Cyklosporoza
Patofizjologia i mechanizm

Cyclospora cayetanensis to obligatoryjny pasożyt wewnątrzkomórkowy jelita cienkiego, wywołujący cyklosporozę, charakteryzującą się przewlekłą biegunką, utratą masy ciała i bólami brzucha. Pasożyt infekuje enterocyty dwunastnicy i jelita czczego, prowadząc do uszkodzenia rąbka szczoteczkowego, atrofii kosmków jelitowych, hiperplazji krypt oraz nacieku zapalnego w błonie śluzowej. Cykl życiowy obejmuje spożycie sporulowanych oocyst, inwazję sporozoitów, fazę merontów typu I i II oraz rozmnażanie płciowe, po którym oocysty są wydalane w kale w formie niesporulowanej i wymagają 7-15 dni sporulacji w środowisku (23-32°C) do uzyskania zakaźności. U osób immunosupresyjnych, zwłaszcza z HIV/AIDS, infekcja może rozszerzać się na drogi żółciowe i przebiegać przewlekle i ciężko. Immunologiczna odpowiedź gospodarza obejmuje produkcję przeciwciał IgA i IgG oraz aktywację limfocytów T CD8+ w błonie śluzowej jelita.

Cyklosporoza – patogeneza i mechanizm działania

Cyclospora cayetanensis jest pasożytniczym pierwotniakiem kokcydialnym, który wywołuje chorobę zwaną cyklosporozą u ludzi. Jest to obligatoryjny pasożyt wewnątrzkomórkowy, który infekuje komórki nabłonkowe jelita cienkiego, szczególnie w dwunastnicy i jelicie czczym, powodując charakterystyczne zmiany patologiczne oraz objawy przewlekłej biegunki.12

Cykl życiowy i mechanizm infekcji

Cyclospora cayetanensis ma złożony cykl życiowy, obejmujący zarówno rozwój płciowy, jak i bezpłciowy w obrębie jednego gospodarza. Infekcja rozpoczyna się od spożycia w pełni sporulowanych oocyst znajdujących się w zanieczyszczonej kałem żywności lub wodzie.1 Po dostaniu się do organizmu gospodarza, oocysty uwalniają sporozoity w świetle jelita cienkiego, które następnie wnikają do komórek nabłonkowych dwunastnicy i jelita czczego.1

Po inwazji do komórek nabłonkowych, sporozoity przekształcają się w trofozoity, które następnie przechodzą w jedną z dwóch form merontów (schizontów):1

  • Meronty typu I – zawierają 8-12 merozoitów i podtrzymują autoinfekcję w organizmie gospodarza1
  • Meronty typu II – zawierają 4 merozoity, które później przekształcają się w mikrogametocyty (mikrogamonty) i makrogametocyty (makrogamonty), inicjując cykl płciowy1

W procesie rozmnażania płciowego mikrogametocyty zapładniają makrogametocyty, co prowadzi do powstania zygoty. Zygoty przekształcają się w oocysty w enterocytach i są wydalane w postaci niesporulowanej w kale.1 Oocysty te nie są od razu zakaźne – muszą przejść proces sporulacji w środowisku zewnętrznym, co zajmuje od 7 do 15 dni w odpowiednich warunkach środowiskowych (temperatura 23-32°C).11 Ta cecha odróżnia Cyclospora od innych ważnych kokcydiów pasożytniczych, takich jak Cryptosporidium, których oocysty są natychmiast zakaźne po wydaleniu.2

Zmiany patologiczne w tkance jelitowej

Inwazja i namnażanie się pasożyta w enterocytach prowadzi do uszkodzenia nabłonka jelita cienkiego, co skutkuje wieloma charakterystycznymi zmianami histopatologicznymi:2

  • Zaburzenie struktury rąbka szczoteczkowego1
  • Utrata błonowych enzymów trawiennych1
  • Stępienie i atrofia kosmków jelitowych1
  • Hiperplazja krypt1
  • Zmiana kształtu komórek nabłonkowych z walcowatych na sześcienne2
  • Wakuolizacja szczytowych części kosmków2

W blaszce właściwej błony śluzowej obserwuje się napływ limfocytów, komórek plazmatycznych i czasami eozynofilów.1 Biopsje jelita czczego wykazują zmiany błony śluzowej w kosmkach jelitowych, rozlany obrzęk i naciek komórkami zapalnymi, reaktywną hyperemię, rozszerzenie naczyń i przekrwienie naczyń włosowatych w obecności pasożyta.11

Te zmiany prowadzą ogólnie do zmniejszenia zdolności absorpcyjnej jelita cienkiego, co skutkuje zmniejszonym wchłanianiem wody, składników odżywczych i elektrolitów.2 Jest to główny mechanizm odpowiedzialny za objawy kliniczne cyklosporozy, takie jak przedłużająca się biegunka wodna, utrata masy ciała, anoreksja, bóle brzucha i wzdęcia.1

