Taenia saginata, Taenia solium

Taenia saginata

Comment lire une taxobox
Taenia saginata
Classification
RègneAnimalia
EmbranchementPlatyhelminthes
ClasseCestoda
Sous-classeEucestoda
OrdreCyclophyllidea
FamilleTaeniidae
GenreTaenia
Nom binominal
Taenia saginata
Goeze1782
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Taenia saginata est appelé ténia inerme en raison de l'absence de crochets sur son scolex, lequel présente en revanche 4 ventouses. Il est également appelé ténia du bœuf. Le corps de l'adulte est un long ruban qui mesure 5 à 10 mètres de long et comporte de 500 à 2 000 anneaux. Son hôte intermédiaire est le bœuf. La contamination de l'homme se fait par ingestion de viande pas assez cuite, et est aujourd'hui beaucoup plus fréquente dans les pays industrialisés que la contamination par Taenia solium. T. saginata est en fait cosmopolite.

Les symptômes sont digestifs (nausées, diarrhées...), avec parfois de l'irritabilité. La maladie provoquée est appeléetæniasis.

Les anneaux mûrs se détachent et sont excrétés en traversant activement le sphincter anal, en dehors de l'émission des selles : on ne retrouve pas d'anneaux dans les selles.

L'autoinfestation par les anneaux ou les œufs (souvent des embryophores) est impossible pour l'homme, contrairement àTaenia solium.

Le diagnostic est aisé, le malade ne pouvant ignorer sa parasitose amène spontanément au médecin les proglotis(anneaux) à ramifications utérines fines, nombreuses et caractéristiques (au microscope en tout cas). Les anneaux gravides se détachent isolément de la chaîne et gagnent le milieu extérieur en franchissant activement, entre les selles, le sphincter anal. Les premiers anneaux apparaissent dans les selles 2 à 3 mois après le repas infectant.

Bandwurm-drawing.jpg

a : Taenia solium - b : Taenia saginata


Sommaire

Morphologie

Blanchâtre, précédé d'une minuscule tête ou scolex piriforme, à 4 ventouses de fixation, le corps de l'adulte est un long ruban (5 à 10 mètres) formé de segments successifs, les anneaux ou proglottis, qui portent un pore génital latéral dont la répartition le long de la chaîne est irrégulièrement alterne. En bout de chaine, les anneaux gravides, plus longs que larges, mesurent 18 mm sur 5 mm.

Biologie

Presque toujours solitaire (immunité "de préséance"), l'adulte, fixé à la muqueuse duodénale par son scolex, vit étiré dans la lumière du grêle.
La zone germinative antérieure bourgeonne sans cesse de nouveaux anneaux qui mûrissent progressivement, acquièrent des organes reproducteurs hermaphrodites, et, en bout de chaîne (et d'évolution), ne sont plus que des sacs bourrés d'embryophores sphériques de 30 à 40 microns de diamètre, à coque épaisse radiée, contenant l'embryon hexacanthe.
Ces anneaux gravides ou cucurbitains se détachent isolément de la chaîne et gagnent le milieu extérieur en franchissant activement, entre les selles, le sphincter anal. Essaimés par dessiccation de l'anneau, les embryophores infectieux souillent la terre et la pâture des bovidés hôtes intermédiaires. Arrivé dans l'intestin du bœuf, l'embryon hexacanthe, libéré par la digestion, traverse la paroi et, par voie sanguine, gagne le tissu musculaire où il se vésicule et s'enkyste, donnant le cysticerque(Cysticercus bovis).

C'est en consommant insuffisamment cuite la viande de bœuf parasitée que l'homme s'infecte. Libéré dans le duodénum, le cysticerque dévagine son scolex, se fixe à la paroi et commence à bourgeonner sa chaîne. Les premiers anneaux apparaissent dans les selles 2 à 3 mois après le repas infectant.

Clinique

Le téniasis à T. saginata est une maladie bénigne, le plus souvent asymptomatique, révélée seulement par la sortie, au troisième ou quatrième mois, des premiers proglottis, et qui cède facilement à un traitement adapté.

Diagnostic

Il est aisé, le malade ne pouvant ignorer sa parasitose et amenant spontanément au médecin les proglottis à ramifications utérines fines et nombreuses, caractéristiques de cette infestation.

Traitement

Le niclosamide (Yomesan*) est le traitement de premier choix des infestations par vers de type Taenia.
Adultes et enfants de plus de 6 ans : 2 gr en une prise.
Enfants de 2 à 6 ans : 1 gr en une prise.
Enfants de moins de 2 ans : 500 mg en une prise.

http://fr.wikipedia.org/wiki/Taenia_saginata

















































































































































Taenia saginata

Taenia saginata
Scientific classification
Kingdom:Animalia
Phylum:Platyhelminthes
Class:Cestoda
Order:Cyclophyllidea
Family:Taeniidae
Genus:Taenia
Species:T. saginata
Binomial name
Taenia saginata
Goeze, 1782
Taenia saginata proglottid stained to show uterine branches. The pore on the side identifies T. saginata as a cyclophyllid cestode.

