"Responses of a bacterial pathogen to phosphorus limitation of its aquatic invertebrate host'.
Stoichiometric conditions of the food, whether living or not, are known to have strong effects on the organism doing the consuming. Nutrient quality has the potential to drive patterns in enemy fitness as well as to reciprocally affect the tolerance of the host or prey. Three main response variables were analyzed during the source of this experiment, whereby invertebrate Daphnia magna hosts were fed on specific nutrient-levels of food and dosed with a set number of spores of the highly effective microparasite Pasteuria ramosa. The theoretical queries at the base of this experiment are whether nutrient poor conditions will limit the pathogen as well as the host, or whether under nutrient poor conditions, the pathogen will become preferentially more efficient at utilizing the limited nutrients, thus having a higher virulence on its host.
The infection rate of the bacterial pathogen was assessed by manipulating the nutrient conditions of the food for Daphnia during the infection period, but thereafter maintaining constant nutrient conditions across all treatments, in order to assess only the ability of the pathogen to infect. A linear relationship between phosphorous content of host food and infection rate was observed, with a higher degree of infection for high phosphorus conditions. Based on previous work the authors believe this result if most likely due to reduced growth of the bascterial spores within the host under low phosphorus conditions rather than due to reduced feeding habits or contact rates.
In contrast to the methodology used to assess infection rate, spore production of the pathogen was measured by maintaining constant nutrient conditions of the food during the infection period, but thereafter altering the food content by treatment. In general more spores were found in hosts fed on phosphorus rich foods, though the relationship was non-linear. This pattern seems to be largely driven by the reduced size of the host fed on nutrient poor foods, however the density of spores within the host was non-constant across treatments. this may be interesting for future work as it could help determine if the pattern of reduced spore counts is in fact fully linked with reduced host size. An interaction may exist whereby larger hosts may still contain a proportionately larger number of pathogens in nutrient rich conditions. An experiment with a higher number of treatments, or hosts that are measured for spore containment more often during the potential growth period, could reduce the irregularities within the results and indicate a more concrete relationship between pathogen density and nutrient conditions in this study system.
The final portion of this study hoped to look at the question of nutrient effects on host reproduction. The difference in reproduction at all nutrient conditions was assessed for both infected and uninfected individuals. not surprisingly, infection reduced host production, period. However, this decrease was more dramatic in hosts fed on a low phosphorus diet, indicating that the virulence effects of the pathogen on its host was in fact higher under nutrient-stressed conditions.
Friday, November 18, 2011
Pradeep Ram, A.S. & Sime-Ngando, T. Environmental Microbiology. (2010).
"Resources drive trade-off between viral lifestyles in the planton: evidence from freshwater microbial microcosms"
Reviewed: 11/18/11
The two possible lifestyles of viruses living in aquatic systems has often been considered as a trade-off. Each lifestyle presenting its benefits and costs under certain environmental conditions, and both lifestyles having persisted across evolutionary time because of this very antagonism in the trade-off. The investigators of this paper chose to look at nutrient conditions might be responsible for the conversion of a lytic cycle pathogen into its lysogenic state. They tested the hypothesis that the addition of organic and inorganic nutrients decreases the presence of the lysogenic lifestyle overall. The experiment was conducted in a laboratory setting on samples collected from a freshwater lake in France.
Mytomycin C is an antibiotic that crosslinks DNA and can initiate a repair pathway within cells. It was this chemical that was used to induce prophages to leave the lysogenic stage. This is a common experimental technique used to determine proportion lysogenic stage (based on difference from lytic). More evidence needs to be collected on its accuracy, but overall it seemed to be a better estimating method than the TEM-based counts used as the alternative by the researchers.
Viral abundance increased under conditions where its host was fed on high nutrient based foods. This result was particularly true for inorganic, as well as organic, carbon additions. This increase however, seemed more closely linked to the benefit that the nutrient additions provided to host growth rates and abundance. researchers also measured the burst size, or internal reproduction of the virus within their hosts. The magnitude of this response was again linked to increased carbon conditions.
