scholarly journals Analysis of Spleen Histopathology, Splenocyte composition and Hematological Parameters in Mice Infected with Plasmodium berghei K173

2021 ◽  
Author(s):  
Huajing Wang ◽  
Shuo Li ◽  
Zhao Cui ◽  
Tingting Qin ◽  
Hang Shi ◽  
...  
Keyword(s):  
Hematological Parameters ◽  
Parasite Burden ◽  
Splenic Macrophages ◽  
Immune Mediated ◽  
Infected Rbcs ◽  
Host Mortality ◽  
Km Mice ◽  
Different Strains ◽  
Host Parasite ◽  
Late Trophozoite

ABSTRACTMalaria is a fatal disease that presents clinically as a continuum of symptoms and severity, which are determined by complex host-parasite interactions. Clearance of infection is believed to be accomplished by the spleen and mononuclear phagocytic system (MPS), both in the presence and absence of artemisinin treatment. The spleen filters infected RBCs from circulation through immune-mediated recognition of the infected RBCs followed by phagocytosis. Using different strains of mice infected with P. berghei K173 (PbK173), the mechanisms leading to splenomegaly, histopathology, splenocyte activation and proliferation, and their relationship to control of parasitemia and host mortality were examined. Survival time of mice infected with PbK173 varied, although the infection was uniformly lethal. Mice of the C57BL/6 strain were the most resistant, while mice of the strain ICR were the most susceptible. BALB/c and KM mice were intermediate. In the course of PbK173 infection, both strains of mice experienced significant splenomegaly. Parasites were observed in the red pulp at 3 days post infection in all animals. All spleens retained late trophozoite stages as well as a fraction of earlier ring-stage parasites. The percentages of macrophages in infected C57BL/6 and KM mice were higher than uninfected mice on 8 dpi. Spleens of infected ICR and KM mice exhibited structural disorganization and remodeling. Furthermore, parasitemia was significantly higher in KM versus C57BL/6 mice at 8 dpi. The percentages of macrophages in ICR infected mice were lower than uninfected mice, and the parasitemia was higher than other strains. The results presented here demonstrate the rate of splenic mechanical filtration and the splenic macrophages likely contribute to an individual’s total parasite burden. This in turn can influence the pathogenesis of malaria. Finally, different genetic backgrounds of mice have different splenic mechanisms for controlling malaria infection.

scholarly journals Analysis of spleen histopathology, splenocyte composition and haematological parameters in four strains of mice infected with Plasmodium berghei K173

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Huajing Wang ◽  
Shuo Li ◽  
Zhao Cui ◽  
Tingting Qin ◽  
Hang Shi ◽  
...  
Keyword(s):  
Plasmodium Berghei ◽  
Parasite Burden ◽  
Splenic Macrophages ◽  
Immune Mediated ◽  
Infected Rbcs ◽  
Host Mortality ◽  
Km Mice ◽  
Different Strains ◽  
Host Parasite

Abstract Background Malaria is a fatal disease that presents clinically as a continuum of symptoms and severity, which are determined by complex host-parasite interactions. Clearance of infection is believed to be accomplished by the spleen and mononuclear phagocytic system (MPS), independent of artemisinin treatment. The spleen filters infected red blood cells (RBCs) from circulation through immune-mediated recognition of the infected RBCs followed by phagocytosis. This study evaluated the tolerance of four different strains of mice to Plasmodium berghei strain K173 (P. berghei K173), and the differences in the role of the spleen in controlling P. berghei K173 infection. Methods Using different strains of mice (C57BL/6, BALB/C, ICR, and KM mice) infected with P. berghei K173, the mechanisms leading to splenomegaly, histopathology, splenocyte activation and proliferation, and their relationship to the control of parasitaemia and host mortality were examined and evaluated. Results Survival time of mice infected with P. berghei K173 varied, although the infection was uniformly lethal. Mice of the C57BL/6 strain were the most resistant, while mice of the strain ICR were the most susceptible. BALB/c and KM mice were intermediate. In the course of P. berghei K173 infection, all infected mice experienced significant splenomegaly. Parasites were observed in the red pulp at 3 days post infection (dpi) in all animals. All spleens retained late trophozoite stages as well as a fraction of earlier ring-stage parasites. The percentages of macrophages in infected C57BL/6 and KM mice were higher than uninfected mice on 8 dpi. Spleens of infected ICR and KM mice exhibited structural disorganization and remodelling. Furthermore, parasitaemia was significantly higher in KM versus C57BL/6 mice at 8 dpi. The percentages of macrophages in ICR infected mice were lower than uninfected mice, and the parasitaemia was higher than other strains. Conclusions The results presented here demonstrate the rate of splenic mechanical filtration and that splenic macrophages are the predominant roles in controlling an individual’s total parasite burden. This can influence the pathogenesis of malaria. Finally, different genetic backgrounds of mice have different splenic mechanisms for controlling malaria infection.