Mechanizmy obronny gospodarza i immunopatologia

Odpowiedź immunologiczna gospodarza na infekcję Cyclospora cayetanensis obejmuje zarówno odporność humoralną, jak i komórkową:2

  • Odporność humoralna – obejmuje produkcję przeciwciał przez komórki B, które mogą neutralizować pasożyta i zapobiegać inwazji komórek gospodarza. Badania wykazały, że pacjenci z cyklosporozą wytwarzają przeciwciała IgA i IgG przeciwko Cyclospora cayetanensis2
  • Odporność komórkowa – angażuje aktywację limfocytów T, które rozpoznają i niszczą zainfekowane komórki gospodarza. U pacjentów z cyklosporozą stwierdzono zwiększoną liczbę komórek T CD8+ w błonie śluzowej jelita2

Stopień nasilenia objawów klinicznych jest powiązany ze stanem immunologicznym gospodarza. U osób immunokompetentnych Cyclospora zazwyczaj ogranicza się do górnego odcinka jelita cienkiego i wywołuje samoograniczającą się chorobę. Natomiast u pacjentów z obniżoną odpornością, szczególnie z infekcją HIV i AIDS, może powodować ektopowe zakażenie dróg żółciowych i pęcherzyka żółciowego oraz przewlekłą, ciężką i nawracającą biegunkę.11

Molekularne podstawy patogenezy

Badania genomiczne wykazały, że Cyclospora cayetanensis posiada podobny zestaw białek związanych z inwazją komórek gospodarza jak inne kokcydia, co sugeruje, że ma podobny proces inwazji do Toxoplasma gondii i Eimeria tenella:1

  • Ślizganie się napędzane przez silnik aktynowy przed inwazją2
  • Interakcje z komórką gospodarza poprzez antygeny powierzchniowe2
  • Tworzenie ruchomego połączenia z szeregiem wydzielanych białek w celu zainicjowania inwazji2
  • Tworzenie struktury wakuoli pasożytniczej wewnątrz komórki gospodarza2
  • Wydzielanie różnych kinaz białkowych, fosfataz białkowych i innych białek katalitycznych w celu modyfikacji szlaków metabolicznych gospodarza, umożliwiając uniknięcie odpowiedzi immunologicznej gospodarza2

W porównaniu z T. gondii, Cyclospora cayetanensis wykazuje znaczne zmniejszenie liczby kinaz białkowych i fosfataz, co sugeruje, że ma ograniczoną zdolność do regulacji szlaków sygnałowych komórek gospodarza i ekspresji genów lub wykorzystuje odmienny system do tego celu.2

Odporność na czynniki środowiskowe

Cyclospora cayetanensis wykazuje znaczną odporność na różne czynniki środowiskowe, co przyczynia się do jej skutecznego rozprzestrzeniania:2

  • Oocysty są odporne na rutynowe procedury dezynfekcji chemicznej stosowane w systemach nawadniania, wodach rekreacyjnych lub stacjach uzdatniania wody pitnej2
  • Pasożyt może być oporny na rutynowe metody dezynfekcji chemicznej, takie jak te wykorzystujące chlor11
  • Oocysty są inaktywowane po ogrzewaniu w temperaturze 60°C przez 1 godzinę2
  • Wysuszenie przez 15 minut powoduje pękanie ścian oocyst2
  • Oocysty mogą przetrwać w wodzie przez 2 miesiące w temperaturze 4°C i 7 dni w temperaturze 37°C2

Ta odporność na warunki środowiskowe, w połączeniu z małym rozmiarem (8-10 μm), niską masą właściwą i wysoką zakaźnością, umożliwia rozprzestrzenianie się zakaźnych oocyst Cyclospora za pośrednictwem wody, gleby i nieprzetworzonych pokarmów, takich jak owoce i warzywa.2

Nietypowe lokalizacje i manifestacje patogenezy

Chociaż Cyclospora cayetanensis zazwyczaj infekuje jelito cienkie, oocysty wykryto również w próbkach pozajelitowych:2

  • W plwocinie pacjentów z HIV z historią gruźlicy płuc, co sugeruje, że Cyclospora może być uważana za patogen oportunistyczny2
  • Przypadki zajęcia dróg żółciowych i pęcherzyka żółciowego u pacjentów z obniżoną odpornością1

Istnieją również doniesienia o związku między zakażeniem Cyclospora a zespołem Guillaina-Barrégo oraz porażeniem Bella, co sugeruje, że cyklosporoza może być zaangażowana w odwracalne uszkodzenie neuronów lub inne nieznane mechanizmy prowadzące do tych chorób neurologicznych.21

Dodatkowo zaobserwowano możliwość przewlekłej kolonizacji jelit przez Cyclospora bez objawów infekcji, co może zmieniać mikrobiotę jelitową i zmniejszać odporność błony śluzowej, prowadząc do rozwoju zakażenia Clostridioides difficile poprzez mechanizm podobny do tego obserwowanego w biegunce wywołanej antybiotykami.1

