Ocular parasitic infections and geographical distribution
Eyes are said to be the windows of body, by which this beautiful world is visualized. Human eye has a unique structure and is vulnerable to numerous infections. Whenever anatomical structures are breached, host defenses come into play, but if infection is severe and not treated timely, it could lead to visual impairment or blindness. Parasitic infections are considered, the significant causes of ophthalmic diseases worldwide. In this chapter, an overview of ocular parasitic infections (OPI) is detailed out, with an initial brief introduction followed by description of anatomy of the human eye and various defense mechanisms to provide better understanding of the parasitic infections affecting different parts of human eye. The last part includes individual details of various human ocular parasitic infections.
- parasitic infections
The ocular parasitic infections (OPI) are considered significant causes of ocular pathologies worldwide . The common protozoal parasites primarily infecting the ocular tissue(s) are
Ocular parasitic infections have been widely reported from different geographical areas (Table 1), mainly depending on the endemicity of the parasite(s). The prevalence depends primarily on the geographical distribution of the parasite, socioeconomic environment and immune status of the patient. The common modes of infection are direct contact (blepharoconjunctivitis caused by
Adult and/or larval stages of the parasites may reside in human ocular tissues externally or in the ocular globe. The clinical symptoms and signs vary, depending on the etiological agent and the ocular tissue/part involved. However, local defense mechanisms and host immune responses play role in establishing the infection. The pathology in the eye can occur due to direct damage by the infecting pathogen, indirectly by toxic products, immune mediated or ectopic localization by ectoparasites. The clinical diagnosis usually mimics other pathologies due to numerous etiologies both infectious and non-infectious, which can cause conjunctivitis, keratitis, uveitis and endopthalmitis . Thus, a high index of clinician suspicion is required for infective parasite etiology in patients having inflammation in the eye. In addition, eye can be involved in various systemic disorders and thorough ocular examination along with history of travel to the endemic area, risk factors and other associated medical illness that help in establishing the preliminary diagnosis. However, confirmatory diagnosis is usually achieved by direct demonstration of parasite in clinical samples and/or pathological changes observed by either slit lamp or biopsy examination [1, 8, 27, 28]. The antigen and antibody detection in ocular fluids and/or serum usually substantiates the clinical diagnosis in few parasitic infections (Toxoplasmosis, malaria, leishmaniasis, ocular gnathostomiasis, cysticercosis, toxocariasis, echinococcosis) [1, 10, 29, 30]. Molecular techniques including detection of parasite DNA by polymerase chain reaction (PCR) have added new dimensions in the diagnosis and species identification [31–36]. The treatment of choice is mostly surgical excision, while in few infections, medical treatment is usually advised either in conjunction with surgical procedure (onchocerciasis, dirofilariasis , cysticercosis , echinococcosis , myiasis, infections due to ticks and mites) or for inoperable patients. Although surgical excision is usually reserved for worms that are large, it is also recommended for space-occupying lesions of the orbit. Drug resistance is posing problem for the effective medical treatment, thus necessitating the discovery of new antiparasitic drugs . Prevention and control measures differ in various infections and usually include proper health education and awareness of various risk factors. The various experimental animal models for few of the ocular infections have been successfully established to study the pathogenic mechanisms, drug efficacy and local immune responses [40, 41].
Although issues mainly are the timely diagnosis and treatment, yet many challenges need to be considered/addressed.
Diagrammatic representation of human eye depicting significant ocular parasitic infections is shown in Figure 1.
The eye balls along with extraocular muscles, nerves, blood vessels and fat are situated in the bony cavities known as orbits. The periosteal covering of the bony orbit fuses with orbital septum and duramater. Abscess due to infectious agent can localize in the space beneath the periostium. The paranasal sinuses are separated from it by the floor, medial wall and roof of the orbit and may act as the source of orbital infection. Lamina papyracea are the thinnest bony walls, which separate orbit from ethmoidal sinuses. Thus, any breach in it causes the ingress of sinus microbiota to orbital tissue leading to infection. Orbital cellulitis can also be caused by direct extension of the infection from the ethmoidal sinuses to the orbital cavity. The lateral wall of the sphenoidal sinus constitutes the medial wall of the optic canal and infection of the former can percolate to the latter causing optic nerve damage and visual loss. There are various apertures present in the orbital cavity, which provides the route of communication with the adjacent structures. The superior and inferior orbital fissures, the lacrimal fossa, nasolacrimal duct and the optic canal constitute such important apertures [1, 42–46].
2.2. Blood supply
The ophthalmic artery and its branches constitute main arterial supply of orbit. The majority of the venous drainage occurs through superior ophthalmic vein, which drains into cavernous sinus that is located just posterior to the orbital apex. Veins from the facial region and many anterior ophthalmic veins anastomose and drain into cavernous sinus through superior orbital vein. Thus, cavernous sinus is prone to infection from facial region and also from the orbital region through the superior ophthalmic vein leading to a serious complication.
The eyelids impart two protective anatomical barriers, i.e., orbital septum and conjunctiva. Former divides the orbit from the eyelid into preseptal and postseptal spaces and provides a physical barrier to infectious agents and latter one is reflected back on itself, which provides protection by hindering the free movement of the material posteriorly from the anterior surface of the globe.
2.4. Lacrimal system
Lacrimal system consists of lacrimal gland, accessory gland and excretory system. Tears are secreted by lacrimal gland, which flows over the cornea and finally drain into nasal cavity by nasolacrimal duct through lacrimal sac. Any obstruction to the nasolacrimal duct can lead to regurgitation of the accumulated fluid onto the ocular surface leading to increased chances of infection.