A ratio of lytic to lysogenic frequencies showed that a higher proportion of lysogens were found in ambient nutrient conditions, as well as for samples that had been experimentally manipulated to contain reduced viral to host ratios. The authors propose that more lysogens can be found in virus-reduced samples because the direct competition between hosts increases, creating poorer host conditions for a potentially lytic-stage virus. This finding was also proposed to be a result of lower contact frequency between host and pathogen stimulating a waiting-type lifestyle (lysogeny), until higher contact rates could be achieved.
Analysis of the Pearson product-moment correlation coefficients shows a very clear antagonism between the frequency of lytic viruses and that of lysogenic ones. This supports the idea that these two lifestyles do in fact represent a distinct trade-off in life-history metrics. The other key result from this experiment, as prevously stated, showed that nutrient additions beyond the ambient increased the proportion of lytic-lifestyle viruses largely as a result of increased bacterial population numbers. However, the study did not demonstrate that decreasing the nutrient conditions within the samples could lead to higher counts of lysogeny. This could be achieved in the future by placing the host species into a broader range of nutrient conditions by chemically manipulating the waters found naturally in the freshwater lake used in this study.
Reviewed: 11/18/11
The two possible lifestyles of viruses living in aquatic systems has often been considered as a trade-off. Each lifestyle presenting its benefits and costs under certain environmental conditions, and both lifestyles having persisted across evolutionary time because of this very antagonism in the trade-off. The investigators of this paper chose to look at nutrient conditions might be responsible for the conversion of a lytic cycle pathogen into its lysogenic state. They tested the hypothesis that the addition of organic and inorganic nutrients decreases the presence of the lysogenic lifestyle overall. The experiment was conducted in a laboratory setting on samples collected from a freshwater lake in France.
Mytomycin C is an antibiotic that crosslinks DNA and can initiate a repair pathway within cells. It was this chemical that was used to induce prophages to leave the lysogenic stage. This is a common experimental technique used to determine proportion lysogenic stage (based on difference from lytic). More evidence needs to be collected on its accuracy, but overall it seemed to be a better estimating method than the TEM-based counts used as the alternative by the researchers.
Viral abundance increased under conditions where its host was fed on high nutrient based foods. This result was particularly true for inorganic, as well as organic, carbon additions. This increase however, seemed more closely linked to the benefit that the nutrient additions provided to host growth rates and abundance. researchers also measured the burst size, or internal reproduction of the virus within their hosts. The magnitude of this response was again linked to increased carbon conditions.
A ratio of lytic to lysogenic frequencies showed that a higher proportion of lysogens were found in ambient nutrient conditions, as well as for samples that had been experimentally manipulated to contain reduced viral to host ratios. The authors propose that more lysogens can be found in virus-reduced samples because the direct competition between hosts increases, creating poorer host conditions for a potentially lytic-stage virus. This finding was also proposed to be a result of lower contact frequency between host and pathogen stimulating a waiting-type lifestyle (lysogeny), until higher contact rates could be achieved.
Analysis of the Pearson product-moment correlation coefficients shows a very clear antagonism between the frequency of lytic viruses and that of lysogenic ones. This supports the idea that these two lifestyles do in fact represent a distinct trade-off in life-history metrics. The other key result from this experiment, as prevously stated, showed that nutrient additions beyond the ambient increased the proportion of lytic-lifestyle viruses largely as a result of increased bacterial population numbers. However, the study did not demonstrate that decreasing the nutrient conditions within the samples could lead to higher counts of lysogeny. This could be achieved in the future by placing the host species into a broader range of nutrient conditions by chemically manipulating the waters found naturally in the freshwater lake used in this study.
Thursday, November 10, 2011
Faruque, S. M. et al. PNAS. (2005).
"Seasonal epidemics of cholera inversely correlate with the prevalence of environmental cholera phages".