Leczenie i kontrola infekcji w kontekscie patogenezy

Zrozumienie patogenezy Cyclospora cayetanensis ma kluczowe znaczenie dla opracowania skutecznych strategii leczenia i kontroli.1 Dotychczas stosowane metody obejmują:

  • Antybiotyki – do leczenia zakażeń Cyclospora stosuje się trimetoprim-sulfametoksazol. U pacjentów immunokompetentnych leczenie kombinacją 160 mg trimetoprimu i 800 mg sulfametoksazolu (tj. tabletka o podwójnej mocy) dwa razy dziennie przez 7 dni kończy chorobę biegunkową i prowadzi do eliminacji pasożytów2
  • Nowe podejścia terapeutyczne – niedawno opracowano nanocząstki lipidowe zawierające nitazoksanid (NTZ-loaded NLCs), które wykazały znaczną skuteczność w leczeniu eksperymentalnej cyklosporozy, osiągając 98% redukcję pasożytów zarówno u myszy immunokompetentnych, jak i immunosupresyjnych1

Mechanizm działania nitazoksanidu opiera się na zakłócaniu cyklu oddechowego pasożyta poprzez hamowanie enzymu oksydoreduktazy pirogronian:ferredoksyna.2 Nowa formulacja w postaci nanocząstek zwiększa rozpuszczalność leku i poprawia jego przenikanie do tkanek, co znacznie zwiększa efektywność terapii.2

Dalsze badania nad biologią, patogenezą i kontrolą zakażenia i transmisji są utrudnione przez trudności z namnażaniem organizmu, brak wiarygodnych testów żywotności i zakaźności oocyst oraz niemożność eksperymentalnego zakażenia zwierząt i ludzkich ochotników.1

Podsumowanie patogenezy cyklosporozy

Patogeneza cyklosporozy jest złożonym procesem obejmującym kilka kluczowych etapów:1

  1. Spożycie: Infekcja rozpoczyna się, gdy osoba spożywa żywność lub wodę zanieczyszczoną oocystami C. cayetanensis
  2. Ekscystacja: Po dostaniu się do jelita cienkiego gospodarza, oocysty uwalniają sporozoity
  3. Inwazja: Sporozoity wnikają do komórek nabłonkowych wyściełających jelito cienkie
  4. Replikacja: Pasożyt namnaża się bezpłciowo wewnątrz wakuoli pasożytniczej
  5. Rozmnażanie płciowe: Po kilku cyklach rozmnażania bezpłciowego pasożyt przechodzi rozmnażanie płciowe
  6. Sporulacja: Zygoty powstałe w wyniku zapłodnienia dojrzewają do oocyst wydalanych w kale
  7. Dojrzewanie środowiskowe: Oocysty nie są natychmiast zakaźne i wymagają dni lub tygodni, aby sporulować w środowisku przed staniem się zakaźnymi

Zmiany patologiczne w jelicie, spowodowane inwazją i namnażaniem się pasożyta, prowadzą do zaburzenia funkcji absorpcyjnej i objawów klinicznych cyklosporozy. Zakażenie najczęściej ogranicza się do górnego odcinka jelita cienkiego u osób immunokompetentnych, ale może powodować zakażenia ektopowe i przewlekłą chorobę u pacjentów z obniżoną odpornością.11

