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.

Feed Mill Capacity Calculations

Silo Capacity Calculator
Silo Capacity = 𝝅 𝟒 × D2h × Stocking Density OR = 𝝅 r2*h
D= Diameter,
r= radius
h= Height


Elevator Capacity (tons/hour) Calculator
Elevator Capacity= 𝝅𝑫𝑽𝑪 ×𝟔𝟎 𝟏𝟎𝟎𝟎*𝑺

D= Pulley diameter (inches)
V= elevator rpm
C= Capacity of one bucket
S= distance between 2 buckets (inches)


Conveyer Capacity (Tons/hour Calculator
Elevator Capacity = 𝑳×𝑾×𝑯×r𝒑𝒎×𝟔𝟎 /𝟏𝟎𝟎𝟎
L= Length
W= Width
H= Working height


Elevator or Conveyor rpm Calculator
rpm= 𝑮𝒆𝒂𝒓 𝒓𝒑𝒎 ×𝑨/ 𝑩
A= No. of cog teeth attached with gear
B= No. of cog teeth attached in opposite direction of A

When choosing the boilers, please pay attention to the capacity of the boiler , the amount of steam required must be not les than 6% of pellet mill

Managemental Diseases in Poultry Part 1

 There are different managemental diseases in Poultry. we will discuss these diseases step by step.

Ventral Prolapse

Egg Bound

Vent Pecking

Ventral Prolapse:

Ventral prolapse is (also known as Oviduct Prolapse, Blowout, Cloacal Prolapse and Pick out) a condition in which lower part of hen's oviduct turns inside out and protrudes through the vent. Prolapse is very serious condition that can be treated if diagnose early, but is likely to recur. 

Causes:

1.   Imbalance Weight:

Under Weight Birds:

    Birds with smaller BW during 3-6 weeks of age, upon reaching maturity have smaller skeletal frame, smaller cloacal diameter. when egg is laid the hen exerts force due to which injuries occur in cloacal muscles. Oviduct come out of cloaca and fail to retract. sometimes oviduct is also accompanied by intestines.

Overweight Birds:

    Overweight in 10-15 weeks of age when photo-stimulated produce larger eggs than the standard. this leads to rupture of cloacal muscles and results in prolapse.

2. Over Photo-stimulation:

    Birds at 13-15 weeks are over photo-stimulated by high intensity and longer duration particularly in under weight birds. Instead of multiple increments of short periods of light duration more light is given in short time. The birds body weight lags its egg production and narrow cloaca is inflicted with injuries leading to Prolapse. 

High light intensity more than 50 lux in open sided houses. More than 15 lux in light-controlled houses also causes Ventral Prolapse. 

3. High Energy High Protein Feed:

    Egg production and size develops at faster rate and larger eggs lead injuries to the cloacal muscles causing Prolapse.

4. Minerals and Vitamin Deficiency:

Calcium Deficiency (Calcium Tetany):

    Birds come into production at a faster rate and lower feed intake causes Ca deficiency in birds. It leads to contraction of cloacal muscles (Ca Tetany). Lesser dilation of cloacal muscles results in injuries and tears of cloacal wall leading to prolapse.

Vit. D3, Phosphorus Deficiency:

    Leads to lesser absorption of Ca.

Prevention and Treatment:

1. Do not overstimulate the birds by increased light duration and intensity.

2. Maintain the BW as per standards of Breed particularly in 3-6 week of age.

3. Do not overweight the birds from 12-16 weeks of age.

4. Provide extra Calcium during peak production. 

5. Do not give high protein high energy feed during production.

A Review about different clays as toxin Binders

 

There are different types of clays like Bentonite, Clinoptilolite, Kaolinite etc. in the market, which are used as toxin binders. Each caly binds aflatoxins and some ochratoxins. But each clay has its own properties and drawbacks.

In this blog we will study the properties and flaws of all clays which are used in the industry as toxin binder.

