’PORK IS HEALTHY’’ BUT BE AWARE OF HUMAN NEUROCYSTICERCOSIS (NCC)-A MAJOR PUBLIC HEALTH PROBLEM IN INDIA
Compiled, & shared by-DR. RAJESH KUMAR SINGH, (LIVESTOCK & POULTRY CONSULTANT), JAMSHEDPUR Post no 1330 Dt 22/07//2019
JHARKHAND,INDIA 9431309542, rajeshsinghvet@gmail.com &
DR AVINASH KUMAR, MD, TATA MAIN HOSPITAL, JAMSHEDPUR
Introduction
Cysticercosis is a global public-health problem, especially so in developing countries including India. It is considered as a “biological marker” of social and economic development. NCC is the most common parasitic infection of the CNS and identified as the most important cause of acquired active epilepsy. However, few recent studies using CT and MRI reveal that NCC is alarmingly high in India especially among the communities w‘ith low socioecomic status with treatment gap of more than 90%. Since cysticercosis is a preventable and eradicable disease, appropriate measures like health education, mass awareness, better medical facilities, mass treatment of T. solium carriers, and restriction on sale of measly pork may help to reduce the disease burden in the endemic areas.
Cysticercosis caused by larval stage of the tapeworm Taenia solium, is a major public health problem, especially in the developing world. Human and pig both acquire cysticercosis through ingestion of eggs excreted in faeces by human T. solium carrier. Cysticercosis is common in communities where pigs are allowed to roam freely, the residents consume undercooked pork and the basic sanitary facilities are lacking
Neurocysticercosis (NCC) is a common cause of seizures and neurologic disease. Although there may be variable presentations depending on the stage and location of cysts in the nervous system, most children (> 80%) present with seizures particularly partial seizures.
Historical perspective
Cysticercosis was first described in pigs by Aristophanes and Aristotle in 3rd century BC. Latter it was noticed in human by Parunoli in 1550. Cysticercosis has also been described in ancient Indian medical book, the Charak Sanhita. NCC was fi rst reported in a coolie from Madras, who died due to seizure and was found to be infected with cyst on autopsy (Armstrong 1888). In 1912, Krishnaswamy (1912) reported cysticerci related case of muscle pains and subcuataneous nodules with abundant cysticerci in the muscles, heart and brain at autopsy. In 1934, high rate of new onset epilepsy related to cysticercosis in the British army deployed in India was noticed
Epidemiology
Cysticercosis has been designated as a “biological marker” of the social and economic development of a community (Carpio et al 1998; Sarti et al 1994). NCC is the single most common cause of seizures/epilepsy in the developing countries (Garcia et al 2003). It is diffi cult to exactly estimate the disease burden of NCC in a community study because (i) of polymorphic presentation of the disease as some patients suffer only one or two seizure(s) in the entire course of their illness while others get recurrent seizures, (ii) in some patients it remains silent throughout its infection (Fleury et al 2003) and (iii) some of the lesions might have disappeared or dissolved. Apart from these clinical features, social stigma associated with epilepsy prohibits the patients or their family member to come openly for medical assistance. On the other hand, some patients with other disorders (like patients with syncope, migraine with aura, somatoform disorders, transient ischemic attack, focal stroke, etc.) may present an acute event of seizure-likesymptoms. NCC is endemic in most developing countries of Asia, Latin America, Central and South Africa (Powell et al 1986). It is also being increasingly reported in the developed countries due to migration of persons with disease or T. solium carriers. Overall NCC is identifi ed as the cause of active epilepsy in 26.3% to 53.8% in the developing world including Latin America (Del Brutto et al 2005; Montano et al 2005; Nicoletti et al 2005). The disease accounts for up to 2% of neurological and neurosurgical admissions in Southern California and more than 1000 cases per year in USA (Schantz et al 1996). Racemose/giant cysticerci, usually uncommon in immunocompetent hosts, had been reported in patients with acquired immunodefi ciency syndrome (AIDS) (Delobel et al 2004). T. crassiceps cysticercosis, usually a rodent disease had also been reported in patients with AIDS (Francois et al 1998, Garg and Kar 2002). Cysticercosis is widespread among swine in Mexico and developing countries of Latin America
Disease burden in India
All the biological markers for transmission of T. solium taeniasis and cysticercosis exist in India. It is likely that the disease is under reported in India because due attention has not been given to this neglected disease and systematic population-based studies are lacking. There are great disparities within the country in geography, ethnicity,religion rituals, income, food habits, personal hygiene, level of education and standards of living, which are likely to infl uence the disease burden. Consequently there are wide variations in the frequency of cysticercosis in India (fi gure 1). There are only few reports from the State of Kerala, where the level of education and standards of hygiene are high, and from Jammu and Kashmir, a Muslim majority State due to prohibition of pork consumption by religion. Before the era of CT scan and magnetic resonance imaging (MRI), National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore reported diagnosis of NCC in 2% of an unselected series of epileptics (Mani et al 1974). At a tertiary referral centre in New Delhi, NCC