Insect immune resistance to parasitoids

Insect host-parasitoid interactions involve complex physiological, biochemical and genetic interactions. Against endoparasitoids, immune-competent hosts initiate a blood cell-mediated response that quickly destroys the intruders and envelops them in a multilayered melanotic capsule. During the past decade, considerable progress has been made in identifying some of the critical components of the host response, mainly because of the use of efficient molecular tools. This review examines some of the components of the innate immune response of Drosophila, an insect that has served as an exceptionally good experimental model for studying non-self recognition processes and immune cell signaling mechanisms. Topics considered in this review include hematopoiesis, proliferation and adhesion of hemocytes, melanogenesis and associated cytotoxic molecules, and the genetic aspects of the host-parasitoid interaction.     

Is xylem cavitation resistance a relevant criterion for screening drought resistance among Prunus species?

Fruit trees are likely to suffer from the effects of severe drought in the future; however, sound criteria for evaluating the species' ability to survive these extreme conditions are largely missing. Here, we evaluated the feasibility of using xylem cavitation resistance as a tool for screening Prunus species for drought resistance. Ten different Prunus species were selected to cover a large range of water requirements, from hydrophilic to xerophilic types. Shoot cavitation resistance was evaluated with the new Cavitron technique. At this inter-specific level, cavitation resistance was related to species drought resistance, with xerophilic species being less vulnerable to cavitation. The Cavitron technique enabled species characterization that required a short time and small amounts of plant material. This technique could be used to evaluate the drought resistance of a limited number of fruit tree genotypes. Genotype screening on a larger scale, however, would likely require another approach. Out of a number of anatomical traits tested, a significant correlation was found between cavitation resistance and inter-vessel wall thickness across species. This anatomical trait is, therefore, suggested as a possible alternative to direct cavitation estimates and could be included as a screening criterion in breeding programs for drought resistance of Prunus genotypes.     

Alarming β-lactamase-mediated resistance in multidrug-resistant Enterobacteriaceae

Resistance to β-lactams and other antibiotics in the Enterobacteriaceae is frequently associated with plasmidic resistance determinants that are easily transferred among species. β-Lactamase-mediated resistance is increasingly associated with plasmid-encoded extended-spectrum β-lactamases (ESBLs) and carbapenemases, specifically the CTX-M family of ESBLs, the KPC family of serine carbapenemases, and the VIM, IMP, and NDM-1 metallo-β-lactamases. Although clonal dispersion of resistant isolates was seen initially, more diverse genetic platforms are being observed as variations of mobile elements are transferred worldwide. These enzymes are now appearing in multiple combinations of ESBLs and carbapenemases, thereby conferring resistance to virtually all β-lactam antibiotics.     

Is flavivirus resistance interferon type I-independent?

Interferon type I comprises a group of major virus-inducible host antiviral factors that control infection with a great number of human and animal viruses. They are ubiquitously expressed cytokines that interfere with virus replication within different cell types by activating a number of host genes and several parallel antiviral pathways. Two major intracellular actors of IFN-I-induced antiviral states are ribonucleic acid-dependent protein kinase and 2'-5'-oligoadenylate synthetases/RNase L, both being induced by IFN-I and activated by viral double stranded ribonucleic acid. In addition, Mx proteins and ribonucleic acid-specific adenosine deaminase have also been implicated in IFN-I-induced antiviral responses to some RNA viruses. Viruses, in turn, have evolved different strategies to escape a control imposed by IFN-I and by IFN-I-induced antiviral factors. The fatal outcome of virus infection as well as the efficiency of IFN-I-based antiviral therapies in its prevention, are determined by complex interactions between viral virulence factors and cellular antiviral IFN-I inducible factors. In the light of these facts and current knowledge on IFN-I involvement in flavivirus infection, I discuss a possible role of IFN-I signalling in resistance to flavivirus infection in a model of congenic mouse strains that express different levels of susceptibility/resistance to common flaviviruses. Specifically, this review emphasizes importance of fully operative 2'-5'-oligoadenylate synthetases/RNase L pathway for the IFN-I-induced stimulation of flavivirus resistance conferred by Flv.     

Why should parasite resistance be costly?

