Toxoplasmosis, a parasitic infection that is widespread throughout the world, is caused by Toxoplasma gondii, an intracellular protozoan parasite. Toxoplasmosis refers to clinical or pathological manifestations of a T. gondii infection, which occurs when the protozoa invade the cells but does not usually cause symptoms in patients with normal immune systems. Conversion of chronic T. gondii infection into active toxoplasmosis occurs primarily in severely immunocompromised hosts.
There are three forms of T. gondii: oocysts, tissue cysts, and tachyzoites. Oocysts are ovalshaped and have been found only in cats; this form of T. gondii can live outside of the host in a warm, moist environment for over a year and therefore may play a major role in transmission of T. gondii infection. Tissue cysts can contain up to 3000 organisms. Tachyzoites are the crescentshaped invasive form of T. gondii: This form is seen in acute T. gondii infection and invades all mammalian cells except non-nucleated red blood cells.
Toxoplasmosis is the most common cause of intraocular inflammation. When the organism reaches the eye via the circulation, an infection may begin in the retina, particularly in immunocompromised individuals. Ultimately, a cyst forms, and because the cyst is resistant to the host’s defenses, a chronic infection develops. When the person’s immune function declines, the cyst wall ruptures and organisms are released into the retina. Other organs can be infected by the organism as well. These organs include the gray and white matter of the brain, the alveolar lining of the lungs, the heart, and the skeletal muscles. Acquired immunodeficiency symdrome (AIDS)–associated Toxoplasma encephalitis can result from reactivation of a chronic infection, and congenital toxoplasmosis may be associated with many fetal anomalies such as microcephaly, microphthalmia, hydranencephaly, and hydrocephalus.
The prevalence of a T. gondii infection seems to be highest in warm, humid climates at lower altitudes; it occurs less frequently in areas at the extremes of temperatures and at high altitudes. The two major routes of T. gondii transmission to humans are oral and congenital. Tissue cysts are found in a large percentage of meat used for human consumption, especially in lamb and pork. Vegetables and other food products contain a large number of oocysts. Exposure to cat feces also plays a major role in transmission of infection.
Nursing care plan assessment and physical examination
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 immunocompromised 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 immunocompetent 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.
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 lymphadenopathy, 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 finding
in immunocompromised patients with toxoplasmosis. During the management of patients 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.
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.
Nursing care plan primary nursing diagnosis: Sensory-perceptual alterations (visual and auditory) related to inflammation and damage of ocular nerves and tissues and the CNS.
Nursing care plan intervention and treatment plan
The challenge in treating toxoplasmosis is that T. gondii protozoa are resistant to many antimicrobial agents, and they typically invade tissue that is difficult for many drugs to reach. The ideal duration for pharmacotherapy has not been established. Acute acquired toxoplasmosis should be treated only if the patient is extremely symptomatic or severely immunodeficient. The duration of treatment for immunosuppressed patients depends largely on the duration of the immunocompromised state. Patients with permanent immunocompromised states, such as AIDS patients, usually need prophylactic antitoxoplasmosis therapy for the rest of their lives. Because the immune-inflammatory response is thought to be responsible for the pathological processes in ocular toxoplasmosis, glucocorticoid steroids may be ordered in some situations. Steroids have been shown to decrease retinochoroiditis and improve vision but cause further decreased immune function in the immunocompromised patient.
Patients with toxoplasmosis do not require any special precautions to prevent the spread of infection; universal precautions are sufficient. There is no evidence that toxoplasmosis can be spread from person to person. The sensory and neurological deficits that are associated with acute disseminated toxoplasmosis present the greatest nursing challenges. Provide adequate safety measures as indicated: side rails up, bed location where the patient can be closely monitored, padding of side rails, and assistance with ambulation or activities of daily living. Reorient the patient as often as necessary, provide opportunities for undisturbed sleep, and ensure appropriate amounts of sensory stimulation. Have the patient talk about topics of interest and importance to him or her, such as hobbies, family, occupation, or current sports and news. Encourage family members to bring pictures and other items from home that help the patient focus on pleasant memories. Institute active or passive range-of-motion exercises to maintain
neuromuscular function and prevent contractures. Initiate seizure precautions for patients with suspected brain involvement.
Because toxoplasmosis can affect virtually every tissue in the body, the patient often experiences pain and nausea. Choice of analgesic and antinausea agents requires close consultation with the physician, taking into consideration actual or potential neurological alterations. Nonpharmacologic pain relief methods can be instituted to augment the effect of analgesics, such
as relaxation techniques, frequent repositioning to level of comfort, soothing music, and massage therapy. If vision is impaired, the patient needs assistance with activities of daily living. Everyone entering the room should identify themselves by name. Referral to social work services or community organizations for the blind may be indicated if ocular involvement is
severe.
Nursing care plan discharge and home health care guidelines
Teach the patient and family about the medications. Pyrimethamine can cause folic acid deficiency. The patient should report bleeding, bruising, visual changes, and feelings of fatigue. Folic acid supplements may be recommended by the physician. Pyrimethamine should be taken just before or after meals to minimize gastric distress. Sulfadiazine can cause decreased white blood cell count, cause fever and rash, and lead to crystals in the urine; it should be taken with a full glass of water, and daily fluid intake should be at least 2000 mL. Sulfadiazine causes increased sensitivity to the sun; the patient should avoid prolonged sun exposure and wear sunscreen when going outdoors.
If the patient has AIDS or some other condition that causes a permanent immunocompromised state, emphasize that these drugs probably are needed throughout the patient’s lifetime. If the patient has neuromuscular defects, teach family members the exercises needed to maintain muscle strength and joint range of motion. If the patient has neurological involvement and is not on antiseizure medications, teach the patient and significant others how to recognize a seizure and what to do if it occurs. Discuss the long-term prognosis for acquired toxoplasmosis; assist the patient and family in drawing up an appropriate plan of action.
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