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  1. 14.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Cyclosporiasis—Updates on Clinical Presentation, Pathology, Clinical Diagnosis, and Treatment
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8471761/
    Cyclospora cayetanensis has a complex life cycle involving both sexual and asexual development within a single host. Infection is initiated by the ingestion of fully sporulated oocysts in fecally contaminated food or water. The oocysts excyst in the lumen of the small intestine, and sporozoites invade the epithelial cells lining the duodenum and jejunum. The sporozoites become trophozoites, which in turn become either Type I meronts (schizonts) or Type II meronts. Type I meronts contain 812 merozoites and perpetuate autoinfection in the host. Type II meronts each contain four merozoites, which go on to form microgametocytes (microgamonts) and macrogametocytes (macrogamonts) to initiate the sexual cycle. A microgametocyte fertilizes a macrogametocyte, resulting in the formation of a zygote. Zygotes become oocysts in the enterocytes and are shed in an unsporulated state in the feces. Parasite invasion and replication within enterocytes damages the small intestinal epithelium, leading to the disruption of the brush border, loss of membrane bound digestive enzymes, and intestinal villous blunting and atrophy. An influx of lymphocytes, plasma cells, and occasionally eosinophils occurs in the lamina propria. These changes have the overall effect of decreasing the small intestinal absorptive capacity, leading to decreased uptake of water, nutrients, and electrolytes. Cyclospora cayetanensis is usually confined to the upper small intestine in immunocompetent hosts, but it can cause ectopic infection of the biliary tree and gall bladder in patients with HIV infection and AIDS.
  • #1 Cyclosporiasis—Updates on Clinical Presentation, Pathology, Clinical Diagnosis, and Treatment
    https://www.mdpi.com/2076-2607/9/9/1863
    Cyclospora cayetanensis has a complex life cycle involving both sexual and asexual development within a single host. Infection is initiated by the ingestion of fully sporulated oocysts in fecally contaminated food or water. The oocysts excyst in the lumen of the small intestine, and sporozoites invade the epithelial cells lining the duodenum and jejunum. The sporozoites become trophozoites, which in turn become either Type I meronts (schizonts) or Type II meronts. Type I meronts contain 8–12 merozoites and perpetuate autoinfection in the host. Type II meronts each contain four merozoites, which go on to form microgametocytes (microgamonts) and macrogametocytes (macrogamonts) to initiate the sexual cycle. A microgametocyte fertilizes a macrogametocyte, resulting in the formation of a zygote. Zygotes become oocysts in the enterocytes and are shed in an unsporulated state in the feces. Oocysts sporulate in the environment, at which time they become infective to other people. Factors affecting sporulation in nature are still unresolved, but the process may be influenced by humidity, soil chemistry, and exposure to ultraviolet light. Under laboratory conditions, sporulation takes approximately 7–14 days at 22 °C and 30 °C.
  • #1 CDC – DPDx – Cyclosporiasis
    https://www.cdc.gov/dpdx/cyclosporiasis/index.html
    Cyclospora cayetanensis is a coccidian protozoan. It appears that all human cases are caused by this species; no animal reservoirs for C. cayetanensis have been identified. […] 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 into type I and type II meronts. Merozoites from type I meronts likely remain in the asexual cycle, while merozoites from type II meronts undergo sexual development into macrogametocytes and microgametocytes upon invasion of another host cell. Fertilization occurs, and the zygote develops to an oocyst which is released from the host cell and shed in the stool. Several aspects of intracellular replication and development are still unknown, and the potential mechanisms of contamination of food and water are still under investigation.
  • #1 Cyclosporiasis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Cyclosporiasis_pathophysiology
    Cyclospora cayetanensis infects epithelial cells of the gastrointestinal tract, especially those of the duodenum and jejunum. It causes histological changes in the infected mucosa, which may include: loss of the brush border appearance, villous atrophy, crypt hyperplasia, and vacuolization of the tips of the villi. […] Unsporulated oocysts of Cyclospora cayetanensis are excreted from infected individuals. When freshly passed in stool, the oocyst is not infective (thus, direct fecal-oral transmission cannot occur, which differentiates Cyclospora from other important coccidian parasites such as Cryptosporidium). Under adequate temperatures (23-32C), oocysts take about 7-15 days to sporulate and become infectious. After ingestion, oocysts excyst to release elongated sporozoites. Sporozoites then infect epithelial cells of the gastrointestinal tract, particularly those of the duodenum and jejunum. The sporozoites undergo asexual reproduction giving rise to meronts type I and II, which then differentiate into gametocytes. Gametocytes are fertilized to produce a zygote.
  • #1 Cyclospora cayetanensis – Wikipedia
    https://en.wikipedia.org/wiki/Cyclospora_cayetanensis