The regulation of host population growth by parasitic species

Parasitology ◽  
1978 ◽  
Vol 76 (2) ◽  
pp. 119-157 ◽  
Author(s):  
R. M. Anderson
Keyword(s):  
Population Growth ◽  
Reproductive Potential ◽  
Parasite Burden ◽  
Host Population ◽  
Parasitic Species ◽  
Regulatory Influence ◽  
Host Mortality ◽  
Parasite Reproduction ◽  
Over Dispersion ◽  
Host Parasite

SummaryThe nature of parasitism at the population level is defined in terms of the parasite's influence on the natural intrinsic growth rate of its host population. It is suggested that the influence on this rate is related to the average parasite burden/host and hence to the statistical distribution of parasites within the host population.Theoretical models of host–parasite associations are used to assess the regulatory influence of parasitic species on host population growth. Model predictions suggest that three specific groups of population processes are of particular importance: over-dispersion of parasite numbers/host, density dependence in parasite mortality or reproduction and parasite-induced host mortality that increases faster than linearly with the parasite burden. Other population mechanisms are shown to have a destabilizing influence, namely: parasite-induced reduction in host reproductive potential, direct parasite reproduction within the host and time delays in the development of transmission stages of the parasite.These regulatory and destabilizing processes are shown to be commonly observed features of natural host-parasite associations. It is argued that interactions in the real world are characterized by a degree of tension between these regulatory and destabilizing forces and that population rate parameter values in parasite life-cycles are very far from being a haphazard selection of all numerically possible values. It is suggested that evolutionary pressures in observed associations will tend to counteract a strong destabilizing force by an equally strong regulatory influence. Empirical evidence is shown to support this suggestion in, for example, associations between larval digeneans and molluscan hosts (parasite-induced reduction in host reproductive potential counteracted by tight density-dependent constraints on parasite population growth), and interactions between protozoan parasites and mammalian hosts (direct parasite reproduction counteracted by a well-developed immunological response by the host).The type of laboratory and field data required to improve our understanding of the dynamical properties of host–parasite population associations is discussed and it is suggested that quantitative measurement of rates of parasite-induced host mortality, degrees of over-dispersion, transmission rates and reproductive and mortality rates of both host and parasite would provide an important first step. The value of laboratory work in this area is demonstrated by reference to studies which highlight the regulatory influence of parasitic species on host population growth.

The influence of Hymenolepis diminuta on the survival and fecundity of the intermediate host, Tribolium confusum

Parasitology ◽  
1980 ◽  
Vol 81 (2) ◽  
pp. 405-421 ◽  
Author(s):  
Anne E. Keymer
Keyword(s):  
Experimental Study ◽  
Intermediate Host ◽  
Parasite Burden ◽  
Tribolium Confusum ◽  
Hymenolepis Diminuta ◽  
Density Dependent ◽  
Host Mortality ◽  
Host Parasite ◽  
The Relationship ◽  
High Parasite

SUMMARYAn experimental study of the effects of parasitism by H. diminuta on the intermediate host, Tribolium confusum, is described. No density- dependent constraints on parasite establishment within individual hosts are evident, although a reduction in cysticercoid size at high parasite burdens is demonstrated. The relationship between parasite burden, host mortality and host fecundity is investigated. Host mortality is linearly related to parasite burden, whereas the relationship between parasite burden and host fecundity is non-linear. There is no difference in viability between eggs from infected and uninfected females. The generative causes of these effects are not investigated experimentally, although it is postulated that survival is related to the degree of damage to the midgut wall caused by parasite penetration, and fecundity to the biomass of parasites harboured by the host. The significance of these effects is discussed in relation to the overall dynamics of the host-parasite association.

