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Abstract
Alpine swifts (Tachymarptis melba) are sub-Saharan migratory birds, which, in Switzerland, nest in colonies that have been continuously monitored for over 40 years. In the summer of 2022, despite favourable environmental conditions, an unexpectedly high number of sudden mortalities (30–80%) occurred in 20 to 45-day-old nestlings from several nesting sites, of which 3 were monitored in detail. Nestlings submitted for post-mortem analysis (n = 5) were in good body condition but exhibited extensive subcutaneous haematomas (n = 5), myocardial petechiae (n = 2) and stunted growth of primary feathers (n = 1). In all birds, 4–5 μm large, amastigote-like protozoans were identified in skeletal and cardiac muscle sections. These tissues tested positive in a PCR targeting the 18S-rRNA gene of Trypanosoma spp. Amplified sequences showed 99.63% identity with sequences of Trypanosoma corvi (JN006854 and AY461665) and Trypanosoma sp. (AJ620557, JN006841). 72 blood smears of 45-day-old nestlings from two colonies were assessed, of which 20 contained trypomastigote forms, some with high parasitaemia (highest average of 56.4 in 10 high power fields, 400x magnification). Trypomastigote morphometrics (n = 36; mean total length = 30.0 μm; length of free flagellum = 5.8 μm) were consistent with those of T. bouffardi. These findings suggest that an avian trypanosomiasis causing mass nestling mortality could be an emerging disease in Swiss Alpine swift populations.
Multi-target drug treatment has become popular as a substitute for traditional monotherapy. Monotherapy can lead to resistance and side effects. Multi-target drug discovery is gaining importance as data on bioactivity becomes more abundant. The design of multi-target drugs is expected to be an important development in the pharmaceutical industry in the near future. This review presents multi-target compounds against trypanosomatid parasites (Trypanosoma cruzi, T. brucei, and Leishmania sp.) and tuberculosis (Mycobacterium tuberculosis), which mainly affect populations in socioeconomically unfavorable conditions. The article analyzes the studies, including their chemical structures, viral strains, and molecular docking studies, when available. The objective of this review is to establish a foundation for designing new multi-target inhibitors for these diseases.
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Swifts (Apodidae) are an unusual group of birds that spend most of their lives in flight, landing only when breeding. Although this aerial lifestyle greatly reduces their likelihood of being bitten by vectors and infected by vector-born parasites, swifts can still be heavily infested during breeding by nest-based vectors such as louse flies (Hippoboscidae). Here, we investigated host, vector, and vector-borne parasite relationships in the three most widespread swift species in the Western Palearctic (WP): common swifts (Apus apus), pallid swifts (A. pallidus), and alpine swifts (Tachymarptis melba), their nest-based louse flies (Crataerina pallida and C. melbae) and avian haemosporidians (genera Haemoproteus, Plasmodium, and Leucocytozoon). Studies of haemosporidian infections in Apodidae remain limited, with clear evidence of infection found to date in just four Neotropical and one Australasian species. The possible role of louse flies in transmitting haemosporidian infections has never been tested in swifts. We assessed the occurrence of haemosporidian infection by PCR screenings of DNA from blood samples from 34 common swifts and 44 pallid swifts from Italy, and 45 alpine swifts from Switzerland. We also screened 20 ectoparasitic louse flies present on 20 birds and identified them by both morphological features and cytochrome oxidase subunit 1 (COI) barcodes. Our results provide no evidence of haemosporidian infection in the 123 swifts tested or in the two louse fly species we identified. Our findings are consistent with available knowledge showing no haemosporidian occurrence in WP swift species and that the most likely infection route for these highly aerial species (via louse fly ectoparasites during nesting) is unlikely.
Avian haemosporidian parasites are widespread and infect birds from a broad variety of avian families with diverse consequences ranging from subclinical infections to severe and fatal disease. This study aimed to determine the occurrence and diversity of avian haemosporidia including associated clinical signs and pathomorphological lesions in captive and free-ranging birds from two zoos and the near environment in Switzerland. Blood samples from 475 birds, including 230 captive and 245 free-ranging individuals belonging to 42 different avian species from 15 orders were examined for the presence of avian haemosporidian DNA by a one-step multiplex PCR designed to simultaneously detect and discriminate the genera Plasmodium, Haemoproteus and Leucocytozoon by targeting mitochondrial genome sequences. Positive samples were additionally tested using a nested PCR targeting the cytochrome b gene of Plasmodium and Haemoproteus. The obtained amplicons were bi-directionally sequenced. This study revealed haemosporidian DNA in 42 of the samples, belonging to ten host species. The most commonly detected lineage was Plasmodium relictum SGS1, which was identified in 29 birds (Phoenicopterus roseus: n = 24, Alectoris graeca: n = 1, Lamprotornis superbus: n = 1, Somateria mollissima: n = 1, Spheniscus demersus: n = 1, Tetrao urogallus crassirostris: n = 1), followed by Haemoproteus sp. STRURA03 in six avian hosts (Bubo bubo: n = 5, Bubo scandiacus = 1), Plasmodium relictum GRW11 in four individuals (Phoenicopterus roseus: n = 3, Spheniscus demersus: n = 1) and Plasmodium elongatum GRW06 in one Alectura lathami lathami. A Phalacrocorax carbo was infected with Plasmodium relictum, but the exact lineage could not be determined. One mixed infection with P. relictum and Haemoproteus sp. was detected in a Bubo scandiacus. Only five individuals (Spheniscus demersus: n = 2, Somateria mollissima: n = 1, Bubo scandiacus: n = 1, Alectoris graeca: n = 1) showed clinical and pathomorphological evidence of a haemosporidian infection.
Louse flies (Hippoboscidae) are permanent ectoparasites of birds and mammals. They have a cosmopolitan distribution with more than 200 described species. The aim of this study was to reveal host–vector–parasite associations between louse flies, birds, and trypanosomes. A total of 567 louse fly specimens belonging to 7 species were collected from birds at several localities in Czechia, including the rare species Ornithophila metallica and Ornithoica turdi. There was a significant difference in the occurrence of Ornithomya avicularia and Ornithomya fringillina on bird hosts according to their migratory status, O. fringillina being found more frequently on long-distance migrants. Trypanosomes were found in four species, namely, Ornithomya avicularia, O. fringillina, O. biloba, and Ornithoica turdi; the later three species are identified in this paper as natural trypanosome vectors for the first time. The prevalence of trypanosomes ranged between 5 and 19%, the highest being in O. biloba and the lowest being in O. fringillina. Phylogenetic analysis of the SSU rRNA gene revealed that a vast majority of trypanosomes from hippoboscids belong to the avian T. corvi/culicavium group B. Four new lineages were revealed in group B, with louse flies being probable vectors for some of these trypanosome lineages. We also confirmed the transcontinental distribution of several trypanosome lineages. Our results show that hippoboscids of several genera are probable vectors of avian trypanosomes.
