The ecology of Chytridium deltanum and other fungus parasites on Oocystis spp.

1971 ◽  
Vol 49 (1) ◽  
pp. 75-87 ◽  
Author(s):  
Margaret J. Masters

Consideration of the population curves of Oocystis crassa and O. lacustris in Lake Manitoba during the summers of 1966 and 1967, and July 1968, indicated that the aquatic fungus Chytridium deltanum was able in two instances to attack growing populations of these algae. This strongly suggested that the fungus was a parasite. However, in July 1965, in Cadham Bay, the fungus bloomed as the host population stopped growing and began to decline. Probably the host cells were slightly senescent at that time and thus more susceptible to fungus attack. Consideration of the composition of the fungus population showed that during one epidemic at least, large numbers of zoospores were released every 7 to 9 days. This suggested a nearly synchronous development of the fungus population. It was also observed that zoospores, able to encyst and successfully infect one host, were sometimes unable to attack another potential host present at the same time. In 1966 and 1967 the fungus appeared a few days after the water had reached 25C. Comparison of culture data for the algae and field studies indicated that Chytridium deltanum most commonly grew on the algae at temperatures above the optimum for the algae.

Parasitology ◽  
1988 ◽  
Vol 96 (3) ◽  
pp. 607-639 ◽  
Author(s):  
T. L. Richie

SUMMARYSeveral species of malarial protozoans commonly parasitize the same host population and often the same individual host. This paper reviews the evidence for interactions among such host-sharing parasites. Field studies measuring the cross-sectional prevalence of malarial species often record fewer mixed infections than expected by chance, suggesting that one parasite has excluded another or suppressed its parasitaemia to undetectable levels. Prevalences may vary reciprocally between seasons, with one species increasing in prevalence while another decreases, despite parallel increases in the transmission rates of both, again suggesting suppression of one species by another. However, longitudinal studies of individual hosts indicate that malarial parasites may also favourably affect the host environment for each other, perhaps due to their depressive effect on the immune system: this is shown by the recrudescence of a latent malarial species immediately before or after the parasitic wave of another species. The suppression hypothesis is supported by data derived from the simultaneous inoculation of twoPlasmodiumspecies into laboratory animals; many studies have shown that one or both species are suppressed. This may be mediated by competition for host cells or nutrients, or by heterologous immunity. However, the suppressed species rebounds after the other species has abated, and may show a prolonged infection. Experimental evidence that one species can facilitate the recrudescence of another is minimal, but this may reflect the paucity of investigations of this phenomenon. Laboratory studies show only minor cross-resistance between host-sharing species, which is consistent with the hypothesis that their co-occurrence has led to antigenic divergence or that species showing strong heterologous resistance cannot co-exist in the same host population. Such complementarity occurs not only with the host immune response but also with many other life-history characteristics of host-sharing parasites, such as host cell preference. I conclude that malarial species have been important in each other's evolution, particularly in the tropics where multi-species complexes are common.


2018 ◽  
Vol 115 (48) ◽  
pp. 12277-12282 ◽  
Author(s):  
Batbileg Bor ◽  
Jeffrey S. McLean ◽  
Kevin R. Foster ◽  
Lujia Cen ◽  
Thao T. To ◽  
...  

Around one-quarter of bacterial diversity comprises a single radiation with reduced genomes, known collectively as the Candidate Phyla Radiation. Recently, we coisolated TM7x, an ultrasmall strain of the Candidate Phyla Radiation phylum Saccharibacteria, with its bacterial host Actinomyces odontolyticus strain XH001 from human oral cavity and stably maintained as a coculture. Our current work demonstrates that within the coculture, TM7x cells establish a long-term parasitic association with host cells by infecting only a subset of the population, which stay viable yet exhibit severely inhibited cell division. In contrast, exposure of a naïve A. odontolyticus isolate, XH001n, to TM7x cells leads to high numbers of TM7x cells binding to each host cell, massive host cell death, and a host population crash. However, further passaging reveals that XH001n becomes less susceptible to TM7x over time and enters a long-term stable relationship similar to that of XH001. We show that this reduced susceptibility is driven by rapid host evolution that, in contrast to many forms of phage resistance, offers only partial protection. The result is a stalemate where infected hosts cannot shed their parasites; nevertheless, parasite load is sufficiently low that the host population persists. Finally, we show that TM7x can infect and form stable long-term relationships with other species in a single clade of Actinomyces, displaying a narrow host range. This system serves as a model to understand how parasitic bacteria with reduced genomes such as those of the Candidate Phyla Radiation have persisted with their hosts and ultimately expanded in their diversity.


