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Microscopic structure of the large intestinal mucosa in piglets during an antibiotic-associated diarrhea
Takamitsu Tsukahara1, Yoshie Iwasaki, Keizo Nakayama
1Laboratory of Animal Science, Kyoto Prefectural University, Shimogamo, Kyoto, Japan.
Abstract:
Antibiotic-associated diarrhea (AAD) is caused by the treatments of broad-spectrum antimicrobials that seriously affect the activity and composition of the large intestinal microflora. The pathogenic bacteria or low concentration of short-chain fatty acids (SCFAs) has been repeatedly discussed in relation to AAD. Recently, we reported the detection of a large amount of succinate and lactate in the diarrheal feces in AAD-induced piglets. In this study, we investigated histologically the large intestinal mucosa in AAD-induced piglets, in which succinate and lactate were accumulated. AAD was induced in the piglets by an oral dose of polymyxin B sulfate (PL) or by an intra-muscular injection of enrofloxacin (ERFX). When the piglets were defecating diarrheal feces with a high concentration of succinate and/or lactate, the large intestine was removed and separated into four segments (cecum, gyri centripetales, gyri centrifugales, and rectum). Healthy piglets were used as the control. In the AAD-induced piglets, the lamina propria was edematous in the gyri centripetales. Piglets treated with ERFX were also edematous in gyri centrifugales. These edematous lamina propria contained larger amounts of inflammatory cells than observed in control tissues. ERFX-treated piglets had a more shallow crypt than PL-treated and control piglets. The mucosal tissue of the large intestine was more seriously damaged in the ERFX- than in the PL-treated piglets, which might have been caused by the high succinate and low SCFAs concentration in the digesta.
Insights
Antibiotic-associated diarrhea (AAD) in piglets is linked to high succinate and lactate levels. Histological analysis revealed significant damage to the large intestinal mucosa, especially with enrofloxacin treatment.
Area of Science:
- Gastroenterology
- Microbiology
- Pathology
Background:
- Antibiotic-associated diarrhea (AAD) disrupts intestinal microflora.
- High succinate and lactate levels are observed in AAD.
- Pathogenic bacteria and low short-chain fatty acids (SCFAs) are implicated in AAD.
Purpose of the Study:
- To investigate the histological changes in the large intestinal mucosa of piglets with antibiotic-associated diarrhea (AAD).
- To correlate mucosal damage with high succinate and lactate accumulation in AAD-induced piglets.
Main Methods:
- AAD was induced in piglets using polymyxin B sulfate (PL) or enrofloxacin (ERFX).
- Large intestinal tissues were collected from diarrheal piglets and controls.
- Histological examination of the large intestinal mucosa (cecum, gyri centripetales, gyri centrifugales, rectum) was performed.
Main Results:
- Edema and increased inflammatory cells in the lamina propria of the gyri centripetales in AAD piglets.
- Enrofloxacin (ERFX)-treated piglets showed edema in gyri centrifugales and shallower crypts.
- More severe mucosal damage was observed in ERFX-treated piglets compared to PL-treated and control piglets.
Conclusions:
- High succinate and lactate concentrations, alongside low SCFAs, contribute to severe large intestinal mucosal damage in AAD.
- Enrofloxacin treatment appears to cause more significant histological damage than polymyxin B sulfate.
- Understanding these histological changes is crucial for managing AAD.