Avian trypanosomes are cosmopolitan and common protozoan parasites of birds; nevertheless , knowledge of their life cycles and vectors remains incomplete. Mosquitoes have been confirmed as vectors of Trypanosoma culicavium and suggested as vectors of T. thomasbancrofti; however, transmission has been experimentally confirmed only for the former species. This study aims to confirm the experimental transmission of T. thomasbancrofti to birds and its localization in vectors. Culex pipiens were fed on blood using four strains of T. thomasbancrofti, isolated from vectors and avian hosts; all strains established infections, and three of them were able to develop high infection rates in mosquitoes. The infection rate of the culicine isolates was 5-28% for CUL15 and 48-81% for CUL98, 67-92% for isolate OF19 from hippoboscid fly, while the avian isolate PAS343 ranged between 48% and 92%, and heavy infections were detected in 90% of positive females. Contrary to T. culicavium, trypanosomes were localized in the hindgut, where they formed rosettes with the occurrence of free epimastigotes in the hindgut and midgut during late infections. Parasites occurred in urine droplets produced during mosquito prediuresis. Transmission to birds was achieved by the ingestion of mosquito guts containing trypanosomes and via the conjunctiva. Bird infection was proven by blood cultivation and xenodiagnosis; mature infections were present in the dissected guts of 24-26% of mosquitoes fed on infected birds. The prevalence of T. thomasbancrofti in vectors in nature and in avian populations is discussed in this paper. This study confirms the vectorial capacity of culicine mosquitoes for T. thomasbancrofti, a trypanosome related to T. avium, and suggests that prediuresis might be an effective mode of trypanosome transmission.
Trypanosoma brucei is a protozoan parasite that causes human and animal African trypanosomiases (HAT and AAT). In the mammalian host, the parasite lives entirely extracellularly, in both the blood and interstitial spaces in tissues. Although most T. brucei research has focused on the biology of blood- and central nervous system (CNS)-resident parasites, a number of recent studies have highlighted parasite reservoirs in the dermis and adipose tissue, leading to a renewed interest in tissue-resident parasite populations. In light of this renewed interest, work describing tissue-resident parasites can serve as a valuable resource to inform future investigations of tissue-resident T. brucei. Here, we review this body of literature, which describes infections in humans, natural hosts, and experimental animal models, providing a wealth of information on the distribution and biology of extravascular parasites, the corresponding immune response in each tissue, and resulting host pathology. We discuss the implications of these studies and future questions in the study of extravascular T. brucei.
Avian malaria is a vector-borne disease caused by Plasmodium species, which may affect a broad spectrum of bird families worldwide. In most endemic and migratory birds, Plasmodium infections seem not to cause severe harm; however, non-indigenous species kept in human care such as penguins may experience high morbidity and mortality rates. Fatal avian malaria may also occur in other non-native seabirds such as puffins (Fratercula spp.), but reported cases are scarce.
The aim of this study was to analyze seven cases of sudden death in captive Atlantic puffins (Fratercula arctica) at Berne Animal Park in Switzerland between 2010 and 2020, and to determine the involvement of haemosporidian parasites in the fatal outcome. In all cases, lymphoplasmacytic inflammation, necrotic lesions in several organs and presence of protozoan stages within tissues/erythrocytes or accumulation of iron-based pigment were observed histologically. A one-step multiplex PCR designed to simultaneously detect and discriminate haemosporidia belonging to the genera Plasmodium, Haemoproteus and Leucocytozoon, and a nested PCR detecting Plasmodium and Haemoproteus infections were performed on DNA extracted from formalin-fixed and paraffin-embedded (FFPE) or fresh liver and spleen tissues from five and two birds, respectively. Plasmodium spp. DNA was detected in the tissues from six of seven birds by the one-step multiplex PCR and in five of seven individuals by the nested PCR protocol. Direct sequencing of the amplification products allowed the molecular identification of Plasmodium relictum SGS1 as the involved species in three individuals and Plasmodium matutinum LINN1 in two of these fatal cases. In one bird, no haemosporidian DNA could be amplified from FFPE tissues despite of suggestive histopathological findings. These results indicate that avian malaria represents an important cause of death in captive puffins and it should be considered as a differential diagnosis in unclear or fatal cases in this threatened bird species.
From September 2012 to May 2018, blood samples from 364 raptors (mostly adults) were collected and screened for trypanosomes and haemosporidians by microscopic examination and nested polymerase chain reactions (PCR). Trypanosoma spp. were identified in 15 birds from eight different species. Light microscopy revealed 14 cases of infection with Trypanosoma cf. corvi, including one each in black-shouldered kite (Elanus caeruleus, n = 49), Brahminy kite (Haliastur indus, n = 50), and spotted owlet (SO, Athene brama, n = 27); two mountain hawk-eagles (Spizaetus nipalensis, n = 3); and three each in Asian barred owlets (ABO, Glaucidium cuculoides, n = 27), barn owls (BO, Tyto alba, n = 65) and collared scops owls (CSO, Otus lettia, n = 41). In addition, one case of infection with T. avium was identified in an oriental scops owl (OSO, Otus sunia, n = 2). All infected raptors showed very low parasitemia levels. The PCR detected more three positives in one CSO, one Japanese sparrowhawk (Accipiter gularis), and one OSO. The sensitivity and specificity of the PCR method were 93.3% and 99.1%, respectively. The overall infection rate was very low (4.9%). The highest infection rate was recorded in cold-dry season (9.9%). Coinfection of Plasmodium with trypanosomes was found in all three ABOs. Coinfection with Haemoproteus spp. was found in one BO, three CSOs, and one SO. Coinfection with Haemoproteus spp. and Leucocytozoon danilewskyi was found in the OSO. Microfilarias were detected in one ABO and one CSO. The ultrastructure of trypomastigotes of T. cf. corvi in an ABO revealed fine structures. All small subunit ribosomal RNA (SSU rRNA) sequences belong to two clades: T. avium and T. corvi-culicavium complex/group. SSU rRNA gene amplification was not successful in one BO. The raptors with trypanosome infections showed normal hematological values and healthy appearance. Furthermore, this is the first report of T. avium in a nocturnal raptor from Thailand.