Parasite resistance is sometimes associated with fitness costs. Costs of resistance are fundamentally important in epidemiology, and in the ecology and evolution of host-parasite interactions. The cost of resistance is often envisioned as the cost of re-allocating limiting resources to resistance machinery from other traits. This popular paradigm has resulted in a spate of research that assumes a fitness cost to resistance. We comment on this trend and propose a working framework of various resistance means and mechanisms. Within these means and mechanisms, we suggest that many are not likely to incur significant fitness costs.     

Three years of insecticide resistance monitoring in Anopheles gambiae in Burkina Faso: resistance on the rise?

ABSTRACT: Background and methods A longitudinal Anopheles gambiae s.l. insecticide-resistance monitoring programme was established in four sentinel sites in Burkina Faso. For three years, between 2008 and 2010, WHO diagnostic dose assays were used to measure the prevalence of resistance to all the major classes of insecticides at the beginning and end of the malaria transmission season. Species identification and genotyping for target site mutations was also performed and the sporozoite rate in adults determined. RESULTS: At the onset of the study, resistance to DDT and pyrethroids was already prevalent in An. gambiae s.l. from the south-west of the country but mosquitoes from the two sites in central Burkina Faso were largely susceptible. Within three years, DDT and permethrin resistance was established in all four sites. Carbamate and organophosphate resistance remains relatively rare and largely confined to the south-western areas although a small number of bendiocarb survivors were found in all sites by the final round of monitoring. The ace-1R target site resistance allele was present in all localities and its frequency exceeded 20% in 2010 in two of the sites. The frequency of the 1014 F kdr mutation increased throughout the three years and by 2010, the frequency of 1014 F in all sites combined was 0.02 in Anopheles arabiensis, 0.56 in An. gambiae M form and 0.96 in An. gambiae S form. This frequency did not differ significantly between the sites. The 1014 S kdr allele was only found in An. arabiensis but its frequency increased significantly throughout the study (P = 0.0003) and in 2010 the 1014 S allele frequency was 0.08 in An. arabiensis. Maximum sporozoite rates (12%) were observed in Soumousso in 2009 and the difference between sites is significant for each year. CONCLUSION: Pyrethroid and DDT resistance is now established in An. gambiae s.l. throughout Burkina Faso. Results from diagnostic dose assays are highly variable within and between rounds of testing, and hence it is important that resistance monitoring is carried out on more than one occasion before decisions on insecticide procurement for vector control are made. The presence of 1014 S in An. gambiae s.l., in addition to 1014 F, is not unexpected given the recent report of 1014 S in Benin but highlights the importance of monitoring for both mutations throughout the continent. Future research must now focus on the impact that this resistance is having on malaria control in Burkina Faso.     

Which came first: insecticides or resistance?

Mutations that confer resistance to insecticides are well documented. However, so far, we have been unable to determine whether these mutations arose before or after the introduction of insecticides. Recently, a landmark study showed that resistance to Malathion can be detected in pinned specimens of Australian sheep blowflies that were collected before the introduction of the insecticide. This finding has numerous implications for our understanding of the prevalence of resistance to new compounds. It also indicates that pre-existing resistance alleles might not carry the fitness cost that is associated with new mutations.     

Expression of pAMα1 tetracycline resistance gene inCorynebacterium glutamicum: Segregation of antibiotic resistance due to intramolecular recombination

Summary AnEscherichia coli/Corynebacterium glutamicum chimeric plasmid has been constructed containing the tetracycline resistance (Tc^R) determinant from pAM1 and the kanamycin resistant (Km^R) determinant from pBD10. The paAM1 tetracycline resistance determinant is expressed inC. glutamicum although the transformed population segregates readily into tetracycline and kanamycin resistant populations. The segregation event is the result of an intramolecular recombination between the pAM1 and pUB110 regions of the chimera.     

Is more better? Polyploidy and parasite resistance

Ploidy-level variation is common and can drastically affect organismal fitness. We focus on the potential consequences of this variation for parasite resistance. First, we elucidate connections between ploidy variation and key factors determining resistance, including allelic diversity, gene expression and physiological condition. We then argue that systems featuring both natural and artificially manipulated ploidy variation should be used to evaluate whether ploidy level influences host-parasite interactions.     

Do xylem fibers affect vessel cavitation resistance?