constituted 2.5% of all intracranial space occupying lesions (Wani et al 1981). With the availability of CT and MRI, the proportion of NCC in seizure disorders dramatically increased. Sawhney et al (1996) reported cerebral cysticercosis in 31% of patients in whom CT was done. In a community survey of 50,617 individuals from South India, the prevalence of active epilepsy was 3.83 per 1000 and NCC was detected in 28.4% of them by CT (Rajshekhar et al 2006). Cysticercosis appears to be more prevalent in the northern States Bihar, Uttar Pradesh through Punjab. In a recent study based on 30 cluster sampling approach suggested by WHO in the rural pig farming community of Mohanlalganj block, Lucknow district, Uttar Pradesh, the prevalence of taeniasis was 18.6%; factors associated with taeniasis were age above 15 years, history of passage of Taenia segment in stool, undercooked pork consumption and poor hand hygiene (Prasad et al 2007). In the same community active epilepsy was identifi ed and clinically confi rmed in 5.8% of the populations during door to door survey and 48.3% of them fulfi lled either defi nitive or probable diagnostic criteria of NCC. Epilepsy in the family and no separate place for pig were identifi ed as risk factors for NCC clustering (Prasad et al 2008b). The single cyst infection (range 47.7% to 53.4%), is the most common in Indian subcontinent (Prasad et al 2008a; Prabhakaran et al 2007). In a study of 156 histologically proven cases of cysticercosis from Patiala, Punjab, 88% patients presented with solitary lesion and the most frequent site being the upper arm, chest wall, eye, abdomen wall and neck (Saigal et al 1984). In a seroprevalence study in and around Chandigarh, anti-cysticercus antibodies was found to be 17.3% with highest prevalence (24%) reported from slum areas; however only 8% of the sero-postives had previous history of seizure (Khurana et al 2006; Saigal et al 1984). Cysticercosis sero-prevalence among the healthy blood donors from Pondicherry was 6.5% using both antigen and antibody detection methods (Parija et al 2005). The prevalence of taeniasis ranged from 0.5-2% in hospitalized patients in northern India, 12–15% in labour colonies where pigs are raised (Mahajan et al 1982). The treatment gap in rural India is above 90% and the probable reasons for such high gap are socioeconomic, lack of knowledge and medical facilities, social prejudice to modern medicine and faith in alternative treatment modalities. Cysticercosis also appears to be widespread among swine in India. In and around Chandigarh, 8–10% of the pigs slaughtered had cysticerci in their muscles and around 0.5% of the pigs reared in Government farms were found to be infected (Mahajan et al 1982). Another survey in slaughter houses of Kolkata (West Bengal) revealed cysticercosis in muscles of 7% of the slaughtered pigs (Ratnam et al 1983). Prasad et al (2002) reported a high frequency of cysticercosis (26%) in swine from Mohanlalganj block of Lucknow district in the State of Uttar Pradesh and 40% of them had cysticerci in the brain.
Life cycle, biology, and transmission
Life cycle of T. solium comprises two natural hosts, humans as the definite and swine as the intermediate host. Human harbours the adult tapeworm; eggs produced by the worm are disseminated to the environment through faeces. The pig ingests some of these eggs, which develop into cysticerci in internal organs like muscle and brain. When human consumes contaminated pork containing cysticerci, they develop into an adult worm in the small intestine (fi gure 2). The adult worm attaches itself to the intestinal mucosa by scolex equipped with four lateral suckers and a rostellum, which bears 25-50 hooklets. T. solium is a hermaphrodite and the gravid proglottides, containing the eggs reach the environment by passive discharge in the faeces. The eggs are spherical and measure 30-40 μm in diameter. After being liberated from the proglottides, the eggs can be ingested by swine and man. Once in the digestive tract, the eggs lose their coat by gastric and pancreatic enzymes and liberate hexacanth embryos or oncospheres. Aided by their hooklets, the oncospheres cross the intestinal wall and local venules, enter systemic circulation and are carried to different organs of the host (skeletal muscles, CNS, subcutaneous tissue, eye, etc.). Here the oncospheres lose their hooklets, acquire a vesicular shape and evolve into cysticerci by gradual evagination of the protoscolex (invaginated scolex) over a period of two months (Escobar and Neito 1972). The life cycle is completed when undercooked pork infested with cysticerci is eaten by human beings. However, man may also become an intermediate host and develop the larval stage of the disease in one of the ways: (i) by heteroinfection, the most common route, in which eggs present in food contaminated by the faeces of Taenia carriers are ingested; (ii) by exogenous autoinfection, due to ano-oral contamination in patients harbouring the adult worm; (iii) by endogenous autoinfection, in which the eggs of the adult tapeworm living in the small intestine return to the stomach due to reverse peristalsis. The last two modes of autoinfection are far less frequent as it is quite uncommon to fi nd patients having simultaneous infestation with cysticercosis and taeniasis in more than 10-15% cases (Rabiela-Cervantes et al 1982). In humans, parasite may get lodged in the CNS and results in NCC (Del Brutto and Satelo 1988). The larval stage also infests other tissues like skeletal muscle, diaphragm, heart and peritoneum, pleura and subcutaneous tissue (Shankar et al 1994). Mammals other than swine have also been reported to harbour cysticerci of T. solium. In Indonesia, examination of two sero-positive dogs revealed cysticerci of T. solium in their brain and heart (Ito et al 2002). C. cellulosae have also been recovered from the brain of a cat
