|Year : 2015 | Volume
| Issue : 1 | Page : 4-13
Spotlight on the brain hydatid cyst and whether its location is accidental or target
Refaat M. A. Khalifa PhD. , Abeer E Mahmoud, Ragaa M Othnman
Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt
|Date of Submission||17-Feb-2015|
|Date of Acceptance||20-Apr-2015|
|Date of Web Publication||24-Aug-2015|
Refaat M. A. Khalifa
Department of Parasitology, Faculty of Medicine, Assiut University, 71526, Assiut
Source of Support: None, Conflict of Interest: None
Hydatidosis of the brain is a rare disease. The diagnosis is usually late because of its slow progression and absence of specific symptoms. This review attempted to throw light on some aspects of cerebral hydatidosis because of deficient clinical suspicion of the disease, and imaging investigations are sometimes inadequate and biopsy reports inconclusive. Thus, the literature pertaining to parasitic causes, the incidence, the pathogenesis, the clinical picture, the diagnosis, and the management of the disease were overviewed. Our intention was to alert parasitologists and neurosurgeons concerning this morbid and rare condition, and to emphasize the fact that parasitic infection should be suspected in cystic lesions affecting the brain, especially in endemic areas of the world. Moreover, we aim to discuss or derive an answer to some amazing aspects of the disease. These include its clear abundance in children and in young age, its unusual huge size in their brains, whether the brain is an accidental or a target location, its extreme rarity in domestic animal's brains, the usual failure of serological and immunological tests used for its diagnosis, the wide range of clinical manifestations and differential diagnoses, and the recent measures used for its treatment and control.
Keywords: accidental or target, brain hydatid disease, management, young age
|How to cite this article:|
Khalifa RM, Mahmoud AE, Othnman RM. Spotlight on the brain hydatid cyst and whether its location is accidental or target. Parasitol United J 2015;8:4-13
|How to cite this URL:|
Khalifa RM, Mahmoud AE, Othnman RM. Spotlight on the brain hydatid cyst and whether its location is accidental or target. Parasitol United J [serial online] 2015 [cited 2018 May 23];8:4-13. Available from: http://www.new.puj.eg.net/text.asp?2015/8/1/4/163403
| Introduction|| |
Cystic hydatid disease (CHD) or cystic echinococcosis (CE) in humans is a zoonotic infection that occurs worldwide. It is caused by the larval stage of a tapeworm of the genus Echinococcus (most commonly Echinococcus granulosus) ,,, . It is most common in agricultural regions, affecting humans and animals worldwide  .
Recently, a WHO strategic plan (2008-2015) added the disease to the list of neglected tropical diseases, which is a collective term used for diseases sharing a few common characteristics such as being more common in tropical countries and that have not received enough importance at national or international levels  . Infection causes considerable human morbidity and mortality and socioeconomic losses in many developing countries. It is not easy to diagnose because of the chronic course of the disease and the lack of proper diagnostic facilities. Diagnostic modalities required to detect this condition are not yet widely available, especially in areas where these infections are most prevalent. Besides, many of the diagnostic techniques such as imaging methods are not affordable. Moreover, chronicity and clinical signs may be evident only after many years, which lead to under-reporting in areas where they are most prevalent  .
Hydatid disease develops in the cystic form over a period of time, provoking symptoms due to local compression and generalized allergic-anaphylactic phenomena  . Most hydatid cysts (HCs) occur in the liver as the first filter (68-75%) or in the lung (27%). Involvement of the brain is rare (1-2%) ,,, . Cerebral HCs constitute up to 3-10% of all intracranial space-occupying lesions, but comprise a significant fraction of all intracranial mass lesions. They are usually single ,,, . However, primary multiple HCs have also been reported  . Primary multiple cerebral HCs are extremely rare, and result from spontaneous, traumatic, or surgical rupture of a solitary primary cyst, or as a consequence of a cyst ruptured elsewhere, followed by the mobilization of hydatid scolices to the brain, but they may arise in the brain itself. In addition, it is believed that multiple cysts may also grow after the rupture of a cyst located in the left cardiac cavity or the great arterial vessels , .
Patients with cerebral HCs may also have cysts in other organs. Less than 20% of the patients with intracranial hydatidosis demonstrate other organ involvement  . In the brain, a HC grows slowly and then presents due to mass effect when quite large  . Tuzun et al.  stated that other organ involvement with brain HC reaches up to 80-90% in post-mortem examinations, whereas in clinical practice, concomitant extracranial cysts were not often demonstrated. As the brain has softer tissue, a HC grows in it faster than in other organs. Thus, when the HC of the brain is large enough to produce symptoms, the cysts in other organs are too small to be detected by clinical and radiological evaluations. Some of these small cysts may not be discovered until 20 to 30 years after the diagnosis of brain HC. Moreover, the immune system can inhibit the growth of larva in other sites, except for the central nervous system, due to limited access to the immune system  .
The parasite, its life cycle, and human infection
Cystic hydatidosis is caused by the larval stage of the tapeworm E. granulosus. Canines are the primary hosts. The life cycle of the parasite involves sheep, cattle, and goats as intermediate hosts, whereas humans may be infected accidently. Adult worms of the tapeworm live in the intestine of definitive host (dogs, foxes, wolves, jackals, and other carnivores) ,, and excrete the eggs in their feces. Sheep, cattle, pigs, and many other domestic livestock are the intermediate host, whereas humans are infected accidentally after the intake of food and water contaminated by the eggs of the parasite or by contact with infected dogs  . Larvae hatching from the ingested eggs in the intestine enter the portal circulation, spreading to different tissues where they produce HCs , . Nine genotypes have been described: seven of them are infective to humans, and most human cases are caused by the sheep strain (G1)  . Infrequently, larvae form solitary cysts in the brain, but in 20% of patients, multiple cysts are found  .
It is now accepted that there are several different genotypes among what had been referred to as E. granulosus  . Molecular methods allowed the discrimination of different genotypes of the parasite (G1-G10 and 'lion strain'); some of them are now considered as separate species. In relation to human infection, the allocation of G-numbers became increasingly difficult due to the additional variability in the genotypic clusters G1-G3 (E. granulosus sensu strict) and G6-G10 (E. canadensis)  . The researchers also demonstrated that G1 (sheep strain) is responsible for a significant majority of human CE worldwide (88.44%), 7.3% of the G6 (camel and goat strain) is found especially in Africa and Asia, and 3.7% of G7 (pig strain) causes a significant number of human infections in eastern European countries. Rare human cases were caused by G5, G8, and G10 genotypes, whereas no human cases infected with G4 were recorded. It is now evident that echinococcal genotypes are different not only in different countries, but also sometimes in different localities of the same country. Thus, G7 is prevalent in Austria  , G1 in central Iran  , and G1, 3, and 6 in Turkey  ; G1 is prevalent in humans, sheep, and cattle; G3 was found for the first time in two human isolates in northwest Iran  ; G5 and G6 are prevalent in India  , and G1, G3, and G6 in Asfahan and Tahran, Iran , . Biological differences between the species and the genotypes of Echinococcus in different localities have the potential to affect the transmission dynamics of the parasite, requiring modification of the methods used in disease control initiatives.
