Ocular Parasitic Infections



Ocular Parasitic Infections


Khalid F. Tabbara



Parasitic infections remain an important cause of ocular and adnexal diseases that are caused by a variety of parasites. Infections of the eye and adnexa may lead to ocular morbidity and, in some cases, cause blindness. Many types of parasitic infections of the eye lead to serious ocular complications. Parasitic infection is a race between the ability of the parasites to multiply, spread and cause disease, and the ability of the host to control and terminate the infection.

The recent increase in the immunocompromised and aged populations has contributed to a corresponding increase in the opportunistic infections of the eye including parasitic infections. Parasites can cause infection in any ocular or adnexal structures, including the eyelids, eyelashes, lacrimal apparatus, orbit, conjunctiva, cornea, iris, anterior chamber, retina, and vitreous. The spread of parasites and invasion of the ocular structures may result from exogenous entry into the eye or endogenous entry via the hematogenous spread.

Tables 79.1 and 79.2 demonstrate the common parasitic infections of the eye or adnexa.








TABLE 79.1. Protozoal Infections of the Eye or Adnexa





















































































Parasite Other Names of Parasite or Disease Ocular Lesion Portal of Entry Mode of Transmission, Intermediate Host, or Vector Laboratory Tests Treatment Geographic Distribution
Leishmania tropica Cutaneous leishmaniasis tropical sore, Oriental sore, Aleppo boil, kala-azar Skin ulcer, interstitial keratitis, nummular keratitis, uveitis Skin Phlebotomus spp. (sandfly) Scrapings of skin lesions Stibogluconate, cryotherapy Middle East, Asia Minor, Central and South America
Leishmania brasiliensis American leishmaniasis, espundia, mucocutaneous leishmaniasis, uta, forest yaws Skin ulcer Skin Phlebotomus spp. (sandfly) Scrapings of skin lesions Stibogluconate Yucatán, Mexico, South America
Entamoeba histolytica Amebiasis Cutaneous amebiasis of the eyelid Skin, mouth Cysts in water contaminated with feces Cysts in stool, trophozoites in purged stool, serologic study, trophozoites in biopsy specimens of lesion Iodoquinol (Diodoquin), paromomycin, dehydroemetine, chloroquine, emetine, tetracyclines, metronidazole Worldwide
Acanthamoeba, Hartmanella Free-living amebae Indolent corneal ulcer, keratitis, uveitis Cornea, nose Contaminated water Trophozoites or cysts in tissue specimens Amphotericin B, natamycin Worldwide
Giardia lamblia Giardiasis, flagellate diarrhea Retinal vasculitis, Retinal hemorrhages   Cysts in food and water contaminated with feces Cysts and trophozoites in stool Metronidazole, quinacrine Worldwide
Toxoplasma gondii Toxoplasmosis Retinochoroiditis, papillitis, retinal vasculitis, uveitis, secondary glaucoma Mouth, transplacental Organ transplantation, accidental skin needle injection in lab workers Transplacental (tachyzoite); infected meat (bradyzoite); cat feces (oocysts); organ transplantation Biopsy, methylene blue dye test, CF, IHA, IF, ELISA, PCR Pyrimethamine with sulfadiazine, clindamycin with sulfa or azithromycin Worldwide
Pneumocystis carinii Pneumonia (new classification: fungus?) Cotton-wool patches in patients with AIDS Respiratory system Respiratory system (?) Sputum exam, microscopy of tissue specimens Pentamidine isethionate, penta-midine methane-sulfonate Worldwide
Microsporida Microsporidiosis Corneal ulcer, scars, uveitis
corneal
epithelial
keratitis
Cornea, skin Contaminated water Corneal tissue specimens Topical fumagillin, fluconazole, or itraconazole Patients with AIDS
CF = complement fixation; ELISA = enzyme-linked immunosorbent assay; IHA = indirect hemagglutination; IF = immunofluorescence
(Tabbara KF, Hyndiuk RA: Infections of the eye, 2nd ed. Boston: Little, Brown & Co, 1996)








