4. Quotations are commonly printed as a means
of inspiration and to invoke philosophical
thoughts from the reader.
4
5. UPSC PYQs
5
1. Describe in detail the clinical
findings , diagnosis , Rx of various
types of ruminal disorders. (2018)
2. Describe the diagnosis & Rx of
ruminal impaction & indigestion in
cattle.(2012)
6. INDIGESTION
DEFINITION- Indigestion is a disturbance occuring in the GI
tract of animals , more commonly in Cattle and rarely in sheep
and goats.
-It is used to describe a wide spectrum of clinical syndromes in
cattle, ranging from excessive fermentation of ingesta & gas
production in bowel to intestinal inflammation and more severe
forms like lactic acidosis.
8. Besides, it has also been classified as:
• Indigestion with acidosis.
• Indigestion with alkalosis.
• Indigestion (simple).
• Indigestion with tympany.
• Indigestion with impaction
• Indigestion with toxaemia.
• Vagus indigestion.
CLASSIFICATION
9. SIMPLE INDIGESTION
▪ DEFINITION- It may be defined as simple digestive
disturbance which is clinically manifested by
inappetance, anorexia, complete or subclinical atony of
rumen; infrequent defecation and constipation
10. ETIOLOGY
▪ Intake of undigestible coarse harmful roughages (bedding, poor straw,
scrub etc.).
▪ Intake of kitchen garbage.
▪ Intake of food containing excessive protein, non-protein nitrogenous
substances and urea.
▪ Intake of mouldy or decomposed food.
▪ Ingestion of too much concentrate feeds.
▪ Sudden changes in the quality and quantity of feeds.
▪ Old age, debility, recovery after disease.
▪ Insufficient mastication.
▪ Depraved appetite (Pica)
11. 11
CLINICAL FINDINGS
• Dullness and depression
• Initially inappetance followed by anorexia.
• Sweet smell may be noticed from breath. Diarrhoea
is seen due to feeding of mouldy feeds.
• Palpation of paralumbar fossa may show doughy
condition.
• Temperature, pulse and respiration are within the
normal range.
• Occasional grinding of teeth.
• Complete atony in later stages.
12. DIAGNOSIS
A simple diagnosis of it is based on –
• History of an abrupt change in the nature
and amount of feed.
• Multiple animals being affected.
The diagnosis is confirmed by collection &
examination of Ruminal fluid, which may have
an abnormal ph , decrease in numbers and
size of protozoa, prolonged MBRT.
13. TREATMENT
I. Rational Treatment
- Correction of ruminal pH to reactivate the
ruminal microbial population. If the pH is
acidic then neutralize it with antacid.
Magnesium hydroxide 400 g or magnesium
carbonate 200 g orally.
- If the pH is alkaline in nature, then neutralize
it with acetic acid, (Vinegar)5-10% solution
200-500 ml orally or 2 ml/kg b. wt, orally.
- Ruminal cud transplantation.
14. TREATMENT ( Contd.)
II. Symptomatic Treatment-
• Rehydrate the animal by 5% Dextrose or normal saline through parenteral
route.
• Use rumenotoric drugs. This will assist in improving the rumen motility.
Nuxomica, ginger, ammonium chloride and tartar emetic (10 g) may be given.
• Saline purgative e.g. Magnesium sulphate 1-2 kg may be given for evacuation
of bowel.
III. Prophylactic Treatment-
• Massage of rumen (downward to upward of left flank).
• Periodical exercise should be given especially in stall fed animal.
• Food should be withheld for 24 hours and then laxative type of foods should be
offered.
15. ALKALINE
INDIGESTION
-Incidence of alkaline indigestion is comparatively less
than other form of indigestion. Protein rich feeds are
the main offenders characterised by anorexia, dull and
depression along with ruminal atony.
16. ETIOLOGY
Intake of excessive protein rich feeds.
-Ingestion of plants containing more protein, barseem,
soyabean etc.
-Abrupt change of ration from carbohydrate to protein.
Exclusive paddy straw feeding over a prolonged period of
time
Feeding of decomposed oil cakes.
Ingestion of herbicide contaminated food.
17. CLINICAL SIGNS
• Inappetance to anorexia.
• Constant drooling of saliva.
• Increased pulse and respiratory rate.