The list of all known locality and host records from the literature on louse flies from Slovakia are summarized, with the addition of new collection data. New locality data are provided for five species. Three species are added to the Slovakian list: Icosta minor (Bigot in Thomson, 1858), which was erroneously cited for Moravia instead of Slovakia in the previous checklist, and Ornithophila metallica (Schiner, 1864) and Ornithomya chloropus (Bergroth, 1901), which were overlooked from the last checklist. As a result,
the louse fly fauna of Slovakia increases to 19 species: 12 autochtonous species and seven rare, non-native species only occasionally imported to Slovakia or migrating to the country with their hosts. This is by far the largest regional fauna of Hippoboscidae in Central Europe, and matches the richest southern European faunas. In total, 78 host-parasite associations concerning 46 bird-host species from eight orders and nine species of mammals, including humans, have been found from a literature review in Slovakia. Two
host-parasite associations are reported from Slovakia for the first time: Ornithomya avicularia (Linnaeus, 1758) on Prunella modularis (Linnaeus, 1758) (Aves: Prunellidae) and Lipoptena fortisetosa Maa, 1965 on Homo sapiens Linnaeus, 1758 (Mammalia: Hominidae).
Abstract African trypanosomes cause human African trypanosomiasis and animal African trypanosomiasis. They are transmitted by tsetse flies in sub-Saharan Africa. Although most famous for their mechanisms of immune evasion by antigenic variation, there have been recent important studies that illuminate important aspects of the biology of these parasites both in their mammalian host and during passage through their tsetse fly vector. This Primer overviews current research themes focused on these parasites and discusses how these biological insights and the development of new technologies to interrogate gene function are being used in the search for new approaches to control the parasite. The new insights into the biology of trypanosomes in their host and vector highlight that we are in a ‘golden age’ of discovery for these fascinating parasites.
African trypanosomosis (AT) is a chronically debilitating parasitic disease of medical and economic importance for the development of sub-Saharan Africa. The trypanosomes that cause this disease are extracellular protozoan parasites that have developed efficient immune escape mechanisms to manipulate the entire host immune response to allow parasite survival and transmission. During the early stage of infection, a profound pro-inflammatory type 1 activation of the mononuclear phagocyte system (MPS), involving classically activated macrophages (i.e., M1), is required for initial parasite control. Yet, the persistence of this M1-type MPS activation in trypanosusceptible animals causes immunopathology with anemia as the most prominent pathological feature. By contrast, in trypanotolerant animals, there is an induction of IL-10 that promotes the induction of alternatively activated macrophages (M2) and collectively dampens tissue damage. A comparative gene expression analysis between M1 and M2 cells identified galectin-3 (Gal-3) and macrophage migration inhibitory factor (MIF) as novel M1-promoting factors, possibly acting synergistically and in concert with TNF-α during anemia development. While Gal-3 enhances erythrophagocytosis, MIF promotes both myeloid cell recruitment and iron retention within the MPS, thereby depriving iron for erythropoiesis. Hence, the enhanced erythrophagocytosis and suppressed erythropoiesis lead to anemia. Moreover, a thorough investigation using MIF-deficient mice revealed that the underlying mechanisms in AT-associated anemia development in trypanosusceptible and tolerant animals are quite distinct. In trypanosusceptible animals, anemia resembles anemia of inflammation, while in trypanotolerant animals’ hemodilution, mainly caused by hepatosplenomegaly, is an additional factor contributing to anemia. In this review, we give an overview of how trypanosome- and host-derived factors can contribute to trypanosomosis-associated anemia development with a focus on the MPS system. Finally, we will discuss potential intervention strategies to alleviate AT-associated anemia that might also have therapeutic potential.
The effect of combined administration of 1000 i.u/100g body weight (bd.wt.) vitamin A and 100 mg/kg bd wt. vitamin C to Trypanosoma brucei brucei-infected rats daily for twenty-one days was investigated. The anaemia caused by T. brucei infection in rats not administered the vitamins was significantly (P vitamins. Indices of hepatic function such as serum alanine- and aspartate transaminases, and serum alkaline phosphatase activities as well as indices of renal function such as serum urea and creatinine levels were all significantly (P prevented the hepatomegaly but only partially prevented the splenomegaly caused by infection. It was concluded that intraperitoneally administered vitamins A and C alleviated T. brucei – induced anaemia and organ damage.
Background
Species of avian malaria parasites (Plasmodium) are widespread, but their virulence has been insufficiently investigated, particularly in wild birds. During avian malaria, several cycles of tissue merogony occur, and many Plasmodium spp. produce secondary exoerythrocytic meronts (phanerozoites), which are induced by merozoites developing in erythrocytic meronts. Phanerozoites markedly damage organs, but remain insufficiently investigated in the majority of described Plasmodium spp. Avian malaria parasite Plasmodium (Giovannolaia) homocircumflexum (lineage pCOLL4) is virulent and produces phanerozoites in domestic canaries Serinus canaria, but its pathogenicity in wild birds remains unknown. The aim of this study was to investigate the pathology caused by this infection in species of common European birds.
Methods
One individual of Eurasian siskin Carduelis spinus, common crossbill Loxia curvirostra and common starling Sturnus vulgaris were exposed to P. homocircumflexum infection by intramuscular sub-inoculation of infected blood. The birds were maintained in captivity and parasitaemia was monitored until their death due to malaria. Brain, heart, lungs, liver, spleen, kidney, and a piece of breast muscle were examined using histology and chromogenic in situ hybridization (ISH) methods.
Results
All exposed birds developed malaria infection, survived the peak of parasitaemia, but suddenly died between 30 and 38 days post exposure when parasitaemia markedly decreased. Numerous phanerozoites were visible in histological sections of all organs and were particularly easily visualized after ISH processing. Blockage of brain capillaries with phanerozoites may have led to cerebral ischaemia, causing cerebral paralysis and is most likely the main reason of sudden death of all infected individuals. Inflammatory response was not visible around the brain, heart and muscle phanerozoites, and it was mild in parenchymal organs. The endothelial damage likely causes dysfunction and failure of parenchymal organs.
Conclusion
Plasmodium homocircumflexum caused death of experimental passerine birds due to marked damage of organs by phanerozoites. Patterns of phanerozoites development and pathology were similar in all exposed birds. Mortality was reported when parasitaemia decreased or even turned into chronic stage, indicating that the light parasitaemia is not always indication of improved health during avian malaria. Application of traditional histological and ISH methods in parallel simplifies investigation of exoerythrocytic development and is recommended in avian malaria research.