Susceptibilities of Various Snail Intermediate Hosts of Schistosoma mansoni to Different Strains of the Parasite

1965 ◽  
Vol 39 (4) ◽  
pp. 363-376 ◽  
Author(s):  
M.F.A. Saoud
Keyword(s):  
Puerto Rico ◽  
Schistosoma Mansoni ◽  
Intermediate Hosts ◽  
Considerable Evidence ◽  
The Past ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Different Strains ◽  
Host Parasite ◽  
Comprehensive Studies

In the past two decades, considerable evidence has accumulated in the literature about the differences in the susceptibility of various intermediate hosts of Schistosoma mansoni to different strains of the parasite. Comprehensive studies on this aspect of host-parasite relationship have been published by Files & Cram (1949), Abdel-Malek (1950) and Files (1951). The results of more recent studies have been reported by Wright (1962) and Saoud (1964).In the present paper, the writer has studied the susceptibility of four intermediate hosts of S. mansoni from Brazil, Puerto Rico, Egypt and Tanganyika to some strains of the parasite.

The use of frequency distributions in an attempt to detect host mortality induced by infections of diplostomatid metacercariae

Parasitology ◽  
1984 ◽  
Vol 89 (2) ◽  
pp. 209-220 ◽  
Author(s):  
C. R. Kennedy
Keyword(s):  
Small Sample Size ◽  
Parasite Burden ◽  
Fish Host ◽  
Small Sample ◽  
Host Age ◽  
Parasite Abundance ◽  
Frequency Distributions ◽  
Host Mortality ◽  
The Mean ◽  
Over Dispersion

SummaryFollowing recent suggestions that a peaked host age–parasite abundance curve, concomitant with a decline in the degree of dispersion of parasites in the older age classes of hosts, can provide evidence of parasite-induced host mortality, the changes in mean abundance and over-dispersion of metacercarial stages of Diplostomum spathaceum, D. gasterostei, Tylodelphys clavata and T. podicipina in relation to fish age were studied in a field locality. The mean parasite burden of D. spathaceum, D. gasterostei and T. clavata increased with host age and the maximum mean burden was found in the oldest hosts. The variance to mean ratio also increased in D. gasterostei, but decreased in the oldest hosts in D. spathaceum and T. clavata. It is concluded that this decrease could be due to parasite-induced host mortality but could equally be due to death of parasites within the host or to changes in infection rate or could be a reflection of the small sample size of the oldest fish. The mean burden of T. podicipina declined gradually with host age, but the variance to mean ratio remained constant and it is concluded that this could be explained by death of the parasites within the host. None of these data or data from other localities provided clear and unambiguous evidence of host mortality induced by heavy infections of any of the four species, although they are consistent with such mortality and do not refute such a possibility. It is concluded that it may be just as difficult to detect and unequivocally demonstrate parasite-induced host mortality in metacercarial digenean–fish host systems as in any other parasite–host systems.

scholarly journals Disentangling non-specific and specific transgenerational immune priming components in host–parasite interactions

2020 ◽  
Vol 287 (1920) ◽  
pp. 20192386
Author(s):  
Frida Ben-Ami ◽  
Christian Orlic ◽  
Roland R. Regoes
Keyword(s):  
Genetic Epidemiology ◽  
Ecological Systems ◽  
High Dose ◽  
Immune Priming ◽  
Specific Effects ◽  
Host Parasite Interactions ◽  
Pasteuria Ramosa ◽  
Different Strains ◽  
Host Parasite ◽  
First Time

Exposure to a pathogen primes many organisms to respond faster or more efficiently to subsequent exposures. Such priming can be non-specific or specific, and has been found to extend across generations. Disentangling and quantifying specific and non-specific effects is essential for understanding the genetic epidemiology of a system. By combining a large infection experiment and mathematical modelling, we disentangle different transgenerational effects in the crustacean model Daphnia magna exposed to different strains of the bacterial parasite Pasteuria ramosa . In the experiment, we exposed hosts to a high dose of one of three parasite strains, and subsequently challenged their offspring with multiple doses of the same (homologous) or a different (heterologous) strain. We find that exposure of Daphnia to Pasteuria decreases the susceptibility of their offspring by approximately 50%. This transgenerational protection is not larger for homologous than for heterologous parasite challenges. Methodologically, our work represents an important contribution not only to the analysis of immune priming in ecological systems but also to the experimental assessment of vaccines. We present, for the first time, an inference framework to investigate specific and non-specific effects of immune priming on the susceptibility distribution of hosts—effects that are central to understanding immunity and the effect of vaccines.

