TOXOCARA Toxocariasis is caused by Toxocara canis and, less frequently, Toxocara catis,which are intestinal nematodes (roundworms) found

in dogs and cats, respectively. In humans, toxocariasis is considered an aberrant infection because humans are incidental hosts, and the parasites cannot completely mature in the human body. Instead, the invasive larvae migrate for months through different organs until they are overcome by the human inflammatory reaction and die. The larvae can survive in tissues for at least 9 years and, possibly, for the life of the host. Three clinical forms of toxocariasis are traditionally described these includevisceral larva migrans (!"#), ocular larva migrans ($"#), and covert toxocariasis. %umerous disease manifestations have also been attributed to these parasites. &iagnosis is based on serologic findings. 'olymerase chain reaction ('()) has been introduced as a diagnostic tool. *xamination of stools has no role in the evaluation of toxocariasis. +hether or not the infection should be treated and, if so, when and how it should be treated is controversial. #ebenda,ole, thiabenda,ole, albenda,ole, and diethylcarbama,ine, among others, are agents used in the treatment. (orticosteroids also have a significant role in therapy. -ee the images below.

&iagram of the Toxocara canis life cycle image. CLINICAL FORMS

The . clinical forms of toxocariasis that are traditionally described include the following/

Visceral larva migrans (VLM)

0eneral/ The classic !"# syndrome consists of episodes of fever, coughing and whee,ing, anemia, eosinophilia, hepatomegaly, and positive Toxocara titers. The patient usually has malaise, asthenia, and vague abdominal symptoms. !"# is diagnosed mainly in children

aged 123 years. -ystemic disease rarely results in ocular disease. #any organs can be involved in !"#. &ermatologic -4in lesions, such as urticaria and nodules, have been described. Toxocariasis can cause chronic idiopathic urticaria, especially when it is associated with eosinophilia. +ell syndrome is an eosinophilic cellulitis of un4nown origin. 5 report described 6 cases with clinical and histologic features of +ell syndrome with positive anti2 Toxocara titers. 7118 %ot only did the symptoms respond to treatment with albenda,ole, but the antibody titer also normali,ed. 9owever, studies of toxocariasis as the cause of chronic urticaria are inconsistent. 5fter an initial study demonstrating T canis antibodies in :;< of patients with chronic urticaria (n=;1), compared with 61< in controls (n=>1), others found a seroprevalence of 6?< in chronic urticaria (n=16>) versus 1.< in controls (n=6.:), a seroprevalence of >< in chronic urticaria (n=11?), a seroprevalence of 1.< in children with the condition, and a seroprevalence of .?< in controls.7168 'ulmonary/ +hee,ing is a common sign of !"#. 'rogression to eosinophilic pneumonia and respiratory failure has been reported. Isolated reports describe diffuse noncavitating pulmonary nodules and pleural effusions. 5 case report that described a :;2year2old previously healthy male with a 62wee4 history of fever and night sweats weight loss eosinophilia high erythrocyte sedimentation rate and abnormal chest radiograph findings that revealed bilateral hilar and mediastinal lymphadenopathy and discrete bilateral pleurisy demonstrates that, in its acute presentation, !"# can be confused with lymphoma. 71.8 9epatic and lymphatic/ !"# is usually associated with hepatomegaly. +hen histologic results are available, they usually reveal granulomatous hepatitis. 'yogenic liver abscess concomitant with Toxocara hepatitis has also been reported. The spleen is enlarged less often than is the liver. 0enerali,ed lymphadenopathy is an infrequent manifestation of toxocariasis. 5 6@2month2old boy in whom lymphedema was the main clinical manifestation of toxocariasis has been reported.71@8 Two cases of isolated eosinophilic ascites due to Toxocarahave been reported.
71;8

)heumatologic/ Arequently, manifestations such as arthralgias, monoarthritis, migratory cutaneous lesions, and small2vessel vasculitis coincidentally occur with !"#. $ne case report describes 9enoch2-chBnlein purpura in a 132year2old male in association with anti2 Toxocara immunoglobulin 0 (Ig0) and Ig* that spontaneously resolved. 71:8 (ardiac/ 5lthough infrequently involved, all layers of the heart can be affected. The most common presentation is myocarditis. 5mong the unusual manifestations described in the literature are "oeffler endomyocarditis7138 and pericardial tamponade.71>8 (%-/ Toxocariasis is one of the causes of eosinophilic meningitis, a form of aseptic meningitis in which the +C(s in the cerebrospinal fluid mainly consist of eosinophils. $ther less common entities described in association with !"# are encephalitis, 7198 larval invasion of the brain parenchyma, solitary mass lesions that cause sei,ures, static encephalopathy, arachnoiditis, and spinal cord lesions.76?8 Ocular larva migrans (OLM) 7618 This refers to eye (usually retinal) involvement during Toxocara infection. Cy chance, the larvae migrate to the eyes, where they induce an eosinophilic inflammatory reaction. #ost of the time, it is unilateral. $cular toxocariasis is an uncommon disease that occurs primarily in young patients. 7668 It affects females and males with approximately equal frequency. #ost patients report a history of recent exposure to puppies or 4ittens. The disease is unilateral in most cases, with mild2to2 moderate intermediate or diffuse inflammation. 'atients with $"# are older than those with !"#. They lac4 systemic symptoms, such as fever, cough, and abdominal pain, and do not have significant eosinophilia. $"# manifests as a loss of visual acuity, leu4ocoria, strabismus, and eye pain. It can be confused with a retinoblastoma.

