BIOS 3010: Ecology Lecture 10: Processes: Parasitism & Diseasehomepages.wmich.edu/~malcolm/BIOS3010-ecology/Lectures/L10-Bios3010.pdf• Cycles have been argued to be caused by either

1

Dr. S. Malcolm BIOS 3010: Ecology Lecture 10: slide 1

BIOS 3010: Ecology Lecture 10: Processes: Parasitism & Disease

•  1. Lecture summary: –  Definition. –  Micro- and

macroparasites. –  Parasite & disease

diversity. –  Host diversity. –  Effects on hosts. –  Disease dynamics.

•  Click (at 48:56 mins):http://www.bbc.co.uk/iplayer/console/p00kmdfy


2. Parasites:

– A parasite is an organism that obtains its nutrients from one or a very few host individuals, normally causing harm but not causing death immediately.

– Probably all organisms on earth have parasites, so more than half of the species on earth must be parasites and much more than half of the individual organisms that exist must be parasites.


3. Micro- and macroparasites: •  Microparasites

–  Small, very numerous like bacteria & viruses. –  Multiply directly in the host. –  Mostly intracellular and so hard to count - therefore counted by

number of infected hosts: •  e.g. measles or malaria outbreaks are measured by the numbers of

infected people. –  Direct or vector transmitted.

•  Macroparasites –  Grow, but do not multiply in hosts. –  Produce infective stages that attack new hosts. –  Live intercellularly between tissues or on hosts. –  Can be counted

•  e.g. tapeworms, ticks and flukes –  Direct or vector transmitted.

2


4. Taxonomic diversity of parasites & diseases:

•  Diseases, ectoparasites and endoparasites: –  Invertebrates:

•  viruses, rickettsiae, bacteria, fungi, protozoa – Microparasites: multiply within their hosts and often result in

either death or some measure of host immunity. •  flukes, roundworms, tapeworms, some crustacea

–  e.g. parasitic copepods •  some arachnids

– mites, kleptoparasitic spiders & ticks. •  some insects

–  lice, bedbugs, fleas, mosquitoes, horseflies & parasitic wasps. – Macroparasites: multiply outside their hosts and host

response varies according to parasite load.


5. Taxonomic diversity of parasites & diseases:

•  Vertebrates: –  Fish

•  lampreys, anglerfish and a catfish. –  Mammals

•  vampire bats.

–  Birds •  blood-feeding finches in the Galapagos.

•  Plants: –  some plants

•  E.g. dodders, mistletoes, louseworts, some orchids, bastard toadflax and Rafflesia which produces the world's largest flower.


6. Parasite diversity:

•  Parasites, especially endoparasites, tend to live in very stable habitats within their hosts.

•  They show ecological emphases on: – Reproduction. – Simplified resource exploitation. – Defenses against the host immune responses. – Reduced movement. – Dispersal is achieved through very high

reproductive output.

3


7. Parasite diversity in fish:

•  1) Solitary salmonid (trout) species had lower parasite diversity than salmonids that school outside the breeding season (Fig. 12.13).

•  2) Species with wider geographical ranges have higher parasite diversity.

•  3) Parasite diversity in cyprinids increases with host size and age (as in Fig. 12.14)

–  So ecological factors such as schooling behavior, distribution and size influence parasite diversity.

–  Diversity and abundance are also influenced by interspecific competition among parasites: •  E.g. possible competitive exclusion among parasites of anole

lizards on Caribbean islands (Figure 12.15).


8. Host diversity:

•  Experimental host diversity mixtures can influence the spread of disease:

– For example, late blight of potatoes (Figure 12.16)

•  Can also limit the spread of disease infections:

– Effectively dilutes the density (or contact rate) of susceptibles in the population and reduces the effectiveness of vectors.


9. Reduced survivorship, growth and fecundity of hosts:

•  Host survivorship is reduced with increasing parasite load – See Figures 12.17 and 12.18

•  Also reduction in: – Age of maturity. – Fecundity. – Population rate of increase.

4


10. Dynamics of parasite populations in hosts:

– Parasites respond to their own density through: •  Intraspecific competition and density dependent effects

on birth and death rates (Fig. 12.8). •  Total weight of parasites may increase and numbers

increase, but individual weights decrease and eggs/parasite decrease, but eggs/host stay the same.

–  Is this just the effect of intraspecific competition or is the host immune response also exercising “bottom up” control?

–  See the immune response of a vertebrate host in Fig. 12.9 that also can include a "memory" in an inducible response (as in plants)(see also Fig. 12.3 in 4th ed.).


11. Dynamics of parasite populations in hosts:

•  Distribution in time and space: – Distributions of parasites within host populations

also tend to be aggregated (Fig. 12.10) with only a few hosts carrying many parasites:

•  Prevalence of infection is the proportion of a host population that is infected

•  Intensity is a measure of the number of parasites in or on a single host (mean intensity is the mean number per host in a population of hosts)

•  Prevalence and intensity are related through various frequency distributions in Fig. 12.11.


12. Disease transmission:

– The net rate of transmission for directly transmitted microparasites is directly proportional to how often infected hosts meet uninfected (susceptible) hosts, which is also a reflection of density and distance between individuals as shown in Fig. 12.6 for a fungal plant disease.