Reviewed: 11/10/11
Cholera epidemics in and around Dhaka, Bangladesh occur seasonally, typically twice a year. Cholera is a human disease that is caused by pathogenic strains of Vibrio cholerae, however the bacteria is a normal component of aquatic ecosystems. Aquatic transmission of the disease-causing bacteria was first noted approximately one hundred and fifty years ago and while many environmental and biological parameters have been associated with the temporally varying disease surges, none have been conclusively linked to the cause or finish of the epidemic (other than the obvious requirement of water). Bacteriophages have been shown to be linked to transmission of toxigenicity in V. cholerae. Data obtained from plaque assays, bacterial cultures, and stool samples randomly obtained from local hospitals were used to demonstrate that the abundance of cholera-inducing bacterial strains was inversely correlated with increases in their own pathogens' numbers.
If the presence of a host-specific bacteriophage was noted within any given water sample collected from local aquatic systems, than its target host was significantly less likely to be found. The percentage of co-occurrences of virus and target host was lower than one that could have been predicted by chance alone.
Cross comparison of monthly collection and analysis for phages in water samples with stool samples showing cholera disease in humans did in fact show an oscillating relationship between the bacteria strains and their viruses. Two strains of bacteria are primarily responsible for the disease in Bangladesh, and six phage types, which can actually be grouped into 4 genetically distinct groups, are associated with them. However, the life modes of these viral types are not all homogenous. The authors propose that the difference between lytic and lysogenic capable phages may be driving a lot of the seasonality of the cholera epidemics.
The model they present begins with epidemics arising during periods of low lytic phage concentrations as described above. Modularity in epidemics may come about from the presence of lysogenic bacteria because lysogeny can build up in bacterial populations via prophages. Prophages make the lysogenic bacteria resistant to superinfection by other viral types and concurrently drive other bacterial strain populations down because they do not have the resistance to the lytic-cycle-dominant phages still present in the system.
This difference in lysogeny or lytic cycle phages, if they are capable of only one cycle or both and what would induce them to choose lysis over lysogeny, is here shown to directly link to the basic pattern of the cholera epidemic.
Other studies have provided evidence on the elimination of a previously dominant V. cholerae strain due to differential infection patterns of a lysogenic virus. It seems that more information on what environmental conditions are necessary to induce a lysogenic pathway in the virus would be useful for researchers hoping to identify natural resevoirs for the virus, or inversely the bacteria. Nutritional treatments could easily be applied to cultures of bacteria and virus in a laboratory setting. Similar methods used to test for prophages as were used in this study (methods such as Southern blots and DNA probes) could potentially provide a lot of information on this globally pervasive disease and the bacteria that causes it.
Reviewed: 11/10/11
Cholera epidemics in and around Dhaka, Bangladesh occur seasonally, typically twice a year. Cholera is a human disease that is caused by pathogenic strains of Vibrio cholerae, however the bacteria is a normal component of aquatic ecosystems. Aquatic transmission of the disease-causing bacteria was first noted approximately one hundred and fifty years ago and while many environmental and biological parameters have been associated with the temporally varying disease surges, none have been conclusively linked to the cause or finish of the epidemic (other than the obvious requirement of water). Bacteriophages have been shown to be linked to transmission of toxigenicity in V. cholerae. Data obtained from plaque assays, bacterial cultures, and stool samples randomly obtained from local hospitals were used to demonstrate that the abundance of cholera-inducing bacterial strains was inversely correlated with increases in their own pathogens' numbers.
If the presence of a host-specific bacteriophage was noted within any given water sample collected from local aquatic systems, than its target host was significantly less likely to be found. The percentage of co-occurrences of virus and target host was lower than one that could have been predicted by chance alone.
Cross comparison of monthly collection and analysis for phages in water samples with stool samples showing cholera disease in humans did in fact show an oscillating relationship between the bacteria strains and their viruses. Two strains of bacteria are primarily responsible for the disease in Bangladesh, and six phage types, which can actually be grouped into 4 genetically distinct groups, are associated with them. However, the life modes of these viral types are not all homogenous. The authors propose that the difference between lytic and lysogenic capable phages may be driving a lot of the seasonality of the cholera epidemics.
