scholarly journals Infection of theBiomphalaria glabrata vector snailbySchistosoma mansoniparasites drives snail microbiota dysbiosis

2018 ◽  
Author(s):  
Anaïs Portet ◽  
Eve Toulza ◽  
Ana Lokmer ◽  
Camille Huot ◽  
David Duval ◽  
...  
Keyword(s):  
Control Strategies ◽  
Amplicon Sequencing ◽  
Biomphalaria Glabrata ◽  
Individual Level ◽  
Host Parasite Interactions ◽  
Bacterial Microbiota ◽  
Rnaseq Data ◽  
16S Rdna Amplicon Sequencing ◽  
The Individual ◽  
Host Parasite

SummaryHost-associated microbiota cari affect the fitness of its host i η a number of ways, including the modification of host-parasite interactions and thus the outcome of disease.Biomphalaria glabratais the vector snail of the trematodeSchistosoma mansoni,the agent of human schistosomiasis, causing hundreds of thousands of deaths every year. Here, we present the first study of the snail bacterial microbiota in response toSchistosomainfection. To examine the interplay betweenB. glabrata, S. mansoniand snail microbiota, snails were infected and the microbiota composition was analysed by massive 16S rDNA amplicon sequencing approach. We characterized theBiomphalariabacterial microbiota at the individual level in both naive and infected snails. Sympatric and allopatric strains of parasites were used for infections and re­infections to analyse the modification or dysbiosis of snail microbiota in different host-parasite co-evolutionary contexts. Concomitantly, using RNAseq data, we investigated the link between bacterial microbiota dysbiosis and snail anti-microbial peptide immune response. This work paves the way for a better understanding of snail/schistosome interaction, and would have critical consequences in terms of snail control strategies for fighting schistosomiasis disease in the field.

scholarly journals Experimental Infection of the Biomphalaria glabrata Vector Snail by Schistosoma mansoni Parasites Drives Snail Microbiota Dysbiosis

2021 ◽  
Vol 9 (5) ◽  
pp. 1084
Author(s):  
Anaïs Portet ◽  
Eve Toulza ◽  
Ana Lokmer ◽  
Camille Huot ◽  
David Duval ◽  
...  
Keyword(s):  
Schistosoma Mansoni ◽  
Control Strategies ◽  
Amplicon Sequencing ◽  
Biomphalaria Glabrata ◽  
Microbiota Composition ◽  
Microbial Composition ◽  
Bacterial Microbiota ◽  
Individual Scale ◽  
The Individual ◽  
Host Parasite

Host-parasite interaction can result in a strong alteration of the host-associated microbiota. This dysbiosis can affect the fitness of the host; can modify pathogen interaction and the outcome of diseases. Biomphalaria glabrata is the snail intermediate host of the trematode Schistosoma mansoni, the agent of human schistosomiasis, causing hundreds of thousands of deaths every year. Here, we present the first study of the snail bacterial microbiota in response to Schistosoma infection. We examined the interplay between B. glabrata, S. mansoni and host microbiota. Snails were infected and the microbiota composition was analysed by 16S rDNA amplicon sequencing approach. We demonstrated that the microbial composition of water did not affect the microbiota composition. Then, we characterised the Biomphalaria bacterial microbiota at the individual scale in both naive and infected snails. Sympatric and allopatric strains of parasites were used for infections and re-infections to analyse the modification or dysbiosis of snail microbiota in different host-parasite co-evolutionary contexts. Concomitantly, using RNAseq, we investigated the link between bacterial microbiota dysbiosis and snail anti-microbial peptide immune response. This work paves the way for a better understanding of snail/schistosome interaction and should have critical consequences in terms of snail control strategies for fighting schistosomiasis disease in the field.

Evolution and function of tandem repeats in the major surface protein 1a of the ehrlichial pathogenAnaplasma marginale

2001 ◽  
Vol 2 (2) ◽  
pp. 163-174 ◽  
Author(s):  
José de la Fuente ◽  
Jose C. Garcia-Garcia ◽  
Edmour F. Blouin ◽  
Sergio D. Rodríguez ◽  
Migel A. García ◽  
...  
Keyword(s):  
Tandem Repeats ◽  
Control Strategies ◽  
Surface Protein ◽  
Single Copy ◽  
Major Surface Protein ◽  
Host Parasite Interactions ◽  
Major Surface ◽  
And Function ◽  
Host Parasite ◽  
Bovine Erythrocytes

