",isbn:"978-1-83969-545-2",printIsbn:"978-1-83969-544-5",pdfIsbn:"978-1-83969-546-9",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"c77f99db5569e8d0325b856cb7d75b17",bookSignature:"Prof. Maged Marghany",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10854.jpg",keywords:"Optical, Radar, Algorithm, Programming, Big Data, Deep Learning, Image Processing, Time Series Data Analysis, Large Scale Methods, Signal Processing, Computer Vision, Remote Sensing",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"February 18th 2021",dateEndSecondStepPublish:"March 18th 2021",dateEndThirdStepPublish:"May 17th 2021",dateEndFourthStepPublish:"August 5th 2021",dateEndFifthStepPublish:"October 4th 2021",remainingDaysToSecondStep:"9 days",secondStepPassed:!1,currentStepOfPublishingProcess:2,editedByType:null,kuFlag:!1,biosketch:'Prof. Marghany was recently ranked among the top two percent scientists in a global list compiled by the prestigious Stanford University. 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1. Introduction
Parasitic zoonoses are becoming increasingly important in the spectrum of emerging and re-emergent diseases for both developed and developing countries, and are typically associated with poor marginalized countries in low-income countries. They are regarded as disease of the poorest among the poor [1, 2, 3]. Taenia solium is found in sub-Saharan Africa, Central Asia and Latin America where domestic pig husbandry is practiced, poverty, illiteracy and deficient sanitary infrastructures are common [1, 4, 5]. Similarly, the disease has been reported in urban areas where most of the infected pigs are transported and consumed. The incidence of the disease in humans is increasing and now is a re-emerging disease in some developed countries and in areas of non-endemicity, due to international travel and immigration [6, 7]. Hence cysticercosis/neurocysticercosis/teaniosis complex caused by the larval stage of T. solium in both pigs and humans remains a significant cause of human morbidity and mortality in many parts of the world. It is seriously affecting pig production and also considered as a public health and economic problem in many developing countries affecting food security and negatively impacts the nutritional and economic well-being of the small holder farming community [8, 9].
2. Life cycle
2.1 Life cycle and pathogenesis
Taenia solium life cycle is sustained where free roaming pigs, have access to contaminated feces of tapeworm carriers. T. solium has a complex two host life cycle and is cyclically transmitted between pigs and man. Humans are the only definitive host and harbor the adult stages of these cestodes following ingestion of insufficiently cooked pork meat infested with cysticerci. Infection with the adult stage is relatively innocuous and carries mild clinical manifestations leading to taeniasis [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11]. Pigs are the natural intermediate host, while human’s acts as the accidental dead-end intermediate host and are both infected with T. solium by ingestion of embryonated eggs from feces of tapeworm carriers from contaminated soil, water, vegetation/foods to form cysticerci. Infection with the cysticerci leads to more severe symptoms including headache and neurocysticercosis when the pathology occurs in the CNS [11].
2.2 Epidemiology
Neurocysticercosis has been considered to be the most common parasitic infestation of the central nervous system and the single most common cause of preventable acquired epilepsy and mortality in developing countries [12, 13, 14], and a strong correlation was reported between the prevalence of epilepsy and seropositivity against T. solium cysticercosis [15]. The association between cysticercosis and epilepsy has been documented as a leading neurological condition worldwide including West Africa. Epilepsy is a frequent chronic neurologic disorder that affects approximately 70 million people of all ages worldwide [15] Studies of [10] in 2010 reported that the median prevalence of active epilepsy was 4.9/1000 (2.3–10.3) for developed countries, 12.7/1000 (3.5–45.5) and 5.9/1000 (3.4–10.2) in rural and urban studies in developing countries. Neurocysticercosis has been associated with 30% of adult onset epilepsy in endemic regions where 10–20% of the general population can have brain lesions consistent with neurocysticercosis on CT scans [16]. Neurocysticercosis creates a tremendous economic burden in endemic areas incurring significant costs due to diagnosis, treatment and disability [17]. Poor sanitary conditions, traditional pig farming, lack of awareness of the disease and poverty play an important role in the perpetuation of the Taenia solium/cysticercosis, and are present in West Africa [18]. Research in the region on Taenia solium cysticercosis and taeniasis in both human and pigs has been limited. Prevalence information of the disease in some countries within the region has been scanty leading to underestimation of the prevalence, epidemiology and clinical impacts of the disease which has made it difficult to make definitive recommendations on control strategies. Data on porcine and human cysticercosis are available from several countries. However, there is no recent information on T. solium taeniasis-cysticercosis complex in some countries including Guinea Bissau, Liberia, Ivory coast and Sierra-Leone [19] as shown in Tables 1 and 2. The aim of this study is to review scientific and gray literature and to identify the empirical data on T. solium taeniasis/human/porcine cysticercosis/neurocysticercosis/epilepsy in West Africa and the risk factors responsible for the epidemiology of T. solium cysticercosis in order to understand the differences in exposure to the parasite in endemic areas around the world. This will give an update and compile the current knowledge on T. solium in Western Africa, including risk factors for infections in pigs and humans cysticercosis (HCC) from endemic communities. The objective of the study will be to review and document data on the prevalence of human cysticercosis/neurocysticercosis in the region with emphasis on epilepsy.
A systematic literature search was done on studies carried out on cysticercosis in humans and pigs, seroprevalence of cysticercosis in humans and pigs, neurocysticercosis/taeniasis, risk factors for transmission of cysticercosis and epilepsy in West Africa published between 1980 and 2019. This search focused on the articles in which data was obtained using the following techniques and protocols: (1) enzyme-linked immunoelectrotransfer blot (EITB), (2) enzyme-linked immunosorbent assay (B158/B60 Ag-ELISA or HP10 Ag-ELISA), (3) copro-antigen ELISA and real-time polymerase chain reaction assay (copro-PCR). Language restriction was applied, the considered languages were English and French. The selected databases for this study were: PubMed (http://www.ncbi.nlm.nih.gov/pubmed/), Google scholar and others. The search was performed from May 22 to August 22, 2019.
2.4 Literature search
The following data were included in this study (1) peer-reviewed studies of T. solium taeniasis/cysticercosis/neurocysticercosis, porcine cysticercosis and epilepsy in West Africa. (2) “Gray literature” on T. solium taeniasis/cysticercosis, neurocysticercosis presence in West Africa which consisted of informally published written materials including reports. We performed a literature search using PubMed (http://www.ncbi.nlm.nih.gov/pubmed/) with date restriction from January 1, 1980 to January 5, 2019 using the following search term: (solium OR Tapeworm OR Taeniasis OR Taeni* OR Taeniosis OR Neurocysticercosis OR Cysticerc* OR epilepsy) AND West Africa (Benin OR Burkina Faso OR Ivory Coast OR Cape Verde OR Gambia OR Ghana OR Guinea OR Guinea Bissau OR Liberia OR Libya OR Malawi OR Mali OR Mauritania OR Niger OR Nigeria OR Senegal OR Sierra Leone OR Togo). We also searched other databases such as Google Scholar (http://scholar.google.com), Cab Direct (http://www.cabdirect.org) and African Journals Online (http://www.ajol.info) using the following keywords: “Taenia solium,” “porcine cysticercosis,” “neurocysticercosis,” “human cysticercosis” and “taeniasis” Epilepsy, West Africa.
