Giardia intestinalis

Giardia intestinalis (Synonyme: G. lamblia, G. duodenalis; Lamblia intestinalis, Cercomonas intestinalis) ist ein einzelliger Parasit aus der Gattung der Giardien, der Menschen (→ Giardiasis), andere Säugetiere (→ Giardiose des Hundes, Giardiose der Katze), Amphibien, Reptilien und Vögel befällt.^[1] Benannt ist der birnen- oder löffelförmige Flagellat mit acht Geißeln nach Alfred Mathieu Giard und Vilém Dušan Lambl. Er gelangt üblicherweise über kontaminiertes Oberflächenwasser, in dem sich seine Dauerformen (Zysten) befinden, oder – seltener – über Kontakte mit Fliegen in den menschlichen Darm. Bei Katzen und Chinchillas gehört Giardia intestinalis zu den Parasiten, die bei Kotuntersuchungen am häufigsten gefunden werden.^[2]

Merkmale

Trophozoiten sind die aktiven Formen des Einzellers im Darm und nur sie pflanzen sich fort. Sie sind oval, langgestreckt und etwa 9–20 µm lang und 5–12 µm breit. Jedes Individuum besitzt zwei Zellkerne und vier Geißelpaare, von denen zwei inmitten der Zelle und zwei weitere seitlich entspringen. Außerdem besitzen die Trophozoiten an der Ventralseite eine Haftscheibe, mit der sie sich im Darmepithel festhalten.

Zysten sind mit einer Schutzhülle versehene Dauerformen und sehr resistent gegenüber Umwelteinflüssen. Sie sind etwa 8–15 µm × 7–10 µm groß. Zysten werden von infizierten Lebewesen ausgeschieden und können bis zu vier Monate in Oberflächenwasser (etwa von Seen) überleben. Im Darm wandeln sich diese wieder in Trophozoiten um.

Besondere Merkmale von Giardia intestinalis sind:

• Giardia intestinalis besitzt keine Mitochondrien und auch keine Peroxisomen, jedoch Eisen-Schwefel-Cluster synthetisierende Mitosomen sowie Erbgut, das Mitochondriengene enthält. Man vermutet, dass Giardien ihre Mitochondrien im Laufe der Evolution wieder verloren haben.
• Das Genom ist sehr variabel. Es enthält 12 Millionen bis etwa 80 Millionen Basenpaare, die auf 8 bis 50 Chromosomen verteilt sind.
• Sexuelle Reifeteilung (Meiose) wurde noch nie beobachtet, aber es wurden Gene für diesen Prozess gefunden.
• Im Jejunum liegen nur Trophozoiten vor, aber im Ileum nur noch Cysten. Fehlendes Cholesterin ist dafür verantwortlich, dass die Trophozoitenoberfläche nicht mehr gebildet werden kann. Dies führt zur Cysten-Bildung (Encystierung).

Mit molekularbiologischen Techniken werden mittlerweile verschiedene Genotypen unterschieden. Während die Genotypen A (zum Teil auch in die Untergruppen AI, AII unterteilt) und B offenbar ein zoonotisches Potenzial besitzen und sowohl den Menschen als auch beispielsweise Hunde und Katzen infizieren können, sind die übrigen Genotypen offenbar wirtsspezifisch. Genotyp C und D kommt bei Hunden (D auch bei Katzen), Genotyp E bei Huftieren, Genotyp F bei Katzen und Genotyp G bei Nagetieren vor. Bei Chinchillas wird vor allem Typ B beobachtet.^[3][4]

Lebenszyklus Giardia

Epidemiologie

Etwa 10 % der Weltbevölkerung sind mit Lamblien infiziert. Vor allem Kinder sind hier die Betroffenen. Unter Tropenreisenden ist es die häufigste Protozoeninfektion.

Erkrankung

Die Infektion mit Lamblien bleibt meist unbemerkt. Manchmal klagen die Patienten über einen Blähbauch, Druckschmerz rund um den Nabel und/oder Durchfälle. Auch Gewichtsverluste sind nicht selten.

Zur Therapie wird Metronidazol oder Paromomycin eingesetzt, bei Therapieversagen auch Albendazol, Nitazoxanid oder Chloroquin.^[5]

Rechtliches

In Deutschland ist der direkte oder indirekte Nachweis von Giardia lamblia namentlich meldepflichtig nach des Infektionsschutzgesetzes, soweit der Nachweis auf eine akute Infektion hinweist. Meldepflicht besteht jedoch nicht in Österreich und der Schweiz.

Einzelnachweise

1. ↑ Giardieninfektionen. (Memento vom 9. Januar 2015 im Internet Archive)
2. ↑ Nico Pantchev u. a.: Endoparasitosen bei Kleinsäugern aus privater Haltung und Igeln. In: Tierärztl Prax, 33(K), 2005, S. 296–306.
3. ↑ Dieter Barutzki u. a.: Die Giardiose des Hundes – eine weit verbreitete Erkrankung. In: Kleintier Konkret, S1, 2008, S. 17–23.
4. ↑ D. Jaros, W. Zygner, S. Jaros, H. Wedrychowicz: Detection of Giardia intestinalis assemblages A, B and D in domestic cats from Warsaw, Poland. In: Polish journal of microbiology / Polskie Towarzystwo Mikrobiologów = The Polish Society of Microbiologists. Band 60, Nummer 3, 2011, S. 259–263, . PMID 22184934.
5. ↑ Marianne Abele-Horn: Antimikrobielle Therapie. Entscheidungshilfen zur Behandlung und Prophylaxe von Infektionskrankheiten. Unter Mitarbeit von Werner Heinz, Hartwig Klinker, Johann Schurz und August Stich, 2., überarbeitete und erweiterte Auflage. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4, S. 292.

