcus granulosus, indicando los distintos estadios del mismo.
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Cystic echinococcosis CE is a complex, chronic and neglected disease with a worldwide distribution. The liver is the most frequent location of parasitic cysts.
CDC – DPDx – Echinococcosis
In humans, its biilogico spectrum ranges from asymptomatic infection to severe, potentially fatal disease. Four approaches exist echhinococcus the clinical management of CE: Allocation of patients to these treatments should be based on cyst stage, ibologico and location, available clinical expertise, and comorbidities.
However, clinical decision algorithms, efficacy, relapse rates, and costs have never been echinococfus evaluated.
This paper reviews recent advances in classification and diagnosis and the currently granulossus evidence for clinical decision-making in cystic echinococcosis of the liver. Cystic echinococcosis CE is a neglected parasitic disease and echinococcal cysts are mostly located in the liver.
Therefore, CE should always be included in the differential diagnosis of cystic lesions of the liver. However, diagnosis and clinical management can be difficult because of the combination of clinical variables cysts stage, size, presence of complications, available expertise and three different treatments that have never been systematically compared. This review summarizes current knowledge and open issues in this field for those hepatologists who have limited or no experience with this complex condition.
Hepatologists may encounter cystic echinococcosis CE in their practice. However, due to its relatively low prevalence in many Western countries, this infection is poorly characterized and its complex management can be difficult for clinicians unfamiliar ggranulosus this condition. Moreover, hepatic CE should be included in the differential diagnosis of focal liver lesions. CE, or hydatidosis, is caused by the larval stage metacestode of Echinococcus granulosus E.
Its life cycle develops in dogs and granulosud canids, which harbor the adult tapeworm in the intestine, and herbivores or humans as dead-end occasional host as intermediate hosts, where the larval metacestode form develops in different organs Figure 1. Once biologlco are ingested by the intermediate host, the oncosphere also named exacanth larvabiokogico released from the keratinized embryophore in the stomach and intestine where it penetrates the small intestine wall via its hook movements.
The oncosphere is then carried via portal flow to the liver and other organs where the metacestode implants. Organs may also be reached through the lymphatic system[ 1 ]. This process results in primary echinococcosis, while secondary echinococcosis follows the spillage of protoscoleces tapeworm heads or small daughter cysts from the original cyst that ruptures following trauma or surgery and their seeding, primarily in the peritoneum for abdominal cysts[ 2 ].
The impact of CE on human health is significant, with an estimated 1. Despite the low mortality rate 0. Despite these figures, the infection is still under-reported and has received to date much less attention than infections of comparing burden[ 5 ]. In humans, its clinical manifestations range from asymptomatic infection to severe, potentially fatal disease.
The lungs are the second most common location; however, CE can present in virtually any other organ, although this rarely occurs[ 12 ]. Echinococcal cysts consist of a bioloogico host tissue pericyst or adventitiawhich surrounds the larval endocyst, and an endocyst itself.
The endocyst is composed of an outer, acellular laminated layer and an inner layer, the germinal layer, which gives rise, in fertile cysts, to brood capsules and protoscoleces[ 6 ]. Each protoscolex may develop into an adult tapeworm if ckclo by a suitable definitive host.
The cyst is filled with clear fluid containing molecules of both parasite and host origin, numerous brood capsules, and protoscoleces. Some cysts may also harbor daughter cysts of variable size Figure 2. The fluid is clear in the early stages Figure 3Abut can be yellowish and turbid, with fragments of endocyst in advanced stages e.
Eurasia, Africa, Australia, and South America show the highest prevalence[ 7 ]. Within endemic zones, the granullsus varies from sporadic to high, with recent studies showing an higher prevalence among females and with increasing age[ 8 ].
File:Ciclo biológico Echinococcus granulosus.jpg
grxnulosus Only a few countries can be regarded as free of E. Currently, 10 genotypic strains of E. Genotypes are grouped into 4 species that constitute the E. Granulosus sensu strictu G1-G3E. The great majority of E.
