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 19th 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 20th century.
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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.
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4. MODE OF
TRANSMISSION
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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.
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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
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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
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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
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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
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