    Cyclospora cayetanensis is a coccidian parasite that causes a diarrheal disease called cyclosporiasis in humans and possibly in other primates. […] The protozoan lives out its lifecycle intracellularly within the host’s epithelial cells and gastrointestinal tract. Infection is transmitted through the fecal-oral route, and begins when a person ingests oocysts in feces-contaminated food or water. Various chemicals in the host’s gastrointestinal tract cause the oocysts to excyst and release sporozoites; generally, two are observed per oocyst. After these sporozoites invade the epithelial cells, they undergo merogony, a form of asexual reproduction that results in many daughter merozoites. These daughter cells may either infect new host cells and initiate yet another round of merogony or take on a sexual track via gametogony: Daughter merozoites become male macrogamonts which form many microgametes and female macrogamonts. After fertilization has occurred via male microgamete fusion with female macrogamont, the zygote matures into an oocyst and ruptures the host cell, from which point it is passed with the stool.
  • #1 Cyclosporiasis and Fresh Produce | FDA
    https://www.fda.gov/food/foodborne-pathogens/cyclosporiasis-and-fresh-produce
    Cyclosporiasis is an intestinal illness caused by the parasite Cyclospora cayetanensis (C. cayetanensis). […] As a parasite, C. cayetanensis behaves differently than other gastrointestinal pathogens that commonly cause foodborne illness. The parasite must be shed by an infected person and remain in the environment for 1-2 weeks before becoming infective to other humans. Once infective, people can become sick by ingesting contaminated food or water and continue the cycle. […] C. cayetanensis needs to spend some time in specific environmental conditions to become infectious and later cause cyclosporiasis; therefore, this parasite is unlikely to be transmitted directly from person-to-person. […] Under experimental conditions, a combination of time and temperature (temperatures from 73 to 77F for 7-15 days) were required for C. cayetanensis to become infectious.
  • #1 Cyclospora cayetanensis
    https://www.k-state.edu/parasitology/cyclospora/cyclospora.html
    Individuals infected with Cyclospora may experience prolonged watery diarrhea, abdominal cramping, weight loss, anorexia, myalgia, and occasionally vomiting and/or fever. […] The small intestine becomes inflamed, and the parasite causes mucosal changes that include villous atrophy and crypt hyperplasia. Mild infections may produce few or no clinical signs.
  • #1 Coccidian parasites -Cyclospora cayetanensis | PPT
    https://www.slideshare.net/slideshow/coccidian-parasites-cyclospora-cayetanensis/250007828
    Coccidian parasites -Cyclospora cayetanensis Dr. Suprakash Das Assit. Prof. Cyclospora cayetanensis C. caytanensis is the only species of the genus that is cause to infection in human. Infection of GI tract in both immunocompetent and immunocompromised hosts. First discovered in 1979 in the human faeces, it has become an important parasite for AIDS patients. […] Small intestine shows acute and chronic inflammation, blunting and atrophy of villi, and hyperplasia of crypts. […] Developmental stages of C. cayetanensis usually occur within epithelial cells of the jejunum and lower portion of the duodenum. Cyclospora infection reveals characteristics of a small bowel pathogen, including upper gastrointestinal symptoms, malabsorption of d-xylose, weight loss, and moderate to marked erythema of the distal duodenum. Histopathology in small bowel biopsy specimens reveals Acute and chronic inflammation, Partial villous atrophy, Crypt hyperplasia.
  • #1
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6780905/
    Cyclospora cayetanensis is a coccidian parasite of humans, with a direct fecal-oral transmission cycle. […] The disease is self-limiting in most immunocompetent patients, but it may present as a severe, protracted or chronic diarrhea in some cases, and may colonize extra-intestinal organs in immunocompromised patients. […] The pathogenesis underlying these symptoms has not been defined. Jejunal biopsies have shown mucosal alterations in intestinal villi, diffuse edema and infiltration by inflammatory cells, reactive hyperemia, vascular dilation and congestion of capillaries in the presence of the parasite, which are compatible with inflammation of the upper intestinal tract.
  • #1 Cyclospora cayetanensis and Cyclosporiasis: An Update
    https://www.mdpi.com/2076-2607/7/9/317
    Cyclospora cayetanensis is a coccidian parasite of humans, with a direct fecal–oral transmission cycle. […] The disease is self-limiting in most immunocompetent patients, but it may present as a severe, protracted or chronic diarrhea in some cases, and may colonize extra-intestinal organs in immunocompromised patients. […] The pathogenesis underlying these symptoms has not been defined. Jejunal biopsies have shown mucosal alterations in intestinal villi, diffuse edema and infiltration by inflammatory cells, reactive hyperemia, vascular dilation and congestion of capillaries in the presence of the parasite, which are compatible with inflammation of the upper intestinal tract.
  • #1 Comparative genomics reveals Cyclospora cayetanensis possesses coccidia-like metabolism and invasion components but unique surface antigens | BMC Genomics | Full Text
    https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-016-2632-3
    Cyclospora cayetanensis is an apicomplexan that causes diarrhea in humans. The investigation of foodborne outbreaks of cyclosporiasis has been hampered by a lack of genetic data and poor understanding of pathogen biology. In this study we sequenced the genome of C. cayetanensis and inferred its metabolism and invasion components based on comparative genomic analysis. […] The similar repertoire of host cell invasion-related proteins possessed by all coccidia suggests that C. cayetanensis has an invasion process similar to the one in T. gondii and E. tenella. However, the significant reduction in the number of identifiable rhoptry protein kinases, phosphatases and serine protease inhibitors indicates that monoxenous coccidia, especially C. cayetanensis, have limited capabilities or use a different system to regulate host cell nuclear activities.
