The gut microbiome of bees is vital for the health of their hosts. Given the ecosystem functions performed by bees, and the declines faced by many species, it is important to improve our understanding of the amount of natural variation in the gut microbiome, the level of sharing of bacteria among co-occurring species (including between native and non-native species), and how gut communities respond to infections. We conducted 16S rRNA metabarcoding to discern the level of microbiome similarity between honey bees (Apis mellifera, N = 49) and bumble bees (Bombus spp., N = 66) in a suburban-rural landscape. We identified a total of 233 amplicon sequence variants (ASVs) and found simple gut microbiomes dominated by bacterial taxa belonging to Gilliamella, Snodgrassella, and Lactobacillus. The average number of ASVs per species ranged from 4.00-15.00 (8.79 ± 3.84, mean ± SD). Amplicon sequence variant of one bacterial species, G. apicola (ASV 1), was widely shared across honey bees and bumble bees. However, we detected another ASV of G. apicola that was either exclusive to honey bees, or represented an intra-genomic 16S rRNA haplotype variant in honey bees. Other than ASV 1, honey bees and bumble bees rarely share gut bacteria, even ones likely derived from outside environments (e.g., Rhizobium spp., Fructobacillus spp.). Honey bee bacterial microbiomes exhibited higher alpha diversity but lower beta and gamma diversities than those of bumble bees, likely a result of the former possessing larger, perennial hives. Finally, we identified pathogenic or symbiotic bacteria (G. apicola, Acinetobacter sp. and Pluralibacter sp.) that associate with Trypanosome and/or Vairimorpha infections in bees. Such insights help to determine bees\' susceptibility to infections should gut microbiomes become disrupted by chemical pollutants and contribute to our understanding of what constitutes a state of dysbiosis.

Tapeworm infection continues to be an important cause of morbidity worldwide. Recent metagenomics studies have established a link between gut microbiota and parasite infection. The identification of gut probiotics is of foremost importance to explore its relationship and function with the parasite in the host. In this study, the gut content of hosts infected with tapeworm Hymenolepis diminuta and non-infected host gut were disected out to determine their Lactic acid bacterial (LAB) population in MRS agar and microbial community was analysed by metagenomics. The bacterial count was calculated on a bacterial counting chamber and their morphology was determined microscopically and biochemically. Further, to determine the safety profile antibiotic resistance test, antimicrobial, hemolytic activity, and adhesion capability were calculated. We found six dominant probiotic strains and a decrease in LAB load from 1.7-2.3 × 107 CFU/mL in the uninfected group to a range of 8.4 × 105 CFU/mL to 3.2 × 105 CFU/mL in the infected groups with respect to an increase in the parasite number from 10-18. In addition, we found a depletion in the probiotic relative abundance of Lactobacillus and an enrichment in potentially pathogenic Proteobacteria, Fusobacteria, and Streptococcus. Phylogenetic analysis of the six probiotics revealed a close similarity with different strains of L. brevis, L. johnsonii, L. taiwansis, L. reuteri, L. plantarum, and L. pentosus. Thus, this study suggests that the parasite inhibits probiotic colonization in the gut during its early establishment of infection inside the host.

Anisakiasis is a parasitic disease caused by Anisakis simplex and has become an emerging zoonosis as preferences for eating raw or undercooked seafood have become more common. Few case reports of asymptomatic anisakiasis have been published to date. A 79-year-old asymptomatic man underwent esophagogastroduodenoscopy (EGD) for gastric cancer screening. The gastroenterologist diagnosed superficial gastritis without any malignant lesions but found an Anisakis larva while reviewing EGD images. The physician performed a second EGD and removed the larva. The patient reported that he ate the flatfish sashimi for dinner on the day before the first EGD. This case indicates the existence of asymptomatic gastric anisakiasis, indicating that anisakiasis incidence may have previously been underestimated.

The establishment of baseline data on parasites from wild primates is essential to understand how changes in habitat or climatic disturbances will impact parasite-host relationships. In nature, multiparasitic infections of primates usually fluctuate temporally and seasonally, implying that the acquisition of reliable data must occur over time. Individual parasite infection data from two wild populations of New World primates, the saddleback (Leontocebus weddelli) and emperor (Saguinus imperator) tamarin, were collected over 3 years to establish baseline levels of helminth prevalence and parasite species richness (PSR). Secondarily, we explored variation in parasite prevalence across age and sex classes, test nonrandom associations of parasite co-occurrence, and assess the relationship between group size and PSR. From 288 fecal samples across 105 individuals (71 saddleback and 34 emperor tamarins), 10 parasite taxa were identified by light microscopy following centrifugation and ethyl-acetate sedimentation. Of these taxa, none were host-specific, Dicrocoeliidae and Cestoda prevalences differed between host species, Prosthenorchis and Strongylida were the most prevalent. Host age was positively associated with Prosthenorchis ova and filariform larva, but negatively with cestode and the Rhabditoidea ova. We detected no differences between expected and observed levels of co-infection, nor between group size and parasite species richness over 30 group-years. Logistic models of individual infection status did not identify a sex bias; however, age and species predicted the presence of four and three parasite taxa, respectively, with saddleback tamarins exhibiting higher PSR. Now that we have reliable baseline data for future monitoring of these populations, next steps involve the molecular characterization of these parasites, and exploration of linkages with health parameters.