Alveolar HD is a morphologically and biologically distinct entity caused by E. multilocularis  . Lesions generally develop in the liver and may spread to the brain and other organs as metastasis , . The incidence of extrahepatic metastasis is around 20%, and it occurs most commonly in the brain , . Alveolar HCs expand and erode the brain tissue, and creep like a crab claw to the surrounding brain region. As for the existence of invasive growth and the tendency and the presence of edema-like malignant tumors, it is difficult to make an evaluation of the actual border around the lesion  .
Cerebral CHD is classified as primary and secondary. Primary intracranial HCs result from direct infestation of the brain from the blood stream into the central nervous system tissues by the larva without any demonstrable involvement of other organs such as the liver and lungs. Primary cysts are usually solitary and fertile, containing brood capsules and scolices, and their rupture may result in recurrent intracranial HCs. Primary multiple cerebral HCs, each containing a pericyst with scolices and brood capsules inside, are quite unusual, resulting from multiple larvae infecting the brain after bypassing the liver and lungs  .
Secondary cysts are generally multiple and result from the rupture of HC in the brain or in another organ of the body  . These cysts may lack a germinal membrane and are usually sterile, with negligible risk of recurrence after their rupture  . Their occurrence may be spontaneous, hematogenous, traumatic, or due to surgical rupture of a primary cerebral or cardiac cyst. Ekici et al.  stressed the concomitant involvement of the heart with the brain.
In 1995, a WHO working group proposed a standardized classification system in which HCs were assembled into three different groups: active, transitional, and inactive. Cysts belonging to these groups differ with respect to the stage at which the cyst is encountered and the ideal treatment options  .
Recently, a MRI classification was proposed for cerebral CHD on the lines of the WHO categorization of hepatic E. granulosus cysts. This categorized the cysts on the basis of their fertility, activity, and imaging morphology. Type 1 cystic echinococcosis (CE1) includes fertile active cysts that appear unilocular and spherical with a clear visible wall. Type 2 cysts (CE2), which are also active, are unilocular mother cysts containing multiple vesicles arranged peripherally along the cyst wall. Type 3 (CE3) are transitional forms containing scolices and are seen as maternal cysts entirely filled by multiple daughter cysts. Type 4 (CE4) cysts show detached membranes giving the water-lily sign and type 5 (CE5) are calcified lesions. Both CE4 and CE5 are inactive cysts that have lost their fertility  .
Prevalence, size, and age incidence
Hydatid disease is a major public health disease with a cosmopolitan spread, the cases being seen in developed as well as developing countries, temperate, subtropical, and tropical zones , . A high prevalence of the parasite can be found in different parts of the world: Africa, Australia, Mediterranean countries, and South America  . It is especially problematic in eastern and southeastern Turkey , and Iran , . However, as a result of the emigration of infected persons, cases also occur in nonendemic areas. Human CE due to E. granulosus is hyperendemic in Libya, Tunisia, and Algeria, and it is endemic in Iran, Iraq, Turkey, Morocco, and Egypt , . Revising the available literature, it was surprising to come across only a single record of brain HCs reported from Egypt  . This may be due to the reporting of cases encountered in local unavailable periodicals, particularly those concerned with central nervous system diseases.
The majority of the cerebral HCs (75%) occur in the pediatric age group, being two to three times more common than in adults , . Khaldi et al.  reported 117 cases from 155 cerebral HC patients in the age range of 2-15 years. They added that the size of the cysts varied from 4 to 13.5 cm and some of them occupied almost the whole hemisphere, inducing cranial deformities. Turgut  reported 137 cases in the pediatric and adolescent age groups in the last century in Turkey. Al-Akayleh  reported five cases from Jordan, with an average age of 9 years, and denoted that the growth rate of the cyst was 1.5-10 cm/year. Duishanbai et al.  reported 30 pediatric cases. Multiple organ HC involvement in a 2-year-old boy was reported by Iyigun et al.  and multiple intracranial HCs in a 15-year-old boy was recorded by Cavusoglu et al.  .
In spite of occurring in pediatric patients and young adolescents, brain HCs often reach a gigantic size ,,,,, as the rate of growth in the brain is usually faster than in any other organ and it is said to be around 4.5 cm/6 months  . As the brain has softer tissue, the HC grows faster than in other organs. Thus, when the HC of the brain is large enough to produce symptoms, the cysts in other organs are too small to be detected by clinical and radiological evaluations. Ninety percent of the cases have solitary lesions  . It was suggested that an underlying patent ductus arteriosus in young children, which might remain for several months after birth, may predispose to systemic inoculation and intracranial localization of E. granulosus larva  . A similar role could be assumed for the patent foramen ovale, which is present in 25-30% of individuals and is suggested as the potential source of cryptogenic emboli to the brain  .
Localization in the brain
Hexacanth embryos released in the upper part of the small intestine are hematogenously taken to the target organ for cyst formation. Obviously, the liver should be the most often parasitized as it is the first organ in which they are filtered. However, practically, it is evident that any organ can be infested at varying rates. One of the rarely affected organs is the brain. As in many cases, when the brain is the sole infected organ, the question arises as to why and how? On the basis of the usual localization of the cysts in a single organ and the rarity of their occurrence in multiple organs, Khalifa et al. , suggested that different E. granulosus organ strains are directed specifically to their target organs; the brain is not an exception. Therefore, they explained that multiple organ infections occur due to the simultaneous uptake of eggs of different echinococcal-specific organ strains.
As early as in 1986, Craig et al.  noticed the variable susceptibility of humans to CE infection, which led to the categorization of humans as susceptible and resistant groups, whereas Romig et al.  related this condition to certain alleles of the HLA system. Recently, the variability of susceptibility to hydatidosis was related to HLA class II ,,, . The researchers illustrated the relation of HLA-DRB1 alleles to resistance and susceptibility markers in hydatidosis patients and their association with the clinical course and the sex. Moreover, Al-Ghoury et al.  related these alleles to the size, the number, and the site of the cysts, targeting them to the liver and lungs of the patients. Hence, we suppose that different alleles of this system might lead the cyst to localize in the brain, and recommend further studies on the alleles of HLA class II that may act as markers of brain infestation.
Recently, it was supposed that certain genotypes of E. granulosus have a higher affinity to localize in the brain than others. Thus, while G1 was supposed to have a predilection for different organs including the liver, the lung, and the brain  , Sajjadi et al.  amplified the molecular characteristics of the target DNA in eight specimens of cerebral and eight hepatic HCs. The researchers concluded that there was a strong indication that G6 has a high affinity to localize in the human brain, whereas G1 was responsible for all liver specimens.
Cerebral HCs are usually supratentorial, whereas infratentorial lesions are quite rare. Supratentorial cysts are common in the parietal lobe due to the major blood supply by the middle cerebral artery  . Dhiman et al.  reported an infratentorial HC as a well-defined rounded hyperdense mass in the right lobe of the cerebrum of a 10-year-old child. Other reported sites included the subarachnoid space, the ventricles, the pons, the cerebellum, the aqueduct of Sylvius, the extradural space, and the diploic space of skull bones ,, .
