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Cysts of Giarida intestinalis (syn. Giardia lamblia)

Giardia intestinalis (Mastigophora) live fecal cyst from dog in Kansas

Giardia intestinalis (Mastigophora) stained cysts from feces of Kansas resident Chist din fecale de om

Giardia intestinalis (syn. Giardia lamblia) trophozoites

view through nuclei (Kansas canine) nucli trofozoitului la cine

ventral adhesive disc (Kansas canine) \ discul adeziv ventral la cine

polychrome IV stain (human) trofozoit la om

Causal Agent:
Giardia intestinalis is a protozoan flagellate (Diplomonadida). This protozoan was initially named Cercomonas intestinalis by Lambl in 1859 and renamed Giardia lamblia by Stiles in 1915, in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague. However, many consider the name, Giardia intestinalis, to be the correct name for this protozoan. The International Commission on Zoological Nomenclature is reviewing this issue.

Life Cycle:

Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.

Geographic Distribution:

Worldwide, more prevalent in warm climates, and in children.

Cryptosporidium

Causal Agent:
Many species of Cryptosporidium exist that infect humans and a wide range of animals. Although Cryptosporidium parvum and Cryptosporidium hominis (formerly known as C. parvumanthroponotic genotype or genotype 1) are the most prevalent species causing disease in humans, infections by C. felis, C. meleagridis, C. canis, and C. muris have also been reported.

Life Cycle:

Life cycle of Cryptosporidium parvum and C. hominis. Click on the image for a large view (31 kb).
Cryptosporidium stages were reproduced from Juranek DD. Cryptosporidiosis. In: Strickland GT, editor. Hunters Tropical Medicine and Emerging Infectious Diseases, 8th ed. Philadelphia: WB Saunders; 2000. Originally adapted from the life cycle that appears in Current WL, Garcia LS. Cryptosporidiosis. Clinc Microbiol Rev 1991;4:325-58.

Click here to see a video clip of an excystation (Adobe Flash format). Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions . Transmission ofCryptosporidium parvum and C. hominis occurs mainly through contact with contaminated water (e.g., drinking or recreational water). Occasionally food sources,

such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum and anthroponotic transmission of C. hominis occur through exposure to infected animals or exposure to water contaminated by feces of infected animals . Following ingestion (and possibly inhalation) by a suitable host , excystation occurs. The sporozoites are released and parasitize epithelial cells ( , ) of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) ( , , ) and then sexual multiplication (gametogony) producing microgamonts (male) and macrogamonts (female) . Upon fertilization of the macrogamonts by the microgametes ( ), oocysts ( , ) develop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host , and the thin-walled oocyst , which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission. Note that oocysts of Cyclospora cayetanensis, another important coccidian parasite, are unsporulated at the time of excretion and do not become infective until sporulation is completed. Refer to the life cycle of Cyclospora cayentanensis for further details.

Geographic Distribution:
Since the first reports of human cases in 1976, Cryptosporidium has been found worldwide. Outbreaks of cryptosporidiosis have been reported in several countries, the most remarkable being a waterborne outbreak in Milwaukee (Wisconsin) in 1993, that affected more than 400,000 people.

Cryptosporidium andersoni (Lindsay et al., 2000, J. Eukaryot. Microbiol. 47: 91-95)

Nomarski interference contrast photomicrograph of oocysts from calf feces. Each oocyst measures about 7.4 x 5.5 micrometers.

Histological section through stomach (gastric glands) of steer showing developmental stages

Scanning electron photomicrographs of Cryptosporidium baileyi (Cryptosporidiidae)

Cryptosporidium baileyi infects the cloaca, bursa, and sometimes respiratory tract of chickens. Heavy infections may develop, but significant clinical disease is usually associated only with respiratory cryptosporidiosis. The first two photos reveal the extent of the infections. The photograph in the upper right shows a single merozoite penetrating a host cell. The photograph in the lower left provides an unusual view of the basal portion of the feeder organelle after the parasite has become dislodged from the host cell. Two type I meronts can be seen in the photograph in the lower, middle panel. The last photograph in the lower right shows a microgamete penetrating a macrogamete.