Diagnosis of NCC
The diagnosis of NCC is impaired by its polymorphic clinical presentations. A definitive or probable diagnosis of NCC can be made on the basis of proposed clinical, radiological and epidemiological criteria (Del Brutto 2001; Garcia et al 2005). Defi nitive diagnosis of NCC is made by direct demonstration of the parasite in tissues or radiological demonstration of scolex in cystic lesions using neuroimaging modalities. However, some reservations had been expressed from India due to presence of large number of single small enhancing CT lesions (SSCTL) in India, that may be due to presence of fungal and tubercular granuloma
Different techniques applied for NCC diagnosis in human
1.Serological techniques
2.Taenia solium cyst fluid antigens based lymphocyte transformation test
3.Neuroimaging techniques
Treatment of NCC
Treatment
• For intestinal infection: Praziquantel or niclosamide (outside the US)
• For neurocysticercosis: Corticosteroids, anticonvulsants, and sometimes albendazole or praziquantel and/or surgery
Treatment of intestinal infection
Intestinal infection is treated with praziquantel 5 to 10 mg/kg po as a single dose to eliminate adult worms. Praziquantel should be used with caution in patients who also have neurocysticercosis because by killing cysts, praziquantel may trigger an inflammatory response associated with seizures or other symptoms.
Alternatively, a single 2-g dose of niclosamide (not available in the US) is given as 4 tablets (500 mg each) that are chewed one at a time and swallowed with a small amount of water. For children, the dose is 50 mg/kg (maximum 2 g) once.
Treatment of neurocysticercosis
The initial treatment goals for symptomatic neurocysticercosis are
• To reduce inflammation associated with degenerating cysticerci documented by MRI
• To prevent seizures if present or if risk is high
• To relieve increased intracranial pressure if present
Corticosteroids (prednisone 60 mg po once/day or dexamethasone 6 mg po once/day) are used to reduce inflammation and increased intracranial pressure.
Conventional anticonvulsants are given to patients who have seizures. These drugs can be used prophylactically in patients at high risk of seizures, particularly those who have multiple degenerating lesions with associated inflammation.
Neurosurgical intervention may be necessary for patients with increased intracranial pressure or intraventricular cysticerci.
Anthelmintic treatment of neurocysticercosis is complicated, and consultation with an expert is recommended. Choice of treatment depends on the location, number, and size of cysticerci; stage of the disease; and clinical manifestations.
Not all patients respond to treatment, and not all patients must be treated (cysts may already be dead and calcified, or the inflammatory response to treatment may be worse than the disease).
When anthelmintic treatment is used, albendazole 7.5 mg/kg po twice/day for 15 days appears to be more effective than the alternative, praziquantel16.6 mg/kg po tid for 15 days, but some patients who have not responded to albendazole have responded to praziquantel. Albendazole given for ≥ 30 days has been used to treat extensive disease and cysts in the subarachnoid space (racemose cysticercosis), which are less responsive to anthelmintic drugs. Occasionally, albendazole and praziquantel are used together.
Either prednisone or dexamethasone is given concurrently with the anthelminthic to reduce the inflammation that occurs in response to dying cysts in the brain. Corticosteroids increase the CSF level of the active metabolite of albendazole but decrease the CSF level of praziquantel.
Neither albendazole nor praziquantel should be used in patients with ocular or spinal cord cysticerci.
The presence of intraventricular cysticerci is a relative contraindication for anthelminthic drugs because the resulting inflammatory response elicited by the dying cysts can cause obstructive hydrocephalus.
Surgery may be necessary for obstructive hydrocephalus (due to intraventricular cysticerci including those in the 4th ventricle) or spinal or ocular cysticercosis. Intraventricular cysticerci are removed endoscopically when possible. Ventricular shunts may be needed to reduce increased intracranial pressure.
Prevention and control
Cysticercosis has been recognized as a potentially eradicable disease. The main method of control in developed countries has been the eradication of swine cysticercosis through improved animal husbandry and meat inspection procedures. This approach has resulted in the successful interruption of transmission of intestinal T. solium in the United States and Western Europe (Ferreira et al 1997). A small number of individuals with tapeworm may infect vast numbers of healthy human beings. Tapeworm carriers are an appealing target for the control of cysticercosis/taeniasis. In the developing world, emphasis has been placed on control of the parasite through health education and mass administration of antihelminthic drugs in areas of endemicity in an attempt to remove tapeworm carriers (Plancarte et al 1999; Garcia et al 2003; Lightowlers 2003).
NB-THE INTENTION OF THIS ARTICLE IS NOT TO DISCOURAGE THE PORK EATING .THIS IS JUST TO MAKE AWARE THE PORK CONSUMING PEOPLE ABOUT THE ALARMING DISEASE- NCC & ENCOURAGE THEM TO EAT HYGENIC PORK BACON.
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