Pathogenic and mutualistic bacteria associated with eukaryotic hosts often lack distinctive genomic features, suggesting regular transitions between these lifestyles. Here we present evidence supporting a dynamic transition from plant pathogenicity to insect-defensive mutualism in symbiotic Burkholderia gladioli bacteria. In a group of herbivorous beetles, these symbionts protect the vulnerable egg stage against detrimental microbes. The production of a blend of antibiotics by B. gladioli, including toxoflavin, caryoynencin and two new antimicrobial compounds, the macrolide lagriene and the isothiocyanate sinapigladioside, likely mediate this defensive role. In addition to vertical transmission, these insect symbionts can be exchanged via the host plant and retain the ability to initiate systemic plant infection at the expense of the plant's fitness. Our findings provide a paradigm for the transition between pathogenic and mutualistic lifestyles and shed light on the evolution and chemical ecology of this defensive mutualism.

This study describes changes in haematological parameters, cytokine profile, histopathology and cortisol levels in Swiss mice experimentally infected with Angiostrongylus costaricensis. Twenty-eight Swiss mice were divided into two groups (G1 and G2) of 14 animals each. In each group, eight animals were infected orally with ten third-stage larvae of A. costaricensis and six were used as a control group. The mice of groups G1 and G2 were sacrificed 14 and 24 days after infection, respectively. Samples were collected for histopathological and haematological analyses and determination of the cytokine profile and cortisol levels. Granulomatous reaction, eosinophilic infiltrate and vasculitis in the intestinal tract, pancreas, liver and spleen were observed with varying intensity in infected animals. Our results showed that the mice developed normocytic and hypochromic anaemia, and that the histopathological lesions caused by the experimental infection influenced increases in cortisol, neutrophil and monocyte levels. In addition to this, we detected increased interleukin-6 and tumour necrosis factor alpha levels in the infected animals.

Abstract Abdominal angiostrongyliasis is caused by Angiostrongylus costaricensis, the definitive and intermediate hosts of which are wild rodents and terrestrial molluscs, respectively. Humans are accidental hosts and can be infected by ingesting the third-stage (infective) larvae (L3). It remains unclear whether the number of L3 inoculated is related to lesion severity. Our aim was to analyse histopathological alterations in Swiss mice infected with different doses of A. costaricensis. Thirty-two mice were randomly divided into four groups (n = 8/group): uninfected, control mice; mice infected with a low dose (five L3); mice infected with an intermediate dose (15 L3); and mice infected with a high dose (30 L3). The frequency of intestinal thrombi, splenitis, eggs/larvae, hepatic infarction and acute pancreatitis differed among the groups, the last being considered a significant finding. We conclude that different infective doses alter the histopathological aspects of the infection in Swiss mice, those aspects being more pronounced at medium and high doses, with no effect on the development of the disease. This experimental model shows that the parasite life cycle can be maintained in Swiss mice through the inoculation of a low dose (five L3).

Abdominal angiostrongyliasis is an endemic zoonosis in southern Brazil caused by the nematode Angiostrongylus costaricensis, which uses terrestrial molluscs as intermediate hosts and wild rodents as final hosts. Humans can be infected by ingesting infectious A. costaricensis larvae. To date, correlations between shedding of first-stage larvae (L1) and different infective doses of third-stage larvae (L3) have not been elucidated. The aim of this study was to assess L1 faecal shedding levels in Swiss mice experimentally infected with different doses of A. costaricensis L3 and to determine whether infective doses are related to mortality. Thirty-two male Swiss mice were divided evenly into a non-infected control (NI-Con); low-dose infection (LD-Inf); medium-dose infection (MD-Inf) and high-dose infection (HD-Inf) groups infected with 0, 5, 15 and 30 A. costaricensis L3, respectively. Faecal samples were collected from each animal, starting at day 20 post infection. HD-Inf mice had greater faecal L1 shedding levels than LD-Inf mice, but not a significantly shortened survival. In conclusion, infective doses of A. costaricensis L3 affect L1 shedding levels without altering mortality in Swiss mice.

This study describes changes in oxidative stress (OS) parameters in mice experimentally infected with Angiostrongylus costaricensis, which causes abdominal angiostrongyliasis. For this, 28 Swiss mice were used, divided into two groups (G1 and G2), with 14 animals each. Of these, eight were infected with ten infective larvae each, by gavage, and six were used as a control group. Mice from G1 and G2 were euthanized at 14 days and 24 days post-infection, respectively. Tissue samples were used for histopathological analysis and blood (serum) samples were taken to assess the levels of proteins, non-protein thiols (NPTs) and nitric oxide (NO), from centrifugation and subsequent collection of aliquots of the supernatant. Among OS parameters, infected mice in both groups had higher NO levels than the control group, due to the presence of: eosinophil infiltrate in the liver and intestine; pancreatitis; and intestinal granuloma. However, the infected mice of both groups showed a reduction in the levels of NPTs, in relation to the control group, due to the presence of: eosinophilic infiltrate in the liver and intestine; and intestinal granuloma. Our results suggest that A. costaricensis infection has important effects on the intestine, liver and pancreas, and the analyses were performed from the tissue of these organs. The mechanisms for these changes are related to the decrease in the body's main antioxidant defences, as demonstrated by the reduction of NPTs, thus contributing to the development of more severe tissue damage. Thus, the objective of the present study was to evaluate the relationship between histopathological lesions and markers for OS.