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   Table of Contents      
BRIEF REPORT
Year : 2006  |  Volume : 54  |  Issue : 2  |  Page : 129-131

Outbreak of ocular toxoplasmosis in Coimbatore, India


Department of Microbiology, Aravind Eye Care System, Aravind Eye Hospital and Post Graduate Institute of Ophthalmology, Avinashi Road, Coimbatore, Tamilnadu, India

Correspondence Address:
Manikandan Palanisamy
Aravind Eye Care System, Aravind Eye Hospital and Post Graduate Institute of Ophthalmology, Avinashi Road, Coimbatore, Tamilnadu - 641 014
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0301-4738.25839

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  Abstract 

Toxoplasma gondii is a protozoan parasite that infects up to a third of the world's population. Infection is mainly acquired by ingestion of food that is contaminated with oocysts. We report an outbreak of ocular toxoplasmosis, which is an acute acquired type rather than reactivation of congenital toxoplasmosis. Our preliminary investigation points to municipal water contamination. This outbreak only proves the need of an effective public health system and health education in curtailing any outbreak.

Keywords: Toxoplasma gondii, waterborne, retinitis, outbreak, toxoplasmosis.


How to cite this article:
Palanisamy M, Madhavan B, Balasundaram MB, Andavar R, Venkatapathy N. Outbreak of ocular toxoplasmosis in Coimbatore, India. Indian J Ophthalmol 2006;54:129-31

How to cite this URL:
Palanisamy M, Madhavan B, Balasundaram MB, Andavar R, Venkatapathy N. Outbreak of ocular toxoplasmosis in Coimbatore, India. Indian J Ophthalmol [serial online] 2006 [cited 2019 Nov 14];54:129-31. Available from: http://www.ijo.in/text.asp?2006/54/2/129/25839



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Toxoplasma gondii is an obligate intracellular protozoan parasite, which can cause severe, life threatening disease, especially in newborns and in immunocompromised patients. It is an important cause of ocular disease in both immunocompromised and immunocompetent individuals.[1],[2] Ocular toxoplasmosis manifests as chorioretinitis in which white focal lesions with intense vitreal inflammatory reaction are seen and recurrent lesions usually arise at the borders of chorioretinal scars in clusters. Ocular lesions are seen in the setting of congenital or postnatally acquired disease as a result of acute infection or reactivation.[1],[2] Infection is mainly acquired by ingestion of food that is contaminated with oocysts shed by cats or by eating undercooked / raw meat containing tissue cysts and also through contact with contaminated soil.[1],[2],[3] Waterborne toxoplasmosis is also documented[4],[5],[6] T. gondii infection can be diagnosed indirectly with serological methods, such as enzyme linked immunosorbent assay (ELISA) immunofluorescent assay, Sabin-Feldman Dye Test and directly by polymerase chain reaction, hybridization, isolation and histology.[2] ELISA is widely used in immunocompetent patients, for detection of both IgG and IgM antibodies. Negative test for IgM essentially rules out recently acquired infection.[2]

Here we report an outbreak of ocular toxoplasmosis, which was an acute acquired type rather than reactivation of congenital toxoplasmosis. This is one of the very few largest reports on outbreak of ocular toxoplasmosis.


  Materials and Methods Top


We have started screening sera for ocular toxoplasmosis in relevant cases since 2001. In September 2004 there was a sudden increase in the seropositive cases in the Uvea clinic [Figure - 1]. All cases presented with abrupt diminution of visual acuity. Ocular examination showed findings consistent with ocular toxoplasmosis - fresh lesions of chorioretinitis with no evidence of old / healed scars [Figure - 2]a. Five ml of blood was collected from all clinically confirmed patients with chorioretinitis and the sera were separated by centrifugation at 3000 rpm for 15 minutes. All the sera were stored at -20o C till further use.

ELISA was done for all the samples to detect both IgG and IgM antibodies of Toxoplasma gondii . Four commercially available separate antigen based kits (Biokit, Spain; Euroimmun, UK; Omega Diagnostics, UK; Equipar Diagnostici, Italy) were used for both IgG and IgM to check for reproducibility of the results. The plates were read using a 450 nm filter with 630 nm as a reference filter.


  Results Top


A total number of 402 sera samples were collected for screening of ocular toxoplasmosis from January 2001 to February 2005. Of these, 249 samples were collected and screened from September 2004. Out of these 249 cases tested during the outbreak, 178 cases had high titres of both IgM and IgG antibodies and 4 cases showed presence of IgM antibodies alone. All age groups were affected but a majority of them were above 20 years of age [Table - 1].