 o o o o o

$ther presentations of $"# include endophthalmitis with secondary retinal detachment, uveitis, vitreous abscess, and optic neuritis. 5mong patients with uveitis, toxocariasis is relatively uncommon. In a review of 6,1>; patients with uveitis, toxocariasis was the etiology in 66 patients (1<). 76.8 The mean patient age was 1:.; years. Inflammation was unilateral in 9?.9<. The most common symptoms caused by Toxocara uveitis were blurred vision in 1> eyes (3;<), pain or photophobia in > eyes (....<), and floaters in @ eyes (1:.3<). The presentation was of a granuloma in the peripheral retina in ;?< of cases, granuloma in the macula in 6;< of cases, and moderate2to2severe vitreous inflammation, mimic4ing endophthalmitis in 6;< of cases. -erum *"I-5 for antibodies to Toxocara was positive in 11 patients (;?<), negative in > patients (.:.@<), and un4nown in . patients (1..:<). The @ patients tested for vitreous or aqueous *"I-5 showed positive titers (6 had negative serologic titers), confirming that seronegativity does not exclude the diagnosis. The primary causes of vision loss were vitreitis, cystoid macular edema, and traction retinal detachment.

Covert toxocariasis
#ost cases of toxocariasis are asymptomatic. The term covert toxocariasis refers to a less specific syndrome that was recogni,ed with the wider use of serodiagnostic assays for Toxocara infection. Dsual symptoms are chronic or recurrent abdominal pain, hepatomegaly, coughing, whee,ing, sleep disturbances, headache, malaise, anorexia, and failure to thrive, among others. *osinophilia is less frequent and less pronounced with this form than with !"# and Toxocara antibody titers are lower.

Clinical mani estations

The clinical manifestations of T canis infections depend on the following factors/ %umber of infective eggs &uration of infection 5natomic location of the larvae 9ost immune response

Pathophysiology
#ost frequently, human toxocariasis is caused by T canis, a canine roundworm. 5dult T canis female worms are usually found in young puppies and lactating female dogs. The adult T canis female worms can excrete as many as 6??,??? eggs per day. These eggs need several wee4s of optimal environmental conditions (1?2.;E(, high soil humidity) to develop from noninfective unembryonated forms to infective embryonated eggs. The embryonated eggs are resistant to free,ing, moisture, and extreme p9 levels. +hen a dog ingests the infective eggs, the larvae hatch in the small intestine, penetrate the intestinal wall, and gain access to the blood and lymphatic circulation. The larvae invade the liver, lungs, and other tissues. In most dogs, the larval maturation process is arrested in most tissues, but in a pregnant female, T canis resumes development and migrates across the placenta, infecting the fetus. 5fter the birth of the puppies, the larvae continue their maturation process, migrating from the lungs to the 0I tract via the trachea they achieve their mature forms in the puppiesF intestinal tracts. Aemale dogs then become reinfected while caring for their puppies. The main sources of eggs, therefore, are puppies younger than . months and lactating female dogs. 9umans are paratenic hosts for T canis. 'aratenic hosts are transport hosts in which the larvae never develop into adult worms. The infection is acquired by ingesting T canis embryonated eggs.

-ources of these eggs include areas where dogs defecate, such as par4s. 5s much as 6?2.?< of soil samples from public par4s and childrenFs sandboxes are contaminated with Toxocara eggs. Infections acquired by ingestion of raw snails and raw lamb have also been reported. The cat roundworm, T catis, has a life cycle similar to that of T canis except that vertical transmission is due to lactation more than transplacental transmission. $ne report documents @ cases of adult T catis intestinal infection in children. 9owever, in most cases, humans are paratenic hosts. T catis causes fewer cases of human infection than T canis, probably because of the defecation patterns of cats, which ma4e environmental infestation less frequent. Tissue damage is due to the host inflammatory reaction more than the infection itself. The larvae produce glycosylated proteins, usually referred to as Toxocaraexcretory secretory antigens. These antigens induce a Th62type (&@G cellular immune response characteri,ed by the production of interleu4in @ that promotes the switching of C2cell isotypes to the production of immunoglobulin * (Ig*) and interleu4in ;. These, in turn, promote eosinophil differentiation and vascular adhesion. 5lthough Toxocara organisms are the most common causes of !"#, case reports have noted other ,oonotic nematodes that cause !"#, including Ascaris suum,718Baylisascaris procyonis (raccoon ascarid), and Lagochilascaris minor (opossum ascarid).