Toxoplasmosis

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Toxoplasmosis
Classification and external resources
DiseasesDB 13208


Disease Entity

Disease

Toxoplasmosis is the most common cause of infectious retinochroiditis in humans.

Etiology

The causative organism, Toxoplasma gondii, is a single-cell, obligate, intracellular protozoan parasite. Cats are the definitive host for T. gondii, however, humans and a wide range of mammals, birds, and reptiles, may also serve as intermediate hosts [1–3,5–10] T. gondii has three forms: (1) the oocyst (soil form), (2) the tachyzoite (active infectious form), and (3) the tissue cyst (latent form).

Epidemiology

T. gondii’s presence in nature is widespread, but human infections are not equally distributed around the world. It has been estimated that 1 billion peopl are infected worldwide.[X] Rates of infection are highest in tropical areas and relatively low in dry, arid areas and cold areas.[X] This likely reflects the environment which are most amenable to the organism's proliferation in the environment.

Risk Factors

Exposure to environments where the infectious organism is found, especially those frequented by felines.

General Pathology

A necrotizing retinitis occurs with vasculitis and destruction of the retina.

Pathophysiology

Infection with Toxoplasma gondii.


Diagnosis

Physical Examination

List of classic and atypical findings which have been reported.

Classic findings

  • White focal retinitis with overlying vitreous inflammation (“headlight in the fog”)
  • Accompanying nearby or adjacent pigmented retinochoroidal scar
  • Vitreous inflammation (mild, moderate, or severe )[3]
  • Secondary nongranulomatous iridocyclitis
  • Granulomatous and stellate keratic precipitates possible [5,6,54,55].
  • Inflammatory ocular hypertension 10% to 15% of cases [8,31,55].
  • Retinal vasculitis (typically near the focus of Retinochoroiditis),

Atypical findings which can accompany retinochoroiditis

  • Papillitis [30,38]
  • Neuroretinitis [30
  • Retrobulbar neuritis [19]
  • Scleritis [36,39]
  • Retinal detachment [68]
  • Punctate outer retinitis [29,31,34]
  • Branch retinal artery occlusion [69];
  • Frosted branch angiitis
  • Coats’-type response [49];
  • Fuchs’-like anterior uveitis [28,33,35,70]
  • Multifocal diffuse necrotizing retinitis [27]

Atypical findings which can exist in absence of retinochoroiditis

  • Retinal vasculitis [1,57]
  • Unilateral neuroretinitis [30] (optic disk edema, macular star)
  • Inflammation in absence of overt necrotizing retinitis [32].
  • Unilateral pigmentary retinopathy mimicking retinitis pigmentosa [37]

Recurrence

Recurrent lesions tend to occur at the margins of old scars, but they also can occur elsewhere in the fundus [3]. Gary’s recurrence article Although 40% of patients have evidence of bilateral infection in the form of retinochoroidal scars, simultaneous bilateral active disease is extremely rare in immunocompetent individuals.

Symptoms

Typical symptoms of active disease are floaters and blurred vision. Eye pain and redness if the patient has a secondary iritis.

Clinical diagnosis

Clinical evaluation and diagnosis is the most important part of diagnosing toxoplasmosis retinitis.

Diagnostic Evaluations

Because of the high prevalence of positive toxoplasma titers in many populations, the use of serology in the diagnosis is mainly limited to reassuring the clinician that toxoplasmosis should remain in the differential. If the IgG titers for toxoplasmosis are completely negative, down to a 1:1 dilution, then toxoplasmosis is completely ruled out in an immunocompetent person. It is possible that an immunosuppressed patient could have a completely negative immunoglobulin titers and have active ocular toxoplasmosis infection.

The development of polymerase chain reaction (PCR) has been very helpful for the diagnosis of atypical or difficult cases. Detection of T gondii DNA by PCR in both aqueous humor and vitreous fluid is both sensitive and specific.[45,61]

Differential diagnosis

Other forms of infectious or autoimmune retinopathy, including viral retinitis, Behcet's disease.

Management

Medical therapy

Systemic Pyrimethamine, sulfadiazine, and corticosteroids

This is the classic triple therapy used in the treatment of toxoplasmosis. In a survey of the American Uveitis Society this combination triple therapy was cited as the treatment of choice by 32% of respondents.[3,63]

Systemic Clindamycin

An additional 27% of American Uveitis society respondents added clindamycin to the previously mentioned therapy. In general, treatment is given until the inflammatory reaction begins to decrease and the retinal lesion shows signs of healing, which is usually 4 to 6 weeks.

Systemic Azythromycin

Rothova et al [64] reported successful treatment of ocular toxoplasmosis in immunocompetent patients with azythromicin alone

Systemic Bactrim

Intravitreal Clindamycin (+/- steroids)

Surgery

Surgical treatment is not indicated for treatment of toxoplasmosis infection.

Surgical treatment may be required for retinal detachements which occur as a complication of toxoplasmosis retinochoroiditis.

Another important consideration when considering surgery in a patient who has had toxoplasmosis, is the use of prophylactic antibiotic treatment to decrease the risk of recurrence of toxoplasmosis at the time of surgery.

Prognosis

Retinochoroiditis is the most frequent manifestation of congenital toxoplasmosis. In a study by Wallon et al, {Wallon, 2004 #432} despite anti-toxoplasmosis treatment in pregnant mothers with toxoplasmosis infection, 24% of children had at least one episode of retinitis during a median followup of six years. Of that group, 29% had at least 1 new event diagnosed up to 10 years after the first lesions were detected.For the children who had final visual acuity data 69% had normal vision and none had bilateral visual impairment.

Patient Education

Clinicians should be aware and should educate parents and older children with congenital infection that late-onset retinal lesions and relapse can occur many years after birth. They should also be reassured that risk of bilateral visual impairment appears to be low. Identifying activation or reactivation early and getting treated will give the best prognosis.

Additional Resources