  Discussion Top


This sudden increase in patients with features of ocular toxoplasmosis and clustering of cases mostly occurring within Coimbatore city and reports from other hospitals in Coimbatore, of an increase in ocular toxoplasmosis cases at the same time support a conclusion that this was an outbreak of acute ocular toxoplasmosis rather than a reactivation or an increased awareness of Ophthalmologists of an ongoing problem. Though at this stage we cannot conclusively say that this was an acute recent infection of ocular toxoplasmosis, as it requires additional serological tests (seroanalysis at reference laboratories), clinical features, age, time and place of the occurrence do not favor a reactivation theory. Though in this series all age groups were affected, most of the patients were adults. Reactivation of congenital infection usually occurs in adolescents.[7] Clustering of cases in a place and at a particular time do not occur in reactivation and the titres are not markedly high as in an outbreak.

We cannot conclusively prove the source of infection. A majority of the cases were found to be located in the areas supplied by one water reservoir and there were negligible cases from areas supplied by the second reservoir. The prima facie evidence suggests that water could be the possible source. The parasite can be transmitted to humans in several ways including ingestion of raw or undercooked meat, contact with soil, eating unwashed fruits or vegetables[1],[3] and drinking water contaminated with oocysts.[4],[5],[6]

Our preliminary investigation points to municipal water contamination. The data collected do not suggest an alternate source, which can account for size and distribution of this outbreak. It may not be possible to fully elucidate the events leading to this outbreak and we may never prove definitely that water is the source of contamination. But we have observed striking similarities in our study to a previous study[4] on outbreak of waterborne toxoplasmosis. The Siruvani reservoir, supplying water to Coimbatore city, might have been contaminated due to the heavy rainfall in catchment areas that preceded the outbreak. Domestic and wild cats infest these catchment areas. Infected cats can shed million of oocysts and the temperature prevailing in this region (20-40o C) can support the survival of sporulated cysts.[1] As chlorination is the only primary mode of disinfection done at the water treatment plant the cysts could have survived to reach the general public.[8]

Access of the reservoir to domestic and wild cats, lack of filtration of water following primary disinfection and little awareness of waterborne diseases among the public were probably the major factors which influenced this outbreak. As the surface water supply can be susceptible to direct or indirect contamination, people are always advised to boil the water before consumption. This outbreak only proves the need of an effective public health system and health education in curtailing any outbreak. We detected the outbreak and alerted the local public health authorities at the start of epidemic. In association with a vigorous campaign for boiling of water before consumption, the number of cases decreased. The other epidemiological parameters are being investigated.

 
  References Top

1.
Holland GN, O'Connor GR, Belfort R Jr, Remington JS. Toxoplasmosis, chapter 85. In : Ocular infection and immunity. Pepose JS, Holland HN, Wilhelmus KR, editors. Mosby: 1996. p. 1183-217.  Back to cited text no. 1
    
2.
Montoya JG and Liesenfeld O. Toxoplasmosis. Lancet 2004;363:1965-76.  Back to cited text no. 2
    
3.
David Dawson. Information on Toxoplasma gondii . In : Foodborne Protozoan Parasites. ILSI Europe Series. Prepared under the responsibility of the ILSI Europe emerging pathogen task force. Accessed at http://www.ilsi.org. 2003. p. 25-8.   Back to cited text no. 3
    
4.
Bowie WR, King AS, Werker DH, Issac-Renton JL, Bell A, Eng SB et al . Outbreak of toxoplasmosis associated with municipal drinking water. Lancet 1997;350:173-7.  Back to cited text no. 4
    
5.
Dubey JP. Toxoplasmosis - a waterborne zoonosis. Vert Parasitol 2004;126:57-72.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.
Bahia-Oliveira, Jones JL, Azevedo-Silva J, Alves CC orefice F, Addiss DG. Highly Endemic, Waterborne Toxoplasmosis in North Rio de Janeiro State, Brazil. Emerg Infect Dis 2003;9:55-62.  Back to cited text no. 6
    
7.
Mets MB, Holfels E, Boyer KM, Swisher CN, Roizen N, Stein L, et al . Eye Manifestations of Congenital Toxoplasmosis. Am J Ophthalmol 1996;122:309-24.  Back to cited text no. 7
    
8.
Suresh K, Smith HV. Tropical organisms in Asia/Africa/South America, Chapter 6. In : World Health Organization (WHO). Waterborne Zoonoses: Identification, Causes and Control. Cotruvo JA, Dufour A, Rees G, Bartram J, Carr R, Cliver DO, Craun GF, Fayer R and Gannon VPJ, editors. IWA Publishing: London, UK; 2004. Accessed at http://www.who.int/water_sanitation_health/diseases/zoonoses/en/. 93-112.  Back to cited text no. 8
    


    Figures

  [Figure - 1], [Figure - 2]
 
 
    Tables

  [Table - 1]


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