Agriculture Reference
In-Depth Information
Other uncommon clinical presentations of OLM include optic disc inflammation (papillitis
or neuroretinitis), motile intraocular nematode (retina, vitreous body and anterior chamber),
keratitis and cataract.
The diagnosis of OLM is usually suggested by the presence of the clinical findings
mentioned above, but the detection of specific antibodies is required. However, serum
antibodies can often be undetectable (Sharkey & McKay, 1993), possibly due to the relatively
low parasite load in these infections (Schantz, 1989). Even low ELISA serum titres may be of
diagnostic value in OLM, but there is no consensus on the cut-off titres for diagnosis.
Specific antibodies can be also detected in the aqueous humor (AH). The intraocular
production of antibodies to
Toxocara
can be assessed by comparing serum and AH samples
obtained simultaneously from the same patients and calculating the Goldmann-Witmer
(GW) coefficient as: ([levels of specific IgG in AH/levels of specific IgG in serum]/[total IgG
in AH/total IgG in serum]). A GW coefficient > 3 indicates intraocular production of
specific antibodies (De Visser et al., 2008).
Sight-threatening ocular inflammation secondary to OLM requires aggressive anti-
inflammatory therapy, combined with albendazole (800 mg for adults and 400 mg for
children daily) over a 2-4 week period. Oral steroids (prednisone 0.5 mg/kg/day) are used
to reduce the inflammatory response induced by larvae. Surgical treatment may be required
for retinal detachment or intravitreal fibrovascular membrane proliferation.
7. Cutaneous larva migrans
CLM is a clinical entity caused in humans by larval migration of zoonotic hookworms,
mainly
Anc. braziliense
but also
Anc. caninum
. Less common clinical manifestations are
eosinophilic pneumonitis, localized myositis, folliculitis and erythema multiforme but eye
involvement is rarely reported. Human infection occurs when infective L3 larvae penetrate
the skin. The infection site may or may not present an erythematous popular or vesicular
rash.
The larvae do not undergo further molts in the human host, but as they migrate across in the
skin, at a rate of 2.7 mm per day, they leave an erythematous, serpiginous track. The
cutaneous lesions can last several weeks and may be severely pruritic, but eventually
resolved spontaneously. Secondary bacterial infection may result from scratching.
The most commonly affected sites are those in close contact with the soil (Araújo et al.,
2000). A recent case series of CLM in Brazil, for example, showed that cutaneous lesions are
more frequently observed on the feet (73.3%), buttocks (14.7%), genital and inguinal areas
(8.0%), legs (2.7%), and hands (1.3%) (Jackson et al., 2006). Other sites, such as the face
(Bouchad et al., 2000) and the scalp (Guimarães et al., 1999), are rarely affected. Clinical
diagnosis is reached based on the typical skin lesions, while biopsies have little diagnostic
value, showing an eosinophilic inflammatory infiltrate. Chemotherapy is seldom needed,
since larvae die out within a matter of weeks if left untreated, but oral albendazol (400-800
mg/day for 3-5 days), oral ivermectin (200 g/kg, single dose) or topical thiabendazole
(10% aqueous suspension four times a day) may be used.
Larval infection of humans with
Anc. ceylanicum
may occasionally give rise to adult worms
that inhabit the small intestine and can cause eosinophilic enteritis (Bowman et al., 2010). In
addition to cutaneous lesions,
Anc. caninum
has also been reported to cause eosinophilic
enteritis and may be a cause of diffuse unilateral subacute neuroretinitis in humans (Sabrosa
& de Souza, 2001).
