•Ocular TB (largely choroidal or retinal) may be seen in 1.4–60% of patients with systemic TB.

•Tuberculosis is the etiological agent in 0.2– 7.9% of patients with all types of intraocular inflammation.

•The HIV epidemic has led to an increase in ocular TB with between 2.8% and 23.5% of HIV/TB coinfections demonstrating ocular lesions.

•The diagnosis of ocular TB is frequently difficult as its manifestations are protean, specimen quantities are limited and often difficult to obtain.

•Ocular evaluation includes clinical examination and collection of specimens from aqueous humor, vitreous humor, uveal or retinal tissue, or subretinal fluid. Processing includes microscopy, culture, or PCR techniques for definitive proof.

•Systemic evaluation includes chest radiography (CT preferred), abdominal radiography, Mantoux testing, and collection/processing of sputum, lymph nodes, and bone marrow as necessary.

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Introduction

Toxoplasmosis is endemic throughout most of the world and affects a large proportion of the adult population [1, 2]. However, the seroprevalence of anti–Toxoplasma gondii differs from country to country [3]. It is estimated, for example, that at least 10% of adults in northern temperate countries and more than half of adults in Mediterranean and tropical regions have been infected [4]. Toxoplasma gondii is a ubiquitous, obligate intracellular protozoan and is considered to be the most common cause of infective retinitis in immunocompetent humans. A number of factors related to regional climate, hygiene, and dietary habits have been identified [5–7].

Toxoplasma gondii was discovered independently by two investigators in 1908. Alfonso Splendore in Brazil identified the organism in laboratory rabbits, while Charles Nicolle and

Louis Manceaux in Tunis observed the organism in the North African rodent Ctenodactylus gondii. Nicolle and Manceaux named the parasite

Toxoplasma gondii – Toxoplasma from the Greek word toxon, meaning arc, describing the small crescent shape of the parasites, and gondii from the animal in which it was found (Fig. 6.1) [8]. The first description of congenital toxoplasmosis (CT) with ocular involvement is attributed to Jankû (Prague 1923), who reported an 11-month- old infant with hydrocephalus, microphthalmia, and a retinal “coloboma” in the macular region; [8, 9] and the first photographic documentation of ocular toxoplasmosis was made in Brazil by Belfort Mattos in 1933 [8].

The course of systemic disease in immunocompetent adults is usually asymptomatic and self-limiting. As soon as infection has occurred, the parasite forms latent cysts in many organs, including the retina, that can reactivate years after the initial infection, giving rise to acute retinochoroiditis and, subsequently, the formation

Fig. 6.1 (a) Gross appearance of a retinal scar in an enucleated eye bank eye with toxoplasmic retinochoroiditis (TRC). (b) Histologic section shows toxoplasmic cysts seen in the neural retina. Note the eccentrically

located tiny nuclei in the cysts. (c) Retina cyst in TRC visualized with electron microscopy (EM). (d) Tachyzoites in lower and higher magnification (with EM; insert)