2.5. Layers of eye ball
The basic structure of eye ball or globe consists of three concentric layers. The outermost covering is composed of sclera and cornea. The middle covering is composed of uveal tract, consisting of choroid, ciliary body and iris. The inner most covering is retina. The sclera is almost avascular except for the presence of superficial small blood vessels. The choroid is a highly vascular structure and provides nutrition and oxygenation to the retina beneath it. Due to these qualities, choroid serves as a fertile area for the proliferation of various pathogens, which spread by hematogenous route.
2.6. Anterior and posterior chambers
Anterior segment of the eye in front of the vitreous humor comprises anterior one-third of the eye and is further divided into anterior chamber and posterior chamber. Anterior chamber is the space between posterior surface of cornea and the iris, whereas posterior chamber is the space between iris and the front of vitreous. The aqueous humor is produced by non-pigmented ciliary epithelium in the posterior chamber and drains through the pupillary aperture into the anterior chamber. Cornea is composed of well-organized collagen fibrils, which is avascular in nature. Lens is also an avascular crystalline structure, which continues to grow throughout life. Thus, aqueous humor fills these spaces and provides nutrition to the surrounding structures.
2.7. Vitreous humor
It is a gel-like substance present in front of retina and posterior to the lens in the posterior segment of the eye. It is optically clear and is composed of collagen framework interspersed with hyaluronic acid. During intraocular inflammation, it becomes hazy and may cause impairment of vision.
2.8. Retina and optic nerve
Retina constitutes the innermost covering of the eye ball and captures the light energy with the help of rods and cones. The outer half of the retina is supplied by central retinal artery, whereas inner half receives its blood supply from the choroid.
The optic nerve is formed by axons of the inner cell layer that exits the globe. It is covered by all the three meningeal coverings, which are direct extensions of the brain coverings. Thus, it is vulnerable to infections originating from both within cranial vault and within orbits.
3. Ocular defense mechanisms
The surface of the eye is well protected by both mechanical and immunological defense mechanisms. To breach the defense mechanism, some form of trauma is essential. The eyelids provide mechanical protection to the surface of eyeball. The eyelashes protect against airborne particles and trauma by initiating blink reflex. The cornea is also sensitive to tactile sensation and helps in the initiation of blink reflex, which is provided by dense sensory nerve endings. The lids direct the tears, particulate debris, allergens and microbes to the lacrimal excretory system by its sweeping action over the anterior surface of the eyeball. Bell’s phenomenon also provides protection to cornea as globe is turned upwards and slightly outwards during eyelid closure to avoid corneal exposure . Meibomian glands secrete lipids, which provide stability to the tear film. The epithelial surface of the cornea and conjunctiva provides anatomical barrier to the pathogens. This function is further strengthened by the impermeability provided by the basement and cellular junctional complexes of the cornea. Indigenous flora of the eye also provides protection by creating a competition for colonization by the pathogens.
Immune defense mechanisms are provided by the vascular supply of the eye. Any breach in the anatomical defense system initiates the ocular inflammatory response, which helps in vasodilation and exudation of immunologically active substances and cells [1, 8, 48–52].
3.1. Defenses of the tear film
There are three layers of the tear film: oil, aqueous and mucous. Majority of the tear film is composed of aqueous layer and pH of the tear film helps in neutralization of toxic substances. Flow of tears help in mechanical flushing of the foreign particles and allergens into the lacrimal excretory system. Mucosal layer helps in entrapment of pathogens. Tear film contains various immunological active substances such as lactoferrin, lysozyme, β-lysin, ceruloplasmin, complement and immunoglobulins.
3.2. Conjunctival defenses
The conjunctival associated lymphoid tissue lies beneath the conjunctiva. It consists of both B and T lymphocytes. B and T cell precursors mature when exposed to foreign particles or allergens, then migrate to regional lymph nodes for further development, and thereafter return to the conjunctiva through blood stream to produce specific immunoglobulins and cellular defense responses.
3.3. Corneal defenses
Although the cornea is avascular, it is provided by limited defense mechanisms in the form of Langerhans cells (dendritic cells) and immunoglobulins. The surface of the cornea is covered by mucous glycoprotein, which helps in cross-linkage of the IgA and protects the anterior surface of the cornea. Immune defense mechanisms are activated whenever injury occurs, leading to recruitment of the polymorphonuclear cells, lymphocytes and fibroblasts.
3.4. Cellular immune responses
Langerhans cells are situated along the peripheral margin of the cornea and conjunctiva. These cells possess receptors, which help in phagocytosis and processing of certain antigens for presentation. Langerhans cells stimulate B and T cells to elicit a strong cellular immune response. During inflammation Langerhans cells migrate toward the cornea, causing increased release of inflammatory substances.
3.5. Leukocyte defense
Polymorphonuclear leukocytes are the hallmark of acute inflammation and are associated with oxygen-dependent pathways for the generation of free radicals that help in killing of the invading pathogens. Another immune defense mechanism operated by the production of defensins is antimicrobial proteins active against wide range of pathogens.
Ocular surface is constantly exposed to environment and foreign bodies, thus there are greater chances of infection. However, robust innate immune system at ocular surface protects the eye from infection. There are several peptides of defensins and cathelicidin families that are present in tear film and secreted by corneal and conjunctival cells. These are not only antimicrobial in nature but also help in the recruitment of immune cells and thus provide a link to adaptive immunity. The important defensins present in human eye are hBD-1 (human beta defensins), hBD-2, hBD-3, CAP37 (Cathelicidin-related antimicrobial peptide), LL37 (type of cathelicidin) and HNP-1, 2, 3 (human neutrophil defensins) .
