Experimental oral administration of pollen beetle (Astylus atromaculatus) to cattle results in an acute lethal gastrointestinal disease.

In the summer of 2023, ingestion of Astylus atromaculatus (pollen beetle) was linked to spontaneous fatal disease in grazing cattle and sheep in Argentina and Uruguay. While the disease was experimentally reproduced in sheep and guinea pigs in the 1970's, no experimental reproductions have been attempted in cattle, and controversy exists as to whether this insect is indeed noxious to cattle and at which dose. Here, we demonstrate that A. atromaculatus causes acute fatal disease in Hereford calves at single oral dosages of 2.5, 4.5, 10.0, and 15.0 g of insect/kg body weight. Death or severe disease necessitating euthanasia occurred at 38 to 48 hours postinoculation regardless of the dose, suggesting that the single fatal dosage is likely <2.5 g/kg body weight (this dose representing approximately 850 mL of intact beetles in a 100 kg calf). Clinically, the disease was characterized by acute anorexia, prolonged recumbency, reluctance to move, listlessness/apathy, depression, ruminal hypomotility and tympany, hypothermia, bruxism with frothing at the mouth, and mucoid diarrhea progressing to death. Hematologic and biochemical alterations included hemoconcentration, stress/acute inflammatory leukogram, negative energy balance, and ketosis. The pathological hallmark of this experimental disease is acute necrotizing omaso-reticulo-rumenitis, fibrinohemorrhagic enteritis, and exfoliative colitis with intralesional chitinous insect fragments. While A. atromaculatus might contain a gastrointestinal toxin or pathogen, extensive toxicological testing failed to identify a causative toxin. Other pathomechanisms such as direct physical damage caused by insect fragments on the alimentary tract seem plausible, although further studies are needed to elucidate the pathogenesis of A. atromaculatus-associated disease.

Growth performance and rumen morphometrics of Nellore and ½ Angus/Nellore feedlot cattle adapted over 9 and 14 days to high-concentrate diets.

The objective of this study was to evaluate the effects of adapting Nellore and ½ Angus/Nellore (AN) feedlot cattle over periods of 9 and 14 days to high-concentrate diets on performance, feeding behaviour, carcass traits and rumen morphometrics. Seventy-two yearling bulls (313.5 kg ± 24.5), 36 Nellore and 36 AN, were randomly allocated in 24 pens (3 animals/pen; 24 m2 and 2.0 m of bunk space/animal) according to a randomized complete block design with a 2 × 2 factorial arrangement of treatments as follows: Nellore adapted for 9 days, Nellore adapted for 14 days, AN adapted for 9 days, and AN adapted for 14 days. Each treatment was composed by 6 pens (considered the experimental unit in this study). The adaptation lasted either 9 or 14 days and consisted of 3 step-up diets. Therefore, yearling bulls received the finishing diet containing 86% concentrate either on day 10 or 15 of the study, which lasted 89 days taking into account adaptation and finishing periods. Cattle were slaughtered in a commercial abattoir, and two 1-cm2 -rumen fragments, one from cranial and another from ventral sac, were collected. The AN cattle outperformed Nellore in terms of average daily gain (1.71 kg/day vs. 1.27 kg/day, p < 0.01), gain:feed ratio (0.137 kg/kg vs. 0.127 kg/kg, p = 0.02) and hot carcass weight (243.64 kg vs. 228.98 kg, p < 0.01). No main effect of the adaptation period was observed for any of the feedlot performance and carcass traits variables evaluated. Compared to feedlot cattle adapted for 9 days, feedlot cattle adapted for 14 days sorted against long (0.68 vs. 0.91, p < 0.01) and for fine particles (1.04 vs. 1.00, p = 0.01). An interaction (p < 0.01) of genotype and adaptation period was observed for rumenitis, where Nellore bulls adapted for 14 days presented the highest scores. In conclusion, there was no evidence that either Nellore or AN cattle benefit from an adaptation period shorter than 14 days.

Inflammatory mechanism of Rumenitis in dairy cows with subacute ruminal acidosis.

