Diseases of the forestomach, inappetence

Question 1

Normal temp. of dairy cattle?

Answer 1

38-39.2’C

(upper limit varies by source)

39.3’C and up is fever

Question 2

Rumen motility can be (3)

Answer 2

increased (hypertony)
decreased (hypotonic)
or absent

Question 3

Normal heart rate for cattle?
Brady?
Tachy?

Answer 3

normal 60-80 beats per min

brady <50
tachy >90-100

Question 4

Normal range of rumen contractions on auscultation?

Answer 4

1-2 contractions in 1 min

Question 5

Cow clinical examination (and anamnesis) should include: (10)

Answer 5

• General condition - fever; heart rate, respiratory rate (observed, not necessarily counted exactly).
• Rumen motility (increased, decreased or absent).
• Rumination activity
• Milk yield (normal or decreased rapidly or slowly)
• Depressed, anorexia
• Obvious distensions of abdomen - left side, right side, both.
• Symptoms of pain and discomfort. Signs of colic.
• Dehydration, mucous membranes
• Feces, defecation process. Diarrhea or scant feces.
• Rectal examination

Question 6

Distention on both left and right sides?

Answer 6

vagus nerve paralysis/
vagal nerve syndrome/
chronic Indigestion Syndrome in Ruminants

Hoflund`s syndrome

Question 7

Answer 7

distension of right side

displaced abomasum, can be with torsion

Question 8

calf with distended right side could indicate…?

Answer 8

abomasal or mesenterial torsion
or abomasal bloat
or intestinal obstruction

Question 9

Indigestion is a common term for

Answer 9

disturbances of the forestomach/s

Question 10

Failure of reticulo-rumen contractions can be seen in…? (4)

Answer 10

Rumen tympany

Traumatic reticuloperitonitis

Vagal nerve paralysis (Hoflund`s
syndrome)

Obstructions

Question 11

Failure of microbial fermentation can be seen in…? (4)

Answer 11

• Simple indigestion
• Rumen acidosis
• Rumen alkalosis
• Rumen parakeratosis

Question 12

Ruminal tympany or bloat is an overdistention of the ruminoreticulum, because cow is not able to eliminate gas from rumen. This is a problem of
eructation!

Explain the two types.

Answer 12

• primary or frothy bloat: a persistent foam mixed with the ruminal contents
• secondary or free-gas bloat:
  free gas separated from the ingesta (often esophageal obstruction involved: potatoes, apples etc.)

Question 13

Bloat can occur on any forage that is low in fiber and high in

Answer 13

protein, but is most common on immature legume pastures (clover, alfalfa etc.). Especially frosty pastures because the extra water content makes the feed digest too faster.

Fermentation activity increases and leads to formation of gas-bubbles and slime get stuck in the rumen content due to saponins.

Question 14

Typical cause of frothy bloat?

Answer 14

too rapid fermentation in rumen due to composition of pasture

or e.g. improper milk feeding techniques, rapid ingestion of milk, or bacterial fermentation in the abomasum in calves.

Question 15

Typical cause of secondary bloat in addition to esophageal obstruction?

Answer 15

hypotony due to parturient paresis and hypocalcemia, or even sedation (in both, contractions are altered as well as potential for obstruction due to positioning - put them on their chest!)

or rumen won’t contract adequately due to other disease process which then causes secondary bloat.

Question 16

How exactly does ruminal tympany kill?

Answer 16

Sudden death due to rupture of diaphragm.

Question 17

Treatment of bloat.

Answer 17

• Walk the cow briskly.
• Massage rumen via flank and give cold water.
• Administration of vegetable/mineral oil 1-2 litre
• Promotion of saliva production - tie a stick in the mouth
• Gas eradication from rumen - emergency
  rumenotomy or cannula/trocar in frothy bloat.
• Passing a stomach tube in cases of free gas tympany.
• Antifoaming agents: polyxene, dimethicone (cuplaton).

After treatment: diet 1-2 days, only hay and water.

Question 18

Clinical signs of esophageal obstruction. (6)

Answer 18

Also known as “choke”.

ptyalism
coughing, retching
extended neck
exaggerated attempts to swallow
secondary bloat
nasal discharge

Question 19

Treatment of esophageal obstruction.

