Autism is associated with gastrointestinal dysfunction and gut microbiota dysbiosis, including an overall increase in Clostridium. Modulation of the gut microbiota is suggested to improve autistic symptoms. In this study, we explored the implementation of two different interventions that target the microbiota in a rodent model of autism and their effects on social behavior: the levels of different fecal Clostridium spp., and hippocampal transcript levels. Autism was induced in young Sprague Dawley male rats using oral gavage of propionic acid (PPA) for three days, while controls received saline. PPA-treated animals were divided to receive either saline, fecal transplant from healthy donor rats, or Bifidobacterium for 22 days, while controls continued to receive saline. We found that PPA attenuated social interaction in animals, which was rescued by the two interventions. PPA-treated animals had a significantly increased abundance of fecal C. perfringens with a concomitant decrease in Clostridium cluster IV, and exhibited high hippocampal Bdnf expression compared to controls. Fecal microbiota transplantation or Bifidobacterium treatment restored the balance of fecal Clostridium spp. and normalized the level of Bdnf expression. These findings highlight the involvement of the gut–brain axis in the etiology of autism and propose possible interventions in a preclinical model of autism.

Autism spectrum disorders (ASD) consist of a range of neurodevelopmental conditions accompanied by dysbiosis of gut microbiota. Therefore, a number of microbiota manipulation strategies were developed to restore their balance. However, a comprehensive comparison of the various methods on gut microbiota is still lacking. Here, we evaluated the effect of Bifidobacterium (BF) treatment and fecal microbiota transplantation (FT) on gut microbiota in a propionic acid (PPA) rat model of autism using 16S rRNA sequencing. Following PPA treatment, gut microbiota showed depletion of Bacteroidia and Akkermansia accompanied by a concomitant increase of Streptococcus, Lachnospiraceae, and Paraeggerthella. The dysbiosis was predicted to cause increased levels of porphyrin metabolism and impairments of acyl-CoA thioesterase and ubiquinone biosynthesis. On the contrary, BF and FT treatments resulted in a distinct increase of Clostridium, Bifidobacterium, Marvinbryantia, Butyricicoccus, and Dorea. The taxa in BF group positively correlated with vitamin B12 and flagella biosynthesis, while FT mainly enriched flagella biosynthesis. In contrast, BF and FT treatments negatively correlated with succinate biosynthesis, pyruvate metabolism, nitrogen metabolism, beta-Lactam resistance, and peptidoglycan biosynthesis. Therefore, the present study demonstrated that BF and FT treatments restored the PPA-induced dysbiosis in a treatment-specific manner.

Autism spectrum disorder (ASD) is a progressively prevalent neurodevelopmental disorder with substantial clinical heterogeneity. Despite the considerable interest in dietary interventions, no consensus has been reached regarding the optimal nutritional therapy. The present study aimed to investigate the possible positive effect of goat’s milk (GM) compared to cow’s milk (CM) on ASD autistic features in a valproic acid (VPA; 600 mg/kg)-induced white albino rat model of autism. All tests were conducted on rats that were divided into four groups (n = 15/group): control with goat milk (GM) treatment, control with cow milk (CM) treatment, autistic with goat milk (GM) treatment, and autistic with cow milk treatment. The casein levels were also measured in GM and CM. Social behavior was assessed by three-chambered sociability to test social interaction after the intervention. After 15 days of intervention, selected biomarkers, such as glutathione (GSH), thiobarbituric acid reactive substance (TBARS), interleukin-6 (IL-6), neurotransmitter dopamine (DA), serotonin (5-hydroxytryptamine, 5-HT), and glutamate (GLU), were measured in blood serum and brain homogenates. The results showed a significant positive effect on social interaction in the VPA rat ASD model fed GM. Blood serum and brain samples showed a positive increase in TBARS in the VPA rat model fed GM, but brain and serum serotonin levels were lower in both VPA-GM and VPA-CM groups. Dopamine in serum was also lower in the VPA-CM group than in the VPA-GM group. IL-6 levels were slightly lower in the VPA-GM group than in the VPA-CM group. In comparison with cow’s milk, goat’s milk was effective in ameliorating the neurotoxic effects of VPA. Goat’s milk may be considered a suitable source of dairy for children diagnosed with ASD. Autistic children with allergies to cow’s milk could possibly convert to goat’s milk. Nevertheless, more in-depth studies and clinical trials are recommended.

Salmonella presents serious risks to human health, causing about 150,000 deaths per year through the consumption of contaminated food, especially chicken eggs. Consequently, risk of salmonellosis from chicken eggs is of significant interest to the Saudi Food and Drug Authority (SFDA). Models that predict the risk of salmonellosis from chicken eggs are valuable tools for protecting public health. After a review of existing models, the SFDA selected the Poultry Food Assess Risk Model (PFARM) for the purpose of evaluating its ability to assess the risk and severity of salmonellosis for a small cohort of chicken egg consumers in Riyadh, Saudi Arabia, as a proof-of-concept and pilot study. The PFARM was selected because it uses novel methods to consider more risk factors for salmonellosis than other models, such as growth potential and zoonotic potential of Salmonella, buffering capacity of the meal, and consumer behavior, health, and immunity. The SFDA examined chicken eggs from retail stores in Riyadh for Salmonella contamination and surveyed 125 consumers to obtain data for simulating how they store, prepare, and consume eggs at home, and their resistance to salmonellosis. The prevalence of Salmonella in chicken eggs at retail was 7% (7/100). The isolated Salmonella serotypes were Cerro (n = 4), Enteritidis, Stanley, and Winston. Salmonella’s mean number (growth units) per contaminated egg was 1.58 log₁₀ (range: 0 to 3.08 log₁₀). The mean category for consumer survey results ranged from 1.1 (very low risk) for meal preparation time to 3.7 (high risk) for home storage time with 34.4% of consumers having low resistance to salmonellosis. Per 100,000 egg meals, the PFARM predicted 88 infections, two illnesses, and no hospitalizations or deaths. The consumers who became ill were exposed to Salmonella Enteritidis, had moderate resistance to salmonellosis but high-risk behaviors for egg storage (temperature abuse), meal preparation (poor hygiene), and consumption (undercooked eggs). These results showed that the studied chicken eggs posed a low risk and severity of salmonellosis for the surveyed consumer cohort in Riyadh, Saudi Arabia, and that the PFARM was fit-for-purpose. The next step is to improve the PFARM and apply it more broadly in Saudi Arabia to better define the problem and its control.