Extra reading Flashcards
Hoberg et al 2001
phylogenetic study of 35 species taenia based on matrix of 28 morphological characters.
mapped extant parasites onto phylogenetic tree whilst considering biogeography.
Shows common ancestor of saginata and asiatica was already in humans.
Used mutation erate of Cytochrome C oxidase sequences to show divergence predates domestication of ungulates.
Although taenia could have faster substitution rates than organisms used to date divergence, they dont have the rapid metabolism and even so would still predate domestication.
Veracx and Raoult 2012
pediculus differences
Morphology and physiology differences -
Capitis - more chitinised, smaller darker. More susceptible to starvation.
Corporis - longitudinal muscles on ventral body wall, longer antennae, larger, perhaps due to larger feed as frequently away from host as clothes discarded.
Different biotopes.
Pair freely when in each others territory, give fertile offspring.
1919 suggested corporis descended from capitis. however genetic studies disagree.
Genomes: small genome - reflects obligate parasitism dependence on host.
Study of 18s RNA gene and mit show 3 cladesof head lice.
Similar genomes, only one gene difference. Expression levels define them.
What has parasite history been able to tell us about human evolution?
only lice and pin worms seemed to evolve with humans.
presence/absence formula to measure parasitological relatedness between hosts, and derive phylogeny of hominids. did not work - human parasite fauns closest to baboons. cant be applied to primates because of wide geographical distribution.
Studying origin of human parasites can suggest where humans diverged from chimps. for many parasites region of origin is unknown but some show ethiopian origin, W and C africa - humans evolve Cameroon or Gabon.
Kittler et al method
molecular clock to date origin of body lice
1 mtDNA, 2 nuclear genes
Sample of 40 head and body lice from 12 locations, 1 chimpanzee louse.
African - greater diversity, suggesting african origin.
Phylogenetic tree deepest clades only contain head lice, suggests body lice originated from headlice.
Aidoo et al method and explanation
studied 1022 children from 1birth cohort in kenya which already had data on malaria morbidity and mortality up to 3-5 years old. Survival analysis using sickle cell traits as a factor.
HbAS sig reduction in all cause mortality between 2-16 months. No reduction in first 2 months - maternally transferred protective immunity and high levels of fetal haemoglobin, poorly supports p. falciparum.
After 16 months - dev of clinical immunity causes lack of association of HBAS with mortality.
Cyrklaff - HbC
Used Cryoelectron tomograms
Infected RBC - extended network of long branched filaments cnnect maurer’scleft with knobs with vesicles attached.
Uninfected RBC - short filaments look like actin rods.
Parasite remodels this membrane skeleton.
HbC and HbS no maurer’s clefts.
Anderson et al
Does ascaris cross infect as infected people report accidental contact with pig waste.
pig and human worms have similar morphology and lack of genetic markers. Frequencies of Ribosomal DNA polymorphic site can distinguish worm populations but not individuals.
Method: used internal transcribed ribosomal region (ITS) and amplified by PCR, electrophoresis and stained with ethidium bromide and UV fluorescence. Hae 111 restriction enzyme showed Hae111 site is polymorphic - either 1 or 2 sites, creating 2 or 3 bands.
Hae111 site in only 2/131 human worms and163/166 pig worms.
Cross infection can occur and worms can reach maturity.
In Guatemala symatric populations are reproductively isolated although very low levels of gene flow.
Peng et al Ascaris in China
Tested if Andersons theory was true in China too.
Method: worm tissue ground up and centrifuged, RNase treatment, DNA precipitated in cold ethanol.
PCR of mtDNA and ITS in rDNA. PCR products digested with endonucleases, electrophoresed and stained w ethidium bromide and UV fluorescence.
Used restriction fragment patterns to define haplotypes.
found sig freq differences in haplotypes, so reproductively isolated in sympatry.
very little/no gene flow between human and pig parasite pops and infection from mature ascaris from pigs unlikely to impose significant health risk to human pops.