Veterinary aspects of brain hydatidosis
Hydatid disease is common in the lungs and the liver and rare in other organs of all livestock species in all North African countries , . . Although the brain of several domestic animals (particularly sheep) is a specific infrequent site for cerebral coenurosis, according to the available literature, HCs were never recorded infesting their brain. This was confirmed in two reports by Khalifa et al. , , who did not record the presence of brain HCs in 6601 camels, 530 cattle, and 685 sheep slaughtered at Misurata abattoir, Libya. Moreover, the same observation was noticed in slaughtered livestock in Australia  , Iran  , Nigeria  , Ethiopia ,,, , Pakistan  , Tanzania  , and Iraq  . All previously mentioned studies did not try to explain the cause of this phenomenon, which needs further research to determine whether it is dependent on specified organ strains of E. granulosus or is due to the presence or the absence of certain humoral genes.
A clinical overview
Cerebral HD patients present late when the cyst grows and becomes large enough to cause mass effect. Headache and vomiting due to increased intracranial tension are the most common presenting features. Other manifestations are seizures, hemiparesis, visual disturbances, speech difficulties, cranial nerve defects, and ataxia. Papilledema is usually present at the time of presentation in children  , and may be due to the increased pressure or due to the interference with the pathway of cerebrospinal fluid flow  . . Infected cysts may induce fever  . Calcification of cerebral HCs is very rare, being less than 1% of all brain hydatidosis  . Calcified HCs of the brain may rarely follow a head trauma  . Clinical manifestations may be convulsive attacks  , epileptic attacks , , intractable seizures and headache  , headache after a head trauma  , and hemiparesis  . However, Choukri et al.  considered calcified HCs as safe and their symptomatology to be the same as that of chronic HCs, whereas Menku et al.  described these cysts as 'dead HCs'.
As an example of HC recurrence, a 10-year-old Indian boy presented with fever, headache, and vomiting for 5 days, with a history of craniotomy for the removal of a large (7.5 cm) HC. Brain computed tomography (CT) performed at the second admission showed new and multiple attached cystic lesions in the right cerebral hemisphere. The larger cyst showed internal septations, suggestive of daughter cysts with a moderate amount of surrounding edema. The right lateral and the third ventricles were compressed and pushed to the left. The patient was treated conservatively  .
As an example of multiple cysts in young age, Radmenesh and Nejat  removed cerebral HCs in 7-year and 10-year-old children from Iran, who were complaining of focal neurological deficits and intracranial hypertension. In another case of secondary brain invasion, a 12-year-old boy from Tehran presented with symptoms of irritability, sleeplessness, and weakness of the extremities. A brain CT scan with contrast media showed large multilocular cystic lesions in the right temporal lobe associated with two other smaller similar cystic lesions in the centrum semiovale bilaterally. Other cysts in the intestinal mesenteric, the cardiac, and the left kidney were found. A serology test (IgE and IgG) was positive for HC. Pathologic findings of all cysts were compatible with HD. Albendazole and praziquantel were started, and cysts were operated  .
As for the different presentations, in children from India aged 8-13 years, with features of increased intracranial pressure, CT findings of large solitary and primary intracerebral cystic lesions with significant mass effect and without any calcification or enhancement were present. The cerebral HC was seen as a homogenous fluid, as an attenuated unilocular cyst (three cases), as a unilocular cyst with a few peripheral daughter cysts (one case), or a cyst filled by multiple daughter cysts (one case). All the cases were operated upon, and cysts were removed completely after craniotomy  . As an example of secondary cysts, a 12-year-old boy with multiple secondary HCs in the brain and heart presented with signs of increased intracranial pressure and left hemiparesis. Cysts were removed, and albendazole was given before surgery  .
Cerebral HC should be considered in children with cystic brain lesions even in nonendemic areas. As serological tests of brain HC frequently yield false-negative results due to an inadequate immune response, the most reliable methods for reaching a diagnosis are radiological and histopathological examinations , . Brain HC is diagnosed on the basis of imaging with CT and MRI. Both are satisfactory for the detection and the localization of cysts in the brain. CT and MRI lead to an early and correct preoperative diagnosis. The usual appearance is a large intraparenchymal nonenhancing hypodense lesion with a well-circumscribed border and no pericystic edema  . MRI is superior to CT for demonstrating neural involvement, multiple cysts, cyst capsule detection, and in delineating the relationship of the cyst with adjacent structures  . A CT scan is also the best imaging method to detect calcification and cyst infection with 90% accuracy  . Calcification of the cyst wall is very rare, seen in around 1% of the cases , . Typical CT features of cerebral HC include spherical or oval homogenous fluid attenuation , . The cystic lesion is usually large, with significant mass effect in the form of ventricular compression and midline shift. No enhancement or perilesional edema is seen in case of uncomplicated E. granulosus cysts , . Enhancement of the cyst and perilesional edema in a case of CE of the brain indicates a complication such as rupture, hemorrhage, or infection  . Alveolar echinococcosis in comparison with CE is seen as a solid or solid-cystic mass that commonly shows calcification and contrast enhancement with perilesional edema  . The diagnosis can be definitely confirmed histopathologically after decompressive surgeries by observing the allergic-type tissue reaction in the surrounding tissue and demonstration of the cyst wall histology and scolices  .
Enzyme-linked immunosorbent assays (ELISA) using the crude HC fluid antigen is used most commonly. Such assays are quite sensitive (95%), but the specificity is low, whereas immunoblot was reported to be more specific, but with less sensitivity  . An immunoblot assay using bovine HC fluid was found to be more sensitive (80%)  . Serological assays such as indirect hemagglutination and intradermal skin test (Casoni's test) are rarely performed now  . Other antibody detection formats that have been evaluated are dot-ELISA and latex agglutination  ; Siavashi et al.  reported dot-ELISA to have 100% sensitivity and 98.7% specificity. Swarna and Parija  evaluated the diagnostic potential of different components of HC and adult E. granulosus in dot-ELISA with no significant difference between them  . Antibody detection assays using crude HC fluid antigen are useful for screening purposes with high sensitivity, but with cross-reactivity with other helminthes  . It is not possible to differentiate between recent and past infections by antibody detection, as they persist for a long time even after clinical and parasitological cure , . Detection of the circulating hydatid antigen in the serum has been found to be useful in the diagnosis of active infection as these antigen levels decrease after chemotherapy or surgical resection of the HCs. ELISA, countercurrent immunoelectrophoresis, reverse passive hemagglutination, and latex agglutination have been used ,,, . Sequencing by PCR of contents from the cyst could also be performed as a more specific test  .
The serologic diagnosis of HC is more of a challenge when located in the brain than in other organs because the antibody response is usually absent or very low, especially if the HC is calcified  . In cases of solitary brain HCs, serological tests usually yield negative results, whereas in rare cases, positive results may be obtained and are explained to occur due to the presence of an undetectable small developing cyst in another organ denoting that negative serological results do not rule out cerebral HCs.