4. Protozoan eye infections
Toxoplasmosis is caused by obligatory intracellular protozoan parasite known as
Approximately, one-third of the world’s population is thought to be infected by
Ocular toxoplasmosis usually manifests in immunocompromised
Congenital ocular toxoplasmosis usually involves both the eyes, whereas acquired ocular toxoplasmosis is usually unilateral [62, 63]. Chorioretinitis is caused by necrotizing inflammation due to the rupture of an older cyst. Intense form of choriretinitis may occur in newborns and patients infected with HIV. In addition, congenital toxoplasmosis patients may present with wide range of ocular symptoms such as strabismus, nystagmus and blindness. Acute, acquired infection may result in photophobia, scotoma and loss of central vision. Ptosis may occur due to oculomotor nerve involvement.
Diagnosis of ocular toxoplasmosis in children with congenital infection is established by recognizing distinctive clinical findings such as focal necrotizing retinitis, vitritis, anterior uveitis and cataract  However, in cases with atypical presentation or having severe fulminant disease, diagnosis is usually established by analyzing the intraocular fluid for the presence of specific antibodies or the presence of parasite DNA by molecular techniques such as PCR or real-time PCR [65, 66]. PCR is performed by targeting the
Antibody detection in serum samples is widely used for establishing the diagnosis of toxoplasmosis [73–76], while its role is limited in establishing the diagnosis of the ocular toxoplasmosis. A rising titer of specific IgG over a period of 3 weeks helps in establishing the diagnosis . The detection of specific antibodies in intraocular fluids by the enzyme-linked immunosorbent assay (ELISA) is the most commonly used test for the diagnosis of toxoplasmosis. The Goldmann-Witmer coefficient (GWC) calculation is a common method to estimate the local versus systemic
An algorithm for the laboratory confirmation of clinically suspected cases of ocular toxoplasmosis has been reported . Reactivated form of ocular toxoplasmosis is considered in patients with typical lesions of toxoplasmic retinochoroiditis, specific IgG seropositive, specific IgM seronegative and responding to anti-
In immunocompetent individuals, toxoplasma retinochoroiditis usually resolves within 2–3 months . Classic therapy or triple therapy with a combination of pyrimethamine, sulfadiazine and systemic corticosteroids is recommended for lesions involving or near to fovea, an area critical for vision. Classic therapy is usually associated with significant side effects, therefore other drugs such as trimethoprim-sulfamethoxazole, clindamycin, atovaquone and azithromycin are being evaluated for the treatment of ocular toxoplasmosis .
Trimethoprim-sulfamethoxazole (Bactrim) appears to be a safe and effective substitute for sulfadiazine, pyrimethamine and folinic acid for the treatment of ocular toxoplasmosis.
Progressive and recurring necrotizing retinitis, with vision-threatening complications such as retinal detachment, choroidal neovascularization and glaucoma, may occur at any time during the clinical course if the infection is not treated on time. Congenital toxoplasmosis can lead to cataract. The aim of the treatment is to arrest parasite multiplication during the active period of retinochoroiditis and to minimize damage to the retina and optic disc .
Animal model(s) can be used to study various aspects of ocular toxoplasmosis .
|Toxoplasmosis||Worldwide particularly in Central America, Asia, Caribbean region, Europe particularly in France|
|Acanthamoeba keratitis||Worldwide significantly in Chicago, San Francisco, Boston, Philadelphia, Sweden, Portland, New Zealand, United Kingdom, India, Africa|
|Chagas disease||Central and South America|
|Malaria||Africa, Central & South America, Middle East and Asia|
|Leishmaniasis||Africa, Mediterranean region, Middle East, Central and South America, parts of Asia|
|Giardiasis||Southeast Asia, South Africa, Europe and USA|
|Onchocerciasis||Africa, South America, Arabian peninsula|
|Loiasis||Central and West Africa|
|Dirofilariasis||Asia, Africa and Europe|
|Gnathostomiasis||South East Asia particularly Thailand, China, Japan and India, Central and South America particularly in Mexico, Guatemala, Peru and Ecuador|
|Thelaziasis||Asia Pacific region - China, India, Thailand, Indonesia, Japan and Korea|
|Toxocariasis||Worldwide particularly in Asia, Japan, Korea, Ireland, Alabama|
|Cysticercosis||Indian subcontinent, Central and South America, Africa and Far East|
|Echinococcosis||South America, Middle East, Mediterranean countries, India and Australia|
|Fascioliasis||France, Spain, Italy, Austria, Belgium, United Kingdom, Algeria, Tunisia, Iran, Uzbekistan, Korea, China, Argentina, Chile, Peru, Brazil, Guatemala|
|Schistosomiasis||Sub-Saharan Africa, China, South Asia|
|Philopthalmosis||Europe (Yugoslavia), Israel, Asia (Thailand, India, Sri Lanka, Japan) and America (i.e., Mexico, and the United States)|
||San Francisco, California|
|Myiasis||Worldwide with greater abundance in poor socioeconomic regions of tropical and subtropical countries, Mediterranean basin and Middle East|
|Phthiriasis palpebrum||Case reports from Tunisia, Taiwan, India, Pakistan, China, Korea, Lebanon, Israel, Brazil, Turkey, United Kingdom, Belgium, Italy, Cyprus, United States of America (USA)|
|Tick infestation||Case reports from Ireland, Turkey and USA|
The diagnosis of AK is difficult as it is usually confused with symptoms of bacterial, fungal or viral keratitis. However, history of contact lens use together with a history of excruciating pain is a strong indication toward the diagnosis of AK. For establishing the clinical diagnosis with high sensitivity, in vivo confocal microscopy can be used, which is a non-invasive procedure. The
Chances of recovery are good if the pathogen is restricted to cornea epithelium but can lead to vision loss, if it invades stroma leading to necrosis and intense inflammation. Medical treatment, if started early, can lead to a significant improvement within 2–3 weeks .