Background:
Anaemia is an important complication of trypanosomiasis. The mechanisms through which trypanosomal infection leads to anaemia are poorly defined. A number of studies have implicated inflammatory cytokines, but these data are limited and inconsistent. In this article, we reviewed the published literature on cytokines associated with Trypanosoma brucei infections and their role in the immunopathology leading to anaemia.
Methodology:
Articles were searched in PubMed through screening of titles and abstracts with no limitation on date of publishing and study design. Articles in English were searched using keywords "African trypanosomiasis", "sleeping sickness", "Trypanosoma brucei", in all possible combinations with "anaemia" and/or "cytokines".
Results:
Twelve articles examining cytokines and their role in trypanosomeinduced anaemia were identified out of 1095 originally retrieved from PubMed. None of the articles identified were from human-based studies. A total of eight cytokines were implicated, with four cytokines (IFN-γ, IL-10, TNF-α, IL-12) showing an association with anaemia. These articles reported that mice lacking TNF-α were able to control anaemia, and that IFN-γ was linked to severe anaemia given its capacity to suppress erythropoiesis, while IL-10 was shown to regulate IFN-γ and TNF-α, providing a balance that was associated with severity of anaemia. IFN-γ and TNF-α have also been reported to work in concert with other factors such as nitric oxide and iron in order to induce anaemia.
Conclusion:
IFN-γ, IL-10, and TNF-α were the three major cytokines identified to be heavily involved in anaemia caused by Trypanosoma brucei infection. The anti-inflammatory cytokine, IL-10, was shown to counter the effects of proinflammatory cytokines in order to balance the severity of anaemia. The mechanism of anaemia is multifactorial and therefore requires further, more elaborate research. Data from human subjects would also shed more light.
The effect of black seed oil (Nigella sativa oil) on parasitaemia, someserum and liver enzymes as well as some haematological parameters inTrypanosoma brucei-infected rats was investigated. The results showthere was low parasitaemia and extension of life span of rats from 12days of the infected untreated (control) rats to 22 days for the infectedblack seed oil-treated rats. Results also show significant increases inactivities of serum alkaline phosphatase as well as glutamateoxaloacetate and glutamate pyruvate transaminases with decreases inthe liver enzyme activities. Protein concentrations show significantdecreases in the serum and increases in the liver. There were alsosignificant increases in the haemoglobin (Hb) concentration, packedcell volume (PCV), red blood cell (RBC), white blood cell (WBC) andplatelet counts of infected oil-treated rats when compared with theinfected untreated. We suggest that black seed oil has trypanocidalproperties and probably stimulate the host immune system to controlparasite proliferation thereby making it a possible agent for managingAfrican sleeping sickness despite possible gradual damage to hostorgans as shown by increases in some serum enzymes.(Afr. J. Biomed. Res. 11: 79 - 85)
The phylogenetic relationships of avian trypanosomes, common parasites of birds, remain ambiguous and validity of many species is questionable. Analyses based on 18S rRNA sequences, dimensions of the kinetoplast disc and the size of kinetoplast (k) DNA minicircles were used to differentiate among large trypanosomes parasitizing birds of the Old World. These trypanosomes with typical striated appearance formed two well-supported groups - the "Trypanosoma avium" clade and the "Trypanosoma corvi" clade. Interestingly, the isolate derived from the Central European hippoboscid fly (Ornithomyia avicularia) is closely related to T. corvi from a raven captured in the U.K., whereas a trypanosome obtained from the blood of a raven of the Central Europe origin (Czech Republic) is a typical member of the "T. avium" clade.
We have investigated the effects of the aqueous leaf extract of P. guajava on reduced glutathione (GSH) and malondialdehyde (MDA) concentrations in rats experimentally infected with Trypanosoma brucei brucei. The results obtained showed that the MDA concentrations in the serum and tissues of the infected animals were significantly increased (P<0.05) relative to the control (Table 2). However there was an insignificant difference in the GSH concentrations in the brain for the infected group and the infected but treated group relative to control (P>0.05) (Table 1). In contrast, a significant decrease (P<0.05) was observed for the GSH concentrations in the liver and kidney for the infected animals compared to the uninfected control and the infected but treated groups. The MDA concentrations in the serum and tissues of the infected but treated animals were significantly reduced when compared to the infected groups (P<0.05) (Table 2). In this study it was demonstrated that the aqueous extract was able to reduce the trypanosomosis associated lipid peroxidation as well as raise the level of GSH in the infected but treated animals significantly (P<0.05). We present evidence that the ability of the leaf extract of P. guajava to lower the MDA concentrations in the treatment group may be attributed to its antioxidant properties.
We have studied the biodiversity of trypanosomes from birds and bloodsucking Diptera on a large number of isolates. We used two molecular approaches, random amplification of polymorphic DNA (RAPD) method, and sequence analysis of the small subunit ribosomal RNA (SSU rRNA) gene. RAPD method divided the isolates into 11 separate lineages. Phylogenetic analysis of the SSU rRNA gene was congruent with the RAPD. Morphometric analysis of kinetoplast width and cell length was in agreement with molecular data. Avian trypanosomes appeared polyphyletic on SSU rDNA tree; thus, they do not represent a taxonomic group. We propose that all lineages recovered by SSU analysis probably represent distinct species of avian trypanosomes. We discuss possible transmission ways and geographical distribution of new avian trypanosome lineages. Finally, we recommend methods that should be used for species determination of avian trypanosomes.
Trypanosoma cruzi, the causative agent of Chagas' disease, which affects a large number of individuals in Central and South America, is transmitted to vertebrate hosts by blood-sucking insects. This protozoan is an obligate intracellular parasite. The infective forms of the parasite are metacyclic and bloodstream trypomastigote and amastigote. Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle. The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types. Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.
The effect of black seed oil ( Nigella sativa oil) on parasitaemia, some serum and liver enzymes as well as some haematological parameters in Trypanosoma brucei -infected rats were investigated. The results show there was low parasitaemia and extension of life span of rats from 12 days of the infected untreated (control) rats to 22 days for the infected black seed oil-treated rats. Results also show significant increases in activities of serum alkaline phosphatase as well as glutamate oxaloacetate and glutamate pyruvate transaminases with decreases in the liver enzyme activities. Protein concentrations show significant decreases in the serum and increases in the liver. There were also significant increases in the haemoglobin (Hb) concentration, packed cell volume (PCV), red blood cell (RBC), white blood cell (WBC) and platelet counts of infected oil-treated rats when compared with the infected untreated. We suggest that black seed oil has trypanocidal properties and probably stimulate the host immune system to control parasite proliferation thereby making it a possible agent for managing African sleeping sickness despite possible gradual damage to host organs as shown by increases in some serum enzymes.