TABLE 79.2. Helminthic Infections of the Eye or Adnexa








































































































































Parasite Other Names of Parasite or Disease Ocular Lesion Portal of Entry Mode of Transmission, Intermediate Host, or Vector Laboratory Tests Treatment Geographic Distribution
Nemathelminthes Nematodes (Roundworms)
Ascaris lumbricoides Roundworm, ascariasis Rare Mouth Viable eggs from soil or contaminated vegetables Eggs in stool, CF, larva in ocular granuloma by histopathologic examination Piperazine, pyrantel pamoate, mebendazole; excision of granuloma Worldwide
Toxocara canis, Toxocara cati Ocular toxocariasis Diffuse uveitis; endophthalmitis; posterior granuloma; peripheral granuloma; retinal detachment Mouth Ingestion of eggs from soil contaminated with dog or cat feces Detection of vitreous, aqueous, and serum antibodies by ELISA Thiabendazole, diethylearbamazine, corticosteroids, photocoagulation, surgical excision, vitrectomy Worldwide
Trichinella spiralis Trichinosis Lid and periorbital edema; extraocular muscle involvement Mouth Undercooked infected pork Skin test, biopsy, serologic study Corticosteroids (symptomatic relief), mebendazole Worldwide
Wuchereria bancrofti (Brugia malayi) Filariasis, elephantiasis lymphangitis Lymphatics of eyelids, and periorbital swelling   Mosquitoes (Culcidae) Blood smear, nocturnal Diethylcarbamazine, surgery W. bancrofti: tropical regions; B. malayi: Japan
Loa loa Eyeworm, loaiasis, Calabar swelling, fugitive swelling Subcutaneous or subconjunctival nodule Skin, conjunctiva Chrysops (deerfly, mango fly) Blood smear Diethylcarbamazine, surgical removal Africa
Onchocerca volvulus River blindness, onchocerciasis onchocercosis Uveitis, keratitis, glaucoma, optic atrophy, corneal scars, nodules on head Skin Simulium (blackfly) Skin biopsy, nodule aspirate Diethylcarbamazine, suramin, ivermectin, mechanical removal from conjunctival sac, surgery Africa, Central and South America, the Orient
Thelazia callipaeda, Thelazia californiensis Thelaziasis Orbital lesion Conjunctiva From dogs and other mammals; life cycle poorly understood; may involve an arthropod intermediate vector Biopsy specimen, identification of worm Mechanical removal, surgery T. callipaeda: Asia, Far East; T. californiensis: United States
Platyhelminthes: Cestodes (Tapeworms)
Taenia brauneri (larva) Coenuriasis Intraocular, superficial, or orbital cyst Mouth Food or drink contaminated with infected dog feces Cansoni intradermal test Surgical excision Worldwide
Multiceps multiceps (larva) Cysticercosis Localized intraocular granuloma Mouth Cysts in pork Skin test, x-ray to detect calcified cysts Surgery, photocoagulation Worldwide
Echinococcus granulosus Hydatid cyst, echinococcosis Orbital cyst (common), intraocular cyst (rare) Mouth Eggs from dog feces Skin test, IHA, x-ray, CT scan, IF Surgery Worldwide
Platyhelminthes: Trematodes (Flukes)
Schistosoma mansoni Schistosomiasis, bilharzia Unknown Skin Cercariae in fresh water, from snail Eggs in stool, rectal or liver biopsy Praziquantel (or oxamniquine) Africa, South America, Puerto Rico
Schistosoma haematobium Schistosomiasis, bilharzia Dacryoadenitis, conjunctival lesion; orbital tumor Skin Cercariae in fresh water, from snail Eggs in urine, cysto-scopy, histopathology of lesion, CT scan Praziquantel Africa, Middle East
Schistosoma japonicum Schistosomiasis, bilharzia Orbital granuloma (rare) Skin Cercariae in fresh water, from snail Eggs in stool, liver biopsy, histopathology of lesion, CT scan Praziquantel China, Japan, Philippines
CF = complement fixation; ELISA = enzyme-linked immunosorbent assay; IF = immunofluorescence; IHA = indirect hemagglutination
(Tabbara KF, Hyndiuk RA: Infections of the eye, 2nd ed. Boston: Little, Brown & Co, 1996)


Types of Parasites

Several descriptive names have been used to denote special types of functions caused by parasites. An ectoparasite lives on the surface of the host. An endoparasite lives within the body of the host, and this is a form of parasitic infection if it produces disease. An obligate parasite is an organism that cannot survive in any other manner, whereas facultative parasite is an organism that can exist either in a free-living state or in association with other organisms or hosts.


