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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 5  |  Issue : 3  |  Page : 174-177

Human cysticercosis


1 Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
2 Department of Clinical Neurosciences, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
3 Department of Neuromicrobiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Date of Web Publication5-Aug-2016

Correspondence Address:
Dr. Sadanandavalli Retnaswami Chandra
Faculty Block, Neurocentre, National Institute of Mental Health and Neurosciences, Bengaluru - 560 029, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-344X.187831

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  Abstract 

Humans and pigs become the intermediate hosts by ingestion of the eggs excreted in feces by human Taenia solium carriers. Neurocysticercosis is the most common parasitic infection of the brain. A gravid segment of the parasite contains about 40,000 eggs and approximately 50 million people suffer world over with 50,000 annual deaths. Disease modifying treatment options have to be carefully chosen in the selected cases. We report a 14-year-old female child who presented with headache, fever, and blindness of 4 months duration she had bilateral papilledema with no perception of light. Investigations showed the whole brain parenchyma filled with cysts of the trophozoite stage sparing the pons, medulla, and spinal cord. Whole body was filled with sheets of cysticercal lesions in the skin, muscles, eyes, liver, and kidney. Patient was treated with steroids and anti-edema measures. Patient made very good recovery with very mild cognitive and behavioral sequelae.

Keywords: Blindness, disseminated cysticercosis, imaging, mismatch between symptoms and signs


How to cite this article:
Chandra SR, Issac TG, Kumar V, Pai A, Patil SA. Human cysticercosis. Int J Health Allied Sci 2016;5:174-7

How to cite this URL:
Chandra SR, Issac TG, Kumar V, Pai A, Patil SA. Human cysticercosis. Int J Health Allied Sci [serial online] 2016 [cited 2021 Feb 26];5:174-7. Available from: https://www.ijhas.in/text.asp?2016/5/3/174/187831


  Introduction Top


Taenia solium and Taenia saginata are the most common human tapeworms in the world. [1] Human beings are the only definitive host of T. solium harboring adult tapeworm in the intestine (Taeniasis), but both man and pig act as intermediate hosts and harbor the larvae in different internal organs including brain. Human and pig both acquire cysticercosis through ingestion of eggs excreted in feces by human T. solium carrier. Neurocysticercosis (NCC) is considered to be the most common parasitic infestation of the central nervous system and the single most common cause of epilepsy in the developing countries. It is a serious but less attended to infection. Relationship between the adult tapeworm and cysticercus was first shown by Kuchenmeister from Germany in 1855. He proved this by feeding prisoners by infected pork and demonstrated tapeworms in their intestine at autopsy. [1] A gravid segment excreted by the infected human being contains around 40,000 eggs and stays alive against all environmental factors for very long time. When the intermediate host happens to feed on that it hatches and enters the blood stream penetrating the gut. Humans become infected by eating inadequately cooked pork and become intermediate hosts by accidental ingestion through unwashed hands, contaminated food, and retrograde peristalsis. What factors help the organism in traversing the intestinal tissue is not very clear. Probably it behaves such as the eukaryotes and probably signals through kinases, second messengers as well as remodeling of the cytoskeleton and alteration in the metabolic changes both in the host and in the organism. [2],[3] Then the organism develops into metacestode in the subcutaneous tissue, muscle, and brain. It is maximum concentrated in the vascular areas. They protect themselves from host immune system by several mechanisms which depend on the production of excretion-secretion proteins and it is important to have an insight into these aspects as this is a stage that determines the success of the organism. [1],[4],[5] The World Health Organization reports approximately 50 million people suffer the world over with about 50,000 annual deaths. [6],[7] The disease is endemic in sub-Saharan Africa, Latin America, and some developing countries and also emerging in the developed European countries due to cross-country migration. [7],[8] In India, commonly cases are reported from Delhi, Uttaranchal, Chandigarh, and Pondicherry though it is prevalent in many other states but not reported. Disseminated cysticercosis presents with painless hypertrophic muscles, palpable subcutaneous nodules often mistaken for other pseudohypertrophic muscle diseases. It is believed that dead larvae act as an irritant to muscles causing inflammatory changes and allergic responses resulting in pseudohypertrophy. Most of these patients suffer from visual symptoms due to (a) raised intracranial tension and (b) optic nerve involvement. [9],[10]

Diagnosis is clinical, epidemiological, radiological, and immunological described by Del Brutto et al. [8] Clinical features depend on the structures involved. In NCC, epilepsy is the most common feature and occurs in 70-90%. Other common neurological symptoms are headache, cognitive, and psychiatric symptoms and blindness. [10],[11] Other complications are secondary to the location of the lesions, like blindness when there is intraocular lesion and hydrocephalus when intraventricular. Usually, other system manifestations are asymptomatic. Treatment is largely symptomatic. Anti-parasitic drugs such as praziquantel and albendazole are very effective in killing the parasite but the death of the organism releases proinflammatory substances which can produce stormy neurological problems if the lesion load is more than 5-10. Disease modifying treatment is absolutely contraindicated when there are intraocular and intraventricular cysts. It is the treatment of choice for intestinal infestation. Cysticidal drugs are not indicated when the cysts have become calcified. However, when active cysts are detected, there is a perennial risk of serious complications. When the intracranial number of lesions is <5 it is relatively safe to use albendazole 15 mg/kg/day for 10-30 days or praziquantel 10-15 mg/kg/day for 1-3 weeks along with steroids. However, if the lesion load is >5, this option is controversial and severe fatal encephalopathy can occur with massive killing of the cyst. [10],[11]