High levels of genetic diversity inNosema ceranaewithinApis melliferacolonies

Parasitology ◽  
2013 ◽  
Vol 141 (4) ◽  
pp. 475-481 ◽  
Author(s):  
TAMARA GÓMEZ-MORACHO ◽  
XULIO MASIDE ◽  
RAQUEL MARTÍN-HERNÁNDEZ ◽  
MARIANO HIGES ◽  
CAROLINA BARTOLOMÉ
Keyword(s):  
Genetic Recombination ◽  
Population Expansion ◽  
Single Copy ◽  
Recent Population Expansion ◽  
Colony Losses ◽  
Bee Colony ◽  
Host Parasite Interactions ◽  
Recent Origin ◽  
Different Strains ◽  
Host Parasite

SUMMARYNosema ceranaeis a widespread honeybee parasite, considered to be one of the pathogens involved in the colony losses phenomenon. To date, little is known about its intraspecific genetic variability. The few studies onN. ceranaevariation have focused on the subunits of ribosomal DNA, which are not ideal for this purpose and have limited resolution. Here we characterized three single copy loci (Actin, Hsp70andRPB1) in threeN. ceranaeisolates from Hungary and Hawaii. Our results provide evidence of unexpectedly high levels of intraspecific polymorphism, the coexistence of a wide variety of haplotypes within each bee colony, and the occurrence of genetic recombination inRPB1. Most haplotypes are not shared across isolates and derive from a few frequent haplotypes by a reduced number of singletons (mutations that appear usually just once in the sample), which suggest that they have a fairly recent origin. Overall, our data indicate that this pathogen has experienced a recent population expansion. The presence of multiple haplotypes within individual isolates could be explained by the existence of different strains ofN. ceranaeinfecting honeybee colonies in the field which complicates, and must not be overlooked, further analysis of host–parasite interactions.

Tissue Uptake of Circulating Thrombopoietin Is Increased in Immune-Mediated Compared With Irradiated Thrombocytopenic Mice

Blood ◽  
1999 ◽  
Vol 93 (8) ◽  
pp. 2515-2524 ◽  
Author(s):  
Mei Chang ◽  
John X. Qian ◽  
Sun min Lee ◽  
John Joubran ◽  
George Fernandez ◽  
...  
Keyword(s):  
Degradation Products ◽  
Inverse Correlation ◽  
Electron Microscopic ◽  
Significant Inverse Correlation ◽  
Thrombocytopenic Purpura ◽  
Tissue Samples ◽  
Electron Microscopic Autoradiography ◽  
Splenic Macrophages ◽  
Immune Mediated ◽  
Total Capacity