Studies to determine the effect of some Nigerian Medicinal plants on some haematological parameters of rats infected with T. b. brucei was carried out. The plants investigated and the dose levels per kilogram body weights used are fresh Momordica balsamina pulp (150mg); fresh Aloe vera pulp (1ml); aqueous extracts of Securidaca longipenduculata root and root bark (100mg) and Annona senegalensis leaves (200mg). All the animals were treated orally for seven consecutive days after establishment of parasitaemia. Parasitaemia and some haematological parameters were determined before and after treatment as well as pathochemical composition of each plant. The result showed a significant (P < 0.05) improvement in Packed Cell Volume (PCV) values of rats treated with M. balsamina; A. vera and S. longipenduculata (root bark) when compared with the positive control. Total leukocyte and lymphocyte counts did not change significantly (P > 0.05) in groups treated with M. balsamina and S. longipenduculata (root bark) but increased in other treated and positive control groups. Similarly, no significant changes (P > 0.05) in neutrophils was observed in M. balsamina and S. longipenduculata (root) treated animals but an increase was seen in S. longipenduculata (root bark), A. vera and infected on treated groups. Treatment with M. balsamina, A. vera and S. longipenduculata (root and root bark) prolonged the lives of animals by 4, 1, 3 and 4 days respectively when compared with the positive control. Differences in the composition of various phytochemical of these plants could be responsible for the varied antitrypanosomal activities. Consequently, these plants have great potential which need to be exploited fully in the management of African trypanosomiasis.
Trypanosoma brucei, Wamba strain, produced an acute infection in mice, and mortality was observed 2 days after the onset of parasitaemia which occurred 3-5 days postinfection. Anaemia was observed in the tail blood of the survivors. When washed erythrocytes from the heart blood were incubated in physiological saline containing 1.5% hydrogen peroxide, the erythrocytes of the infected mice produced significantly greater amounts of by-products of lipid peroxidation (measured as thiobarbituric acid reactive substances) than the erythrocytes of the control mice. This observation suggested that the infected mice may have a reduced ability in the prevention of free radical mediated lipid peroxidation in the erythrocyte membrane. It is concluded that peroxidative injury to the erythrocytes may contribute to the pathogenesis of anaemia in trypanosomosis.
Isolates of Trypanosoma brucei and Trypanosoma congolense from the blood of cattle were used to infect growing rats. Despite the use of similar infective doses, T. brucei parasitaemia appeared earlier than T. congolense parasitaemia. After the same period of parasitaemia, the degrees of anaemia, splenomegaly and hepatomegaly were similar in both infections. The percentage decrease in packed cell volume was not correlated with splenic and hepatic weights. Neither infection significantly affected the weight gain of the rats. It was concluded that both organisms caused diseases of comparable severity and that the mere enlargement of the spleen and liver made no significant contribution to the development of the anaemia.
Different stages of Trypanosoma cruzi are seen during mammalian infection. Histologic sections of infected hearts have shown amastigotes and, when using immunohistochemistry (IHC), parasite antigens; however, demonstration of trypomastigotes in these tissues has proven elusive. Using a mouse strain that develops chagasic cardiomyopathy (histologically similar to human infection) 70 days after injecting T. cruzi-Brazil strain, we studied the distribution of parasite stages and the extent of inflammation. All organs had varying amounts of mononuclear inflammation by day 10, which peaked between day 20 and day 30, and decreased by day 50. Amastigotes were detected in myocytes, histiocytes, acinar pancreatic cells, astrocytes and ependymal cells by day 10, and the number of amastigotes peaked on day 30. Immunohistochemistry demonstrated trypomastigotes in sinusoids, vessels and interstitial tissues of several organs between day 15 and 50. Abundant parasite antigens (granular staining) were detected in connective tissues throughout the infection. The burden of amastigotes and trypomastigotes during the acute phase seems to correlate with the degree of inflammation and granular staining in the chronic stage.
Birds from three National Parks (Bwindi Impenetrable, Kibale, and Queen Elizabeth) in western Uganda were surveyed during the dry season in July 2003 and investigated for hematozoa by microscopic examination of stained blood films. Of 307 birds examined, representing 68 species of 15 families and four orders, 61.9% were found to be infected with blood parasites. Species of Haemoproteus (15.3% prevalence), Plasmodium (20.5%), Leucocytozoon (40.1%), Trypanosoma (11.4%), Hepatozoon (2.6%), Atoxoplasma (0.3%), and microfilariae (3.9%) were recorded. Except for Haemoproteus spp. infections, the overall prevalence of hematozoa belonging to all genera was significantly higher in this study than was previously reported in Uganda. Thirty-six species of birds were examined for blood parasites for the first time and 112 new host-parasite associations were identified. Eighty-one were at the generic and 31 at the specific level of the hematozoa. Hepatozoon and Atoxoplasma spp. were detected for the first time in Uganda.
For migratory birds optimal timing of the onset of reproduction is vital, especially when suitable conditions for reproduction occur only for a short while during the year. With increasing latitude the suitable period becomes shorter and we expect the organization of annual cycle to be more synchronized to the local conditions across individuals of same population. This should result in low variation of arrival and departure date in breeding sites at higher latitudes. We quantify the temporal and geographical variation in pre‐ and post‐breeding migration between individuals from four different populations of alpine swifts (Tachymarptis melba) along a latitudinal gradient. We tracked 215 individuals in three years with geolocators. The two western and two eastern populations showed separate migratory flyways and places of residence in Africa. Length of stay at the breeding sites was negatively correlated with latitude and differed by more than a month between populations. Duration of migration was similarly short in all populations (median 6.2 days in autumn and 8.7 days in spring). However, variation in timing of migration was unrelated to latitude and individuals everywhere arrived in the same asynchrony at the breeding site.
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Trypanosomes and leishmanias are widely known parasites of humans. However, they are just two out of several phylogenetic lineages that constitute the family Trypanosomatidae. Although dixeny - the ability to infect two hosts - is a derived trait of vertebrate-infecting parasites, the majority of trypanosomatids are monoxenous. Like their common ancestor, the monoxenous Trypanosomatidae are mostly parasites or commensals of insects. This review covers recent advances in the study of insect trypanosomatids, highlighting their diversity as well as genetic, morphological and biochemical complexity, which, until recently, was underappreciated. The investigation of insect trypanosomatids is providing an important foundation for understanding the origin and evolution of parasitism, including colonization of vertebrates and the appearance of human pathogens.