BACKGROUND: Subacute ruminal acidosis (SARA) is a metabolic disease in high-producing dairy cattle, and is accompanied by rumenitis. However, the mechanism of rumenitis remains unclear. Therefore, the aim of this study was to investigate the molecular mechanism of rumenitis in dairy cows with SARA. RESULTS: The results showed that SARA cows displayed high concentrations of ruminal volatile fatty acids, lactic acid and lipopolysaccharide (LPS). Furthermore, the blood concentrations of LPS and acute phase proteins haptoglobin, serum amyloid-A, and LPS binding protein were significantly higher in SARA cows than in control cows. Importantly, the phosphorylation levels of nuclear factor-kappaB (NF-κB) p65, inhibitor of NF-κB (IκB), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 1/2 (ERK1/2) were significantly higher in the rumen epithelium of SARA cows than those of control cows. The ruminal mRNA and protein levels of NF-κB- and mitogen-activated protein kinase (MAPK)s -regulated inflammatory cytokines, tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and interleukin 1ß (IL-1ß), were markedly higher in SARA cows than in control cows. Similarly, serum concentrations of TNF-α and IL-6 were also significantly higher in SARA cows. CONCLUSIONS: These results indicate that SARA results in high concentration of ruminal LPS, which over activates the NF-κB and MAPKs inflammatory pathways and then significantly increases the expression and synthesis of pro-inflammation cytokines in the rumen epithelium, thereby partly inducing rumenitis.

Pollen beetle (Astylus atromaculatus)-associated gastroenteric disease in cattle: report of 6 natural outbreaks.

Astylus atromaculatus is a pollen beetle native to South America, commonly found in crop flowers. Experimental intoxication of sheep and guinea pigs by this beetle resulting in fibrinonecrotizing enteritis has been reported. We describe here 6 natural outbreaks of intoxication in cattle associated with consumption of alfalfa (5 of 6) and mixed native (1 of 6) pastures heavily contaminated with A. atromaculatus. The outbreaks occurred during the summer (January-February) of 2023 in Argentina (n = 4) and Uruguay (n = 2), in beef cattle under extensive or semi-extensive rearing systems, with overall cumulative incidence and mortality of 22.3% and 17.8%, respectively. The main clinical signs included acute onset of anorexia, lethargy, hyperthermia, hindlimb weakness, reluctance to move, and diarrhea, for up to 15 d. In 2 outbreaks, sudden death was observed. Eight Hereford, Angus, and/or crossbreed heifers, cows, steers, and/or calves were autopsied. Gross and microscopic findings included multifocal necrosis with fibrinous pseudomembranes in the forestomachs and/or small and large intestines. Fragments or whole specimens of A. atromaculatus were identified in the ruminal content of all animals. Testing for multiple gastroenteric pathogens was negative as was testing of A. atromaculatus for cantharidin and batrachotoxin. GC-MS and LC-MS/MS performed on the beetles did not identify any known toxic compounds. Based on the exposure to A. atromaculatus-contaminated pasture, gross and microscopic lesions, and negative results of all testing for multiple gastroenteric pathogens, a diagnosis of intoxication by A. atromaculatus is proposed. Disease caused by A. atromaculatus consumption has not been reported previously in cattle, to our knowledge.

Development of an experimental model for liver abscess induction in Holstein steers using an acidotic diet challenge and bacterial inoculation.

Holstein steers (n = 40; initial BW = 84.9 ±â€…7.1 kg) were used to study the genesis of liver abscesses (LA) using an acidotic diet challenge with or without intraruminal bacterial inoculation. Steers were housed in individual pens inside a barn and randomly assigned to one of three treatments: (1) low-starch control diet comprised primarily of dry-rolled corn and wet corn gluten feed (CON); (2) high-starch acidotic diet with steam-flaked corn (AD); or (3) acidotic diet plus intraruminal inoculation with Fusobacterium necrophorum subsp. necrophorum (9.8 × 108 colony forming units [CFU]/mL), Trueperella pyogenes (3.91 × 109 CFU/mL), and Salmonella enterica serovar Lubbock (3.07 × 108 CFU/mL), previously isolated from LA (ADB). Steers in AD and ADB were fed the acidotic diet for 3 d followed by 2 d of the CON diet, and this cycle was repeated four times. On day 23, ADB steers were intraruminally inoculated with the bacteria. At necropsy, gross pathology of livers, lungs, rumens, and colons was noted. Continuous data were analyzed via mixed models as repeated measures over time with individual steer as the experimental unit. Mixed models were also used to determine the difference in prevalence of necropsy scores among treatments. Ruminal pH decreased in AD and ADB steers during each acidotic diet cycle (P ≤ 0.05). LA prevalence was 42.9% (6 of 14) in ADB vs. 0% in AD or CON treatments (P < 0.01). Ruminal damage was 51.1% greater in ADB than in AD (P ≤ 0.04). Culture of LA determined that 100% of the abscesses contained F. necrophorum subsp. necrophorum, 0% contained T. pyogenes, 50% contained Salmonella, and 50% contained a combination of F. necrophorum subsp. necrophorum and Salmonella. The F. necrophorum subsp. necrophorum was clonally identical to the strain used for the bacterial inoculation based on phylogenetic analysis of the whole genome. This experimental model successfully induced rumenitis and LA in Holstein steers and confirms the central dogma of LA pathogenesis that acidosis and rumenitis lead to the entry of F. necrophorum into the liver to cause abscesses. Our findings suggest that an acidotic diet, in conjunction with intraruminal bacterial inoculation, is a viable model to induce LA. Further research is needed to determine the repeatability of this model, and a major application of the model will be in evaluations of novel interventions to prevent LA.

