Exoerythrocytic stages of avion and reptilian malarial parasites

Huff, Clay G.

doi:10.1016/0014-4894(69)90176-3

Cited by 28 publications

(16 citation statements)

References 116 publications

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“…1b); they cannot infect the blood cells, so there is no parasitaemia after maturation of the cryptozoites. These merozoites induce the second generation of primary exo-erythrocytic meronts (metacryptozoites), which develop in reticuloendothelial cells, particularly in macrophages, and can be found all over the body; they are often reported in spleen, liver and lungs [2, 7, 8, 54, 55, 61, 69, 74, 93, 126]. Metacryptozoites are covered by a thin wall; they look similar to cryptozoites, but are larger and produce a greater number of merozoites (Fig.…”

Section: Resultsmentioning

confidence: 99%

Exo-erythrocytic development of avian malaria and related haemosporidian parasites

Valkiūnas

Iezhova

2017

Malar J

108

159

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Background: Avian malaria parasites (Plasmodium spp.) and related haemosporidians (Haemosporida) are responsible for diseases which can be severe and even lethal in avian hosts. These parasites cause not only blood pathology, but also damage various organs due to extensive exo-erythrocytic development all over the body, which is not the case during Plasmodium infections in mammals. However, exo-erythrocytic development (tissue merogony or schizogony) remains the most poorly investigated part of life cycle in all groups of wildlife haemosporidian parasites. In spite of remarkable progress in studies of genetic diversity, ecology and evolutionary biology of avian haemosporidians during the past 20 years, there is not much progress in understanding patterns of exo-erythrocytic development in these parasites. The purpose of this review is to overview the main information on exo-erythrocytic development of avian Plasmodium species and related haemosporidian parasites as a baseline for assisting academic and veterinary medicine researchers in morphological identification of these parasites using tissue stages, and to define future research priorities in this field of avian malariology. Methods:The data were considered from peer-reviewed articles and histological material that was accessed in zoological collections in museums of Australia, Europe and the USA. Articles describing tissue stages of avian haemosporidians were included from 1908 to the present. Histological preparations of various organs infected with the exo-erythrocytic stages of different haemosporidian parasites were examined. Results:In all, 229 published articles were included in this review. Exo-erythrocytic stages of avian Plasmodium, Fallisia, Haemoproteus, Leucocytozoon, and Akiba species were analysed, compared and illustrated. Morphological characters of tissue stages that can be used for diagnostic purposes were specified. Conclusion:Recent molecular studies combined with histological research show that avian haemosporidians are more virulent than formerly believed. The exo-erythrocytic stages can cause severe disease, especially in non-adapted avian hosts, suggesting the existence of a group of underestimated malignant infections. The development of a given haemosporidian strain can be markedly different in different avian hosts, resulting in significantly different virulence. A methodology combining the traditional histology techniques with molecular diagnostic tools is essential to speed research in this field of avian malariology.

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Section: Resultsmentioning

confidence: 99%

Exo-erythrocytic development of avian malaria and related haemosporidian parasites

Valkiūnas

Iezhova

2017

Malar J

108

159

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“…While EEF of avian and reptilian malaria parasites develop in the reticulo-endothelial or hematopoietic systems [43–45], a major evolutionary change occurred with the mammalian malaria parasites, whose EEF mature in hepatocytes. Perhaps the nutritionally rich and immunologically privileged hepatic environment offers advantages, but it also presents a problem for merozoites released from EEFs into hepatic sinusoids: unless they invade an erythrocyte very quickly they face a gauntlet of highly phagocytic Kupffer cells.…”