Giardia duodenalis, also known as Giardia intestinalis and Giardia lamblia, is a flagellated parasitic microorganism of the genus Giardia that colonizes the small intestine, causing a diarrheal condition known as giardiasis.^[1][2][3] The parasite attaches to the epithelium by a ventral adhesive disc or sucker, and reproduces via binary fission.^[4] Giardiasis does not spread via the bloodstream, nor does it spread to other parts of the gastrointestinal tract, but remains confined to the lumen of the small intestine.^[5] Giardia has an outer membrane that makes it possible to retain life, even when outside of the host body, and which can make it tolerant to chlorine disinfection. Giardia trophozoites absorb their nutrients from the lumen, and are anaerobes. If the organism is split and stained, its characteristic pattern resembles the familiar "smiley face" symbol.^[6]

Chief pathways of human infection include ingestion of untreated drinking water (which is the most common method of transmission for this parasite),^[3] food, and soil contaminated with human feces, as well as ingestion of sewage, a phenomenon particularly common in many developing countries.^[7][3] Contamination of natural waters also occurs in watersheds where intensive grazing occurs.

Giardia infections occur worldwide. It is the most commonly identified intestinal parasite among children in day-care centers, hikers, family members, and immunocompromised adults in the United States and Canada . About 20,000 cases per year in the United States are reported.^[8]

Life cycle

Lifecycle of Giardia lamblia

G. duodenalis takes on two morphologically distinct forms during its lifecycle. The replicative form is a motile, pear-shaped cell that survives only in host small intestines called a trophozoite.^[9] Trophozoites swim through the intestinal mucus until they eventually adhere to the host intestinal epithelium.^[10][9] Adhered trophozoites then divide by binary fission, forming either more trophozoites or the nonreplicative cyst stage.^[9] Cysts pass through the host's large intestine and are shed in the feces.^[9] The G. duodenalis cyst is the environmentally stable stage in the parasite life cycle. This stage facilitates the transmission of cysts in the environment when a host of G. duodenalis transfers cysts into the environment through their feces which is then consumed by a new host. The cysts can have a prolonged survival of weeks to months in the environment because they have a slower metabolic rate than trophozoites. This allows them to be resistant to environmental stressors and survive best in cool and moist environments.^[11] Cysts remain dormant until ingested by a host animal. In the new host, environmental conditions trigger the cyst to produce two trophozoites, which then attach to epithelial cells, starting the cycle anew.^[9]

Structure of G. duodenalis

The trophozoite has an elaborate structure with two nuclei and eight pairs of flagella which allow it to move around the host easily. It uniquely has an adhesive disk that enables it to adhere to the intestinal epithelium. There are no Golgi in the cell body and its mitosomes are a result of degenerated mitochondria. These mitosomes don’t have any mitochondrial genomes but contain proteins from former mitochondrial genes that migrated to the nucleus. The trophozoite encysts into a cyst when it comes into contact with environmental stressors such as a high pH. The form of the cyst primarily contains the nucleus and evolves to not have structures of the trophozoites such as the flagella and adhesive disks. This allows the cyst to stay dormant until it is ingested by a new host and evolves back into the trophozoite form for infection.^[12]

Prevalence and ecology

G. duodenalis causes an infection called giardiasis. The disease infects around 200 million people worldwide each year, resulting in 500,000 deaths. The most affected demographic is children 0 to 4 years of age. Globally G. duodenalis is the most commonly identified protozoal intestinal parasite. In high-income countries, there is an infection rate between 2-5%, and in low and middle-income countries there is an infection rate between 20-30%.^[13]

The cyst can survive for weeks to months in cold water,^[14] so can be present in contaminated wells and water systems, especially stagnant water sources, such as naturally occurring ponds, storm-water storage systems, and even clean-looking mountain streams. Cysts can also be found on surfaces, soil, food, or water that have been contaminated with feces from infected humans or animals.^[15] They may also occur in city reservoirs and persist after water treatment, as the cysts are resistant to conventional water-treatment methods, such as chlorination and ozonolysis.^[14] Zoonotic transmission is also possible, so Giardia infection is a concern for people camping in the wilderness or swimming in contaminated streams or lakes, especially the artificial lakes formed by beaver dams (hence the popular name for giardiasis, "beaver fever").

In addition to waterborne sources, fecal–oral transmission can also occur, for example in day-care centers, where children may have poor hygiene practices. Those who work with children are also at risk of being infected, as are family members of infected individuals. Not all Giardia infections are symptomatic, and many people can unknowingly serve as carriers of the parasite.