Possible mechanical and hydraulic costs to increased cavitation resistance were examined among six co-occurring species of chaparral shrubs in southern California. We measured cavitation resistance (xylem pressure at 50% loss of hydraulic conductivity), seasonal low pressure potential (P(min)), xylem conductive efficiency (specific conductivity), mechanical strength of stems (modulus of elasticity and modulus of rupture), and xylem density. At the cellular level, we measured vessel and fiber wall thickness and lumen diameter, transverse fiber wall and total lumen area, and estimated vessel implosion resistance using (t/b)(h)(2), where t is the thickness of adjoining vessel walls and b is the vessel lumen diameter. Increased cavitation resistance was correlated with increased mechanical strength (r(2) = 0.74 and 0.76 for modulus of elasticity and modulus of rupture, respectively), xylem density (r(2) = 0.88), and P(min) (r(2) = 0.96). In contrast, cavitation resistance and P(min) were not correlated with decreased specific conductivity, suggesting no tradeoff between these traits. At the cellular level, increased cavitation resistance was correlated with increased (t/b)(h)(2) (r(2) = 0.95), increased transverse fiber wall area (r(2) = 0.89), and decreased fiber lumen area (r(2) = 0.76). To our knowledge, the correlation between cavitation resistance and fiber wall area has not been shown previously and suggests a mechanical role for fibers in cavitation resistance. Fiber efficacy in prevention of vessel implosion, defined as inward bending or collapse of vessels, is discussed.     

Does glycoprotein IIB/IIIA resistance exist?

Platelet function testing is not embedded into routine clinical practice, because no optimal, easy, reproducible and multipathway platelet aggregation test can be accomplished in vitro. Only recently, the relationship between the level of platelet aggregation inhibition by platelet inhibitors and clinical outcome in acute myocardial infarction became more clear.1-5 High platelet reactivity was found in patients who experienced stent thrombosis, and patients with clopidogrel resistance were at increased risk of recurrent atherothrombotic events.1,2 Furthermore, in ST-elevation myocardial infarction (STEMI) increased levels of platelet aggregation were found compared with unstable angina or control patients.4 In a thrombolysis study, higher platelet receptor occupancy was coupled with better angiographic and electrocardiographic outcome.     

Can resistance against quorum-sensing interference be selected?

Quorum-sensing (QS) interference is a novel therapy to fight bacterial infections that, unlike conventional antibiotic treatments, is focused on reducing the damage caused by pathogens (virulence) rather than focused on inhibiting their growth. Given this ideal, it was predicted that this approach will be impervious to or at least much less prone to resistance in bacterial populations. However, recently, resistance mechanisms against well-characterized quorum quenchers (QQs) have been found in the laboratory as well as in clinical strains, demonstrating that the rise of resistance against these kinds of compounds is possible. Nevertheless, it has been argued that even if resistance mechanisms against QS interference exist, this fact does not guarantee that resistance will spread. In the present work, we discuss recent insights derived from the latest experiments to address this question. In addition, we explain how environmental conditions like the stress produced by the host immune system may influence the selection of resistance and eventually lead to the selection of QS interference-resistant bacteria in a clinical setting.     

Does multiple paternity influence offspring disease resistance?

It has been suggested that polyandry allows females to increase offspring genetic diversity and reduce the prevalence and susceptibility of their offspring to infectious diseases. We tested this hypothesis in wild‐derived house mice (Mus musculus) by experimentally infecting the offspring from 15 single‐ and 15 multiple‐sired litters with two different strains of a mouse pathogen (Salmonella Typhimurium) and compared their ability to control infection. We found a high variation in individual infection resistance (measured with pathogen loads) and significant differences among families, suggesting genetic effects on Salmonella resistance, but we found no difference in prevalence or infection resistance between single‐ vs. multiple‐sired litters. We found a significant sex difference in infection resistance, but surprisingly, males were more resistant to infection than females. Also, infection resistance was correlated with weight loss during infection, although only for females, indicating that susceptibility to infection had more harmful health consequences for females than for males. To our knowledge, our findings provide the first evidence for sex‐dependent resistance to Salmonella infection in house mice. Our results do not support the hypothesis that multiple‐sired litters are more likely to survive infection than single‐sired litters; however, as we explain, additional studies are required before ruling out this hypothesis.