Preventive measures include thorough and adequate disinfection of contact lenses. It is recommended to remove contact lenses before any activity involving contact with water, including showering, using a hot tub, or swimming. Hands should be washed with soap and water and dried before handling contact lenses. Contact lenses should not be rinsed with tap water and should be cleaned and stored as per manufacturer’s guidelines. It is suggested that the increased awareness about the other predisposing factors (corneal injury, fall of foreign body in eye) among the general public may enable early and frequent recognition and proper management of AK in patients other than contact lens wearers .
4.3. Chagas disease
Chagas disease or American trypanosomiasis is caused by
The diagnosis of acute Chagas disease is established by the direct demonstration of trypomastigotes in the blood/buffy coat preparation. Parasites can also be isolated by direct culturing of blood on NNN medium (Novy, MacNeal, Nicolle’s medium). It may take 7 to 10 days for culture to become positive. Diagnosis may also be established by xenodiagnosis. During acute phase, the role of serology is limited in the diagnosis as antibodies take time to develop and false positive results have also been known to be associated with serological tests due to cross-reaction of antibodies to non-pathogenic
Acute cases of Chagas disease are treated by nifurtimox and benznidazole. Benznidazole is given as 5–7.5 mg/kg per day orally in two divided doses for 60 days. Nifurtimox is given as 8–10 mg/kg per day orally in three or four divided doses for 90 days [91, 94].
Within few weeks, symptoms of acute Chagas disease such as Romana’s sign fade away, but infection persists. The average life-time risk of developing complications of chronic phase is around 30%. It may take more than 20 years to develop chronic complications. However, trypanocidal therapy did not significantly reduce cardiac clinical deterioration through 5 years of follow-up as documented by randomized trial of benznidazole for chronic Chagas’ cardiomyopathy [95, 96].
Leishmaniasis is caused by protozoan parasite that belongs to genus
Diagnosis of leishmaniasis can be achieved by the direct demonstration of parasites in the tissue smears and/or biopsy samples, culture technique(s), antigen and/or antibody detection and molecular technique(s). However, each technique has its own merits and demerits. Amastigotes can be easily identified in the cutaneous and mucocutaneous lesions but are not easily identified in cases with ocular disease [103, 117, 118]. Molecular techniques such as PCR/real-time PCR can identify the genome of parasite with greater sensitivity (100%) and specificity (100%) [119, 120]. The treatment of leishmaniasis depends on several factors such as clinical form of the disease. The antileishmanial drugs include pentavalent antimony, sodium stibogluconate, liposomal Amphotericin B, miltefosine and paromomycin [118, 121].
Ocular lesions do not heal without treatment and could lead to vision loss if conjunctiva is involved due to severe ulceration. Healing occurs without visual impairment if treatment is initiated early during the course of infection and vigorous treatment is required to prevent blindness [121, 122].
Malaria is caused by the parasites of Genus
Wide range of ocular symptoms has been reported in patients suffering from malaria. Uncomplicated malaria is usually not associated with significant ocular findings but rarely may be associated with edema and hyperemia of the eyelids, chemosis of conjunctiva, conjunctival hemorrhage and anterior uveitis . On the other hand, severe ocular manifestations may occur in cerebral malaria due to
Diagnosis of malaria is established by light microscopy or by rapid antigen detection kits. Light microscopic examination of Giemsa-stained peripheral blood smear is considered as gold standard for the diagnosis of malaria with a threshold of about 50–100 parasites/µL . However, in addition, ocular examination may provide clue to the diagnosis as specific retinal changes can be seen directly [129, 134, 135].
Treatment depends on the species of
If not treated, malarial retinopathy is associated with serious consequences as reports indicate that the severity of retinopathy is related to prolonged death and coma. After antimalarial treatment and resolution of coma in severe malaria, malarial retinopathy resolves after some time [132, 137].
Microsporidiosis is the term used to denote the infection caused by microsporidia belonging to phylum Microspora . Microsporidia were once thought to be protists but are now known to be fungi. Although it is classified as a protozoal disease in ICD-10, their phylogenetic placement has been resolved to be within the fungi . Microsporidiosis is considered as an opportunistic infection in AIDS/HIV-infected individuals and is prevalent worldwide (Table 1) . Microsporidia are small, unicellular, spore forming, obligate intracellular pathogens. Important genera responsible for ocular manifestations are Encephalitozoon and Nosema. Another species, Septata, has also been reported to cause keratoconjunctivitis . The prevalence of microsporidiosis ranges from 2 to 50% among severely immunocompromised, HIV-infected patients found in North America, western Europe and Australia. The prevalence data for microsporidiosis is limited among non-HIV-infected persons .
The life cycle of parasite involves three stages (Figure 8):
The resistant spore (infective form)
The spore injects the infective sporoplasm into the host cell. Inside the host cell, sporoplasm undergoes multiplication either in the cell cytoplasm or inside parasitophorous vacuole. Microsporidia develop to mature spores by sporogony that are released by disruption of cell membrane. The free mature spores are the infective forms.
Ocular manifestations caused by
Diagnosis is established by direct demonstration of the spores by microscopy or electron microscopy of the corneal scrapping or biopsy specimens. Isolation of the parasites in culture has also been attempted . There are no reports on use of serological tests to detect antibodies in serum or tears in ocular microsporidiosis . Lesions usually heal after 1–2 weeks as it is self-limiting. Treatment of microsporidial keratoconjunctivitis with polyhexamethylene biguanide does not offer any significant advantage but treatment with topical fumagillin showed significant improvement [141–143].