2.5 Data extraction and collection
Presence of T. solium in this study was defined as a documented case of disease related to the tapeworm, whether it was diagnosed and documented as human cysticercosis, neurocysticercosis, porcine cysticercosis, taeniasis or epilepsy. Initially, we reviewed all titles and abstracts, if accessible, and excluded studies outside West Africa, and studies with no specified diagnostic technique, studies written in languages other than English and French, and studies not having full paper, that is, abstracts only experimental studies were also excluded.
2.6 Study selection
Figure 1 describes the review process and the number of articles selected at each stage of the review. From an initial number of 550 articles, only 121 were eventually used. The search selected by removal of duplicate studies from the title selection and studies performed before 1980. Secondly, another set of articles were excluded due to: (1) parasites other than T. solium; (2) studies performed in non-west African countries; (3) articles written in languages other than French and English; (4) studies not presenting original data and/or the techniques and protocols performed on their studies and (5) studies not related to T. solium epidemiology and epilepsy in West African countries. Finally, when full texts were read, the following were selected. Community-based studies, case reports, HCC prevalence reports available, HCC diagnosis using the EITB and Ag ELISA, porcine cysticercosis using carcass inspection and Ab and Ag ELISA, Taeniasis studies based on Copro-Ag ELISA and stool microscopy, and epilepsy studies based on questionnaire, medical or non-medical sources.
Figure 1.
Flow diagram.
3. Results
The search identified 66 studies that reported the prevalence of T. solium taeniasis/cysticercosis/neurocysticercosis and epilepsy in West Africa from 1980 to 2019.The study identified porcine cysticercosis in 18 countries, human cysticercosis in 19 countries, taeniasis in 4 countries and epilepsy was reported in 25 countries(Tables 1 and 2). Figure 1 shows the flow chart of the selection of literature for the informed prevalence estimations of studies included in this review; 8 from Benin (1PC/7HCC/PWE), 11 from Burkina Faso (3PC/8HCC/PWE), 1 from Gambia (PC), 4 from Ghana (2PC/1EP/1TE), 2 from Liberia (PWE), 1 from Mali (PWE), 1 from Mauritania (PWE), 24 from Nigeria (PC10/HCC/PWE14), 3 from Senegal (1PC/2PWEI) and 4 from Togo (4 PWE).
3.1 Porcine cysticercosis in West Africa
One epidemiological studies from Benin [20] used carcass inspection to determine the prevalence of porcine inspection and obtained a prevalence of 0.06–0.69% among a total of 118,073, slaughtered pigs. Two studies from Burkina Faso used carcass inspection to determine the prevalence of porcine cysticercosis and obtained a prevalence of 0.22–0.57% in a total of 179,337 pigs [21, 58]. One study used B158/B60 Ag-ELISA to determine the prevalence of active cysticercosis in pigs and obtained a seroprevalence of 32.5–39.6% among 336 pigs [22]. Two studies from Ghana determined the prevalence of porcine cysticercosis by carcass inspection and obtained the prevalence of 2.31–11.70% [59, 60], among a total of 4181 pigs. A total of 10 studies in Nigeria determined the prevalence of porcine cysticercosis by carcass inspection and obtained a prevalence of 1–20% [23, 24, 25, 26, 61, 62, 63, 64, 65] among a total population of 12,781 pigs. While one study determined the seroprevalence of porcine cysticercosis and obtained a seroprevalence of 46% IgG antibodies among 115 pigs [66]. A study in Senegal determined the prevalence of porcine cysticercosis by lingual inspection and obtained a prevalence of 0.1–1.0%, while Ag-ELISA gave a seroprevalence of 4.8% [67]. All the data are presented in Table 1.
3.2 Human cysticercosis, taeniasis and epilepsy in West Africa
Sero-epidemiological studies from 16 countries were selected for the West African region, 3 studies [29] from Benin used Ab-ELISA, skull/muscle X-ray and pathology of cysts and a study used both Ab-ELISA and EITB [30]. The total number of individuals sampled for serological testing in this region was 4387. Prevalence of circulating antibodies ranged from 1 to 4%. Detailed description of each study is given in Table 2. The total number of individuals examined for epilepsy survey in the region was 27,848, excluding 1443 individuals that were involved in the serological study by [29]. Three studies used door-to-door method of survey in estimating the prevalence of epilepsy [27, 30, 31]. Two of the authors used capture/recapture method. They used questionnaires/neurologist to diagnose epileptics [27, 30, 31] and according to definition by the ILAE 1989, and PAANS [68, 69]. The prevalence of epilepsy in the country ranged from 8.08/1000 to 20.1/1000. A study [29] linked the 1.5% seroprevalence epilepsy to the prevalence of human cysticercosis. A 0–29% human cysticercosis seroprevalence in Burkina Faso was obtained from six studies using Ag-ELISA [32, 33, 34, 36, 37] and the prevalence of epilepsy in the region ranged from 4.5 to 14% per 1000. The total individuals sampled for seroprevalence studies were 13,413. Three of the studies associated the prevalence of epilepsy to cysticercosis [36, 37]. Two studies [34, 38] estimated the prevalence of epilepsy only, with a total individuals sample size of 29,315 excluding studies that associated the prevalence of epilepsy with cysticercosis.
