Published Date: 2003-10-05 23:50:00
Subject: PRO/AH> Cysticercosis - India (02)
Archive Number: 20031005.2501
CYSTICERCOSIS - INDIA (02)
A ProMEDmail post
ProMEDmail is a program of the
International Society for Infectious Diseases
Date: Fri, 3 Oct 2003
From: Dr Subhash Chandra Parija <email@example.com>
Comment on cysticercosis in India
Intestinal taeniasis and cysticercosis are the 2 distinct clinical entities
caused by the adult worm and cyst of _Taenia solium_, respectively.
Intestinal taeniasis is a mild intestinal infection but is potentially
serious because of the possibility that cysticercosis will develop in the
same infected host. Man acquires _T.solium_ infection orally by ingestion
of undercooked or improperly cooked infected pork. The cyst (_Cysticercus
cellulosae_) is the infective stage of intestinal taeniasis; raw or
undercooked pork infected with the cyst is the source of infection.
In contrast, cysticercosis is potentially a dangerous systemic disease with
variable clinical manifestations, depending on the sites in which
cysticerci are found. The egg is the infective stage for cysticercosis, and
human feces are the chief source of infection. Man acquires cysticercosis
by: 1) ingestion of food, vegetables, or water contaminated by the eggs
present in the infectious feces of a _Taenia_ carrier; 2) anus-hand-mouth
transfer of the eggs by contaminated hands of persons with poor personal
hygiene (endogenous autoinfection); or 3) reverse peristalsis in which eggs
produced by _T.solium_ are thrown back to the duodenum, where they hatch
and cause tissue infection (autoinfection).
Cysticercosis is increasingly reported from different parts of India. In
India, the first 2 [modes of transmission] are [probably] the major factors
responsible for transmission of cysticercosis.
In cysticercosis, the cysticerci are found most often in subcutaneous and
intermuscular tissues, followed by the eye and then the brain. The
incubation period is variable; symptoms may appear 15 days to even many
years after the infection.
Cysticercosis in humans can be of the following types:
- Muscular and subcutaneous cysticercosis: Any muscle mass may be involved
in the condition. Most patients are asymptomatic. Symptomatic cases present
as acute myositis [muscle inflammation]. Cysticerci in muscles often are
associated with neurocysticercosis. Subcutaneous nodules are mostly
- Ocular cysticercosis: Cysticerci are present in an eye in about 20 percent
of cases. Most cysts are found in the vitreous, subretinal space, and
conjunctiva. The condition may present as iritis, uveitis, and palpebral
[eyelid] conjunctivitis. The cysts in subconjunctival or subretinal sites may
present as slowly growing nodules, [presenting the possibility of confusion]
with tumors. Occasionally, subretinal eye cysts may lead to blindness due to
detachment of the retina. Fundoscopic examination may show free-floating
cysticerci in the anterior chamber and vitreous chamber. This helps in the
visual identification of the movements and morphology of larval forms. Larvae
may be found attached to subretinal tissues.
- Neurocysticercosis (NCC): This is the most serious form of cysticercosis.
The condition is seen in 60-90 percent of cases of cysticercosis. NCC is a
common cause of neurological disease in India. It is one of the common
causes of epilepsy in children. It is second only to tuberculosis as the most
common important space-occupying lesion of the brain.
The clinical manifestations in the CNS are highly variable and depend on the:
1) Number, location and viability of cysts(s);
2) Stage of development of the cyst -- whether young and mature or intact
and degenerated; and
3) Host response against the cyst.
NCC is of two types: parenchymal and extraparenchymal disease. Parenchymal
disease is caused by infection of the brain parenchyma with cysticerci.
This is the most common form of NCC. Extraparenchymal disease is caused by
location of cysts in the cerebrospinal fluid (CSF) of the ventricles,
cisterns, and subarachnoid space or in the spinal cord. Commonly, 1 to 5
cysts are found, but in some patients as many as 200 cysts have been reported.
Convulsions and/or seizures, intracranial hypertension, and psychiatric
disturbances are the 3 important manifestations of the NCC .These may occur
separately or in combination. Onset can be insidious or abrupt. Convulsions
and/or seizures are caused by the presence of cysticerci in the brain
parenchyma. Seizures are the most common clinical manifestations and occur in
70-90 percent of cases. Seizures in children are focal with acute onset.
In endemic areas, cysticercosis is the most common cause of epilepsy.
Meningeal cysts may manifest as meningitis. The cysts of intramedullary
spinal cord cysts can produce motor or sensory disorders. Intracranial
hypertension is caused by obstruction of CSF by the cysts, which are found
in the ventricles of the brain. Headache, nausea, vomiting, vertigo, and
altered mental status are the presenting symptoms. Intracranial herniations,
stroke, and status epilepticus are the most important complications of
The prognosis of neurocysticercosis is highly variable .Nearly 10 percent
of patients with cerebral lesions die within 5 years to 10 years of
[developing the] illness.
The specific diagnosis of intestinal taeniasis is made by demonstration of
gravid proglottids of _T.solium_ passed in the feces. Eggs of _T. solium_
and _T. saginata_ are morphologically indistinguishable.