Neuroimaging - computerized tomography (CT) and magnetic resonance imaging (MRI) are fairly sensitive in picking up the lesions. CT can detect most cases because of their tendency for calcification except lesions in ventricles and basal cisterns. MRI is extremely useful as it can identify the higher water content of the cyst and can detect the early stages of the parasite and it can be used to assess the response to treatment when disease-modifying agents are used. [10] Serological tests consist of detecting antibodies against cysticercus using ELISA. Its sensitivity is as high as 94%.

Histopathology of the muscles or the nodule will show the cysticerci along with inflammatory changes. Ultrasonography (USG) of the muscles and eyes also reveal the lesions.

Our patient had very few lesions in the visceral organs and no lesions in the pons, medulla, and spinal cord. Identifying the factors which determine the invasiveness of the organism and potential resistance of some structures like spinal cord as well as the factors protecting the neuraxis of the pig might give us important clues to protect the humans from NCC. Identifying the invasiveness determining antigens is likely to pave the way for potential vaccine against NCC. This case is being presented for the extremely severe invasion of the brain, eyes, and muscles and significant improvement following treatment.


  Case Report Top


A 14-year-old female child from Dharamapuri District, Tamil Nadu, South India presented with fever, headache, and vomiting, loss of weight and appetite since 4 months. She had blurring of vision from the beginning of the illness, and she became totally blind since 2 weeks. She was started on antituberculous treatment for 3΍ months along with steroids at regional hospital and did not result in any improvement and therefore referred to our center. At the time of admission, the patient was restless and apprehensive. She had no perception of light. There was bilateral proptosis with papilledema. There was no intraocular cyst detected by indirect ophthalmoscopy. Her plantar responses were extensor. No other neurological features present. There was a single nodule in the right upper eyelid, and discrete lesions were seen in the subcutaneous plane in the right side of the neck. No other systemic signs were noticed. The patient used to take mixed diet but denied consuming pork. The patient had the habit of takin nonhomemade Street food like Pani puri. Investigations done showed cerebrospinal fluid (CSF) - 150 cells, 95% lymphocytes and protein - 93 mg/dl, antinuclear antibody was first positive (6.5) and later negative. Serum glutamic oxaloacetic transaminase - 15 IU/L, serum glutamate-pyruvate transaminase - 14 IU/L, total bilirubin 0.7 mg/dL, serum urea 24 mg/dL, serum creatinine - 0.4 mg/dL, random blood sugar - 106 mg/dl, serum electrolytes-sodium - 129 mEq/L, potassium - 3.63 mEq/L, chloride - 94 mmol/L, hemoglobin - 12.6 g/dL, Total Count (TC)- 13,700/mm 3 , Differential Count (DC)- Neutrophils (72), Lymphocytes (14), Monocytes (5), Eosinophils (8), Basophils (1), platelet count 4.5 lakh/mm 3 , mean corpuscular hemoglobin/mean corpuscular hemoglobin concentration/mean corpuscular volume - 28.9 pg/ml/33.2 g/dl/87.1 FL respectively. In our center, CSF finding showed clear, CSF with increased CSF pressure, 6 cells, all lymphocytes, protein - 68 mg/dl, sugar 54 mg/dl, chloride - 122 mEq/L, USG abdomen was normal. Visual evoked potential was abnormal in both eyes.

CT scan brain done outside showed multiple small white specks throughout the brain with ironed out the appearance of the brain. MRI of the brain showed multiple cystic lesions seen throughout the brain except brainstem and spinal cord. There were large number of intraocular and intraorbital cysts as well as the muscles of the face, tongue, neck, trunk, upper-, and lower-limbs [Figure 1]. There were also lesions in the liver and kidney, though they were very few. Muscle biopsy was done from the left biceps [Figure 2]. Which showed multiple whitish cystic lesions which could be easily pulled out. Histopathological examination revealed the following. Large viable cysticercal cysts abutting the perimysium and burrowing into the muscle present. Cyst wall has a thinned out cellular layer and underlying reticular layer with dilated ductules. Thin collagenous capsules derived from perimysium with aggregates of histiocytes were seen around forming ill-formed granulomas. There was occasional eosinophils and thick rim of lymphocytes. Muscles around showed atrophy especially involving type 2 fibers.
Figure 1: Magnetic resonance imaging of the brain showed multiple cystic lesions seen throughout the brain except brainstem and spinal cord. There were large number of intraocular and intraorbital cysts as well as the muscles of the face, tongue, neck, trunk, upper-, and lower-limbs, (a-c) depicts starry sky appearance in MRI, (d and e) depicts sheets of cysticercus in all muscle planes