Echinococcus granulosus – Viquipèdia, l’enciclopèdia lliure
Acute infection in humans has never been documented[ 9 ], thus all available data come from experimental studies in animal intermediate hosts.
Cavity formation and the development of both germinal and laminated layers of the cyst wall occur 10 to 14 d post infection in the mouse model[ 10 ]. Formation of brood capsules and protoscoleces requires a longer time period in sheep, from 10 mo to 4 years[ 11 ]. Based on clinical observations using ultrasound USthe cysts progress from a fluid-filled biolgoico cavity to a pseudo-solid, eventually calcified lesion.
The sequence of cyst development between these 2 stages is poorly understood[ 12 ]. Preliminary observations suggest that cysts that have reached the CE4 stage as a result of treatment may revert to CE3b more often than those reaching the inactive garnulosus spontaneously; this may occur many years after apparently successful granuolsus 14 ] Junghanss, personal communication.
The origin and fate of CE2 and CE3b stages are less clear. CE2 may represent a relapsed CE3a, and CE3b a relapsed CE4, but long-term observations of large cohorts of patients are needed to bioologico this hypothesis. The growth rate of cysts is variable. The presentation of human CE is protean. Potential presentations may be due to the mechanical effect of a large graunlosus on surrounding tissues, dw of a cyst biolofico an acute hypersensitivity reaction, or complications such as biliary obstruction or embolism.
The cyst is often asymptomatic and diagnosed accidentally during radiographic examination, surgery, or during evaluation of other clinical diagnoses. Common symptoms are upper abdominal discomfort and pain and poor appetite. Physical findings are hepatomegaly, presence of an abdominal palpable mass and abdominal distension.
Cysts in the liver should be included in the differential diagnosis of several conditions, such as jaundice, colicky pain, portal hypertension, ascites, compression of the inferior vena cava and Budd-Chiari syndrome and can be misdiagnosed as non-parasitic cysts, single or multiple hemangiomas, pyogenic or amebic liver abscess, hematoma, adenoma, adenocarcinoma, hepatocellular carcinoma, metastases, focal or diffuse lymphoma, alveolar echinococcosis, and textiloma[ 2021 ].
As the infection may remain silent for years before the enlarging cysts cause symptoms, the clinical diagnosis of CE is often difficult and requires a combination of physical examination, imaging techniques, in particular US, and serology; the latter plays a supportive role in diagnosing CE despite the development of sensitive serodiagnostic tests and dr use of different antigen sources.
Imaging techniques have revolutionized the diagnosis and clinical management of CE. Gharbi et al[ 22 ] developed the first US classification for CE in Other classifications were subsequently produced but were not widely adopted. Inthe WHO Informal Working Group developed an international standardized US classification that could be universally applied to replace the plethora of classifications in use.
This classification, d in [ 23 ], differs from Gharbi original classification by introducing a cystic lesion CL category to include cysts of unclear origin, and by reversing the order of CE types 2 and 3 Figure 4. CL cysts are not included as a type of CE, as they require further evaluation before being classified as CE[ 24 ].
CE1 and 2 are active, biologco fertile cysts containing viable protoscoleces. CE3 are cysts entering a transitional stage where the integrity of the echinocofcus has been compromised either by the host or by chemotherapy. CE4 and CE5 are inactive cysts that have lost their fertility grsnulosus are degenerating. Cicl more recent amendment to the WHO classification clarifies that calcifications are not limited to CE5 cysts, but may be present to a various extent in all cystic stages and are therefore not indicative of cyst death[ 25 ].
Data on long-term follow-up of cysts treated with albendazole and percutaneous treatment provide ground for a further sub-classification of CE3 transitional cysts into CE3a with detached endocyst and CE3b predominantly solid with daughter vesicles.
This has important implications for clinical decision-making and prognosis[ 26 ]. The sub-classification of CE3 into CE3a and CE3b is supported a recent work using high-field 1 H magnetic resonance spectroscopy evaluating the metabolic profile of cysts contents ex vivo [ 27 ]. This study confirmed findings from optical granuloosus that CE3a are equally likely to ecjinococcus viable or non-viable, whereas CE3b are consistently viable.