AbstractThe major surface protein (MSP) 1a of the ehrlichial cattle pathogenAnaplasma marginale, encoded by the single-copy genemsp1α, has been shown to have a neutralization-sensitive epitope and to be an adhesin for bovine erythrocytes and tick cells.msp1αhas been found to be a stable genetic marker for the identification of geographic isolates ofA. marginalethroughout development in acutely and persistently infected cattle and in ticks. The molecular weight of MSP1a varies among geographic isolates ofA. marginalebecause of a varying number of tandemly repeated peptides of 28–29 amino acids. Variation in the sequence of the tandem repeats occurs within and among isolates, and may have resulted from evolutionary pressures exerted by ligand–receptor and host–parasite interactions. These repeated sequences include markers for tick transmissibility that may be important in the identification of ehrlichial pathogens because they may influence control strategies and the design of subunit vaccines.

scholarly journals Host age modulates within-host parasite competition

2015 ◽  
Vol 11 (5) ◽  
pp. 20150131 ◽  
Author(s):  
Rony Izhar ◽  
Jarkko Routtu ◽  
Frida Ben-Ami
Keyword(s):  
Evolutionary Dynamics ◽  
Parasite Prevalence ◽  
Host Age ◽  
Individual Level ◽  
Pasteuria Ramosa ◽  
Age Dependent ◽  
The Individual ◽  
Host Parasite ◽  
Parasite Exposure ◽  
Age At Exposure

In many host populations, one of the most striking differences among hosts is their age. While parasite prevalence differences in relation to host age are well known, little is known on how host age impacts ecological and evolutionary dynamics of diseases. Using two clones of the water flea Daphnia magna and two clones of its bacterial parasite Pasteuria ramosa , we examined how host age at exposure influences within-host parasite competition and virulence. We found that multiply-exposed hosts were more susceptible to infection and suffered higher mortality than singly-exposed hosts. Hosts oldest at exposure were least often infected and vice versa. Furthermore, we found that in young multiply-exposed hosts competition was weak, allowing coexistence and transmission of both parasite clones, whereas in older multiply-exposed hosts competitive exclusion was observed. Thus, age-dependent parasite exposure and host demography (age structure) could together play an important role in mediating parasite evolution. At the individual level, our results demonstrate a previously unnoticed interaction of the host's immune system with host age, suggesting that the specificity of immune function changes as hosts mature. Therefore, evolutionary models of parasite virulence might benefit from incorporating age-dependent epidemiological parameters.

scholarly journals Parasite-mediated anorexia increases or decreases virulence evolution, depending on dietary context

2018 ◽  
Author(s):  
J. L. Hite ◽  
C. E. Cressler
Keyword(s):  
Food Intake ◽  
Population Level ◽  
Parasite Development ◽  
Infection Prevalence ◽  
Individual Level ◽  
Physiological Processes ◽  
Gastrointestinal Conditions ◽  
The Individual ◽  
Spread Of Infection ◽  
Host Parasite

AbstractParasite-mediated anorexia is a ubiquitous, but poorly understood component of host-parasite interactions. These temporary but substantial reductions in food intake (range: 4-100%) limit exposure to parasites and alter within-host physiological processes that regulate parasite development, production, and survival, such as energy allocation, immune function, host-microbiota interactions, and gastrointestinal conditions. By altering the duration, severity, and spread of infection, anorexia could substantially alter ecological, evolutionary, and epidemiological dynamics. However, these higher-order implications are typically overlooked and remain poorly understood — even though medical (e.g., non-steroidal anti-inflammatory drugs, vaccines, targeted signaling pathways, calorie restriction) and husbandry practices (e.g., antibiotic and diet use for rapid growth, nutrient supplementation) often directly or indirectly alter host appetite and nutrient intake. Here, we develop theory that helps elucidate why reduced food intake (anorexia) can enhance or diminish disease severity and illustrates that the population-level outcomes often contrast with the individual-level outcomes: treatments that increase the intake of high quality nutrients (suppressing anorexia), can drive rapid individual-level recovery, but inadvertently increase infection prevalence and select for more virulent parasites. Such a theory-guided approach offers a tool to improve targeting host nutrition to manage disease in both human and livestock populations by revealing a means to predict how nutrient-driven feedbacks will affect both the host and parasite.

