61BL3313 Population and Community Ecology

Lecture 10 Disease- and parasite-host interactions Spring 2013 Dr Ed Harris 61BL3313Population and Community Ecology

This time: Host-parasite interactions -introduction -factors affection parasite oppulations -modeling host-parasite intercations -disease dynamics -immunization -metapopulations and disease -social parasites

Host-parasite interactions: introduction Disease parasites have had a profound role on human natural and evolutionary history

Host-parasite interactions: introduction Disease parasites have had a profound role on human natural and evolutionary history Smallpox, now eradicated

Host-parasite interactions: introduction Disease parasites have had a profound role on human natural and evolutionary history Malaria, still a problem

Host-parasite interactions: introduction Disease parasites have had a profound role on human natural and evolutionary history bubonic plague, unknown

Host-parasite interactions: introduction -Here we consider a specific instance of multi-species population growth model -Micro-parasite and hosts population dynamics -not surprisingly, there has been much research to understand this interaction

Host-parasite interactions: introduction A few interesting characteristics of this type of system: -tremendous population growth of disease parasite in host -this growth is checked by host death or mounting immunity -surviving hosts may become immune

Host-parasite interactions: introduction Different modeling approaches SIR -hosts are classified as either Susceptible, Infected, or Recovered -many elaborations are possible and have been devised for SIR -models must account for abundance within hosts and host to host variation in infection

Host-parasite interactions: introduction Different modeling approaches -another factor is that some hosts have very complicated life cycles -e.g. Schistosomes (schistosomiasis); est. ~100,000,000 people cary at least one worm

Host-parasite interactions: introduction

Host-parasite interactions: factors affection parasite oppulations 3 main factors moderate interaction between parasite and host 1.course of infection within host 2.mode of transmission between hosts 3.behaviour and demography of hosts

Host-parasite interactions: factors affection parasite oppulations The course of an infection includes a latent period after exposure to the source of the infection. During this period the virus, for example, will increase exponentially. The next stage includes the infectious period, during which time the host develops the symptoms of the disease. Meanwhile, as the parasite population is building its numbers, the host immune system begins developing speciﬁc antibodies.

Host-parasite interactions: factors affection parasite oppulations As the antibody numbers increase, the parasite population plummets and the symptoms of the illness subside. The host ceases to be infectious at some point during the illness and the previously susceptible individual passes from S (susceptible) to I (infected) to R (recovered and immune). Some infected individuals may die during the course of the disease, and some recovered individuals may eventually lose their immunity.

Host-parasite interactions: factors affection parasite oppulations Other important factors affecting the natural history of the infection include: -the length of the infectious period -the time-lag derived from the latent period -the development of immunity by the host (thereby removing susceptible individuals from the host population) -the ability of some parasites to remain latent and undetected in host individuals (for example, herpes), only to reappear at some later date.

Host-parasite interactions: factors affection parasite oppulations 2 basic modes of transmission 1.vertical - mother to offspring 2.horizontal – from individual to individual Which is more common?

Host-parasite interactions: factors affection parasite oppulations Horizontal transmission – direct or indirect E.g., 1.close contact (common cold, the flu, measles) 2.sexual contact (hepatitis B, HIV, syphilis) 3.contaminative contact (cholera, tetanus, typhoid)

Host-parasite interactions: modeling host-parasite intercations Let's look at a SIR model, we assume: N = total host population density S = susceptible host density I = infected host density R = recovered (immune) host density b = host birth rate m = natural host mortality rate unrelated to disease mortality

Host-parasite interactions: modeling host-parasite intercations Let's look at a SIR model, we assume: alpha = disease-induced mortality rate beta = transmission rate of disease from one host to another n = recovery rate, or the per capita rate of passage from the infected (I) to the recovered (R) classes. This is usually the inverse of the average infectious period g = rate at which recovered individuals lose their immunity. That is, the rates at which individuals return to the susceptible class (S) from the R class.

Host-parasite interactions: modeling host-parasite intercations Let's look at a SIR model, we assume: The total population size, consisting of susceptible, infected and recovered:

Host-parasite interactions: modeling host-parasite intercations The growth rate of each segment of the population can be visualized separately The increase in the number of susceptible individuals is based on the birth rate (bN) and the rate at which recovered individuals lose immunity (γR). Losses are due to the host mortality rate unrelated to the disease (mS), and to the conversion of individuals from the susceptible to infected classes (βSI).

Host-parasite interactions: modeling host-parasite intercations The growth rate of each segment of the population can be visualized separately The growth rate of infected individuals equals the product, βSI, minus losses due to the combined effects of natural and disease-caused mortality (m + α), as well as recovery rate (from I to R), ν

Host-parasite interactions: modeling host-parasite intercations The growth rate of each segment of the population can be visualized separately The growth rate of the recovered class equals νI minus the death rate unrelated to disease and the loss of immunity, γR

Host-parasite interactions: modeling host-parasite intercations Thus we can add up all the previous equation to model the overall population growth <some math happens> Therefore we see that the growth of the population is diminished by the “natural” death rate, m, and by the mortality rate due to infections, αI

Host-parasite interactions: disease dynamics Spreading of a disease, that is, an epidemic, requires that the number of infected individuals remain steady or increases. This means that dI/dt ≥ 0. Since dI/dt = βSI − (m + α + ν)I Simplifying to

Host-parasite interactions: disease dynamics The rates m, α, and ν are all time-dependent. They represent rates at which a susceptible individual either dies or moves from the infected to the recovered class. The inverse of (m + α + ν) can be thought of as the length of the infectious period, D (Nokes 1992). If we substitute D for m + α + ν

Host-parasite interactions: disease dynamics If we deﬁne the product, βSD, as equal to R0, the basic reproductive number (BRN) or parameter for this disease

Host-parasite interactions: disease dynamics R0, the mean number of new infections caused by a single infective individual, is an important parameter. If this value is > 1, then dI > 1 and the disease incidence will increase. If R0 < 1, the epidemic fails. R0 is directly proportional to the rate at which an infection spreads, βS. It also depends on the mean amount of time an infection is active, D. For an infection to spread, it must have the right combination of susceptible hosts (S), a reasonably high transmission rate (β), and a sufﬁciently long period of transmission.