Of note, CE3a and Echinococccus also respond differently to non-surgical treatments[ 2829 ]. In light of these features, CE3b cysts should be considered as active, while CE3a are the transitional cysts sensu stricto.
Another study showed how a CE1 brain cyst, in in vivo magnetic resonance spectroscopy matched the profile of an active stage before the medical treatment with albendazole ABZ and that of an inactive one after ABZ[ 30 ].
CE2 and CE3b cysts tend to relapse both after PAIR puncture, granulosud, injection of a scolecidal agent, and reaspiration and ABZ[ 262829 ], and several studies suggest that a strong Th2 response correlates with susceptibility to disease active cystwhereas a Th1 response correlates with protective immunity inactive cysthowever this is not clear cut[ 31 – 36 ].
Computed tomography CTincluding spiral or multidetector CT, with multiplanar reformations, and magnetic resonance imaging MRIwith at least a T2-weighted imaging sequence, and if necessary cholangiopancreatography, have distinct indications: Despite CE being a helminthic infection, eosinophilia is usually moderate or absent. Despite the development of sensitive laboratory tests and the use of different antigen sources, serology remains complementary to imaging in the diagnosis of Tranulosus.
Currently, lipoprotein antigen B AgB and Ag5, the major components of cystic fluid, have received the most attention with regard to diagnosis, but purified cyst exhinococcus fluid is still the most widely used in current assays for immunodiagnosis of CE, which are not standardized[ 4142 ]. The result of a single test is not considered diagnostic, and the two tests are generally run in parallel. False positives result from cross-reactivity, most commonly with other cestode infections E.
Serologic testing for CE is hampered by many problems[ 41 – 4345 ]. These include low sensitivity, partially dependent granulisus the location of the cysts in the body and the cystic stage, and rchinococcus inability of serology to clearly distinguish between active and inactive cysts when US is inconclusive[ 43 biollogico. In addition, patients with multiple cysts are generally seropositive. This may lead inexperienced clinicians to prescribe unnecessary treatment and cause unjustified anxiety to the patient.
New antigens are under investigation which promise to have higher diagnostic performances in these situations[ 53 ]. When US and serology are inconclusive, a direct analysis of the material obtained by percutaneous aspiration is needed. The procedure must be performed with the assistance of an anesthesiologist because of the very low but nonetheless present risk of anaphylaxis[ 54 ].
The presence of protoscoleces or their components or of antigens specific to Ce. There is no standard treatment for hepatic CE.
Matters are further complicated by the dearth of randomized clinical trials evaluating treatment options, and the ensuing low level of evidence to support one therapeutic modality over another[ 5758 ]. Surgery has long been considered the best, if not the only, option in the treatment of CE. While surgery is increasingly being replaced by other options in uncomplicated cysts, it maintains a central role in complicated cysts i.
Surgery can be performed as an open procedure, with either radical or conservative techniques, or laparoscopically. There are still controversies as to the safest and most effective technique, and in which cases it should be applied[ 576061 ].
As a rule, perioperative ABZ prophylaxis, from 1 wk prior to surgery until 4 wk postoperatively, is necessary to minimize the risk of secondary echinococcosis from seeding of protoscoleces in the abdominal cavity[ 59 ]. In conservative procedures, only the parasitic material is removed while part or all of the pericyst is left in place and the residual cavity is managed with different techniques, such as omentoplasty, capitonnage, or external drainage.
It is commonly perceived that the more radical the surgery, the higher the operative risk but the lower the risk of relapses and vice versa. Recurrence, both local and as secondary echinococcosis, is associated with spillage during removal of the cyst, incomplete removal of the endocyst, and possibly the presence of unnoticed exophytic cyst development[ 6369 ]. For the latter, intraoperative US has been shown to be an important tool to improve the quality of hepatic surgery[ 70 ].
Infection and biliary communication with the cyst i. Cyst diameter is a factor associated with a high risk of biliary-cyst communication in clinically asymptomatic patients.