scholarly journals Three tick species parasitizing a rock python in Sri Lanka

2012 ◽  
Vol 4 (1) ◽  
pp. 54-56
Author(s):  
T.S.P. Fernando ◽  
H.K.A.V.A. Kulasena Fernando

Parasitism is a relationship where one of the parties (the parasite) either harms its host or lives at the expense of it. Host parasite interactions are important driving forces in population dynamics and even extinction. These interactions are also indicators of ecosystem health and they are important in stabilizing food webs. A parasite may cause mechanical injury, stimulate a damaging inflammatory or immune response, or simply rob the host of nutrition. However in the wild most parasites must live in harmony with their hosts. If the parasites kill the host, they themselves would ultimately die without shelter and nutrition. Reptiles become hosts to a number of parasitic organisms ranging from protozoans to arthropods. Among these, ticks (hard and soft) are the most common arthropod group that parasitizes reptiles.

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0165293 ◽  
Author(s):  
Ute Stenkewitz ◽  
Ólafur K. Nielsen ◽  
Karl Skírnisson ◽  
Gunnar Stefánsson

2008 ◽  
Vol 5 (25) ◽  
pp. 919-928 ◽  
Author(s):  
Sabrina Gaba ◽  
Sébastien Gourbière

The life cycle of many endoparasites can be delayed by free-living infective stages and a developmental arrestment in the host referred to as hypobiosis. We investigated the effects of hypobiosis and its interaction with delay in the free-living stages on host–parasite population dynamics by expanding a previous attempt by Dobson & Hudson. When the parasite life cycle does not include free-living stages, hypobiosis destabilizes the host–parasite interactions, irrespective of the assumptions about the regulation of the host population dynamics. Interestingly, the destabilizing effect varies in a nonlinear way with the duration of hypobiosis, the maximal effect being expected for three to five months delay. When the parasite life cycle involves free-living stages, hypobiosis of short or intermediate duration increases the destabilizing effect of the first time delay. However, hypobiosis of a duration of five months or more can stabilize interactions, irrespective of the regulation of the host population dynamics. Overall, we confirmed that hypobiosis is an unusual time delay as it can stabilize a two-way interaction. Contrary to the previous conclusions, such an atypical effect does not require self-regulation of the host population, but instead depends on the existence of free-living stages.


Oikos ◽  
2001 ◽  
Vol 95 (3) ◽  
pp. 431-440 ◽  
Author(s):  
C. D. M. Muller-Graf ◽  
E. Jobet ◽  
A. Cloarec ◽  
C. Rivault ◽  
M. van Baalen ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Yue Yuan ◽  
Jianping Zhao ◽  
Min Chen ◽  
Huifang Liang ◽  
Xin Long ◽  
...  

Schistosomiasis is a parasitic disease endemic to freshwater areas of Southeast Asia, Africa, and South America that is capable of causing serious damage to the internal organs. Recent studies have linked exosomes to the progression of schistosomiasis. These structures are important mediators for intercellular communication, assist cells to exchange proteins, lipids, and genetic material and have been shown to play critical roles during host–parasite interactions. This review aims to discuss the pathophysiology of exosomes in schistosomiasis and their roles in regulating the host immune response. Understanding how exosomes are involved in the pathogenesis of schistosomiasis may provide new perspectives in diagnosing and treating this neglected disease.


2019 ◽  
Author(s):  
Devon Keller ◽  
Devin Kirk ◽  
Pepijn Luijckx

AbstractDespite its pivotal role in evolutionary and ecological processes the genetic architecture underlying host-parasite interactions remains understudied. Here we use a quantitative trait loci approach to identify regions in the Daphnia magna genome that provide resistance against its microsporidium parasite Ordospora colligata. The probability that Daphnia became infected was affected by a single locus and an interaction between two additional loci. A fourth locus influenced the number of spores that grew within the host. Comparing our findings to previously published genetic work on Daphnia magna revealed that two of these loci may be the same as detected for another microsporidium parasite, suggesting a general immune response to this group of pathogens. More importantly, this comparison revealed that two regions previously identified to be under selection coincided with parasite resistance loci, highlighting the pivotal role parasites may play in shaping the host genome.


