Veterinary Internal Medicine.docx

8/17/2019 Veterinary Internal Medicine.docx

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DISEASES OF CIRCULATORY SYSTEM

1. Diagnostic approach:

2. Principles of circulatory failure :

Heart failure Peripheral failure

Due to: due to:

- Defect in heart filling -Loss of fluid- Abnormality in myocardium -Dilatation of peripheral vessels.

r in conducting system

- !"cessive #or$ load -Pooling of blood in

- %ombination of above peripheral system

Consequences

1. !ither complete or partial hamper in& - !"changes of fluid& electrolytes& o"ygen& ' nutrients

' e"cretory substances.2. (he first critical system is nervous system to be affected.

Diagnostic approach

i) History& inspection& palpation ' percussion need especial e"periences.

ii) Auscultation by stethoscope or phonendoscope reveal about heart sounds& sometimes position of heart also.

(achycardia * increased rate of heart beat

+radycardia - Decreased rate of heart beat

(ransient sound * ,ormal& 1st& 2nd& rd& ' th&

/urmur sound - abnormal sound or adventitives

Pericardial rub - Pericardial heart sound.

0hythm * 0egularity of successive pulse.

0hythmic * deviation in rhythm.

iii) +lood pressure in animal not easy&it has been tried in dog ' house by

Dog * tibia artery


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House - /iddle coceygeal artery.

Done man * +rachial artery.

+y sphygonometer

Pressure

ystolic Diastolic

3entricular contraction) 3entricular rela"ation.)

Hypertension * increased Pressure

Hypo-tension - decreased Pressure

iv) Angiography

Electro cardiogram is not common in livestock done in human.

PERICARDITIS

4nflammation of pericardium is called 5. 4t may be acute or chronic and effusive& 6ibrinous or

adhesive traumatic Pericarditis is #idely prevalent in cattle but not in house.

Aetiology

1. (0P in cattle is most fre7uent.

2. Locali8ation of blood borne diseases- in all sps.. !"tension of inflammation from pleurisy ' myocardium- in all sps.

Symptoms

Bacteria

i) Pasteurellosis


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ii) heptococcus sps

iii) almonella * spp

iv) Leptospira- sppv) /ycoplasmal spp

vi) /ycobere ferium spp.

vii) 9lassers disease in pig.

Viral

i. 4nfectious feline peritonitis

ii. %anine distemper

Fungal

i) %occidioisomycosisii) Actonomycosis

Others chronic uremia may set up pericardial lesion.

Clinical in!ings

i) Pain& reluctant to move ' abducted elbo#s& arching of bac$ ' shallo# abdominal

respiration

ii) 1; to 1;


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%ongenital defects the cardial cycle brea$s

iii) /uffling sounds due to pleurisy %areful e"amination reveals pulmonary emphysema

iv) Hydro pericardium Aspiratory puncture may accompanying #ith edema.

i) (0D * Leu$ocytosis ' shift to the left.

Treatment

?se of specific antibiotic for specific causative agent.

i) ,on specific treatment is use of broad-spectrum antibiotic ' salt

ii) Paracentesis ' use of diuretics is use fuel.

iii) alt free diet ' use of fribrinolytic drugs li$e o"alate

%&OCARDITIS'

4nflammation of heart muscle is $#on as /yocarditis

Aetiology

1. (on inecti)e' due to Auto-immune condition and to"icity of heavy metals e7.Arsenic&hg&lead& copper etc.

*# Inecti)e agent

a) 3irus - 6/D virus in young one.i.e. !7uine infections anaemia&%anine parvo virus&'

canine distemper. b) +acteria * Clostridium chauvoei, steptococcous staphy bococess.

c) 6unfus * cryptocossus.d) Parasiles * e7. %yst& trypanosoma& to"oplasma& strongyless etc.

Pathogenesis

- 4neffective cardiade output ' passive verous congestion.