Human taeniasis from Ghana was obtained from a study performing the Katao Khazt method and obtained a prevalence of 13.3% in a total sample size of 44 individuals [39]. Human cysticercosis in Ghana was obtained from a study by western blot and obtained a prevalence of 0.01% and the same study estimated the prevalence of epilepsy as 10.1/1000 in a total population size of 586,607 [40]. Human cysticercosis from Nigeria was obtained from two studies [47, 48] by using Ab ELISA with prevalence of cysticercosis ranging from 9.6 to 14.3% in a total of 425 individuals. There were five studies selected for epilepsy [43, 44, 51, 70] with prevalence ranging from 4.3/1000 to 20.8/1000 in a total of 64,979 individuals for the epilepsy study. Five studies in the region were case report of cysticercosis [45, 49, 50, 71] involving the ocular and breast cysticercosis. Human taeniasis was obtained from two studies by stool microscopy [25, 46] with a prevalence ranging from 8.6 to 40% among a total of 1953 individuals in the region. Human cysticercosis in Senegal was obtained from one study performing antigen and antibody ELISA [42]. The total number of individuals in the study were 403, and prevalence of both antigen and antibody was 7.6%.The prevalence of epilepsy in the country was obtained from two selected studies [52, 53] and the prevalence of epilepsy ranged from 8.3/1000 to 14.2/1000 in a total of 12,182 individuals. Prevalence of epilepsy from Liberia was obtained from two studies [41, 54] and the prevalence of epilepsy across the region ranged from 28.0/1000 to 43.0/1000 among a total of 7169. Prevalence of epilepsy from Mauritania was obtained in one study [55] with a prevalence of 34.7/1000 in a total of 236 individuals. Human cysticercosis was obtained from two sero-epidemiological studies from Togo by antibody ELISA and gave a prevalence of 23.3 [57] and cysticercosis 38/1000 [56] among a total of 14,419 individuals. The two studies also estimated the prevalence of epilepsy and obtained 16/1000 and 18.6/1000 [56, 57] among a total of 6607. A detailed description of each study is given in Table 2.
3.3 Risk factors for human cysticercosis in West Africa
Out of the selected articles reviewed, 16 identified risk factors associated with the prevalence of Taenia solium cysticercosis, taeniasis, epilepsy and porcine cysticercosis. Lack of proper meat inspection, clandestine slaughtering of pigs and illegal sales of meat leading to poor sanitary control were all risk factors that were associated with an increased prevalence of cysticercosis in Benin Republic [30] as it will promote sale of infected pork carcass to unsuspecting consumers (since condemnation cannot be carried out) and predispose them to infection by these parasites (taeniasis) which increases transmission of infection in the community while increase age, stigma and lack of medical facilities were associated with increase prevalence of epilepsy, people with epilepsy may hide their true identity due to fear of marginalization and may not get proper health care [31]. In Burkina Faso, being a male, pig farming including percentage of soil in sand, residing in poor homes, lack of latrine. Males may have poor hygiene compared with females as they are likely to eat improperly washed fruits or vegetables after purchase and may eat food from food vendors prepared outside the home who might be carriers of the adult tapeworm. The authors also thought the acidic nature of the gastrointestinal tract might have made the eggs tolerate slightly more acidic soil. The higher soil (sandy) percentage might have favored spread of taenid eggs unto vegetation and water by wind. Carabin et al. [32] and living in communities with higher percentage of traditional pig husbandry [32, 36] were risk factors associated with the seroprevalence of cysticercosis [32]. Other factors include pig ownership, preparation method of pork by mothers, access to latrine [33] and pork consumption, pork consumption is associated with cysticercosis either by self-infection or through ingestion of contaminated food and water [32, 37]. Interestingly, previous consumption of pork, being a paid worker or trader as against farmer and housewives was also associated with the seroprevalence of cysticercosis [22, 37]. It was also observed that free roaming pigs in the rainy season and knowledge of porcine cysticercosis was associated with an increase prevalence of porcine cysticercosis. Free roaming pigs get exposed to infected human feces deposited in the bush or open field thereby increasing the chance of infection and spread of porcine cysticercosis. Being a residence with more than one individual having epilepsy was associated with higher prevalence of active cysticercosis. Refs. [34, 36] observed that NCC and epilepsy were observed in older people compared with people with epilepsy without NCC. In addition, NCC was associated with epilepsy in communities where pig husbandry is practised and higher prevalence of NCC was observed in people with epilepsy. In Ghana, pork consumption and consumption of measly pork and pork soups lightly cooked were risk factors for taeniasis [39], while hypertension and exposure to Taenia solium infection were risk factors responsible for adult onset of epilepsy [40]. In Nigeria, pork preparation method and history of epilepsy was associated with seroprevalence of cysticercosis. Heat generated from boiling or frying is likely to kill the metacestode compared with heat from roasting or barbecuing [48]. Others include type and availability of toilets, open defecation, lack of personal hygiene after toilet use, pork consumption and traditional system of pig management [47]. One of the risk factors for epilepsy was history of febrile convulsions [70], purchasing home slaughtered pigs, lack of toilet facilities [64], sourcing pig from the northern part of the country and local breed of pigs [26]. It was observed in Senegal that the risk factor for seropositivity to cysticercosis was older age group and lack of latrine [42].
4. Discussion
Majority of studies on epilepsy use various combination of screening questionnaires, clinical confirmation by neurologists, general practitioners or medical students to identify cases of epilepsy with screening questionnaires developed by World Health Organization (WHO) [72] and Limoges Institute of Epidemiology and Tropical Neurology IENT questionnaire [69]. Epileptic seizures, which are the most common presentation of neurocysticercosis, have been documented in developing countries, which is three to six times higher than those in developed countries [68]. Causes of epilepsy are highly variable across different regions of sub-Saharan Africa and depend on geographical, climatic, political, social and hygienic conditions [73]. The main and most important causes of epilepsy seem to be very similar throughout sub-Saharan Africa showing that hypertension [40]. A genetic predisposition, a past history of febrile convulsions, perinatal neurological disorders, head injuries, cerebrovascular accidents and infections of the central nervous system account for most cases of epilepsy [73] Other presumed causes include witch craft/spiritual [43, 74], brain tumor [75], blood transmission and birth trauma due to self-delivery. Also included are protozoon and helminthic infections, including admission to hospital with malaria, exposure to T. canis, T. gondii, O. volvulus and T. solium [40] of which Taenia solium has received attention in sub-Saharan Africa over the past few years. Neurocysticercosis is a common cause of epilepsy in pig breeding area [76], however the wide variation in the frequency of epilepsy in the continent could be due to different definitions and type of epilepsy including the population studied and type of sample [44]. Some studies in the region showed the association between epilepsy and cysticercosis using different diagnostic criteria both for epilepsy and cysticercosis. These include three studies in Burkina Faso, of which some researchers [34] showed a seropositivity between cysticercal antigens and active epilepsy with a prevalence odds ratio (POR) of 2.40 (95%). A second study [36] showed 68 of the subjects confirmed with epilepsy by CT scan and 20 were diagnosed with definitive NCC (for a proportion of 45.5–46.9% in two of the study villages). The third study [37] showed that 39 of 70 positive were confirmed with epilepsy for a lifetime prevalence of 4.5% and epilepsy was associated with cysticercosis by Ag-ELISA (POR = 3.1, 95% BCI = 1.0; 8.3). All three studies confirmed epilepsy by ILAE definition/physician. In Senegal, a study [42] showed that one of 10 CT-scan positives individual by Ag-ELISA and EITB was reported to have epileptic seizures, and cerebral CT-scans showed that 23.3% of the seropositive were affected by neurocysticercosis. In Togo, a previous study [57] showed that cysticercosis (confirmed by ELISA, anatomopathological examination, cranial or muscle X-ray) caused 29.5% epilepsy in sufferers. A study by [40] in five Health and Demographic Surveillance System centeres in Kintampo Ghana and four other countries (Kenya, South Africa, Uganda and Tanzania) showed that epilepsy was significantly associated with exposure to T. solium (odds ratios 7·03, P = 0·002), in adults epilepsy confirmed by questionnaire/clinician and cysticercosis was confirmed by detection antibody by Western Blot, while active convulsive epilepsy in the study was defined as two or more unprovoked convulsive seizures (occurring at least 24 h apart, with at least one seizure in the preceding 12 months).