Parasitic Diseases of Wild Birds provides thorough coverage of major parasite groups affecting wild bird species. Broken into four sections covering protozoa, helminths, leeches, and arthropod parasites, this volume provides reviews of the history, disease, epizootiology, pathology, and population impacts caused by parasitic disease. Taking a unique approach that focuses on the effects of the parasites on the host, Parasitic Diseases of Wild Birds fills a unique niche in animal health literature.
Being airborne is considered to be energetically more costly as compared with being on the ground or in water. Birds migrating or foraging while airborne are thought to spend some time resting on the ground or water to recover from these energetically demanding activities. However, for several decades ornithologists have claimed that some swifts may stay airborne for almost their whole lifetime. Here we present the first unequivocal evidence that an individual bird of the Alpine swift (Tachymarptis melba) can stay airborne for migration, foraging and roosting over a period of more than 6 months. To date, such long-lasting locomotive activities had been reported only for animals living in the sea. Even for an aerodynamically optimized bird, like the Alpine swift, flying requires a considerable amount of energy for continuous locomotive control. Our data imply that all vital physiological processes, including sleep, can be perpetuated during flight.
Summary 1. Parasitism is a non-negligible cost of reproduction in wild organisms, and hosts are selected to partition resources optimally between current and future reproduction. While parents can compensate for the cost of parasitism by increasing their current reproductive investment, such change in resource allocation is expected to carry-over costs on future reproduction. 2. Life history theory predicts that because long-lived organisms have a high residual reproductive value, they should be more reluctant to increase parental effort in response to parasites. Also, when rearing successive infested broods, the cost of parasitism can cumulate over the years and hence be exacerbated by past infestations. 3. We tested these two predictions in the alpine swift Apus melba , a long-lived colonial bird that is infested intensely by the nest-based blood sucking louse-fly Crataerina melbae . For this purpose, we manipulated ectoparasite load over 3 consecutive years and measured reproductive parameters in successive breeding attempts of adults assigned randomly to 'parasitized' and 'deparasitized' treatments. 4. In current reproduction, fathers of experimentally parasitized broods produced a similar number of offspring as fathers from the deparasitized treatment, but the rearing period was prolonged by 4 days. Fathers that were assigned to the parasitized treatment in year x produced significantly fewer fledglings the following year x + 1 than those of the deparasitized treatment. The number of young produced by fathers in year x + 1 was correlated negatively with the number of days they cared for their brood in the previous year x . We also found a significant interaction between treatments performed over 2 successive years, with fathers of parasitized broods suffering a larger fitness loss if in the past they had already cared for a parasitized brood rather than for a deparasitized one. Similar effects of parasitism, although partly non-significant (0·05 < P -values > 0·10), were found in mothers. 5. Altogether, our results show that parasites can modify resource allocation between current and future reproduction in long-lived hosts, and that the cost of parasitism can cumulate over the years. It emphasizes the fact that effects of parasites can depend on past infestations and become apparent in future reproduction only.
Development plasticity is a common evolutionary and phenotypic response to poor growth condition, in particular in organisms with determinate growth such as most birds and mammals. Because various body structures can contribute differently to overall fitness, natural selection will adjust the degree of plasticity of each structure to its proportionate contribution to fitness at a given life stage.
Two non‐mutually exclusive mechanisms can account for plasticity in the growth of offspring to compensate for the effect of parasites. First, if parasite infestation levels fluctuate over the nestling period, parasitized young may show reduced growth until peak parasite infestation, and accelerated growth once the conditions improve (the accelerated growth hypothesis). Secondly, if the period of tissue maturation is not fixed in time, hosts may grow slower than parasite‐free hosts but for a longer period of time (the delayed maturation hypothesis).
To test whether hosts compensate for the effects of parasites on their development, the load of the blood‐sucking louse‐fly Crataerina melbae Rondani in the nests of Alpine swifts, Apus melba Linnaeus, was increased or decreased experimentally. Parasite prevalence was 100% in both treatments, but intensity (no. of parasites per nestling) was significantly lower for deparasitized nestlings. In both treatments, parasite intensity increased up to halfway through the rearing period (i.e. 30 days of age) and decreased afterwards.
In line with the accelerated growth hypothesis, wings of parasitized nestlings grew at a lower rate than those of deparasitized ones before the peak of parasite infestation, but at a greater rate after the peak. Louse‐flies had no significant effect on the growth of body mass. In agreement with the delayed‐maturation hypothesis, wings of parasitized nestlings grew for 3 additional days and were of similar size at fledging as in deparasitized birds.
In summary, the present study shows in a wild bird population that nestling hosts can compensate for the effect of parasitism on their phenotype. It emphasizes the need to take the dynamics of parasite populations into account in studies of host–parasite relationships, and to investigate the effect of parasites on host development over the entire growing period rather than only at fledging, as employed traditionally.
Little is known on the occurrence and magnitude of faster than normal (catch‐up) growth in response to periods of undernutrition in the wild, and the extent to which different body structures compensate and over what timescales is poorly understood.
We investigated catch‐up growth in nestling Alpine Swifts, Apus melba , by comparing nestling growth trajectories in response to a naturally occurring 1‐week period of inclement weather and undernutrition with growth of nestlings reared in a good year.
In response to undernutrition, nestlings exhibited a hierarchy of tissues preservation and compensation, with body mass being restored quickly after the end of the period of undernutrition, acceleration of skeletal growth occurring later in development, and compensation in wing length occurring mostly due to a prolongation of growth and delayed fledging.
The effect of undernutrition and subsequent catch‐up growth was age‐dependent, with older nestlings being more resilient to undernutrition, and in turn having less need to compensate later in the development.
This shows that young in a free‐living bird population can compensate in body mass and body size for a naturally occurring period of undernutrition, and that the timing and extent of compensation varies with age and between body structures.
The present report describes a novel etiological agent of cutaneous leishmaniasis in horses that, at least for some cases, sporadically appeared as autochthonous infections in geographically distant regions of Germany and Switzerland. The infection was initially diagnosed upon clinical and immunohistological findings. Subsequent comparative sequence analysis of diagnostic PCR products from the internal transcribed spacer 1 (ITS1) of ssrRNA classified the respective isolates as neither Old World nor New World Leishmania species. However, four isolates subjected to molecular analyses all exhibited a close phylogenetic relationship to Leishmania sp. siamensis, an organism recently identified in a visceral leishmaniasis patient from Thailand. Future investigations will demonstrate if this form of leishmaniasis represents an emerging, and perhaps zoonotic, disease of European, or even global, importance.