The model they present begins with epidemics arising during periods of low lytic phage concentrations as described above. Modularity in epidemics may come about from the presence of lysogenic bacteria because lysogeny can build up in bacterial populations via prophages. Prophages make the lysogenic bacteria resistant to superinfection by other viral types and concurrently drive other bacterial strain populations down because they do not have the resistance to the lytic-cycle-dominant phages still present in the system.
This difference in lysogeny or lytic cycle phages, if they are capable of only one cycle or both and what would induce them to choose lysis over lysogeny, is here shown to directly link to the basic pattern of the cholera epidemic.
Other studies have provided evidence on the elimination of a previously dominant V. cholerae strain due to differential infection patterns of a lysogenic virus. It seems that more information on what environmental conditions are necessary to induce a lysogenic pathway in the virus would be useful for researchers hoping to identify natural resevoirs for the virus, or inversely the bacteria. Nutritional treatments could easily be applied to cultures of bacteria and virus in a laboratory setting. Similar methods used to test for prophages as were used in this study (methods such as Southern blots and DNA probes) could potentially provide a lot of information on this globally pervasive disease and the bacteria that causes it.
Suttle, C.A. Nature Reviews., (2007).
"Marine viruses - major players in the global ecosystem".
Reviewed: 11/10/11
Viruses are the most abundant player in the oceans when it comes to quantity of genetic information. Viruses in general are a unique class of organisms to consider due to their ability to infect hosts at multiple trophic levels. They have the potential to exert controlling forces on autotrophs and the heterotrophic grazers that feed on them. The author of this review presents information on different aspects of viral ecology as they relate to the specifics of a marine system, as well as the molecular techniques that have been developed to quantify their abundance.
It appears as though marine virus ecology might be fundamentally different from its terrestrial counterpart. It seems to me as if marine viruses can be thought of as existing in one gigantic pool, floating and dispersing after lytic events of their host species. Whereas as in terrestrial systems we usually think about viruses as being vectored or transmitted in some more organized fashion. Along with this idea is a lack of understanding about the way that viruses are transmitted in the ocean. A significant amount of data, involving genetic sampling in many diverse aquatic habitats around the globe, seems to show that their exists hotspots for certain virus families in differential parts of the ocean. It is possible to identify commonalities in different viral lineages as well. The VHSV virus is associated with a disease in trout farms of Europe, but has also been identified in marine fish and in some lakes in North America.
Interest in amassing more data on the specific roles of viruses in the ocean can be linked to their role in turnover and shuttling of carbon and other limiting nutrients as they infect and lyse their hosts. Particulate and dissolved organic matter arising after these events increases the amount of respiration done by decomposers in the photic zone.
The author also presents an interesting analysis of the spectrum of r and K selection in both the host species of the ocean and the viruses that infect them. While it appears that the abundance of marine prokaryotes and eukaryotes is weighted towards k strategists, who are slow growing and resistant to infection, the abundance curves and r-K spectrum is the opposite in the viral community. The most abundant viruses appear to genrally fall under the header of r-selected species, those with rapid replication and generally more virulent. This contrast of host and pathogen has important implications as it indicates that the rarer host species, those that are more r-strategists and are the most susceptible to infection, are controlled by a highly abundant, rapidly-replicating pathogen community. This does not mean that r-selected host species never undergo periods of release where they rapidly reproduce and expand in concentration, but it does imply that viruses are an important control to bring the overall marine ecosystem back to a more equilibrium state. It would be interesting to attempt to quantify both the affect that viruses have on the grazer populations ability to control other dominant eukaryotes or prokaryotes and how viral effects on these lower trophic order species affects the grazers who might feed on them.
Reviewed: 11/10/11
Viruses are the most abundant player in the oceans when it comes to quantity of genetic information. Viruses in general are a unique class of organisms to consider due to their ability to infect hosts at multiple trophic levels. They have the potential to exert controlling forces on autotrophs and the heterotrophic grazers that feed on them. The author of this review presents information on different aspects of viral ecology as they relate to the specifics of a marine system, as well as the molecular techniques that have been developed to quantify their abundance.