Bentonite:

Bentonites are the clay rocks altered from glassy igneous material such as a volcanic ash or tuff. Bentonites have been used as palletizing iron ores, foundry bond clay, ceramic, drilling mud, sealant, animal feed bond, bleaching clay, agricultural carrier, cat box adsorbent, adhesive, catalyst and catalyst support, desiccant, emulsion stabilizer, cosmetic, paint, pharmaceutical, civil engineering, clay organoclay and polymer-clay nanocomposites.

    Bentonites are greatly affected from the acid activation, ion exchange, heating and hydrothermal treatments, and some other physicochemical processes. For example, physicochemical properties such as strength, swelling, plasticity, cohesion, compressibility, particle size, cation-exchange capacity, pore structure, surface area surface acidity and catalytic activity as well as the mineralogy can change considerably by modifications.

    Commercial importance of bentonites depends on the contents of their clay and nonclay minerals. Dominant clay minerals in bentonites are smectites such as montmorillonite, beidellite, saponite, nontronite and hectrorite. Bentonites are seldom found as monomineralic clays and may contain other clay and nonclay minerals and also some organic impurities.

Structures of Smectite:

    Smectite is a 2:1 layer clay mineral and has two silica tetrahedral bonded to a central alumina octahedral (O) sheet as seen in Fig. 2:

    The net negative charge of the 2:1 (TOT) layers arising from the isomorphic substitution in the octahedral sheets of Fe²⁺ and Mg²⁺ for Al³⁺ and in tetrahedral sheets of Al³⁺ for Si⁴⁺ is balanced by the exchangeable cations such as Na⁺, and Ca²⁺ located between the layers and around the edges. The mineral is called Na- smectite (NaS) or Ca-smectite (CaS) corresponding to the exchangeable cation which in Na⁺ or Ca²⁺. Industrial bentonites predominantly contain either Na-montmorillonite or Ca-montmorillonite. The equivalent amount of exchangeable cations in one kilogram smectite as well as other clay minerals and clays is defined cation exchange capacity (CEC).

Swelling:

                The physical state of smectite and corresponding bentonite may be changed with increasing water content, from anhydrous solid to a hydrated material, semi-rigid plastic, gel and suspension respectively.

                The change in the physical state of a bentonite from an anhydrous solid to gel is called swelling. The swelling of smectites occurs between the 2:1 (TOT) layers in agglomerated particles.

Porous Structure:

Smectites are porous clay minerals. The voids in a solid located amoung and within particles are caleed pore. The shape of the pores having different sizes can be cylindrical, parallel-sided slit, wedge, cavity and ink-bottle.

Adsorption Non-Polar Molecules:

                Smectites and other clay minerals do not adsorb non-polar molecules such as nitrogen, argon and ethane at elevated temperatures. These molecules can be adsorbed on smecitites at their liquefaction temperatures but cannot penetrate between the 2:1 (TOT) layers.

Adsorption Polar Molecules:

    A montmorillonite consists of 15-20 elements. Between the different elements, there are cations (next to crystal water), which are easy to be exchanged by other cations or positively charged molecules.

The cation exchange capacity (CEC Value) describes the capacity of clay minerals to exchange cations.

 

Clinoptilolite (Zeolite):

    Clinoptilolite is a natural zeolite composed of a microporous arrangement of silica and alumina tetrahedral. Among a high number of natural zeolites, clinoptilolite is best known. Zeolites are classified as tectoaluminosilicates with large pores and channels in the structures containing loosely bound water molecules (so called zeolite water) and alcalic cations (Na⁺, K⁺, Li⁺ Cs⁺, Ca²⁺, Mg²⁺, Ba²⁺, Sr²⁺). They can selectively adsorb gas and steam molecules, reversibly adsorb and desorb water, or based on ion selectivity they can exchange own cations for other ones.

     Zeolites are also used as effective adsorbents of toxic agents, particularly aflatoxins from the feed. They effectively minimize adverse effects of aflatoxins on feed intake, performance and nutrient conversion, and reduce mycotoxin concentration in the livers of affected animals. A lower concentration (15g/kg) of zeolite in the diet seems more effective than a higher concentration (25g/kg) as it was describe by Oguz snf Kurtoglu.