Taenia saginata, also known as Taeniarhynchus saginata or the beef tapeworm, is a parasite of both cattle and humans, causing taeniasis in humans. Taenia saginata occurs where cattle are raised by infected humans maintaining poor hygiene, human feces are improperly disposed of, meat inspection programs are poor, and where meat is eaten without proper cooking. The disease is relatively common in Africa, some parts of Eastern Europe, the Philippines, andLatin America.[1]

Contents

Description

T. saginata is normally 3 m to 5 m in length, but can become very large, over 20 m long in some situations. The body is whitish in colour, divided into the anterior scolex, followed by a short neck and a highly extended body proper called strobila. The strobila is composed a series of ribbon-like segments called proglottids. Unlike other tapewormsthe scolex does not have a rostellum or scolex armature. The scolex is composed of 4 powerful suckers. The segments are made up of mature and gravid proglottids. T. saginata is the largest of genus Taenia consisting between 1000 to 2000 proglottids and can also have a lifespan of 25 years in a hosts intestine.[2] The mature proglottid contains the uterus (unbranched), ovarygenital pore, testes, and vitelline gland. It does not have adigestive system, no mouth, no anus, or digestive tract. It is also an acoelomate, meaning that it does not have a body cavity. In the gravid proglottid, the uterus is branched and is filled with eggs. The gravid segments detach and are passed in the feces. Each of these segments can act like a worm. When they dry up, the proglottid ruptures, and the eggs are released. The egg can only infect cattle, the intermediate host. Inside the cow'sduodenum the oncosphere hatches with the help of the gastric and intestinal secretions and migrates through theblood to the muscle. There it develops into infective cysticercoid cysticerci.[3]

Life cycle

The life cycle is indirect and complicated, and is completed in humans as the definitive host and cattle as theintermediate host. The adult worm inhabits the small intestine of humans. Fertilized eggs are released through the faeces along with the gravid proglottid which gets detached from the strobila. Cattle ingest the infective embryo while grazing. The digestive enzymes will break the thick shell of the egg and allow formation of thezygotes called "oncospheres". These zygotes then penetrate the mucous layer of the digestive tract and enter the circulation of the host. This is where the young larval stages form a pea-sized, fluid filled cyst, also known as “Cysticercus” and these cysts seem to form in the muscular fibers and are sometimes seen in specific organs like the lungs and liver. Humans acquire the infective larvae from eating undercooked meat. The digestive enzymes break down the cysticercus and the larval cyst is released and the inverted scolex is able to come out and attach to the host’s intestine. Adult tapeworm soon develop, and within three months it can reach 5 m long.[2]

Epidemiology

The disease is relatively common in Africa, some parts of Eastern Europe, the Philippines, and Latin America.[1] Humans become infected when they eat beef that is not cooked fully. Prevention is easy. Cook beef until it is no longer pink inside because cysticerci die at 56 degrees Celsius. Also, if beef is frozen at -5 degrees Celsius it is considered to be safe to consume.[3]

This parasite is found anywhere where beef is eaten, even in countries like the United States where there are strict federal sanitation policies. In the U.S. the incidence of becoming infected is low, however, 25% of infected cattle are still sold.[3]

Symptoms

Tapeworms are usually asymptomatic. However heavy infection often result in intestinal upset, weight loss, dizzinessabdominal paindiarrheaheadachesnausea,constipation, or chronic indigestion, and loss of appetite. There can be intestinal obstruction in humans and this can be alleviated by surgery. The tapeworm can also expel antigens that can cause an allergic reaction in the individual.[3]

Diagnosis

The basic diagnosis is done from a stool sample. Feces are examined to find parasite eggs. The eggs look like other eggs from the family Taeniidae, so it is only possible to identify the eggs to the family, not to the species level. Since it is difficult to diagnose using eggs alone, looking at the scolex or the gravid proglottids can help identify it as Taenia saginata.[3] Proglottids sometimes trickle down the thighs of infected humans and are visible with unaided eye and aid with identification. When the uterusis injected with India ink, its branches become visible. Counting the uterine branches enables some identification (Taenia saginata uteri have twelve or more branches on each side, while other species like Taenia solium only have five to ten).[1]

It is notoriously difficult to differentiate the species from other species of Taenia such as T. solium and T. asiatica because of their close morphological resemblance, and their eggs are more or less exactly identical. Identification often requires histological observation of the uterine branches and PCR detection of ribosomal 5.8S gene.[4] T. saginata’s uterus stems out from its center forming 12 to 20 branches, but in contrast to its closely related Taenia species, the branches are much less in number and comparatively thicker; in addition the ovaries are bilobed and testes are twice as many.[5]

Treatment

Treatment for cestode infection can be done with the drug praziquantel. Praziquantel opens membrane calcium channels causing paralysis of the worm, aiding the body in expelling the parasite through peristalsisNiclosamide, used to treat many different kinds of infections with trematodes and adult tapeworms, is quite effective.

See also

External links

http://en.wikipedia.org/wiki/Taenia_saginata











































































Taenia solium

Comment lire une taxobox
Taenia solium
 Le scolex d'un Tenia solium
Le scolex d'un Tenia solium
Classification
RègneAnimalia
EmbranchementPlatyhelminthes
ClasseCestoda
Sous-classeEucestoda
OrdreCyclophyllidea
FamilleTaeniidae
GenreTaenia
Nom binominal
Taenia solium
Linnaeus, 1758
 cycle de contamination de Taenia solium

cycle de contamination de Taenia solium

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Le Taenia solium (ou ténia armé ou ténia du porc) est l'espèce de Ténia dont l'hôte intermédiaire est le porc et l'hôte définitif, l'homme. Il a aujourd'hui presque disparu des pays industrialisés en raison de la facilité pour les services vétérinaires à le détecter. En effet, la viande de porc touchée par cette parasitose se retrouve criblée de larves cysticerques et celle-ci est retirée des chaînes de production.

Taenia solium est un cestode très voisin du Taenia saginata mais qui possède la particularité de parasiter l'homme non seulement à l'état adulte (taeniasis) mais aussi à l'état larvaire, entraînant alors la cysticercose humaine.

Son scolex est différent de celui du Taenia saginata.

Les symptômes de la présence d'un Taenia solium dans l'organisme sont:

  • présence rare d'anneaux dans les selles (à la différence de T. saginata qui possède des anneaux musculeux qui peuvent franchir la marge annale n'importe quand, les anneaux de T. solium sortent uniquement lors des selles et sont eclatés dans les selles. Un examen coprologique afin de retrouver les oeufs est nécessaire.
  • troubles digestifs: diarrhées, maux de ventre, etc.

