Poultry litter is a good crude protein supplement for ruminants but must be treated to kill pathogens before feeding. Composting effectively kills pathogens but risks loss of ammonia due to uric acid degradation. The objectives of this study were to test the ability of tannins to reduce pathogens and preserve uric acid during poultry litter composting. In two experiments, poultry litter was mixed with phosphate buffer and distributed to 50-ml tubes (three tubes/treatment per sample day) amended with 1 ml buffer alone or buffer containing pine bark, quebracho, chestnut, or mimosa tannins. Treatments achieved 0.63% (wt/wt) quebracho, chestnut, or mimosa tannins in experiment 1, or 4.5% pine bark or 9% quebracho, chestnut, or mimosa tannins in experiment 2. Tubes were inoculated with a novobiocin- and nalidixic acid-resistant Salmonella typhimurium, closed with caps, and incubated at successive 3-day increments at 22, 37, and 42°C, respectively. In experiment 1, bacterial counts in contents collected on days 0, 6, and 9 revealed a treatment by day effect (p < 0.03), with the Salmonella challenge being 1.3 log10 CFU/g higher in quebracho-treated composts than in untreated controls after 6 days of composting. After 9 days of composting, Salmonella, wildtype Escherichia coli, and total aerobes in untreated and all tannin-treated composts were decreased by about 2.0 log10 CFU/g compared to day 0 numbers (3.06, 3.75, and 7.77 log10 CFU/g, respectively). Urea and ammonia concentrations tended (p < 0.10) to be increased in chestnut-treated composts compared to controls and concentrations of uric acid, urea, and ammonia were higher (p < 0.05) after 9 days of composting than on day 0. Despite higher tannin application in experiment 2, antibacterial effects of treatment or day of composting were not observed (p > 0.05). However, treatment by time of composting interactions was observed (p < 0.05), with quebracho- and chestnut-treated composts accumulating more uric acid after 24 h and 9 days of composting and chestnut-, mimosa- or quebracho-treated composts accumulating less ammonia than untreated composts. Results demonstrate that composting may effectively control pathogens and that tannin treatment can help preserve the crude protein quality of composting poultry litter.

The minimal effective dose of sodium chlorate as an intervention to reduce the carriage of pathogenic bacteria in food-producing animals has not been clearly established. The effect of low-level oral chlorate administration to ewes was assessed by comparing the diversity of prominent bacterial populations in their gastrointestinal tract. Twelve lactating crossed Pelibuey and Blackbelly-Dorper ewes (average body weight, 65 kg) were randomly assigned (four per treatment) to receive a control treatment (TC; consisting of 3 g of NaCl per animal per day) or one of two chlorate treatments (T3 or T9; consisting of 1.8 or 5.4 g of NaClO3 per animal per day, respectively). Treatments were administered twice daily via oral gavage for 5 days. Ruminal and fecal samples were collected daily, starting 3 days before and ending 6 days after treatment, and were subjected to denaturing gradient gel electrophoresis of the 16S rRNA gene sequence amplified from total population DNA. For ruminal microbes, percent similarity coefficients (SCs) between groups varied from 23.0 to 67.5% and from 39.4 to 43.3% during pretreatment and treatment periods, respectively. During the treatment period, SCs within groups ranged from 39.4 to 90.3%, 43.3 to 86.7%, and 67.5 to 92.4% for TC, T3, and T9, respectively. For fecal microbes, SCs between groups varied from 38.0 to 85.2% and 38.0 to 94.2% during pretreatment and treatment periods, respectively. SCs for fecal populations during treatment were most varied for TC (38.0 to 67.9%), intermediate for T9 (75.6 to 92.0%), and least varied for T3 (80.6 to 90.6%). Heterogeneity within and between groups provided no evidence of an effect of chlorate treatment on ruminal or fecal microbial populations.

The objective of this study was to evaluate the efficacy of oral sodium chlorate administration on reducing total coliform populations in ewes. A 30% sodium chlorate product or a sodium chloride placebo was administered to twelve lactating Dorper X Blackbelly or Pelibuey crossbred ewes averaging 65 kg body weight. The ewes were adapted to diet and management. Ewes were randomly assigned (4/treatment) to one of three treatments which were administered twice daily by oral gavage for five consecutive days: a control (TC) consisting of 3 g sodium chloride/animal/d, a T3 treatment consisting of 1.8 g of sodium chlorate/animal/d, and a T9 treatment consisting of 5.4 g sodium chlorate/animal/d; the latter was intended to approximate a lowest known effective dose. Ruminal samples collected by stomach tube and freshly voided fecal samples were collected daily beginning 3 days before treatment initiation and for 6 days thereafter. Contents were cultured quantitatively to enumerate total coliforms. There were no significant differences in total coliform numbers (log10 cfu/g) in the feces between treatments (P = 0.832). There were differences (P < 0.02) in ruminal coliform counts (log10 cfu/mL) between treatments (4.1, 4.3 and 5.0 log10/mL contents in TC, T3 and T9 Treatments, respectively) which tended to increase from the beginning of treatment until the 5th day of treatment (P < 0.05). Overall, we did not obtain the expected results with oral administration of sodium chloride at the applied doses. By comparing the trends in coliform populations in the rumen contents in all treatments, there was an increase over the days. The opposite trend occurred in the feces, due mainly to differences among rumen contents and feces in ewes administered the T9 treatment (P = 0.06). These results suggest that the low chlorate doses used here were suboptimal for the control of coliforms in the gastrointestinal tract of ewes.

Poultry litter, produced by intensive poultry production systems, is a potentially valuable crude protein feedstuff for ruminants if effectively treated to kill pathogens before feeding. Composting effectively kills pathogens but risks losses of ammonia during uric acid degradation. To test if hop extracts may help preserve uric acid concentrations during composting, 11-g portions of used wood chip litter (WCL, 88% dry matter) were treated with 6 mL water containing Galena or Chinook hop extracts to achieve 0.06 g of either extract/g WCL. Control WCL was treated with buffer alone. The WCL was distributed to 50-mL tubes (3 tubes/treatment), capped and incubated in Gas Pac jars for 8 days at 30oC, followed by 3 days at 37oC and an additional 2 days at 42oC to simulate a 13-day compost period. A repeated measures analysis of variance revealed a treatment by day interaction on uric acid (P &lt; 0.05), with concentrations being highest upon initiation of composting (41.9 ± 3.6 µmol/g), lowest on day 13 for the untreated compost (17.5 ± 9.2 µmol/g) and intermediate for Galena and Chinook hop-treated compost (28.0 ± 4.7 and 25.8 ± 0.8 µmol/g, respectively). Effects of treatment, day of composting or their interaction, however, were not observed (P &gt; 0.05) on concentrations of ammonia and urea, which averaged 1.2 ± 1.0 and 2.9 ± 0.6 µmol/g, respectively. As expected, an effect of day-of composting on survivability (P &lt; 0.05) of select bacterial populations was confirmed, with counts being decreased more than 3.0 log10 units after 13 days composting than on day 0 for enterococci, staphylococci, lactic acid bacteria, coliforms and total aerobes (6.7 ± 0.09, 9.0 ± 0.01, 5.8 ± 0.16, 5.9 ± 0.09 and 9,9 ± 0.06 log10 CFU/g, respectively). These results indicate that hops-treatment may help preserve crude protein within WCL during composting.