- /ycocardial degeneration leads to acute cardial failure ' death.

Clinical in!ings

i) 4ncreased Pulse rate ' arrhythmia.

ii) Dyspnoea ' #ea$ness.

iii) !"haustion ' increased temperature in infective condn.

iv) %hronic venous congestion ' heart failure.v) yncope ' death.

vi) Acute death i.e. #ithout sign ' symptom)


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Diagnosis

Difficulty by %linical symptoms.

D# Diagnosis

i) !lectro-cardiography.!%9)

ii) Difficult to differentiable from endocardium

Treatment

i) (reatment of primary cause.ii) ymptomatic treatment but in large animal may not be useful.

E(DOCARDITIS

4nflammation of endocardium #ith interference in blood e=ection or valvular stenosis is

!ndocarditis #hich is characteri8ed clinically by it is manifestation and murmur sound of heart.

Aetiology

Farm animal * +acteria strep to& %orynebacterium& clostridium& /ycoplasma& erycepaothri"&

and !scherichia coli )

3irus also i.e. influen8a

+orse' above cause as #ell as migrating strongylus larvae.

Pathogenesis

Due to implantation of bacteria on to the valves from the blood stream result bacteremia or

embolism of the valve capillaries leads to myocardial disease may cause inflammation of

endothelium& its damage or edema of valve. %ongenital cardiac defect may also predispose valve problem or stressful #or$ of valve ' endocarditis& vegetative and ulcerative type of lesions may

cause problems on blood e=ection ' flood. 6ragments of vegetative lesions after detaching may

come into circulation ' result embolic end arteritis military Pulmonary abscesses& abscesses on

myocardium& $idney ' =oints chronic lesions on value results adhesions of cusps. hrin$ing

distortion and thic$ening of the valve cusps. At this stage inference of blood flood occurs '

congestive heart failure al#ays results.


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In)ol)ement

%attle: - /ost fre7uently right arterio-ventricular value and left arterio-ventricular.

Horse * Aortic semi lunar valves most fre7uent value of aorta origin) and pulmonary

value * origin of pulmonary artery #hich each value consists three flap cusps)& less

fre7uently left a tro- ventricular value.

Clinical fndings

i) /urmur sound on auscultation at the cardiac over and poor e"ercise tolerance.ii) /oderate fluctuating fever@

iii) econdary involvement of other organs result Peripheral lymphadenitis& embolic

pneumonia& nephritis& arthritis& tenosynovitis& or /yocarditis.

iv) Loss of condition pale mucous membrane ' increased heart rate.v) 4n cattle additional symptoms are 9runting respiration& moderate ruminal tympany&

scouring or constipation& blindness& facial paralysis& muscle #ea$ness& recumbency&

=aundice ' sudden death. Distension of =ugular vein& general edema and a systolic 'diastolic murmur sound in many cases. Periodic ill thrill is common history.

vi) 4n horse- =ugular proment in terminal stages ' hot edema.

vii) 4n s#ine * Agalactia& loss of #t& intolerance in e"ercise ' dyspnoea at rest.

Diagnosis

i) Difficult from clinical symptoms.

ii) Phonocardiography: - (echni7ue for recording heart sounds ' murmurs. (hese are pic$ed

up by microphone placed over the heart.

Dierential !iagnosis

!ndocarditis ' Pericarditis and other causes of cardiac failure are confusion. 4n cattle *

confusion mostly occur in lympomatosis

i) 4n endocarditis.Acute - lencocytosis ' shift to the left /onocytes increased& increased

macrophages ' severe anaemia in

%hronic: - Hyper-gamma-globulinemia in bacterial inf n. 0epeated e"amination of

urine gives proteinuria ' bacteria in urine.


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ii) !chocardiography * reveals about echoes from vegetative lesion ' defect

abnormal value movement.