Answer 19

secondary bloat must be relieved by
trocarization through the left sublumbar fossa.

solid objects (eg, potatoes) may often be
massaged free or spontaneously dislodge

can be managed with standing
esophageal lavage via orogastric tube or while under general anesthesia

Large foreign bodies can often be pushed into the rumen without further
problems.

Rare cases of esophageal obstruction with foreign bodies may be
treated with esophagotomy.

Question 20

Vagal indigestion syndrome is also known as?

Answer 20

Hoflund´s syndrome

Chronic Indigestion Syndrome in Ruminants

Question 21

Hoflund’s syndrome is characterized by

Answer 21

disturbance in the passage of ingesta
through the
- reticulo-omasal orifice (fAILURE OF OMASAL TRANSPORT)

OR
- pylorus (PYLORIC STENOSIS OR ABOMASAL REFLUX SYNDROME)

An outflow abnormality of reticulorumen and abomasum.

PROGNOSIS IS UNFAVORABLE, BUT YOU NEED A CORRECT DIAGNOSIS and sometimes to relieve the cow’s condition.

Question 22

Clinical signs of Hoflund’s syndrome. 7

Answer 22

Progressive Abdominal Distention, papple shape, L-shaped rumen

Reduced Appetite
Decreased Rumen Motility
Weight Loss

Scant Feces (reflecting poor digestion)
Weakness and Lethargy
Bradycardia

Question 23

ddx for “papple” shaped cows

Answer 23

most common causes are underlined in red.

hardware disease and diffuse peritonitis can cause compression of the vagus nerve by way of abscesses etc.

abomasal volvulus and impaction (compression of vagus nerve leading to neuropathy)

secondary impaction
(decreased abomasal emptying due to hardware dz or perforated abomasal ulcers)or a foreign body can obstruct flow of ingesta.

Question 24

type of vagus indigestion

Answer 24

Type II: Omasal Transport Failure

Signs: Severe distention of the rumen and reticulum, often with fluid accumulation. The cow may appear constipated with scant, firm feces.

Cause: Impaired passage of ingesta from the reticulum to the omasum, leading to an accumulation of fluid and ingesta in the rumen and reticulum.

Question 25

type of vagus indigestion

Answer 25

Type III: Pyloric Outflow Obstruction

Signs: Severe distention of the abdomen with fluid (ruminal and abomasal) accumulation, dehydration, and marked metabolic alkalosis. Feces are scant and often dark.

Cause: Obstruction or dysfunction at the pylorus or abomasum, leading to fluid and ingesta accumulation in the stomachs.

Question 26

type of vagus indigestion

Answer 26

Type IV: Abomasal Displacement or Obstruction

Signs: Distention primarily on the right side, signs of early satiety, and discomfort.

Cause: Abomasal obstruction or growing uterus displaces the abomasum, leading to similar symptoms as in Type III, but more related to physical obstruction rather than functional paralysis.

Question 27

Treatment of Hoflund’s syndrome. (5)

Answer 27

• Rumen lavage for emptying the rumen or
  rumenotomy for diagnostic purposes.
• Diagnostic laparotomy for finding adhesions.
• Fluid and electrolyte therapy: treatment of metabolic alkalosis, hypochloremia and hypokalemia.
• Laxatives to get the excess water moving (vegetable oil or Mg sulfates)
• Good quality hay and water

Question 28

Why might Hoflund’s syndrome see metabolic alkalosis and not acidosis?

Answer 28

metabolic alkalosis is more commonly observed than acidosis due to the disruption in normal gastrointestinal function, particularly in the abomasum and the pylorus.

The abomasum secretes hydrochloric acid (HCl) for digestion, and normally, this acid is neutralized by bicarbonate in the small intestine.

When outflow is obstructed, the acidic contents are trapped in the abomasum, preventing loss of hydrogen ions (H⁺) into the intestines.