Diagnosis of cerebral HCs presents a difficult diagnostic situation , . Brain CT needs to differentiate between porencephalic cyst, arachnoid cyst, brain abscess, and cystic neoplasm , . Porencephalic and arachnoid cysts are not spherical and are not surrounded entirely by the brain parenchyma. A porencephalic cyst shows signs of volume loss and gliosis in the adjacent white matter. An arachnoid cyst is extra-axial in location, whereas intra-axial HC is surrounded by brain parenchyma all around. Cystic tumors and brain abscesses show definite contrast enhancement in the wall and or mural nodule; perilesional edema is also present in case of abscesses , .
Cerebral HCs are slow growing (1.5-10 cm/year), and so patients usually present later when the cysts become large enough to cause manifestations  . Skull bones over the cysts are extremely thin. The brain cyst is transparent and the opposite brain matter is discernible  . Microscopically, the outer membrane appears laminated and acellular, staining amphophilic with hematoxylin and eosin stain and pink with periodic acid Schiff stain. The inner germinal layer is composed of polygonal to cuboidal cells with a foamy appearance. At places, these cells proliferate to form bud-like protoscolices showing hooklets. Multiple developing protoscolices within the vesicle of the germinal membrane comprise brood capsules that may rupture to discharge the larvae. Thus, the granular sand is composed of brood capsules, protoscolices, and hooklets that are refractile on light microscopy and stain prominently with Ziel Nielson stain. Spillage of the fluid content into the surrounding tissue causes a foreign body granulomatous inflammation. These brood capsules, which are attached to the germinal membrane, develop to form daughter cysts, whereas the rest degenerate and undergo calcification  . As almost all cases of cerebral HCs were reported by neurosurgeons, pathological changes in surrounding brain tissues were not mentioned.
The treatment of cerebral HC is surgical with the aim of complete excision without rupture. The cyst contains hundreds, even thousands, of protoscolices, each of which can form a new HC ,,, .The most commonly utilized surgical procedure to remove the cyst intact is by irrigating saline into the interface between the cyst wall and the brain. A pericystic hydraulic method (the Dowling-Orlando technique) with a large craniotomy was used , in which the surrounding surgical field was packed with mops to prevent local spillage. It is recommended that the cyst can be sterilized by injection of a scolicidal solution to prevent intraoperative dissemination. For this reason the use of hypertonic NaCl, cetrimide, or ethanol solution is recommended by the WHO  . Surgical treatments are occasionally contraindicated because of proximity to adjacent vital structures  . Many of the measures such as surgery or puncture, aspiration, injection of scolicidal agent, and reaspiration (PAIR) may be associated with complications, which add to the hospitalization and treatment costs  . In the PAIR technique, metronidazole could also be used with an effect similar to that of hypertonic saline on the membrane of a HC  .
For curing cerebral HCs, a few reports mention the efficacy of drug therapy with albendazole (10-15 mg/kg/day), in two divided doses, given in cycles of 4 weeks; or mebendazole (40-50 mg/kg/day), for 1-3 months, administrated perioperatively or postoperatively to prevent dissemination or recurrence ,, . However, drug therapy is better combined with surgery in case of accidental cyst rupture ,, .
Accordingly, HD should be treated with either albendazole and surgery or albendazole and PAIR to extract the cyst without any complications ,, .
It has been suggested that albendazole can decrease the recurrence of the disease; meanwhile, it can be used in the treatment of inoperable cysts. Because of the high frequency of recurrent hydatid disease after treatment with only surgery or only albendazole, a multidisciplinary approach is recommended and continuing medical treatment for at least 3 months postoperatively is also suggested. This regimen is continued for several cycles depending on the severity of the disease or the improvement of patients  .
Mebendazole could also be considered as an alternative drug, but it is less effective because of poor absorption. Praziquantel, an isoquinoline anthelmintic, is a potent protoscolicidal agent in vitro ,,, .
The reported recurrence rate in the brain due to cyst rupture at surgery was 40.7% , . It was recommended that patients should be followed up regularly in order to recognize possible recurrence, dissemination, or complications of the disease  .
Prevention and control
There are many environmental, economic, and social factors involved in the transmission of CE in populations lacking basic sanitation and living in close proximity to livestock  . Special control measures against infected dogs should be undertaken by periodical stool analysis and treatment of pet dogs. It is important to stress on avoiding feeding stray dogs on untreated offal and, if necessary, their merciful extermination  . Some of the newer approaches for the control of these conditions include the use of effective ovine vaccines for CE  . Vaccination of the intermediate hosts is important to interrupt the transmission cycle, especially in sheep. Along these lines, recombinant DNA technology has been used for the production of antigens derived from the parasite oncosphere of E. granulosus , . Cloned recombinant antigen EG95 has been found to be highly immunogenic in sheep and goats. Vaccines using this antigen have entered clinical trials in many countries such as Australia, Argentina, and China. This particular vaccine is very promising because two doses were found to confer protection for at least one year. It has also been demonstrated that this postvaccination immunity is also passively transferred to neonates  . However, recent investigations have revealed that this protective vaccine developed against G1 genotype E. granulosus proved to be immunogenetically different in cases with G6 genotype infections. Hence, further research studies will be required to determine whether the current vaccine would be effective against the G6 and the G7 genotypes or whether it will be necessary, and possible, to develop genotype-specific vaccines  .
| Conclusion|| |
The majority of the cerebral HCs (75%) occur in the pediatric age group, being two to three times more common than in adults. In spite of that, the cysts often reach a gigantic size as the rate of their growth is usually more rapid than in any other organ due to the soft tissue of the brain. The rate is said to be around 4.5 cm per 6 months.
It seems that localization in the brain is targeted and not accidental. We suppose that different alleles of the HLA class II might lead the cyst to localize in the brain, and recommend further studies on the alleles of this system that may act as markers to brain infestation. Moreover, it is now believed that some echinococcal genotypes, particularly G6, have an affinity to localize in the brain. Although the brain of several domestic animals worldwide (particularly sheep) is a specific infrequent site for cerebral coenurosis, HCs were never recorded infesting their brain.
Cerebral HC should be considered in children with cystic brain lesions even in nonendemic areas. As serological tests of brain HC frequently yield false-negative results due to an inadequate immune response, especially in calcified cysts, the most reliable methods in reaching a diagnosis are radiological and histopathological examinations. In cases of solitary brain HCs, serological tests usually yield negative results, whereas in rare cases, positive results may be obtained and explained as due to the presence of an undetectable small developing cyst in another organ. This denotes that negative serological results do not rule out cerebral HCs.
Hydatid disease should be treated with either albendazole and surgery or albendazole and PAIR to extract the cyst without any complications. The reported recurrence rate of 40.7% is due to cyst rupture at surgery. Patients should be followed up regularly in order to recognize possible recurrence, dissemination, or complication of the disease. Some of the newer approaches for the control of cerebral HD include the use of effective ovine vaccines. Vaccination of the intermediate hosts is important to interrupt the transmission cycle, especially in sheep. Moreover, future studies should be conducted to determine whether some echinococcal genotypes have an affinity to localize in the brain, requiring modifications of control initiatives.
| Acknowledgements|| |
Conflicts of interest
There are no conflicts of interest.
| Author contribution|| |
Refaat M.A. Khalifa, designed the study and reviewed the manuscript. Abeer E. Mahmoud and Ragaa M. Othman collected the references and wrote the manuscript.
| References|| |
Krajewski R, Stelmasiak Z. Cerebral hydatid cysts in children. Childs Nerv Syst 1991; 7:154-155.
