A brief discussion on Cysticercosis and how the affect the human body.

Slides on Cysticercosis
Gives more insight on how the disease occurs it’s treatment and prevention

1. UNIVERSITY OF CAPE COAST COLLEGE OF HEALTH AND ALLIED SCIENCES SCHOOL OF MEDICAL SCIENCES ( PHYSICIAN ASSISTANT STUDIES ) COMMUNITY AND PUBLIC HEALTH PRESENTATION PHA 227 NEGLECTED TROPICAL DISEASES & EMERGING DISEASES CYSTICERCOSIS GROUP THREE AH/PAS/22/0071 AH/PAS/22/0104 AH/PAS/22/0110 AH/PAS/22/0009 AH/PAS/22/0092 AH/PAS/22/0044 OUTLINE INTRODUCTION EPIDEMIOLOGY PATHOPHYSIOLOGY CLI. MANIFESTATIONS MODE OF TRANSMISSION LAB. INVESTIGATIONS DIAGNOSIS TREATMENT PREVENTION & CONTROL

2. INTRODUCTION Cysticercosis is parasitic tissue infection. Disease infects skeletal muscles, subcutaneous tissues, eyes, central nervous system (CNS) and other tissues. Results from ingestion of Taenia solium eggs (pork tapeworm). Clinical syndromes caused by T solium are categorized as either cysticercosis (tissue) or taeniasis (intestine). Neurocysticercosis – CNS infection with T solium. Commonest type of cysticercosis. Division of Neurocysticercosis- Parenchymal & extra parenchymal diseases. The first case of cysticercosis was in 1558 in an epileptic patient by Rumler . He associated this new finding to be a type of epilepsy. Further research and investigations by German pathologists during the 19 th century led to the discovery of cysticercosis which was then related to Rumler’s finding in the epileptic patient. The disease was suspected to be endemic but became non-endemic in the 20 th century. 2

3. EPIDEMIOLOGY Estimated 50-100 million people are infected with cysticercosis worldwide. WHO estimates suggests 2.56-8.30 million cases of neurocysticercosis globally since its discovery. Areas of endemic disease includes Central & South America, India, China, Southeast Asia & Sub-Saharan Africa. Neurocysticercosis is the most frequent preventable cause of epilepsy worldwide-30%. In 2015, WHO Foodborne Disease Burden Epidemiology Reference Group identified T solium as a leading cause of death from foodborne diseases- 2.8 million disability-adjusted life-years. Patients with cysticercosis are typically aged 10-40 years. Most patients with parenchymal cysticercosis either remain asymptomatic or develop a self-limited seizure disorder. 3

4. MODE OF TRANSMISSION 4

5. PATHOPHYSIOLOGY When humans ingest undercooked pork containing cysticerci of T solium, the scolex . The scolex, evaginates from cyst and develops into an intestinal tapeworm (taeniasis). When pigs ingest the eggs, the eggs hatch, penetrate the pigs’ intestinal wall and spread to the skeletal muscles. The eggs (larvae) mature into encysted cysticerci over 2-3 months . The cysticerci suppress the host inflammatory response and survive in tissues for months. The life cycle is completed when humans ingest inadequately cooked pork that contains viable cysticerci . Humans are accidental hosts of the larvae stage and develop cysticercosis similar to that in pigs. Cysticercosis is a foodborne infection and can be acquired in the absence of pork consumption. 5

6. CLINICAL MANIFESTATIONS Symptoms vary depending on location & type of cysticerci. Neurocysticercosis seizures intracranial hypertension & headache focal neurological signs stroke hydrocephalus Ophthalmic cysticercosis blurred vision retinitis vision loss Subcutaneous cysticercosis lumps 6

7. LABORATORY INVESTIGATIONS Serologic studies can be helpful in the diagnosis of cysticercosis but are limited in their usefulness in a community setting by general lack of availability. An enzyme linked immunoblot transfer assay (ELISA) can demonstrate serum or CSF anti-cysticercosis antibodies. Highly specific for exposure of T solium - 94% in extra-parenchymal infection & 28% in parenchymal infection. Polymerase chain reaction (PCR) tests can detect the DNA of T solium in clinical samples. No tests are available till date. Imaging scans- computed tomography (CT) scan & magnetic resonance imaging (MRI) Radiological studies - X-rays & ultrasound for detection of cysts in soft tissues & organs 7

8. DIAGNOSIS Diagnosis of cysticercosis is often based on clinical presentation, abnormal findings on neuroimaging and serology . Occasionally more invasive procedures are required (brain biopsy). Differential diagnoses Brain Abscess Parasitic lesions Tuberculoma Tumors vasculitis 8

9. TREATMENT, PREVENTION & CONTROL Treatment For asymptomatic patients- diagnosis before treatment For ocular cysticercosis patients- treatment with albendazole & corticosteroids or surgery For subcutaneous cysticercosis patients- treatment with anti-inflammatory drugs or cysticerci excision For neurocysticercosis patients- treatment with antiepileptic drugs, anti-inflammatory drugs & shunt surgery for hydrocephalus. Anti-parasitic drugs are important but should never be considered emergently. Prevention & control Personal hygiene Food hygiene especially meat (pork) Proper preparation of meat, vegetables & fruits Serologic screening 9

10. REFERNCES Trevian C., Sotiraki S., laranjo-Gonzalez M., Dermauw V., et al. (2018). Epidemiology of Taeniasis/cysticercosis in Europe, a systemic review: parasite vectors, 11(1), 569. Carpio, A., Escobar, A., & Hauser, W. A. (1998). Cysticercosis and epilepsy: a critical review: Epilepsia, 39 (10), 1025- 1040. Wallin M.T., Kurtzke J.F. (2004). Neurocysticercosis in the UK: review of an important emerging infection, Neurology , 1559-64. THANK YOU 10