Treatment:-

i. ,ot so hopeful.

ii. +lood culture ' drug sensitivity test. ?se of specific or broad spectrumantibiotics.

iii. Streptococcus infn in cattle is difficult because its resistance so procaine ben8yl

penicillin 2;;;; unitsB$gCdailyCfor -1; days or longer.iv. Amino glycoside are combined form first five days if temperature not reduces&

infection is under control. Again days or more treatment must be continued.

v. (reatment #ith macrolides e7. !rythromycin) ' ampicillin is effective but theyare e"pensive.

vi. %hances of relapse is move& of signs of congestive heat failure prognosis is

unfavorable.

+&PERTOP+& A(D DI,ATIO( OF +EART

Compensatory result

Hypertrophy and dilatation of heart can collectively be called cardiac enlargement. Physiological

hypertrophy of heart is the normal physiological enlargement of heart in race or athletic animals.

!nlargement o heart is due to Persistent increased #or$ loads that are associated #ith

cardiovascular disease& the heart may respond

%ardiac hypertrophy is due to increased pressure load

By !ilatation- hypertrophy or com.ination o .oth

Cardiac hyper tropy Cardiac dilation

?sual response of - ?sual response

- 4ncreased pressure load ' in this there is increased volume load ' probably

4ncrement of individual fibre& si8e results from fiber re-arrangement.

4ncrease in total mass. - +y this increased volume of blood

- %ompensatory mechanism can be e=ected by single contract)

fos coronary circulation or per unit contraction.

4n state of cardiac insufficiency -Depends on laplace loud #hich


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4ncreased tension re7uest for producing

4ncreased inside chamber

Cardiac reserve the normal heart has the capacity to in release body weight

several olds in response to normal physiological demands created byexercise and to a less extent by pregnancy by lactation ! by digestion.

Collectively this response comprise the cardiac reserve

.

Clinical fndings

o Degree of enlargement is a good indication of degree of cardiac embarrassment but accurate

measurement is impracticable.

o 4ncreased Pressure on heart& flo# load@;.

o Presence of myocardial diseased increased of cardiac reserve.

Diagnosis

+y careful auscultation ' palpation of ape" beat of heart.

D# Diagnosis

• Displacement heat by space occmpying lesions.

• 3entral collapse of lung ' up# and displacement of heat

• 0adiography ' eco-cariographic.

Treatment

(reatment of primary causes.

C"#$E%T&'E (E)*T +)&,*E

6ailure of the heart to maintain circulatory e7uilibrium at rest and congestion of venous circuit

accompanied by dilation of vessels& edema of the lungs of periphery& enlargement of the heart

#ith increased rate is $no#n as 5. Pulmonary circulation implies left sided heart failure and

systemic venous circulation implies right sided heart failure.

Aetiology

1. Any factor or disorder #hich causes /yocarditis& endocarditis or Pericarditis #hich interfere

in blood flood.

2. Any disease #hich #ea$ens the face of myocardial contractionmay be due to nutrition). Any type of alveolar diseases e.g. tenosis& congenital defect persistent defect arteries&

rupture of value or aortic valued effect


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. /yopathy or myocardial infarction.

E. %hronic pulmonary emphysema or disease eg. 6ibrosis of lungs& emphysema.


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o Ascites& hydrothora"& hydro pericardium.

o !nlarged liver ' palpable at right costal arch #ith thic$ened ' rounded

edge.

o liguria& concentrated urine ' presence of albumen.

o Lose 6aeces& decreased #eight of body #ith due to edema but rapid loss of

condition.o Dilated superficial veins mainly the =ugular.

!pista"is in horses may be)

Diagnosis

+y clinical symptoms.

i) !%9.electro-cardiography)

D# Diagnosis

i) Peritonitis :- n Paracentesis presence of bacteria ' Leu$ocytosis

- Absence of cardiac involvement.

ii) 0uptured bladder :-- liguria

- +?,+lood urea nitrogen) ' peritoneal flood nitrogen

- Abdominal pain ' strain to /icturation .iii) Hepatic fibrosis :

- Gaundice ' photosensiti8ation.

