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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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 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