Feeder organelle Cryptosporidium parvum

The electron micrograph on the left is of the desmosome-like junction and feeder organelle of Cryptosporidium parvum. Developmental stages occur between the microvilli and are attached to epithelial cells. During penetration of host cells by sporozoites or merozoites, an electron-dense layer forms at the point of attachment and is morphologically reminiscent of a desmosome. A thin layer of host cell cytoplasm envelops the parasite, which may be derived from fused microvilli. As the parasite rounds up and begins to differentiate, finger-like folds of the parasite cytoplasm extend to the level of the electron dense desmosome-like layer, and these folds have been termed the

"feeder organelle" (1978, Vet Pathol 15: 417-427). It is often postulated that the feeder organelle and desmosome-like junction somehow facilitate nutrient transport by the parasite. Though likely, experimental data to support this is as yet lacking.

Life-cycle of Cryptosporidium parvum

Oocysts ingested. Four infective sporozoites exit through suture. Sporozoites penetrate epithelial cells, especially along the ileum. Multiple fission (=merogony) occurs, resulting in the 8 Type I merozoites within a Type I meront. Meronts rupture, releasing free merozoites. Merozoites penetrate new cells and undergo merogony to form additional meronts. Type I merozoites are thought to be capable of recycling indefinitely (autoinfection).

Some Type I merozoites form Type II meronts, which contain 4 merozoites. Type II merozoites rupture out, enter new cells, and form macrogametes (=macrogametocyte) or microgametocytes containing 16 nonflagellated microgametes. Microgametes fertilize macrogametes. A resistant oocyst wall is then formed around the zygote, meiosis occurs, and 4 sporozoites are formed (sporogony). Oocysts are passed in the feces. About 20% of the oocysts are devoid of a wall and are sometimes termed "thin-walled oocysts." It is believed that the resulting sporozoites produced from thinwalled oocysts can excyst while still within the gut and infect new cells in a second autoinfective cycle.

Some miscellaneous Apicomplexa

Cryptosporidium parvum (host: Bos taurus) acid fast stain (oocysts red; yeast and bacteria blue)

Gregarina cuneata (host Tenebrio molitor) oocysts in strings following dehiscence

Gregarina sp. (host: mealworm) gametes in syzygy

Cryptosporidium parvum

Histological section of developmental stages within intestine of suckling mouse, 4 days postinfection

Acid fast stain showing oocysts (dark red) as differentiated from yeast (dark blue) from feces of calf

Developmental stages within intestine of suckling mouse, 4 days post-infection. Numerous type I merozoites can be seen.

Lower magnification showing the extent of developmental stages within intestine of suckling mouse, 4 days postinfection

Cryptosporidium varani (syn. C. saurophilum) from leopard geckos (Eublepharis macularis)

Wasting syndrome due to chronic intestinal infection

Cryptosporidium oocysts fecal smear, acid fast stain (oocysts reddish)

Histological section of small intestine showing developmental stages (dark dots) projecting into lumen of gut

Causal Agent:
The coccidian parasite, Cystoisospora belli, infects the epithelial cells of the small intestine, and is the least common of the three intestinal coccidia that infect humans.

Life Cycle:

At time of excretion, the immature oocyst contains usually one sporoblast (more rarely two) . In further maturation after excretion, the sporoblast divides in two (the oocyst now contains two sporoblasts); the sporoblasts secrete a cyst wall, thus becoming sporocysts; and the sporocysts divide twice to produce four sporozoites each . Infection occurs by ingestion of sporocysts-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate schizogony . Upon rupture of the schizonts, the merozoites are released, invade new epithelial cells, and continue the cycle of asexual multiplication . Trophozoites develop into schizonts which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes . Fertilization results in the development of oocysts that are excreted in the stool .

Geographic Distribution:
Worldwide, especially in tropical and subtropical areas. Infection occurs in immunodepressed individuals, and outbreaks have been reported in institutionalized groups in the United States.

Cyclosporiasis
Causal Agent:
The causal agent has been only recently identified as a unicellular coccidian parasite. The species designation Cyclospora cayetanensis was given in 1994 to Peruvian isolates of human-associated Cyclospora. It appears that all human cases are caused by this species.
References:

1. 2. 3.

Herwaldt BL. Cyclospora cayetanensis: a review, focusing on the outbreaks of cyclosporiasis in the 1990s. Clin Infect Dis 2000;31:1040-1057. Ortega YR, Gilman RH, Sterling CR. A new coccidian parasite (Apicomplexa: Eimeriidae) from humans. J Parasitol 1994;80:625-629. Pieniazek NJ, Herwaldt BL. Reevaluating the molecular taxonomy: Is human-associated Cyclospora a mammalian Eimeria species? Emerg Infect Dis 1997;3:381-383.

