Cysticercosis diagnosis & management.pptx

1. Cysticercosis

2. T aenia solium , also known as the pork tapeworm, causes two different infections in children. CYSTS EGGS In its normal life cycle, children can acquire the tapeworm form by ingestion of undercooked pork containing the larval cysts In the intestines, the cyst converts into the tapeworm form. Children are also susceptible to infection by the eggs shed by tapeworm carriers.

3. Infection with the cystic form is termed cysticercosis , and involvement of the central nervous system (CNS) is termed Neurocysticercosis . The tapeworm form only develops after ingestion of undercooked pork. Ingestion of pork is not necessary to develop cysticercosis I ndividuals harboring an adult worm may infect themselves with the eggs by the fecal-oral route

4. PATHOLOGY Living, intact cystic stages usually suppress the host immune and inflammatory responses. Intact cysts can be associated with disease when they obstruct the flow of cerebrospinal fluid. Most cystsremain asymptomatic for a few years. Symptoms typically develop as the cysticerci begin to degenerate, associated with a host inflammatory response. The natural history of cysts is eventually to resolve by complete resorption or calcification, but this process may take years. Cysticerci can also present as subcutaneous nodules, ocular infection or spinal lesions with myelopathy or radiculopathy

5. CLINICAL MANIFESTATIONS Presenting findings in the vast majority of children with neurocysticercosis : Seizures Headache Less common manifestations include Hydrocephalus D iffuse cerebral edema Focal neurologic findings.

6. It is important to classify neurocysticercosis on the basis of anatomic location, clinical presentation, and radiologic appearance. T he prognosis and management vary with location Parenchymal Intraventricular Subarachnoid Spinal O cular

7. Parenchymal neurocysticercosis T ypically presents with seizures. The seizures are usually focal, but becomes generalize. Children may present with a single seizure or recurrent epilepsy. Mild neuro - cognitive defects have been documented from cysticerci alone but are more commonly associated with poorly controlled seizures. A fulminant encephalitis-like presentation may rarely occur after a massive initial infection associated with cerebral edema

8. Intraventricular neurocysticercosis U p to 20% of cases Associated with O bstructive hydrocephalus A cute, subacute , or intermittent signs of increased intracranial pressure, usually without localizin signs. Ocular neurocysticercosis D ecreased visual acuity because of cysticerci in the retina or vitreous R etinal detachment I ridocyclitis .

9. Subarachnoid neurocysticercosis Rare in children. It can be associated with Basilar arachnoiditis Can present with signs of Meningeal irritation Communicating hydrocephalus Cerebral infarction Spinal disease with radiculitis or transverse myelitis . Cysticerci in the tissues may present with focal findings from mass effect.

10. DIAGNOSIS S hould be suspected in a child W ith sudden onset of seizures or hydrocephalus History of residence in an endemic area Care provider from an endemic area. The most useful diagnostic study for parenchymal disease is MRI of the head. CT can also done to look for calcified lesions.

11. MRI P rovides the most information about C yst location C yst viability A ssociated inflammation. The scolex can appear as a 1-2 mm nodule attached to the cyst wall, and, when identified, is diagnostic for cysticercosis T1-weighted MRI demonstrating two parenchymal cysts with scolices .

12. The MRI also better detects Basilar arachnoiditis Intraventricular cysts Cysts in the spinal cord. T1-weighted MRI of cysticercal basilar arachnoiditis T1- weighted MRI showing a cyst below the fourth ventricle

13. T2-weighted MRI showing a cysticercus above the optic nerve

14. CT is best for identifying calcifications. A solitary parenchymal cyst, with or without contrast enhancement, or CNS calcifications are the most common findings in children Plain films may reveal calcifications in muscle or brain consistent with cysticercosis .

15. In children from endemic regions, the presentation which is highly specific for neurocysticercosis A single enhancing lesion that is round and <2 cm in diameter Absence of symptoms or signs of other diseases (e.g., no fever or lymph nodes) N o focal findings N o evidence of increased intracranial pressure

16. Serologic diagnosis using the enzyme-linked immunotransfer blot is available commercially in the United States but not in India . Serum antibody testing is highly specific but is frequently negative in children with single lesions or just calcifications. Antigen-detection assays and polymerase chain reaction assays show promise for diagnosis of ventricular and sub- arachnoid disease but not available commercially. Serological tests are not recommended for diagnosis and management of children with NCC. Routine screening of family members of children with NCC is not recommended

17. Differential Diagnosis Neurocysticercosis is often confused clinically with other seizure disorders. Clinical suspicion is based on Travel history H istory of contact with an individual who might carry an adult tapeworm Suggestive imaging studies. The imaging appearance can be confused Brain abscess G ranulomas (TB , fungal infections, LCH and toxoplasmosis) Tumors

