Latent Toxoplasmosis Essay

In latent toxoplasmosis, bradyzoites are present in the tissue as cysts. Individuals with latent toxoplasmosis are asymptomatic. Despite the lack of symptoms, it is important to keep in mind that a chronic, lifelong infection has been established. If an individual with latent infection becomes immunocompromised later in life, he or she may be at risk for disease reactivation and increased morbidity and mortality without appropriate treatment.18, 28

Acute, or primary, toxoplasmosis is caused by the invasion of tachyzoites into neural and muscle tissue. Acute toxoplasmosis is often asymptomatic in healthy individuals, although some patients may experience flu-like symptoms, such as fever, malaise, and myalgia. Signs and symptoms of acutely
infected immunocompromised patients may include altered mental status, blurred vision, headaches, lung disorders resembling pneumocystis pneumonia, poor coordination, seizures, and in rare cases, varicella-like lesions. Lymphadenopathy is the most common manifestation of acute toxoplasmosis. Swelling occurs primarily under the chin and in the neck, although swelling in the groin is also possible. It may occur at different times during the initial infection, persist for months, and/or recur independently post-treatment.

Cerebral toxoplasmosis is the acute infection of the brain and is most commonly seen in immunocompromised patients. Clinical manifestations include altered mental status, focal neurologic signs, headaches, intracranial hypertension, and seizures. Additionally, neural cyst formation may cause lesions along cerebrospinal fluid channels, resulting in hydrocephalus. Encephalitis is the most common manifestation of cerebral toxoplasmosis, especially in patients living with HIV/AIDS. Isolated cerebellar toxoplasmosis has also been observed in some patients, although its occurrence is rare. Signs and symptoms of cerebellar toxoplasmosis include clipped speech, gait ataxia, and poor coordination.

In congenital toxoplasmosis, tachyzoites invade the placenta and, subsequently, infect the fetus.
The risk of transmission is lowest in the first trimester (10 - 15%) increases as the pregnancy progresses (risk in third trimester approximately 60 - 90%); however, first trimester infection is associated with increased fetal neurological dysfunction leading to physical and mental disabilities. Congenital toxoplasmosis is also associated with increased miscarriages and stillbirths. Clinical manifestations include cerebral calcifications, chorioretinitis and other forms of ocular inflammation, deafness, hydrocephalus, psychomotor retardation, seizures, and microcephaly due to the pathogen’s interference with normal brain development. Additionally, the infant may be born with signs of systemic infection, such as fever, hepatosplenomegaly, and rash. Congenitally infected infants may also show no signs or symptoms of toxoplasmosis at birth but may develop them later in life. Conversely, infants displaying signs and symptoms of acute infection at birth may become latent and asymptomatic. It should be noted that mothers with latent infection cannot transmit the infection to the fetus, as bradyzoites are not transmitted
transplacentally.

Ocular toxoplasmosis is caused by bradyzoite cyst formation in ocular tissue, such as the retina. Clinical manifestations include choreoretinitis, which is most commonly associated with congenital toxoplasmosis, neuroretinitis, retinal scarring leading to scotoma, strabismus, and uveitis/panuveitis. Severe ocular lesions may cause permanent blindness.