Assessment

HISTORY. Signs of low-grade T. gondii infection include fever of unknown origin, asymptomatic lymph node enlargement, malaise, headache, sore throat, rash, and muscle soreness. Question mothers of infants about potential exposure or manifestations of T. gondii infection that may have occurred during pregnancy. Explore the presence of conditions that cause an immunocom-promised state, such as AIDS, organ transplantation accompanied by immunosuppressive therapy, cancer chemotherapy, and hematologic malignancies.

If you suspect congenital toxoplasmosis, which is transmitted in utero from mother to fetus, ask the parent(s) to describe any central nervous system (CNS) or ocular dysfunction. Clinical manifestations may include microcephalus, hydrocephalus, strabismus, cataracts, glaucoma, deafness, or psychomotor retardation. The term acquired toxoplasmosis is reserved for immuno-competent individuals who have developed clinical manifestations in response to acute infection. Ask about enlarged lymph nodes; a rash; or problems with the heart, liver, lungs, brain, or muscles. Because ocular toxoplasmosis occurs in both acquired and congenital toxoplasmosis, ask the patient if she or he has experienced blurred vision, pain, photophobia, and visual impairment.

PHYSICAL EXAMINATION. In infants with congenital toxoplasmosis, you may note changes in the shape of the head denoting microcephalus or hydrocephalus, or you may find jaundice and a rash. When you palpate the infant's abdomen, you may feel an enlarged liver or spleen. There may also be signs of myocarditis, pneumonitis, and lymphadenopathy (enlarged lymph nodes).

In patients with acquired toxoplasmosis, the most common finding is asymptomatic lym-phadenopathy, either confined to a single area or region or generalized. Usually, the lymph nodes normalize within a few weeks, but the problem may recur over several months. You may be able to see a rash and palpate an enlarged liver and spleen. Some patients also have signs of dysfunction of the organ or tissue involved (heart, liver, lungs, brain, or muscle).

Ocular toxoplasmosis, which occurs in both acquired and congenital toxoplasmosis, typically causes a lesion on the retina that leads to inflammation of the retina and choroid (retinochoroiditis). An ophthalmoscopic examination reveals patches of yellow-white, cottonlike lesions on the retina. The area around the lesions is usually engorged with blood. Acute toxoplasmosis in the immunocompromised patient is associated with a unique set of clinical manifestations. The patient may have any of the signs and symptoms seen in patients with normal immunity but is more likely to have serious organ involvement as well. More than 50% of these patients have manifestations of CNS involvement, such as altered consciousness, motor impairment, neurological deficits, and seizures. These findings indicate a large T. gondii brain abscess, or meningoencephalitis. Severe myocarditis and pneumonitis are also common findings in immunocompromised patients with toxoplasmosis. During the management of patients

904 Toxoplasmosis with acute neurological changes, assess the neurological status at least hourly. Include assessments of orientation, memory, and thought processes; the strength and motion of the extremities; sensory alterations; pupil response; and the patient's speech, emotional response, and behaviors.

PSYCHOSOCIAL. Death is a real possibility in toxoplasmosis patients with immune dysfunction. Fear of death and feelings of despair or hopelessness may evolve; patients and families should be encouraged to discuss these openly. Mothers of infants with congenital toxoplasmosis may experience feelings of guilt because of their transmission of the infection.

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