In the laboratory, adults of D. melanogaster and related species are susceptible to entomopathogenic fungi such as Beauveria bassiana. Nothing is known about the rate of infection of Drosophila by Beauveria or other such fungi in the field, although genetic variation for resistance against Beauveria does exist both among and within natural populations (Tinsley et al., 2006).
Typically, infected flies die 5-28 days after exposure to fungal spores (Fytrou et al., 2006; Tinsley et al., 2006; Kraaijeveld and Godfray, 2008). Once infected, flies continue to produce eggs for several days (Kraaijeveld and Godfray, 2008). The costs of launching an immune response against fungal infection are unknown, and it can not be ruled out that the use of resources for the production of the relevant antimicrobial peptides contributes to the early death of infected flies.
Artificial selection for increased resistance to Beauveria results in evolutionary change in D. mela-nogaster, but in an unexpected way. Interestingly, there is no difference in life span after infection between selection and control flies. Instead, infected selection flies continue laying eggs for longer than infected control flies (Kraaijeveld and Godfray, 2008). This results in the fecundity of infected selection flies, from infection to death, being higher than that of control flies, despite both types of flies succumbing to the fungus after the same amount of time. Thus, it seems that the selection regime selects for some kind of tolerance more than actual resistance. Even though the precise mechanism underlying this tolerance is still unknown, comparison of uninfected control and selection flies suggests a cost of tolerance: selection flies have lower lifetime fecundity than control flies when uninfected (Kraaijeveld and Godfray, 2008).
Laboratory populations of D. melanogaster have been reported to be infected by a few species of Microsporidia, of which Tubulinosema kingi (formerly Nosema kingi) is the best studied (Armstrong and Bass, 1989a, 1989b; Franzen et al, 2006; Futerman et al., 2006; Vijendravarma et al., 2008, 2009). Typically, larvae (younger instars are especially susceptible) ingest spores coming from infected cadavers; pathogen load remains low in subsequent larval instars, but increases rapidly in adult flies (Futerman et al., 2006; Vijendravarma et al., 2008). Nothing is known about the prevalence of T. kingi or other Microsporidia in natural Drosophila populations, and the only two infected flies reported from the field are likely to have been escapees from the nearby laboratory (Futerman et al, 2006).
Infected flies show decreases in several fitness parameters, from developmental rate to survival probability to adult size (Armstrong and Bass, 1989a, 1989b; Futerman et al., 2006). The fitness parameter which seems to suffer most after infection by T. kingi is fecundity, which is reduced by 33-66%, depending on Drosophila species (Armstrong and Bass, 1989b; Futerman et al, 2006). Very little is known about the resistance mechanism of Drosophila against Microsporidia, although both cellular and humoral mechanisms appear to play a role in other insect species (Hoch et al., 2004; Tokarev et al., 2007). Nothing is known about the costs of launching an immune response (whatever this response may be) against Microsporidia.
Experimental evolution, in which fly populations were exposed to microsporidian spores on their food, resulted in evolutionary changes. As the resistance mechanism is unknown, fecundity was taken as a proxy measure of resistance in these experiments. Flies from selection lines suffer less of a reduction in fecundity after exposure to microsporidian spores than flies from control lines, and spore loads are lower in infected selection flies than in infected control flies (Vijendravarma et al.,
2009), suggesting that they indeed evolved higher levels of resistance.
Comparison of uninfected selection and control flies suggests that this increase in resistance bears costs: larvae from the selection lines are poorer competitors for food than larvae from the control lines (Vijendravarma et al., 2009). On top of this, adult flies from the selection lines have lower early-life fecundity than adult flies from the control lines (Vijendravarma et al., 2009).
Very little is known of the abundance of pathogenic bacteria in Drosophila populations in the field, but the overall bacterial community associated with D. melanogaster in natural populations appears to be quite variable (Corby-Harris et al., 2007). Most work in the laboratory has used pricking with bacteria-infected needles as the means of inoculation, and this leads to high levels of mortality within a few days (Lazarro et al., 2004). However, when natural (oral) means are used to inoculate flies with such seemingly highly pathogenic bacteria (e.g. Serratia marcescens), the bacterium does not appear to have any negative fitness effects (Lazarro et al., 2004). However, one species of pathogenic bacterium has been identified which causes death to larvae and adults 1-4 days after oral inoculation: Pseudomonas entomophila (Vodovar et al., 2005).
Genetic variation in resistance against bacteria after inoculation by 'dirty needles' has been found in natural populations (Lazarro et al., 2004; Corby-Harris and Promislow, 2008). Using a genetic correlation approach, McKean et al. (2008) showed that resistance to the bacterium Providencia rettgeri has maintenance costs. In the absence of infection, there was a negative correlation among families between fecundity and resistance. Interestingly, this cost is environment-dependent, as it is only found when food is limited and not when food is plentiful. They also reported a cost of actual resistance, but this seems to be a cost of wounding the fly during the infection process rather than the cost of the immune system launching a response against the bacterial infection itself.
Wolbachia is an unusual bacterium in that it is intracellular. It is a widespread symbiont of arthropods and nematodes, and induces male-killing, feminizing, and/or cytoplasmic incompatibility (Werren, 1997) in its host in order to further its own spread in the host population. Here we will focus solely on the bacterium as a potential pathogen of the individual it has infected. Wolbachia infection in D. melanogaster populations is common and widespread (Fry et al, 2004; Riegler et al, 2005). The fitness effects it has on D. melanogaster and related species (e.g. Drosophila simulans) are variable, but reductions in size, fecundity, sperm competitiveness, and immune response to parasitoid eggs have all been reported (Fry et al, 2004; Champion de Crespigny and Wedell, 2006; Fytrou et al, 2006). Whether Drosophila launches an immune response to combat Wolbachia infection is unknown, and so nothing is known about any resistance mechanism nor about any costs of resistance.
At least half a dozen RNA viruses are known from natural populations of D. melanogaster, with up to 40% of flies infected (Carpenter et al., 2007). C virus is not pathogenic after natural (oral) infection, although it is highly pathogenic when injected (Thomas-Orillard et al., 1995). An additional effect of the virus on its host is to increase fecundity (Thomas-Orillard et al., 1995). Infection by X virus renders flies very sensitive to lack of oxygen (death occurs when flies are exposed to pure carbon dioxide; Zambon et al., 2005). Sigma virus is host-specific to D. melanogaster and widespread in natural populations (Carpenter et al., 2007). Unlike the other viruses, it is vertically transmitted. Flies infected by Sigma virus suffer the same effect as those infected by X virus (extreme sensitivity to anoxia) and, in addition, infected eggs have a lower viability and infected adults a lower survival (Carpenter et al., 2007; Tsai et al, 2008).
The resistance mechanism of D. melanogaster against viruses is not fully understood, although several immune pathways (Toll, Janus kinase/ signal transduction and activators of transcription (JAK/STAT)) appear to be involved (Dostert et al, 2005; Zambon et al, 2005; Tsai et al, 2008). Nothing is known about the costs of mounting an immune reaction against viruses or of the costs of the antiviral resistance mechanism itself.
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