Giardia infects humans, but is also one of the most common parasites infecting cats, dogs, and birds. Mammalian hosts also include dozens of species,^[16] including cattle, sheep,^[17] and goats.^[17]

Cats can be cured easily, and lambs usually simply lose weight, but in calves, the parasites can be fatal and often are not responsive to antibiotics or electrolytes. Carriers among calves can also be asymptomatic. This parasite is deadly for chinchillas, so extra care must be taken by providing them with safe water. Dogs have a high infection rate, as 30% of the population under one year old are known to be infected in kennels. The infection is more prevalent in puppies than in adult dogs. Infected dogs can be isolated and treated, or the entire pack at a kennel can be treated together regardless. Kennels should also be then cleaned with bleach or other cleaning disinfectants. The grass areas used for exercise should be considered contaminated for at least one month after dogs show signs of infection, as cysts can survive in the environment for long periods of time. Prevention can be achieved by quarantine of infected dogs for at least 20 days and careful management and maintenance of a clean water supply.

Cell biology

Giardia trophozoites stained with Giemsa; 100x magnification.

G. duodenalis trophozoites are pear-shaped cells, 10 to 20 μm long, 7 to 10 μm across, and 2 to 4 μm thick.^[9][10] They are motile by way of four pairs of flagella, which propel the trophozoites through the intestine.^[10] Notably, each G. duodenalis cell has two nuclei, both of which actively transcribe genes.^[9] Adjacent to the nucleus, G. duodenalis cells have an endoplasmic reticulum that extends through much of the cell.^[18] Trophozoites about to differentiate into cysts also contain prominent vesicles termed encystation-specific vesicles that disappear once cyst wall construction begins.^[18] Unlike most other eukaryotes, G. duodenalis cells contain no visible mitochondria, but instead contains a substantially reduced metabolic organelle termed a mitosome.^[10] Additionally, cells appear to contain no Golgi bodies, and instead the secretory system consists entirely of the endoplasmic reticulum and numerous vesicles spread throughout the cell, termed peripheral vesicles.^[18] Peripheral vesicles are responsible both for taking up extracellular nutrients, and expelling waste outside the cell.^[19] Each cell also contains a pair of rigid structures called median bodies which make up part of the G. lamblia cytoskeleton.^[9] Trophozoites adhere to host epithelial cells via a specialized disk-shaped organelle called the ventral disk.^[9]

Cysts are oval-shaped cells slightly smaller than trophozoites.^[10] They lack flagella, and are covered by a smooth, clear cyst wall.^[10] Each cyst contains the organelles for two trophzoites: four nuclei, two ventral disks, etc.^[10]

Multiple views of a G. lamblia cyst imaged by confocal microscopy: Bar = 10 micrometers
(A) Cyst imaged by transmission (differential interference contrast)
(B) Cyst wall selectively imaged through use of fluorescent-labelled antibody
(C) Cyst imaged through use of carboxy fluorescein diacetate, a viability stain
(D) Composite image of (B) and (C)
(E) Composite image of (A), (B), and (C)

Metabolism

G. lamblia primarily generates its energy by breaking down glucose via glycolysis, as well as the arginine dihydrolase pathway.^[20] It is unable to synthesize nucleotides on its own, instead salvaging them from its host.^[20] Synthesis of iron-sulfur clusters is done in a double-membrane-bound compartment called the mitosome, which is likely a remnant of mitochondria.^[20] Each cell contains 25 to 100 mitosomes divided into two categories - peripheral mitosomes, which are scattered throughout the cell, and central mitosomes, which gather at the center of the cell for unknown reasons.^[21] As in mitochondria, proteins with a certain peptide signal sequence are trafficked to and imported into the mitosome.^[20] Unlike mitochondria, mitosomes have no genome of their own. All mitosomal genes are encoded by the Giardia nuclear genome.^[20]

Genetics

Giardia and the other diplomonads are unique in their possession of two nuclei that are similar in appearance, DNA content, transcription, and time of replication. Five chromosomes occur per haploid genome. The genome has been sequenced and was published in 2007, although the sequence contains several gaps. The sequence is about 12 million base pairs and contains about 5000 protein-coding genes.^[22] The GC content is 46%. Trophozoites have a ploidy of four and the ploidy of cysts is eight, which in turn raises the question of how Giardia maintains homogeneity between the chromosomes of the same and opposite nuclei. Modern sequencing technologies have been used to resequence different strains.^[23]

Immunology

Infections with Giardia are self-limited, showing that it can be controlled by the host immune system in few weeks, generally chronic giardiasis is developed in humans with immunodeficiency disorders. During the infection different mechanisms from the innate and adaptive response are activated. The first physical barrier is the mucus layer where interacts with epithelial, immune cells, and some antimicrobial peptides released by those cells as well as nitric oxide and pro-inflammatory cytokines like IL-6. TLR2 and TLR4 also can be activated by Giardia.^[24] T-cell response in giardiasis, includes CD4+Th17 cells and CD8+T cells. While the production of IgA by B cells helps to eliminate the infection.^[25]

Evolution

Giardia had been assumed to be primitively asexual and with no means of transferring DNA between nuclei. These assumptions made explaining the remarkably low level of allelic heterozygosity (< 0.01%) in the genome isolate, WB, very difficult, but all those assumptions of asexuality are now in doubt, with population genetics providing evidence for recombination^[26] and the identification of meiotic genes, evidence for recombination among isolates and the evidence for exchange of genetic material between nuclei during the process of encystation.^[27]

These findings on sexuality in Giardia, above, have important implications for understanding the origin of sexual reproduction in eukaryotes. Though sexual reproduction is widespread among extant eukaryotes, until recently, sex seemed unlikely to be a primordial and fundamental feature of eukaryotes. A probable reason for the view that sex may not be fundamental to eukaryotes was that sexual reproduction previously appeared to be lacking in certain human pathogenic single-celled eukaryotes (e.g. Giardia) that diverged from early ancestors in the eukaryotic lineage.

