Sub-acute rumen acidosis (SARA)

 

(SARA) Sub-acute rumen acidosis is related to high levels of ruminal LPS. The lipopolysaccharides (LPS) cause inflammation and participate to different metabolic disorders and diseases. Different policies and solutions can be pragmatic to reduce the rumen microbiota and prevent this risk.

In sub-acute rumen acidosis (SARA), the amount of free lipopolysaccharides (LPS) coming from G-ve bacteria increases noticeably. These LPS pass the ruminal wall and intestine, passing into the circulation. The negative effects on the health of the animal are then revealed in decreased productive and reproductive performance.

The LPS are released during the lysis of G-ve bacteria which die due to the low pH, and these bacteria are mainly responsible for the production of propionic acid for the energy yield that is obtained. It is essential to preserve ruminal balance between G+ve & G-ve bacteria such that there is no excess of LPS.

Nutritional requirement for lactating cows effected with SARA:

During first phase of lactation (about 1 week after calving), the cow needs a high energy level to meet the large demand for milk production. This energy demand is often not fully satisfied and feed intake falls short. This shortage leads to the need to provide as much energy as possible per feed ration.

Suppose a 650 kg live weight cow, producing about 35 kg of milk per day with a fat percentage of 3.7 and a protein percentage of 3.2. To achieve this production level and fulfill its maintenance requirements, this animal needs a feed intake of 22 kg of dry matter (DM) per day, with an energy level of 21 UFL equal to 36,000 Kcal/day of NE l (Net Energy Lactation)).

To obtain an energy supply of this type, it is necessary to provide rations with a high content of cereals rich in nonstructured carbohydrates (NSC). This will allow the animals to obtain the maximum efficacy in getting the NE I from the metabolizable energy (ME) expressed as kl*.

*kl expresses the effectiveness in passing from EM to EN l net of the heat dissipated by the animal, therefore kl = ENl/EM (Van Es 1978).

Compared to a diet rich in NDF (Neutral Detergent Fiber), this type of diet promotes and stimulates certain strains of bacteria to the detriment of others, shifting the balance towards a greater population of bacteria that produce propionic acid instead those which produce acetic acid. This change also determines a greater share of Gram- compared to Gram+.

Definition of rumen acidosis:

Rumen acidosis is that “pathology” whereby the volume of SCFA (Short Chain Fatty Acids) produced by the rumen bacteria is greater than the ability of the rumen itself to absorb and neutralize them. Rumen acidosis is mainly caused by the amylolytic and saccharolytic bacterial flora (Streptococcus bovis; Selenomonas ruminantium, Bacteroides amylophilus, Bacteroides ruminicola and others) responsible for the production of lactic acid. Unlike the other most representative volatile fatty acids (acetic, butyric and propionic), lactic acid has a lower pKa: 7 (3.9 versus 4.7). This means that for the same amount of molecules produced, lactic acid releases a number of ions H+ in the fluid ten times greater than other AGVs, with evident effects on the pH.

Therefore we can define the Sub-Acute Rumen Acidosis (SARA) when the rumen pH falls below 5.6 for at least 180 minutes a day.

Effects of rumen acidosis:

In such situations, a series of negative consequences can be triggered in the lactating cow. Investigations (for instance, using fistulated cows) can reveal, among others, the following alteration in the rumen:

• Shift in total microbiome rumen profile (density; diversity; community structure)
• Shift in protozoa population (increase in ciliates protozoa after 3 weeks of SARA; increase in the GNB population)
• Shift in fungi population (decreasing the fungi population with high fibrolytic enzymes, which are sensitive to low pH)
• Rise in LPS rumen concentration (increasing the GNB strain and their lysis)
• Influence on the third layer of Stratified Squamous Epithelium (SSE) (desmosomes and tight junctions)
• Influence on ruminal fiber degradation (reduction in the number of cellulolytic bacteria which are less resistant to acid pH)
• Reduction of the total production of fatty acids (propionic, acetic, butyric), therefore less available energy
• Lower rumen motility (also as a consequence of the smaller number of protozoa)
• Greater hemoconcentration due to the greater osmotic pressure of the rumen area

The last point is extremely important, as it enables an easier passage of fluids from the blood to the pre-stomachs, greatly influencing the fermentation processes.