Le Taenia solium peut entraîner une maladie, la cysticercose. Dans certains cas, l'homme devient l'hôte intermédiaire du T. solium et héberge alors les larves cysticerques. Cependant chez ce dernier les larves cysticerques vont avoir un tropisme différent de celui retrouvé chez le porc, ainsi les larves ne vont pas rester dans le tissu musculaire mais vont migrer dans le cerveau (60% des cas) ou encore dans la région proche des yeux.

Le Taenia solium qui, comme les autres ténias, se développe d'environ un mètre tous les 6 mois pour atteindre une dizaine de mètres. Ce cestode est très sensible aux traitements à base de Niclosamide ( exemple: Trédémine). Après le traitement (1 jour de traitement pour le Taenia saginata et solium, 7 pour les ténias nains), vous devrez vérifier pendant 3 mois la présence d'anneaux, et au bout de ces 3 mois, faire une analyse cytobactériologique de vos selles.

Sommaire

Répartition géographique et importance

Commun autrefois dans tous les pays où l'on consommait de la viande de porc, il a disparu pratiquement d'Europe sous l'influence de trois facteurs principaux :

  • l'élevage industriel du porc, limitant sa coprophagie ;
  • la surveillance vétérinaire, efficace par le langueyage ;
  • la cuisson "à cœur", devenue traditionnelle pour la viande de porc.

L'affection persiste par foyers en Extrême-Orient, en Afrique, et en Amérique du Sud.

Morphologie

Un peu moins long que le Taenia saginata, il s'en distingue aisément par son scolex, globuleux, armé de 2 couronnes de crochets en plus de 4 ventouses et la disposition régulièrement alternée des pores génitaux latéraux.

Biologie

Parasite spécifique de l'homme comme le Taenia saginata, l'adulte vit dans l'intestin grêle d'où les anneaux gravides s'éliminent passivement avec les selles, par fragments de chaîne. Le porc, hôte intermédiaire volontiers coprophage, s'infecte en déglutissant les embryophores (indiscernables de ceux du ténia inerme). Le cycle, en tous points semblable, aboutit à l'enkystement, dans les muscles, des cysticerques infectieux (Cysticercus cellulosae). C'est en consommant la chair insuffisamment cuite ou mal conservée des porcs ladres (qui ont des cysticerques de ténia dans les muscles) que l'homme s'infecte.

Clinique

Le rôle pathogène est double :

  • Le développement normal de l'adulte dans l'intestin n'entraîne qu'un téniasis banal.
  • Au contraire la possibilité d'évolution des embryophores déglutis accidentellement (souillure alimentaire ou auto-infestation) permet l'installation d'une cysticercose, véritable "ladrerie" humaine, qui fait toute l'importance de la parasitose.

La localisation musculaire, bien tolérée, sauf si elle est massive, est souvent un diagnostic de radiographie systématique ou d'autopsie; elle existe certainement plus souvent qu'on ne la signale. Ce sont en effet l'œil et l'encéphale qui paraissent être les lieux d'élection de la cysticercose, se partageant à peu près également plus de 80% des cas décrits. Dans l'œil, le cysticerque joue le rôle de corps étranger avec selon sa localisation, exophtalmiestrabismeiritis ou troubles visuels, fréquemment assortis de céphalées et de douleurs locales. Dans le cerveau, le tableau évoque une tumeur intra-crânienne évolutive : les céphalées, vertiges et autres petits troubles du début (cysticerques vivants) aboutissant à des troubles de la parole, des épisodes confusionnels, des crises d'ataxie ou d'épilepsie bravais-jacksonienne (réaction expansive autour des cysticerques morts). L'évolution peut se faire vers le coma et la mort.

Diagnostic

Le diagnostic du téniasis à Taenia solium se fait facilement sur la morphologie des anneaux retrouvés dans les selles et examinés par transparence (ramifications utérines épaisses et peu nombreuses). Encore faut-il les y chercher, car la clinique n'oriente pas et le malade ignore le plus souvent sa parasitose.

  • Le diagnostic direct n'est possible que par biopsie, mais, en dehors des rares localisations sous-cutanées, celle-ci est le plus souvent impraticable.
  • La radiographie n'objective les cysticerques qu'une fois morts et calcifiés.
  • La sérologie est encore à l'étude.

En fait, c'est presque toujours sur pièce opératoire ou prélèvement nécropsique que l'examen anatomo-pathologique confirmera ou révèlera l'étiologie cysticerquienne.

Traitement

Contre l'adulte, on utilisera la niclosamide aux doses indiquées pour taenia saginata.
Contre les cysticerques mal tolérées, le traitement est chirurgical principalement. On peut utiliser le praziquantel ( Biltricide*) 50mg/kg/jour en trois prises pendant quinze jours.

http://fr.wikipedia.org/wiki/Taenia_solium


Cysticercose

Comment lire une taxobox
Taenia solium
 Le scolex d'un Tenia solium
Le scolex d'un Tenia solium
Classification
RègneAnimalia
EmbranchementPlatyhelminthes
ClasseCestoda
Sous-classeEucestoda
OrdreCyclophyllidea
FamilleTaeniidae
GenreTaenia
Nom binominal
Taenia solium
Linnaeus, 1758
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La cysticercose , ou neurocysticercose, est la plus fréquente des infections parasitaires du système nerveux central dans le monde entier. Il est provoqué par les larves d’un ver platTaenia solium normalement retrouvées dans le porc. Les larves, appelées cysticerci ( pluriel de cysticercus) ; se transforment en kystes dans l’organisme. Si ces vers sont retrouvés dans l’intestin, elles provoquent une maladie différente qui s'appelle le taeniasis, qui est traitée dans les articles Taenia solium et de Taenia saginata.