- Liver function test.

iv) !dema: - /ay occur in mare ' condition near to calving date.- (here is no =ugular engorgement. ' evidence of cardiac involvement.

- /ay be due to endo parasites or hypo-proteinuria. Dyspnoea * /ay be due

to pulmonary edema- Pulmonary emphysema

- Allergic or anaphylactic stage

- 6og fever of cattle

,ine o Treatment

1. Provide rest so that there is less demand of blood.

2. Perform specific causative agent treatment.

. ?se salt free diet in edematous condition. ?se diuretics to treat edematous condition.

E. 4n severe condition vein section is suggested as an emergency treatment -ml blood B$g body #t at a time. 4t cannot be repeated before days.


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Treatment

1. ince there is no specific treatment& symptomatic treatment should be follo#ed. (o reduce

the spasm or cramp and to sooth the nerves anti-spasmodic li$e chlorproma8ine&Phenobarbitone& etc. are used.

2. (o correct neurological disorders methyldopa lardopa) E;;mg I tab once daily follo#ed by

I tabB#ee$ can be given. r trihe"ypnendyl hcl pecitane-lederle) 2 mg 1 tab) +.4.D. orally.. 3it. + .comple" J vitamin c. should be given.

revention

"# ince the disease is a se7ulae of Distemper& it should treat #ith additional 1; days after theapparent symptoms manifestation causes.

Simple Indigestion in Ruminants

(Mild dietary indigestion)

Simple indigestion is a minor disturbance in ruminant GI function that occurs most

commonly in cattle and rarely in sheep and goats. Simple indigestion is a diagnosis

of exclusion and is typically related to an abrupt change in the quality or quantity of

the diet.

Etiology

Almost any dietary factor that can alter the intraruminal environment can cause

simple indigestion. The disease is common in hand-fed dairy and beef cattle

because of variability in the quality and quantity of their feed. airy cattle may

suddenly eat excessive quantities of highly palatable feeds such as corn or grass

silage! beef cattle may eat excessive quantities of relatively indigestible" poor-

quality roughage during #inter. uring drought" cattle and sheep may be forced to

eat large quantities of poor-quality stra#" bedding" or grain. Simple indigestion can

result from suddenly changing the feed" using spoiled or fro$en feeds" introducing


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urea to a ration" turning cattle onto a lush cereal grain pasture" or introducing

feedlot cattle to a high-level grain ration.

Simple indigestion is usually associated #ith a sudden change in the p% of the

ruminal contents" such as a decrease in ruminal p% due to excessive fermentation

or an increase in ruminal p% due to putrefaction of ingested feed. It can also result

from the accumulation of excessive quantities of relatively indigestible feed that

may physically impair rumen function. &ultiple animals are usually simultaneously

affected because simple indigestion has a nutritional basis" although the severity of

the clinical signs can vary among animals.

Clinical Fin!ings

The clinical signs depend on the type of animal affected and cause of the disorder.

Silage overfeeding causes anorexia and a moderate drop in mil' production in dairycattle. The rumen is usually full" firm" and doughy! primary contractions are

decreased in rate or absent" but secondary contractions may be present although

usually decreased in strength. Temperature" pulse" and respiration are normal. The

feces are normal to firm in consistency but reduced in amount. Recovery usually is

spontaneous #ithin ()*)+ hr.

Simple indigestion due to excessive feeding of grain results in anorexia and ruminal

hypomotility to atony ,stasis. The rumen is not necessarily full and may contain

excessive fluid. The feces are usually soft to #atery and foul smelling. The affectedanimal is bright and alert and usually begins to eat #ithin () hr. A more severe

digestive upset due to excessive feeding of grain is described as grain overload

,see Grain verload in Ruminants.