Oxidant stress is an imbalance between radical-generating and radical-scavenging activity, resulting in oxidation products and tissue damage. The present study aimed to estimate oxidation and antioxidant status in blood of camels naturally infected with Trypanosoma evansi. Blood samples from T. evansi-infected and healthy (control) female camels were used to determine the free radical nitric oxide (NO) generation in serum, malondialdehyde production in serum (sMDA) and erythrocyte (eMDA) as a biomarker of lipid peroxidation, blood methemoglobin formation (MetHb, a biomarker of hemoglobin oxidation), the antioxidants serum ascorbate and albumin levels, erythrocytic glutathione concentration (GSH), superoxide dismutase (SOD) and catalase (CAT) activities. The infected camels were characterized by macrocytic hypochromic anemia. Trypanosomiasis in camels resulted in significant (P<0.001) stimulation of serum NO (78.93%), eMDA (110.04%), sMDA (67.39%) and MetHb (1.5-fold) coupled with significant reduction (P<0.001) of albumin (27.6%), ascorbate (25.38%), GSH (43.36%), SOD (32.47%) and non-significant increase in CAT (7.06%, P=0.322) compared to control values. In infected camels, a significant positive correlation of NO with eMDA (r=0.546, P=0.009) and MetHb (r=0.490, P=0.021) was detected. By contrast, NO was inversely correlated with RBC (r=-0.546, P=0.009), PCV (r=-0.427, P=0.048) and Hb (r=-0.612, P=0.002). On the other hand, eMDA was inversely correlated with RBC (r=-0.596, P=0.003), PCV (r=-0.516, P=0.014) and Hb (r=-0.613, P=0.002). In addition, methemoglobinemia was negatively correlated with RBC (r=-0.560, P=0.007), PCV (r=-0.470, P=0.027) and Hb (r=-0.585, P=0.004). Our results suggest that chronic T. evansi infection in camels is associated with a state of oxidative process.
The ability of three species of avian trypanosome, Trypanosoma corvi, T. bouffardi and T. everetti, to protect against heterologous and homologous challenge has been studied in susceptible birds. None protects against challenge with either or both of the other two species and mixed infections can be obtained experimentally. With T. bouffardi, both apparently sterile and premune states exist after initial infection and the host is immune to challenge with homologous strains; heterologous strains sometimes break this immunity and produce shorter, lower parasitaemias. T. everetti remains in the circulating blood for long periods at low levels and challenge doses with the homologous strain result in a slightly elevated parasitaemia for a few days. T. corvi produces a degree of immunity after the initial infection which usually results in a reduced second parasitaemic peak of shorter duration when birds are challenged with a homologous strain.
The fine structure of the bloodstream forms of the avian trypanosome Trypanosoma bouffardi has been studied; it differs in several features from the structure of mammalian trypanosomes in having: an undulating membrane and an intraflagellar contribution to this structure; a highly cristate plate like mitochondrial system with many finger like mitochondrial profiles running longitudinally parallel to and just below the subpellicular microtubules for the whole length of the parasite; a very large number of ribosomes in the cytoplasm and general lack of an extensive detectable reticulum system; ribosomal concentrations in the nuclear pore sites in the nuclear envelope, and the frequent presence of myelin figures in the cytoplasm. Similarities between the mammalian trypanosomes and T. bouffardi include: the presence of a distinct surface coat; the capability of plasmaneme production; the method of flagellar attachment through maculae adherences and the presence of a flagellum associated reticulum; the method of uptake of material by endocytosis through omega spiny coated vesicles in the reservoir and the presence of many cytoplasmic inclusions similar to those found in mammalian species of trypanosome.
Trypanosoma bouffardi Leger & Blanchard, 1911, is described from naturally infected Lagonosticta s. senegala, Estrilda b. bengalus, Vidua chalybeata, Estrilda t. troglodytes and Amadina f. fasciata , all of which are new host records for Nigeria; Vidua chalybeata is a new host record for trypanosomes.
There was no significant morphological difference between populations of this trypanosome in the various natural and experimental vertebrate hosts.
T. bouffardi was transmissible to nine species of Ploceidae belonging to the three subfamilies Estrilinae, Ploceinae and Viduinae; but not to Pycnonotus barbatus , chickens or pigeons.
The parasitaemia produced by infections of T. bouffardi reached 4·1 × 10 ⁵ parasites/mm ³ of blood.
Reproduction of the trypanosomes was synchronous and discontinuous and occurred in the blood by unequal binary fission of trypomastigotes. Occasionally longitudinal equal binary fission of trypomastigotes also took place. There was no concentration of dividing forms in the tissues.
T. bouffardi did not grow on NNN medium although it has been grown for a short time on the medium described by Yesufu (1970).
Experimental infections of canaries with an avian trypanosome, Trypanosoma bouffardi, isolated from West Africa demonstrated that these infections can cause pathological changes in tissues. Enlargement of the spleen coincided with peak parasitaemia but no other gross changes were observed. Histopathological examination of infected and control birds revealed focal myocarditis and lymphoid hyperplasia, in infected birds, which are consistent with trypanosome infection. Avian trypanosome infections are not usually regarded as pathogenic but our results suggest that pathological changes occur which are similar to those observed in mammals infected with salivarian trypanosomes.
Linear measurements and derived indices from striated trypanosomes in nine species of sub-Saharan birds representing seven families of the Passeriformes, were compared. The dimensions of the striated trypomastigotes from the Carduelinae, Estrildidae, Nectarinidae, Passeridae, Pycnonotidae, Turdinae and Zosteropidae were similar to each other as well as to those of the striated trypanosomes from the boreal owl (Strigidae). All these trypanosomes were considered to be Trypanosoma avium Danilewsky, 1885. A further 20 avian species were considered to harbour T. avium, thus greatly extending the reported host range of this trypanosome. Non-striated trypanosomes from the estrildid Uraeginthus angolensis closely resembled Trypanosoma bouffardi Leger & Blanchard, 1911 in appearance and dimensions, and were considered to be of this species. Additional host records for T. bouffardi from an additional nine avian species have been reported. The uniquely small and stumpy Trypanosoma everetti Molyneux, 1973 was reported from an additional 18 avian species. A large non-striated trypanosome from the laughing dove, Streptopelia senegalensis, was identified as Trypanosoma hannae Pittaluga, 1905 and this species was re-described. An infection of this parasite was also found in a single Streptopelia capicola and a single Streptopelia semitorquata. Two trypanosomes seen in the francolin, Francolinus natalensis, were identified as Trypanosoma calmettei Mathis & Léger, 1909.