At the same time, bicarbonate (HCO₃⁻) from the pancreas and saliva continues to be absorbed into the bloodstream as part of normal physiology, but without the corresponding loss of H⁺, this leads to an increase in systemic bicarbonate levels.

Question 29

Why is hypochloremia seen in Hoflund’s syndrome?

Answer 29

due to the disruption in normal gastrointestinal function, particularly in the abomasum and the pylorus, obstruction may occur.

The obstruction causes chloride ions (Cl⁻) to be sequestered within the abomasum, leading to hypochloremia (low blood chloride levels). Chloride is needed to balance the production of bicarbonate.

Result: The loss or sequestration of chloride, coupled with the continued generation and absorption of bicarbonate, leads to an alkaline shift in the blood pH.

Question 30

Clinical signs of traumatic reticuloperitonitis. (6)

Answer 30

Sudden onset: signs develops within 12 hours.

• Marked drop of milk yield (day before 40 kg, now only 2 kg).
• Complete anorexia, no rumination and decreased reticulo-rumen movements.
• Subacute abdominal pain.
• Free gas bloat due to lack of rumen contractions.
• Fever 39,5-40’C
• Defecation is painful and results in constipation and scant feces.

Question 31

Clinical exam findings in traumatic reticuloperitonitis.

Answer 31

• Ruminal stasis
• No „pings“, rumen tympany maybe.
• Cow should demonstrate signs of abdominal pain! deep palpation of ventral
  abdomen with your knee.
• Use „pinch and grunt tests“

Question 32

Lab analysis findings in traumatic reticuloperitonitis.

Answer 32

• Fibrinogen is elevated
• Glutavac- test (used on whole blood for the diagnosis of acute inflammation (increased fibrinogen concentration) and chronic inflammatory infections (increased immunoglobulin concentration)

(glutaraldehyde reacts with fibrinogen, coagulation speed is less than 3 min)

• Abdominocentesis (inflammation, bacteria!). Can even use california mastitis test cow-side on the fluid retrieved.

Question 33

Treatment of traumatic reticuloperitonitis.

Answer 33

Conservative:
Administration of reticular magnet at the
early stage of disease. If clinical signs disappear - prognosis is good. For prevention also!

Antimicrobial therapy broad spectrum
antimicrobials 5-7 days.

Surgical removal of foreign body -
rumenotomy.

Question 34

Traumatic reticulopericarditis can be diagnosed by

Answer 34

cardiac auscultation

It’ll sound like a washing machine or crackling if it includes fibrin.

Question 35

Describe an animal with chronic local reticuloperitonitis.

Answer 35

• Usually cow has been treated with AB due to unknown fever some week ago.
• Milk yield is still low, cow is depressed.
• Body condition is poor.
• Secondary ketosis and scant feces.
• Rumination activity is infrequent, rumen is small.
• Moderate bloat
• Grunting test may have positive or negative.
• Fever may fluctuate
• VERY UNPLEASANT SITUATION FOR VET, due to vagueness of condition.

Question 36

What do microbes provide to the ruminant? (5)

Answer 36

• Digestion of cellulose and hemicellulose by cellulolytic bacteria.
• Provision of high quality protein by proteolytic bacteria.
• Production of VFAs - these are the energy source of the cow!
• Provision of B vitamins by rumen bacteria.
• Detoxification of toxic compounds.

Question 37

Name the 3 main volatile fatty acids produced by rumen bacteria.

Answer 37

acetic (65%)
butyric (10%)
propionic (25%)

also lactic acid

Question 38

Which part of cattle feed produces propionic and lactic acids?

Answer 38

Grain, potatoes etc. provide starch, sugars and thus propionic acid & lactic acid.

pH 5,5-6

gram positive
Streptococcus spp.(Str. bovis)
Lactobacillae. lactococci etc.

Question 39

Which part of cattle feed produces acetic and butyric acids?

Answer 39

Hay, silages, forages provide cellulose,
hemicellulose and thus acetate and butyrate.

pH 6-7

Gram-negative bacteria

Question 40

Ruminal acidosis can be caused by too much what in the ration?

Answer 40

Too much starch and sugars aka too much grain.

Too much propionic and lactic acid.