Life Cycle:

Some of elements of this figure were created based on an illustration by Ortega et al. Cyclospora cayetanensis. In: Advances in Parasitology: opportunistic protozoa in humans. San Diego: Academic Press; 1998. p. 399-418.

When freshly passed in stools, the oocyst is not infective (thus, direct fecal-oral transmission cannot occur; this differentiates Cyclospora from another important coccidian parasite,Cryptosporidium). In the environment , sporulation occurs after days or weeks at temperatures between 22C to 32C, resulting in division of the sporont into two sporocysts, each containing two elongate sporozoites . Fresh produce and water can serve as vehicles for transmission and the sporulated oocysts are ingested (in contaminated food or water) . The oocysts excyst in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine . Inside the cells they undergo asexual multiplication and sexual development to mature into oocysts, which will be shed in stools . The potential mechanisms of contamination of food and water are still under investigation.

Geographic Distribution:
Cyclosporiasis has been reported in many countries, but is most common in tropical and subtropical areas. Since 1990, at least 11 foodborne outbreaks of cyclosporiasis, affecting approximately 3600 persons, have been documented in the United States and Canada.

Causal Agents:
The term microsporidia is also used as a general nomenclature for the obligate intracellular protozoan parasites belonging to the phylum Microsporidia. To date, more than 1,200 species belonging to 143 genera have been described as parasites infecting a wide range of vertebrate and invertebrate hosts. Microsporidia, are characterized by the production of resistantspores that vary in size, depending on the species. They possess a unique organelle, the polar tubule or polar filament, which is coiled inside the spore as demonstrated by its ultrastructure. The microsporidia spores of species associated with human infection measure from 1 to 4 m and that is a useful diagnostic feature. There are at least 14 microsporidian species that have been identified as human pathogens: Brachiola algerae, B. connori, B. vesicularum, Encephalitozoon cuniculi, E. hellem, E. intestinalis, Enterocytozoon bieneusi Microsporidium ceylonensis,M. africanum, Nosema ocularum, Pleistophora sp., Trachipleistophora hominis, T. anthropophthera, Vittaforma corneae. Encephalitozoon intestinalis was previously named Septata intestinalis, but it was reclassified as Encephalitozoon intestinalis based on its similarity at the morphologic, antigenic, and molecular levels to other species of this genus. Based on recent data it is now known that some domestic and wild animals may be naturally infected with the following microsporidian species: E. cuniculi, E. intestinalis, E. bieneusi. Birds, especially parrots (parakeets, love birds, budgies) are naturally infected with E. hellem. E. bieneusi and V. corneae have been identified in surface waters, and spores of Nosema sp. (likely B. algerae) have been identified in ditch water.

Life Cycle:

The infective form of microsporidia is the resistant spore and it can survive for a long time in the environment . The spore extrudes its polar tubule and infects the host cell . The spore injects the infective sporoplasm into the eukaryotic host cell through the polar tubule . Inside the cell, the sporoplasm undergoes extensive multiplication either by merogony (binary fission) or schizogony (multiple fission) . This development can occur either in direct contact with the host cell cytoplasm (e.g., E. bieneusi) or inside a vacuole termed parasitophorous vacuole (e.g., E. intestinalis). Either free in the cytoplasm or inside a parasitophorous vacuole, microsporidia develop by sporogony to mature spores . During sporogony, a thick wall is formed around the spore, which provides resistance to adverse environmental conditions. When the spores increase in number and completely fill the host cell cytoplasm, the cell membrane is

disrupted and releases the spores to the surroundings infect new cells thus continuing the cycle.