Furthermore, with diets low in NDF, the level of chewing and salivation is certainly lower, with a consequent lower level of salivary buffers that enter the rumen and which would maintain an appropriate pH under normal conditions.

Rumen acidosis: a rich place for LPS

In a trial conducted by Ametaj et al., R. Bras. Zootec. in 2010, as a function of lowering the rumen pH, we see an increase in the number of LPS in the rumen measured as ng / ml (nanograms / milliliter) of rumen fluid. This lowering of pH is directly proportional to the quantity of NSC present in the diet (% of grains) and inversely correlated with the increase in the quantity of LPS in the rumen.

Figure 1. The increase in the level of endotoxins in the rumen is directly correlated with an increase in ration concentrates

In the graph  below, note how many Gram bacteria are extremely influenced by the pH of the surrounding environment. In the rumen, the presence of Gram- bacteria is very significant. Many species of these bacteria are crucial for the production of SCFA and therefore of energy. 

 

Figure 2. Activity of main bacteria in the rumen in function of pH

It is therefore necessary to pay close attention to the energy level of the ration as an energy input (generally around 1500 – 1700 Kcal/kg of DM intake). At the same time, we need to ensure that the animal does receive and ingest that daily amount of DM. If ingestion is negatively influenced by acidosis (clinical or sub-clinical), this can lead to endotoxemia, with harmful consequences for the animal’s health and production performance.

We can therefore note that the level of LPS (endotoxins) present in the rumen is directly correlated with the pH of the rumen itself and with a symptomatologic picture dating back to SARA. This occurs when the mortality and lysis of Gram- bacteria is high and through the consequent imbalance created with diets containing excess fermentable starches, compared to diets with higher fiber content.

In fact, it was shown that the transition from a concentrated fodder ratio of 60:40 to a more stringent ratio of 40:60 caused the level of free LPS in the rumen to go from 410 to 4.310 EU / ml.

Effect on cow pathology when endotoxins enter in bloodstream

Once the LPS enter the bloodstream, they are transported to the liver (or other organs) for the detoxification. However, sometimes this is not enough to neutralize all the endotoxins present in blood. The remaining excess can cause issues such as the modification of the body’s homeostasis or cause that cascade of inflammatory cytokines responsible for the most common pathologies typical in cows in the first phase of lactation. The most common symptoms are the increase of somatic cells in milk or claws inflammation.

Pro-inflammatory cytokines as TNF, IL6 and IL8 induced by LPS-related inflammation are able to stimulate the production of ACTH (adrenocorticotropic hormone).

ACTH, together with cortisol and the interleukins, inhibit the production of GnRH and LH, with serious effects on milk production. The productivity and the fertility of the animal are thus compromised.

To this fairly impactful clinical picture we can also add the amount of prostaglandins (stimulated by LPS receptors) which are responsible for the increase in body heat (fever) and ruminal stasis (5).

A very important pathological picture linked to the presence of bacterial endotoxins is certainly the one that leads to puerperal metritis and clinical endometritis. In these pathological forms there is a massive presence in the uterus of Gram- such as E. coli, F. necrophorus, Bacteroides spp. and Prevotella spp, which massively release LPS.

Severe endotoxemia can also cause fetal abortion, however there is no evidence that endotoxemia as a consequence of SARA can lead to this problem.

Preventive measures of rumen acidosis

The solution to these massive risks is a prudent and proactive approach by the nutritionist towards all situations that can cause a rapid increase of Gram- in the rumen. It is therefore necessary to avoid cases of clinical and sub-clinical acidosis (SARA) in order to avoid the issues listed above. This would also help avoid stressful conditions for the animal that would lead to decreased performance and health.

To maintain balance and a healthy status of the animal, the use of additives such as toxin binders is suggested in the first phase of lactation, starting from 15 days before giving birth.