Iyigun O, Uysal S, Sancak R, Hokelek M, Uyar Y, Bernay F, Ariturk E. Multiple organ involvement hydatid cysts in a 2-year-old boy. J Trop Pediat 2004; 50:374-376.
Behrman RE, Kliegman RM, Beds JH. Nelson textbook of pediatrics
. 16th ed. Philadelphia: WB Saunders; 2008. 1079-1081.
Rokni MB. Echinococcosis/hydatidosis in Iran. Iranian J Parasitol 2009; 4:1-16.
Eckert J, Deplazes P. Biological, epidemiological and clinical aspects of echinococcosis: a zoonosis of increasing concern. Clin Microbiol Rev 2004; 17:107-135.
Feasey N, Wansbrough-Jones M, Mabey DC, Solomon A. Neglected tropical diseases. Br Med Bull 2010; 93:179-200.
Budke CM, White AC, Garcia HH. Zoonotic larval cestode infections: neglected tropical diseases? PLoS Negl Trop Dis 2009; 3:e319.
Papanikolaou A. Osseous hydatid disease. Trans R Soc Trop Med Hyg 2008; 102:233-238.
Kocaman S, Ersahin Y, Mutluer S. Cerebral hydatid cysts in children. J Neurosci Nurs 1999; 31:270-277.
Gupta S, Desai K, Goel A. Intracranial hydatid cyst: a report of five cases and review of literature. Neurol India 1999; 47:214-217.
Limaiem F, Bellil S, Bellil K, Chelly L, Mekani A, Khaldi M, et al.
Primary hydatidosis of the central nervous system: a retrospective study of 39 Tunisian cases. Clin Neurol Neurosurg 2010; 112:23-28.
Duishanbai S, Jiafu D, Guo H, Liu C, Liu B, Aishalong M, et al.
Intracranial hydatid cyst in children: report of 30 cases. Child Nerv Syst 2010; 26:821-827.
Ersahin Y, Mutluer S, Guzelbag E. Intracranial hydatid cysts in children. Neurosurg 1993; 33:219-225.
Tuzun M, Altinors N, Arda IS, Hekimoglu B. Cerebral hydatid CT and MR findings. Clin Imaging 2002; 26:353-357.
Daskas N, Aggelopoulos E, Tzoufi M, Kosta P, Siamopolou A, Argyropoulou MI. Accidental drainage of a cerebral hydatid cyst into the peritoneal cavity. Ped Infec Dis J 2004; 23:685-686.
Binesh F, Mehrabanian M, Navabi H. Primary brain hydatidosis. BMG Case Rep 2011, 8:1-4. doi: 10.1136/bcr.06.2010.3099
Per H, Kumandaº S, Gümüº H, Kurtsoy A. Primary solitary and multiple intracranial cyst hydatid disease: report of five cases. Brain Dev 2009; 31:228-233.
Cataltepe O, Tahta K, Colak A, Erbengi A. Primary multiple cerebral hydatid cysts. Neurosurg Rev 1991; 14:231-234.
Turgut M, Benli K, Eryilmaz M. Secondary multiple intracranial hydatid cysts caused by intracerebral embolism of cardiac echinococcosis: an exceptional case of hydatidosis. Case report. J Neurosurg 1997; 86:714-718.
Turgut M. Intracranial hydatidosis in Turkey: its clinical presentation, diagnostic studies, surgical management and outcome. A review of 276 cases. Neurosurg Rev 2001; 24:200-208.
Bukte Y, Kemaloglu, S, Nazaroglu, H, Ozkan, U, Ceviz, A, Simsek, M. Cerebral hydatid disease: CT and MR imaging findings. Swiss Med Wkly 2004; 134:459-467.
Ameli NO, Abbassioun K. Hydatid disease of central nervous system
. 1st ed (Persian). Tehran: Ketabsara; 1995.
Aleksic-Shihabi A, Vidolin EP. WHO/OIE manual on cystic echinococcosis of the heart and brain: a case report. Acta Med Okayama 2008; 62:341-344.
Eckert J, Gemmell M, Meslin X, Pawlowski Z. Echinococcosis in humans and animals: a Public Health Problem of Global Concern. WHO/OIE publications; 2002.
Mamishi S, Sagheb S, Pourakbari B. Hydatid disease in Iranian children. J Microbial Immunol Infect 2007; 40:428-431.
Chatterjee KD Textbook of parasitology. 12th ed. Calcutta, India: Chatterjee Medical Publications; 1995.
Col C, Col M, Lafci H. Unusual localizations of hydatid disease. Acta Med Austriaca 2003; 30:61-64.
Kiresi D, Karabacakoglu A, Odev K Karakose S. Uncommon locations of hydatid cysts. Acta Radiol 2003; 44:622-636.
Reuter, S, Seitz HM, Kern P, Junghanss T. Extrahepatic alveolar echinococcosis without liver involvement: a rare manifestation. Infection 2000; 28:187-192.
Nakao H, Yanagida T, Okamoto M, Knapp J, Nkouawa A, Sako Y, et al
. State-of-the art Echinococcus
phylogenetic taxonomy of human-pathogenic tapeworms and its application to molecular diagnosis. Infect Genet Ecol 2010; 10:444-452.
Alvares Rojas CA, Romig T, Lightowers MW. Echinococcus granulosus
sensu lato genotypes infecting humans - review of current knowledge. Int J Parasitol 2014; 44:9-18.
Schneider R, Gollackner B, Schindl M, Tucek G, Auer H. Echinococcus canadiensis
G7 (pig strain): an underestimated cause of cystic echinococcosis in Austria. Am J Trop Med Hyg 2010; 82:871-874.
Kia Eb, Rahimi H, Sharbatkhori M, Talebi A, Harandi MF, Mirhendi H. Genotype identification of human cystic echinococcossis in Asfahan, central Iran. Parasitol Res 2010; 107:757-760.
Simsek S, Kaplan M, Ozercan IH. A comprehensive molecular survey of Echinococcus granulosus
in formalin-fixed paraffin-embedded tissues in human isolates in Turket. Parasitol Res 2011 109:411-416.
Pezeshki A, Akhlaghi L, Sharbatkhoori M, Razmjou E, Oormazdi H, Mohebali M, et al.
Genotyping of Echinococcus granulosus
from domestic animals and humans from Ardabil Province, northwest Iran. J Helminthol 2013; 87:387-391.
Sharma M, Sehgal R, Fomda BA, Malhotra A, Malla N. Molecular characterization of Echinococcus granulosus
cysts in north Indian patients: identification of G1, G3, G5 and G6 genotypes. PLos Negl Trop Dis 2013; 13:e2262.
Pestechian N, Hosseini Safa A, Tajedini M, Rostami-Nejad M, Mousayi M, Yousof H, et al
. Genetic diversity of Echinococcus granulosus
in center of Iran. Korean J Parasit 2014; 52:413-418.