    Zeolite supplemented diets are well tolerated by the animals; they support biomas production and improve the health status of the animals.  Clinoptilolite in the diet of layer hens (50g/kg) increased the number of laid eggs, stability of eggshell and efficiency of food utilization; however, neither the onset of the egg lay cycle, nor egg weight were affected (Olver, 1997).

Kaolin:

    Kaolin is a plastic raw material, particularly consisting of the clay mineral kaolinite. The chemical formula is Al₂O₃.2SiO₂.2H₂O (39.5% Al₂O₃, 46.5% SiO₂, 14.0% H₂O). Kaolinite ranks among phyllosilicates, are classified into the main groups according to the type of the layers, interlayer content, charge of the layers and chemical formulas.

Structure of Kaolinite clay

Physical Properties:

                The 1:1 platelets of kaolinite are held together strongly via hydrogen bonding between the OH of the octahedral layer and the O of the tetrahedral layer. Due to this strong attraction these platelets do not expand when hydrated and kaolinite only has external surface area. Also, kaolinite has very little isomorphic substitution of Al for Si in the tetrahedral layer. Accordingly, it has a low cation exchange capacity. Kaolinite easily adsorbs water and forms a plastic, paste-like substance.

Happy Teachers Day

 

Bovine Ephemeral Fever (Three Days Sickness Disease)

 

Three Days Sickness Disease

Key Points

• Bovine ephemeral fever is a disease of cattle and water buffalo caused by a rhabdovirus and transmitted by flying, biting insects.

• Because of the inflammatory nature of the disease, NSAIDs are very effective at relieving clinical signs and pain.

• Vaccine effectiveness varies. Inactivated vaccines provide only short-term immunity and should be administered at least three times to gain some effectiveness in prevention of clinical signs.

Bovine ephemeral fever (also known as 3 days sickness disease) is an arthropod-borne viral disease of cattle and water buffalo that causes milk production losses, recumbency, and sometimes death.

Bovine ephemeral fever is an insect-transmitted, noncontagious, viral disease of cattle and water buffalo that is seen in Africa, the Middle East, Australia, and Asia. Inapparent infections can develop in Cape buffalo, hartebeest, water-buck, wildebeest, deer, and possibly goats, sheep, and gazelles. Low levels of antibody have been recorded in several other antelope species, giraffe, and even in pigs and elephants, but the specificity has not been confirmed.

Etiology and Epidemiology

Bovine ephemeral fever virus (BEFV) is classified as a member of the genus Ephemerovirus in the family Rhabdoviridae (single-stranded, negative sense RNA). The virus is ether-sensitive and readily inactivated at pH levels below 5 and above 10. Although BEFV is considered to exist as a single serotype worldwide, antigenic variation has been demonstrated by cross-neutralization tests, monoclonal antibody panels, and epitope mapping. Several closely related ephemeroviruses (including Berrimah virus, Kimberley virus, Malakal virus, Adelaide River virus, Obodhiang virus, Puchong virus, Kotonkan virus, Koolpinyah virus, and Mavingoni virus) have been identified. However, of these, only Kotonkan virus (isolated in Nigeria) has been associated with clinical ephemeral fever in cattle.

BEFV can be transmitted from infected to susceptible cattle by IV inoculation; as little as 0.005 mL of blood collected during the febrile stage is infective. To date, infection by virus obtained from virus culture has never succeeded. Although the virus has been recovered from several Culicoides species and from anopheline and culicine mosquito species collected in the field, the identity of the major vectors has not been proved. Transmission by contact or fomites does not occur. The virus does not appear to persist for long periods in recovered cattle, though it was detected in lymphoid tissue one week after cessation of viremia. Infection results in long term immunity.

The prevalence, geographic range, and severity of the disease vary from year to year, and epidemics occur periodically. During epidemics, onset is rapid; many animals are affected within days or 2–3 weeks. Bovine ephemeral fever is most prevalent in the wet season in the tropics and in summer to early autumn in the subtropics or temperate regions (when conditions favor multiplication of biting insects); it disappears abruptly in winter. Virus spread appears to be associated with winds and transportation of animals. Morbidity may be as high as 80%; overall mortality is usually 1%–2%, although it can be higher in lactating cows, bulls in good condition, and fat steers (10%–30%). However, reported overall mortality rates have exceeded 10% in outbreaks in several countries in recent years.