Sommaire

Cycle parasitaire

Cycle parasitaire de Taenia solium . Cliquer sur l’image pour agrandir

La cysticercose se produit quand des oeufs de Taenia solium pénètrent dans l'estomac avec de la nourriture ou de l'eau contaminées par des matières fécales humaines infectées. En outre, les personnes porteuses de ténias adultes dans l’intestin (teniasis) peuvent s’autoinfecter elles-mêmes par la cysticercose en vomissant, ce qui refoule des œufs dans l'estomac. Quand les œufs reviennent dans les intestins, les vers éclosent et migrent dans les muscles squelettiques, le cœur, l’œil et même le cerveau et moelle épinière. Une fois en place, ils forment de petits kystes encapsulés contenant le ver.

Symptômes

Dans les muscles, les kystes provoquent un œdème ou créent des nodules sous la peau. Si les kystes se forment dans l'œil, ils peuvent altérer la vision en flottant dans le globe oculaire et entraîner une cécité par œdème et décollement de la rétine. Les lésions cardiaques peuvent provoquer des troubles du rythmeou une défaillance cardiaque (rare). Les symptômes les plus dangereux sont le résultat de l'enkystement dans le système nerveux central.

Selon le département des maladies parasitaires des Centers for Disease Control and Prevention, dans la neurocysticercose (cysticercose du cerveau), les crises d’épilepsie, et les céphalées sont les symptômes les plus fréquents. Cependant, la confusion, le déficit d'attention aux gens et à leur entourage, les troubles de l'équilibre, la dilatation des ventricules du cerveau (appeléehydrocéphalie) peuvent également se produire. Souvent, il y a peu de symptômes jusqu'à ce que le parasite meure1. Quand le parasite meurt, lesystème immunitaire de l’hôte détecte les débris du ver et les attaque, entraînant de l’œdème et une cicatrisation. C'est ce qui provoque la plupart des symptômes observés. Les lésions de la moelle épinière peuvent conduire à la perte partielle de la commande motrice, à l’altération de l’état général, et également à la paralysie. Quand la mort se produit, elle est le plus souvent due à l’atteinte du cerveau avec pour résultat l’hydrocéphalie, l’œdème cérébral, la compression du cerveau, ou les crises epileptiques2

Diagnostic

La Neurocysticercose est difficile à diagnostiquer à sa phase initiale et peut ne devenir évidente qu’au début des premiers symptômes neurologiques, ou quand unscanner, ou une IRM du cerveau, est pratiqué pour une raison quelconque.

La recherche d’Anticorps ou la biopsie de la zone atteinte peuvent être nécessaires pour affirmer le diagnostic.

Traitement

Des médicaments antiparasitaires tel que le Praziquantel et l’Albendazole peuvent être utilisés pour traiter la neurocysticercose. Les Stéroïdes et les médicaments anti-inflammatoires sont également souvent prescrit en complément pour réduire l’œdème cérébral qui résulte des attaques du système immunitaire contre les vers morts. La question de savoir si les patients tirent bénéfice du traitement est encore controversée, parce que les cysticerques vivants ne provoquent pas de crises d’épilepsie ; seuls les parasites morts ou mourants suscitent une réponse inflammatoire et des crises. En théorie, donc, le traitement d'un patient avec des drogues qui tuent les parasites vivants peut induire des crises chez quelqu'un qui était auparavant en bonne santé et ne présentait pas de crise ; de même, traiter quelqu'un qui présente des crises peut n’avoir aucun effet positif parce que les parasites sont déjà morts et qu’aucune amélioration ne peut être espérée. Une méta-analyse de 11 essais cliniques suggère qu'il y a probablement un léger avantage pour les patients qui ont des lésions actives, mais aucun avantage pour ceux qui ont seulement des lésions mortes ou inactives. 3

Si le kyste est localisé dans certains endroits, tels que l'œil ou le cerveau, les stéroïdes peuvent être prescrits quelques jours avant le traitement antiparasitaire, afin d'éviter les problèmes provoqués par l’œdème. Si l’œdème et la réaction immunitaire ne sont pas jugulés, le traitement lui-même peut avoir des conséquences mortelles, ainsi le médicament est-il donné à faible dose pendant plusieurs jours. Parfois la chirurgie peut être nécessaire pour enlever la zone infectée ou les kystes, mais ceci peut être impossible quand ils sont situés dans des régions dont l'accès chirurgical est difficile ou dangereux. En outre, il existe des médicaments pouvant traiter certains symptômes, tels que les crises ou les troubles du rythme cardiaque sans atteindre les vers.

Si les cysticerques sont calcifiés dans le cerveau, ou s'il y a seulement une lésion, le traitement n'est pas indiqué1

Prévention

Il est possible de prévenir l'infection par le T.solium en évitant la consommation de porc insuffisamment cuit et de nourriture ou d’eau contaminée par les déjections humaines. Une attention particulière devrait accordée aux règles d’hygiène là où elles sont défectueuses et aux lois qui rendent obligatoire l’inspection des viandes. La congélation du porc infesté pendant une période prolongée tuera également les cysticerques.

Si une personne est déjà atteinte du T.solium , elle peut éviter la cysticercose en traitant précocement l'infection dans l’intestin, en n'ingérant pas ses propres matières fécales, et en évitant les vomissements, toutes circonstances qui introduisent des œufs dans l'estomac pour qu'ils deviennent des cysticerques dans l’intestin.