  • #1 Cyclospora | FDA
    https://www.fda.gov/food/foodborne-pathogens/cyclospora
    Cyclospora cayetanensis is a parasite that is so small it can only be seen under a microscope. When people eat food or drink water thats contaminated with Cyclospora, they can get an intestinal illness called cyclosporiasis. […] Cyclospora is generally transmitted when infected feces contaminate food or water. Its unlikely to be transmitted directly from person to person because the Cyclospora parasite needs time (days to weeks) after being passed in a bowel movement to become infectious for another person. […] The time between becoming infected and becoming sick is usually about one week. Cyclospora infects the small intestine (bowel) and usually causes watery diarrhea, with frequent, sometimes explosive, bowel movements. Other common symptoms include loss of appetite, weight loss, stomach cramps/pain, bloating, increased gas, nausea, and fatigue. […] Based on current information available Cyclospora may be resistant to routine chemical disinfection methods such as those using chlorine.
  • #1 Cyclospora
    https://www.ecolab.com/expertise-and-innovation/resources/microbial-risks/cyclospora
    Cyclospora is a parasite that infects the small intestine, causing cyclosporiasis. […] Cyclosporiasis cannot be transmitted from person to person. An infected person sheds non-infective Cyclospora oocysts, which then need up to 14 days in suitable environmental conditions to become infective. […] This mechanism could make imported produce an ideal host for Cyclospora oocysts because it generally travels for many days before consumption. […] Cyclospora oocysts are resistant to common disinfectants such as chlorine and iodine, and there are no EPA guidelines for demonstrating product performance against Cyclospora.
  • #1 Cyclospora – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Infectious_diseases/Cyclospora/
    Cyclospora is an intestinal parasite that can cause a variety of symptoms including watery diarrhea, fatigue, anorexia, myalgia, abdominal cramps, flatus, nausea, dehydration, and weight loss. It is spread through the ingestion of contaminated food or water that has come into contact with feces. […] Cyclospora cayetanensis is an intestinal parasite that is spread by ingesting food or water that has been contaminated with feces (CDC 2013). It has a worldwide distribution but is most common in developing areas (Suh et al. 2015). C. cayetanensis is a common cause of traveler’s diarrhea, but it has become a concern as an emerging disease due to several large-scale food-borne outbreaks in the late 1990s in the United States and Canada (Shields and Olson 2003). C. cayetanensis infection is sometimes asymptomatic, but common symptoms are watery diarrhea, vomiting, headache, fever, and other flu-like-symptoms (CDC 2013). It is also of concern because it has been associated with more serious sequelae including Guillain-Barré syndrome, reactive arthritis syndrome, and cholecystitis (Shields and Olson 2003).
  • #1
    https://journals.lww.com/ajg/fulltext/2024/10001/s2769_cyclospora_cayetanensis_or_clostridioides.2770.aspx
    Cyclospora cayetanensis, a parasite causing human enteritis, has been rarely reported from healthcare laboratories, despite its universal presence. […] While it is usually responsible for self-limiting diarrhea in immunocompetent individuals, we present a case where the patient suffered from severe, unrelenting diarrhea despite having no obvious immune defects. […] Another possibility is chronic gut colonization by Cyclospora without infection, which may have altered the gut microbiota and decreased mucosal immunity, leading to the patient developing C. difficile colitis via a mechanism similar to that seen in antibiotic-induced diarrhea. […] This case report serves as a unique opportunity to explore the possible mechanisms, if any, regarding how Cyclospora infection or colonization may predispose individuals to C. difficile infection.
  • #1
    https://link.springer.com/article/10.1007/s11908-009-0016-4
    Cyclosporiasis is a food- and water-borne infection that affects healthy and immunocompromised individuals. […] Further understanding of the biology, pathogenesis, and control of infection and transmission has been hindered by the difficulty of propagating the organism, lack of reliable oocyst viability and infectivity assays, and inability to experimentally infect animals and human volunteers. […] Ortega YR, Nagle R, Gilman RH, et al.: Pathologic and clinical findings in patients with cyclosporiasis and a description of intracellular parasite life-cycle stages. […] Sun T, Ilardi CF, Asnis D, et al.: Light and electron microscopic identification of Cyclospora species in the small intestine. Evidence of the presence of asexual life cycle in human host. […] Eberhard ML, Ortega YR, Hanes DE, et al.: Attempts to establish experimental Cyclospora cayetanensis infection in laboratory animals.
  • #1 Potent efficiency of the novel nitazoxanide-loaded nanostructured lipid carriers against experimental cyclosporiasis | PLOS Neglected Tropical Diseases
    https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011845
    Cyclosporiasis is a ubiquitous infection caused by an obligate intracellular protozoan parasite known as Cyclospora cayetanensis (C. cayetanensis). The disease is characterized by severe diarrhea which may be regrettably fatal in immunosuppressed patients. The results demonstrated that NTZ-loaded NLCs represented the highest significant parasite percent reduction of (98% reduction) in both immunocompetent and immunosuppressed mice designating successful tissue penetration and avoiding recurrence of infection at the end of the study. Oocysts treated with NTZ-loaded NLCs demonstrated the most mutilated rapturing morphology via scanning electron microscope examination as well as representing the most profound improvement of the histopathological picture. In conclusion, NTZ-loaded NLCs exhibited the uppermost efficacy in the treatment of cyclosporiasis. The safe nature and the anti-parasitic effect of the novel formulation encourage its use as a powerful treatment for human cyclosporiasis.
