Zaporozhyan state medical university departement of infectious diseases

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intestine of human scolex comes out from cysticercus and attaches to mucous 

membrane. In 2 months helminth becomes sexually mature and starts detaching 

and releasing segments.  

Susceptibility to Taeniosis is common. Immunity isn’t formed. 

Human can be as definitive as intermediate host for T. solium. Oncospheres 

can enter human body by two ways. The first one is with vegetables and verdure 

(green onion, dill, parsley) contaminated with patient’s faeces. The second one is 

due to entering mature segments into stomach from intestine during reversed 

peristalsis (for example, in case of vomiting). Oncospheres entered into stomach 

release embryos which penetrate the intestinal wall and are carried with blood all 

over the body. In human body cysticercus is often found in brain and eye and 

rarely in skin, muscles and other tissues.Therefore human with Taeniasis can be 

course of Cysticercosis invasion for himself and other people.  

Pathogenesis is the same as in case of Taeniarhynhosis. 

Clinical features. Invasion with T. solium may be asymptomatic and 

patients become aware of the infection by noting passage of proglottids in their 

faeces. Some patients complain of nausea, abdominal pain, weakness and sleep 

disorders. Symptoms are not associated with pruritus ani. The proglottids do not 

migrate actively per anum. 

Specific diagnostics of taeniosis. The main method of examination is 

macroscopical which can reveal released gravid proglottids in the faeces (often in 

short chains). Mature segment of T. solium has 8–10 uterine branches. The eggs of 

T. solium and T. saginatus have similar structure therefore if only eggs are found 

laboratory gives conclusion that these are eggs of teniid. 

Clinical features of cysticercosis. The clinical manifestations of 

cysticercosis are variable and depend on localization and number of parasites. 

Cysticerci can be found anywhere in the body but are most commonly detected in 

the brain, skeletal muscle, subcutaneous tissue, or eye. The most often cysticerci 

are localized in brain. Epilepsy, the most common presentation of 

neurocysticercosis, is usually the primary or sole manifestation of the disease. 

Seizures occur in 50 to 80 per cent of patients with parenchymal brain cysts or 

calcifications but are less common in other forms of the disease. Seizures may be 

generalized, focal, or Jacksonian. Other common focal signs include pyramidal 

tract signs, sensory deficits, signs of brainstem dysfunction, and involuntary 

movements. These manifestations usually follow a subacute or chronic course, 

making neurocysticercosis difficult to differentiate clinically from neoplasms or 

other infections of the central nervous system. Focal signs may occur abruptly in 

patients who develop a cerebral infarct as a complication of subarachnoid 

neurocysticercosis. When cysticerci develop at the base of the brain or in the 

subarachnoid space, they may cause chronic meningitis or arachnoiditis, 

communicating hydrocephalus, or strokes. 

Neurocysticercosis may present with increased intracranial pressure, usually 

from hydrocephalus secondary to cysticercotic arachnoiditis, granular ependymitis, 

or ventricular cysts. In these cases, intracranial hypertension develops subacutely 

and progresses slowly. Signs of increased intracranial pressure, including 

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headache, nausea, vomiting, changes in vision, dizziness, ataxia, or confusion, are 

often evident. Patients with hydrocephalus may develop papilledema or display 

altered mental status. Lymphatic pleocytosis with prevalence of eosinophils and 

elevated level of protein are found in CSF in patients with neurocysticercosis. 

Cysticercosis of eye causes visual impairment and sometimes results in 

blindness. Lesion of orbit leads to exophthalmus.  

Muscular pseudohypertrophy, a rare presentation, is caused by heavy 

cysticercal infection of skeletal muscles giving a 'Herculean' appearance. The few 

cases reported are all from India. Muscular and subcutaneous cysticerci are far less 

common in American than in African or Asian patients with neurocysticercosis 

(See table).  

The clinical manifestations of cystecercosis 

in dependence on localization of cyctecercs  

 

Brain  

 

 

 

Symptoms 

Eyes  

Cereb

ral 

hemispheres  

IV  

 Ventri

cle  

Basis   

Headache  

 +  +   

Dizziness 

 

   

 +  +   

Nausea 

 

   

 +  + 

 

Vomiting 

 

   

 +  + 

 

Epileptic attacks    

 + 

 

 

Disorders of psychics  

(dimension, gallucinations) 

  

 

+ 

Dispnoe  

 

 

+ 

 

The harsh of the state in impairment 

the change of the body position 

 

 

+ 

 

Disorder of vestibular conduction 

 

 

  

 

+ 

Paresis, paralyses   

  

+  

Progressive impairment of the vision 

+ 

 

 

 

Specific diagnostics of Cysticercosis. Immunological tests such as immune 

enzyme analysis with cysticerci diagnosticum, instrumental methods such as 

computed tomography (CT), magnetic resonance imaging (MRI), ophthalmoscopy 

and ultrasound examination. 

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