eMedicine Specialties > Emergency Medicine > Infectious Diseases

Cysticercosis: Treatment & Medication

Author: Ryan Tenzer, MD, FAAEM, Clinical Assistant Professor of Emergency Medicine, Penn State College of Medicine; Consulting Staff, Department of Emergency Medicine, Lehigh Valley Hospital
Coauthor(s): Howard A Blumstein, MD, FAAEM, Assistant Professor, Surgery; Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine
Contributor Information and Disclosures

Updated: Apr 28, 2009

Treatment

Prehospital Care

Patients present with seizure activity, altered mental status, headache, or other neurologic complaints. Prehospital treatment involves standard supportive care including ensuring that adequate airway support, oxygenation, ventilation, and perfusion are maintained. Administration of anticonvulsants may be necessary for prolonged or repeated seizure activity. Empiric naloxone may be given for coma. Hypoglycemia should be corrected.

Emergency Department Care

  • Secure airway, oxygenation, circulation, adequate glucose delivery, and proper monitoring. 
  • Administer supportive care for those presenting with seizure activity.
  • Correct metabolic abnormalities.
  • Anticonvulsants are reliably effective in controlling seizures secondary to cysticercosis. Most patients will respond to first-line agents.
  • Steroids, osmotic agents, and/or diuretics are indicated with evidence of increased ICP.
  • Analgesics may be administered for pain control.
  • Initiate diagnostic procedures, including blood work and imaging.
  • Consult appropriate specialists.

Consultations

  • Consultations may include neurosurgery, neurology, infectious diseases, and ophthalmology. Neurosurgical procedures are frequently required to relieve intracranial pressure. Biopsy or surgical removal of lesions may be necessary.

Medication

Antihelminthic agents are the mainstay of definitive treatment. Controversy exists as to whether antiparasitic treatment of cysticercosis is necessary in most cases. Some authors claim that patients do well without antiparasitic therapy since symptomatology is produced by pericystic inflammation, which portends imminent involution of the parasite. This suggests that the presence of clinical symptoms is predictive of a subsequent self-limited disease course.

In addition, the calcific lesions of "inactive" disease may not be clinically silent but rather epileptogenic and can thereby confer significant morbidity. A randomized controlled study of 300 patients with neurocysticercosis over several years found that those treated with a course of albendazole plus corticosteroids and anticonvulsants developed significantly more lesional calcification on follow-up imaging than those treated with anticonvulsants alone.4 During the first year, this treatment group also had a significantly higher incidence of seizures and thereafter displayed a trend toward such. These investigators concluded that antihelminthic treatment may result in more long-term seizure activity since complete resolution of lesions may be more likely when cysts are allowed to spontaneously resolve. They therefore recommend treatment with anticonvulsants alone, with careful clinical and radiologic follow up.

Despite lively controversy surrounding the matter, a preponderance of the literature positively supports treatment with antihelminthics.5,6 Several randomized controlled trials have demonstrated benefit of antihelminthic therapy, particularly in reducing the number of active cysts. Benefit seems to be greatest during the first weeks of therapy. As mentioned previously, treatment with antihelminthic medication will initially worsen clinical symptoms as faltering parasite defenses lead to increasing perilesional inflammation. Therefore, in nearly all trials, antiparasitic medication has been combined with steroid therapy. In addition, patients are usually maintained on concomitant anticonvulsant therapy for an indefinite period of time.

Caution is particularly warranted in patients with significant pretreatment encephalitis, hydrocephalus, or vasculitis, since treatment may cause increasing inflammation as cysts involute, leading to worsening clinical states. CSF shunting may be indicated before medical treatment begins since intracranial hypertension may worsen upon administration of antiparasitics.   

Anthelmintics

Parasite biochemical pathways differ sufficiently from those of the human host so as to allow selective interference by chemotherapeutic agents in relatively small doses. Many patients may require more than one course of treatment to entirely eliminate active cysts.

The more effective agent, albendazole, has upstaged praziquantel as the traditional therapeutic agent. Subarachnoid and intraventricular neurocysticercosis (NCC) may be relatively more resistant to treatment. In these cases, repeat courses of medication are usually needed, and there is limited evidence that higher-dose albendazole treatment (30 mg/kg/d) may be beneficial.7


Praziquantel (Biltricide)

Increases cell membrane permeability in susceptible worms, resulting in a loss of intracellular calcium, massive contractions, and paralysis of their musculature. In addition, produces vacuolization and disintegration of the schistosome tegument. This is followed by attachment of phagocytes to the parasite and death.

