Empirical evidence for specificity and specific interactions

For specific interactions (Figure 14.1a) to materialize within a host-parasite system, two conditions must be met. There must not only be polymorphisms between hosts in their immune defences, but the suite of responses effective against different parasite types should not entirely overlap. In other words, they should be specific to the parasite type. Whole-organism infection studies, and more recently genetic and molecular work, have shown that invertebrate hosts demonstrate such specificity. Using the snail Biomphalaria glabrata and its parasite Schistosoma masoni, host lines were separately selected for either resistance or susceptibility to two different parasite strains. While the selected lines responded as expected to the parasite strain they were exposed to, no concomitant change in resistance was found to the other parasite strain (Webster and Woolhouse, 1998). Similarly, quantitative trait loci (QTL) studies of the encapsulation of malaria parasites by mosquitoes has shown that a major QTL for the encapsulation of one parasite strain contributed little to the encapsulation of another (Carton et al., 2005). It can be concluded that in these systems resistance is parasite-strain-specific, in that the suite of defences effective against one parasite type are not similarly effective against a second distinct parasite type. Relating to the idea that different immune defence components are specific against particular infections are more detailed mechanistic studies of immune defence pathways, and their importance for combating pathogens. For instance, a plethora of work on Drosophila using mutants of certain immune system components has demonstrated specificity on a coarse level. Particular sets of recognition, signalling, and effector molecules are required for defence against certain classes of microbes but not others (Hultmark, 2003). For example, the two best-studied signalling pathways in Drosophila immunity, Toll and Imd, have been shown to be differentially required for an effective immune response depending on the microbe in question (Hultmark, 2003). Furthermore, post-genomic studies show different patterns of gene expression on exposure to distinct pathogens and parasites. When Drosophila received a fungal, protozoan, viral, or bacterial infection, 64% of the upregulated genes were specific to the infection type (Roxstrom-Lindquist et al., 2004). Further evidence concerning the differential use and importance of immune system components, based on a coarse level of specificity between parasite types, can be found in Chapters 2 and 4. A mechanistic basis for a finer degree of immune specificity can be found in Chapter 5.

Note from the examples thus far that 'specificity' does not necessarily mean that resistance against one parasite type is traded-off with resistance to another, a pattern that would emerge as a negative co-variation between the two resistance components. While this trade-off could take place between two immune pathways or immune genes, an alternative is that alleles at a particular gene confer resistance or susceptibility depending on the parasite type. In this case, specific resistance against one parasite type will be antagonistic to resistance against another.

For many years, evolutionary ecology studies of host-parasite systems have strongly hinted that specificity exists within the immune defence of invertebrates. Several studies (Table 14.1) have demonstrated the existence of specific interactions between host and parasite types (see Figure 14.1a). Taking the evolutionary ecology perspective of immunity, as any host trait that influences the infection level of that individual (see Box 14.1), such host-parasite interactions would not manifest if the immunity of invertebrates were homogeneous and not specific. Instead, genotypic differences in hosts would relate to across-the-board resistance or susceptibility to parasites. This is not the case, and therefore the empirical evidence offers strong support for the existence of specific immune responses in invertebrates. This inference derived from macroscopic infection experiments is now being strongly corroborated by the discovery of specific immune mechanisms based on different principles than those found in vertebrates (see Chapter 5).

Table 14.1 Exampl

es of specific interactions between invertebrate hosts and their parasites. The presence of such interactions hints strongly at the

existence of specific immune responses.





Daphnia magna

Two bacterial and three

Interaction between host clones and parasite species in

Decaestecker et al. (2003)


measures of virulence, infectivity, and spore production.

Pasteuria ramosa (bacterium)

Interactions between host clones and parasite clones with

Carius et al. (2001)

respect to virulence and infectivity.

Bombus terrestris

Crithidia bombi (protozoan)

Interaction between host colony (relatedness between

Schmid-Hempel (2001)

individuals = 0.75) and parasite isolate with respect to

transmissible cells shed in the faeces.

Interaction between host colony and parasite isolate with

Mallon et al. (2003)

respect to infection intensity in the gut.


Serratia marcescens

Interaction between host and parasite strains in respect to

Schulenburg and Ewbank



virulence (expressed as survival).



Plasmodium falciparum

Interaction between host family and parasite isolate with

Lambrechts et al. (2005)



respect to the likelihood and intensity of infection.

Examples of specific host-parasite interactions have been found across the invertebrates, including insects, and for a variety of different parasite types. In an infection experiment with nine different clones of the host Daphnia magna and nine different isolates of the bacterial parasite, Pasteuria ramosa, the interaction term between host clone and parasite isolate was significant in determining resistance (Carius et al., 2001). In other words, the influence of host clone on the outcome of infection was dependent on the parasite isolate it was infected with. No clone was completely susceptible or completely resistant to all parasite strains. The same was also true for the infection ability of parasite isolates. Similarly, when different isolates of the trypanosome Crithidia bombi were passed through a number of different colonies of its bumblebee host, Bombus terrestris, a clear association of different parasite isolates with a given host colony was found (Schmid-Hempel et al., 1999). Furthermore, controlled infection experiments of host individuals with different parasite isolates yield results comparable to the Daphnia example above. Infection intensity is dependent on an interaction between the host origin and parasite isolate (Schmid-Hempel, 2001). A genetic screen of the naturally infecting C. bombi populations also supports this finding. This showed the population of the parasite to be highly structured and genetically diversified, a pattern that is expected to result from strong genotypic host-parasite interactions (Schmid-Hempel and Reber Funk, 2004). In light of the above results and those presented in Table 14.1, there is little doubt that many systems show specificity at the macroscopic level of infection and susceptibility.

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