Types of Hosts

There are three main types of hosts for parasites. A definitive host, in general, is a host in which parasites reach their sexual maturity. An intermediate host serves as a source of shelter for the asexual phase of the life cycle of the parasite, or is an arthropod that may play a role in the transmission of the disease to man. An incidental host is a host in which the parasite does not ordinarily live. The host may or may not show harmful effects from this relationship.1

A parasite is defined as an organism that takes aboard on or in a certain host for the purpose of procuring food or shelter.


Host-Parasite Relationship

The ocular tissues are not the natural habitat of many parasites. Some parasites gain access to ocular tissues from the external environment whereas others reach the ocular structures by way of the blood stream. Parasitism is a relationship in which one organism derives all the benefits from the association and the host suffers from the functional and organic disorders. The relationship between the parasite and its host may change from time to time, and the parasite may at times exhibit other than a parasitic association, namely, mutualism, in which both organisms benefit from each other, and commensalism, an association that is beneficial to one partner and at least not harmful to the other. Organisms that are unable to obtain food except in mutual association with members of another species establish a relationship known as symbiosis.


Host-Parasite Interaction

The parasite can injure the host in a variety of ways. In general, parasites injure host tissues by secreting toxic products. Certain parasites cause destruction of tissue by means of their proteolytic enzymes; others may induce an inflammatory reaction in the host that produces damage.

Cell-mediated immunity and humoral immunity play important roles in the defense mechanisms against parasitic infections. The same mechanisms may also participate in tissue damage.2 Parasites often establish mechanisms that permit survival in the host. Some parasites undergo antigenic alteration in their surface membrane, allowing them to evade the immune response of the host. Other parasites secrete minimal antigen, thus evoking little host reaction or immune tolerance. Some parasites produce substances that cause an inhibition of macrophage activity. In certain instances (e.g., Toxoplasma), parasites can cause immunosuppression of the host or may escape the immune mechanisms of the host by forming cysts within the tissue. The cyst wall may be composed of an outer layer from the host’s own tissue, thus escaping recognition by the immune system.3

The outcome of parasitic infection depends on the parasite itself and the immune status of the host. The natural defense mechanisms of the host may be compromised by disease or therapy. Parasitic infections that commonly occur in patients with acquired immunodeficiency syndrome (AIDS) include toxoplasmosis, pneumocystosis, microsporidiosis, cyclosporiasis, isosporiasis, cryptosporidiosis, and disseminated strongyloidiasis.


Classification of Parasites

The animal parasites of most vertebrates and mammals are classified into two distinct groups: Protozoa, the unicellular parasites; and Metazoa, the multicellular parasites. Protozoa, or the single-cell parasites, have been divided into a number of phyla, including Sarcomastigophora, Apicomplexa, Microspora, and Ciliophora. The multicellular Metazoa consist of helminths including the phylum platyhelminths (flatworms) and the Aschelminthes, of which the most important to us is the class Nematoda, or round worms. The Acanthocephala (thorny-headed worms) and the Arthropoda (the insects, spiders, mites, and ticks) are the other two important phyla of human parasites. All these phyla contain both parasitic and free-living forms, except for the Apicomplexa, Microspora, and Acanthocephala. Each phylum is subdivided into classes, and the classes are divided into orders. Each order is divided into families containing one or more genus and species.


Phylum Sarcomastigophora

The phylum Sarcomastigophora is divided into two subphyla: the Sarcodina (amebae) and the Mastigophora (flagellates). The ameboflagellates are a group of organisms that have the characteristic of both the amebae and the flagellates. The Sarcodina subphylum contains those forms that move by pseudopodia and includes all free-living amebae, as well as those that are symbiotic in the intestinal tract and elsewhere in the body. This subphylum contains the entamebae and Acanthamoeba organisms. Mastigophora is a subphylum of a group of organisms that have specialized structures known as the flagella. Flagella arise from small intracytoplasmic granules known as blepharoplasts that help to propel the organism. The location and number of flagella may vary from one species to another.


Phylum Apicomplexa

Members of phylum Apicomplexa have a complex life cycle, with a reproduction characterized by sexual and asexual phases. The genera in this group of parasites include the Plasmodium, which is the cause of malaria, and species of the genera Isospora, Cryptosporidium, and Sarcocystis, which are parasites of the intestinal mucosa; and Toxoplasma, Pneumocystis, and Sarcocystis, which are found as parasites of tissues and organs.


Phylum Microspora

The phylum Microspora includes a group of parasites that used to be classified under Protozoa. Microspora are tiny intracellular parasites that may infect vertebrates and invertebrates. Microsporida are becoming an important cause of morbidity in immunocompromised persons and AIDS patients.


