Lifecycle of Taenia solium - COnnecting REpositories · 2016. 8. 6. · Intestinal pathology: Taeniasis[9] encephalitis Dementia Chemotaxis Stroke/transient Cerebral pathology: Neurocysticercosis

Intestinal pathology: Taeniasis[9]

Cerebral pathology: Neurocysticercosis

Larvae suffer some pathological changes until its death. This evolution can be described in four stages:

1.Vesicular stage 2.Colloidal vesicular stage 3.Granular nodular stage 4.Calcified nodular stage These pathology is characterized by a natural progression of innate (neutrophils and macrophages), early induced (NK cells and γδ T cells) and adaptive immune response (αβ T cells and B cells) in infected mice.Th1 response

It depends on the number, size, stage and localization of cysts and the patient’s immune response.

Possible explanation of relation between brain injury, inflammation and epilepsy [6]

General information:

Taenia solium:

Norm

al l

ifec

ycl

e of

Taen

ia S

oli

um

A

ber

rant

cycl

e

EPILEPSY

Brain injury

Head trauma

Stroke Cortical

malformations

Perinatal

injury

Brain inflammati

on

Microglia Macrophages

Astrocytes Neurons

Innate immunity

Altered excitability

Neuronal death

BBB Lymphocytes

Adaptative immunity

Dichotomous role of inflammation

Infection Seizures Unknown

Reference 1. Willingham AL 3rd, Wu HW, Conlan J, Satrija F. Combating Taenia solium cysticercosis in Southeast Asia an opportunity for improving human health and livestock production. Adv Parasitol. 2010;72:235-66 2. Marcia Ramos Monteiro da Silva, et al. Recombinant expression of Taenia solium TS14 antigen and its utilization for immunodiagnosis of neurocysticercosis. Acta Trop. 2006;100(3):192-8. 3. Oscar H. Del Brutto. Neurocysticercosis: A review. Surg Neurol. 2005;63(2):123-32. 4. Astrid E.Cardona et al. Development of an Animal Model for Neurocysticercosis: Immune Response in the Central Nervous System Is Characterized by a Predominance of γδ T Cells. J Immunol. 1999;162(2):995-1002 5. Sumit Sinha, B.S Sharma. Neurocysticercosis: A review of current status and management. J.Clin.Neurosci. 2009;16(7):867-76.

Affected countries: Latin America, India, Asia and Sub-Saharan Africa. Imported cases: Europe, Australia, USA and Canada. 1/1000 for human teaniasis Incidence 1-10% for humans CC 20-40% for pig CC Age of infection: 5-15 years old Age of manifestation: 25-35 years old Problems: high poverty, warm weather, illiteracy...

Immunodiagnosis Medical imaging

EITB ELISA RMN TAC

Lifecycle of Taenia solium

• Neurocysticercosis is endemic in many parts of the world, specially in developing countries. However we have to take into consideration the diagnosis in developed countries by immigration of endemic countries. •Neurocysticercosis is the most common cause of symptomatic epilepsy worldwide. Despite the severity of the disease, most people don’t give the importance to it, since it principally affects developing countries. •Treatment and diagnosis works well, but can be improved. •This parasitic disease is potentially eradicable, but to be effective we need eradication programs that consists: 1. Interrupt the tape worm-host cycle. 2. The vaccination of pig against infection with the parasite, which indirectly reduce the appearance of new cases of the disease. 3. Public health and awareness. 4. Possible vaccination for human. But the best alternative is the education and the health promotion, specially in developing countries.

Taenia solium Cerebral symptoms Surgery

Albendazol Praziquantel Epilepsy Inflammation

•Dose: 50 mg/kg/day

•Duration: 15 days

•Efficacy: 60-70% in

parenchymatous cyst

•Dose: 15 mg/kg/day

•Duration: 3 weeks

•Efficacy: 80% of the cyst

•Enhance GABA channel (fenobarbiturate and benzodiazepine) •Inhibit Sodium channel (carbamazepine) •Inhibit Calcium channel (gabapentin)

•Corticosteroid: Prednisolone

8.Conclusions 7.Treatment

4.Diagnosis

Clinical manifestation [5]

Pathology

Epilepsy

Pericyst inflammation, granuloma formation

Raised intracranial pressure

Hydrocephalus (arachnoiditis, ependymitis, ventricular cysts), pseudotumor (edema), giant cysts, cysticercal encephalitis

Focal deficits

Direct compression by large or multiple cysts

Meningitis

Widespreas subarachnoid inflammation

Myelo radiculopathy

Inlammation, local mass effect, vasculitis

Others Dementia

Multiple parenchymatous cysts

Encephalitis

Intense inflammation and edema

Subarachnoid haemorrhage

Inflammatory aneurysm

Trigeminal neuralgia

Arachnoiditis

Subdual hematoma

Collection of multiple cysts

Stroke/transient ischemia attack

Angiitis

Dizziness

Intermittent CSF obstruction

Endocrinological or ophthalmic symptoms

Sellar/intraocular cysts

1.Diagnostic criteria [3] Absolute criteria • Histologic demonstration of the parasite from biopsy of a brain or spinal cord lesion •Cystic lesions showing the scolex on CT or MRI •Direct visualization of subretinal parasites by funduscopic examination