A wide variety of serological tests are available to detect anti-cysticercus
antibodies in serum or CSF. The 2 most commonly used tests are enzyme-linked
immunosorbent assay (ELISA) and enzyme-linked immunoelectrotransfer blot
(EITB). These tests are used for diagnosis of cases of NCC and for the
epidemiological study of cysticercosis.
ELISA is a useful method for demonstration of antibodies in the serum as well
as in the CSF, but detection of antibodies in CSF provides better
reliability. The test has a low sensitivity (75 percent) and specificity
(85 percent). It shows false positive reactions with sera from other
helminthic infections. ELISA is useful to diagnose NCC patients with few
CNS lesions and relatively mild disease.
EITB assay using a purified fraction of glycoprotein (Gp) is highly
specific (100 percent) for detection of antibodies both in the serum and
CSF. The presence of 1-7 specific glycoprotein (Gp) bands is considered
diagnostic of _T.solium_ infection. The test is more than 90 percent
sensitive in NCC patients with more than 2 cysticerci in the brain;
sensitivity declines to 50-70 percent with a single cysticercus. The assay,
therefore, is of limited value in children, because most of them in India
have a single lesion. A serum immunoblot assay is more sensitive than the
test using CSF.
Antibody detection in cysticercosis has 2 important disadvantages: Firstly,
it may indicate only exposure to infection. It does not indicate whether
the patient has established and viable recent infection. Secondly,
antibody titres continue to persist in the serum even after the parasite
has been eliminated through the immune mechanism and/or following drug
therapy. Detection of antigen in serum or CSF indicates recent or viable
infection. Antigen can be detected in the serum or CSF by ELISA using
specific monoclonal antibodies. These antigen detection tests are highly
sensitive and specific.
Imaging methods supplement the diagnosis of NCC. These include traditional
x-ray and newer imaging methods such as computed tomography (CT) and
magnetic resonance imaging (MRI). Plain x-ray of the soft tissues in arms,
thigh, chest, and neck may show dead calcified oval or elongated cysts. A
central calcified scolex surrounded by a calcified cyst wall is
pathognomonic. X-ray of the skull may demonstrate cerebral calcification
and reveal intracranial lesions [produced by] neurocysticercosis.
CT and MRI are the main imaging methods used now for the diagnosis of
neurocysticercosis. They help to i) identify the cysticerci, and ii)
demonstrate the number, site, and stage of the cysticerci present in the
brain. CT is the best method for detecting dead, calcified, and multiple
cysts. The dead worms are visible as round hypodensities, often with the
protoscolex [mouth] of the parasite appearing as an eccentric dot of calcium.
CT is superior to MRI in the detection of intracerebral calcification. A
central calcified scolex surrounded by a calcified cyst is pathognomonic of
neurocysticercosis. A CT scan with contrast shows a ring-enhancing image
(signifying edema) surrounding an involuting living cysticercus.
MRI is superior to a CT for demonstration of a) non-calcified cysts; b)
cysts in the brain parenchyma, particularly near base of the brain; and c)
cysts in extraparenchymal sites (intraventricular and cisternal cysts). MRI
shows a mural nodule within the cyst, which is pathognomonic for NCC.
Praziquantel and niclosamide, as given for _T.saginata_ taeniasis, also are
effective for the treatment of intestinal taeniasis caused by _T.solium_.
Asymptomatic neurocysticercosis requires no treatment. Treatment for
symptomatic NCC is chemotherapy by albendazole or praziquantel -- the latter
is the drug of choice. The drug is given in an oral dose of 50 mg/kg body
weight in 3 divided doses for 15 days. Praziquantel is usually given along
with corticosteroids to reduce the inflammatory reactions caused by the dead
Surgery is indicated for cysticercosis of ocular, ventricular, and spinal
cord, because treatment with anthelminthic drugs can provoke irreversible
Measures to prevent and control _T.solium _ intestinal taeniasis include:
1) Avoidance of eating raw or insufficiently cooked pork
2) Inspection of pork for the cysticerci
3) Implementation of sanitation facilities, and
4) Treatment of infected persons.
Cysticercosis can be prevented by:
1) Avoidance of food (e.g., raw vegetables grown in field fertilised with
human feces) contaminated with eggs of _T.solium_
2) Treatment of infected persons, and
3) Improvement of personal hygiene.
The latter 2 measures prevent intestinal auto-infection, and are important
in the strategy to control the infection in India.
Dr Subhash Chandra Parija
Professor and Head
Department of Medical Microbiology
Jawaharlal Institute of Postgraduate Medical Education & Research
[ProMED thanks Professor Parija for his description of the basic biology of
infection with _Taenia solium_. The first posting (29 Sep 2003, referenced
below) on the subject indicated a large increase in cases of epilepsy due
to cysticercosis in India, and we would be very grateful if someone could
present data on the incidence of cysticercosis, especially the incidence of
neurocysticercosis. An increase in neurocysticercosis could, as mentioned
above, be due to the increased used of human fecal material as fertilizer for
vegetables, and any information on such use in Northern India would be
appreciated. - Mod.EP]