Phylum Ciliophora

The phylum Ciliophora includes a variety of free-living and symbiotic species. The organisms have cilia, which are structurally similar to flagella but are shorter and more numerous. An example of these parasites is Balantidium coli, which is found in the intestinal tract. These organisms do not cause significant ocular disorders.


Phylum Platyhelminthes

The phylum Platyhelminthes, or flatworms, contains parasites that are flat and have a symmetric body. Most of these flatworms have both male and female reproductive systems. The adult worm may range in length from 1 mm to several meters. Most members of this phylum live either on or in the body of their host. The trematodes (flukes) and cestodes (tapeworms) exist in parasitic form only. The trematodes are elongated, slender organisms that attach to the host tissue with hooks or cup-shaped muscular depressions called suckers. They have a simple digestive tract. Members of the class Cestoda have a ribbonlike, elongated, segmented body and an anterior specialized attachment organ, or scolex. They have no digestive system. Adult cestodes inhabit the small intestines. Intermediate hosts are required for the development of cestodes.


Phylum Aschelminthes

The phylum Aschelminthes contains the nematodes, or roundworms, which are elongated and cylindrical in shape. Each worm is either male or female (i.e., the sexes are separate), and the male is frequently smaller than the female. A well-developed digestive tract is present. Intermediate hosts are necessary for the larval development of their forms. Some of the nematodes are free living, but a large number of species are parasitic to humans and animals.


Phylum Acanthocephala

Worms in the phylum Acanthocephala are endoparasitic and have modified hooks and a retractable proboscis to facilitate attachment. The heads are thorny. The cycle requires an intermediate host. The sexes are separate, and the male is smaller than the female.


Phylum Arthropoda

The phylum Arthropoda contains parasites that have jointed, paired appendages (“feet”). They have a tough, chitinous exoskeleton, a symmetric body, and a well-developed digestive tract. The sexes are separate. There are several classes in this phylum, many of which are of medical importance. Some genera cause parasitic infections of the eye (e.g., Pediculosis, Myiasis), produce venom, cause damage to the tissues, or can be fatal. Arthropods may serve as vectors for infectious organisms, yet others provide shelter for parasites or serve as intermediate hosts for the development of other parasites.


Phylum Pentastomida

The parasites in the phylum Pentastomida are endoparasites. They can cause diseases of the lungs, but they do not usually produce ocular disease.


Infections Caused by Protozoa


Microsporidiosis

Microsporidiosis is an infection caused by the obligate intracellular parasite of the order Microsporidia. The four principal genera that may produce disease in man are (i) Pleistophora; (ii) Nosema; (iii) Encephalitozoon; and (iv) Enterocytozoon. Because these parasites are tiny, they stain poorly in tissue sections and show little tendency to produce inflammatory reactions in the tissues. The organisms are difficult to identify, and subclinical infections are common. Human cases of ocular microsporidiosis have been reported in children and in healthy adults and contact lens wearers.4,5,6,7 Immunocompromised patients and patients with AIDS are susceptible to microsporidiosis.8,9 Declining incidence of microsporidiosis is noted after the introduction of the highly active antiretroviral therapy (HAART).8,10

The organism belongs to the phylum Microspora, class Microsporea, and order Microsporidia. The two suborders are Pansporablastina and Apansporoblastina. The first sporulates in the host cell with the sporocyst, and the latter lacks a pansporoblastic membrane. The Pleistophora species belongs to the suborder Pansporablastina, whereas the Nosema, Encephalitozoon, and Enterocytozoon species belong to the suborder Apansporoblastina.

Microsporidia are, as mentioned, obligate intracellular parasites. They are characterized by two developmental stages inside the host cell: (i) the feeding, or schizogonic, stage; and (ii) the sporulation, or sporogenic, stage.

