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DNA chip-assisted diagnosis of a previously unknown etiology of intermediate uveitis- Toxoplasma gondii.

Basu S, Sharma S, Kar S, Das T - Indian J Ophthalmol (2010 Nov-Dec)

Bottom Line: Ltd., Bangalore, India).The enzyme-linked immunosorbent assay (ELISA) detected elevated serum antitoxoplasma IgG levels in both.They responded to the antitoxoplasma therapy with oral co-trimoxazole (and additional intravitreal clindamycin in patient 1), with no recurrence during follow-ups of 6 and 8 months, respectively.

View Article: PubMed Central - PubMed

Affiliation: Retina-Vitreous Service, LV Prasad Eye Institute, Bhubaneswar, Orissa, India. basu@lvpei.org

ABSTRACT
We report the use of DNA chip technology in the identification of Toxoplasma gondii as the etiological agent in two patients with recurrent intermediate uveitis (IU). Both patients had recurrent episodes of vitritis (with no focal retinochoroidal lesion) over varying time intervals and were diagnosed to have IU. The tuberculin test was negative in both. Blood counts, erythrocyte sedimentation rate, and serum angiotensin convertase enzyme levels were normal. In both cases, the vitreous fluid tested positive for the T. gondii DNA sequence by using a uveitis DNA chip (XCyton Pvt. Ltd., Bangalore, India). It contained complimentary sequences to "signature genes" of T. gondii, Mycobacterium tuberculosis, M. chelonae, and M. fortuitum. The enzyme-linked immunosorbent assay (ELISA) detected elevated serum antitoxoplasma IgG levels in both. They responded to the antitoxoplasma therapy with oral co-trimoxazole (and additional intravitreal clindamycin in patient 1), with no recurrence during follow-ups of 6 and 8 months, respectively.

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The DNA chip, showing a positive reaction at the position of T. gondii (B1 gene sequence) and the positive control (β-globin gene)
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Figure 0001: The DNA chip, showing a positive reaction at the position of T. gondii (B1 gene sequence) and the positive control (β-globin gene)

Mentions: Tuberculosis and sarcoidosis were considered unlikely etiologies, as tuberculin test, serum ACE levels, and chest X-ray were normal. The possibility of a masquerade syndrome was not investigated further, considering the complete response to steroids on previous occasions and rarity of the condition. Since the disease followed a pattern of multiple recurrences on tapering of steroids, we suspected an underlying infectious etiology. A vitreous biopsy was done for DNA amplification using the multiplex polymerase chain reaction (PCR) technique. To identify the amplified DNA, we used a DNA chip (XCyton Diagnostics Pvt. Ltd., Bangalore, India; Fig. 1), containing complimentary sequences to “signature genes” of Toxoplasma gondii, Mycobacterium tuberculosis, M. chelonae, and M. fortuitum [Table 1]. We got a positive reaction for the B1 gene sequence of T. gondii [Fig. 1]. Subsequently, the enzyme-linked immunosorbent assay (ELISA) detected very high antitoxoplasma IgG levels. Oral steroids were stopped. We advised oral co-trimoxazole (960 mg twice daily) and a single dose of intravitreal clindamycin (1 mg/0.1 ml). This led to a sharp reduction in vitreous inflammation and an improvement in the visual acuity to 20/50 after 2 weeks. No focal lesions were seen in the fundus. There was no recurrence over the next 6 months of follow-up.


DNA chip-assisted diagnosis of a previously unknown etiology of intermediate uveitis- Toxoplasma gondii.

Basu S, Sharma S, Kar S, Das T - Indian J Ophthalmol (2010 Nov-Dec)

The DNA chip, showing a positive reaction at the position of T. gondii (B1 gene sequence) and the positive control (β-globin gene)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2993989&req=5

Figure 0001: The DNA chip, showing a positive reaction at the position of T. gondii (B1 gene sequence) and the positive control (β-globin gene)
Mentions: Tuberculosis and sarcoidosis were considered unlikely etiologies, as tuberculin test, serum ACE levels, and chest X-ray were normal. The possibility of a masquerade syndrome was not investigated further, considering the complete response to steroids on previous occasions and rarity of the condition. Since the disease followed a pattern of multiple recurrences on tapering of steroids, we suspected an underlying infectious etiology. A vitreous biopsy was done for DNA amplification using the multiplex polymerase chain reaction (PCR) technique. To identify the amplified DNA, we used a DNA chip (XCyton Diagnostics Pvt. Ltd., Bangalore, India; Fig. 1), containing complimentary sequences to “signature genes” of Toxoplasma gondii, Mycobacterium tuberculosis, M. chelonae, and M. fortuitum [Table 1]. We got a positive reaction for the B1 gene sequence of T. gondii [Fig. 1]. Subsequently, the enzyme-linked immunosorbent assay (ELISA) detected very high antitoxoplasma IgG levels. Oral steroids were stopped. We advised oral co-trimoxazole (960 mg twice daily) and a single dose of intravitreal clindamycin (1 mg/0.1 ml). This led to a sharp reduction in vitreous inflammation and an improvement in the visual acuity to 20/50 after 2 weeks. No focal lesions were seen in the fundus. There was no recurrence over the next 6 months of follow-up.

Bottom Line: Ltd., Bangalore, India).The enzyme-linked immunosorbent assay (ELISA) detected elevated serum antitoxoplasma IgG levels in both.They responded to the antitoxoplasma therapy with oral co-trimoxazole (and additional intravitreal clindamycin in patient 1), with no recurrence during follow-ups of 6 and 8 months, respectively.

View Article: PubMed Central - PubMed

Affiliation: Retina-Vitreous Service, LV Prasad Eye Institute, Bhubaneswar, Orissa, India. basu@lvpei.org

ABSTRACT
We report the use of DNA chip technology in the identification of Toxoplasma gondii as the etiological agent in two patients with recurrent intermediate uveitis (IU). Both patients had recurrent episodes of vitritis (with no focal retinochoroidal lesion) over varying time intervals and were diagnosed to have IU. The tuberculin test was negative in both. Blood counts, erythrocyte sedimentation rate, and serum angiotensin convertase enzyme levels were normal. In both cases, the vitreous fluid tested positive for the T. gondii DNA sequence by using a uveitis DNA chip (XCyton Pvt. Ltd., Bangalore, India). It contained complimentary sequences to "signature genes" of T. gondii, Mycobacterium tuberculosis, M. chelonae, and M. fortuitum. The enzyme-linked immunosorbent assay (ELISA) detected elevated serum antitoxoplasma IgG levels in both. They responded to the antitoxoplasma therapy with oral co-trimoxazole (and additional intravitreal clindamycin in patient 1), with no recurrence during follow-ups of 6 and 8 months, respectively.

Show MeSH
Related in: MedlinePlus