2010 ◽  
Vol 7 (50) ◽  
pp. 1311-1318 ◽  
Author(s):  
Igor Volkov ◽  
Kim M. Pepin ◽  
James O. Lloyd-Smith ◽  
Jayanth R. Banavar ◽  
Bryan T. Grenfell

The evolution of viruses to escape prevailing host immunity involves selection at multiple integrative scales, from within-host viral and immune kinetics to the host population level. In order to understand how viral immune escape occurs, we develop an analytical framework that links the dynamical nature of immunity and viral variation across these scales. Our epidemiological model incorporates within-host viral evolutionary dynamics for a virus that causes acute infections (e.g. influenza and norovirus) with changes in host immunity in response to genetic changes in the virus population. We use a deterministic description of the within-host replication dynamics of the virus, the pool of susceptible host cells and the host adaptive immune response. We find that viral immune escape is most effective at intermediate values of immune strength. At very low levels of immunity, selection is too weak to drive immune escape in recovered hosts, while very high levels of immunity impose such strong selection that viral subpopulations go extinct before acquiring enough genetic diversity to escape host immunity. This result echoes the predictions of simpler models, but our formulation allows us to dissect the combination of within-host and transmission-level processes that drive immune escape.


The development of vector-transmitted disease models and their application to field studies is reviewed. The key concepts of the basic rate of reproduction and disease transmission threshold are explained, and their application to disease control briefly illustrated. The complications involved in producing appropriate models are discussed for the case of the trypanosomatid parasites Leishmania and Trypanosoma that frequently have more than one vertebrate host and are often fatal in the human host. A two-species, vector-borne disease model allows a quantification of the role of animal reservoirs in maintaining human diseases. Human prevalence may be determined more by the parasitological characteristics of wild reservoir species, about which little is generally known, than by any other single feature of the complex interaction between parasites, vectors and hosts. Domestic animals are often ideal reservoirs, maintaining large numbers of vectors and considerably enlarging the parasite pool. When vector-transmitted diseases are fatal to the human host, human and vector dynamics interact in ways which may cause epidemic cycles, low-level endemic equilibria or disease extinction. For both leishmaniasis and trypanosomiasis it is suggested that a very small number of chronic human cases can maintain the disease in the human population over long periods of time between epidemic outbreaks. They may also be important in the maintenance of geographically distinct foci, characteristic of human trypanosomiasis in Africa. Finally there is a plea to establish a tradition of field observation leading to, and being directed by, mathematical models which in turn are modified as the observations accumulate. All too often, one-way traffic between the two results in slow, or misguided, progress.


2020 ◽  
Author(s):  
Sarah Jane Charles ◽  
Valerie van Mulukom ◽  
Miguel Farias ◽  
Jennifer Brown ◽  
Romara Delmonte ◽  
...  

The ‘brain-opioid theory of social attachment’ (BOTSA) has been proposed as providing the neurobiological underpinnings of social bonding. Endorphins are activated in the brain by a variety of social activities, including social touch, laughter, singing, dancing and feasting. Several of these seem to be involved in the processes of bonding whole communities by allowing large numbers of individuals to be bonded simultaneously. It has been suggested that religious rituals may also be part of this bonding toolkit. We tested this hypothesis in a series of field studies carried out during religious rituals in the UK and Brazil. We found that taking part in the service increased both pain threshold (a standard proxy for endorphin activation) and positive affect, and that between them these enhanced the sense of bonding to the religious group. The results suggest that one of the key functions of religious ritual may be to increase community bonding.


2011 ◽  
Vol 21 (1) ◽  
pp. 97-107 ◽  
Author(s):  
Patricia Gerbarg ◽  
Gretchen Wallace ◽  
Richard Brown

Treatment for the psychological consequences of mass disasters is essential to the recovery of individuals and communities. Little is known about how to provide effective mental health interventions when there are thousands of victims and little, if any, access to care. Post-disaster research and program evaluations suggest that mind-body practices can provide significant relief of anxiety, depression, posttraumatic stress, and physical ailments. Mind-body programs are inexpensive, adaptable to different cultures and conditions, and can be taught rapidly to large numbers of people, including community leaders, to create a sustainable resource for local mental health needs. The challenges of doing research in disaster areas are illustrated using examples from field studies. Potential risks of administering programs to vulnerable populations are discussed, with program design recommendations. The development of safe, effective, trauma-sensitive, culturally appropriate, sustainable programs requires research and collaboration among healthcare professionals, mind-body trainers, researchers, academic institutions, government agencies, and non-governmental humanitarian organizations.