– Rates of transmission of microparasites are dependent upon the basic reproductive rate Rp (like Ro)

5


13. Disease transmission:

– Microparasites - Rp is the average number of new cases of the disease (secondary infections) that arise from a single infectious host introduced into a population of susceptible hosts.

– Macroparasites - Rp is the average number of established, reproductively mature offspring produced by a mature parasite in a population of uninfected hosts.

– Transmission threshold - Rp = 1, an infection will die out if Rp < 1 and will spread if Rp > 1


14. Rp and directly transmitted microparasites:

– The basic reproductive rate Rp increases with: •  (1) L = average period of time an infected host

remains infectious. •  (2) S = density of susceptible individuals in the

population. •  (3) β = transmission rate of the disease.

–  Also depends on infectiousness or the probability that contact leads to transmission and the probability of contact.

•  So overall, •  Rp = SβL and is host density dependent, and the

critical threshold density ST ,where Rp = 1, is, ST = 1/βL


15. Epidemic and endemic phases of disease:

– When Rp >1 there is a rapid increase in the incidence of disease with rapid infection of susceptibles and the disease is epidemic.

– When Rp ≈ 1 the disease is in an endemic phase because its rate of spread is much reduced by increased immunity, mortality and decreased density of susceptibles

6


16. Epidemic and endemic phases of disease:

– Because Rp = SβL •  Highly infectious diseases (high β), or those with long

infectiousness periods (high L) will have high Rp values even in small populations (low ST) and will persist:

–  like endemic Herpes viruses.

•  Conversely, low β and low L diseases will only persist in large, dense populations:

–  like measles epidemics above a threshold density of 300,000 individuals - see Figure 12.17

–  Fig. 12.17 also shows cycling of host infections due to the introduction of new susceptible hosts through births and immigration


17. Disease immunity and vaccination:

–  Given Rp = SβL, the critical proportion of a population that needs to be vaccinated (pc) to provide herd immunity and bring Rp down to 1 or less is defined in terms of the typical number of susceptibles before immunization (So) and ST is the number still susceptible and not immunized after immunization, then pc (proportion immunized) is:

•  pc = 1 - ST / So (e.g. 1 - 2/10 = 0.8, or 1 - 8/10 = 0.2) •  so if ST = 1/βL and So = Ro/βL, then •  pc = 1 - 1/ Ro •  see Fig. 12.18 for the relationship between pc and Ro, to

bring Ro to <1


18. Parasites and population dynamics of hosts:

– Parasites can dampen cycles of host abundance and reduce host density (Fig. 12.27a, b).

– Case of red grouse in Britain and their nematode parasites:

•  Birds show regular cycles of abundance (Fig. 12.27d) •  Cycles have been argued to be caused by either

fluctuations in food quality (heather) or the influence of a parasitic gut nematode, Trichostrongylus tenuis.

–  Fig. 12.31 shows density dependent increase in grouse mortality with increased parasite load (perhaps through fox predation of more susceptible individuals) and decreased fecundity with increased parasite load.

7


Figure 12.13 (3rd ed.): Species richness of parasites in solitary and social salmonids


Figure 12.14 (3rd ed.): Species richness of cyprinid fish increases with size


Figure 12.15 (3rd ed.): Reduced anole lizard parasite load in mixed infections.

8


Figure 12.16 (3rd ed.): Mixing host susceptibility slows potato blight spread in potatoes.


Figure 12.17 (3rd ed.): Host survivorship and parasite load.

(a) (i) Nematode in mosquitoes, (ii) flukes in sheep; (b) people in LDCs and MDCs


Figure 12.18 (3rd ed.): Hydrometra fitness decreases with parasitic mite load.

9


Figure 12.8 (3rd ed.): Parasite density dependent responses

(a) Ascaris in humans, (b) tapeworm in humans, (c, d) tapeworm in mice


Figure 12.9 (3rd ed.): Vertebrate immune response - antibody memory.


Figure 12.10 (3rd ed.): Aggregated distributions of parasites

10


Figure 12.11 (3rd ed.): Relationship between prevalence & intensity of infection.


Figure 12.6 (3rd ed.): Parasite rate of infection increases with

host density.


Figure 12.17: Cases of (a) measles and (b) pertussis in England & Wales

Mass vaccination began

11


Figure 12.18: Vaccination level required for eradication at different combinations of disease transmission (pc) and reproductive rate (Ro)


Figure 12.27 (see Fig 12.23 4th ed):

Host population cycle dampening by parasites: (a) protozoan in flour beetle, (b) virus in meal moth, (c) virus in larch budmoth, (d) nematodes in red grouse and cycles without nematode.


Figure 12.31: Density dependent effects of Trichostrongylus tenuis on red grouse winter mortality and brood size

(See Fig. 12.24 4th ed.)

Documents

BIOS 3010: Ecology Lecture 10: Processes: Parasitism & Diseasehomepages.wmich.edu/~malcolm/BIOS3010-ecology/Lectures/L10-Bios3010.pdf• Cycles have been argued to be caused by either