The stigmatization and marginalization of epilepsy is also enormous n many African countries, epileptic patients are cast out because it is considered a contagious or shameful disease [28, 43, 69, 77]. Those affected go through social seclusion and people will not marry PWE unless both parties have epilepsy. For example, consanguineous marriage is forbidden by culture in South East Nigeria [43], and may potentially force them to intermarry thereby promoting genetic transmission of epilepsy [43, 44]. Other beliefs include that inheriting properties from PWE will get one infected but if a medicine man performs burial rites for the dead person and takes away their properties and burn it then it stops. Burial of PWE far away from home prevents people from getting epilepsy. Eating, sleeping together or wearing same clothes with PWE is said to be a source of infection [43, 44]. Eating of pork by someone with epilepsy promotes cysticercosis and corroborates with a study that found a significant link between cysticercosis occurrence and epilepsy [78]. In West Africa, T. solium cysticercosis in pigs and man has been reported and reports have shown the prevalence’s of porcine cysticercosis across the west African countries varies from 0.05 to 46% for both carcass inspection and serological studies and prevalence of taeniid eggs were found to be between 8.6 and 40% based on stool microscopy while copro-antigen ELISA gave a prevalence of 30% [65] as shown in Tables 1 and 2. Difference in severity of infection caused by T. solium could also explain the differences in prevalence of epilepsy. In addition, the extent of the presence of other environmental factors such as use of bad hygiene practices, close contact of humans and pigs and consumption of inadequately cooked pork affects the differences in prevalence of epilepsy [31] including free roaming pigs [43]. Abattoirs and approved slabs are the only approved places for slaughter and inspection of pork meat for consumption, however most carcasses are sold uninspected hence, lack of inspection and large scale clandestine slaughter of pigs promote spread of cysticercosis [32, 34]. The poor knowledge of T. solium, poor hand washing practices, not treating drinking water and handling of raw pork with bare hands promote spread of cysticercosis [65]. Reports in the region indicate that home slaughter conditions were normally substandard because they are makeshift and not constructed to actually meet the requirements of ideal slaughter premises [48]. There was also strong association between knowledge of cysticercosis and occupation and could be attributed to the fact that people in certain occupations are considered to be more knowledgeable about the disease than others [48].
5. Conclusions
The high prevalence of porcine and human cysticercosis and epilepsy in the region indicates that there is a need to get more updated prevalence data of cysticercosis in rural areas where epilepsy is suspected to be more prevalent, compared to urban regions due to parasitic infection. Studies determining the association between epilepsy and cysticercosis should be carried out in countries where it has not been done. The conditions necessary for the parasite to thrive and be transmitted in the region is present in West Africa. Interventions studies including Health education has only been done recently in Burkina Faso, such intervention measures should be carried out in other parts of the region so as to enlighten the populace on the menace caused by the parasite and how it could be prevented.
6. Limitations
The present study has some limitations as the criteria for inclusion and exclusion of articles might have increased or reduced the number of studies used in the region and not all risk factor s and causes of epilepsy were discussed. The study did not determine the prevalence of epilepsy and both porcine and human cysticercosis, in the region as the aim of the study was to show data on studies done by other researchers in the region.
Acknowledgments
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Conflict of interest
The authors declare no conflict of interest.
Notes/thanks/other declarations
We wish to thank the management of National Veterinary Research Institute Vom for assistance rendered during the preparation of the manuscript.
\n',keywords:"Taenia solium, epilepsy, human, pigs, West Africa, literature search, epidemiology",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/69511.pdf",chapterXML:"https://mts.intechopen.com/source/xml/69511.xml",downloadPdfUrl:"/chapter/pdf-download/69511",previewPdfUrl:"/chapter/pdf-preview/69511",totalDownloads:277,totalViews:0,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,dateSubmitted:"June 11th 2019",dateReviewed:"September 5th 2019",datePrePublished:null,datePublished:"April 22nd 2020",dateFinished:null,readingETA:"0",abstract:"Taenia solium taeniasis/cysticercosis/neurocysticercosis is a neglected zoonotic disease endemic in sub-Saharan Africa, Latin-American and Asia and is an emerging public health and economic problem. The association between cysticercosis and epilepsy has been documented worldwide including West Africa. Poor sanitary conditions, traditional pig farming and poverty play an important role in perpetuation of Taenia solium. There has been limited research undertaken in T. solium in human and pigs in some West African countries, where prevalence of taeniasis was up 40%, human cysticercosis 10.3%, porcine cysticercosis 32.5–39.6% and epilepsy 28.0/1000–43.0/1000. The study identified porcine cysticercosis in 18 countries, human cysticercosis in 19 countries, taeniasis in 4 countries and epilepsy was reported in 25 countries. The aim of this study is to review scientific literature on the epidemiology of T. solium infections in pigs and humans in Western Africa and document data on the prevalence of epilepsy in the region. The objective is to document occurrence of disease in West Africa so as to offer options available for control. The study conducted literature search of online international databases of published resources for information on T. solium in Western Africa and Epilepsy from 1990 to 2018.