TOXOPLASMOSIS


GENERAL FEATURES


• Toxoplasmosis is a parasitic disease caused by the protozoa Toxoplasma gondii that intracellularly infects body tissues and fluids.


• The cat serves as the definitive host and transmits the protozoa through its feces. Humans consume water or food that has been directly contaminated, or they consume poorly cooked meat from previously infected mammals.


• T gondii can also be transmitted transplacentally (but only when the mother is acutely infected during the pregnancy) or, rarely, through organ transplantation.


• Infections can be acute (active), chronic (inactive), or reactivated.


• Prevalence correlates with the eating and hygiene habits of a population.


• Congenital infection, acquired only through acute maternal infection, may result in spontaneous abortion, stillbirth, or neonatal disease with a wide variety of manifestations including neurologic and ophthalmic disorders.


CLINICAL ASSESSMENT


• History and physical examination


–Most immunocompetent patients will be asymptomatic, but some will present with nonspecific malaise that may resemble mononucleosis. Nontender cervical or occipital lymphadenopathy is the most common finding in immunocompetent patients.


–Patients who have had previous infection may experience a reactivation of the infection when they enter an immunocompromised state. 


–HIV is a significant contributor to symptomatic toxoplasmosis in the United States.


–Immunocompromised patients may present with signs and symptoms ranging from pneumonia to full-blown sepsis. 


–Abnormal neurologic findings such as hemiparesis and speech abnormalities are common secondary to CNS lesions, especially in those with concomitant HIV infection.


–Patients of all immune states can acquire retinochoroiditis. It can manifest in infants and adults and in acute or reactivated infections. Patients with retinochoroiditis may complain of eye pain, photophobia, and visual changes.


–Funduscopic examination may reveal white retinal lesions that appear foggy due to overlying inflammation in the vitreous fluid ("headlight in the fog" lesion).


DIAGNOSIS


• Tests for IgG and IgM antibodies should be ordered in immunocompetent patients. A positive IgG finding can indicate chronic disease while a positive IgM finding can indicate acute disease.


• Acute infection can be diagnosed by isolating T gondii from tissue 
or body fluids. Inoculation of tissue culture or mice can aid in identification.


• If the patient is immunocompromised, polymerase chain reaction (PCR) can be performed on any affected fluid or tissue to detect 
T gondii DNA. 


• Congenital infection can be determined prenatally through PCR of amniotic fluid. Acute infection should be diagnosed in the mother first.


• Retinochoroiditis can be diagnosed through PCR of vitreous fluid.


• Although it cannot show the cause of the lesion, MRI can help to determine the presence of possible brain lesions in patients with neurologic changes.


TREATMENT


• Treatment is indicated in pregnant patients with acute infection and in immunocompromised patients with reactivated infection. Immunocompetent patients with either acute or chronic infection or retinochoroiditis generally do not require treatment.


• The combination of pyrimethamine (Daraprim), sulfadiazine (Microsulfon), and folinic acid (leucovorin) is standard treatment.


• Prophylactic treatment with trimethoprim-sulfamethoxazole (Bactrim, Septra, Sulfatrim, generics) is indicated in asymptomatic immunocompromised patients who have positive IgG test results. It is also indicated for all HIV-positive patients who are seropositive for T gondii and have a CD4 count of <100 cells/μL.


• Prevention is through thoroughly cooking meat and good hygiene.