2003 ◽  
Vol 38 (2) ◽  
pp. 300-313 ◽  
Author(s):  
R. E. Webb ◽  
G. B. White ◽  
K. W. Thorpe

Previous observations show that gypsy moth, Lymantria dispar L., mortality induced by the fungus Entomophaga maimaiga Humber, Shimazu & Soper is quickly manifested as host population density increases. However, the gypsy moth nucleopolyhedrovirus (LdMNPV) lags behind the rebounding gypsy moth population. In this study, egg masses were contaminated with virus to successfully augment LdMNPV in gypsy moth populations in Virginia. Laboratory bioassays determined the approximate LdMNPV dose to apply to egg masses with and without the addition of the virus enhancer Blankophor BBH to the spray mixture. The highest dose of virus (5.3 × 105 PIBs/mL) tested without Blankophor BBH gave 82.3% mortality. Mortality for this virus dose increased to 91.8% when 1% Blankophor BBH was added. Field studies established that application of virus at an earlier date (04 April) was as efficacious as an application made at a later date (12 April); this study also included a further assessment of the addition of Blankophor BBH to the spray mixture. While application of LdMNPV + Blankophor BBH resulted in faster kill, levels of kill were similar (88.0% for early treatment and 78.8% for later treatment for virus applied alone versus 87.8% for early treatment and 89.1% for later treatment for virus + Blankophor BBH). However, a higher than expected number of cadavers in the LdMNPV + Blankophor BBH treatments had few or no polyhedral inclusion bodies (PIBs). Finally, virus infection resulting from the application of LdMNPV to pupae in June 1998 was compared with infection levels seen after the application of virus to egg masses in April 1999. The April 1999 treatment to egg masses clearly resulted in a higher kill of emerging larvae (=79.3% mortality) compared to the June 1998 treatment to female pupae (with virus incorporated into the egg masses laid by females after adult emergence) (=13.7% mortality). The virus was recovered season-long from larvae collected from populations in the treated plots (but not from control plots), indicating within season spread.


2010 ◽  
Vol 192 (23) ◽  
pp. 6182-6190 ◽  
Author(s):  
Wesley Loftie-Eaton ◽  
Douglas E. Rawlings

ABSTRACT Plasmids pRAS3.1 and pRAS3.2 are natural variants of the IncQ-2 plasmid family, that except for two differences, have identical plasmid backbones. Plasmid pRAS3.1 has four 22-bp iterons in its oriV region, while pRAS3.2 has only three 6-bp repeats and pRAS3.1 has five 6-bp repeats in the promoter region of the mobB-mobA/repB genes and pRAS3.2 has only four. In previous work, we showed that the overall effect of these differences was that when the plasmid was in an Escherichia coli host, the copy numbers of pRAS3.1 and pRAS3.2 were approximately 41 and 30, respectively. As pRAS3.1 and pRAS3.2 are likely to have arisen from the same ancestor, we addressed the question of whether one of the variants had an evolutionary advantage over the other. By constructing a set of identical plasmids with the number of 22-bp iterons varying from three to seven, it was found that plasmids with four or five iterons displaced plasmids with three iterons even though they had lower copy numbers. Furthermore, the metabolic load that the plasmids placed on E. coli host cells compared with plasmid-free cells increased with copy number from 10.9% at a copy number of 59 to 2.6% at a copy number of 15. Plasmid pRAS3.1 with four 22-bp iterons was able to displace pRAS3.2 with three iterons when both were coresident in the same host. However, the lower-copy-number pRAS3.2 placed 2.8% less of a metabolic burden on an E. coli host population, and therefore, pRAS3.2 has a competitive advantage over pRAS3.1 at the population level, as pRAS3.2-containing cells would be expected to outgrow pRAS3.1-containing cells.


2010 ◽  
Vol 8 (56) ◽  
pp. 377-394 ◽  
Author(s):  
Brian N. Cox

The direction of migration of a cell invading a host population is assumed to be controlled by the magnitude of the strains in the host medium (cells plus extracellular matrix) that arise as the host medium deforms to accommodate the invader. The single assumption that invaders are cued by strains external to themselves is sufficient to generate network structures. The strain induced by a line of invaders is greatest at the extremity of the line and thus the strain field breaks symmetry, stabilizing branch formation. The strain cue also triggers sprouting from existing branches, with no further model assumption. Network characteristics depend primarily on the ratio of the rate of advance of the invaders to the rate of relaxation of the host cells after their initial deformation. Intra-cell mechanisms that govern these two rates control network morphology. The strain field that cues an individual invader is a collective response of the combined cell populations, involving the nearest 100 cells, to order of magnitude, to any invader. The mechanism does not rely on the pre-existence of the entire host medium prior to invasion; the host cells need only maintain a layer several cells thick around each invader. Consistent with recent experiments, networks result only from a strain cue that is based on strain magnitudes. Spatial strain gradients do not break symmetry and therefore cannot stabilize branch formation. The theory recreates most of the geometrical features of the nervous network in the mouse gut when the most influential adjustable parameter takes a value consistent with one inferred from human and mouse amelogenesis. Because of similarity in the guiding local strain fields, strain cues could also be a participating factor in the formation of vascular networks.


Sign in / Sign up

Export Citation Format

Share Document