Références

  1. Centers for Disease Control and Prevention Division of Parasitic Diseases fact sheet
  2.  Sorvillo FJ, DeGiorgio C, Waterman SH, « Deaths from cysticercosis, United States », dans Emerg Infect Disvol. 13, no 2, 2007, p. 230–5 [texte intégral]
  3.  Del Brutto OH, Roos KL, Coffey CS, Garcia HH, « Meta-analysis: Cysticidal drugs for neurocysticercosis: albendazole and praziquantel », dans Ann Intern Med,vol. 145, no 1, 2006, p. 43–51

The webpage of a network of scientists and professionals aiming to control Taenia solium in Mexico. http://www-lab.biomedicas.unam.mx/cistimex/http://www.taeniasolium.unam.mx/

http://fr.wikipedia.org/wiki/Cysticercose


Taenia solium

Taenia solium
Scolex of Taenia solium
Scientific classification
Kingdom:Animalia
Phylum:Platyhelminthes
Class:Cestoda
Order:Cyclophyllidea
Family:Taeniidae
Genus:Taenia
Species:T. solium
Binomial name
Taenia solium
Linnaeus, 1758

Taenia solium, also called the pork tapeworm, is a cyclophyllid cestode in the family Taeniidae. It infects pigs and humans inAsiaAfricaSouth America, parts of Southern Europe, and pockets of North America. Like all cyclophyllid cestodesT. soliumhas four suckers on its scolex ("head"). T. solium also has two rows of hooks.

Contents

Description

T. solium has a very similar life cycle to Taenia saginata,Cysticerci have three morphologically distinct types.[1] The common one is the ordinary "cellulosecysticercus which has a fluid filled bladder that is 0.5 cm to 1.5 cm in length and an invaginatedscolex. The intermediate form has a scolex while the "racemose" has no evident scolex but are believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid and 13% of patients might have all three types in the brain. Humans are usually infected through eating infected pork, fostering adulttapeworms in the intestine, and passing eggs through feces, but autoinfection is also possible. In that case, a cysticercus (a larva sometimes called a "bladder worm") develops in the human and the human acts like an intermediate host. This happens if eggs get to the stomach, usually as a result of contaminated hands, but also due toretroperistalsisCysticerci often occur in the central nervous system, which can cause major neurological problems like hydrocephalusparaplegymeningitis,convulsions and even death. The condition of having cysticerci in one's body is called cysticercosis.

Eggs can be diagnosed only to the family (biology) level, but if a proglottid's uterus is stained with India ink, the number of visible uterine branches can help identify the species: unlike the Taenia saginata uteri, T. solium uteri have only five to ten uterine branches on each side.

Infection with T. solium adults is treated with niclosamide, which is one of the most popular drugs for adult tapeworm infections, as well as for fluke infections. Ascysticercosis is a major risk, it is important to wash one's hands before eating and to suppress vomiting if a patient may be infected with T. solium. If neurocysticercosisoccurs the drug of choice is either albendazole or praziquantel. These drugs damage the parasites skin internally causing it to disintegrate and is then removed by the host's immune system.

Infection may be prevented with proper disposal of human feces around pigs, cooking meat thoroughly, and/or freezing the meat at -10oC for 5 days. Most cases occur because infected food handlers contaminate the food.

Life cycle

Life cycle of T. solium. Click the image to see it full-size

This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier. Pigs and humans become infected by ingesting eggs or gravid proglottids. Humans are infected either by ingestion of food contaminated with feces containing eggs, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine, invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other tissues, where they develop into cysticerci. In humans, cysts can cause serious sequelae if they localize in thebrain, resulting in neurocysticercosis. The parasite life cycle is completed, resulting in human tapeworm infection, when humans ingest undercooked pork containing cysticerci. Cysts evaginate and attach to the small intestine by their scolex. Adulttapeworms develop, (up to 2 to 7 m in length and produce less than 1000 proglottids, each with approximately 50,000 eggs) and reside in the small intestine for years.


Pathogenesis

Ingestion of T. solium eggs or proglottid rupture within the host intestine can cause larvae to migrate into host tissue and cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed including headaches, dizziness and occasional seizures. In more severe cases, dementia or hypertension due to perturbation of the normal circulation of cerebrospinal fluid can occur. The severity of cysticercosisdepends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements and brain system dysfunction. In children ocular location of cysts is more common than cystation in other locations of the body. If a person is heavily infected with T. solium, it can lead to neurocysticercosis which can lead to epilepsyseizureslesions in the brain, blindness and tumors like growths. This kind of patients will also show the low level of eosinophils when they run the blood test.

Diagnosis

Diagnosis requires biopsy of the infected tissue and examination of feces. T. solium eggs and proglottids found in feces diagnoses taeniasis and not cysticercosis.Cysticercosis is diagnosed primarily on confirming the prescence of hooks on the scolex of T. solium. Radiological test such as X-ray, CT scans and MRIs can also be used to detect diseases. X-rays are used to identify calcified larvae in the subcutaneous and muscle tissues and CT scans and MRI’s are used to find lesions in the brain.

Treatment

PZQ (praziquantel) is the drug of choice for the treatment of T. solium infection. For cysticercosis, one can be treated with albendazole combining with steroid to reduce the inflammation. In some cases like tumors in the brain, treating with drugs is not enough and they need to be surgically removed as necessary. Albendazoleappears to be more effective and a safe drug for Neurocysticercosis, infection of the brain with T. solium larvae.[2][3]

Prevention and Control

The best way to control of getting tapeworms is by eating fully cooked pork. Moreover, high level of personal hygiene and prevention of fecal contamination with pig foods also play major roles in prevention of getting the parasites.

Epidemiology

Stained T. solium proglottid.

T. solium is found worldwide, however, it has shown to be more common in cosmopolitan areas. Because pigs areintermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigsand eat undercooked porkCysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil or water supplies. Prevalence rates in the United States have shown that immigrants from Mexico, Central and South Americaand South-east Asia account for most of the domestic cases of cysticercosis.[4] Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier via gravid proglottids, and thus can occur in populations that neither eat pork nor share environments with pigs, although, as stated, the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork.