. These free mature spores can

Geographic Distribution:
Microsporidia are being increasingly recognized as opportunistic infectious agents worldwide. Cases of microsporidiosis have been reported* in developed as well as in developing countries, including: Argentina, Australia, Botswana, Brazil, Canada, Czech Republic, France, Germany, India, Italy, Japan, The Netherlands, New Zealand, Spain, Sri Lanka, Sweden, Switzerland, Thailand, Uganda, United Kingdom, United States of America, and Zambia. http://www.dpd.cdc.gov/dpdx/Default.htm

Some miscellaneous ciliates

Balantidium coli cyst (intestine of swine) 40-60 micrometers in diameter

Ichthyophthirius multifiliis trophozoite (in skin of freshwater fish) up to 1 mm long

Nyctotherus sp. trophozoites (Geochelone dendriculata)

Balantidium coli trophozoites (Ciliophora)

Above: oil immersion photomicrographs of individual trophozoites

High dry objective photomicrographs of trophozoites

Balantidium coli intestinal ulceration

Numerous trophozoites in intestinal tissue

Causal Agent:
Balantidium coli, a large ciliated protozoan parasite.

Life Cycle:

Cysts are the parasite stage responsible for transmission of balantidiasis . The host most often acquires the cyst through ingestion of contaminated food or water . Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine . The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur . Trophozoites undergo encystation to produce infective cysts . Some trophozoites invade the wall of the colon and multiply. Some return to the lumen and disintegrate. Mature cysts are passed with feces .

Geographic Distribution:
Worldwide. Because pigs are an animal reservoir, human infections occur more frequently in areas where pigs are raised. Other potential animal reservoirs include rodents and nonhuman primates.

Blastocystis hominis

Blastocystis hominis is an anaerobic intestinal protozoan originally allied with the amoebae and more recently with the alveolates (Apicomplexa, dinoflagellates, and Ciliophora). Numerous morphologically similar forms exist in different animals and the number of true species is not yet known. At least three distinct morphological types can be found in feces, including the common vacuolar stage (above) which divides, an amoeboid stage which may be invasive and is capable of budding, and a granular or cystic form which is thought to give rise to numerous new organisms when conditions become unfavorable. Heavy infections are linked to diarrhea and intestinal discomfort, but whether the parasite is a causative agent of intestinal distress or responds favorably to an opportunistic situation is still unclear. Certainly the detection of high numbers in fecal smears is an indicator that something is amiss. The parasite seems to be susceptible to numerous drugs, including trimethoprim/sulfamethoxazole, metronidazole, and pentamidine. Causal Agent:
The taxonomic classification of Blastocystis hominis is mired in controversy. It has been previously considered as yeasts, fungi, or ameboid, flagellated, or sporozoan protozoa. Recently, however, based on molecular studies, especially dealing with the sequence information on the complete SSUrRNA gene, B. hominis has been placed within an informal group, the stramenopiles (Silberman et al. 1996). Stramenopiles are defined, based on molecular phylogenies, as a heterogeneous evolutionary assemblage of unicellular and multicellular protists including brown algae, diatoms, chrysophytes, water molds, slime nets, etc. (Patterson, 1994). Cavalier-Smith (1998) considers stramenopiles to be identical to his infrakingdom Heterokonta under the kingdom Chromista. Therefore, according to Cavalier-Smith, B. hominis is a heterokontid chromista.
References:

1. 2. 3.

Silberman JD, Sogin ML, Leipe DD, Clark CG. Human parasite finds taxonomic home. Nature 1996;380:398. Patterson DJ. Protozoa, evolution and systematics. In: Housmann K, Hulsmann N, editors. Progress in Protozoology. Stuttgart: Fischer; 1994. p. 1-14. Cavalier-Smith T. A revised six-kingdom system of life. Biol Rev Camb Philos Soc 1998;73:203-266.

Life Cycle:

Blastocystis hominis stages were reproduced from Singh M, Suresh K, Ho LC, Ng GC, Yap EH. Elucidation of the life cycle of the intestinal protozoan Blastocystis hominis. Parasitol Res 1995;81:449. Copyright held by Springer-Verlag and reproduced here by permission of Springer-Verlag and M. Singh.

Knowledge of the life cycle and transmission is still under investigation, therefore this is a proposed life cycle for B. hominis. The classic form found in human stools is the cyst, which varies tremendously in size from 6 to 40 m . The thick-walled cyst present in the stools is believed to be responsible for external transmission, possibly by the fecal-oral route through ingestion of contaminated water or food . The cysts infect epithelial cells of the digestive tract and multiply asexually ( , ). Vacuolar forms of the parasite give origin to multi vacuolar and ameboid forms. The multi-vacuolar develops into a pre-cyst that gives origin to a thin-walled cyst , thought to be responsible for autoinfection. The ameboid form gives origin to a pre-cyst , which develops into thick-walled cyst by schizogony . The thick-walled cyst is excreted in feces .