Abstract We have previously demonstrated a significant inverse correlation between circulating thrombopoietin (TPO) levels and peripheral platelet (PLT) counts in patients with thrombocytopenia secondary to megakaryocytic hypoplasia but not in patients with immune thrombocytopenic purpura (ITP; Chang et al, Blood 88:3354, 1996). To test the hypothesis that the differences in the circulating TPO levels in these two types of thrombocytopenia are caused by differences in the total capacity of Mpl receptor-mediated TPO clearance, thrombocytopenia was induced in female CD-1 mice either by sublethal irradiation (irradiated) or rabbit antimouse PLT serum (RAMPS) for 1 day (1 d RAMPS) and 5 days (5 d RAMPS). A well-characterized murine model of autoimmune thrombocytopenic purpura, male (NZW × BXSB) F1 mice (W/B F1), was also included in this study. All thrombocytopenic mice and their controls received trace amounts of 125I-recombinant murine TPO (125I-rmTPO) intravenously and were killed 3 hours postinjection. Blood cell-associated radioactivity was significantly decreased in all 4 groups of thrombocytopenic mice. Significantly increased plasma and decreased whole spleen-associated radioactivity was observed in the irradiated group compared with controls (P < .05). While a lesser but still significant increase in plasma and decrease in whole spleen-associated radioactivity was observed in the 1 d RAMPS mice (P < .05), there were no significant differences between the 5 d RAMPS nor the W/B F1 male mice compared with controls, although whole spleen-associated radioactivity was higher in the W/B F1male. A significant inverse correlation of plasma and whole spleen-associated radioactivity was demonstrated in W/B F1male mice (r = −.91, n = 6, P < .05). There was also a decrease in bone (femur)/blood-associated radioactivity in the irradiated group compared with controls (P < .05), but a significant increase in 1 d and 5 d RAMPS mice (P < .01). Furthermore, the 125I-rmTPO uptake capacity within the spleen and marrow of immune thrombocytopenic mice appeared to be associated with a higher megakaryocytic mass when tissue samples were examined by light microscopy. Internalization of 125I-rmTPO by megakaryocytes and PLTs in the spleens and marrows of ITP mice was also demonstrated directly using electron microscopic autoradiography. Labeled PLTs were also found within splenic macrophages. Additionally, the mean PLT volumes of RAMPS mice were significantly higher than those of the control and irradiated mice (P < .05), as was the bound 125I-rmTPO (cpm) per million PLT (P < .05). Finally, significantly decreased 125I-rmTPO degradation products were only found in the plasma of the irradiated mice compared with control animals (P < .05). These data suggest that the lack of Mpl+ cells in the mice with thrombocytopenia secondary to megakaryocytic hypoplasia (irradiated) results in decreased uptake and degradation of TPO and higher circulating TPO levels. Furthermore, these data also suggest that, after a brief TPO surge in response to immune thrombocytopenia (1 d RAMPS), the lack of an inverse correlation of circulating TPO with PLT counts during steady-state immune thrombocytopenic mice (5 d RAMPS + W/B F1 male) is due, at least in part, to its uptake and degradation by the high PLT turnover and increased mass of megakaryocytes.

Hyperparasitism, a Mutualistic Phenomenon

1963 ◽  
Vol 95 (7) ◽  
pp. 716-720 ◽  
Author(s):  
S. E. Flanders
Keyword(s):  
Mortality Factor ◽  
Phytophagous Insect ◽  
Primary Parasite ◽  
Host Mortality ◽  
Continuous Reproduction ◽  
Host Parasite

AbstractHyperparasitism is a mortality factor that generally is beneficial to the continuous reproduction of the species involved.The parasites of a primary parasite of a phytophagous insect may exhibit two distinctive types of secondary relations to that insect. These types are defined as follows:Direct secondary parasitism: that type of host-parasite symbiosis where only the primary's parasitized host or the primary itself is attacked.Indirect secondary parasitism: that type of host-parasite symbiosis where the primary's phytophagous host is attacked whether parasitized or not parasitized.The host mortality caused by direct secondary parasitism may greatly exceed that caused by indirect secondary parasitism, this being manifested when the percentage of the primary parasitization of the phytophagous host is minimal.

The population dynamics of Gyrodactylus bullatarudis (Monogenea) within laboratory populations of the fish host Poecilia reticulata

Parasitology ◽  
1984 ◽  
Vol 89 (1) ◽  
pp. 159-194 ◽  
Author(s):  
Marilyn E. Scott ◽  
R. M. Anderson
Keyword(s):  
Poecilia Reticulata ◽  
Acquired Resistance ◽  
Parasite Burden ◽  
Fish Host ◽  
Time Interval ◽  
Helminth Parasites ◽  
Short Period ◽  
Laboratory Populations ◽  
Host Mortality ◽  
Transmission Stage

SummaryExperiments were undertaken to investigate the factors which influence the transmission dynamics of Gyrodactylus bullatarudis within populations of laboratory guppies. The parasites possess a number of biological attributes which are almost unique amongst helminth parasites of vertebrates. These include the ability to reproduce viviparously and directly on the surface of the host, the ability to survive death of the host (for a short period of time) and the ability to transfer between hosts (despite the absence of a specialized transmission stage in the parasite's life-cycle). Long-term laboratory experiments demonstrated the inability of the parasite to persist within populations of the host in the absence of the continual introduction of naive susceptible fish. With regular addition of susceptible fish, the parasite population exhibited recurrent epidemic behaviour. The magnitudes of the epidemics and the time interval between them, were dependent on the rate at which fish were added to the populations. The parasite was over-dispersed in its distribution within the experimental fish populations and was a significant cause of host mortality (in a manner related to parasite burden). The experimental results suggest that acquired resistance to infection is an important factor determining epidemic behaviour.

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