I. Ruminal Acidosis c.

Pathogenesis
Ruminal acidosis has 2 forms, the Acute and
Subacute Ruminal Acidosis (SARA).
Acute and subacute forms of ruminal acidosis differ
in the severity of pH depression and the visibility of
clinical signs. Acute acidosis has a more severe pH
depression and more prominent clinical signs. This form
is commonly observed in feedlots. In contrast, SARA is
more common, with pH depression primarily caused by
the accumulation of volatile fatty acids alone, without a
significant contribution from lactic acid accumulation,
Normal rumen physiology
and is more frequently seen on dairy farms.
Stability of ruminal pH is maintained by the
rapid absorption of organic acids. Volatile fatty acids
a. Etiology
(VFAs) in the rumen are passively absorbed across the
SARA develops when ruminal buffering is not
ruminal wall. Passive absorption is enhanced by
adequate to contrast the volatile fatty acids (VFAs)
fingerlike papillae that project away from the rumen
production. This may be due to the following reasons:
wall. The length of these papillae increases when the
● Feeding cattle concentrated feeds, such as
animal is fed high-grain diets; increasing ruminal surface
fermentable grains
area and absorptive capacity, consequently protecting
● Switching rapidly from high forage to feed
against acid accumulation in the rumen.
with high concentrate
● Mechanisms by which animals resolve ruminal
● Feeding cattle a low-fiber diet
acidosis:
● The presence of mold and spores that
- Selecting long forage particles (preferential
produce mycotoxins in the body
feeding of long, dry hay or sorting through
mixed ration for longer forage)
b. Economic importance
- Decrease overall feed intake (may be mediated
Subacute ruminal acidosis is the most important
by pH/osmolality receptors or due to pain caused
nutritional disease in dairy cattle since it can negatively
by rumenitis)
impact the dairy industry by decreasing dry matter
intake, milk production, and profitability, and increasing
Subacute ruminal acidosis
culling rate and death loss
SARA occurs when ruminal pH falls below
5.8 (pH < 5.8) and remains below the threshold for over
3 hours within a 24-hour period. The bacterial species
decrease and ciliated protozoa populations in the rumen
are depleted, making the ruminal microflora less stable
and less able to maintain normal pH levels. Low acid
pH levels may lead to
laminitis, rumenitis, and erosion & ulceration of ruminal d. Clinical Findings
epithelium. Bacteria colonize the papillae and leak into ● Acute
portal circulation causing abscessation in the liver; - Often results in death
which eventually leads to peritonitis around abscessed - although illness and liver abscesses may be
areas. Damage to the ruminal epithelium may frequently
seen beforehand
be followed by fungal colonization resulting in mycotic
- Cattle may become depressed, go off feed,
rumenitis.
have an elevated heart rate, or have diarrhea.
If SARA is not corrected, it progresses into acute
● Subacute
ruminal acidosis.
- Reduced feed intake
- Poor body condition and weight loss
Acute ruminal acidosis
- Unexplained diarrhea
Carbohydrate fermentation in the rumen shifts to
- Pulse rate and respiratory rate may rise
lactate production at pH levels below 5.5 (pH < 5.5;
- Lethargy
range: 4.5 - 5.0) due to the proliferation of
- increased temperature
Streptococcus bovis.
As pH levels continue to decrease (pH < 4.5;
e. Diagnosis
range: 4.0 - 4.5) S. bovis population declines while D-
Rumenocentesis: consists of percutaneous needle
lactate synthesizing bacteria (Lactobacillus spp.)
aspiration of rumen fluid from the caudoventral rumen.
increases D-lactate production. An increase in lactic acid
The disadvantage associated with this method is that it is
and VFA subsequently increases oncotic pressure which
quite invasive, and can result in abscesses at the site of
increases water accumulation, leading to dehydration
puncture.
and diarrhea. Consequently, increased lactate production
Oral-Stomach Tube Technique: it is not considered
causes lactate-using bacteria (Megasphaera elsdenii
a reliable technique because pH may vary depending on
and Selenomonas ruminantium) to proliferate.
intra-ruminal localization, time of sampling in relation to
Normally, these convert lactate to VFAs that are easily
feeding, and saliva contamination.
protonated and absorbed. However, the turnover time of
lactate synthesizers is faster than lactate users, causing
f. Treatment
overproduction of D-lactate and continued pH decrease
Mild cases
which may lead to death.
● the affected animal should be removed from the
In cases of liver abscess rupture, caudal vena
source of the offending feed
cava syndrome is observed. Septic emboli released from
● provide a source of good-quality fiber
the abscesses travel through the caudal vena cava to the