Section: Discussionmentioning

confidence: 99%

Release of Hepatic Plasmodium yoelii Merozoites into the Pulmonary Microvasculature

et al. 2007

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Plasmodium undergoes one round of multiplication in the liver prior to invading erythrocytes and initiating the symptomatic blood phase of the malaria infection. Productive hepatocyte infection by sporozoites leads to the generation of thousands of merozoites capable of erythrocyte invasion. Merozoites are released from infected hepatocytes as merosomes, packets of hundreds of parasites surrounded by host cell membrane. Intravital microscopy of green fluorescent protein–expressing P. yoelii parasites showed that the majority of merosomes exit the liver intact, adapt a relatively uniform size of 12–18 μm, and contain 100–200 merozoites. Merosomes survived the subsequent passage through the right heart undamaged and accumulated in the lungs. Merosomes were absent from blood harvested from the left ventricle and from tail vein blood, indicating that the lungs effectively cleared the blood from all large parasite aggregates. Accordingly, merosomes were not detectable in major organs such as brain, kidney, and spleen. The failure of annexin V to label merosomes collected from hepatic effluent indicates that phosphatidylserine is not exposed on the surface of the merosome membrane suggesting the infected hepatocyte did not undergo apoptosis prior to merosome release. Merosomal merozoites continued to express green fluorescent protein and did not incorporate propidium iodide or YO-PRO-1 indicating parasite viability and an intact merosome membrane. Evidence of merosomal merozoite infectivity was provided by hepatic effluent containing merosomes being significantly more infective than blood with an identical low-level parasitemia. Ex vivo analysis showed that merosomes eventually disintegrate inside pulmonary capillaries, thus liberating merozoites into the bloodstream. We conclude that merosome packaging protects hepatic merozoites from phagocytic attack by sinusoidal Kupffer cells, and that release into the lung microvasculature enhances the chance of successful erythrocyte invasion. We believe this previously unknown part of the plasmodial life cycle ensures an effective transition from the liver to the blood phase of the malaria infection.

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“…7. This reflects Plasmodium phylogeny in that avian and reptilian Plasmodium species, which do not have a life cycle stage in hepatocytes, invade and replicate in Kupffer cells and other cells of the mononuclear macrophage system (Bray, 1957; Huff, 1969). It is reasonable to postulate that the evolutionarily more recent mammalian species retain the ability to recognize and safely enter Kupffer cells while acquiring new mechanisms to continue their journey across the space of Disse and invade parenchymal cells, which offer special advantages for the first stage of replication in the mammalian host.…”

Section: Discussionmentioning

confidence: 99%

Kupffer cells are obligatory for Plasmodium yoelii sporozoite infection of the liver

et al. 2007

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SummaryPrevious studies suggested Plasmodium sporozoites infect hepatocytes after passing through Kupffer cells, but proof has been elusive. Here we present new information strengthening that hypothesis. We used homozygous op/op mice known to have few Kupffer cells because they lack macrophage colony stimulating factor 1 required for macrophage maturation due to a deactivating point mutation in the osteopetrosis gene. We found these mice to have 77% fewer Kupffer cells and to exhibit reduced clearance of colloidal carbon particles compared with heterozygous phenotypically normal littermates. Using a novel quantitative reverse transcription polymerase chain reaction assay for P. yoelii 18S rRNA, we found liver infection of op/op mice to be decreased by 84% compared with controls. However, using another way of limiting Kupffer cells, treatment with liposomeencapsulated clodronate, infection of normal mice was enhanced seven-to 15-fold. This was explained by electron microscopy showing temporary gaps in the sinusoidal cell layer caused by this treatment. Thus, Kupffer cell deficiency in op/op mice decreases sporozoite infection by reducing the number of portals to the liver parenchyma, whereas clodronate increases sporozoite infection by opening portals and providing direct access to hepatocytes. Together these data provide strong support for the hypothesis that Kupffer cells are the portal for sporozoites to hepatocytes and critical for the onset of a malaria infection.

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Exoerythrocytic stages of avion and reptilian malarial parasites

Cited by 28 publications

References 116 publications

Exo-erythrocytic development of avian malaria and related haemosporidian parasites

Exo-erythrocytic development of avian malaria and related haemosporidian parasites

Release of Hepatic Plasmodium yoelii Merozoites into the Pulmonary Microvasculature

Kupffer cells are obligatory for Plasmodium yoelii sporozoite infection of the liver

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