In addition to the evidence cited above for recombination in Giardia, Malik et al.^[28] reported that many meiosis specific genes occur in the Giardia genome, and further that homologs of these genes also occur in another unicellular eukaryote, Trichomonas vaginalis. Because these two species are descendants of lineages that are highly divergent among eukaryotes, Malik et al.^[28] suggested that these meiotic genes were present in a common ancestor of all eukaryotes. Thus, on this view, the earliest ancestor of eukaryotes was likely capable of sexual reproduction. Furthermore, Dacks and Roger^[29] proposed, based on phylogenetic analysis, that facultative sex was present in the common ancestor of all eukaryotes. Bernstein et al. also reviewed evidence in support of this view.^[30]

Eight genotype assemblages of G. duodenalis have been recognized to date (A-H).^[16] Genotyping of G. duodenalis isolated from various hosts has shown that assemblages A and B infect the largest range of host species, and appear to be the main (or possibly only) G. duodenalis assemblages that undeniably infect human subjects.^[16]

Research

Frances Gillin of the University of California, San Diego, and her colleagues cultivated the entire lifecycle of this parasite in the laboratory, and identified biochemical cues in the host's digestive system that trigger Giardia's lifecycle transformations.^[31][32] They also uncovered several ways in which the parasite evades the defences of the infected organism. One of these is by altering the proteins on its surface, which confounds the ability of the infected animal's immune system to detect and combat the parasite (called antigenic variation). Gillin's work reveals why Giardia infections are extremely persistent and prone to recur. In addition, these insights into its biology and survival techniques may enable scientists to develop better strategies to understand, prevent, and treat Giardia infections.

In December 2008, Nature published an article showing the discovery of an RNA interference mechanism that allows Giardia to switch variant-specific surface proteins to avoid host immune response.^[33] The discovery was made by the team working at the Biochemistry and Molecular Biology Laboratory, School of Medicine, Catholic University of Cordoba, Argentina, led by Dr. Hugo Lujan.

The main congress about Giardia is the International Giardia and Cryptosporidium Conference. A summary of results presented at the most recent edition (2019, in Rouen, France) is available.^[34]

History

A Giardia trophozoite, drawn by Vilém Lambl and published in 1859

Drawings of a Giardia trophozoite and cyst by Charles E. Simon in 1921

The first likely description of Giardia was in 1681 by Antonie van Leeuwenhoek, who in a letter to Robert Hooke, described "animalcules" resembling Giardia trophozoites in his stool.^[9][35] The next known description of Giardia wasn't until 1859, when Czech physician Vilém Lambl published a description of the trophozoite stages he saw in the stool of a pediatric patient. Lambl termed the organism Cercomonas intestinalis.^[36] In 1888, Raphaël Blanchard renamed the parasite Lamblia intestinalis in Lambl's honor.^[36] In 1915, Charles Stiles renamed the organism Giardia lamblia in honor of both Lambl and Professor Alfred Mathieu Giard of Paris.^[36][37] In 1921, Charles E. Simon published a detailed description of the parasite's morphology.^[9]

See also

• List of parasites of humans
• 1998 Sydney water crisis

References

Giardia lamblia, intestinalis o duodenalis es un protozoo flagelado perteneciente al orden Diplomonadida. Es parásito de varios mamíferos, incluyendo el ser humano. Vive en el intestino delgado y provoca una patología denominada giardiosis, giardiasis o lambliasis.

Morfología

• Presenta un tamaño inferior a 20 μm.
• Carece de ciertos orgánulos como son las mitocondrias y el aparato de Golgi, sin embargo posee vestigios de estos orgánulos, como los mitosomas y un sistema de transporte similar al del aparato de Golgi.^[1]​
• Únicamente tiene un hospedador (monoxeno), es cosmopolita y tiene dos formas de vida en su ciclo vital:
  • Trofozoíto: presenta un tamaño en torno a 20 μm de longitud y 15 μm de ancho con una morfología piriforme y una simetría bilateral. Proyectada en un plano se asemeja a una pera. Posee 8 flagelos, 2 anteriores, 2 posteriores, 2 ventrales y 2 caudales, cuya función es la motilidad celular. En la cara ventral presenta una estructura con forma de disco bilobulado, cuya función es permitir la fijación del parásito a la superficie del epitelio intestinal. En la cara dorsal y coincidiendo en posición con el disco bilobulado se sitúan dos núcleos ovalados con grandes endosomas. A lo largo de la superficie ventral se disponen unos elementos denominados cuerpos mediales, cuya función aún permanece desconocida. El trofozoito es la forma vegetativa que se alimenta y se reproduce.

Quiste de Giardia con tinción de lugol

• • Quiste: presenta un tamaño en torno a 15,4 μm de longitud y 9,7 μm de ancho con una morfología ovalada. Posee 4 núcleos que siempre aparecen dispuestos en alguno de los polos. No presenta flagelos aunque se pueden apreciar los axonemas flagelares (restos de los flagelos) y los cuerpos mediales duplicados con respecto al trofozoito. La pared es transparente y muy resistente tanto a factores físicos como químicos. El quiste es la forma vegetativa infectante y de resistencia.
• Alimentación por fagocitosis y pinocitosis del contenido intestinal a través de la superficie dorsal

Ciclo vital e infección

Ciclo vital de Giardia lamblia.