• Tremor, ataxia and convulsion.
• Passage of semisolid faeces. in frequency and
amplitude.
• Depressed rumen motility .
18. TREATMENT
Evacuation of ruminal contents through lavage or
rumenotomy in emergency cases.
Correction of ruminal pH (alkalosis)- 5-10%. Acetic acid
@ 5-10 ml/kg body weight orally. 5-10% solution of Acetic
acid 200-500 ml orally or intra ruminally.
Oral antibiotic Penicillin or tetracyline or neomycin (10-20
mg/kg) to prevent further production of ammonia.
Transplantation of cud .
B-vitamins and liver extract to reactivate ruminal bacteria.
Ringer's lactate, 5% dextrose saline-to avoid toxaemia
and help hepatic detoxification.
Provision of digestible carbohydrate (molasses, grain)
20. DEHYDRATION
According to W.H.O., dehydration
denotes loss of water and dissolved salts
from the body. occurring, for instance, as
a result of diarrhoea. It may be due to
water and electrolyte deprivation or loss
of body fluids. Water is lost from the
body through respiration, skin, faeces
and urine.
21. CLINICAL MANIFESTATIONS
• Acidemia
• Renal ischemia
• High rise of temperature.
• Other changes – Loss of S/C elasticity , sunken
eye balls , dry mucous membranes , twitching
of muscles.
• Death occurs when 40% of body H2O is lost.
24. ISOTONIC DEHYDRATION
(Water or solute depletion)
There is loss of water and salt in a iso-osmolarity i.e. isotonic
sodium and fluid loss. Isotonic dehydration produces reduced
extracellular fluid (E.C.F.) volume due to acute gastro-intestinal
disorders, fluid and food deprivation, and profuse sweating.
TREATMENT
(a) Restoration of E.C.F. by means of normal saline or Ringer's
lactate. This will improve circulation and renal function.
(b) Administration of 0.45% NaCl will make up the deficit from
loss from gastro-intestinal (G.1.) tract. Otherwise, 5%
Glucose in water preferred.
25. HYPOTONIC DEHYDRATION
( Sodium depletion)
25
There is loss of salt in excess of water i.e. severe dehydration with
severe hyponatraemia.
It is characterised chemically by low concentration of plasma Na'
and CI and clinically by rigidity, apathy, fatigue, weakness, debility,
moist mucous membrane, sunken eye ball, shock and coma.
TREATMENT
• Minor Na deficiency requires addition of salt to fluid and food
in diet.
• Moderate deficiency requires 0.9% Sodium Chloride
parenterally .
• Marked deficiency requires 5% Sodium Chloride for rapid
restoration of plasma volume and renal circulation.
26. HYPERTONIC DEHYDRATION
(Water depletion)
26
There is deprivation of water without Na" loss. Water deficiency is
induced by insufficient water intake, in case of G.I disorders and
diabetes insipidus.
TREATMENT
Administration of water and fluid orally.
Intravenous injection of electrolyte free water.
5% Glucose through I.V. followed by,
Saline or Ringer's solution in vomiting and comatosed animal.
Water deficiency may be corrected by 5% Glucose solution
supplememed with electrolyte and Vitamin B-complex.
27. STROKE
27
DEFINITION- It is a term commonly used for
hyperthermia or elevated body temperature that
can have varied causes.
PREDISPOSING FACTORS -
• Hot day, high humidity
• Ill ventilation.
• Over crowding
28. CLINICAL SIGNS
28
• Panting and open mouth breathing.
• Frothy discharge from mouth.
• Tachycardia & cardiac arrythmia.
• 106-110 deg C .
TREATMENT
1. Supportive & management
2. Keep Animal at Ventilated & shady place
3. Cold bath in ice water
4. Give ice block to lick / water to drink
5. Ice cold rectal enema
6. Steroid (dexamethasone)
7. Prevent central oedema & shock
8. Sodium benzoate 5-10 gm s/c => cattle
9. Tranquilliser to sedate anima
10. Broad spectrum antibiotics.
29. POISONING
29
Poisoning occurs when a toxic substance is swallowed ,
inhaled, absorbed after coming in contact with skin, eyes,
mucous membranes. Also called as INTOXICATION.