Question 41

What volatile fatty acids are behind acidosis?

Answer 41

propionic and lactic acid

pH 5,5-6

Question 42

Main stabilizer of rumen pH?

Answer 42

180 litres of saliva (pH 8,5) produced per day contains approximately 2.5 kilograms of bicarbonate. Neutralize rumen pH!

Ruminants require fibre in the diet to maximise saliva production.

With high grain–low fibre diets; chewing decreases, the production of salivary buffers is reduced and organic acid production exceeds the buffering capacity of the rumen.

Question 43

Normal rumen pH.

Answer 43

pH 6.2 to 7.0 (neutral to slightly acid) — ideal for all rumen microbes.

A pH below 6.2—fibre-digesting bacteria slow down.

A pH below 5.4—fibre-digesting bacteria die out, lactic acid bacteria increase, and acidosis results.

Question 44

SARA stands for

Answer 44

subacute rumen acidosis

Question 45

Farmer has a herd problem,
that milk fat percentage has decreased
cows have diarrhea and
milk yield has declined also.

What do you suspect?

Answer 45

subacute rumen acidosis (due to improperly balanced rations)

Question 46

Rumen acidosis is

Answer 46

a metabolic disease of cattle when the pH of the rumen falls to less than 5.5 (normal is 6.5 to 7.0).

In many cases the pH can fall even lower.

The change in acidity changes the rumen flora, with acid-producing bacteria taking over. They produce more acid, making the acidosis worse.

The increased acid is then absorbed through the rumen wall, causing metabolic acidosis, which in severe cases can lead to shock and death.

Also known as grain overload and barley poisoning.

Question 47

Clinical signs of acute acidosis (5)

Answer 47

a static rumen with gurgling fluid sounds (due to gas),
watery diarrhea,
ataxia, and
a normal temperature
—are characteristic.

Progressive dehydration, complete anorexia and depression as well.

+ Endotoxemia – endotoxic shock caused by dying gram negative bacteria that can’t handle acidotic conditions.

Diarrhea due to water movement into GI lumen, third spacing.

• Weakness
• Abdominal distension

Question 48

What is used as a prognostic indicator for a cow with ruminal acidosis?

Answer 48

Heart rate in a cow with clinical ruminal acidosis can be used as a prognostic
indicator.

Cattle with a heart rate greater than 120 beats per minute generally have a
grave prognosis, despite treatment.

Question 49

Treatment of ruminal acidosis.

Answer 49

• Restore ruminal and systemic acidosis, prevent further production of lactic acid- rumenotomy in early stage.
• Maintenance and correction of fluid deficit and acidosis.
• Replacement fluids = bodyweight kg x dehydration% + maintenance 100 ml/ kg BW

Question 50

Estimating degree of dehydration in cows.
ca 8% standing, with sunken eyes
<10% standing
>10% lateral on the ground
ca 14%

Answer 50

Mild Dehydration (5-6%):
prolonged turgor
eyes begin to sink
mm tacky
lethargy

Moderate Dehydration (7-9%):
prolonged turgor
eyes moderately sunken
mm dry
crt delayed
lethargic, showing signs of weakness.

3. Severe Dehydration (10-12%)
   very prolonged turgor
   Eyes are deeply sunken.
   mm very dry
   crt severely delayed
   cow is very weak, possibly recumbent, and may be unresponsive.

Question 51

Calculation of base deficit (bicarbonate
requirements).

Answer 51

• Total requirement of bicarbonates (mEq) = base deficit (mEq/l) x 0,3 (conversion factor) x body weight (kg).
• In calves, the conversion factor could also be 0,5 due to large size of extracellular fluid space.
• In practice, where laboratory measurement can not be
  used, the base deficit (BD) is set at 10 mEq/l.

Question 52

default base deficit?

Answer 52

In practice, where laboratory measurement can not be used, the base deficit (BD) is set at 10 mEq/l.

Question 53

Supportive treatment for ruminal acidosis?