Nikmanesh B, Mirhendi H, Ghalavand Z, Alebouyeh M. Genotyping of Echinococcus granulosus
isolates from clinical samples based on sequencing of mitochondrial genes in Iran, Tehran. Iranian J Parasitol 2014; 9:20-27.
Aydinli B, Aydýn, U, Yazici, P, Ozturc, G, Ombas, O, Oplat, KY. Alveolar echinococcosis of liver presenting with neurological symptoms due to brain metastases with simultaneous lung metastasis: a case report. Turky Parazitol Derg 2008; 32:371-374.
Isik N, Silav G, Cerci A, Karabagli P, Elmaci I, Kalelioglu M. Cerebral alveolar echinococcosis. A case report with MRI and review of the literature. J Neurosurg Sci 2007; 51:145-151.
Ma L, Liu WK, Mao BY, Zhang YK. An echinococcosis multilocularis
presenting as a giant anterior cranial basilar tumor. J Neurol Sci 2009; 30:247-249.
Senturk S, Oguz KK, Soylemezoglu F, Inci S. Cerebral alveolar echinoccosis mimicking primary brain tumor. Am J Neuroradiol 2006; 27:420-422.
Tappe D, Weise D, Ziegler U, Müller, A, Mullges W, Stich A. Brain and lung metastasis of alveolar echinococcosis in a refugee from a hyperendemic area. J Med Microbiol 2008; 57:1420-1423.
Wang J, Yao W, Yi B, Liu S, Zhang D, Jiang C, et al.
Proton magnetic resonance spectroscopy in the evaluation of infiltration zone of cerebral alveolar echinococcosis. Chin Med J (Engl) 2012; 125:2260-2264.
Popli M, Khudale B. Primary multiple hydatid cysts of the brain. Australas Radiol 1998; 42:90-91.
Abdel Razek AA, El-Shamam O, Abdel Wahab N. Magnetic resonance appearance of cerebral cystic echinococcosis: World Health Organization (WHO) classification. Acta Radiol 2009; 50:549-554.
Ekici M, Ekici A, Per H, Tucer B Kumandaº S, Kurtsoy A. Concomitant heart and brain hydatid cyst without other organ involvement: a case report. DAJPN 2011; 24:155-159.
WHO Informal Working Group. International classification of ultrasound images in cystic echinococcosis for application in clinical and field epidemiological settings. Acta Trop 2003; 85:253-261.
Craig PS, McManus DP, Lightowlers MW, Chabalgoity JA, Garcia HH, Gavidia CM, et al
. Prevention and control of cystic echinococcosis. Lancet Infect Dis 2007; 7:385-394.
King C, Mandle G, Benet J, Dolin R. Douglas and benett′s principles and practice of infectious diseases
. 6th ed. Philadelphia: Churchill Living Stone; 2005
Bergos R, Varela A, Castedo E. Pulmonary hydatidosis: surgical treatment and follow up of 240 cases. Eur J Cardiothorac Surg 1999; 16:628-634.
Altimors N, Bavbek M, Caner H, Erdogan B. Central nervous system hydatidosis in Turkey: a cooperative study and literature survey analysis of 458 cases. J Neurosurg 2000; 93:1-8.
Turgut M. Hydatidosis of central nervous system and its coverings in the pediatric and adolescent age groups in Turkey during the last century: a critical review of 137 cases. Child′s Nerv Syst 2002; 18:670-683.
Rokni MB. The present status of human helminthic diseases in Iran. Ann Trop Med Parasitol 2008; 102:283- 295.
Sadjjadi SM, Sedaghat F, Hosseini SV, Sarkari B. Serum antigen and antibody detection in echinococcosis: application in serodiagnosis of human hydatidosis. Korean J Parasitol 2009; 47:153-157.
Geramizadeh B. Unusual locations of the hydatid cyst: a review from Iran. IJMS 2013; 38:2-14.
Guzel A. Primary cerebral intraventricular hydatid cyst: a case report and review of literature. J Child Neurol 2008; 23:585-588.
Khaldi M, Mohamed S, Kallel J, Khaouja N. Brain hydatidosis: report of 117 cases. Child′s Nerv Syst 2000; 16:765-769.
Al-Akayleh A. Intracranial hydatid cysts: diagnosis and treatment. Bahrain Med Bull 2003; 35:91-94.
Cavusoglu H,Tuncer O, Ozdilmac A, Aydin Y. Multiple intracranial hydatid cysts in a boy. Turk Neurosurg 2009; 19:203-207.
Ozkan U, Kemaoglu MS, Selcuki M. Gigantic intracranial mass of hydatid cyst. Clilds Nerv Syst 2001; 17:623-625.
Tatli M, Guzel A, Altimors N. Large primary cerebral hydatid cysts in children. Neurosci (Riyadh) 2006; 11:318-321.
Kayaoglu CR. Giant hydatid cyst in the posterior fossa of a child: a case report. J Int Med Res 2008; 36:198-202.
Yi U, Ucar D, Basar N, Bastemir M. Gigantic hydatid cyst of the brain. Deu Tip Facul Dergisi 2008; 22:161-163
Nemati A, Kamagarpour A, Rashid M, Nazen S. Giant cerebral hydatid cyst in a child. Report and review of literature. Br J Med Pediat 2010; 3:a338.
Cece H, Sogut O, Kaya H. Primary giant intracranial extracerebral hydatid disease in a child. J Pakistan Med Assoc 2011; 61:826-827.
Kemaloglu S, Ozkan U, Bukte Y, Acar M, Ceviz A. Growth rate of cerebral hydatid cyst, with a review of the literature. Childs Nerv Syst 2001; 17:743-745.
Ray M, Singhi PD, Pathak A, Khandelwal NK. Primary multiple intracerebral echinococcosis in a young child. J Trop Pediatr 2001; 51:59-61.
Griffin BP. Transesophageal echocardiography. In: Griffin BP, Topol EJ, editors. Textbook of cardiovascular medicine
. 2nd ed; Philadelphia: Saunders Elsevier Ltd., chapter 86; 2002. 1175.
Khalifa R, Mazen N, Marwan A, El-Majdoub L. Light and scanning electron microscopy of the hooklets of hydatid cyst infecting sheep and camels from Misurata (Libya) and their possible role in parasite strain recognition. Egypt Ger Soc Zool, 44D, Invertebrate Zool, Parasitol 2004a; 44D:1-19.
Khalifa R, Mazen, N, Marwan A, El-Majdoub, L. Abnormal presentation of cystic hydatid cysts from livestock in Misurata- Libya. Bull Fac Sci, Assiut Univ 2004b; 33:71-79.
Craig PS, Zeyhle E, Romig T. Hydatid disease: research and control in Turkana. II. The role of immunological techniques for the diagnosis of hydatid disease. Trans Roy Soc Trop Med Hyg 1986; 80:183-192.
Romig T, Zeyhe E, Macpherson C, Rees P, Were J. Cyst growth and spontaneous cure in hydatid disease. Lancet 1986; 327:861-862.