18. TREATMENT The initial management of cysticercosis should focus on Symptomatic therapy for S eizures and/or Hydrocephalus Seizures can usually be controlled using standard antiepileptic drugs. If the lesions resolve, antiepileptic drugs can often be tapered and stopped. Indications for prolonged or lifelong antiepileptic therapy. Frequent seizures T he development of calcified lesions

19. The natural history of parenchymal lesions is to resolve spontaneously with or without antiparasitic drugs, but this process is often prolonged (months to years). Solitary parenchymal cysts resolve slightly more rapidly with antiparasitic therapy. Antiparasitic drugs also decrease the frequency of recurrent seizures. Other forms of the disease are less common in children. In adults with cystic lesion an overall 50% decrease in recurrence of generalized seizures with albendazole treatment. The benefit to children is significantly less, perhaps because most of these infections were with only one to two cysts.

20. The most commonly used antiparasitic A lbendazole DOSE : 15 mg/kg/day orally D ivided twice daily It should be taken with a fatty meal to improve absorption. The most common duration of therapy is 7 days for single parenchymal lesions. However, longer duration (months), higher doses (up to 30 mg/kg/day), or combination therapy with praziquantel is often required for Multiple lesions S ubarachnoid disease

21. 2 ND DRUG : Praziquantel DOSE : 50-100 mg/kg/ day DURATION : 28 days Used as an alternative to albendazole . First-pass metabolism is common with corticosteroids or antiepileptic drugs. Cimetidine can be used in conjunction with praziquantel to blunt the first- pass metabolism

22. CORTICOSTEROIDS A worsening of symptoms can follow the use of either drug based on the host’s inflammatory response to the dying parasite. Patients should be medicated with Parental : Prednisone 1-2 mg/kg/day or O ral : Dexamethasone 0.15 mg/kg/day B eginning before the first dose of antiparasitic drugs Continuing for at least 2 weeks Corticosteroids likely also decrease seizure frequency

23. I mproved resolution with combination therapy with Corticosteroids : Dexona or Prednisolone Albendazole : 15 mg/kg/day orally divided twice daily P raziquantel (50 mg/kg/day PO divided three times daily for 14 days)

24. Antihelminthics are not recommended in more than five viable cysts and/or cysticercal encephalitis [“starry-sky” appearance in contrast-enhanced computed tomography (CECT)/ MRI brain], to avoid worsening of perilesional edema leading to raised intracranial pressure. Intravenous steroids are the mainstay of therapy in children with cysticercal encephalitis. There is no role of routine prophylaxis with antiseizure medications (ASMs) in children with NCC who do not present with seizures

25. Most patients with hydrocephalus require neurosurgical interventions. Some cases require emergent placement of a ventriculostomy . But most can be managed by cystectomy alone. For obstructive hydrocephalus caused by ventricular cysticercosis , many patients can be cured by minimally invasive surgery. Neuroendoscopy is the preferred approach to cysticerci in the lateral or third ventricle. Cysticerci in the fourth ventricle can be removed by a suboccipital craniotomy.

26. Adherent cysticerci that cannot be removed can be treated by placement of a ventriculoperitoneal shunt (VPS). However, there is a high rate of shunt failure, which can be minimized somewhat by treatment with antiparasitic drugs plus corticosteroids.

27. Subarachnoid disease has a poor prognosis. The prognosis is much improved by aggressive therapy, including antiparasitic drugs, antiinflammatory treatment, and neurosurgical procedures for hydrocephalus(e.g., VPS placement). However, the duration of antiparasitic and antiinflammatory therapy often needs to be prolonged. Methotrexate can be used as a steroid-sparing agent in patients requiring prolonged anti-inflammatory therapy. Ocular cysticercosis is usually treated surgically, although there are reports of cure using medical therapy alone.

28. Follow up Repeat CECT/CE-MRI should be done after 6 months of the first scan. If follow-up scan is suggestive of resolution of lesion, then ASMs can be tapered and stopped. If the lesion is calcified, then continue ASMs for 2 years seizure-free interval. If there is the persistence of lesion, then retreatment with albendazole or a combination of albendazole and praziquantel can be used.

29. PREVENTION In areas with evolved public health systems, cysticercosis can largely be eliminated by Meat inspection Condemnation of infected meat Thorough cooking of pork Improved sanitation. This approach has not worked in countries where most meat is butchered informally.

30. Decrease or elimination of transmission Mass chemotherapy for tapeworm carriers Mass treatment of pigs Improved personal hygiene Screening family members and those preparing food for index cases for cysticercosis has a very low yield, in part because of the poor sensitivity of current tests. Those who have noted passing material consistent with taeniasis should be treated with praziquantel regardless of the results of stool studies. Veterinary vaccines for several cestode infections have a high degree of efficacy and have a potential role in decreasing parasite transmission