Giardia lamblia vive en forma de trofozoito en la luz del intestino delgado (principalmente en el duodeno) adherido a las vellosidades intestinales por medio de los discos bilobulados. Se alimenta y se reproduce hasta que el contenido intestinal inicia el proceso de deshidratación, momento en el que comienza el enquistamiento del trofozoito. Pierde los flagelos, adquiere una morfología ovalada, se rodea de una pared quística y madurez. Los quistes expulsados junto a las heces ya son infectantes. Cuando dichos quistes son ingeridos por un nuevo hospedador, llegan al duodeno, donde se disuelve la pared quística, dando así lugar a un individuo tetranucleado que se divide inmediatamente en dos trofozoitos binucleados que se anclan al epitelio intestinal, cerrando así su ciclo vital.

Patogenia

La patología originada por G. lamblia se debe principalmente a los efectos que causan la acción mecánica de adherirse y fijarse al epitelio intestinal. Dichos efectos producen una alteración de las microvellosidades, que disminuyen su superficie de exposición al ser engrosadas, y esto conlleva la aparición de diversas alteraciones fisiológicas más o menos graves, según el mayor o menor deterioro del proceso de absorción. Cabe mencionar que la sustracción de alimento producida por el parásito no parece ser relevante en la patogénesis. La patogenicidad también se ve muy influenciada por el tipo de cepa y el estado inmunitario del hospedador y es totalmente aeróbica.

Sintomatología

Los síntomas producidos por una giardiasis pueden ser desde inexistentes hasta presentar una sintomatología grave. En caso de que la infección curse con síntomas, estos aparecen tras un período de incubación que dura en torno a 1-3 semanas, y consisten principalmente en diarreas mucosas, sin restos de sangre y meteorismo, dolor abdominal y anorexia (síntoma).

En los casos más severos se puede llegar a producir el síndrome de malabsorción, debido a la destrucción de las células epiteliales del intestino delgado. Esto obliga a un constante reciclaje de los epitelios con células inmaduras, que aún no son capaces de absorber o digerir ciertas moléculas, lo que determina una malabsorción de lípidos, glúcidos y proteínas. Está caracterizada por la aparición de esteatorrea (heces grasas y copiosas) y, posteriormente, de deficiencias proteicas y vitamínicas (sobre todo vitaminas liposolubles).

La duración de la fase aguda de la infección es de unos 3 o 4 días y va desapareciendo a medida que actúa el sistema inmunitario del hospedador a través de los linfocitos T. En algunos individuos, principalmente aquellos inmunodeficientes, la enfermedad puede hacerse crónica, pudiendo prolongarse los síntomas durante años.

También es frecuente la presencia de flatulencias, eructos, náuseas, vómitos, distensión abdominal y retortijones.

Tratamiento

Las infecciones humanas son tratadas convencionalmente con metronidazol, tinidazol o nitazoxanida.^[2]​ Aunque metronidazol es la primera opción de tratamiento, es mutagénico en bacterias y carcinogénico en ratones, por lo que debe ser evitada en el embarazo.^[3]​

Tabla adaptada de Huang, White.^[3]​

Profilaxis

La principal medida de profilaxis es hervir y/o filtrar el agua, cuando no se esté seguro de su procedencia. El tratamiento de agua para impedir infecciones por Giardia suele implicar procesos de filtración de alta eficiencia; la Giardia es resistente a la desinfección química por cloración, por lo cual debe prestarse especial cuidado a los procesos de floculación y filtración de tratamiento de aguas, los cuales se deshacen efectivamente de muchos parásitos y quistes, así como la desinfección por radiación ultravioleta, la cual es muy efectiva en la inactivación de este parásito.

Epidemiología

Aunque su distribución es mundial solo es endémica en los países con condiciones sanitarias deficientes. La prevalencia de la giardiasis varía entre el 1% y el 60% según la región y está directamente relacionada con las condiciones sanitarias. Su incidencia es mayor en niños debido a su predisposición a ingerir alimentos o líquidos sin control. Se estima que unos 200 millones de seres humanos son infectados anualmente por este parásito.

Reseña histórica

Giardia lamblia fue el primer parásito microscópico demostrado en la especie humana, descubierto por Anton van Leeuwenhoek al parecer cuando observaba con el microscopio una muestra de su materia fecal. Pero fue hasta 1882 que Kunster creó el nombre genérico de Giardia para designar a protozoos flagelados que observó en el intestino de batracios. Más tarde Alexeif señaló que la especie encontrada en el hombre pertenecía a este género. En 1888 Blanchard había sugerido que el parásito fuera denominado lamblia para honrar a Lambl, investigador checo que lo redescubrió 200 años después de Leeuwenhoek, nombre utilizado todavía en la mayor parte de los países de Europa Oriental. En 1915, atendiendo al criterio de prioridad, Stiles propuso la unificación de la terminología con la designación binominal de Giardia lamblia.

Véase también

• Enteromonas hominis.
• Chilomastix mesnili.
• Retortamonas intestinalis.
• Trichomonas vaginalis.
• Trichomonas tenax.
• Pentatrichomonas hominis.
• Dientamoeba fragilis.
• Blastocystis hominis.