Giardiasis is caused by
Barraquer was the first to report the ocular manifestation (iridiocyclitis, choroiditis and retinal hemorrhages) in patients who were suffering from diarrhea due to
The diagnosis is established by direct demonstration of the parasite in the fecal samples by microscopy. Concentration techniques of the samples yield higher sensitivity. Nitroimidazole group of drugs are highly effective against
5. Nematode infections
Onchocerciasis, also known as “river blindness”, is caused by
Onchocerciasis mainly occurs in tropical countries and majority of the cases (99%) have been reported from sub-Saharan Africa. It is also found in some countries of the Middle East and Latin America such as Brazil, Guatemala, Mexico and Venezuela (Table 1, Figure 11). Approximately, 25 million people are known to be affected by onchocerciasis worldwide, and it is known to cause visual impairment and blindness in approximately 800,000 and 300,000 people, respectively [148, 150]. The inflammatory response initiated against dying microfilariae causes gradual and progressive loss of vision due to sclerosal keratitis [149, 151]. Apart from causing keratitis, clinical features may also manifest as iridiocyclitis, chorioretinitis and optic atrophy. Autoimmune mechanisms have also been postulated to cause inflammation in the posterior eye. Accumulation of retinal and retinoic acids, strong eosinophilic response and immune reaction against
The filarial parasites of major medical importance in humans contain the symbiotic bacterium
Diagnosis is difficult to establish in light infections. Skin snips can be subjected to microscopy for visualizing the larvae, but it yields very low sensitivity. Infections of the eye can be diagnosed with direct demonstration of the parasite by slit-lamp examination or by demonstrating the parasite in sclerocorneal punch biopsy. Newer techniques such as skin-snip PCR can establish the diagnosis if larvae are not visualized . Antibodies can be detected by ELISA or EIA, but these tests cannot distinguish between past and current infections [156, 157]. Skin-snip PCR has 84–91% sensitivity and 100% specificity . The sensitivity and specificity of serum antibody detection has been reported to be 78–99% and 95–100%, respectively . A promising antigen detection by dipstick assay was recently developed, but its specificity was found to be low in high endemic areas due to cross reaction with urine filarial antigen [158, 159]. Xenodiagnosis (exposing possible infected tissue to a vector and then examining the vector for the presence of microorganism) has also provided clue in some cases.
If the infection is not treated on time, it can progress toward blindness . Drug of choice for the treatment is ivermectin, given 150 to 200 µg /kg body weight, every 6 months to prevent the skin damage and blindness. Treatment with ivermectin has been shown to decrease visual field loss and severity of keratitis. Ivermectin only kills the larvae but not the adult worms. Doxycycline can be used to kill the adult worm. The mechanism of action is that it kills the
The best method to get the protection from insect bite is the use of insect repellent. Community-directed treatment with ivermectin (CDTI) along with vector control measures is the main approach to control onchocerciasis. Ivermectin kills microfilariae and also prevents adult worms from producing more microfilariae for few months following treatment, so reduces transmission .
Loiasis is caused by
Ocular manifestations may occur due to the presence of both microfilariae and adult worms. The adult worms may survive up to 15 years and have been found in the conjunctiva, vitreous, eyelid and anterior chamber. Calabar swellings  may occur as a result of localized angioedema due to intense atopic reaction. Retinal hemorrhages may occur due to aneurysmal dilatation of the retinal vessels due to the invasion of the retinal and choroid vessels by the microfilariae present in blood stream. Perivascular inflammation can also be present, and ocular examination under slit lamp examination is useful in establishing the diagnosis.
The diagnosis is usually confirmed by the direct demonstration of the microfilariae in the blood by visualizing Giemsa-stained slides under the microscope. However, many of the individuals having visible worm in the eye may test as amicrofilaraemic . Blood should be drawn during the midday as this time coincides with the periodicity of the microfilariae in the blood. The microfilariae can also be demonstrated in unstained blood smear. Adult worm extraction establishes the diagnosis in patients having conjunctival involvement . Antibody detection  may aid in establishing the diagnosis, but its presence cannot differentiate between recent and past infection. Eosinophilia and high IgE also indicate active infection .
Eye worm if not treated causes very little damage to eye as it lasts less than one week (often just hours). Surgical removal relieves eye symptoms, in addition medical treatment is required for treating loiasis . Therapy involves manual removal of adult worms and administration of diethylcarbamazine (DEC), which kills both adult worms and microfilariae.
Dirofilariasis is caused by nematodes belonging to the genus
There are several cases that document ocular involvement due to dirofilariasis [37, 171–173]. Ocular symptoms depend on the site of infection. Eyelid involvement  leads to edema, pain, pruritus and congestion of conjunctiva, whereas intraocular  involvement leads to foreign body sensation, diplopia, photophobia and floaters.
Diagnosis can be established by the direct demonstration and identification of the adult worm. Intraocular presence of the parasite can be confirmed by ophthalmoscopy. Serological techniques are not useful in establishing the diagnosis due to the cross reaction with other parasitic helminths, particularly
Without treatment, worm remains in eye causing symptoms due to its presence . Surgical excision is the treatment of choice; however use of diethylcarbamazine (DEC) has also been reported with some success [37, 178].