Azab ME, Bishara SA, Helmy H, Oteifa NM, El-Housseiny LM, Ramzy RM, et al
. Association of some HLA-DRB1 antigens with Echinococcus granulosus
specific humoral immune response. J Egypt Soc Parasitol 2004a; 34:183-196.
Azab ME, Bishara SA, Ramzy RM, Oteifa NM, El-Hosseiny LM, Ahmed MA. The evaluation of HLA-DRB1 antigens as susceptibility markers for cystic echinococcosis in Egyptian patients. Parasitol Res 2004b; 92:473-477.
Al-Ghoury AA, El-Hamshary EM, Azazy AA, Hussein EM, Rayan HZ. HLA class II alleles: susceptibility or resistance to cystic echinococcosis in Yemeni patients. Parasitol Res 2010; 107:355-361.
Hussein E, Al-Mohammed H, Al-Mulhem A, Abolmagd E. HLA class II DRB1 resistance and susceptible markers in hydatidosis Saudi patients in association to clinical course and gender. J Egypt Soc Parasitol 2012; 42:573 - 582.
Sajjadi SM, Mikhaeili F, Karamian M, Maraghi S, Sajjadi FS, Shariat-Torbaghan S, et al
. Evidence that the Echinococcus granulosus
G6 genotype has affinity for the brain in humans. Int J Parasitol 2013; 43:875-877.
Ali M, Mahmood K, Khan P. Hydatid cysts of the brain. J Ayub Med Coll Abbottabad 2009; 21:152-154.
Dhiman DS, Sharama YP, Sarin NK, Thakur RC. Radiological quiz: neuroradiology. Ind J Radiol Imag 1999; 9:77-78.
Cemil B, Tun K, Gurcay AG, Uygur, A, Kaptanoglu E. Cranial epidural hydatid cysts: clinical report and review of the literature. Acta Neurochir (Wien) 2009; 151:659-662.
Furtado S, Visvanathan K, Nandita G, Reddy K, Hegde A. Multiple fourth ventricular hydatidosis. J Clin Neurosci 2009; 16:110-112.
Ibrahim M, Gusbi A. Cystic echinococcosis in North Africa (excluding Morocco) veterinary aspects. In Compendium on cystic echinococcosis in North Africa and in middle eastern countries with special references to Morocco. Brigham Young Provo 1997; 207:207-222.
Haridy FM, Ibrahim BB, Morsy TA. Sheep-dog-man. The risk zoonotic cycle in hydatidosis. J Egypt Soc Parasitol 2000; 30:423-429.
Banks D, Copeman D, Skerratt L, Molina E. Prevalence of Echinococcus granulosus
in Australian cattle. Assiust Vet J 2006; 84:303-307.
Daryani A, Shrif M, Amouei A, Nasrolahei M. Fertility and viability rates of hydatid cysts in slaughtered animals in the Mazandaran Province, Northern Iran. Trop Anim Health Prod 2009; 41:1701-1705.
Tijjani A, Musa H, Astranda N, Mamman, B. Prevalence of hydatidosis in sheep and goats slaughtered at Damaturi abattoir, Yobe State, Nigeria. Nig Vet J 2010; 31:71-75.
Kebede W, Hagos A, Girma Z, Lobago F. Echinococcosis/hydatidosis: its prevalence, economic and public health significance in Tigray region, North Ethiopia. Trop Anim Health Prod 2009; 41: 865-871.
Fufa A, Desta A, Alemayehu R, Bekete M, Elana D. Major Metacestodes in cattle slaughtrered at Nekemte Municipal abattoir, Western Ethiopia: prevalence, cyst viability, organ distribution and socioeconomic implications. Biomirror 2011; 2:1-7.
Fufa A, Fentaye S, Megresa B, Regassa, A. Prevalence of bovine hydatidosis in Kombolcha Elfora abattoir, North Eastern Ethiopia. Open J Animal Sci 2012; 2:281-286.
Bizuwork A, Kebede N, Tibat T, Tilahun G, Kassa T. Occurrence and financial significance of bovine cystic echinococcosis in Southern Wollo, Northeastern Ethiopia. J Vet Med Animal Health 2013; 5:51-56.
Khan M, Tanveer A, Younus, M, Shafiq M, Saeed K, Anmara H, Gill T. Prevalence, organ specificity and economic impact of hydatidosis in the cattle slaughtered in the Lahore abattoir. IJAVMS 2010; 4:38-40.
Swai E, Schoonman L. A survey of zoonotic diseases in trade cattle slaughtered at Tunga city abattoir: a cause of public health concern. Asian J Trop Biomed 2012; 2:55-60.
Jarjees M, Al-Bakri H. Incidence of hydatidosis in slaughtered livestock at Mosul, Iraq. Iraqi J Vet Sci 2012; 26:21-25.
Gana R, Skhissi M, Maaqili F, Bellakhdar F. Multiple infected cerebral hydatid cysts. J Child Neurosci 2008; 15:5815-5893.
Alvares F, Blazequez M, Oliver B, Manrique M. Calcified cerebral hydatid cyst. Surg Neurol 1982; 17:163-164.
Menku A, Kurtsoy A, Tucer B, Durak A, Akdemer H, Travmas K, et al
. Calcified cerebral hydatid cyst following had trauma: case report. Turk Neurosurg 2004; 14:36-40.
Choukri M, Bertal A, Lakhdar A, Ashouri M, Ouboukhlik A, el Kamar A. Calcified cerebral hydatid cyst. Report of a case. J Neuroradiol 2001; 28:261-263.
Boaziz M. Calcified cerebral hydatid cyst: a case report. Cahieresd′etudeset de recherché francophones/Sante 2005; 15: 129-132.
Abderrahmen K, Aouidj ML, Khallel J, Khaldi MM. Calcified cerebral hydatid cyst. Neurochirurgie 2007; 53:371-374.
Tyagi D, Balasubramaniam S, Sawant H. Primary calcified hydatid cyst of the brain. J Neurosci Rural Pract 2010; 1:115-117.
Koktekir E, Erdem Y, Gokcek C, Karatay M, Yilmaz A, Bayar M, et al
. Calcified intracranial hydatid cyst: case report. Turkiye Parazitol Derg 2011; 35:220-223.
Palani A. Partially calcified giant intracebral hydatid cyst in a pediatric child. Neurol India 2012; 60:260-262.
Sandhu P, Saggar K, Sodhi KS. Multiple hydatid cysts of the brain after surgery. J Neurol Neurosurg Psychiatry 2000; 68:97.
Radmenesh F, Nejat F. Primary cerebral hydatid cyst: two cases report. Iran J Pediatr 2008; 18:83-86.
Sabouni F, Ferdosian F, Mamishi S, Nejat F, Monnajemzadeh M, Rezaci N. Multiple organ involvement with hydatid cysts. Iranian J Parasitol 2010; 5:65-70.
Wani N, Kousar T, Gojwari T, Robban I, Singh M, Ramazan A, et al
. Computed tomography findings in cerebral hydatid disease. J Turk Neurosurg 2011; 21:347-351.
Najjar M, Rajab Y, El-Beheiri Y. Intracranial hydatid cyst. Dilemma in diagnosis and management. Neurosci 2007; 12:249-252.