During acute Trypanosoma vivax infection of calves, produced by intravenous inoculation, the mean packed cell volume and red blood cell counts of the infected animals decreased significantly (P < 0.05) between Days 6 and 13 post-infection (pi). The moderately severe normocytic anaemia started to develop during the first wave of parasitaemia which occurred from Day 2 pi and peaked between Days 4 and 5 pi. The mean erythrocyte glutathione (GSH) concentration of the infected calves decreased significantly (P < 0.05) from 58.4 +/- 11.4 mg 100ml-1 red blood cells (RBC) on Day 0 pi to 44.5 +/- 12.8 mg 100ml-1 RBC on Day 5 pi. As the GSH values recovered on Day 6 pi and increased thereafter, another slight decrease (P > 0.05) in GSH concentration occurred on Day 12 pi at the second peak of parasitaemia followed by a significant (P < 0.05) increase to 79.1 +/- 14.6 mg 100ml-1 RBC on Day 13 pi. In the uninfected calves, the mean GSH values ranged from 47.7 +/- 7.0 to 60.8 +/- 6.8 mg 100ml-1 RBC. When washed, erythrocytes of the infected and uninfected calves were separately challenged with hydrogen peroxide. They produced comparable amounts of thiobarbituric acid reactive substances as a measure of by-products of lipid peroxidation. This suggested that the ability of the erythrocytes to prevent peroxidative injury was not reduced, because GSH regeneration was probably enhanced and the antioxidant capacity of the erythrocytes was maintained.
We looked for louse flies (Diptera, Hippoboscidae) in a mixed colony of 9 species of birds from 1991 to 1997. Alpine swifts (Apus melba) exhibited an unusually high prevalence (85.9%) by Crataerina melbae (Rondani, 1879). No birds from the other 8 breeding bird species were parasitized by this louse fly. We suggest that the number of potential swiftlike hosts as well as the size of hosts may account for the differential prevalence of the louse flies within the colony.
Trypanosome infections in their natural hosts are frequently difficult to detect by microscopy, and culture methods are unreliable and not suitable for all species of Trypanosoma. A nested PCR strategy for detecting and identifying Trypanosoma species, suitable for detecting both known and unknown trypanosomes, is presented. Thirty-two blood samples from 23 species of Australian birds and mammals were screened by a nested PCR for the presence of Trypanosoma sp. ssrRNA. Three infections were detected, one in an eastern grey kangaroo (Macropus giganteus), one in a common wombat (Vombatus ursinus) and one in a platypus (Ornithorhynchus anatinus). The kangaroo and wombat are new host records for Trypanosoma sp.; the platypus parasite was Trypanosoma hinneyi. The three parasites could be distinguished by restriction fragment length polymorphisms of the amplified fragment of the ssrRNA gene. The kangaroo and wombat parasites were also isolated in a semi-solid blood agar medium. The culture forms of the kangaroo trypanosome had an expanded flagellar sheath in which structures similar to hemidesmosomes were detected by EM. The nested PCR was at least as sensitive as culture, and analysis of the PCR products gave parasite-specific fingerprints. Therefore this method could be suitable for rapidly screening host animals for the presence of trypanosomes and identifying the infecting strain.
The course of Trypanosoma congolense infections in African grey duiker (Sylvicapra grimmia) and sheep and goats were studied. Several parameters suggested that the grey duiker was much more resistant to trypanosomosis than sheep and goats. They showed increases in weight during infection, had a much longer pre-patent period, and their peak parasitaemia levels were about 100-fold lower than those of sheep and goats. Parasites were no longer detected in grey duiker blood 35 days after infection. Anaemia, measured as drops in packed cell volume (PCV), haemoglobin (Hb) concentration and erythrocyte (RBC) counts were not observed in the grey duiker. In contrast, sheep and goats suffered severe weight losses and had continuously high parasitaemia levels. Sheep and goats developed progressively severe normocytic normochromic anaemia and leucopenia from day 14 post-infection onwards. Serum levels of total protein, globulin and albumin of grey duiker did not change significantly throughout the course of infection, while the levels of total serum protein, globulin and gamma -globulin exhibited significant increases from day 21 post-infection onwards in sheep and goats, with peak values recorded on 28 and 35 days post-infection in sheep and goats, respectively. There were inconsistent variations in albumin levels in sheep and goats throughout the course of infection. There were no significant changes in erythrocyte activities of AST and ALT, while there were transient but significant elevations of ALP level on day 35, and GGT levels between 14 and 35 days post-infection in grey duiker. Conversely, the levels of all the enzymes were progressively depressed, especially from 14 to 49 days post-infection. In vitro erythrocyte peroxidation remained relatively unchanged throughout the period of the experiment in the grey duiker, except for slight but significant increase on day 42 post-infection.
1. It is shown that Ornithomyia avicularia L. (Diptera, Hippoboscidae) is a vector of Trypanosoma avium in this country.
2. The metacyclic trypanosomes develop in the insect's hind-gut, and infect birds by penetrating the membranes of buccal cavity and/or oesophagus and crop.
3. The opportunity for infection to take place occurs when birds ingest infected insects.
4. The significance of this finding in connexion with other reports of ( a ) vectors of avian trypanosomes, and ( b ) trypanosomes transmitted by hippoboscids, is discussed.
5. Attempts to obtain development of T. avium in a few nymphs of Rhodnius prolixus and one adult Culex molestus , failed. Mites from an infected bird were examined for the presence of flagellates, with negative results.
Leishmania are dimorphic protozoan parasites that live as flagellated forms in the gut of their sandfly vector and as aflagellated forms in their mammalian hosts. Although both parasite forms can infect macrophages and dendritic cells, they elicit distinct responses from mammalian cells. Amastigotes are the parasites forms that persist in the infected host; they infect cells recruited to lesions and disseminate the infection to secondary sites. In this review I discuss studies that have investigated the mechanisms that Leishmania amastigotes employ to harness the host cell's response to infection. It should be acknowledged that our understanding of the mechanisms deployed by Leishmania amastigotes to modulate the host cell's response to infection is still rudimentary. Nonetheless, the results show that amastigote interactions with mammalian cells promote the production of anti-inflammatory cytokines such as IL-10 and TGF-beta while suppressing the production of IL-12, superoxide and nitric oxide. An underlying issue that is considered is how these parasites that reside in sequestered vacuolar compartments target host cell processes in the cytosol or the nucleus; does this occur through the release of parasite molecules from parasitophorous vacuoles or by engaging and sustaining signalling pathways throughout the course of infection?
Jan 1960
H Arn-Willi
Arn-Willi, H., 1960. Biologische studien am Alpensegler, vol. 19. Vogt-Schild.