2012 ◽  
Vol 279 (1741) ◽  
pp. 3234-3240 ◽  
Author(s):  
Alex Best ◽  
Gráinne Long ◽  
Andy White ◽  
Mike Boots

By definition, parasites harm their hosts, but in many infections much of the pathology is driven by the host immune response rather than through direct damage inflicted by parasites. While these immunopathological effects are often well studied and understood mechanistically in individual disease interactions, there remains relatively little understanding of their broader impact on the evolution of parasites and their hosts. Here, we theoretically investigate the implications of immunopathology, broadly defined as additional mortality associated with the host's immune response, on parasite evolution. In particular, we examine how immunopathology acting on different epidemiological traits (namely transmission, virulence and recovery) affects the evolution of disease severity. When immunopathology is costly to parasites, such that it reduces their fitness, for example by decreasing transmission, there is always selection for increased disease severity. However, we highlight a number of host–parasite interactions where the parasite may benefit from immunopathology, and highlight scenarios that may lead to the evolution of slower growing parasites and potentially reduced disease severity. Importantly, we find that conclusions on disease severity are highly dependent on how severity is measured. Finally, we discuss the effect of treatments used to combat disease symptoms caused by immunopathology.


Food Webs ◽  
2016 ◽  
Vol 6 ◽  
pp. 1-8 ◽  
Author(s):  
Thomas G. Jephcott ◽  
Telesphore Sime-Ngando ◽  
Frank H. Gleason ◽  
Deborah J. Macarthur

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Sussie Dalvin ◽  
Christiane Eichner ◽  
Michael Dondrup ◽  
Aina-Cathrine Øvergård

Abstract Background The salmon louse (Lepeophtheirus salmonis) is a parasite of salmonid fish. Atlantic salmon (Salmo salar) exhibit only a limited and ineffective immune response when infested with this parasite. Prostaglandins (PGs) have many biological functions in both invertebrates and vertebrates, one of which is the regulation of immune responses. This has led to the suggestion that prostaglandin E2 (PGE2) is important in the salmon louse host–parasite interaction, although studies of a salmon louse prostaglandin E2 synthase (PGES) 2 gene have not enabled conformation of this hypothesis. The aim of the present study was, therefore, to characterize two additional PGES-like genes. Methods Lepeophtheirus salmonis microsomal glutathione S-transferase 1 like (LsMGST1L) and LsPGES3L were investigated by sequencing, phylogenetics, transcript localization and expression studies. Moreover, the function of these putative PGES genes in addition to the previously identified LsPGES2 gene was analyzed in double stranded (ds) RNA-mediated knockdown (KD) salmon louse. Results Analysis of the three putative LsPGES genes showed a rather constitutive transcript level throughout development from nauplius to the adult stages, and in a range of tissues, with the highest levels in the ovaries or gut. DsRNA-mediated KD of these transcripts did not produce any characteristic changes in phenotype, and KD animals displayed a normal reproductive output. The ability of the parasite to infect or modulate the immune response of the host fish was also not affected by KD. Conclusions Salmon louse prostaglandins may play endogenous roles in the management of reproduction and oxidative stress and may be a product of salmon louse blood digestions. Graphic Abstract


2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
John J. Dennehy

The outcomes of host-parasite interactions depend on the coevolutionary forces acting upon them, but because every host-parasite relation is enmeshed in a web of biotic and abiotic interactions across a heterogeneous landscape, host-parasite coevolution has proven difficult to study. Simple laboratory phage-bacteria microcosms can ameliorate this difficulty by allowing controlled, well-replicated experiments with a limited number of interactors. Genetic, population, and life history data obtained from these studies permit a closer examination of the fundamental correlates of host-parasite coevolution. In this paper, I describe the results of phage-bacteria coevolutionary studies and their implications for the study of host-parasite coevolution. Recent experimental studies have confirmed phage-host coevolutionary dynamics in the laboratory and have shown that coevolution can increase parasite virulence, specialization, adaptation, and diversity. Genetically, coevolution frequently proceeds in a manner best described by the Gene for Gene model, typified by arms race dynamics, but certain contexts can result in Red Queen dynamics according to the Matching Alleles model. Although some features appear to apply only to phage-bacteria systems, other results are broadly generalizable and apply to all instances of antagonistic coevolution. With laboratory host-parasite coevolutionary studies, we can better understand the perplexing array of interactions that characterize organismal diversity in the wild.


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