Pedrosa I, Saiz A, Arrazola J, Ferraires J, Pedrosa C. Hydatid disease: Radiological and pathological features and complications. Radiographics 2000; 20:795-817.
McCorkell S, Lewall D. Computed tomography of intracerebral echinococcal cysts in children. J Comput Assist Tomogr 1985; 9: 514-518.
Rudwan MA, Khaffaji S. CT of cerebral hydatid disease. J Neuroradiol 1988; 30:496-499.
Demir K, Karsli AF, Kaya T, Devrimci E, Alkan K. Cerebral hydatid cysts: CT findings. J Neuroradiol 1991; 33:22-24.
Karak P, Mittal M, Bhatia S, Mukhopadhyay S, Berry M. Isolated cerebral hydatid cyst with pathognomonic CT sign. J Neuroradiol 1992; 34:9-10.
Topal U, Parlak M, Kilic E, Sivri Z, Sadikoglu M, Tuncel E. CT and MRI findings in cerebral hydatid disease. Eur Radiol 1995; 5:244-247.
El-Shamam O, Amer T, El-Atta M. Magnetic resonance imaging of simple and infected hydatid cysts of the brain. Magn Reson Imaging 2001; 19:965-974.
Tunaci M, Tunaci A, Engin G, Ozkorkmaz B, Ahishali B, Rozanes I. MRI of cerebral alveolar echinococcosis. J Neuroradiol 1999; 41:844-846.
Gavidia C, Gonzalez A, Zhang W, Garcia N, Rodenquez S, Verastegui M, et al
. Diagnosis of cystic echinococcosis, central Peruvian Highlands. Emerg Infect Dis 2008; 14:260-266.
Parija S, Rao R. Evaluation of combined use of indirect haemagglutination and Casoni′s skin test in diagnosis of hydatid disease. Indian J Pathol Microbiol 1987; 30:117-121.
Siavashi MR, Taherkhani H, Rezaei K, Deligani MR, Assmar M. Comparison of Dot-ELISA and sandwich ELISA diagnostic tests in detection of human hydatidosis. Iran Biomed J 2005; 9:91-94.
Swarna SR, Parija SC. Dot-ELISA for evaluation of hydatid cyst wall, protoscolices and hydatid cyst fluid antigens in the serodiagnosis of cystic echinococcosis. Rev Inst Med Trop Sao Paulo 2008; 50:233-236.
Carmena D, Benito A, Eraso E. Antigens for the immunodiagnosis of Echinococcus granulosus
infection: An update. Acta Trop 2006; 98: 74-86.
Devi CS, Parija SC. A new serum hydatid antigen detection test for diagnosis of cystic echinococcosis. Am J Trop Med Hyg 2003; 69: 525-528.
Sunita T, Khurana S, Malla N, Dubey ML. Immunodiagnosis of cystic echinococcosis by antigen detection in serum, urine and saliva samples. Trop Parasitol 2011; 1:33-38.
Ravinder PT, Parija SC, Rao KS. Evaluation of human hydatid disease before and after surgery and chemotherapy by demonstration of hydatid antigens and antibodies in serum. J Med Microbiol 1977; 46:859-864.
Parija SC, Ravinder P, Rao, K. Detection of hydatid antigen in urine by countercurrent immunoelectrophoresis. J Clin Microbiol 1997; 35: 1571-1574.
Ferragut G, Ljungström I, Nieto A. Relevance of circulating antigen detection to follow-up experimental and human cystic hydatid infections. Parasite Immunol 1998; 20:541-549.
Parija SC, Mishra D. Evaluation of reverse passive hemagglutination (RPHA) test for the detection of antigen in serum for the diagnosis of cystic echinococcosis. J Parasit Dis 2007; 131:155-158.
Prabhakar MM, Acharya AJ, Modi DR, Jadav B. Spinal hydatid disease: a case series. J Spinal Cord Med 2005; 28:426-431.
Vicidomini S, Cancrini G, Gabrielli S, Naspetti R, Bartoloni A. Muscular cystic hydatidosis: case report. BMC Infect Dis 2007; 30:23.
Goswami S, Pandya S, Desai R, Chafekar N. Primary intradural extramedulary hydatid cyst of spine. GMJ 2011; 66:83-84.
Negovetic L, Lupret V, Smiljanic D, Arsenic B. Cranial vault and gigantic intracranial hydatid cyst in a young woman. J Neurosurg 1990; 27: 480-482.
Ciurea A, Fountas K, Coman T, Machinis T, Kapsallaki E, Fezoulidis N, et al
. Long-term surgical outcome in patients with intracranial hydatid cyst. Acta Neurochir 2006; 148:421-426.
Fares Y, El-Zaatari M, Haddad G, Kanj A. Cerebral hydatid cyst: Successfully managed. PAN Arab J Neurol 2011; 15:9-13
Gottstein B, Reichen J. Echinococcosis/hydatidosis. In: Cook GC, Zumla AI, editors. Manson′s tropical diseases
. 22nd ed. Saunders Elsevier; 2009:1549.
Karaoglanoglu M, Akinci O, Bozkurt S, Karatas G, Coskun A, Ziylan S. Effect of different pharmacologic and chemical agents on the integrity of hydatid cyst membranes. Am J Roentgenol 2004; 183:465-469.
Ciurea AV, Vasilescu G, Nuteanu L, Carp N. Cerebral hydatid cyst in children. Experience of 27 cases. Childs Nerv Syst 1995; 11:679-685.
Metanat M, Sharifi B, Sandoghi M. Osseous hydatid disease. Iranian J Parasitol 2008; 3:60- 64.
Deka B, Wilson DJ, Dever LL. Disseminated echinococcosis involving the pulmonary artery. Psychiatric times 2009; 26:1-5.
Craig PS, Rogan MT, Allan JC. Detection, screening and community epidemiology of taeniid cestode zoonoses: cystic echinococcosis, alveolar echinococcosis and neurocysticercosis. Adv Parasitol 1996; 38:169-250.
Lightowlers M, Jenkins D. Hydatid disease - still a global problem. Microbiol Australia 2012; 33:157-159.
Allan JC, Craig PS, Garcia Noval J, Mencos F, Liu D, Wang Y, et al.
Copro antigen detection for immunodiagnosis of echinococcosis and taeniasis in dogs and humans. Parasitol 1992; 104:347-355.
Lightowlers M, Flisser A, Gauci C, Heath D, Jensen O, Rolfe R. Vaccination against cysticercosis and hydatid disease. Parasitol Today 2000; 16:191-196.
Lightowlers MW, Lawrence SB, Gauci CG, Young J, Ralston MJ, Maas D, et al
. Vaccination against hydatidosis using a defined recombinant antigen. Parasite Immunol 1996; 18:457-462
Giri S, Parija SC. A review on diagnostic and preventive aspects of cystic echinococcosis and human cysticercosis. Trop Parasitol 2012; 2:99-108.
Todorov T, Vutova K, Petkov D, Balkanski G. Albendazole treatment of multiple cerebral hydatid cysts: case report. Trans R Soc Trop Med Hyg 1988; 82:150-152.