Clinical Findings

Bovine Ephemeral fever signs occur suddely and vary in severity, which include:

• biphasic to polyphasic fever (40°–42°C [104°–107.6°F])

• shivering

• inappetence

• tearing

• serous nasal discharge

• drooling

• pulmonary emphysema

• increased heart rate

• tachypnea or dyspnea

• atony of forestomachs

• depression

• stiffness and lameness

• a sudden decrease in milk yield

Clinical signs are generally milder in water buffalo. Affected cattle may become recumbent and paralyzed for 8 hours to >1 week. After recovery, milk production can fail to return to normal levels until the next lactation. There are anecdotal reports of abortions. This might be an indirect consequence of the disease, because the virus does not appear to cross the placenta or affect the fertility of the cow. Apparently, bulls, heavy cattle, and high-lactating dairy cows are the most severely affected, but spontaneous recovery usually occurs within a few days. More insidious losses may result from decreased muscle mass and lowered fertility in bulls.

Lesions

Bovine ephemeral fever is an inflammatory disease. The most common lesions include:

• polyserositis affecting pleural, pericardial, and peritoneal surfaces

• serofibrinous polysynovitis, polyarthritis, polytendinitis, and cellulitis

• focal necrosis of skeletal muscles

Histomorphologic abnormalities in peripheral nerves and brain have been detected as well. Generalized edema of lymph nodes and lungs, as well as atelectasis, also may be present.

Diagnosis

• Clinical signs

• PCR identification of the virus

Diagnosis of bovine ephemeral fever is based almost entirely on clinical signs in an epidemic. Whole blood should be collected from sick and apparently healthy cattle in affected herds and must be sufficient to provide two air-dried blood smears, 5 mL of whole blood in anticoagulant (not EDTA), and ~10 mL of serum. A differential WBC count on blood smears can either support or refute a presumptive field diagnosis. The majority of clinical cases have a neutrophilia with the presence of many immature forms, although this is not pathognomonic. Plasma fibrinogen rises on the day of peak fever and remains elevated for at least 7 days. Hypocalcemia may occur one day after fever onset.

Timely laboratory confirmation is mostly performed by PCR and rarely by virus isolation. Serum neutralization is diagnostic in retrospect. A 4-fold rise in antibody titer between paired sera collected 2–3 weeks apart confirms infection.

Virus is best isolated by inoculation of mosquito (Aedes albopictus) cell cultures with defibrinated blood, followed by transfer to baby hamster kidney (BHK-21 or BHK-BSR) or monkey kidney (Vero) cell cultures after 15 days. Suckling mice may also be used for primary isolation by intracerebral inoculation. Isolated viruses are identified by PCR and sequencing, neutralization tests using specific BEFV antisera, and ELISA using specific monoclonal antibodies.

Treatment and Control

• NSAIDs

• Supportive care for recumbent cows

Complete rest is the most effective treatment for bovine ephemeral fever, and recovering animals should not be stressed or worked because relapse is likely. Anti-inflammatory drugs given early and in repeated doses for 2–3 days are effective. Oral dosing should be avoided unless the swallowing reflex is functional. Signs of hypocalcemia are treated as for milk fever. Antibiotic treatment to control secondary infection and rehydration with isotonic fluids may be warranted.

There is conflicting evidence regarding the effectiveness of the commercially available attenuated or inactivated BEFV vaccines. Although an attenuated BEF vaccine showed high effectiveness in Australia, reports from other countries indicate lower effectiveness of the same vaccine. Inactivated virus vaccines have not produced longterm protection against experimental challenge with virulent virus and cannot guarantee lasting immunity. In field studies, they were 50% effective only after at least three vaccinations. Although a subunit vaccine that protects against field and laboratory challenge has been described, it is not commercially available. The efficacy of vector control remains uncertain, because the insect vectors have not been fully identified. There is no evidence that people can be infected.