Referencias

Giardia intestinalis, aussi anciennement appelé Giardia duodenalis, Giardia lamblia, et Lamblia duodenalis, est une espèce de protozoaires flagellés responsable d'une parasitose intestinale, la giardiase (aussi appelée giardiose ou lambliase), dans les espèces humaine, canine et féline.
Les Giardias sont des organismes anaérobies, dénués de mitochondries, assurant l'oxydation des composés organiques. À la place, ils possèdent un organite particulier, appelé mitosome.

Il s'agit du premier parasite intestinal découvert en 1681.

Histoire de l'espèce

Le germe a été décrit pour la première fois par Antoni van Leeuwenhoek en 1681^[1]. Le biologiste tchèque Vilém Dušan Lambl le décrit en 1859^[2] et lui attribue le taxon Cercominas intestinalis. En 1888, Raphaël Blanchard le renomme Lamblia intestinalis^[3] en l'honneur de ce biologiste.

Le genre Giardia est défini par Johann Künstler en 1882, en l'honneur d'Alfred Giard.

En 1915, Kofoid & Christiansen écrivent que le genre Giardia doit se substituer à Lamblia^[4]. Cette même année, Charles Wardell Stiles et al. introduisent le taxon Giardia lamblia.

Description

Morphologie

Schéma d'un kyste (à gauche) et d'un trophozoïte (à droite) de G. intestinalis

Trophozoïtes de G. intestinalis observés au microscope optique

La forme végétative, le trophozoïte, mesure 15 μm. Elle se présente sous la forme d'un cerf-volant vue de face et sous la forme d'une cuillère vue de profil. Elle possède un noyau bilobé ainsi que huit flagelles, tous dirigés vers l'arrière : une paire antérieure, une paire postérieure et deux paires médianes. Ces flagelles partent de deux blépharoplastes (corpuscules) situés entre les noyaux et traversent l'axe de la cellule formant l'axostyle. Un ou deux corps parabasaux en virgule sont parfois visibles à la partie moyenne de la cellule.

La forme kystique se retrouve dans le côlon et mesure environ 10 μm. Ovalaire, elle est entourée d'une coque lisse, réfringente, à double paroi et peu épaisse. Elle est composée de quatre noyaux, reliquat de flagelles en forme de S très allongé, et de deux corps parabasaux en virgule. C'est la forme infestante qui vit dans le côlon et qu'on retrouve dans les selles.

Cycle de vie

Par intervalles, tous les six à douze jours, les trophozoïtes s'immobilisent dans le duodénum, se fixent aux microvillosités des entérocytes grâce à leurs disques ventraux qui agissent comme des ventouses, s'enkystent puis sont rejetées à l'extérieur, en grand nombre, avec les selles.

Bourrées alors de kystes caractéristiques, ces selles sont directement infestantes, elles vont permettre le diagnostic de certitude. La négativité des selles entre ces phases de rejet justifie l'envoi au laboratoire de selles récoltées selon la méthode "des 8 jours". Les kyste vont garder leur pouvoir pathogène au moins deux mois dans le milieu extérieur, ils sont très résistants, la stérilisation habituelle des eaux de boisson n'est pas suffisante mais l'ébullition et la congélation les détruisent.

S'il est ingéré via des aliments souillés, le kyste arrive dans le duodénum où il subit l'action des enzymes duodénales. La maturation des deux trophozoïtes du kyste s'achève et celui-ci libère deux Giardias végétatifs qui s'installent sur place. Ceux-ci se multiplient ensuite par fission binaire.

Répartition

On sait actuellement que c'est un parasite cosmopolite, touchant 10 à 20 % des populations vivant en climats tempérés et chauds, et que son taux de fréquence augmente en France et en Europe, surtout chez l'enfant. Différent en cela des autres parasites intestinaux, si habituellement associés, le giardia est volontiers rencontré seul et, quoique bien toléré par 70 % des porteurs, n'en est pas moins responsable de troubles importants chez bon nombre des autres...

Clinique

Trophozoïtes observés en cytologie

Pathogénie et symptômes

Le rôle pathogène de Giardia intestinalis est conditionné à la fois par l'état réceptif du terrain et par l'action propre du parasite :

• Si 70 % des porteurs de Giardias sont des "porteurs sains", 30 % présentent une symptomatologie nette et, parmi eux, 10 à 12 % sont de vrais malades dont la vie, en dehors de toute thérapeutique, est gravement perturbée par leur parasitose.
• Le tableau clinique moyen de l'adulte est celui d'une diarrhée "au long cours" apparaissant par crises mais durant parfois plusieurs semaines d'affilée avec cinq à six émissions par jour de selles abondantes.
• L'enfant fait, en général, une forme plus sévère avec douleurs périombilicales, nervosisme et troubles de la croissance.
• Les formes graves ou malignes surviennent sur des terrains fragilisés ou déficients immunologiques (surtout en IgA sécrétoires). Sans appétit, digérant mal, le malade est lassé par sa diarrhée qui persiste depuis de longs mois ; il a des crises de palpitations, des douleurs précordiales, des lipothymies, parfois de l'asthme ou des poussées d'urticaire. Insomniaque, asthénique, nettement amaigri, c'est, enfin, un psychasthénique dont le visage plombé, fripé, anxieux, traduit les angoisses.

