Parasitism and diseaseDefinitionCategories of parasitesAnother way of categorizing parasitesModes of parasite/disease transmissionThere are all combinations of parasite type and transmission modeMacroparasites include:Microparasites with indirect life cyclesCharacteristics of parasite populations: boundariesCharacteristics of parasite populations: measures of abundanceCharacteristics of parasite populations: distribution of parasites among host individualsCharacteristics of parasite populations: transmission ratesOther factors affecting transmission ratesCharacteristics of parasite populations: density-dependence responsesEffects of parasites on individual hostsMore effects of parasites on individual hostsAcanthocephalansSimplest A & M (1981) model: directly transmitting parasite between invertebrate hosts with no immune response (Persistent InfThere are lots of variants on this simple model that incorporate such complexities as free-living stages, immune responses, anBasic reproductive rate for a parasite (R0)Conditions for parasite persistencePredictions about parasite life histories These life history relationships guide vaccination programsEvolution of virulenceWhat’s going on?IB 153 Parasitism and disease 10/12/20061Host-parasite population dynamicsAnderson and May modelsSome terms:H = total # of hosts (X + Y)X = # susceptible hostsY = # infected (or infectious) hostsa = per capita host birth rateb = rate of host mortality due to factors other than diseaser = a – b (host intrinsic rate of increase)α = disease-induced mortality rate (pathogenicity)β = transmission coefficientγ = rate of host recovery from infectionSimplest A & M (1981) model: directly transmitting parasite between invertebrate hosts with no immune response (Persistent Infection Model)dX/dt = a(X + Y) – bX – βXY + γYdY/dt = βXY – (α + b + γ)YdH/dt = rH – αYAssumptions:• Per capita birth rate “a” is same for infected and uninfected individuals• Sources of mortality are additive in their effect• Does not consider intensity of infection, only prevalence• No vertical transmission• All parameters are constants• No density-dependence in host population growth (grows exponentially in the absence of parasites)There are lots of variants on this simple model that incorporate such complexities as free-living stages, immune responses, and alternate hostsSome general predictions:1. High rates of host reproduction reduce the impact of parasites on host population density.2. Higher rates of transmission cause greater reduction in host population density. If too low, parasite goes extinct.3. Maximum degree of host population depression occurs at intermediate pathogenicity (α). If it is < r, then host population escapes control, but if it is very high, hosts are killed before the parasite can be effectively transmitted, so parasite declines, eventually going extinct.4. Aggregation or clumping of parasites tends to reduce their impact on host populations. Since most parasites are in a few individual hosts, the parasite population drops when these individuals die and control of the host population is reduced. On the other hand, a random distribution of parasites can cause too strong a suppression of the host population, leading to destabilization and parasite extinction.5. Direct reproduction in the host leads to greater suppression of the host population.R0> 1: parasite will establish and increase in number and prevalence within a host populationR0< 1: parasitic infection will die outWhat are determinants of R0?1. Density of susceptibles host individuals (S)2. Transmission rate of the parasite (β)3. Fraction of hosts that survive long enough to become infectious themselves (f)4. Average time over which an infected host remains infectious (L)Conditions for parasite persistenceR0= SβfL [your book: SβL]Critical threshold susceptible host density where parasite population maintains itself(R0= 1)ST= 1 / βfL [your book: βL]Predictions about parasite life histories 1. Diseases that are very infectious (high β), unlikely to kill host (large f), or have long periods of infectiousness (high L) will have a high R0and be able to persist in small host populations (low ST).2. Diseases that have low infectivity (low β), are likely to kill host quickly (highly pathogenic, low f), or have short periods of infectiousness (low L) will have small R0and can only persist in large populations of hosts (high ST).IB 153 Parasitism and disease 10/12/20062Case 1: protozoans in invertebrates – long-lasting infections in a host individual (large L) because of short-lived immune response, so parasite can persist in small populations (low ST).Case 2: viral or bacterial infections – induce a strong immune reaction which makes the infection transient within individual hosts (low L), thus requires a large population of susceptibles to persist (high ST). For example: for measles, susceptible population must be ~ 500,000!What’s going on?Isn’t it “bad” for a parasite to kill its host? Won’t a parasite gradually evolve into a mutualist?The answers are in R0= SβfLIf β, f, and L all varied independently, the a reduction in virulence (low f) would inevitably lead to a higher R0and parasites would evolve into mutualists. But…These parameters often covary in a specific way: virulence is a consequence of the production of transmission stages (cell damage, toxic metabolic wastes)So, lower β means lower virulence (high f); also lower virulence means fasater recovery, so lower β means lower L.A parasite can have a high R0if it kills quickly (small f), but produces many infective stage (high β)Or it can have an equally high R0if produces fewer infective stages (low β), but is less virulent (large f)More than one way to “skin a cat” – evolution can push virulence in different directions. In Myxoma, intermediate virulence strains are the most fit (highest