Gnathostomiasis is a food-borne zoonotic parasitic infection, caused by ingestion of raw or undercooked freshwater fish, pork, chicken, frog and snake [179, 180] contaminated with the third-stage larvae of
Ocular manifestations occur due to the migration of the parasite and its metabolites, leading to inflammatory response. Conjunctiva and corneal infection may lead to congestion of the conjunctiva and corneal ulceration, respectively. Intraocular involvement may lead to glaucoma, uveitis, retinitis and vitreous hemorrhage [182, 183]. In severe cases, retinal detachment has also been reported due to the fibrinous scarring along the migratory path.
Diagnosis is difficult to establish and high index of suspicion is required. Patients may present with marked eosinophilia  and elevated IgE levels . ELISA for specific antibody detection and histopathological examination of the biopsy samples may assist in establishing the diagnosis [186–188]. ELISA for antibody detection reported to have low sensitivity, ranging from 59 to 87%, with a specificity of 79–96% [189, 190]. If parasite is not removed, it leads to persistence of visual disturbances such as floaters. Surgical treatment is curative and only modality available .
Thelaziasis is caused by nematode
Without treatment, worm remains in eye causing symptoms due to its presence . Treatment is surgical removal of worms along with the topical application of thiabendazole. Preventive measures include use of bed nets at night, maintenance of personal hygiene and keeping surroundings clean to control the vector population responsible for the transmission of infection .
Toxocariasis is caused by
High index of suspicion is required for establishing the diagnosis of OLM during ocular examination . Marked eosinophilia along with positive serology by ELISA  helps in confirming the diagnosis . Detection of specific antibodies in the vitreous fluid also helps in differentiating it from retinoblastoma . ELISA based on the excretory-secretory antigens of
Albendazole and mebendazole are the drugs of choices for the treatment of VLM [214, 215]. However, there is a limited role of antiparasitic drugs in the treatment of OLM. Photocoagulation along with steroids has been recommended for the treatment of OLM.
6. Cestodes infections
Cysticercosis is caused by the larval cysts of the tapeworm
Ocular involvement is well documented and several case reports have documented the orbital, intraocular, subretinal and optic nerve involvement due to cysticercosis [219, 220]. Free-floating cyst can be found in vitreous or anterior chamber of the eye. Cranial nerve or intraocular muscles lesions may result in gaze palsies [221–223].
Diagnosis is usually established by ophthalmoscopic examination along with imaging evidence of ultrasonography, CT scan or MRI scan. Although serology is easy to perform, it is usually negative in isolated ocular cysticercosis patient . Molecular techniques such as conventional PCR, real-time PCR  and loop-mediated isothermal amplification (LAMP)  can be utilized for establishing the diagnosis of ocular cysticercosis and for genotyping [30, 226]. However, it requires a sophisticated molecular laboratory setup, which is not available widely in developing nations.
Without treatment, symptoms related to visual disturbances persist. Symptoms resolve with surgical and medical treatment . Albendazole along with steroids are the main drugs used in the treatment. Steroid treatment decreases the inflammatory response associated with the antihelminthic therapy around the lesions. Surgical removal of large cysts is recommended where there is an impairment of the vision .
Echinococcosis/hydatidosis is caused by infection of the larval stages of the
The symptoms and signs depend on the location of the cyst in the target organ. Most common ocular finding is the development of proptosis due to the presence of intraorbital space occupying lesion. This may further lead to exposure to keratitis and ulceration of the cornea. Other complications due to the local invasion of the expanding cyst may lead to erosion of orbital wall, optic atrophy and optic neuritis. Subretinal hydatid cyst has been reported. In severe cases, blindness may also occur .
The diagnosis depends on the clinical findings suggestive of hydatid cyst on ocular examination and confirmed by radiological techniques such as ultrasonography, CT scan and/or MRI [232, 233]. “Double wall” sign is a characteristic of orbital hydatid cyst seen by ultrasonography . Serology may also aid in diagnosis. However, in majority of the commercially and in-house serological assays, hydatid fluid is the main antigenic component and sensitivity of IgG-ELISA reported in various studies varies from 64.8 to 100%, while specificity varies from 87.5 to 100%. Purified and recombinant antigens are also being tried for developing ELISA with high sensitivity and specificity . Fine needle aspiration cytology can also be performed for establishing the diagnosis .
Symptoms persist if not treated . Surgical removal of the cyst is the treatment of choice. Medical therapy includes administration of albendazole or mebendazole to prevent the recurrences due to the contents of the cyst leaking into the surgical sites . If the cyst is accidently ruptured, in situ irrigation with hypertonic saline should be performed. However, it causes local inflammatory reaction that may lead to atrophy of optic nerve .
7. Trematodes infections
Fascioliasis is a food-borne parasitic infection caused by trematodes that mainly affect liver. It is acquired by eating metacercaria of
Opthalmofascioliasis is the term used for those cases in which eye infection is directly caused by migrant ectopic fasciolid fluke. All other patients with ocular manifestations due to fasciolids located in liver or other organs should be classified as fascioliasis with ocular implications. Although ocular involvement in fascioliasis is rare, cases have been reported from France, Spain, Italy, Austria, Belgium, United Kingdom, Algeria, Tunisia, Iran, Uzbekistan, Korea, China, Argentina, Chile, Peru, Brazil and Guatemala (Figure 20) . Symptoms and signs usually relate to the affected eye and may cause conjunctival hyperaemia, corneal oedema, dilated episcleral vessels, paralysis of extraocular muscles, decrease in perception of light, deep anterior chamber with flare, uveitis and so on. Diagnosis is established directly by visualization of leaf-shaped like organism in the eye or by studying the morphological features of the surgically removed worm. Eosinophilia, positive serology by ELISA or presence of eggs in stools may aid in diagnosis. Severe complications may occur if not treated. Early surgical intervention is associated with rapid response and reasonable final visual acuity . Thus, ophthalmological manifestations have been known to be cured with surgical treatment without any antiparasitic treatment . However, triclabendazole is the drug of choice if medical treatment is required.