  • #1 Cyclospora cayetanensis | medtigo
    https://medtigo.com/pathogen/cyclospora-cayetanensis/
    The pathogenesis of Cyclospora cayetanensis involves several steps: […] Ingestion: The infection begins when a person ingests food or water contaminated with the oocysts of C. cayetanensis. […] Excystation: Once inside the host’s small intestine, the oocysts release sporozoites, which undergo excystation to become the infective form of the parasite. […] Invasion: The sporozoites invade the epithelial cells lining the small intestine, where they establish a parasitophorous vacuole and begin to reproduce. […] Replication: The parasite replicates asexually inside the parasitophorous vacuole, forming large multinucleated structures called meronts. […] Sexual Reproduction: After several rounds of asexual reproduction, the parasite undergoes sexual reproduction, forming microgametes (male) and macrogametes (female).
  • #2 Cyclospora cayetanensis | Johns Hopkins HIV Guide
    https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_HIV_Guide/545047/all/Cyclospora_cayetanensis
    C. cayetanensis is an obligate intracellular, coccidian parasite that infects epithelial cells of the small intestine, destroys the intestinal brush border, and alters mucosal architecture. […] Transmission occurs by ingestion of fecally contaminated soil, food and water. […] Humans are the only known host and reservoir. Human-to-human transmission is unlikely as excreted oocysts must sporulate before becoming infectious.
  • #2 Cyclospora cayetanensis – Wikipedia
    https://en.wikipedia.org/wiki/Cyclospora_cayetanensis
    The oocysts that are passed are not, however, immediately infectious. Sporulation can take from one to several weeks, meaning person-to-person transmission is not a likely event. This differentiates C. cayetanensis from Cryptosporidium parvum, a closely related organism that causes a similar disease since C. parvum oocysts are immediately infectious upon release from the host.
  • #2 Cyclosporiasis—Updates on Clinical Presentation, Pathology, Clinical Diagnosis, and Treatment
    https://www.mdpi.com/2076-2607/9/9/1863
    Parasite invasion and replication within enterocytes damages the small intestinal epithelium, leading to the disruption of the brush border, loss of membrane bound digestive enzymes, and intestinal villous blunting and atrophy. An influx of lymphocytes, plasma cells, and occasionally eosinophils occurs in the lamina propria. These changes have the overall effect of decreasing the small intestinal absorptive capacity, leading to decreased uptake of water, nutrients, and electrolytes.
  • #2 Cyclosporiasis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Cyclosporiasis_pathophysiology
    C. cayetanensis oocysts have also been isolated from non-gastrointestinal sites, such as sputum, especially in immunocompromised patients with HIV and concomitant TB. This led to the hypothesis that C. cayetanensis may be an opportunistic pathogen. […] C. cayetanensis infects epithelial cells of the small intestine, especially those of the jejunum. Infected patients may have evidence of intestinal injury on endoscopy such as mucosal erythema. Histologic samples of small bowel of these patients demonstrate involvement of the lamina propria and neutrophilic infiltration in some cases. Cyclosporiasis may demonstrate evidence of chronic inflammation, with plasma cells observed in mucosal samples of infected patients. […] Infected epithelial cells of the gastrointestinal tissue may demonstrate the following changes: Loss of brush border appearance, Vacuolization of the tips of the villi, Epithelial changes from columnar to cuboid, Villous atrophy (partial), Crypt hyperplasia, Increased length of crypts and increased mitosis, Shortened villi, Absence of parasitic vacuoles in biopsied samples.
  • #2 Cyclospora cayetanensis | medtigo
    https://medtigo.com/pathogen/cyclospora-cayetanensis/
    Sporulation: The zygotes formed by fertilization mature into oocysts excreted in feces. […] Environmental maturation: The oocysts are not immediately infectious and require days to weeks to sporulate in the environment before becoming infectious. […] Infection: The infectious oocysts are ingested by another host, and the cycle continues. […] […] […] Humoral immunity entails the production of antibodies by B cells, which can neutralize the parasite and prevent its invasion of host cells. Studies have shown that patients with cyclosporiasis produce IgA and IgG antibodies against Cyclospora cayetanensis, indicating that humoral immunity may contribute to host defense. […] Cell-mediated immunity involves activating T cells, which can recognize and kill infected host cells. Studies have also shown that T cells are involved in the immune response to Cyclospora cayetanensis. Patients with cyclosporiasis have been found to have enhanced numbers of CD8+ T cells in the intestinal mucosa, which may play a role in controlling the infection. […] Other immune response components, such as cytokines and natural killer cells, may also be involved in host defense against Cyclospora cayetanensis.
  • #2 Comparative genomics reveals Cyclospora cayetanensis possesses coccidia-like metabolism and invasion components but unique surface antigens | BMC Genomics | Full Text
    https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-016-2632-3