Horizontal transmission of a parasite is influenced by infected host phenotype and density

Parasitology ◽  
2014 ◽  
Vol 142 (2) ◽  
pp. 395-405 ◽  
Author(s):  
K. E. ROBERTS ◽  
W. O. H. HUGHES
Keyword(s):  
Control Strategies ◽  
Horizontal Transmission ◽  
Population Level ◽  
Pathogen Transmission ◽  
Parasite Transmission ◽  
Microsporidian Parasite ◽  
Female Workers ◽  
Host Parasite Interactions ◽  
The Social ◽  
Host Parasite

SUMMARYTransmission is a key determinant of parasite fitness, and understanding the dynamics of transmission is fundamental to the ecology and evolution of host–parasite interactions. Successful transmission is often reliant on contact between infected individuals and susceptible hosts. The social insects consist of aggregated groups of genetically similar hosts, making them particularly vulnerable to parasite transmission. Here we investigate how the ratio of infected to susceptible individuals impacts parasite transmission, using the honey bee, Apis mellifera and its microsporidian parasite Nosema ceranae. We used 2 types of infected hosts found simultaneously in colonies; sterile female workers and sexual males. We found a higher ratio of infected to susceptible individuals in groups resulted in a greater proportion of susceptibles becoming infected, but this effect was non-linear and interestingly, the ratio also affected the spore production of infected individuals. The transmission level was much greater in an experiment where the infected individuals were drones than in an experiment where they were workers, suggesting drones may act as intracolonial ‘superspreaders’. Understanding the subtleties of transmission and how it is influenced by the phenotype of the infected/susceptible individuals is important for understanding pathogen transmission at population level, and for optimum targeting of parasite control strategies.

Current control strategies for infectious diseases in low-income countries

2018 ◽  
Author(s):  
Fréric Pagè ◽  
Dominique Maison ◽  
Michael Faulde
Keyword(s):  
Infectious Diseases ◽  
Low Income ◽  
Control Strategies ◽  
Current Control ◽  
Low Income Countries ◽  
Years Of Life Lost ◽  
Middle Income ◽  
Climate Conditions ◽  
Individual Level ◽  
The Individual

The burden of communicable diseases is ten times higher in low- and middle-income countries (LMICs) in terms of mortality rate and of years of life lost. Most of the LMCIs are in tropical or subtropical areas with vector-favorable climate conditions and poverty impeding access to improved water supply, sanitation, and efficient health care coverage. Public health strategies to control infectious diseases can be sorted by prevention level. Infectious diseases control strategies often combine actions from different prevention levels according to the stage of a disease. At the individual level, actions and interventions are succeeding in a logical cascade following the stage of the disease as community-level actions are implemented. We present strategies that have been implemented to control infectious diseases, their limits and the needs to attain successful control of infectious diseases in LMICs.

scholarly journals Linking Bioenergetics and Parasite Transmission Models Suggests Mismatch Between Snail Host Density and Production of Human Schistosomes

2019 ◽  
Vol 59 (5) ◽  
pp. 1243-1252 ◽  
Author(s):  
Matthew Malishev ◽  
David J Civitello
Keyword(s):  
Host Density ◽  
Population Level ◽  
Immune Defense ◽  
Parasite Transmission ◽  
Host Snail ◽  
Individual Level ◽  
High Resource ◽  
Parasite Ecology ◽  
The Individual ◽  
Host Parasite

Abstract The consequences of parasite infection for individual hosts depend on key features of host–parasite ecology underpinning parasite growth and immune defense, such as age, sex, resource supply, and environmental stressors. Scaling these features and their underlying mechanisms from the individual host is challenging but necessary, as they shape parasite transmission at the population level. Translating individual-level mechanisms across scales could inherently improve the way we think about feedbacks among parasitism, the mechanisms driving transmission, and the consequences of human impact and disease control efforts. Here, we use individual-based models (IBMs) based on general metabolic theory, Dynamic Energy Budget (DEB) theory, to scale explicit life-history features of individual hosts, such as growth, reproduction, parasite production, and death, to parasite transmission at the population level over a range of resource supplies focusing on the major human parasite, Schistosoma mansoni, and its intermediate host snail, Biomphalaria glabrata. At the individual level, infected hosts produce fewer parasites at lower resources as competition increases. At the population level, our DEB–IBM predicts brief, but intense parasite peaks early during the host growth season when resources are abundant and infected hosts are few. The timing of these peaks challenges the status quo that high densities of infected hosts produce the highest parasite densities. As expected, high resource supply boosts parasite output, but parasite output also peaks at modest to high host background mortality rates, which parallels overcompensation in stage-structured models. Our combined results reveal the crucial role of individual-level physiology in identifying how environmental conditions, time of the year, and key feedbacks within host–parasite ecology interact to define periods of elevated risk. The testable forecasts from this physiologically-explicit epidemiological model can inform disease management to reduce human risk of schistosome infection.