Schistosomiasis, or bilharziasis, is caused by trematode flatworm of the genus
Ocular involvement is not the usual site that is involved in schistosomiasis, but cases have been reported where Schistosoma ova or even the adult worm can reach the systemic circulation and can lodge itself at ectopic sites such as eyes. Although schistosomiasis is very common, ocular cases are rare. It can cause uveitis or subretinal granuloma . Diagnosis is established by direct demonstration of eggs/cercariae in the eye. Detection of eggs in the urine and feces may aid in establishing the diagnosis. Symptoms persist if not treated. Praziquantel is the drug of choice for all forms of schistosomiasis .
7.3. Other rare ocular infections by trematodes
The cases of acute nodular conjunctivitis and anterior chamber granuloma formation have been documented, which are caused by endemic water-borne trematode infection. The identification of the remnants of parasites aspirated from such cases revealed that these parasites belong to the genus
8. Eye infections caused by ectoparasites
Myiasis is an infection caused by larvae of flies. It is common in tropical and subtropical areas. It is known as ophthalmomyiasis when ocular structures are involved. Ophthalmomyiasis is categorized into three clinical categories (ophthalmomyiasis externa, ophthalmomyiasis interna and orbital myiasis), depending on the location of larvae in the eyes. Several genera have been reported to cause myiasis such as
Diagnosis is established by the identification of the maggots. Treatment usually involves the surgical removal of the maggots. Medical treatment involves just one oral dose (150 to 200 µg/kg of body weight) of ivermectin . However, the use of ivermectin for the treatment of myiasis is an off-label treatment in many countries and should be used for selected cases. The side effects such as dermal eruptions, fever, dizziness, migraines and muscular pains are common. Antibiotics and steroids may also be required to prevent the inflammation and superadded bacterial infection. Opthalmomyiasis interna  is caused by the invasion of the ocular structures leading to uveitis, lens dislocation and retinal detachment. Diagnosis is established by visualizing the migratory tracks along subretina by the ophthalmoscopy. Symptoms persist if not treated. Serious complications may also occur such as lens dislocation and retinal detachment due to invasion of tissue . Steroid therapy is advocated if there is severe inflammation, and surgical removal is performed in severe cases. Orbital myiasis is seen in patients who are not able to maintain good personal hygiene . Treatment is directed at removal of maggots and control of secondary infection. Preventive measures include maintenance of good sanitation conditions and proper disposal of waste material to control the flies in surrounding areas.
Important genera of the lice causing human infestation belong to
Ticks belonging to the class Arachnida are important vectors for the transmission of several infections to humans . Geographical regions where ticks’ infestation has been reported are depicted in Table 1 and Figure 21. Ticks complete their life cycle in three different stages, i.e. larva, nymph and adult, and all the life cycle stages require blood meals. Ticks have been reported to attach to ocular structures that may appear as meibomian gland mass. Symptoms persist if not treated. Treatment includes removal of ticks, and tick bite granuloma may resolve after several weeks.
Ocular parasitic infections are of medical importance worldwide because of significant morbidity rates, and if not diagnosed and treated on time could lead to vision loss. High index of clinical suspicion is required to establish the diagnosis for further confirmation by laboratory techniques followed by specific treatment. Direct demonstration of the parasite is possible in few ocular parasitic infections, while in few, specific clinical features such as changes in retina on direct ocular examination may point toward specific diagnosis. Serology has limited role in the diagnosis as most of the ocular parasitic infections are localized in the eye. Utility of different diagnostic techniques in various parasitic ocular infections has been summarized in Table 2. Although reports reveal that the serology for antibody detection and/or molecular techniques for parasite DNA detection, when applied directly on the ocular tissues, aqueous or vitreous humor usually confirm the diagnosis, these techniques have its own merits and demerits. IgG immunoblot technique has been applied for the diagnosis of ocular toxoplasmosis with some success, and it is suggested that local antibody production is presumed to have occurred, if immunoreactive bands are detected in the aqueous humor but not in the serum . Future reports in this direction may throw further light on its utility. Moreover, application of Western blotting technique may be possible only in limited diagnostic centers.
Report on “Diagnostic Approach to Ocular Toxoplasmosis” revealed in conclusion that the clinical diagnosis of ocular toxoplasmosis may be supported by laboratory tests in 60–85% of cases, depending on the time of sampling. Analysis of the aqueous humor is particularly helpful in patients with atypical lesions or in individuals who are irresponsive to specific therapy. Even so, a laboratory confirmation of the clinical diagnosis is not achieved in 15–40% of cases .
In general, it can be concluded that the clinical awareness and multiple approaches/techniques for the confirmatory diagnosis of clinically suspected ocular parasitic infections may yield higher sensitivity and diagnostic efficacy, as suggested earlier .
Treatment depends on the causative agent and may involve surgical removal and/or medical treatment with antiparasitic drugs (Table 2). In few infections, steroids are also prescribed to prevent the damage from the inflammatory response associated with the dying parasites. Preventive strategies depend on the type of parasitic infection and mainly include control of vector population for vector borne parasitic infections, maintenance of good personal hygiene and providing awareness to people about ocular parasitic infections through information, education and communication (IEC).
The need of increased awareness and clinical suspicion of OPI for prompt and specific diagnosis followed by application of sensitive and specific diagnostic technique(s) for confirmation and effective treatment are the main challenges.