    Our findings indicate that C. cayetanensis possesses coccidia-like metabolism and invasion components but unique surface antigens. […] The similar repertoire of host cell invasion-related proteins possessed by all coccidian parasites suggests that C. cayetanensis has host cell receptors and invasion process similar to that of T. gondii and E. tenella: gliding powered by an actin motor before invasion, interactions with the host cell through surface antigens, forming a moving junction with a series of secreted proteins to initiate invasion, forming a PV structure inside the host cell, and secreting various protein kinases, protein phosphatases, and other catalytic proteins to modify the host metabolic pathways for the evasion of host immune responses. […] Compared with T. gondii, the dramatic reduction in protein kinases and phosphatases suggests that C. cayetanensis and E. tenella have only limited capacity to regulate host cell signaling pathways and gene expression, or use a divergent system to do so.
  • #2 Cyclospora’s Mode of Infection | Marler Clark
    https://marlerclark.com/foodborne-illnesses/cyclospora/cyclosporas-mode-of-infection
    Cyclospora oocysts have been detected in non-gastrointestinal samples. There have been reports of oocysts in the sputa of HIV patients with a history of pulmonary tuberculosis, suggesting that Cyclospora could be considered an opportunistic pathogen. Travel to rural areas and ingestion of contaminated foods could be modes of infection. Accidental inhalation of oocysts has also been suggested. […] The dissemination of infective Cyclospora oocysts via water, soil, and unprocessed foods (e.g., fruits and vegetables, including ready-to-eat salads) is enabled by their small size (810 m), low specific gravity, and high infectivity. Such oocysts can survive for weeks to months in water and food, depending on the environmental temperature, and are resistant to the routine sanitization or chemical disinfection procedures used in irrigation systems, recreational waters, or drinking water treatment plants.
  • #2 Pathogen Safety Data Sheets: Infectious Substances – Cyclospora spp. – Canada.ca
    https://www.canada.ca/en/public-health/services/laboratory-biosafety-biosecurity/pathogen-safety-data-sheets-risk-assessment/cyclospora-pathogen-safety-data-sheet.html
    The oocysts are excreted unsporulated, requiring 7-13 days of optimal conditions outside of the host to mature. After an incubation of 2-11 days, immunocompetent patients experience a self-limited, but prolonged, relapsing watery diarrhea. […] Cyclospora are resistant to chemicals such as chlorine used for treating water. […] The Cyclospora oocysts are inactivated after heating at 60C for 1 h. Oocysts cannot be induced to sporulate at minus 18C for 24 h. Desiccation for 15 minutes causes the oocysts walls to rupture. […] Cyclospora spp. require 7-15 days in the environment to sporulate, showing that they are able to survive in soil. Oocysts have been noted to survive in water for 2 months at 4C and 7 days at 37C.
  • #2 Cyclosporiasis – Wikipedia
    https://en.wikipedia.org/wiki/Cyclosporiasis
    In 2007, Indian researchers published a case report that found an association between Cyclospora infection and Bell’s palsy. This was the first reported case of Bell’s palsy following chronic Cyclospora infection. In addition to other extra-intestinal reports, cyclosporiasis might be involved in either reversible neuronal damage or other unknown mechanisms to lead to Guillain-Barr syndrome or Bell’s palsy.
  • #2 Cyclospora – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Infectious_diseases/Cyclospora/
    Cyclospora, a recently recognized coccidian protozoan parasite, has been reported to cause diarrheal illness, often prolonged, in the United States and other countries (26). TMP-SMX is effective in treating diarrheal disease caused by cyclospora (27). In immunocompetent patients, treatment with a combination of 160 mg of trimethoprim and 800 mg of sulfamethoxazole (i.e., a double-strength tablet) twice daily for 7 days ended diarrheal illness and led to clearance of the parasites (28). In patients infected with the human immunodeficiency virus, treatment with one double-strength tablet of TMP-SMX four times a day for 10 days leads to a rapid resolution of diarrhea (29). Symptomatic cyclosporiasis may recur in the following weeks, but it can be prevented by the administration of TMP-SMX three times weekly. […] The recommended treatments for all other apicomplexan parasites (including malaria, toxoplasmosis, Cyclospora, and Cystoisospora) involve combinations of antiparasitic drugs.
  • #2 Potent efficiency of the novel nitazoxanide-loaded nanostructured lipid carriers against experimental cyclosporiasis | PLOS Neglected Tropical Diseases
    https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011845
    The main objective of the present study was to prepare a novel formula composed of a lipid nanocarrier (NLCs) to deliver the loaded drug (NTZ) in a nanometric size in order to enhance the biological activity and tissue permeability of the drug. […] The loading of NTZ on NLCs added a great value in achieving a nano-metric sustained release formula along with increasing the drug solubility which remarkably improved the drug tissue permeability and efficiency. This coincides with other studies that proved the efficacy of nanoparticles in lowering the parasite burden compared to the conventional drugs. […] Most of the examined treated oocysts exhibited loss of the spherical shape and smooth surface. Several disfigurements were noticed in the form of ridges, furrows, erosions, and/or ulcerations. However, mice treated with NTZ-loaded NLCs showed noteworthy mutilation with deep cavitations and appeared even rupturing. This may be attributed to the mechanism of action of NTZ in disturbing the respiratory cycle through inhibition of the pyruvate ferredoxin oxidoreductase enzyme.