Diagnostic

Chez les malades, il faut penser à une giardose devant une diarrhée prolongée.
Le diagnostic de certitude est obtenu par le laboratoire : soit en trouvant des formes végétatives dans le liquide de tubage duodénal, soit en trouvant des kystes dans les selles par examen parasitologique répété journalier ou, mieux, par l'examen d'une selle "des 8 jours". Dans 70 % des cas, le diagnostic sera une découverte de laboratoire.

Traitement

La molécule la plus utilisée est le métronidazole. En cas de ré-infestation ou d'échec, il est préconisé une cure après une semaine de repos, et un traitements des contacts familiaux. En cas d'échecs répétés, on peut, chez l'adulte, avoir recours à la quinacrine.

Voir aussi

• André G. Buret, Simone M. Cacciò, Loïc Favennec et Staffan Svärd, « Update on Giardia: Highlights from the seventh International Giardia and Cryptosporidium Conference », Parasite, vol. 27,‎ 2020, p. 49 (ISSN , PMID , PMCID , DOI , lire en ligne )

Notes et références

• (en) Référence NCBI : Giardia intestinalis (taxons inclus)

Giardia lamblia (nota anche come G. intestinalis e G. duodenalis) è un organismo unicellulare anaerobico appartenente al genere Giardia (Protozoi Flagellati Diplomonadini). È un parassita dell'intestino tenue dell'uomo e di altri mammiferi (in particolare dei primati e del maiale), responsabile della giardiasi.

Struttura

Il ciclo vitale di Giardia lamblia prevede l'alternanza di due forme, una quiescente (cisti) e una vegetativa (trofozoite), durante la quale, attraverso un paio di ventose si ancora all'organismo ospite. La riproduzione è scissipara e avviene all'interno dell'intestino dell'ospite.

Struttura delle cisti

La forma quiescente, presente in cibo e acqua contaminati da materia fecale ma anche in torrenti e specchi d'acqua montani, da dove può essere assorbita per ingestione nell'organismo ospite, è costituita da cisti ovoidali, rigide, di circa (11-15 µm x 7-10 µm), dotate di 4 nuclei. Le cisti sono protette da una parete esterna spessa 0,3-0,5 µm, formata da uno strato esterno rifrangente composto da una rete di filamenti lunghi da 7 a 20 µm e da uno strato interno composto da due membrane. Sulla parete esterna sono state individuate 4 distinte proteine da 29, 75, 88 e 102 kDa; la componente glucosidica, ritenuta in un primo tempo costituita da chitina, risulta invece in prevalenza N-acetilgalattosamina (GalNAc).

Una cisti di Giardia lamblia in microscopia confocale.

La figura mostra un'unica cisti di Giardia lamblia osservata al microscopio confocale, con vari accorgimenti strumentali. La linea bianca misura 10 µm.

• A osservazione per semplice trasmissione (contrasto differenziale interferenziale).
• B parete della cisti evidenziata mediante uno specifico anticorpo con marcatore fluorescente (TRITC).
• C cisti marcata con diacetato di carbossifluoresceina (CFDA), un indicatore di vitalità.
• D immagine composta da B e C.
• E immagine composta da A, B, e C.

Struttura dei trofozoiti

La forma vegetativa è costituita da trofozoiti a simmetria bilaterale con aspetto di piccola pera, lunga 10-20 µm e larga 5-10 µm. Sulla faccia ventrale si trovano quattro paia di flagelli (anteriore, posteriore, caudale e ventrale) e un disco ventrale, nonché uno o due corpi mediani in forma di artiglio. I due nuclei sono privi di nucleoli e contornati da dischi adesivi simili a occhiali. Il disco ventrale aderisce alla mucosa intestinale dell'ospite, dalla quale assume il nutrimento per pinocitosi.

Attività patogena

Generalmente la presenza del parassita nell'intestino non causa alcuna sintomatologia, ma in circa il 10% dei casi può causare, dopo un periodo di incubazione di 12-19 giorni: diarrea (con feci schiumose ricche di grassi), dolori epigastrici, anoressia, nausea e meteorismo.

Nel caso di cronicizzazione i sintomi sono attenuati. In bambini e in soggetti con deficit immunitari possono causare steatorrea, astenia e calo ponderale. La prognosi è comunque sempre favorevole.

Bibliografia

• Rodney D. Adam, Biology of Giardia lamblia, Clinical Microbiology Reviews, luglio 2001, p. 447-475, Vol. 14, No. 3 [1]

A giárdia (Giardia lamblia) é um protozoário microscópico parasitário flagelado que parasita o intestino delgado dos mamíferos, inclusive dos seres humanos, causando uma doença diarreica conhecida como giardíase. Nos humanos, costuma parasitar o intestino delgado, principalmente em segmentos de duodeno e jejuno. G. lamblia, G. intestinalis ou G. duodenale são os sinónimos dados à espécie.^[1][2]

O parasita se liga ao epitélio por meio de um disco adesivo ventral ou ventosa, e se reproduz por fissão binária.^[3] A giardíase não se espalha pela corrente sanguínea, nem se espalha para outras partes do trato gastrointestinal, mas permanece confinada ao lúmen do intestino delgado.^[4] Giardia possui uma membrana externa que permite se manter viva, mesmo fora do corpo do hospedeiro, e que pode torná-la tolerante à desinfecção com cloro. Os trofozoítos de Giardia absorvem nutrientes do lúmen e são anaeróbios.^[5]

As principais vias de infecção humana incluem a ingestão de água potável não tratada (que é o método mais comum de transmissão deste parasita),^[6] alimentos e solo contaminados com fezes humanas. A contaminação das águas naturais também ocorre em bacias hidrográficas onde ocorre o pastoreio intensivo. Este flagelado pode viver no estado livre, em lagos ou ribeiras, durante bastante tempo.