OBJECTIVE: LPS-responsive beige-like anchor protein (LRBA) deficiency is a combined immunodeficiency and immune dysregulation. The authors present a case report of LPSresponsive beige-like anchor protein (LRBA) deficiency with the history of autoimmunity, enteropathy and visceral leishmaniasis. Sirolimus therapy was started for autoimmunity and enteropathy but was discontinued due to recurrent leishmaniasis. Therefore, a common side-effect of many immunosuppressive drugs in patients with LRBA deficiency is increased susceptibility to infections.
METHODS: Whole exome sequencing was performed to detect the underlying genetic mutation and Leishmania DNA was detected by the PCR technique in this patient.
RESULTS: Whole exome sequencing of the patient reported a homozygous frameshift deletion mutation in the LRBA gene (NM_006726: exon29: c.4638delC, p. S1546fs). Leishmania DNA PCR was positive in this case.
CONCLUSIONS: Parasite infections manifestations report in LRBA deficiency. Leishmania infections in patients with chronic diarrhea and autoimmunity should be considered for immunodeficiency.

The goal of immunotoxicity testing is to obtain data useful for immunotoxicity safety assessment. Guidance in the performance of immunotoxicity safety evaluations is provided in documents from the US EPA for chemicals and the ICH S8 document for pharmaceuticals. The ICH S8 document outlines a tiered approach that includes (1) standard toxicity studies with associated hematology, immune system organ weights, and histopathology data; (2) functional assays, such as cytotoxic T lymphocyte (CTL) assays, natural killer (NK) cell assays, respiratory burst, phagocytosis, and T-cell-dependent antibody response (TDAR) assays; and (3) host resistance assays. Host resistance assays are considered the gold standard in immunotoxicity testing and provide a critical overview of the extent to which innate, adaptive, and homeostatic regulatory immune functions are integrated to protect the host. Both comprehensive and targeted host resistance assays are available, each with distinct advantages. This chapter serves to provide a general overview of the various assays that may be used, as well as a summary of procedures.

Genome editing by programmable nucleases represents a promising tool that could be exploited to develop new therapeutic strategies to fight infectious diseases. These nucleases, such as zinc-finger nucleases, transcription activator-like effector nucleases, clustered regularly interspaced short palindromic repeat (CRISPR)-CRISPR-associated protein 9 (Cas9) and homing endonucleases, are molecular scissors that can be targeted at predetermined loci in order to modify the genome sequence of an organism. Areas covered: By perturbing genomic DNA at predetermined loci, programmable nucleases can be used as antiviral and antimicrobial treatment. This approach includes targeting of essential viral genes or viral sequences able, once mutated, to inhibit viral replication; repurposing of CRISPR-Cas9 system for lethal self-targeting of bacteria; targeting antibiotic-resistance and virulence genes in bacteria, fungi, and parasites; engineering arthropod vectors to prevent vector-borne infections. Expert commentary: While progress has been done in demonstrating the feasibility of using genome editing as antimicrobial strategy, there are still many hurdles to overcome, such as the risk of off-target mutations, the raising of escape mutants, and the inefficiency of delivery methods, before translating results from preclinical studies into clinical applications.

In this study we show that four arginase isoforms (arg1a, arg1b, arg2a, arg2b) exist in rainbow trout (Oncorhynchus mykiss) and Atlantic salmon (Salmo salar). We have characterised these molecules in terms of a) sequence analysis, b) constitutive expression in different tissues, and modulated expression following c) stimulation of head kidney macrophages in vitro, or d) vaccination/infection with Yersinia ruckeri and e) parasite infection (AGD caused by Paramoeba perurans and PKD caused by Tetracapsuloides bryosalmonae). Synteny analysis suggested that these arginase genes are paralogues likely from the Ss4R duplication event, and amino acid identity/similarity analyses showed that the proteins are relatively well conserved across species. In rainbow trout constitutive expression of one or both paralogues was seen in most tissues but different constitutive expression patterns were observed for the different isoforms. Stimulation of rainbow trout head kidney macrophages with PAMPs and cytokines also revealed isoform specific responses and kinetics, with arg1a being particularly highly modulated by the PAMPs and pro-inflammatory cytokines. In contrast the type II arginase paralogues were induced by rIl-4/13, albeit to a lesser degree. Vaccination and infection with Y. ruckeri also revealed isoform specific responses, with variation in tissue expression level and kinetics. Lastly, the impact of parasite infection was studied, where down regulation of arg1a and arg1b was seen in two different models (AGD in salmon and PKD in trout) and of arg2a in AGD. The differential responses seen are discussed in the context of markers of type II responses in fish and paralogue subfunctionalization.

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