Geographic Distribution:
Worldwide.

Dientamoeba fragilis

Dientamoeba fragilis is an amoeboflagellate and, though forming no flagella, is most closely allied with the flagellates. It is currently placed within the family Monocercomonadidae. Trophozoites are small, 5-12 micrometers in length, and 60-80% are binucleate. Good staining reveals a mitotic spindle interconnecting the two nuclei. No cysts are formed and the parasite is unable to survive passage through the stomach. Like most intestinal amoebae (or in this case amoebae-like organism), Dientamoeba fragilis can cause mild to moderate diarrhea and abdominal discomfort. However, it is not known to be invasive like Entamoeba histolytica. Studies have shown that D. fragilis can survive in the eggs of the human pinworm, Enterobius vermicularis (1956, Am. J. Trop. Med. Hyg. 5: 258-265; 1977, Am. J. Trop. Med. Hyg. 26: 16-22). Thus, like the closely related Histomonas meleagridis, it is likely that transmission of this protozoan is also through ingestion of pinworm ova. One recent study (2000, J Clin Microbiol 38: 4653-4654) has revealed two distinct genetic variants. These may or may not represent distinct, morphologically similar species.
The complete life cycle of this parasite has not yet been determined, but assumptions were made based on clinical data. To date, the cyst stage has not been identified in D. fragilis life cycle, and the trophozoite is the only stage found in stools of infected individuals . D. fragilis is probably transmitted by fecal-oral route and transmission via helminth eggs (e.g.,Ascaris, Enterobius spp.) has been postulated . Trophozoites of D. fragilis have characteristically one or two nuclei ( , ), and it is found in children complaining of intestinal (e.g., intermittent diarrhea, abdominal pain) and other symptoms (e.g., nausea, anorexia, fatigue, malaise, poor weight gain).

Geographic Distribution:
Worldwide.

Macroscopic cysts of a Sarcocystis sp. in the breast muscle of a Green-winged teal collected in Brazos County, Texas
Members of the genus Sarcocystis possess a heteroxenous life-cycle. Asexual multiplication occurs in the intermediate host resulting in the formation of resistant tissue cysts containing thousands of bradyzoites. Some species produce microscopic tissue cysts whereas other species, such

as the one on the left, produces rice grain-like macroscopic cysts. Metrocytes are present within these cysts, which are globular, irregularly shaped cells that undergo endodyogeny and eventually give rise to infective bradyzoites. Once the tissue cyst is ingested by the appropriate definitive host, bradyzoites are liberated, penetrate intestinal cells, and undergo gamogony. Merogony does not occur within the intestinal tract of the definitive host. The resulting oocysts sporulate endogenously and are thin-walled, often rupturing and releasing free sporocysts in the feces. Although not all members are pathogenic, some species are and heavy infections in the intermediate host can lead to anemia, premature parturition, abortion, weight loss, diarrhea, anorexia, and death. The traditional name for macroscopic cysts of Sarcocystis spp. in anseriform birds has been Sarcocystis "rileyi". However, this actually represents a complex of multiple Sarcocystis spp. Definitive hosts for these various species include Didelphis virginiana (opossum) and Mephitis mephitis (striped skunk), and it is likely that future studies will reveal a number of additional medium-sized mammals as hosts.

Tissue cysts of 3 Sarcocystidae

Besnoita darlingi (opossum) many cysts macroscopic

Hammondia hammondi (mouse) this cyst 103 x 44 micrometers

Sarcocystis tenella (sheep) some up to 700 micrometers long

Some miscellaneous flagellates

Opalina sp. (Opalinata) trophozoite from Pseudacris streckeri

Trichonympha campanula trophozoites from termite gut

Trichomonas vaginalis (Mastigophora) trophozoites from culture

Trichomonas vaginalis (Mastigophora) longitudinal binary fission

ausal Agent:
Trichomonas vaginalis, a flagellate, is the most common pathogenic protozoan of humans in industrialized countries.

Life Cycle:

Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate , where it replicates by binary fission . The parasite does not appear to have a cyst form, and does not survive well in the external environment. Trichomonas vaginalis is transmitted among humans, its only known host, primarily by sexual intercourse .

Geographic Distribution:
Worldwide. Higher prevalence among persons with multiple sexual partners or other venereal diseases.