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Figure 2: Left biceps biopsy of the patient showing live cyst. (a and b) shows live cysts in the Biceps muscle. The white dot depicts the scolex. (c and d) shows the separated cysts in the biopsy specimen

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The patient was treated with pulse methyl prednisolone followed by oral methyl prednisolone (0.9 mg/kg), anti-edema and anticonvulsant drugs. Cysticidal drugs were not started in view of the massive lesions visualized. She steadily improved in her vision and cognition and at the time of discharge 2 weeks after admission, she could read with acuity of about 6/60 in both eyes. Members of the treating team visited a nearby place and were surprised to get a sample of measly pork from which we could separate the cysts [Figure 3] and [Figure 4].
Figure 3: (a and b) shows Pork fully infected with cysticercus (measly pork), (c) shows extracted cysticercus from measly pork, (d) shows Scolex under light microscopy

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Figure 4: Histopathological picture of a cysticercus cyst inside the muscle

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  Discussion and Conclusion Top


Disseminated cysticercosis is a relatively rare, potentially fatal form of infection by the larval form of cysticercus called cysticercus cellulosa. The worst form is the neurological with ocular involvement where cysticidal drugs cannot be used. Surprisingly patients are generally quiet though they may manifest with repeated seizures hydrocephalus and neuropsychiatric manifestations including dementia. The unique feature in our patient is as against the cases reported in the literature, relatively very few lesions in the skin but very severe involvement of the muscles and brain converting the patient into a human cysticercosis. Our patient had very few lesions in the visceral organs and no lesions in the pons, medulla, and spinal cord. Identifying the factors which determines the invasiveness of the organism and potential resistance of some structures like spinal cord as well as the factors protecting the neuraxis of the pig might give us important clues to protect the humans from NCC. Identifying the invasiveness determining antigens is likely to pave the way for potential vaccine against NCC. The number and location the lesions probably is not the only cause for the sequelae seen in some of these patients as our patient in spite of having been converted into a "human cysticercosis" had very little sequelae with reference to her cognitive-behavioral symptoms and did not have any motor features or seizures. What protected the pons, medulla, and the spinal cord also cannot be explained. This could be probably related to the relatively less direct vascular supply to these structures. In addition, indirect and direct ophthalmoscopy may not detect intraocular cysts always even if they are in large numbers. Therefore, in patients with low lesion load when disease-modifying treatment is planned, it is mandatory to do MRI of the orbit.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Garcia HH, Del Brutto OH. Taenia solium cysticercosis. Infect Dis Clin North Am 2000;14:97-119, ix.  Back to cited text no. 1
    
2.
Aguilar-Díaz H, Bobes RJ, Carrero JC, Camacho-Carranza R, Cervantes C, Cevallos MA, et al. The genome project of Taenia solium. Parasitol Int 2006;55;S127-30.  Back to cited text no. 2
    
3.
Almeida CR, Stoco PH, Wagner G, Sincero TC, Rotava G, Bayer-Santos E, et al. Transcriptome analysis of Taenia solium cysticerci using Open Reading Frame ESTs (ORESTES). Parasit Vectors 2009;2:35.  Back to cited text no. 3
    
4.
Victor B, Kanobana K, Gabriël S, Polman K, Deckers N, Dorny P, et al. Proteomic analysis of Taenia solium metacestode excretion-secretion proteins. Proteomics 2012;12:1860-9.  Back to cited text no. 4
    
5.
Hewitson JP, Grainger JR, Maizels RM. Helminth immunoregulation: The role of parasite secreted proteins in modulating host immunity. Mol Biochem Parasitol 2009;167:1-11.  Back to cited text no. 5
    
6.
Lorenzo S, Daumerie D. Working to Overcome the Global Impact of Neglected Tropical Disease. WHO Report. Geneva: WHO; 2010. p. 1-169.  Back to cited text no. 6
    
7.
Rajshekhar V, Joshi DD, Doanh NQ, van De N, Xiaonong Z. Taenia solium taeniosis/cysticercosis in Asia: Epidemiology, impact and issues. Acta Trop 2003;87:53-60.  Back to cited text no. 7
    
8.
Del Brutto OH, Rajshekhar V, White AC Jr., Tsang VC, Nash TE, Takayanagui OM, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001;57:177-83.  Back to cited text no. 8
    
9.
Nash TE, Del Brutto OH, Butman JA, Corona T, Delgado-Escueta A, Duron RM, et al. Calcific neurocysticercosis and epileptogenesis. Neurology 2004;62:1934-8.  Back to cited text no. 9
    
10.
Jena A, Sanchetee PC, Tripathi R, Jain RK, Gupta AK, Sapra ML. MR observations on the effects of praziquantel in neurocysticercosis. Magn Reson Imaging 1992;10:77-80.  Back to cited text no. 10
    
11.
Bandyopadhyay D, Sen S. Disseminated cysticercosis with huge muscle hypertrophy. Indian J Dermatol 2009;54:49-51.  Back to cited text no. 11
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