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/69511",risUrl:"/chapter/ris/69511",book:{slug:"overview-on-echinococcosis"},signatures:"Rebecca Weka, Pam Luka, Ndudim Ogo and Paul Weka",authors:[{id:"254446",title:"Dr.",name:"Ndudim",middleName:null,surname:"Ogo",fullName:"Ndudim Ogo",slug:"ndudim-ogo",email:"ogoendy@yahoo.com",position:null,institution:null},{id:"308010",title:"Dr.",name:"Rebecca",middleName:null,surname:"Weka",fullName:"Rebecca Weka",slug:"rebecca-weka",email:"bekkyweka@gmail.com",position:null,institution:null},{id:"311177",title:"Dr.",name:"Pam",middleName:null,surname:"Luka",fullName:"Pam Luka",slug:"pam-luka",email:"pamluka08@gmail.com",position:null,institution:null},{id:"311178",title:"Mr.",name:"Paul",middleName:null,surname:"Weka",fullName:"Paul Weka",slug:"paul-weka",email:"lawunka1@gmail.com",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Life cycle",level:"1"},{id:"sec_2_2",title:"2.1 Life cycle and pathogenesis",level:"2"},{id:"sec_3_2",title:"2.2 Epidemiology",level:"2"},{id:"sec_4_2",title:"2.3 Methods",level:"2"},{id:"sec_5_2",title:"2.4 Literature search",level:"2"},{id:"sec_6_2",title:"2.5 Data extraction and collection",level:"2"},{id:"sec_7_2",title:"2.6 Study selection",level:"2"},{id:"sec_9",title:"3. Results",level:"1"},{id:"sec_9_2",title:"3.1 Porcine cysticercosis in West Africa",level:"2"},{id:"sec_10_2",title:"3.2 Human cysticercosis, taeniasis and epilepsy in West Africa",level:"2"},{id:"sec_11_2",title:"3.3 Risk factors for human cysticercosis in West Africa",level:"2"},{id:"sec_13",title:"4. Discussion",level:"1"},{id:"sec_14",title:"5. Conclusions",level:"1"},{id:"sec_15",title:"6. Limitations",level:"1"},{id:"sec_16",title:"Acknowledgments",level:"1"},{id:"sec_19",title:"Conflict of interest",level:"1"},{id:"sec_16",title:"Notes/thanks/other declarations",level:"1"},{id:"sec_17",title:"Acronyms and abbreviations",level:"1"}],chapterReferences:[{id:"B1",body:'WHO. A Rationale for Investment and Action World Health Organization 2016, WHO/HTM/NTD/NZD/2016; 2016'},{id:"B2",body:'Gabriël S, Dorny P, Mwape KE, Trevisan C, Braae UC, Magnussen P, et al. Control of Taenia solium taeniasis/cysticercosis: The best way forward for sub-Saharan Africa? Acta Tropica. 2016;165:252-260'},{id:"B3",body:'Torgerson PR, Macpherson CN. The socioeconomic burden of parasitic zoonoses: Global trends. Veterinary Parasitology. 2011;182:79-95'},{id:"B4",body:'Fleury A, Sciutto E, de Aluja AS, Carpio A. Cysticercosis: A preventable, but embarrassing neglected disease still prevalent in non-developed countries. In: Zoonoses-Infections Affecting Humans and Animals. 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Seizure. 2013;22(7):572-576'},{id:"B76",body:'Phiri IK, Ngowi H, Afonso S, Matenga E, Boa M, Mukaratirwa S, et al. The emergence of Taenia solium cysticercosis in eastern and southern Africa as a serious agricultural problem and public health risk. Acta Tropica. 2003;87(1):13-23'},{id:"B77",body:'Adewuya AO. Parental psychopathology and self-rated quality of life in adolescents with epilepsy in Nigeria. Developmental Medicine and Child Neurology. 2006;48:600-603'},{id:"B78",body:'Quet F, Rafael F, Ngoungou EB, Diagana M, Druet-Cabanac M, Preux PM. Investigating epilepsy in Africa: 10 years of data collection using a standardized questionnaire in 2,269 peoples with epilepsy. Epilepsia. 2011;52(10):1868-1876'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Rebecca Weka",address:"bekkyweka@gmail.com",affiliation:'
Ministry of Agriculture and Rural Development, Nigeria
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1. Introduction
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Allergic diseases are the most common chronic condition in childhood. Epidemiological studies observed increase in the prevalence of allergic diseases from the middle of the twentieth century, which is explained by environment and lifestyle changes and improvements in modern Westernized societies. At the beginning of the twenty-first century, stagnation in the prevalence of asthma while increase in the prevalence of food allergy was noticed, which announced the second wave of allergy epidemics [1, 2, 3]. The first atopic phenotype that starts in early infancy is atopic dermatitis (AD). It is estimated that it affects up to 20% of children. Disrupted integrity of the skin barrier contributes to the development of sensitization to food and aeroallergens and also increases the risk for the development of food allergy. It is considered that 30% of children with AD have food allergy, and 30% develop asthma and 75% allergic rhinitis [4]. About 3–5% of children have been diagnosed with food allergy, and up to 50% of them have AD [1]. AD and food allergy can coexist and can also appear independently in infancy and in the first years of life. In the following years, wheezing induced by viruses like respiratory syncytial virus or rhinovirus and sensitization to inhalational allergens can be observed. As the child grows up, respiratory symptoms are more common and occur outside of the infection; introduction of anti-inflammatory drugs is needed, i.e., the signs of asthma occur. Preschool and school age are the time of appearance of allergic sensitization to pollen of grass, weed and tree pollen, and the beginning of allergic rhinoconjunctivitis which persists in adolescence and the young adult age.
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At the same time, remission of atopic dermatitis and food allergy is noticed, while asthma and rhinitis symptoms continue. Sensitizations to pollen and cross-reactions to nuts, fresh fruits and vegetables may induce oral allergy syndrome, the type of food allergy that occurs in the school age. Asthma may disappear in teenage years, but after some period of remission, skin and respiratory symptoms can appear once again. In early adulthood, skin and lung symptoms are related to tobacco smoking, occupational exposures and lifestyle, and they manifest like contact dermatitis or asthma-chronic obstructive pulmonary disease overlap syndrome [5].
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Atopic dermatitis, food allergy, asthma and allergic rhinitis in childhood share the common genetic, epigenetic and environmental risk factors, while the underpinning pathogenesis is marked with disrupted skin, lung and gut barriers, altered microbiome and local and systemic Th-2-driven immunological pathways. Those allergic conditions can comanifest or occur in temporal sequence. The hypothesis that has been proposed to clarify time sequence and associations of allergic disease is called allergic march. This concept means that allergic disorder starts in early infancy with the first hallmark of atopy and atopic dermatitis and then appears food allergy, and later in childhood comes asthma and allergic rhinitis. Some investigators presumed that the underlying allergic inflammation of the skin could progress from atopic dermatitis to asthma. In addition, some preventive measures like improving skin barrier before skin disease onset can reduce the risk for respiratory allergy. Those observations support the causal link between atopic dermatitis and asthma. Although described longitudinal appearance of all allergic diseases was noticed only in small proportion (~7%) of children [6, 7], others had different trajectories of one or more allergic diseases which can occur in different point of time in childhood. Last explanations are talking about a cluster of coexistence-related allergic diseases rather than a progression.
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2. Atopic dermatitis, disrupted skin barrier and allergic sensitization: is it the beginning?