Host-parasite interactions: disease dynamics One conclusion we may draw from this analysis is that for a disease to succeed, it needs a dense population of hosts. For mosquito-borne diseases like malaria, BRN depends on: (i) vector (mosquito) abundance; (ii) focused feeding (the tendency to bite speciﬁc hosts and nothing else; (iii) vector longevity (the equivalent of D)

Host-parasite interactions: disease dynamics

Host-parasite interactions: disease dynamics Mean age in years at time of infection

Host-parasite interactions: immunization A main goal of immunization is to reduce the number of susceptible individuals in a host population, thereby lowering R of the disease to less than one

Host-parasite interactions: immunization The estimated fraction needed for successful immunization against several diseases, in a dense (>50,000) New York State population in 1918–19. A is average age of infection, R0 is the reproductive parameter for the disease, and p is the proportion that would need to be immunized for eradication of the disease. Average life span estimated at 55 years.

Host-parasite interactions: immunization Which comes from

Host-parasite interactions: immunization This reasoning has been used to set vaccination targets in many countries for many diseases More complex models would include equations for a host that has a very long latent period during which time it is not yet infectious, or for hosts that never reach a state of total immunity and continue to be infectious throughout the remainder of their lives (various venereal diseases or typhoid, for example)

Host-parasite interactions: metapopulations and disease Most modern conservation has as goals: 1.many populations 2.high migration between populations However, if disease is a concern, is this a good approach?

Host-parasite interactions: metapopulations and disease Another concern is "spillover", where there is transfer of disease amongst different, more abundant host species. E.g., domestic dogs are the probable source of diseases that have threatened African wild dogs (Lycaon pictus), African lions (Panthera leo), Baikal seals (Phoca sibirica), grey wolves (Canis lupus), and arctic foxes (Alopex lagopus semenovi)

Host-parasite interactions: metapopulations and disease S is the proportion of susceptible host patches (host population present, no disease) I is the proportion of infected patches (host population and disease present) The extinction rates of susceptible and infected populations are xS and xI The migration rate between susceptible and infected populations is ψ. When an infected disperser arrives at a susceptible patch, it infects the resident population with the probability of δ. Infection spreads at the rate of ψδIS. Now imagine the infection rate from an “outside source,” g. Start by setting g to zero, then ran a number of simulations showing the important effects when g is a non-zero parameter.

Host-parasite interactions: metapopulations and disease Model the proportion of patches occupied in the S and I states

Host-parasite interactions: metapopulations and disease

Host-parasite interactions: metapopulations and disease When g = 0.4 there is a reasonably large chance of infection from an “outside source.”

Host-parasite interactions: social parasites -parasites by definition lower host fitness -one reason is that many parasite consume the flesh of hosts -another is through behavioural parasitism

Host-parasite interactions: social parasites Brood or nest parasites When the eggs hatch, the host parents feed the parasitic chicks, even in preference to their own offspring. The chicks are large and aggressive, and since the parents often make no distinction among the chicks, the cowbird or cuckoo chicks get a majority of the food provided by the parents. In most cases the host raises few young of their own species when a parasitic chick is present in the nest. Moreover, cuckoo and cowbird females often remove host eggs prior to the laying of their own eggs, and in a nest still containing host eggs a cuckoo chick will eject host eggs from the nest.

Host-parasite interactions: social parasites Brood or nest parasites In some instances, the host makes an attempt to distinguish among the eggs and dumps the parasite eggs from the nest. Social parasites, including several species of cuckoos, cowbirds, African honeyguides, and ﬁnches have responded by laying “mimetic” eggs. That is, eggs which look like those of the host species. Furthermore, according to the “Maﬁa hypothesis,” (Zahavi and Zahavi 1997), some nest parasites retaliate against “dumpers” by destroying all of the eggs in the nest and perhaps even the nest itself. This parasite makes the host birds an offer they “can’t refuse.” That is, “raise one of my chicks or lose all of your children and your house!”

Host-parasite interactions: social parasites Brood or nest parasites: social insects

Host-parasite interactions: social parasites Social parasitism also occurs among social insects. In the so-called slave-making ants, a queen of the species Lasius reginae enters the nest of another species (L. alienus), kills the resident queen, and forces the workers to care for her own offspring. In such a case the workers are unable to distinguish the foreign ant queen from their own (Faber 1967). This parasitism is temporary, however, during colony foundation, and L. reginae workers eventually take over foraging and management of the nest. In other cases, however, the parasitic species produces no workers, a condition termed inquilinism. Here, socially parasitic species spends its entire life in the nest of its host species. Workers are lacking or are degenerate in normal foraging behavior.

Host-parasite interactions: social parasites Conclusions: The complexities of parasite–host interactions rival those of mutualisms. Parasites range from endoparasitic viruses to ectoparasitic ticks, and we lack an understanding of the life cycle of most parasites in organisms other than humans. What we do know is often based on models of human diseases and their modes of transmission. Parasitism can also involve complex behavioral interactions such as brood parasites or slave-making ants. In general, we know little about disease-host interactions, and ecologists may well have been guilty of underestimating their importance.

61BL3313 Population and Community Ecology