|Year : 1991 | Volume
| Issue : 3 | Page : 136-137
Toxoplasmic retinochoroiditis and hydrocephalus
Gulbir Singh Rekhi, DP Sharma, Pramod Sharma, Girish Prabhakar
Department of Ophthalmology, SMS Hospital, Jaipur, India
Gulbir Singh Rekhi
A-201, Malaviya Nagar, Jaipur 302017, Rajasthan
Source of Support: None, Conflict of Interest: None
A child presenting with hydrocephalus with extensive inactive retinochoroiditis and his mother with a healed toxoplasmic scar is being discussed. Maternal ocular examination in each case of hydrocephalus is recommended, as uveitis work up of the child is often unrewarding.
|How to cite this article:|
Rekhi GS, Sharma D P, Sharma P, Prabhakar G. Toxoplasmic retinochoroiditis and hydrocephalus. Indian J Ophthalmol 1991;39:136-7
|How to cite this URL:|
Rekhi GS, Sharma D P, Sharma P, Prabhakar G. Toxoplasmic retinochoroiditis and hydrocephalus. Indian J Ophthalmol [serial online] 1991 [cited 2019 Jun 20];39:136-7. Available from: http://www.ijo.in/text.asp?1991/39/3/136/24449
| Introduction|| |
Toxoplasmosis is due to infestation by an obligatory intracellular protozoan parasite called Toxoplasma gondii. The disease can be acquired in utero or in adult life. The triad of convulsions, intracranial calcification and chorioretinitis characterizes congenital toxoplasmosis.
Beginning with the discovery by Wolf and coworkers of toxoplasmosis in man in 1938 , followed by toxoplasmin skin test , and toxoplasmin dye test , various authors have emphasized the ocular and neurological aspects of the disease. Feldman (1953)  reported an incidence of 94% of chorioretinal lesions in 150 cases of toxoplasmosis. Feldman (1956) [5 ] has agayn reported hydrocephalus in 22% of 147 cases of toxoplasmosis.
| Case report|| |
A one year old male child was brought to the out patient department of paediatric surgery with the parents complaining of gradual enlargement of the head of the child since birth. The child was born after 38 weeks of gestation and weighed 2 Kg. at birth. The labor and delivery were uneventful with the good cry and suck reflex at birth. Parents first noticed abnormal enlargement of the head after about 2 1/2 months. Since then there has been a gradual enlargement of the head and the child was brought to us at the present age.
The parents suspected that the child had some difficulty in vision and not having the normal physical and mental growth. The mother gave a history of having had some ocular problem for which she had taken some treatment at a peripheral health centre.
On examination the head circumference of the child was 65 cms. Anterior fontanelle was widely open and tense and sunset sign of eyes was positive. On-percussion crack-pot sound was elicited (positive Mcewans sign). The physical and mental milestones of the child were delayed for the age. Vision could not be confirmed.
| Investigations|| |
Routine haemogram and urine analysis were normal. X Ray of the skull revealed abnormal enlargement of the skull and thinning of the skull bones. No intracranial cacification could be seen. Ultrasonogram of the skull revealed dilatation of both the lateral ventricles and third ventricle. There were areas of increased echogenicity in the brain parenchyma.
In the child - extensive bilateral inactive chorioretinitis involving the macular area and periphery. The child had pendular nystagmus in each eye, and the discs were pale bilaterally. Complete uveitis work up was negative.
In the mothe r- Bilateral healed typical punched out lesions were observed with hyperpigmented margins suggestive of healed toxoplasmic retino choroiditis. The mother and child were negative for toxoplasmin dye test. The lumbar puncture of the child revealed -elevated CSF pressure, sugar of 50 mg%, proteins 55 mg% and cell count of 20. Culture of CSF was negative. Chest films and VDRL of both mother and child were negative.
The child was managed by putting a ventriculoperitoneal shunt (Upadhyaya shunt) and at the time of the last follow up (after 6 months of operation), the head had stopped enlarging but the physical and mental milestones remain delayed.
| Discussion|| |
Various authors ,, have reported the association of choriorentinitis and cerebral damage. This case deals with one manifestation of cerebral damage, hydrocephalus and its association with chorioretinal inflammatory disease, presumably due to toxoplasmosis. The toxoplasmic infestation in utero is known to cause aqueductal stenosis thus leading to hydrocephalus later on. This case is presented to ,emphasize the importance of maternal ocular examination in all hospitalized hydrocephalic patients since an extensive uveitis diagnostic work up of the child may even fail to implicate a specific etiology.
| References|| |
Wolf, A., Cowan, D., and Paige, B.H.: Human toxoplasmosis: Occurrence in infants as encephalomyelitis; verification by transmission to animals. Since, 89: 226-227 (Mar.) 1939.
Frenkel, J.K.: Dermal hypresensitivity to toxoplasma antigens. Proc. Soc. Exper. Biol. & Med.. 68:639 (Dec.10) 1948.
Sabin. A.B., and Feldman, H.A.: Dyes as microchemical indications of a new immunity phenomenon affecting a protozoon parasite (Toxoplasma) Science, 108: 663, 1948.
Feldman, H.A., and Miller, L.7: Congenital human toxoplasmosis. Ann. N.Y. Acad. Sci., 64: 180-184 (July 5) 1956.
Feldman, H.A., and Miller, L.T: Congenital human toxoplasmosis. Ann. N.Y. Acad. Sci., 64:180-184 (July 5) 1956.
Burns, R.P: Cytomegalic inclusion disease uveitis: Report of case with isolation from aqueous humor of virus in tissue culture. AMA Arch. Ophth., 61:376-387, 1959.
Weller, TH., Macauley, I.C., Craig, J.M., and Wirth, P : Isolation of intraocular inclusion producing agents from infants with illnesses resembling cytomegalic inclusion disease. Proc. Soc. Exper. Biol.& Med., 94:4-12 (Jan.) 1957.
Christensen, L., Beeman. H.W., and Allen, A: Cytomegalic inclusion disease. AMA Arch. Opth., 57:90-99 (Jan.) 1957.
[Figure - 1], [Figure - 2], [Figure - 3]