Major criteria •Lesions highly suggestive of neurocysticercosis on neuroimaging studies •Positive serum EITB for the detection of anticysticercal antibodies •Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel •Spontaneous resolution of small single enhancing lesions

Minor criteria • Lesions compatible with neurocysticercosis on neuroimaging studies • Clinical manifestations suggestive of neurocysticercosis •Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens •Cysticercosis outside the CNS

Epidemiologic criteria •Evidence of a household contact with Taenia solium infection •Individuals coming from or living in an area where cysticercosis is endemic •History of frequent travel to disease-endemic areas

Basic protein

NK T cell

Chemotaxis

Mast cell

Mast cell

Macrophage

C3b

IL-4 IL-3 IL-5

Plasma cell

IgE

Mediators

Inflammation

C3b

C3a C5a

C3a C5a

C

C Eosinophil

Neutrophil

Platelets

PAF NCF

IL-4

ECF

(Th 1)

Th 2

Mediators

IFN-γ

Activation and differentiation of naive CD4 T cells in the presence of IL-4 into Th 2 cells.

Taenia solium cause the synthesis and secretion of IL-4 by NK T cells

Is a cestode that belongs to the Cyclophyllidea order and the Taeniidae family. Tree Stage: egg, larvae and adult tapeworm. Target tissues: CNS, eye, skeletal and heart muscles, subcutaneous tissues.

Brain parenchyma

Time p.i IL-2 IL-12 INF-γ TNF-α IL-5 Il-1,6,13 Il-4,10

2 days - - - ND - - -

3 days - - - ND - - -

5 days - - - ND - - -

1 wk - - - - - - -

3 wk - + - - - - -

5 wk - + + - + - -

8 wk - + + - - - -

11 wk + + - - - - -

13 wk + + - - - - -

Cytokines were detected in immunohistochemistry reaction.-, undetectable;+, 1-100 positive cells per section; ++, 100-300 positive cells; +++, 300-500 positive cells;++++, >500 positive cells. MHC class II expression=I-Ad.[4]

Possible causes of epilepsy:

Cytokines: IL-1β, IL-6 and TNFα

Permeability of blood–brain barrier

Gliosis

Neuronal death

ELISA results using HISTS14 antigen. In (A) serum sample from patients and in (B) CFS sample.[2]

Left: RMN showing one cyst. Right: TAC showing multiple parenchymal brain calcification.[5, 10]

2. Degrees of certainty for the diagnosis [3]

Definitive diagnosis

• Presence of one absolute criterion •Presence of two major plus one minor and one epidemiologic criterion Probable diagnosis

•Presence of one major plus two minor criteria •Presence of one major plus one minor and one epidemiologic criterion •Presence of three minor plus one epidemiologic criterion

Diagnostic criteria

Map illustrates the distribution of Neurocysticercosis.[1]

3.Introduction

1. Objective

Neuroinfections are important brain diseases and they affect a lot of people all over the world, but not all the people know about their existence. The aim of this work is to deepen in the pathological, biochemistry and clinical aspects of Neurocysticercosis, an helminthic disease that affects the central nervous system. It is caused by larvae of Taenia solium, who lives in the small intestine of humans.

2.Sources and methods

Sources Articles, books and scientific reviews about Neurocysticercosis. Methods •Search all the information. •Read general articles about the topic to get a general idea, and then more specifics articles. •Sum up all the important aspects of the pathology.

5.Immuno response 6.Clinical Manifestations

1.Adult Taenia solium in small intestine

2.Taenia solium eggs in human feces

3.Taenia solium eggs ingested by pork

4.Cysticerci in pork muscles

5.Infected pork meat ingested by humans

6.Larvae evagination in human stomach

9.Neurocysticercosis

8.Taenia solium eggs ingested by humans

7.Auto contamination Contaminated water Contaminated food

Body (proglottids) Neck Scolex

Subcutaneous tissues

CNS

Eyes

Muscles

Taenia solium

Places affected

Larvae

6. Annamaria Vezzani, Tiziana Granata. Brain inflammation in epilepsy: experimental and clinical evidence. Epilepsia. 2005;46(11):1724-43. 7. Hector H.Garcia et al. Current Consensus Guidelines for Treatment of Neurocysticercosis. Clin Microbiol Rev. 2002;15(4):747-56. 8. Pramod Kumar Mishare and Judy M Teale. Transcriptome analysis of the ependymal barrier during murine neurocysticercosis. J Neuroinflammation 2012;9:141. 9. Thomas J. Kindt. Kuby Immunology, sixth edition. W. H. Freeman, 2007 10.Eric T.Kimura-Hayama, et al. Neurocysticercosis: Radiologic-Pathologic Correlation. Radiographics. 2010;30(6):1705-19.