It appears as though marine virus ecology might be fundamentally different from its terrestrial counterpart. It seems to me as if marine viruses can be thought of as existing in one gigantic pool, floating and dispersing after lytic events of their host species. Whereas as in terrestrial systems we usually think about viruses as being vectored or transmitted in some more organized fashion. Along with this idea is a lack of understanding about the way that viruses are transmitted in the ocean. A significant amount of data, involving genetic sampling in many diverse aquatic habitats around the globe, seems to show that their exists hotspots for certain virus families in differential parts of the ocean. It is possible to identify commonalities in different viral lineages as well. The VHSV virus is associated with a disease in trout farms of Europe, but has also been identified in marine fish and in some lakes in North America.
Interest in amassing more data on the specific roles of viruses in the ocean can be linked to their role in turnover and shuttling of carbon and other limiting nutrients as they infect and lyse their hosts. Particulate and dissolved organic matter arising after these events increases the amount of respiration done by decomposers in the photic zone.
The author also presents an interesting analysis of the spectrum of r and K selection in both the host species of the ocean and the viruses that infect them. While it appears that the abundance of marine prokaryotes and eukaryotes is weighted towards k strategists, who are slow growing and resistant to infection, the abundance curves and r-K spectrum is the opposite in the viral community. The most abundant viruses appear to genrally fall under the header of r-selected species, those with rapid replication and generally more virulent. This contrast of host and pathogen has important implications as it indicates that the rarer host species, those that are more r-strategists and are the most susceptible to infection, are controlled by a highly abundant, rapidly-replicating pathogen community. This does not mean that r-selected host species never undergo periods of release where they rapidly reproduce and expand in concentration, but it does imply that viruses are an important control to bring the overall marine ecosystem back to a more equilibrium state. It would be interesting to attempt to quantify both the affect that viruses have on the grazer populations ability to control other dominant eukaryotes or prokaryotes and how viral effects on these lower trophic order species affects the grazers who might feed on them.
Friday, November 4, 2011
Refardt D. ISME Journal. (2011).
"Within-host competition determines reproductive success of temperate bacteriophages".
Reviewed: 11/04/11
Parasites compete with one another just like species in any other trophic level in the ecosystem. This study approached parasitism from this perspective, in a competitor-on-competitor and resource-limited fashion. The results are important ecologically as they suggest that the conceptual tools already present in the field of ecology to think about traditional competition may apply to coinfected parasites within a common host as well.
The study organisms were the ubiquitous E. coli bacteria and 11 bacteriophages. Bacteria are easily cultured and many different molecular and genetic techniques have been previously developed to control their growth in a laboratory setting. Bacteriophages infect by two related but slightly different mechanisms. One involves the lytic cycle, where the parasite hijacks the host machinery to reproduce its own genetic material and then initiates cell rupture and death. The second is the lysogenic cycle, where the phage inserts its DNA into the host DNA, becoming a prophage. The prophage stays internal, and gets replicated with each cell division, until external pressures induce the lytic cycle and cell death. A secondary infection of a prophage into a bacteria already infected with a prophage must be a constant threat, as premature stimulus of the lytic cycle could lower reproductive output for either or both bacteriophages.
This concept shapes the basis of this experiment. Baseline performance of uni-infected prophages was analyzed first in order to note deviations from the normal pattern of growth when coinfected with a secondary prophage. Productivity, phages released per lysed cell, and lysis time, length of the rupture process from moment of externally applied signal, were the primary response variables analyzed.
In the majority of the coinfections, baseline productivity was not maintained by both phages at the same time, indicating a potential hierarchy of competitive ability. Total combined productivity of the two phages was close to 100% in most cases. This lends support to the idea that a high degree of resource/exploitative competition was taking place. However, there was a significant loss of total productivity that could not be explained by the sharing of resources alone, indicating some direct/interference competition between the two coinfected prophages, though the mechanism is not known.