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Atopic dermatitis is the most common chronic skin disorder in childhood. It appears in early childhood with dry, itchy skin and eczema on the cheeks, wrists and other parts of the body. Up to 20% of children experience AD in childhood. The majority outgrows eczema, but one proportion of them continues to have symptoms into adulthood [8]. According to the recently published cohort, six latent classes representing subphenotypes of AD were identified. These classes can be summarized in four classes as follows: unaffected individual or transient AD (61.9%); early-onset-persistent AD (10.7%); early-onset late resolving, early-onset early resolving and mid-onset resolving by age 11 years of age (16.5%); and later-onset AD after age 3.5 years (10.9%) [9].
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AD is a systemic disorder characterized by disrupted skin barrier. It is considered that factors associated with damage of skin barrier are complex and influenced by a combination of structural, genetic, environmental and immunological factors. Structural changes are caused by altered lipid composition, decreased structural proteins, increased skin pH and reduced skin microbiome diversity. Cutaneous permeability defects can be assessed by measuring transepidermal water loss (TEWL) which correlates with disease severity. Several genetic defects encoding skin barrier proteins contribute to the breakdown of skin barrier. Inherited loss-of-function mutations in filaggrin gene, which encodes structural epidermis proteins, are associated with early-onset AD that is more often persistent and closely related with asthma and food allergy [10]. Polymorphisms in the thymic stromal lymphopoietin (TSLP) gene, SPINK5 gene and corneodesmosin have also been linked to AD and the development of food allergy [11, 12, 13]. The inflammatory responses induced by AD are manifested by increased production of Th2 cytokines such as IL-4, IL-13, IL-25, IL-33 and TSLP. TSLP is one of the major inductors of systemic Th2 response, and it is considered that it could be the link between skin and respiratory allergy. It is expressed in skin keratinocytes, pulmonary airway and intestinal epithelium, while increased expression was observed in the skin of AD patients and respiratory epithelium of asthma patients [14].
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Skin microbiome dysbiosis is characterized by the dominance of Staphylococcus aureus which through various mechanisms worsens chronic skin inflammation [15]. Skin barrier dysfunction is associated with innate immune activation that results in dysregulated immune response to environmental antigens (like allergens and bacteria) and skin inflammation leading to the evolution of allergic sensitization [16]. Several studies on animals and humans support the concept that damaged skin promotes sensitizations. In mouse, exposure to egg and peanuts through disrupted skin induces sensitization [17] and, after exposure to egg aerosol, could induce asthma-like airway hyperresponsiveness [18]. In children, applications of peanut oil to inflamed skin were positively associated with the development of peanut food allergies [19], and the use of wheat-containing facial soap was positively associated with the development of wheat food allergy [20]. Application of oat-based creams on the skin of children with AD can induce oat sensitization in one third of children [21]. The concept of allergic march has been supported by cross-sectional and longitudinal birth cohort studies. Several birth cohorts have shown associations between early-onset AD and development of asthma and allergic rhinitis in school age [22, 23]; risk is greater in children with early-onset persistent AD phenotype [24]. Children with AD and allergic sensitization had increased risk of food allergy, asthma and allergic rhinitis compared to non-sensitized children without AD [25]. Food sensitizations in the first 2 years of life were associated with increased risk of asthma and allergic rhinitis in school age [26]. Peanut, milk and egg food allergy also increased the risk of developing asthma and rhinitis later in childhood [27]. Meta-analyses of birth cohort studies which investigated atopic march observed that early-life food sensitization was associated with an increased risk of infantile eczema, childhood wheeze/asthma, eczema and allergic rhinitis and young adult asthma [28].
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The development of sensitization is complex, and except skin barrier defect and environmental allergen exposure, the presence of other factors is important because they may function as adjuvants, and some of them are bacterial colonization of the skin, allergens with intrinsic protease activity and exogenous adjuvants [29].
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3. Why is allergy increasing? Hypothesis-driven strategy
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Allergic diseases of the skin, gut and lung are complex disorders with multiple phenotypes and underlying genotypes. They occur as a result of environmental exposures during early life in individuals with genetic susceptibility to allergy. Gene-environment interactions are accountable for different influences of the environment on individual level. There are several hypotheses of allergy increase in the twentieth century. According to the hygiene hypothesis, decreased exposure to microorganisms in modern society, through increased hygiene and decreased prevalence of infection in early life, disrupts immune tolerance and directs immunological reaction toward Th2 direction [30].
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The beginning of hygiene hypothesis can be found in the David Strachan study from 1989. He observed that children who grew up in large families, with large number of older siblings, have less allergy and concluded that exposure to infection in early life (prenatally and early childhood) can prevent allergy [31]. This was confirmed by subsequent studies which linked less allergies with viral, bacterial or protozoic pathogens, transmitted by the fecal-oral route [32]. In 1990 hygiene hypothesis was supported by the observation that growing up on farms, regular contact with farm animals, stables and drinking unpasteurized milk were protective against allergy [33]. Farms are microbe-rich environment. Endotoxin, lipopolysaccharide, part of the outer layer of Gram-negative bacteria, is a marker of microbe surroundings. Its protective effect on atopy is produced by stimulation of immune system in Th1 direction. Preventive effect of endotoxin was seen only for early-life exposure (prenatal and early childhood, before development of allergic sensitization) [33, 34].
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In the past 20 years, hygiene hypothesis was expanded by “old friends hypothesis” and “biodiversity hypothesis” [35, 36]. According to that hypothesis, contact with natural environment and its species (included microbes and parasites) protects against allergy. Children are exposed to the environment indirectly (through mother during prenatal life) and directly through the skin, gut and lung. Changes in the microbiome of the gut, skin and nose reduced microbiome diversity, and loss of symbiotic relationship with parasites and bacteria increased the risk for allergic disease [37]. Stability and diversity of gut microbiome are developed during early life (first 1000 days of postnatal life). This process can be influenced with different factors like mode of birth, infant feeding, fiber content in the mother’s and child’s diet and older siblings and exposure to pets and/or farm animals during childhood. Environment and dietary habits of mother and previous generations can change microbe diversity of neonate’s trough epigenetic modification [38, 39, 40, 41, 42].
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The second hypothesis dual-allergen exposure hypothesis is based on observations that allergic sensitization occurs through disrupted skin in AD, while early ingestion of food (before development of sensitization) allows development of oral tolerance [43]. Delayed introduction of solid food in infancy, which were recommended at the end of the twentieth was not protective for food allergy development [44]. This hypothesis was confirmed by several randomized clinical trials like Learning Early About Peanut Allergy (LEAP) and Enquiring About Tolerance (EAT). EAT was looking at the early introduction of six common food allergens at 3 months of age alongside breastfeeding compared to exclusive breastfed infants. It found that prevalence of egg allergy was lower among infants with early introduction [45]. LEAP assessed oral tolerance induction of peanut in group of high-risk infants between 4 and 11 months of age. It compared early and regular peanut consumption, average of 6 grams of peanut protein a week, in relation to completely avoiding peanut protein until 60 months of age. Early introduction of peanut protein results in significant reduction in peanut allergy. LEAP-On study was an extension of LEAP, in which protective effect of early introduction on peanut allergy was observed, even after cessation of peanut consumption [46, 47]. According to the findings from the studies like LEAP and EAT, guidelines for complementary feeding were remarkably changed. Pediatric and allergy societies have published consensus statements about early introduction of peanuts in high-risk infants. Also, current recommendations advise against delayed introduction of allergenic food into infant diet [48, 49].