● give an oral buffer such as magnesium oxide,
lungs where bacteria proliferate in lung tissue and
or sodium bicarbonate
ultimately invade pulmonary vessels. These vessels
rupture and cause massive pulmonary hemorrhage;
Severe cases
clinically manifested as hemoptysis and peracute death.
● intravenous fluid therapy
 ● emergency surgery may be necessary to
empty the rumen contents (Rumenotomy).
g. Control and Prevention
To prevent subacute ruminal acidosis (SARA), it
is crucial to enable the rumen to adapt to high-grain diets
and control the intake of easily fermentable
carbohydrates. This can be achieved through proper diet
formulation, ensuring a balance between fiber and non-
fiber carbohydrates, and maintaining excellent feed bunk
management. Even with well-formulated diets, animals
are still susceptible to SARA if they consume large
meals due to excessive competition for bunk space or
after periods of feed deprivation.
II. Rumen Alkalosis
Rumen alkalosis is an Indigestion resulting from
a change in pH of ruminal fluid exceeding 7.5 is referred
to as alkaline indigestion or ruminal alkalosis
(Vijayakumar et al., 2010). Alkaline indigestion occurs
usually due to excess and sudden intake of protein rich
feed, urea feeding, abrupt change of ration, drinking of
contaminated and sewage water and excessive feeding of
straw over a prolonged period of time (Misra and
Tripathy, 1963). Most of the times Soyabean meal is
commonly fed to dairy cows and growing cattle due to
its high energy and nitrogen content leading to alkalosis
(Sauvant et al., 2002).
A. Etiology
When there is excess production of ammonia,
the microbes cannot utilize it. But ammonia which is not
utilized for microbial synthesis is absorbed beyond the
gastrointestinal tract. The increased level of ruminal
ammonia
results in an increased rate of absorption (Huntington,
1986). The excess ammonia reaches the portal
circulation, is transported to the liver, and is converted to
urea. The urea is then excreted via the kidney through
urine or recycled into the rumen by way of saliva or
blood. As a result of an enormous intake of protein, there
will be an excessive accumulation of ruminal ammonia,
and nitrogen and a decrease in VFA leading to an
alkaline pH of ruminal fluid. Excessive alkaline pH will
inhibit ruminal contractions which can cause paresis of
rumen musculature. The paresis of rumen musculature
and high ruminal fluid pH bring about inappetence and
interfere with cellulose digestion (Chakrabarti, 2014).
Rumen alkalosis is caused by one of these reasons:
● Excess and sudden intake of protein-rich feed
● Urea feeding
● Abrupt change of ration
● Drinking of contaminated and sewage water
● excessive feeding of straw
B. Economic Importance
Ruminal Alkalosis importance is that it can
negatively impact the dairy industry by decreasing dry
matter intake, milk production, and profitability, and
increasing culling rate and death loss
C. Pathogenesis
Excess feeding of protein > In rumen excess production
of ammonia that the microbes cannot utilize > Non-
utilized ammonia for microbial synthesis, absorbed
beyond the GIT > The increased level of ruminal
ammonia > Increased rate of absorption > The
excess ammonia >
Reaches the portal circulation >transported to liver
> converted to urea.
F. Treatment
Urea > excreted via the kidney through urine or recycled
into the rumen by way of saliva or through blood. The primary cause should be treated and strictly follow
the correct dosage; a slight increase or decrease may
Urea = Excessive accumulation of ruminal ammonia, affect the animals' recovery.
nitrogen
● Use of different ruminal acidifiers for the

> Decrease in Volatile fatty acids (VFA) treatment of alkaline indigestion in cattle.
● 5 % Acetic acid in 250 ml water orally once a
>Alkaline pH of ruminal fluid day can be used
● 0.9% NS for chloride-responsive metabolic
>Inhibits ruminal contractions
alkalosis @ 50 – 100ml/hrs until urinary
>Cause paresis of rumen musculature chloride rises to > 25 mEq/L (> 25 mmol/L) and
urinary pH normalizes.
D. Clinical findings
● Underlying conditions are treated with the
The principal signs of alkaline indigestion include:
correction of hypovolemia and hypokalemia.
● For urgent correction of blood pH by
● Anorexia,
hemofiltration or hemodialysis is an option
● Moderate decrease in milk yield,
● Depression,
● Increased pulse and respiratory rate,
● Constipation & semi-solid or pasty feces,
● Hepatic, renal, circulatory, and nervous
disturbances
● The ruminal fluid color changed to khaki
brown
● Ruminal fluid consistency changed to
watery
● Decreased ruminal protozoan activity

E. Diagnosis

● Case history and clinical symptoms

● Laboratory findings as high blood pH,
bicarbonate with a low level of Co2
 Kumbhar, N. (2018). Occurrence, etiological studies and
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