Crucially this study found that coinfection alters productivity of the parasites and that this alteration is differential based on competitive ability. However, coexistence of phages still occurs in nature; one super-phage has not outcompeted all other phages in all settings. This may be because a small proportion of the variance in productivity was explained by the specific combination of the two coinfected phages, and not just a sum of their main effects. The results of this study would also benefit by testing a similar experiment across an array of nutrient conditions and/or host genotype or species. The phages in this experiment resided within a host that was largely not stressed by external environmental factors up until the lytic cycle was induced. An experiment involving staggered pH level differences, or deviations in nutrient content from the idealized petri plate, would be highly applicable to natural world microbial communities, as well as to larger questions about coinfection as drivers in ecological processes.
Reviewed: 11/04/11
Parasites compete with one another just like species in any other trophic level in the ecosystem. This study approached parasitism from this perspective, in a competitor-on-competitor and resource-limited fashion. The results are important ecologically as they suggest that the conceptual tools already present in the field of ecology to think about traditional competition may apply to coinfected parasites within a common host as well.
The study organisms were the ubiquitous E. coli bacteria and 11 bacteriophages. Bacteria are easily cultured and many different molecular and genetic techniques have been previously developed to control their growth in a laboratory setting. Bacteriophages infect by two related but slightly different mechanisms. One involves the lytic cycle, where the parasite hijacks the host machinery to reproduce its own genetic material and then initiates cell rupture and death. The second is the lysogenic cycle, where the phage inserts its DNA into the host DNA, becoming a prophage. The prophage stays internal, and gets replicated with each cell division, until external pressures induce the lytic cycle and cell death. A secondary infection of a prophage into a bacteria already infected with a prophage must be a constant threat, as premature stimulus of the lytic cycle could lower reproductive output for either or both bacteriophages.
This concept shapes the basis of this experiment. Baseline performance of uni-infected prophages was analyzed first in order to note deviations from the normal pattern of growth when coinfected with a secondary prophage. Productivity, phages released per lysed cell, and lysis time, length of the rupture process from moment of externally applied signal, were the primary response variables analyzed.
In the majority of the coinfections, baseline productivity was not maintained by both phages at the same time, indicating a potential hierarchy of competitive ability. Total combined productivity of the two phages was close to 100% in most cases. This lends support to the idea that a high degree of resource/exploitative competition was taking place. However, there was a significant loss of total productivity that could not be explained by the sharing of resources alone, indicating some direct/interference competition between the two coinfected prophages, though the mechanism is not known.
Crucially this study found that coinfection alters productivity of the parasites and that this alteration is differential based on competitive ability. However, coexistence of phages still occurs in nature; one super-phage has not outcompeted all other phages in all settings. This may be because a small proportion of the variance in productivity was explained by the specific combination of the two coinfected phages, and not just a sum of their main effects. The results of this study would also benefit by testing a similar experiment across an array of nutrient conditions and/or host genotype or species. The phages in this experiment resided within a host that was largely not stressed by external environmental factors up until the lytic cycle was induced. An experiment involving staggered pH level differences, or deviations in nutrient content from the idealized petri plate, would be highly applicable to natural world microbial communities, as well as to larger questions about coinfection as drivers in ecological processes.
Jolles, A.E. , Ezenwa, V.O., Etienne, R.S., Turner, W.C., & Olff, H. Ecology. (2008).
"Interactions between macroparasites and microparasites drive infection patterns in free-ranging African buffalo".
Reviewed: 11/04/11
Infection by both macro- and micro- parasites in wild populations occurs at an astonishingly high rate. Among the buffalo herds described in this study the prevalence of Bovine tuberculosis and helminth infection reached as high as 72.5% for TB, and 87.5% for the worms. With such high prevalence of disease it is only natural to assume that some hosts face the double pressure of coinfection; it is also possible to imagine the concept of a herd that contains a higher proportion of coinfected individuals. This study hoped to identify the primary drivers of disease dynamics in buffalo at both the host and host population level.
Worm prevalence in buffalo was found to be highly negatively correlated with TB prevalence. Demographic factors such as sex and age, as well as proportionate amounts of certain individuals within the population, were found to be partial drivers of this pattern. Age plays a role in infection patterns at young ages fro both worms and TB, but males were only slightly less likely to be infected with worms than females.