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Recent researches report about the important role of vitamin D in the pathogenesis of allergy. Vitamin D has positive impact on foetal lung development and an immunomodulatory effect; it stimulates differentiation of T lymphocytes, induction of Treg, while its deficiency induces Th2 response [50]. It was observed that rise in allergy prevalence occurs with increasing vitamin D deficiency especially among populations less exposed to the sun [51]. Deficit of vitamin D is associated with increased risk of peanut and egg food allergy, atopic dermatitis and asthma. The severe form of the diseases was observed with higher vitamin D deficiency [52, 53].
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4. Allergic march: causal link or cluster of related diseases
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The allergic march is a real phenomenon, but there is a great debate about underlying mechanisms. Some researchers argue that there is a causal link between AD and other allergic diseases in childhood, in which AD is the first disease with local and systemic immunological response. Systemic response could trigger multisystem allergic disease. Longitudinal, prospective population-based cohorts or cohorts of high-risk infants reported about increased risk of asthma and allergic rhinitis among children with previous or current AD [54, 55, 56, 57, 58, 59].
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Meta-analysis of 13 prospective birth cohort studies reported that odd ratio of asthma among children with AD in the first 4 years of life was 2.14% (95% CI 1.67–2.75), while the prevalence of asthma at the age of 6 years in eczema cohort studies was 29.5% (95% CI, 28.2–32.7%). The conclusion was that only one in every three children with eczema develops asthma during later childhood [4]. According to the results of high-risk birth cohort, 26.7% children with AD developed AR at 7 years of age, while the risk is higher among children with persistent and late-onset AD (OR 2.68, 95% CI 0.97–7.41) [57]. Sensitization to food allergen increased the risk for AR (OR 1.2, 95% CI 0.6–2.2), but the associations is stronger among children who had co-sensitization to both food and aeroallergens (OR 3.1, 95% CI 1.2–7.8) [28]. In the PASTURE study, children with early-persistent AD phenotype and those with late phenotype had an increased risk of developing allergic rhinitis. Early AD phenotype did not associate with AR, while the risk increased among children with early AD and food allergy [60]. According to these results, there was a new question: can we predict which phenotype of AD will be linked to asthma? More information come from longitudinal cohorts which analyzed different phenotypes of AD based on disease course and determined which classes are at highest risk for other atopic diseases [9, 60, 61]. According to the results from those studies, the early-onset, severe, persistent phenotype is associated with the highest risk for allergic comorbidities. Polysensitization, atopic heredity and filaggrin loss-of-mutation contribute to increased risk [62]. Children with high-risk phenotype of AD are candidates for preventive measures, which could delay or stop the occurrence of asthma and allergic rhinitis. But, it is considered that there is not enough evidence that AD causes asthma and allergic rhinitis. Paller et al., in recent review, presumed existence of inherited predisposition to one or more atopic disorders. Occurrence of the disease is a result of complex interplay between different underlying genotypes and environmental exposures during maturation of immune system, with tissue-specific peak time of clinical manifestation. Allergic diseases have different phenotypes and different trajectories that form clusters [62].
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Simultaneously with AR, local allergic rhinitis (LAR) can appear in the preschool age. This entity of rhinitis is marked with local synthesis of specific IgE but without systemic allergy (allergic sensitizations and specific IgE). It was observed that LAR is a separate, well-defined phenotype of noninfectious rhinitis, which is stable over time [63, 64]. But, among younger patients and children, LAR can be the first step in the natural evolution to classical AR, especially when starting in the first two decades of life and in polysensitized patients [65]. In the German Multicentric Allergy Study, it was observed that over one third of the children developing a typical grass pollen-related seasonal AR had no serum-specific IgE to pollen. These children develop a systemic IgE sensitization to grass pollens in the second or third pollen season following the onset of their rhinitis symptoms [66, 67]. If patients with LAR have AR over time, this supports atopic march.
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5. Can we prevent and/or stop atopic march?
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Better understanding of underpinning mechanisms of atopic dermatitis and atopic comorbidities as well as environmental risk factors induces further researches of preventive interventions aimed at stopping atopic march. Those interventions could be started during pregnancy and early life among healthy or high-risk infants before onset of disease (primary prevention) or among children with one atopic disease in order to prevent appearance of other atopic comorbidities (secondary prevention).
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Disrupted skin barriers promote sensitizations and increase the risk for allergic disease. Improvement in skin barrier through regular application of emollients beginning in the neonatal period can prevent AD among high-risk children. Protective effect was observed if treatment lasted up to 6–8 months of age [68, 69, 70]. There was favorable effect at the 12 months of age, even after treatment was ceased [69]. These researches support original hypothesis of skin barrier dysfunction as a beginning of atopy march, but it is still unclear if this protective effect is long-lasting or onset of AD is delayed. The effect of emollients on food allergy was unclear. Only one research showed a trend for decreased food sensitization at 6 and 12 months of age [69], while two other were not powered to measure food sensitization [68, 70]. Some of undergoing studies aim to investigate the effect of emollients in prevention of AD among general population.
\n
Local and system inflammatory response is a hallmark of AD, and anti-inflammatory therapy is effective in control of exacerbations, but study of Schneider et al. showed ineffectiveness of pimecrolimus in stopping atopic march [71]. Skin microbiome dysbiosis can increase the risk for onset or exacerbation of AD and comorbidities [72]. Recent researches showed that topical application of skin commensal bacteria can improve lesions in AD [73, 74]. Apart from local use of bacteria, the great interest of researchers is the role of probiotics in protection of allergy. Several studies have shown positive effect of probiotics like that adding Lactobacillus rhamnosus in diet of pregnant women can reduce the risk of AD [75]. Adding probiotics like Bifidobacterium lactis, Lactobacillus salivarius or Lactobacillus GG to the infant formula reduced the severity of AD [76]. But recent randomized control trial has shown opposite result. The study concluded that early supplementation with LGG in the first 6 months of life does not appear to prevent eczema at 2 years of age [77]. However, systematic reviews and meta-analyses report protective effect of the probiotics for the primary prevention of atopic dermatitis [78, 79, 80]. Probiotics are ineffective in prevention of asthma, food allergy and allergic rhinitis. Medical societies like the American Academy of Pediatrics, the European Academy of Allergy and Clinical Immunology and the European Society for Pediatric Gastroenterology, Hepatology and Nutrition do not recommend the use of probiotics for primary prevention of allergic disease [49, 81, 82, 83]. The World Allergy Organization recommends the use of probiotics in diet of mothers of high-risk infants during pregnancy and lactation and in diet of those infants in order to prevent AD [84]. There is no consensus for the most effective specific strain of probiotics. The strain, dosage, timing of introduction and duration of probiotics usage are still uncertain. These questions are the aim of the future investigations.