Microsporidia may vary in size from 1 to 18 μm in length, but most pathogenic organisms are approximately 2 μm in size. The spores of Microsporidia are oval or spheric, and each spore consists of sporoplasm with a polar filament and varying numbers of coils and tubules, depending on the species. The existence of a polar filament identifies the organism as microsporidian.11 The infection is transmitted by the fecal-oral route. In corneal infection, direct inoculation may be responsible for the disease and the keratitis.12,13 The most common ocular manifestation of microsporidiosis is keratitis.13,14,15 Cases of microsporidiosis have been reported in association with AIDS. Patients with microsporidiosis present with conjunctival hyperemia, irritation, photophobia, and foreign-body sensation. Involvement of the cornea may lead to a decrease in vision. Conjunctival hyperemia and edema are associated with papillary hypertrophy. Biomicroscopy of the cornea shows tiny, punctate epithelial keratitis.6,8,9,14 The diagnosis of corneal and conjunctival involvement may be confirmed by corneal scrapings or by obtaining biopsy specimens, which are then subjected to electron microscopic studies.16 These organisms may not be visible on routine microscopy. With a hematoxylin and eosin stain, the Microsporidia organisms may appear refractile, having a clear cytoplasm and basophilic nucleus that makes it hard to identify. Giemsa staining may be helpful. The organisms have variable staining with acid-fast stain and appear to be gram-positive. The cell wall stains with Gomori methenamine silver (GMS) stain. The polar granule of Microsporidia can be demonstrated by periodic acid-Schiff (PAS) stain.

Acid-Fast stain (1%) and Gram’s chromotrope stain are ideal for the detection of Mirosporidia.16

Electron microscopy shows typical coiled polar filaments with one or two nuclei in the sporoblast and spores. Several nuclei are seen in the schizont. These stages do not show mitochondria. The organism may be differentiated from other protozoa, such as Toxoplasma, Leishmania, and Cryptosporidium. For example, Toxoplasma is larger (approximately 6 to 7 μm in length) and does not stain with GMS. Leishmania does not stain with GMS and is larger than Microsporidia. Cryptosporidium is similar to Microsporidia in size, but is found extracellularly and does not invade the cells. Serologic tests for microsporidiosis are available, including enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescent assay, but the sensitivity and specificity of these tests have not been established. The most frequently encountered genus causing microsporidiosis in patients with AIDS is Encephalitozoon. Several species have been identified. A species of Microsporidia, Encephalitozoon hellem can be isolated from the cornea of AIDS patients with keratoconjunctivitis.

The diagnosis of Microsporidia keratitis is made on the basis of clinical findings by slit-lamp biomicroscopy, which typically shows multiple intraepithelial white-gray opacities throughout the epithelium. Confocal microscopy and the chromotrope stain may allow rapid confirmation of the diagnosis and the initiation of therapy.15 The diagnosis is confirmed by examining corneal scrapings, which show organisms within the epithelial cells. These organisms measure 1 to 2 μm in length and contain PAS-positive anterior granules. Diagnosis can also be made by examining corneal and conjunctival scrapings. This has been facilitated by the use of immunofluorescein techniques using antisera against Encephalitozoon hellem. The scrapings usually do not show evidence of inflammatory reaction, and epithelial cells are seen containing the organisms. In conjunctival tissue, biopsy specimens of inflammatory cells may be seen, and the organisms are normally present within the conjunctival macrophages.

Immunocompetent patients may develop keratitis and conjunctivitis secondary to microsporidiosis.4,5,15 Microsporidial keratitis occurred in contact lens wearers.5,6

It also occurs following treatment with topical steroids.

The treatment of microsporidiosis in AIDS patients has improved after the HAART era.8,10 Treatment includes the topical use of fumagillin (Fumidil B).17,18 Fluconazole and itraconazole are alternative therapy in patients with microsporidiosis.9,18 Albendazole is given to treat intestinal microsporidiosis.18


Giardiasis

Giardiasis is caused by the protozoan Giardia lamblia. The disease has a worldwide distribution and is considered to be a leading cause of intestinal parasitic disease. Giardiasis may occur in the absence of clinical signs and symptoms, and the parasite may stay in the intestines in a subclinical form. The parasite is transmitted through the fecal-oral route. Drinking water is the most common mode of transmission.19,20 Person-to-person transmission has been reported in day care centers and among homosexual men.

The trophozoites of G. lamblia are pear-shaped and measure 8 to 20 μm in length and 5 to 15 μm in width. The organism has two nuclei with prominent karyosomes, and four pairs of flagella with two ventral suckers. The cyst of the parasite is oval and measures 10 to 20 μm in longest diameter. Each cyst has four nuclei but does not possess flagella or suckers. Upon excystation, the organism becomes a trophozoite with two nuclei and starts dividing by binary fission.

The most frequently encountered clinical symptoms are recurrent episodes of diarrhea, malaise, weakness, abdominal distention and cramps, nausea, vomiting, anorexia or weight loss, fever, and occasional constipation.