scholarly journals Bacterial Microbiota in Unfed Ticks (Dermacentor nuttalli) From Xinjiang Detected Through 16S rDNA Amplicon Sequencing and Culturomics

Zoonoses ◽  
2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Kai Song ◽  
Yuxin Ji ◽  
Surong Sun ◽  
Xihong Yue ◽  
Cheng Wang ◽  
...  
Keyword(s):  
16S Rdna ◽  
Bacterial Species ◽  
Amplicon Sequencing ◽  
Zoonotic Diseases ◽  
Comprehensive Understanding ◽  
Bacterial Microbiota ◽  
Western Tianshan ◽  
Rdna Sequencing ◽  
16S Rdna Amplicon Sequencing ◽  
Acinetobacter Pittii

Background: Ticks are a major arthropod vector of zoonotic diseases affecting both humans and domestic animals worldwide. Thus, studying tick microbiota would aid in understanding of the potential threats posed by ticks. Methods: Approximately 8,000 unfed ticks, identified as Dermacentor nuttalli, were collected from the sylvosteppe in the western Tianshan mountains. To investigate their potential pathogens, we divided the ticks into 36 groups of 200–300 individuals each for examination with culturomics and 16S rDNA amplicon sequencing. Results: A total of 237 bacterial genera were identified with the two methods. Culturomics identified 46 bacterial species from 23 genera, predominantly Pseudomonas, Pantoea, and Bacillus, whereas 16S rDNA sequencing identified 461 OTUs from 233 genera, predominantly Pseudomonas (53.8%), Coxiella (17.2%), and Pantoea (6.4%). Coxiella, Rickettsia, and ten other genera were discovered only by sequencing, because optimal cultivating conditions were not used for their isolation, whereas Arthrobacter and three other genera were discovered only through culturomics. Conclusions: Several of the identified bacteria, such as line-related sepsis-causing Delftia acidovorans and the pneumonia agent Acinetobacter pittii, can cause human diseases. Thus, both sequencing and culturomics methods are crucial for comprehensive understanding of the microbiota of D. nuttalli.

Dynamics of anti-Borreliaantibodies in Black-legged Kittiwake (Rissa tridactyla) chicks suggest a maternal educational effect

2006 ◽  
Vol 84 (4) ◽  
pp. 623-627 ◽  
Author(s):  
Julien Gasparini ◽  
Karen D. McCoy ◽  
Vincent Staszewski ◽  
Claudy Haussy ◽  
Thierry Boulinier
Keyword(s):  
Maternal Antibodies ◽  
Maternal Transfer ◽  
Rissa Tridactyla ◽  
Host Parasite Interactions ◽  
Borrelia Burgdorferi S.L ◽  
Experimental Approaches ◽  
The Individual ◽  
Evolutionary Consequences ◽  
Host Parasite ◽  
Parasite Challenge

In the presence of parasites, mothers can transfer specific immunoglobulins to their offspring. These antibodies are typically thought to provide protection until the juvenile produces its own immune response, but they may also act to educate the developing immune system so as to prepare the individual for future parasite challenge. We examined this hypothesis in a natural host–parasite system involving the Black-legged Kittiwake ( Rissa tridactyla (L., 1758)), the seabird tick ( Ixodes ( Ceratixodes ) uriae White, 1852), and the Lyme disease bacterium ( Borrelia burgdorferi s.l. (Johnston, 1984)). We compared the dynamics of anti-Borrelia antibodies in chicks between ages 5 and 20 days that received a large amount of maternal anti-Borrelia antibodies to those that did not. The results suggest that the presence of maternal antibodies against Borrelia increases the overall production of anti-Borrelia immunoglobulins by chicks and support the existence of an adaptive maternal effect. Experimental approaches are now called for to better appraise the ecological and evolutionary consequences of the maternal transfer of antibodies in host–parasite interactions.

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