Morfologia

Os trofozoítos tem 20 micrómetros de comprimento e 10 µm de largura, forma de pêra e são móveis, possuindo quatro pares de flagelos (anterior, posterior, ventral e caudal) e dois núcleos, dois corpos parabasais, e ainda dois axonemas cada um; enquanto os cistos são arredondados, com dois ou quatro núcleos, quatro corpos parabasais, quatro axonemas e com parede celular grossa, imóveis, mas por essas condições, se tornam mais resistentes e com maior potencial patológico. A reprodução dos trofozoítos é assexuada - por divisão binária longitudinal- e têm a capacidade de variar as suas proteínas de superfície, evadindo o sistema imunitário.^[7][8]

Trofozoítos: célula afilada na extremidade posterior, com 8 flagelos (dois anteriores, quatro médios e dois posteriores), dois discos de adesão, dois núcleos e dois corpos semilunares.

Cistos: elipsoidal, com a presença de corpos escuros em formato de meia lua, axonemas de flagelos, presença de 2 ou 4 núcleos e membrana externa deslocada do citoplasma.

Ciclo de vida

Ciclo de vida de Giardia lamblia

G. duodenalis possui duas formas morfologicamente distintas durante seu ciclo de vida: a forma ativamente móvel, chamada trofozoíto, e a forma infectante, chamada de cisto. O trofozoíto possui cerca de 20 µm de comprimento e 10 µm de largura, possuindo formato de pera e simetria bilateral. É a forma replicativa e móvel do parasita, sobrevivendo apenas dentro do intestino delgado de seus hospedeiros.^[7] Os trofozoítos nadam através do muco intestinal até eventualmente aderirem ao epitélio intestinal do hospedeiro,^[8], onde então se dividem por fissão binária, formando mais trofozoítos ou cistos não-replicativos. Os cistos passam pelo intestino grosso do hospedeiro e são liberados pelas fezes.^[7] Os cistos de G. lamblia são resistentes aos estressores ambientais e podem sobreviver no ambiente por semanas a meses se mantidos úmidos.^[8][7] Os cistos permanecem dormentes até serem ingeridos por um animal hospedeiro. No novo hospedeiro, as condições ambientais fazem com que o cisto produza dois trofozoítos, que então se ligam às células epiteliais, iniciando o ciclo novamente.^[7]

História

Anton van Leeuwenhoek (1681) observou animalúnculos móveis (trofozoíto) em suas próprias fezes. Todavia, o médico checo Vilém Dušan Lambl, em 1859, o descreveu com mais pormenores. Este gênero foi criado por Kunstler (1882) ao verificar a presença de um flagelado no intestino de girinos.^[9]

Epidemiologia

Os principais riscos de infecção pela giárdia é pelo consumo de alimentos contaminados por água não tratada, além de auto-infecção ou manipulação de alimentos de forma inadequada. A infecção pode ocorrer também através de relações sexuais.

A giárdia (Giardia lamblia) costuma ser encontrada em diversos lugares do mundo, afetando, principalmente, crianças na faixa de 6 anos - interessante ressaltar que este fato é devido a proximidade de criança brincarem em parques, nas ruas, entre outros lugares que possam conter o cisto, ou a própria ingestão de alimentos contaminados - podendo assim ocorrer surtos em creches, por exemplo, aonde as pessoas desta faixa etária se contaminam com maior facilidade, devido ao contato direto.

Patogenia

Giárdia (Giardia lamblia) causa diarreia e dificuldades na absorção intestinal, por aderir e diminuir as microvilosidades do intestino, dificultando a absorção de nutrientes; e por possuir proteases que agem em glicoproteína, levando lesões à mucosa, desencadeando também uma resposta inflamatória.

Infecção

Na fase aguda da infecção, ocorre diarréia aquosa até o desenvolvimento da imunidade. Na fase crônica, quando já aderida ao intestino do hospedeiro, forma uma espécie de tapete impedindo a absorção dos nutrientes. Sua aderência é graças aos discos de adesão presentes bilateralmente. A liberação de toxinas pode causar destruição das microvilosidades do epitélio intestinal, assim como o desencadeamento de reação inflamatória. Infecções crônicas podem impedir e muito a absorção intestinal, causando doenças nutricionais como a síndrome da ma absorção, que pode levar adultos e principalmente crianças (ou filhotes) a altos graus de desnutrição e até à morte.

Diagnóstico

O diagnóstico é confirmado a partir do achado de cistos ou trofozoítas nas fezes. Por haver pequena quantidade em amostras, é de difícil diagnóstico, por isso deve-se ter ao menos três amostras do paciente suspeito ou contaminado. Uma maneira mais direta, porém menos quantitativa, é a pesquisa de antígeno por ELISA nas fezes. Tendo um alto grau de sensibilidade (de 85 % a 95%) e de especificidade ( 90% a 100%).

Referências