No abstract

Aspergillus flavus and Aspergillus parasiticus are fungi that produce toxic secondary metabolites known as aflatoxins. These toxins can contaminate various food and feed products, including grains and nuts, before or after they are harvested. This contamination is most commonly found in tropical countries. Many studies have demonstrated that clay additions can reduce animal aflatoxin toxicity. The objective of this research was to study how the usage of Pacitan's local bentonite, located in East Java, Indonesia, could potentially decrease the harmful effects of aflatoxin B1 in native chicken species. The Masking Gel Calcification method was used to create bentonite nanoparticles at the Center for Ceramics in Bandung, West Java, Indonesia. The in vivo study was conducted at a native chicken farm in Bantul, Yogyakarta, Indonesia, with 1200 unsexed Kampung Unggul Balitbangtan (KUB) chickens. Kampung Unggul Balitbangtan chickens were divided into 4 treatments and 6 replications, each containing 50 chickens. The diets in the treatments were named as T0 (the control group in which chickens were fed basal diet, without aflatoxin B1), T1 ( T0 + 200 µg/kg aflatoxin B1), T2 (T0 + 200 µg/kg aflatoxin B1 + 1 g/kg Factory Feed with standard factory absorbent), and T3 (T0 + 200 µg/kg aflatoxin B1 + 1 g/kg nano bentonite). Aspergillus flavus isolates from PAU Universitas Gadjah Mada were created using crude aflatoxin (FNC 2262). This study found a significant difference in KUB chicken performance, specifically in feed conversion ratio (FCR). Compared to T0, the findings indicated that T1 had the highest FCR value, followed by T2 and T3. It can be concluded that nanoparticle bentonite has a looser structure because of decreased packing density with the lowest FCR. Based on hematology analysis, it can suppress aflatoxin B1 toxicity in KUB chickens.

Background and Aim: Staphylococcus aureus produces various superantigen exotoxins, including staphylococcal enterotoxin B (SEB). It causes fatal anaphylactic reactions and toxic shock. This study aimed to evaluate the reaction of leukocytes and histopathological changes in the respiratory organs of Balb/c mice after intranasal infection with enterotoxigenic S. aureus (SEB). Materials and Methods: The presence of the seb gene in S. aureus was established in this study using polymerase chain reaction-specific primer. Two groups of 8-week-old male Balb-c mice consist of six mice in each group. The treated group was infected with 50 μL and 100 μL of SEB intranasal on days 1 and 14, respectively. NaCl was administered in the second group and was considered as a control group. Blood samples were collected through the retro-orbital plexus on days 1, 4, 7, 14, and 22 after infections. Total cell counts were analyzed with an independent sample t-test and compared using the statistical package for the social sciences (SPSS) version 16.0 (IBM Corp., NY, USA). The infected tissues of the respiratory organ were observed descriptively and compared to the control group. Results: The seb gene with a molecular size of 478 bp, indicating the SEB strain, is present in S. aureus used in this study. Intranasal administration of SEB showed increased leukocytes, lymphocytes, monocytes, and eosinophils on day 22 post-infection. Significant leukocytosis was seen on days 6 and 14; lymphocytosis on days 1, 4, 6, and 16; and eosinophilia on days 6, 14, and 22 compared with the control group (p > 0.05). In contrast, the neutrophil decreased after an increase of immature band cells compared to the control group, indicating a severe acute infection with SEB. The lungs and trachea of the test group had an inflammatory cell accumulation in the respiratory organ. Conclusion: Intranasal route infection of S. aureus containing seb gene significantly induced the cellular immune response and caused pathological changes in the respiratory tissues of the Balb/c mice model. The hematological changes were aligned with marked pathological changes in the respiratory tract. Balb/c mice could be an excellent experimental model to study toxic and anaphylactic shock against SEB to define the future therapeutic agents.