Stear et al, components of resistance to T. circumcincta in sheep
No variation in innate responses in flock.
2 stages of genetic control of aquired immunity
1. reduction in egg production per worm, associated w IgA.
2. Control of worm burden, associated w production of globule leukocytes.
3-6 months lamb most variation in immunity - maybe not all have developed immune response yet.
Mean eritability of egg count averaged at 0.33 between 3-6months.
V strong negative correlation of FEC and live weight.
Control of FEC may be important genetic determinant of growth in naturally grazing sheep.
DRB1 locus has major effect on FEC, allele G2 has only 2 % FEC of G1.
MHC evolution and sheep MHC associated with parasite resistance and survival.
Genetic diversity in MHC maintained by antagonistic coevolution.
MHC allelic variation associated with juvenile survival and resistance to int nematodes.
Balancing selection due to nonsynonymous substitutions exceeds the rate of synonymous so favours new MHC variants.
2 types of selective mechanism: 1. reproductive - MHC biased mating
2. Parasite driven - MHC role in vertebrate immunity.
Negative freq dependent selection.
sheep - mortality highest in juveniles, survivorship at this age likely to be a strong predictor of fitness
OLADRB satellite lies in an intron in MHC. OLADRB 257 allele is sig ass w decreased parasite resistance and decreased survival in lambs
OLADRB 263 - increased resistance and survival.
Gemill et al why parasites have sex.
- sexual rep by parasites may counter somatic evolution of immune response
- immunity determined sexuality in S ratti.
- Parasites have sex to evade parasites of their own, and counter immune response.
- Short generation time of parasites facilitates selection of parasites very closely adapted to host genotype.
- However, many have no within host replication- helminths.
- sexual rep less common when no immune response, greater when targeted.
Viney et al
can effects of immunisation on worms be reversed with immunosupression?
Previous studies shown that effects of host immune response on worms (shorter length, lower fecundity, distribution in gut) can be reversed when transplanted into a naive host.
Also shown that worms transplanted from immunised host to naive host can recover.
4 groups, each w 28 female rats. A- Immunised then immuno supressed B- Immunised only C - Immunosupressed only D- Naive.
Dosed with S ratti, collected faeces and determined total rep output of worms. Rats killed and worms recovered.
Worms from immunised rats shorter, less gonads in body.
Immunised had lowest per capita fecundity, but immunised them immuno suppressed were similar to naive rats.
immunisation dependent reduction in per capita fecundity was fully reversed upon immune suppression.
how does chloropuinine therapy affect plasmodium?
investigated using mice and rodent malaria - P chaubaudi, subcurative dose of chloroquinine.
Earlier peak of gametocyte production compared to untreated control.
changes in infectivity of mosquitoes but not proportion of mos infected.
worried that drugs causing DNA synthesis blocking drugs cause stress response of parasites, = greater fecundity and switch to sexual stages.
after CQ treatment found lower asexual and gametocytes than control but higher proportion of gametocytes.
later treatment caused greater parasite death due to a higher abundance of parasites coupled w greater immune response.
Why are schistosomes affected by the immune response?
S. mansoni has alternative developmental pathway in immune def hosts. Attenuated forms which prolong survival of host and schistosomes.
Schistosomes exploit endocrine and immune signals.
In mice lacking RAG1 or Prkdc cells had flukes w delayed sexual maturity and less eggs accumulated in liver.
Also deficient in IL-7 had impaired schistosome growth.
Lacking aB cells had more effect than B or gdB cells.
how can helminths affect microparasites
Bottom up control when helminth causes anaemia - limits RBC available for protozoa. Reduce SA for microparasite attachment.
Top down control - helminths can impair immune system, suppress IFN Y response. Also alter efficacy of predation on microparasites.
Perhaps antihelmintic drugs can alter severity of disease such as malaria.