Liver abscesses (LA) in feedlots are costly to the beef industry. At harvest, LA cause an increase in liver condemnations, carcass trimming, and a decrease in quality grade. The objective of this research was to develop an experimental LA model in Holstein steers using an acidotic diet with and without intraruminal inoculation of bacteria involved in LA formation. These data suggest acidotic diet challenges in conjunction with bacterial inoculation were able to induce LA in Holstein steers. The acidotic diet alone caused reduced rumen content pH and caused rumen wall inflammation and damage, observed at harvest. Nonetheless, the addition of bacteria had a compounding effect on rumen damage. Both bacteria inoculated were isolated from 57% of LA suggesting they may work in synergy to form LA.

Pathogenesis of Liver Abscesses in Cattle.

Liver abscesses are a bacterial infection, which occurs because of entry, via portal vein, of pyogenic bacteria into the hepatic parenchyma. Liver abscesses are a polymicrobial infection; however, Fusobacterium necrophorum, a ruminal bacterium, is the primary etiologic agent. Ruminal acidosis disrupts the protective barrier function of the ruminal epithelium and facilitates entry and colonization of F. necrophorum in the ruminal wall and subsequent entry into the portal circulation. Virulence factors of F. necrophorum contribute to the evasion of host defense mechanisms and cause tissue damage to set up an infection in the liver. The potential role of the hindgut in pathogenesis remains to be investigated.

Acute lead arsenate poisoning in beef cattle in Uruguay.

We describe and illustrate lesions in an outbreak of lead arsenate poisoning in beef cattle that ingested pesticide residues stored in an abandoned building of a former orange orchard. Of 70 exposed cattle, 14 had diarrhea, paresis, ataxia, recumbency, and/or seizures. Ten of the affected animals died after a clinical course of 12-18 h. Pathologic findings in 3 steers included extensive necrohemorrhagic, ulcerative rumenitis, omasitis, and abomasitis; lymphocytolysis in lymphoid organs; and nephrosis. Hepatic arsenic and lead levels in cases 1-3 were 20, 24, and 31 ppm, and 8.3, 25, and 9.4 ppm, respectively. Lesions in the forestomachs and lymphoid tissues have been rarely reported in cases of lead arsenate poisoning. In southern South America, these lesions are indistinguishable from those produced by Baccharis coridifolia, a toxic plant that contains macrocyclic trichothecenes, thus these conditions should be considered in the differential diagnosis of necrotizing lesions in alimentary and lymphoid organs.

Diagnosis and Treatment of Clinical Rumen Acidosis.

Clinical rumen acidosis is an important cause of morbidity and mortality in both large and small ruminants. Feeding and management practices that lead to the consumption of large amounts of readily fermentable carbohydrates precipitate clinical disease. The fermentation of carbohydrates into volatile fatty acids and lactate causes acidosis (local and systemic), rumen ulceration, cardiovascular compromise, and organ dysfunction. Animals affected with acidosis can suffer from numerous sequelae. Treatment of animals with clinical rumen acidosis is focused on addressing plasma volume deficits, correcting acid-base disturbances, and restoring a normal rumen microenvironment.