References

  1. ^ Rabiela MT, Rivas A, Flisser A (1989). Morphological types of Taenia solium cysticerci. Parasitol. Today 5: 357-359.
  2. ^ Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH, Herrera G, Evans CA, Gonzalez AE, Cysticercosis Working Group in Peru. (2004). "A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis.". N Engl J Med. 350 (3): 249-258. PMID 14724304.
  3. ^ Matthaiou DK, Panos G, Adamidi ES, Falagas ME. (2008). "Albendazole versus praziquantel in the treatment of neurocysticercosis: a meta-analysis of comparative trials.". PLoS Negl Trop Dis. 2 (3): e194. PMID 18335068.
  4. ^ Flisser A. (1988). Neurocysticercosis in Mexico. Parasitol. Today 4: 131-137.

See also

 This article incorporates public domain material from websites or documentsof the Centers for Disease Control and Prevention.

External links

http://en.wikipedia.org/wiki/Taenia_solium


Cysticercosis

Cysticercosis
Classification and external resources

Magnetic resonance image of a patient with neurocysticercosis demonstrating multiple cysticerci within the brain.
ICD-10B69.
ICD-9123.1
DiseasesDB3341
MedlinePlus000627
eMedicineemerg/119med/494ped/537
MeSHD003551

Cysticercosis, or neurocysticercosis, is the most common parasitic infestation of thecentral nervous system worldwide.[1] Humans develop cysticercosis when they ingesteggs of the tapeworm Taenia solium. The eggs are usually found in fecally-contaminated water or food. Autoinfection as a result of the entry of eggs into stomach due toretroperistalsis or as a result of accidental ingestion of eggs from the host's own feces due to contaminated hands is also possible.[2]

Contents

Agent

The cause of human cysticercosis is the larval form of Taenia solium (pork tapeworm). T. solium is a member of Phylum Platyhelminthes, class Cestoda, Order Cyclophyllidea and family Taeniidae. The common larval stage of T. solium was also known as Cysticercus cellulosae.

History of discovery

The earliest reference to tapeworms were found in the works of ancient Egyptians that date back to almost 2000 BC.[3] The description of measled pork in the History of Animals written by Aristotle (384–322 BC) showed that the infection of pork with tapeworm was known to ancient Greeks at that time.[3] It was also known toearly Muslim physicians and was one of the reasons for pork being forbidden by Islamic dietary laws.[4] Recent examination of evolutionary histories of hosts and parasites and DNA evidence show that over 10,000 years ago, ancestors of modern humans in Africa became exposed to tapeworm when they scavenged for food or preyed on antelopes and bovids, and later passed the infection on to domestic animals such as pigs.[5]

Cysticercosis was described by Johannes Udalric Rumler in 1555; however, the connection between tapeworms and cysticercosis had not been recognized at that time.[6] Around 1850, Kuchenmeister fed pig meat containing cysticerci of T. solium to humans awaiting execution in a prison, and after they had been executed, he recovered the developing and adult tapeworms in their intestines.[3][6] By the middle of the 19th century, it was established that cysticercosis was caused by the ingestion of the eggs of T. solium.[7]

Transmission

Pigs and humans are T. solium reservoirs. Humans can be infected by ingesting the eggs or larvae from eating undercooked pork that contains viable cysticercosis larvae or from fecally contaminated food or water.[8] The adult tapeworm develops in humans after the ingestion of infected meat; however cysticercosis occurs after the ingestion of eggs, either from external sources or from their own feces.[8] Pigs get infected with cysticerci when they ingest human feces. The incubation period ranges from months to over ten years.[9]

Morphology

T. solium worms may reach a length of several meters.[8] The scolex has four suckers, and a double crown of prominent hooks, which attach to the intestinal mucosa.[8] T. solium eggs are spherical and 30 to 40 µm in diameter.[9]

The cysticercus larva completes development in about 2 months. It is semitransparent, opalescent white, and elongate oval in shape and may reach a length of 0.6 to 1.8 cm.[8]

Life cycle

Life cycle.gif

The life cycle involves humans as a definite host and pigs as an intermediate host. Pigs ingest contaminated food or water that contains eggs or proglottids from human’s feces. The ova develop into cysticercus in pig muscles. Human becomes infected when they ingest raw or undercooked “measly pork” that contains viable cysticercus. Upon reaching the small intestine, the scolex attaches to the intestinal wall and a proglottid chain grows. T. soliumreleases three to six proglottids/day, bearing 30,000 to 70,000 eggs (ova) per proglottid into the intestine. Nearly 250,000 ova are passed daily into the human feces and to the environment, and the cycle continues.[9] Infections with cysticercus occur after humans consume the ova from exogenous sources or through self-infection via the fecal-oral route. Humans, in this case, are intermediate hosts. Ova are digested in the stomach and release oncospheres which penetrate the intestinal wall and reach the bloodstream.[10] These oncospheres develop into cysticerci in any organ but are common in brain, subcutaneous tissue, or eyes.

Clinical Presentations in humans

Cysticercosis in muscles

Cysticerci can develop in any voluntary muscle in humans.[8] Invasion of muscle by cysticerci can cause myositis, with fever, eosinophilia, and muscular pseudohypertrophy, which initiate with muscle swelling and later progress to atrophy and fibrosis.[8] In most cases, it is asymptomatic since the cysticerci die and become calcified.

Neurocysticercosis

Neurocysticercosis presents in many forms, depending on the localization of the cysts and disease activity.[8] 60% of the patients with cysticerci are found to have them in the brain.[8]As the stage of cysticerci reflect the signs, symptoms and treatment of neurocysticercosis, it is important to understand the natural history of CNS cysts.[9] In the case of cysticerci in the brain parenchyma, four major stages have been classified: [9] In stage 1, immature cysts appear within 1–4 weeks during which the oncosphere lodges to the brain and finally expands into a cyst. It is mainly asymptomatic, although flu-like illness, rare seizures, rare increased intracranial pressure from massive infestation has been recorded. In stage 2, the cysticerci become mature and viable about 2 months after egg ingestion. The cyst possesses a protoscolex with the cyst bladder and causes no or minimal surrounding inflammation or edema. The cysticerci also down-regulate host cellular immunity. Stage 2 cysts are also asymptomatic, and can persist for more than 10 years.