30. PESTICIDE TOXICITY
30
Chemical pesticides were introduced as an important tool
for pest control and have been used extensively in human
health operations and agricultural applications since late
1940s.
• The poisoned animal shows clinical signs referable to
nervous excitement, hypersalivation, diarrhoea and
vomiting.
• The chronic cases show myelin degeneration and
neurotransmission defects
31. HEAVY METAL TOXICITY
31
• Pollution of the environment with heavy metals is a
serious problem that is recognized in most countries of the
world.
• Various anthropogenic activities such as burning of fossil
fuel, mining and metallurgy, industries and transport
sectors redistribute toxic heavy metals into the
environment, which persist for a considerably longer
period.
• These toxicants are accumulated in the vital organs
including liver and kidney and exert adverse effects on
domestic and wild animal populations
32. ARSENIC
32
It is a widely distributed environmental pollutant that gets
released into the environment through industrial processes
and agricultural usage.
Chronic ingestion of arsenic contaminated drinking water is
associated with skin lesions like spotted melanosis,
hyperkeratosis, leucomelanosis, rain drop depigmentation,
gangrenous extremities, hepatomegaly, splenomegaly,
cognitive impairments as well as cancers of different organs.
33. CLINICAL SIGNS
33
Signs of arsenic toxicity in cattle vary from gastrointestinal to
nervous signs.
In acute cases, abdominal pain, restlessness, respiratory distress,
grinding, ruminal stasis, even vomition are seen.
Increased heart rate, dehydration and oliguria are the common
manifestations of arsenic toxicity.
Chronic arsenic toxicityis mostly manifested by weight loss,
capricious appetite, conjunctival and mucosal erythema, bucal
ulceration and reduced milk yield in cows.
British anti laucide (BAL)is the choice of antidote against
arsenic.
34. LEAD
34
• It is common cause of poisoning in cattle.
• It causes encephalopathy, gastroenteritis and degeneration of peripheral nerves.
• In acute poisoning, animals reveal muscle tremors, champing of jaw, salivation
,blindness, muscular twitching, convulsion, hyperasthesia and death.
• In chronic cases, head pressing, long standing posture, circling, excitement,
blindness and mania, grinding of teeth, ruminal stasis, gastroenteritis and
abdominal pain are noticed.
• Animals die as a result of respiratory failure during convulsions..
• The animals can be treated with calcium versenate (calcium EDTA) given @ 100 200
mg/kg body weight intravenously thrice daily for 3-4 days.
• Thiamine given @ 2 mg/kg body weight subcutaneously also helps in its
treatment.
• Simultaneous use of Ca EDTA and vitamin B has synergistic effect.
35. MERCURY
35
• The metal is biologically non-essential but being used
in various industries, released in environment from
both natural and anthropogenic sources.
• Man-made sources such as coal combustion, non-
ferrous metal production, waste disposal etc. release
substantial quantities of mercury resulting in eco-
toxicity.
• Methyl-mercury is the most toxic and stable form of
mercury
• The mercury poisoning can be treated symptomatically.
36. SELENIUM
36
• Selenium toxicity due to pollution of environment has
been reported in animals.
• Relationship between selenium toxicity and plant
selenium level has been established and selenium
excess was considered as one of the factors causing
Degnala disease that affected thousands of cattle and
buffaloes in India and Pakistan.
37. CADMIUM
37
• Like lead and mercury, cadmium is also non-essential
biologically.
• Several reports demonstrate increasing concentration
of cadmium in liver and kidneys of wild small mammals,
viz. bank voles, wood mouse, short tailed field voles,
common shrew, meadow voles and European voles
from contaminated habitats.
39. FLUOROSIS
39
• Continual ingestion of small amount of fluoride through feed or
water leads to fluorosis in animals.
• Usually 200-400 ppm of it in dry ration produces disease in bovines.
• Due to its ingestion, hydrofluoric acid is formed in the rumen
resulting in irritation of mucosae.
• Due to excessive ingestion of fluorine, animals show anorexia,
vomition, ruminal stasis, diarrhoea, weakness, muscle tremors,
constant chewing movement, dilatation of pupil and hyperasthesia.
• Due to chronic ingestion, mottling and pigmentation of teeth occur.
• The animals reveal lameness, stiffness and painful gait. The bones
are enlarged, show exostoses, and pain is elevated on palpation.