Researchers also tested the role of a mortality hypothesis in driving disease dynamics using both empirical data and a simple theoretical model to qualitatively assess expected outcomes from different initial conditions. They found that coinfected individuals did indeed have a poorer body condition than those hosts who were singly infected. They also found that individuals with a higher concentration of fecal eggs, a metric of worm pressure, occurred less frequently in TB positive individuals, indicating an increased mortality rate. This pattern was true at the herd level as well based on proportionate amounts of infected individuals. Theoretical work supported a higher mortality rate alone being a partial driver of the negative correlation between worms and TB at the herd level, but only the addition of immunological heterogeneity into the model compared with the disease patterns at the individual level. Individuals infected with worms have a higher immunity to TB infection because of the self-regulation of the immune system in mammals to microparasitic and macroparasitic pathways. The immunity of worm infected individuals to TB reduced the infection rate of TB differentially in the worm-hosts than in regular susceptibles, reducing the total number of coinfections, which have a higher mortality anyways.
This study is interesting because it shows how different kinds of parasites interact and coexist with one another via multiple mechanisms. Differential infection in a shared host population based on sex and age shows niche differentiation, but antagonism between the two parasites was still present in this study. The two immunological pathways within the host reduced the secondary infection of TB when worms were present, though interestingly this was not true in the opposite direction. The result has evolutionary implcations as well, implying that parasites that come in and can reduce their host's risk of infection to a potentially more dangerous potential parasite would have an evolutionary advantage. These same immunological pathways are conserved across mammal species indicating a long occurring pattern of coinfection in the natural world.
Reviewed: 11/04/11
Infection by both macro- and micro- parasites in wild populations occurs at an astonishingly high rate. Among the buffalo herds described in this study the prevalence of Bovine tuberculosis and helminth infection reached as high as 72.5% for TB, and 87.5% for the worms. With such high prevalence of disease it is only natural to assume that some hosts face the double pressure of coinfection; it is also possible to imagine the concept of a herd that contains a higher proportion of coinfected individuals. This study hoped to identify the primary drivers of disease dynamics in buffalo at both the host and host population level.
Worm prevalence in buffalo was found to be highly negatively correlated with TB prevalence. Demographic factors such as sex and age, as well as proportionate amounts of certain individuals within the population, were found to be partial drivers of this pattern. Age plays a role in infection patterns at young ages fro both worms and TB, but males were only slightly less likely to be infected with worms than females.
Researchers also tested the role of a mortality hypothesis in driving disease dynamics using both empirical data and a simple theoretical model to qualitatively assess expected outcomes from different initial conditions. They found that coinfected individuals did indeed have a poorer body condition than those hosts who were singly infected. They also found that individuals with a higher concentration of fecal eggs, a metric of worm pressure, occurred less frequently in TB positive individuals, indicating an increased mortality rate. This pattern was true at the herd level as well based on proportionate amounts of infected individuals. Theoretical work supported a higher mortality rate alone being a partial driver of the negative correlation between worms and TB at the herd level, but only the addition of immunological heterogeneity into the model compared with the disease patterns at the individual level. Individuals infected with worms have a higher immunity to TB infection because of the self-regulation of the immune system in mammals to microparasitic and macroparasitic pathways. The immunity of worm infected individuals to TB reduced the infection rate of TB differentially in the worm-hosts than in regular susceptibles, reducing the total number of coinfections, which have a higher mortality anyways.
This study is interesting because it shows how different kinds of parasites interact and coexist with one another via multiple mechanisms. Differential infection in a shared host population based on sex and age shows niche differentiation, but antagonism between the two parasites was still present in this study. The two immunological pathways within the host reduced the secondary infection of TB when worms were present, though interestingly this was not true in the opposite direction. The result has evolutionary implcations as well, implying that parasites that come in and can reduce their host's risk of infection to a potentially more dangerous potential parasite would have an evolutionary advantage. These same immunological pathways are conserved across mammal species indicating a long occurring pattern of coinfection in the natural world.
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