The ocular manifestations appear to be secondary to hypersensitivity reactions to Giardia antigens. The ocular manifestations that have been reported include anterior uveitis, choroiditis, and hemorrhagic retinopathy. Salt-and-pepper retinal changes with normal electroretinogram have been reported.21,22 The correlation between ocular manifestations and intestinal giardiasis has been circumstantial. Several patients have reported improvement in their ocular symptoms after being treated for giardiasis. The presumptive association between giardiasis and ocular manifestations has been met with skepticism. Mantovani and associates23 studied 90 children in Italy with symptomatic giardiasis, 10 of whom had ocular manifestations. Eight of these children presented with a diffuse salt-and-pepper appearance of the fundus with retinal pigment epithelial involvement in the midperiphery in both eyes. In one of the eight children, atrophic areas of the retinal pigment epithelium were noted as well as small, hard exudates in one eye. Of the remaining two children, one had evidence of chorioretinitis, and the other had hyperemia of the optic nerve head. After therapy with tinidazole 50 mg/kg (single dose), patients were followed up for 1 year. The child with chorioretinitis recovered after treatment with systemic corticosteroids, and the retinal pigment epithelial changes in the other patients remained the same. The results were compared with healthy children: none of the 200 children with gastrointestinal symptoms that were unrelated to giardiasis had evidence of salt-and-pepper changes in the fundus. Ocular manifestations that were observed in the giardiasis group were not observed in any of the control groups.

Treatment of giardiasis includes the administration of tinidazole; furazolidone (Furoxone); metronidazole (Flagyl); or quinacrine hydrochloride (Atabrine).


Pneumocystosis

Pneumocystosis is a disease caused by species of the genus Pneumocystis. The organism found in rodents, however, differs ontogenetically from the species found in man.

The organism is a recognized cause of pneumonia in infants and immunocompromised patients. In the last quarter of the 20th century, there was an increase in the incidence of Pneumocystis jiroveci (formerly carinii) pneumonia, partly because of the increase in AIDS cases.24,25,26 In AIDS, Pneumocystis jiroveci pneumonia is probably the result of reactivation of a latent subclinical infection.

Pneumocystis jiroveci has been classified as a protozoan, but the taxonomic classification of the organism has been the topic of debate for many years. Pneumocystis is regarded as a protozoan because it enters both a cyst stage and the trophozoite stage during development. The organism possesses pseudopodia and can attach to the host cell. Previous studies, including ribosomal RNA-sequencing studies, have indicated that Pneumocystis is closer to fungi than to protozoa.

Reclassification of Pneumocystis as a fungus followed the application of the 2005 Vienna Code. Validity of the name for the human pathogen Pneumocystis jiroveci was re-established from its 1976 publication under the zoological code, contrary to interpretation under the botanical codes.27 Pneumocystis jiroveci is lectotypified and epitypified. The rat parasite Pneumocystis carinii is neotypified separating it from Pneumocystis wakefieldiae.27

Three developmental stages of this organism have been recognized: precyst, cyst, and trophozoite. The cyst has a thick wall and contains eight sporozoites (intracystic bodies). After excystation, the sporozoites become trophozoites. The trophozoite measures 1.5 to 5 μm in length. It has two cell membranes, which measure approximately 25 nm. The cellular contents of the organism include a nucleus with a rough endoplasmic reticulum, vacuoles, a round body, and mitochondria. On electron microscopy of clinical specimens, the trophozoite appears as a round structure. The cyst wall consists of three layers and measures approximately 0.25 μm in thickness. The inner surface of the wall demonstrates focal thickening, having parenthesis-shaped inclusions that can stain with a silver-containing stain such as GMS. The sporozoite measures approximately 1 to 1.5 μm in diameter and contains the same organelles as the trophozoite.

Pneumocystis jiroveci may cause interstitial pneumonia in the immunocompromised host. Kwok and colleagues28 identified Pneumocystis organisms in the area of cotton-wool spots in a patient with AIDS. The report of this association, however, has been questioned because the organism did not take the silver stain, the intracystic bodies contained no nuclei, and no cyst wall could be demonstrated by electron microscopy.29 Choroiditis in patients with AIDS has been suggested to be caused by Pneumocystis jiroveci. Freeman and co-workers30 reported on Pneumocystis jiroveci choroidopathy. Clinical, histopathologic, and electron microscopic studies of Pneumocystis jiroveci choroiditis have been reported.31,32,33

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Jul 11, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Ocular Parasitic Infections

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