Stage 3 is typified by colloid or degenerating cysts with thick cystic fluid, thickened capsule, and appear two to 10+ years after the cyst becomes mature. The cyst no longer prevents a host immune response and its antigens leak from the bladder wall. The intense inflammation is provoked around the degenerating cyst. Most patients bearing stage 3 develop clinical signs and symptoms such as seizures, occasional focal neurological signs, headaches, nausea, vomiting, lethargy from increased intracranial pressure and altered mental status.[9] At stage 4, the cyst is calcified. The surrounding inflammation drops since the dead cyst no longer produces foreign antigens. Common clinical features includes persistent non-provoked seizures although most of the patients are asymptomatic.[9]

In meningeal cysticercosis, cysticerci often do not develop into typical cysts, and become racemose, lacking a scolex and becoming lobes in thin-walled bladders. These cysts increase and slowly leak their antigen into the subarachnoid CSF producing meningitis and can further develop into arachnoiditis, which may lead to obstructive hydrocephalus, cranial nerve involvement, intracranial hypertension, arterial thrombosis and stroke.[8][9]

In intraventricular cysticercosis, the cysts occur in the lateral, third or fourth ventricles which may be asymptomatic or if they block the flow of CSF, they may cause increased intracranial pressure.[9]

Ophthalmic Cysticercosis

In some cases, cysticerci may be found in the globe, extraocular muscles, and subconjunctiva. Depending on the location, they may cause visual difficulties that fluctuate with eye position, retinal edema, hemorrhage, a decreased vision or even a visual loss.[8][9]

Subcutaneous Cysticercosis

Subcutaneous cysts are in the form of firm, mobile nodules, occurring mainly on the trunk and extremities[11]. Subcutaneous nodules are sometimes painful.

Diagnosis

The traditional method of demonstrating T. solium eggs in stool samples diagnoses only taeniasis.[10] Though the presence of T. solium eggs or proglottids in the feces does not necessary mean the infection with cysticercus, those patients should be evaluated serologically, since autoinfection via fecal-oral route can potentially result in cysticercosis.

In CDC’s immunoblot assay, cysticercosis-specific antibodies can react with structural glycoprotein antigens from the larval cysts of T. solium.[10] Therefore, the serum samples from patients with other microbial infections do not react with any of the T. solium derived antigens. The positions of the seven diagnostic glycoproteins are marked and selected based on how fast they can move in SDS-PAGE. The test is so far 100% specific and has higher sensitivity than any other immunoassay systems.

Neuroimaging with CT or MRI is the most useful method to diagnose neurocysticercosis.[9] CT scan shows both calcified and uncalcified cysts, as well as distinguishing active and inactive cysts (2). MRI can detect intraventricular cysts while CT scan cannot.[9]

Management and Therapy

Treatment must be tailored to the specific needs of the patient and may include medical drugs such as antihelminthic drugs and corticosteroids or surgery.[12]

Surgical treatment includes direct excision of ventricular cysts, shunting procedures, and removal of cysts via endoscopy.[8][9] Albendazole is preferable overpraziquantel due to its lower cost and corticosteroids and anticonvulsants do not reduce CSF and brain drug levels.[9] Moreover, the results from meta-analysis study have shown that albendazole is more effective than praziquantel in terms of clinically important outcomes in patients with neurocysticercosis.[13] In the case of brain parenchymal cysticercosis, treatment depends on the stage of cyst development. In immature cyst stage (stage 1), high-dose corticosteroids are administered to reduce the edema but antihelminth drugs have been found to be harmful.[9] Vesicular or viable cysts (stage 2) are often asymptomatic, and usually are not treated with antihelminth drugs, while surgical removal of the cyst, along with albendazole is indicated in the colloid cyst stage (stage 3). No antihelminthic treatment is administered in dead calcified cysts stage (stage 4).[9]

In the case of cysts in globe, surgical cyst removal is necessary, while antihelminth drug with steroids alone might be sufficient to treat cysts outside globe.[9] Treatment recommendations for subcutaneous cysticercosis includes surgery, praziquantel and albendazole.[11]

Public Health and Prevention Strategies

Cysticercosis is considered as “tools-ready disease” according to WHO [14]. International Task Force for Disease Eradication in 1992 reported that cysticercosis is potentially eradicable.[15] It is feasible because there are no animal reservoirs besides humans and pigs. The only source of T. solium infection for pigs is from humans, a definite host. Theoretically, breaking the life cycle seems easy by doing intervention strategies from various stages in the life cycle..[16]

For example,

  1. Massive chemotherapy treatment of infected humans, improving sanitation, and education humans are major ways to discontinue the cycle at step 1, in which eggs from human feces are transmitted to other humans and/or pigs.
  2. Cooking of pork or freezing it and inspecting meat are effective means to cease the life cycle at step 3.
  3. The management of pigs by treating them or vaccinating them is another possibility to intervene step 4 of the life cycle.

