(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
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.