Adult

50 mg/kg/d PO divided tid for 2 wk

Pediatric

<4 years: Not established
>4 years: Administer as in adults

Hydantoins may reduce serum praziquantel concentrations, possibly leading to treatment failure

Documented hypersensitivity; ocular cysticercosis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Destruction of parasite within eyes can cause irreparable lesions (ocular cysticercosis should not be treated with praziquantel); caution while driving or performing other tasks requiring alertness on the day of and following treatment; minimal increases in liver enzymes reported; when schistosomiasis or fluke infection associated with cerebral cysticercosis, hospitalize patient for duration of treatment


Albendazole (Albenza)

Broad-spectrum anthelmintic that decreases ATP production by the worm causing energy depletion, immobilization, and finally, death.

Adult

15 mg/kg/d PO divided bid/tid for 2 wk

Pediatric

10 mg/kg PO qid

Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity

Documented hypersensitivity; ocular cysticercosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue use if LFTs increase significantly (resume when levels decrease to pretest values)

Corticosteroids

A temporary increase in pericystic inflammation often is observed during treatment of NCC, as the dying parasite no longer can escape host defenses. For this reason, it is often recommended that corticosteroids be administered in combination with, or instead of, antihelminthics. This practice is controversial and should be tailored to the individual patient according to the number and location of cysticerci. Steroids are more likely indicated in cases involving extraparenchymal cysts.


Prednisone (Orasone, Meticorten, Deltasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Adult

1 mg/kg/d PO

Pediatric

Not established

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use


Dexamethasone (Decadron, Dexone)

For various allergic and inflammatory diseases. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Adult

4-6 mg IV q4-6h

Pediatric

Not established

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization

Documented hypersensitivity; active bacterial or fungal infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use

Anticonvulsants

Anticonvulsant therapy should proceed as in other epileptiform states. Benzodiazepines are first-line agents for active prolonged or repeated seizures. They should generally be followed by a more definitive anticonvulsant such as phenytoin. Barbiturates may be needed in more refractory cases.


Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Important to monitor blood pressure after administering dose. Adjust as necessary.

Adult

0.05-0.15 mg/kg IV

Pediatric

Not established

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson's disease


Phenytoin (Dilantin)

May act in motor cortex, where it may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited. Dose to be administered should be individualized. Administer larger dose before retiring if dose cannot be divided equally.

Adult

18 mg/kg IV loading dose followed by 100-150 mg/dose at 30-min intervals; not to exceed 1500 mg/24 h

Pediatric

Not established

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, valproic acid

Documented hypersensitivity; sinoatrial block, second- and third-degree AV block, sinus bradycardia, or Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugar level); discontinue use if hepatic dysfunction occurs


Phenobarbital (Solfoton, Luminal, Barbita)

Elevates seizure threshold, limits the spread of seizure activity, sedative.

Adult

10-30 mg/kg IV loading dose followed by 5 mg/kg/dose q15-30min; not to exceed 40 mg/kg

Pediatric

Not established

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritic patients

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia since adverse reactions can occur; caution in myasthenia gravis and myxedema

More on Cysticercosis

Overview: Cysticercosis
Differential Diagnoses & Workup: Cysticercosis
Treatment & Medication: Cysticercosis
Follow-up: Cysticercosis
Multimedia: Cysticercosis
References

References

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Further Reading

Keywords

cysticercosis, undercooked pork, tapeworm, pork tapeworm, tapeworm treatment, tapeworm symptoms, tapeworm causes, neurocysticercosis, NCC, larval cysts, Taenia solium infestation, T solium, cysticerci

Contributor Information and Disclosures

Author

Ryan Tenzer, MD, FAAEM, Clinical Assistant Professor of Emergency Medicine, Penn State College of Medicine; Consulting Staff, Department of Emergency Medicine, Lehigh Valley Hospital
Ryan Tenzer, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Howard A Blumstein, MD, FAAEM, Assistant Professor, Surgery; Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine
Howard A Blumstein, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Barry J Sheridan, DO, Chief, Department of Emergency Medical Services, Brooke Army Medical Center
Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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