\n
Early introduction of allergenic food like peanut and egg can prevent food allergy, but the effect on other allergic diseases is not known. Exposure to furry pets in home like dogs and cats in early life can prevent sensitization, but this protective effect can be modified by endotoxin exposure [85]. Deficiency of vitamin D has been associated with onset and exacerbation of allergy. According to this immunomodulatory effect, it has been assumed that supplementation of vitamin D might protect against allergy. But recent researches does not support protective role of vitamin D in allergy [86, 87].
\n
In the prevention of allergic diseases, protective effect was observed for antihistamines. In infants with atopic dermatitis or with high risk for allergy, ketotifen treatment was associated with lower incidence of asthma [88], while the use of cetirizine decreased the risk for asthma in grass pollen-sensitized children [89]. Allergen immunotherapy (AIT) has been used over the last 100 years and is the only therapy with disease-modifying effect. The role of AIT in primary and secondary prevention was investigated in several studies. Sublingual AIT applied for the primary prevention of allergy among high-risk infants has no protective effect on the developing of first allergic disease [90]. Oral AIT decreased the risk of asthma, among children with grass pollen allergic rhinitis [91]. Recent systematic review and meta-analysis found no evidence that AIT decreased the risk for developing a first allergic disease. However, AIT reduced the risk of asthma among patients with allergic rhinitis. This effect was observed 2 and more years after the AIT was completed. AIT can reduce the onset of new sensitizations, but the evidence was not clear [92, 93].
\n
\n
\n
6. Conclusion
\n
Allergic diseases like atopic dermatitis, asthma and allergic rhinitis have sequential appearance with typical peaks of incidence during childhood. This temporal association is observed in the whole children population, and it starts with atopic dermatitis and food allergy in infancy, followed with asthma in the preschool age and finishes with allergic rhinitis. During growing up, the remission of atopic dermatitis and asthma was noticed, while symptoms of allergic rhinitis persist through adolescence and young adult age. The occurrence of all allergy diseases among the same child in temporal appearance was noticed only in smaller proportion of children in which causal link between AD, asthma and AR can be presumed; while, among others, common occurrence of allergic diseases follows different trajectories, without typical allergic sequence. For those children, complex interplay of allergic predisposition, systemic and local immunological responses and environmental influences during maturation of immune system triggers the appearance of those coexistence of allergic disease.
\n
\n\n',keywords:"allergic march, atopy, children",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/68312.pdf",chapterXML:"https://mts.intechopen.com/source/xml/68312.xml",downloadPdfUrl:"/chapter/pdf-download/68312",previewPdfUrl:"/chapter/pdf-preview/68312",totalDownloads:294,totalViews:0,totalCrossrefCites:0,dateSubmitted:"December 17th 2018",dateReviewed:"February 28th 2019",datePrePublished:"September 6th 2019",datePublished:"December 4th 2019",dateFinished:null,readingETA:"0",abstract:"Atopy is an inherited tendency of producing immunoglobulin E on common proteins from the environment like pollen, house mites and food. The presence of atopy represents a risk for the development of allergic diseases like atopic dermatitis, asthma, allergic rhinitis and food allergy, although atopy can also be present only in the form of asymptomatic sensitization. Allergic diseases share common inherited and environmental risk factors, immunologic patterns of allergen-specific Th2 response and efferent phase of immunologic reaction characterized with the production of IgE and activation of granulocytes. The presence of one disease increases the risk for developing other diseases. Allergic diseases demonstrate characteristic sequence of incidence in childhood which is called allergic/atopic march and starts with atopic dermatitis in early infancy. Disrupted integrity of the skin in atopic dermatitis contributes to the development of sensitization and increases the risk for development of other allergic diseases. The discovery of filaggrin gene mutation opens the possibility for causative incidence of allergic diseases and for prevention of development of atopic march. But, the causal link from atopic dermatitis to asthma is still a matter of debate.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/68312",risUrl:"/chapter/ris/68312",signatures:"Blaženka Kljaić Bukvić, Mario Blekić and Marija Pečnjak",book:{id:"7062",title:"Rhinosinusitis",subtitle:null,fullTitle:"Rhinosinusitis",slug:"rhinosinusitis",publishedDate:"December 4th 2019",bookSignature:"Balwant Singh Gendeh and Mirjana Turkalj",coverURL:"https://cdn.intechopen.com/books/images_new/7062.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"67669",title:null,name:"Balwant Singh",middleName:null,surname:"Gendeh",slug:"balwant-singh-gendeh",fullName:"Balwant Singh Gendeh"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"289739",title:"Dr.",name:"Blaženka",middleName:null,surname:"Kljaić Bukvić",fullName:"Blaženka Kljaić Bukvić",slug:"blazenka-kljaic-bukvic",email:"blazenka.bukvic@gmail.com",position:null,institution:null},{id:"296533",title:"Dr.",name:"Marija",middleName:null,surname:"Pečnjak",fullName:"Marija Pečnjak",slug:"marija-pecnjak",email:"mpecnjak@gmail.com",position:null,institution:null},{id:"296535",title:"Dr.",name:"Mario",middleName:null,surname:"Blekić",fullName:"Mario Blekić",slug:"mario-blekic",email:"blekic1978@yahoo.com",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Atopic dermatitis, disrupted skin barrier and allergic sensitization: is it the beginning?",level:"1"},{id:"sec_3",title:"3. Why is allergy increasing? Hypothesis-driven strategy",level:"1"},{id:"sec_4",title:"4. Allergic march: causal link or cluster of related diseases",level:"1"},{id:"sec_5",title:"5. Can we prevent and/or stop atopic march?",level:"1"},{id:"sec_6",title:"6. Conclusion",level:"1"}],chapterReferences:[{id:"B1",body:'Boyce JA et al. Guidelines for the diagnosis and management of food allergy in the United States: Summary of the NIAID-sponsored expert panel report. The Journal of Allergy and Clinical Immunology. 2010;126(6):1105-1118'},{id:"B2",body:'Nwaru BI et al. Prevalence of common food allergies in Europe: A systematic review and meta-analysis. Allergy. 2014;69(8):992-1007'},{id:"B3",body:'Prescott S, Allen KJ. Food allergy: Riding the second wave of the allergy epidemic. 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