Toxoplasmosis is azoonotic infection in humans caused by the protozoal intracellularparasiteToxoplasmagondii,sporozoan protozoa in the genus of Toxoplasma. Cats are the primaryhosts, while humans and other mammals serve as intermediate hosts.Infection withTgondii iscommon among humans, and it is estimated that one third of theworld's population has been exposed. The seroprevalence varies widelyin different regions and depends on socio-economic status,environmental factors and meat-cooking habits.1 Indian studies of prevalence of toxoplasmosis reveal a wide variationand one study reported prevalence, as high as 77% in women ofreproductive age group. The average prevalence among Indian pregnantwomen is 7.7%. There is no published data on the disease prevalencein Kerala. A pilot study done in Kozhikode district revealed asero-prevalence of 27.16%.
There is a closerelationship between the incidence of toxoplasmosis and theseroprevalence of toxoplasma antibodies within a population.Infection with the parasite occurs among all age groups and as aconsequence, serological evidence of the infection increases withincreasing age. Most infections are however sub clinical and diseasetypically becomes apparent only as a congenitally acquired infectionand in patients with significant immunodeficiency such as in acquiredimmunodeficiency syndrome (AIDS).
The protozoan wasfirst discovered by Nicolle and Manceaux in 1908. He first isolatedit from African rodents Ctenodactylusgundii. It was identified as anagent of infectious disease in 1932. In 1983 toxoplasmosis was morewidely recorded as a cause of morbidity in immune deficient patientsincluding AIDS and idiopathic CD4 cytopenia syndrome.
Toxoplasma gondii occurs in 3 stages.
Humans acquireinfectionvia eating undercooked or raw meat infected with tissue cysts,via ingestionof food or water contaminated with infected cat feces carryingsporulated oocysts. Maternal to fetus transmission can also occur.Rare cases of individuals becoming infected through bloodtransfusions or organ transplantation have also been reported.
Sporozoits fromoocysts and bradyzoites from tissue cysts invade intestinal mucosaand in epithelial cells multiply as tachyzoites .Tachyzoites spreadto mesenteric lymph nodes and thenvia blood stream and lymphatics reach organs such as brain, eye, liver,spleen, heart, skeletal muscle, lymph nodes and placenta of pregnantmother. Focal areas of necrosis develop in these organs.2
With the developmentof immunity tachyzoites are destroyed and acute infection resolves.Some of the tachyzoites may still persist and develop into tissuecysts containing bradyzoites, which remain viable for years. Whenthere is suppression of immune system, infection is reactivated.
Development of bothhumoral and cellular immunity alter the course of toxoplasmainfection and its clinical manifestations. Humoral immunity ischaracterized by the production of specific circulating antibodies,both IgM and IgG. Toxoplasma specific Ig M antibodies appear first,hence its detection is suggestive of an acute infection. IgGantibodies appear late and persist, and is suggestive of a chronicinfection. Cell mediated immunity through activated macrophages andmonocytes is suggested to play an important role in conferringresistance to re-infection as well as in the development of initialresistance in toxoplasmosis in co-operation with humoral antibodies.This stage is associated with the disappearance of tachyzoites fromvarious tissues, especially from extra neural tissues and formationof tissue cysts. The tachyzoites may persist in the central nervoussystem and in the eye due to the absence of circulating antibodies inthe tissues.
In humans,asymptomatic or benign toxoplasmosis is the rule in immunocompetentpatients. Eighty to ninety percent ofTgondii infections in immunocompetent hosts are asymptomatic. Generally, whenacute infection is symptomatic, manifestations include symmetricfever, nonspecific rash and lymphadenopathy. The most common presentation of symptomatic postnatally acquiredtoxoplasmosis in immunocompetent patients is painless cervicaladenopathy. When fever and lymphnode enlargement persist, moreoften it ends in biopsy studies and the common histologic picture isnecrosis with granulomas. In majority of cases the clinical courseis benign and symptoms and signs resolve within a few weeks. However,severe manifestations of infection, including chorioretinitis, canoccur in some immunocompetent hosts.3
Chorioretinitis or oculartoxoplasmosis is a relatively common manifestation ofTgondii infection. Ocular toxoplasmosis occurs when cysts deposited in ornear the retina become active, producing tachyzoites. Focalnecrotizing retinitis is the characteristic lesion, but retinal scarsfrom prior reactivation are typically present. Clinical presentationusually is with eye pain and decreased visual acuity. Adults who hadacquired disease in infancy usually present with bilateral eyeinvolvement. Adults with acute infection generally present withunilateral ocular involvement.4
Figure 1. Whitefocal lesions with inflammation of vitreous humor (the classic‘headlight in the fog’ appearance) seen onophthalmoscopic examination in a patient with ocular toxoplasmosis.
Depending on thelocation and severity of toxoplasmic chorioretinitis, infection canresult in permanent retinal scarring and loss of visual acuity.Recurrent episodes are common, resulting in multiple areas of retinalscarring and functional loss.
Studies have shownthat in high endemic areas there is an association between a typicalgenotype and severe toxoplasmosis acquired by immune competentadults. It has also been recently reported that an unusual abundanceof atypical strains in the environment is associated with humanocular toxoplasmosis and with severe forms of congenitaltoxoplasmosis.
Approximately 10-20%of pregnant women infected withTgondii have clinical symptoms of the disease. The most common signs ofinfection are lymphadenopathy and fever. If the mother was infectedprior to pregnancy, there is virtually no risk of fetal infection, aslong as she remains immunocompetent. If the infection is acquiredduring the pregnancy, there is risk of infection to the fetus. Therate of trans-placental infection has been estimated to be 50% foruntreated mothers and 25% for treated mothers.
The rate of fetalinfection varies with trimester with 10-25% of infections occurringin the first trimester, 30% in the second trimester, and 50% in thethird trimester. Infection during the first or second trimestersappears to be most severe. The clinical features of congenitallyacquiredTgondii infection include chorioretinitis, blindness, seizures, microcephaly,anemia, and encephalitis. Infections acquired during the thirdtrimester are usually subclinical; however, clinical disease maystill occur later in life. 75% of infants congenitally infected withTgondii manifest no symptoms, 14% had evidence of chorioretinitis and 9%demonstrate signs of CNS involvement.