Intervention by concurrent treatment of humans and pigs

The intervention strategies to eradicate cysticercosis includes surveillance of pigs in foci of transmission and massive chemotherapy treatment of humans.[15] In reality, control of T. solium by a single intervention, for instance, by treating only human population will not work because the existing infected pigs can still carry on the cycle. The proposed strategy for eradication is to do multilateral intervention by treating both human and porcine populations.[17] It is feasible because treatment pigs with oxfendazole have been shown to be effective and once treated, they are protected from further infections for at least 3 months.[18]

Limitations

Even with the concurrent treatment of humans and pigs, complete elimination is hard to achieve. In one study conducted in 12 villages in Peru, both humans and porcine were treated with praziquantel and oxfendazole, with the coverage of more than 75% in humans and 90% in pigs [19] The result shows a decreased in prevalence and incidence in the intervention area; however the effect did not completely eliminate T. solium. The possible reason includes the incomplete coverage and re-infection.[20]Even though T. solium could be eliminated through mass treatment of human and porcine population, it is not sustainable.[17] Moreover, both tapeworm carriers of humans and pigs tend to spread the disease from endemic to non-endemic areas resulting in periodic outbreaks of cysticercosis or outbreaks in new areas.[21][22]

Vaccine against porcine cysticercosis

Given the fact that pigs are part of a life cycle, vaccination of pigs is another feasible intervention to eliminate cysticercosis. Research studies have been focusing on vaccine against cestode parasites, since many immune cell types are found to be capable of destroying cysticercus.[23] Many vaccine candidates are extracted from antigens of different cestodes such as T. soliumT. crassicepsT. saginataT. ovis and target oncospheres and/or cysticerci. In 1983, Molinari et al. reported the first vaccine candidate against porcine cysticercosis using antigen from cysticercus cellulosae drawn out from naturally infected.[24] Recently, vaccines extracted from genetically engineered 45W-4B antigens have been successfully tested to pigs in an experimental condition.[25] This type of vaccine can protect against cysticercosis in both Chinese and Mexican type of T. solium. However, it has not been tested in endemic field conditions, which is important because the realistic condition in the field differ greatly from experimental condition, and this can result in a great difference in the chances of infection and immune reaction.[23]

The S3PVAC Vaccine

The vaccine constituted by 3 peptide synthetically produced (S3Pvac) has proven its efficacy in natural conditions of transmission.[26] The S3PVAC vaccine so far, can be considered as the best vaccine candidate to be used in endemic areas such as Mexico (20). S3Pvac consists of three protective peptides: KETc12, KETc1 and GK1, whose sequences belong to native antigens that are present in the different developmental stages of T. solium and other cestode parasites.[23][27]

Non-infected pigs from rural villages in Mexico were vaccinated with S3Pvac and the vaccine reduced 98% the number of cysticerci and 50% the number of prevalence.[26][28]. The diagnostic method involves necropsy and tongue inspection of pigs. The natural challenge conditions used in the study proved the efficacy of the S3Pvac vaccine in transmission control of T. solium in Mexico.[23] The S3Pvac vaccine is owned by the National Autonomous University of Mexico and the method of high scale production of the vaccine has already been developed.[23] The validation of the vaccine in agreement with the Secretary of Animal Health in Mexico is currently in the process of completion.[29] It is also hoped that the vaccine will be well-accepted by pig owners because they also lose their income if pigs are infected cysticercosis.[29] Vaccination of pigs against cysticercosis, if succeeded, can potentially have a great impact on transmission control since there is no chance of re-infection once pigs receive vaccination.

Limitations of vaccines

Even though vaccines have been successfully generated, the feasibility of its production and usage in rural free ranging pigs still remains a challenge. If a vaccine is to be injected, the burden of work and the cost of vaccine administration to pigs will remain high and unrealistic.[23] The incentives of using vaccines by pig owners will decrease if the vaccine administration to pigs takes time by injecting every single pig in their livestock. An oral vaccine is proposed to be more effective in this case as it can be easily delivered to the pigs with the food, though no one has ever achieved it yet.[23]

Other types of interventions and Limitations

Cysticercosis can also be prevented by routine inspection of meat and condemnation of measly meat by the local government.[30] However, in areas where food is scarce, cyst-infected meat might be considered as wasted since pork can provide high quality protein.[31] At times, infected pigs are consumed within the locality or sold at low prices to traffickers who take the uninspected pigs at urban areas for sale.[32]

Due to these limitations, cysticercosis has not been eliminated in any endemic areas.

Epidemiology

The tapeworm that causes cysticercosis is endemic to many parts of the world including China, Southeast Asia, India, sub-Saharan Africa, and Latin America.[33] Some studies suggest that the prevalence of cysticercosis in Mexico is between 3.1 and 3.9 percent. Other studies have found the seroprevalence in areas of Guatemala, Bolivia, and Peru as high as 20 percent in humans, and 37 percent in pigs.[34] In Ethiopia, Kenya and the Democratic Republic of Congo around 10% of the population is infected, in Madagascar 16%. The frequency has decreased in developed countries owing to stricter meat inspection, better hygiene and better sanitary facilities. The distribution of cysticercosis coincides with the distribution of T. solium.[35] Cysticercosis is the most common cause of symptomatic epilepsy worldwide.[36]

In Latin America, an estimated 75 million persons live in endemic areas and 400,000 people have symptomatic disease.[37] Cysticercosis is also found to be associated with Hispanic ethnicity, immigrant status, and exposure to areas of endemicity.[8] In the US, the disease is found in immigrants from Mexico, Central and South America. Current livestock for pigs in the U.S do not play a role in the transmission of Taenia solium, and thus cysticercosis in the U.S is an imported disease.[16]

In the USA during 1990–2002, 221 cysticercosis deaths were identified. Mortality rates were highest for Latinos and men. The mean age at death was 40.5 years (range 2–88). Most patients, 84.6%, were foreign born, and 62% had emigrated from Mexico. The 33 US-born persons who died of cysticercosis represented 15% of all cysticercosis-related deaths. The cysticercosis mortality rate was highest in California, which accounted for ˜60% of all deaths.[38]

In popular culture

  • The first patient on the television show House suffered from cysticercosis.
  • In the crossover of the series Grey's Anatomy (season 5) and Private Practice (season 2), Archer Montgomery, brother of Addison Forbes Montgomery, suffered from neurocysticercosis. He was cured via the surgical removal of the cysts by his former brother-in-law Derek Shepherd.

External Links

http://en.wikipedia.org/wiki/Cysticercosis
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