NEUROCYSTICERCOSIS:ETIOLOGY AND PATHOGENESIS

Cysticercosis is a disease caused by cysticerci, the larval (metacertode) stage of human tapeworm Taenia solium or Taenia Saginata in subcutaneous, muscle or central nervous system tissues. Cysticercosis is a public health problem in many tropical and developing countries where swine, the intermediate host, are raised in non hygienic conditions. Swine becomes infected by ingesting eggs or proglottids containing eggs from human feaces. The larvae are released from the eggs, penetrate the intestinal mucosa, and encyst in muscles, resulting in cysticercosis. The cysticercus, or larval stage, then may be transmitted to human beings who ingested undercooked, infected pork. People also may become infected by ingesting food contaminated with human feaces. The eggs and larval mature into tapeworm, T. Solium in the intestine (taeniasis) or larvae may be distributed hematogenously invading a wide variety of tissues (human cysticercosis). Eventually, people are accidental intermediate hosts.
                                                     CLINICAL SIGNS
In humans, cysticerci have an apparent affinity for the brain. Larval cysts have been found in the leptomeninges, ventricle, cerebrum and cerebellum. The cysts not only cause compression & congestion of surrounding brain tissue, but also may induce a marked inflammatory response. In human beings & dogs, seizures, locomotory imbalances, dementia, focal neurologic deficits, & death caused by acute intracranial hypertension have been reported, as have histopathologic changes such as meningitis and basal arachnoids. Clinical signs in dog, and inability to maintain balance, were most likely result of parasitic compression within the brain stem. In general, brain stem lesions may result in central vestibular signs such as vertical or positional nystagmus, head tilt, falling and rolling, loss of balance, and deficits in cranial nerves V, VI and VII and possible mental depression and hemiparesis. Neurologic signs tend to be ipsilateral to the lesion. In the dog, the cysts of the left occipital lobe do not contribute to the signs of ataxia.
                                                       DIAGNOSIS
Antemortem diagnosis of cysticercosis in dogs has not been reported. Cysticercosis in dogs has been diagnosed via postmortem examination. Diagnosis of cysticercosis in human beings is made on the basis of clinical findings, result of computerized tomography (CT), Magnetic resonance imaging (MRI), serological testing and biopsy or autopsy findings. The preferred serologic test for human beings is an enzyme Linked immune electro transfer blot assay. Imaging techniques including CT and MRI, are used extensively for diagnosis and evaluation of cysticercosis in human beings. These techniques allow for identification and localization of cysts; And also inflammation, oedema and mineralization associated with cysticercosis.
                                                       TREATMENT
Recent recommended treatment of human cysticercosis includes Praziquantel or albendazole in conjunction with corticosteroids. A severe localized inflammatory response often accompanies the degeneration and death of the cysticercus; which is enhanced by treatment with Praziquantel or albendazole. Although somewhat controversial, many people believe corticosteroids are indicated to suppress the inflammatory response and minimize subsequent adverse reactions to the parasitic death. Praziquantel and albendazole have resulted in marked improvement of resolution of clinical signs, with disappearance of the lesions on subsequent CT and or MRI studies in human beings.