The future research priorities need to be directed to study exact host-pathogen mechanisms, local immune responses and to establish more sensitive and specific diagnostic techniques. The molecular techniques can provide rapid diagnosis of multiple ocular parasitic infections and species identification for specific therapy. Multiplex PCR assay, if developed, can add new dimensions in the diagnosis. Efforts to develop animal models are desired that may further help to study the exact host-pathogen mechanisms, local immune responses and in developing new treatment strategies.
|Toxoplasmosis||Serology – IgM, IgG, IgA
Molecular: PCR, Real-time PCR
|a. Pyrimethamine and sulfadiazine plus corticosteroids
b. Trimethoprim/sulfamethoxazole plus oral prednisolone
c. Intravitreal clindamycin (1-1.5mg) injection and dexamethasone
d. Surgery reserved for severe complicated cases
|Acanthamoeba keratitis||Microscopy, culture on non-nutrient plates (coated with bacteria)/ in flasks (PBS+Bacteria), PCR, Real-time PCR||a. Biguanides – PHMB (0.02%)
b. Chlorhexidine 0.02% in combination with aromatic diamidines such as 0.1% propamidine isethionate, 0.15% dibromopropamidine, hexamidine 0.1% and neomycin (Topical antimicrobials should be administered every hourly for first several days and there after frequency reduced to every 3 hours with a minimum duration of therapy of 3-4 weeks
c. Surgical treatment includes keratoplasty or its variation known as DALK (Deep Anterior Lamellar Keratoplasty)
|Chagas disease||Blood smear, Buffy coat, culture, xenodiagnoses and PCR||a. Benznidazole 5-10 mg/kg daily in 2-3 divided doses for 60 days
b. Nifurtimox 15 mg/kg daily in 3 divided doses for 60-90 days
|Malaria||Thin and thick blood film for microscopy, antigen detection, PCR||a.
|Leishmaniasis||Microscopy of tissue smears, culture on NNN media, PCR||Pentavalent antimonial compounds, liposomal amphotericin B, miltefosine (dose is weight dependent), paromomycin, azoles such as ketoconazole, itraconazole and fluconazole|
|Microsporidiosis||Microscopy, Immunofluorescence assay, PCR||Topical fumagillin bicylohexylammonium (Fumidil B) 3 mg/mL in saline (fumagillin 70 µg/mL) eye drops: two drops every 2 hours for 4 days, then two drops four times daily (investigational use only in United States) plus albendazole 400 mg orally twice daily for management of systemic infection.|
|Giardiasis||Confirming by intestinal infection||Metronidazole, tinidazole, and nitazoxanide. Others include paromomycin, quinacrine, and furazolidone|
|Ocular nematode infections|
|Onchocerciasis||Slit-lamp examination, Biopsy of skin to identify larvae, skin nodules examination for identification of adult worms, PCR, antibody detection||a. Ivermectin: given every 6 months for the life span of the adult worm or as long as infected person has evidence of skin or eye infection
b. New treatment: Doxycycline, before starting treatment infection with
c. Removal of adult worms
|Loiasis||a. Surgical removal of the worm under the skin or across the eye
b. Diethylcarbamazine (DEC) is the drug of choice
c. Albendazole is given to patients not responding to DEC
|Dirofilariasis||a. Surgical removal of the worm
b. DEC is given for medical treatment
|Gnathostomiasis||Identification of the removed worm
Serology to detect antibodies
|a. Surgical removal of worm|
|Thelaziasis||b. Identification of worm removed from conjunctival sac
c. Eggs and larvae may be seen by microscopy of tears and other eye secretions
|Removal of worm|
|Toxocariasis||Histological demonstration of toxocara larva
Serology by ELISA
|d. Topical and systemic corticosteroids are useful in managing intraocular inflammation
e. Role of anthelmintic therapy in ocular toxocariasis remains unclear
f. Recommended drugs for systemic toxocariasis are:
g. Albendazole 400mg given twice daily for 7-14 days
h. Diethylcarbamazine - given at 3-4 mg/kg/day for 21 days
|Ocular cestode infections|
|Cysticercosis||Imaging with MRI, CT scan and USG
|a. Antiparasitic drugs – Albendazole 15mg/kg/day for 4 weeks, Praziquantel
b. Corticosteroids in tapering dose over a period of 1 month
|Echinococcosis||Imaging||a. Surgical removal
b. Albendazole is given as an anti-infective prophylaxis
|Ocular trematode infections|
|Fascioliasis||Detection of adult worm in the eye
Other features such as eosinophilia, stool examination and serology may help
|a. Surgical removal of worm
b. Triclabendazole 10mg/kg body weight as a single dose
|Schistosomiasis||Stool and urine examination for detection of parasitic eggs or detection of eggs or cercariae in eye
|Praziquantel 40-60mg/kg per day in two to three divided doses for one day|
|Philopthalmosis||Identification of the remnants of parasites aspirated from such cases||a. Conjunctival nodules heal spontaneously and anterior chamber nodules can be treated with topical/ oral corticosteroids.
b. Surgical removal is recommended in cases having large nodules
|Ocular infections by ectoparasites|
|Myiasis||a. Identification of the maggots
b. Visualizing the migratory tracks along sub retina
|a. Surgical removal of the maggots
b. Ivermectin 150-200 µg/kg of body weight in single dose
c. Steroid therapy
|Phthiriasis palpebrum||a. Excoriation marks along with small erythematous papules
b. Nits can be found at the base of eyelashes
|a. Eyelid disease is treated by petrolatum
b. Non-eyelid involvement may be treated with lindane, permethrin, pyrethin or malathion
|Tick infestation||Biomicroscopy may reveal ticks||Removal of ticks|
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