Answer 53

• Restore fluid and electrolyte losses. Hypertonic 5% Na-bicarbonate solutions (5-6L) IV during 30 minutes, then 1,3%
  150 ml/kg BW.
• NSAIDs for treatment of endotoxemia. Flunixin meglumine, meloxicam
• B1-vitamiin (thiamine). Thiminase has released from Str. bovis and degraded thiamine. Lack of B1- vitamin causes
  polyencephalomalacia.
• Antibiotics including penicillins, tylosin, potentiated sulphonamides and tetracycline should be given to reduce the
  risk of liver abscessation.
• Ca-gluconate and magnesium for treatment of secondary hypocalcemia.

Question 54

Lack of B1- vitamin causes

Answer 54

polioencephalomalacia.

a common neurologic disease of ruminants. The main clinical signs reflect dysfunction of the cerebrum and include wandering, circling, cortical blindness, incoordination, head pressing, recumbency, nystagmus, and seizure activity.

PEM has been associated with two types of dietary risks: altered thiamine status and high sulfur intake.

Question 55

Why does ruminal acidosis cause laminitis?

Answer 55

Acute laminitis may be present and is most common in those animals not severely affected; chronic laminitis may develop weeks or months later.

Ruminal acidosis leads to laminitis primarily through the absorption of lactic acid and endotoxins into the bloodstream, causing systemic inflammation and vascular damage. The resulting disruption in blood flow to the sensitive laminae leads to the painful and debilitating condition of laminitis.

Question 56

Why does ruminal acidosis cause epistaxis?

Answer 56

ruminal acidosis can cause rumenitis,
rumenitis can lead to bacteremia and endotoxemia,
above can lead to liver abscesses,
the abscesses can erode nearby blood vessels and cause septic emboli,
the septic emboli can lodge in the lungs causing pulmonary abscesses,
if the above erode into blood vessels, it can manifest as epistaxis

Question 57

What fraction of milk decreases in subacute ruminal acidosis?

Answer 57

milk fat begins to decrease

milk fat is made from acetate and acetate is made by rumen bacteria that feed on cellulose/hemicellulose from silages and forages

remember that in ruminal acidosis there is too much lactic (&propionic) acid from too much starch and sugar

Question 58

What causes cold ears in milk fever cows?

Answer 58

When blood calcium levels are low, the muscles, including those that control the blood vessels, cannot function properly.

This leads to vasoconstriction (narrowing of blood vessels), reducing blood flow to peripheral areas like the ears.

Question 59

Why is hypocalcemia seen in ruminal indigestion?

Answer 59

primarily due to disruptions in the rumen’s microbial activity and the resultant effects on calcium metabolism.

ruminal indigestion can lead to secondary metabolic disorders like hypomagnesemia or displaced abomasum, which further complicates calcium homeostasis and exacerbates hypocalcemia.

Magnesium is crucial for the activation of parathyroid hormone (PTH), which regulates calcium levels in the blood. In ruminal indigestion, magnesium absorption can also be impaired, leading to reduced PTH activity and, consequently, lower calcium levels.

Question 60

How does severe ruminal acidosis cause blindness?

Answer 60

Through polioencephalomalacia.

altered rumen microbial population produces thiaminase,
thiamine is rapidly degraded, leading to a deficiency.
its deficiency impairs energy production in brain cells.
brain cells undergo necrosis,
These lesions are characteristic of polioencephalomalacia (PEM).

The visual cortex is particularly susceptible to damage from thiamine deficiency. Lesions in this area can lead to cortical blindness.

Question 61

How does rumen acidosis cause kidney failure and azotemia?

Answer 61

through systemic metabolic acidosis, dehydration, reduced renal perfusion (from hypovolemia), direct nephrotoxic effects of endotoxins, and severe electrolyte imbalances that strain renal function further.

Question 62

How does lactic acidosis cause dehydration?

Answer 62

The accumulation of lactic acid in the rumen creates a hyperosmolar environment, drawing water from the bloodstream into the rumen.

This fluid shift can lead to cellular dehydration and reduced circulating blood volume (hypovolemia).

Question 63

Metabolic acidosis often leads to hyperkalemia, why?

Answer 63

in acidosis cells exchange intracellular potassium for extracellular hydrogen ions in an attempt to buffer the acidosis.