Diagnosis

A diagnosis of simple indigestion is based on a history of an abrupt change in the

nature or amount of the diet" multiple animals being affected" and the exclusion of

other causes of forestomach dysfunction. The diagnosis is confirmed by collection

and examination of ruminal fluid" #hich may have an abnormal p% ,/0 or 12"

decrease in the numbers and si$e of proto$oa" or prolonged methylene blue

reduction time ,a measure of bacterial activity.

The systemic reaction and painful responses to deep palpation of the xiphoid in

traumatic reticuloperitonitis are not seen. The history and the absence of 'etonuria

help eliminate 'etosis from consideration. The possibility of left displaced

http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_ruminant_forestomach/grain_overload_in_ruminants.htmlhttp://www.merckmanuals.com/vet/digestive_system/diseases_of_the_ruminant_forestomach/grain_overload_in_ruminants.html


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abomasum usually can be eliminated by simultaneous percussion and auscultation.

3agal indigestion" abomasal volvulus" and cecocolic volvulus become more readily

detectable as they progress. Grain overload is differentiated from simple indigestion

by its greater severity and the pronounced fall in the p% of the rumen contents to

/4.4.

Treatment

Treatment is aimed at correcting the suspected dietary factors. Spontaneous

recovery is usual #hen animals are fed a typical ruminant diet. Administration of

∼(5 6 of #arm #ater or saline via a stomach tube" follo#ed by vigorous 'neading of the rumen" may help restore rumen function in adult cattle. &agnesium hydroxide

7 may be useful #hen excessive amounts of grain have been ingested" but

magnesium hydroxide should only be administered to cattle #ith lo# ruminal p%,/0" other#ise excessive forestomach and systemic al'alini$ation can result.

7urported rumenatorics ,eg" nux vomica" ginger" tartar emetic"

parasympathomimetics are not recommended as ancillary treatments. If too much

urea ,see 8onprotein 8itrogen 7oisoning or protein has been ingested" vinegar

,acetic acid may be administered 7 to return rumen p% to the normal range. If the

number or activity of ruminal microbes is reduced" administration of )*+ 6 of ruminal

fluid from a healthy co# #ill help. ,see Ruminal 9luid Transfer . ral or intravenous

electrolyte solutions may be needed to correct electrolyte and acid-base

abnormalities" particularly in dehydrated cattle.

Grain verload in Ruminants

(Lactic acidosis, Carbohydrate engorgement, Rumenitis)

Grain overload is an acute disease of ruminants that is characteri$ed by rumen

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hypomotility to atony" dehydration" acidemia" diarrhea" toxemia" incoordination"

collapse" and in severe cases" death.

Etiology an! Pathogenesis

The disease is most common in cattle that accidentally gain access to large

quantities of readily digestible carbohydrates" particularly grain. Grain overload also

is common in feedlot cattle #hen they are introduced to heavy grain diets too

quic'ly. :heat" barley" and corn are the most readily digestible grains! oats are less

digestible. 6ess common causes include engorgement #ith apples" grapes" bread"

batter;s dough" sugar beets" potatoes" mangels" or sour #et bre#er;s grain that #as

incompletely fermented in the bre#ery. The amount of feed required to produce

acute illness depends on the 'ind of grain" previous experience of the animal #ith

that grain" the nutritional status and condition of the animal" and the nature of the

ruminal microflora. Adult cattle accustomed to heavy grain diets may consume


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?arbohydrate engorgement results in conditions ranging from simple indigestion

,see Simple Indigestion in Ruminants to a rapidly fatal acidemia and strong ion

,metabolic acidosis. The interval bet#een overeating and onset of signs is shorter

#ith ground feed than #ith #hole grain" and severity increases #ith the amount

eaten. A fe# hours after engorgement" the only detectable abnormality may be an

enlarged rumen and possibly some abdominal pain ,manifest by belly 'ic'ing or

treading of the hindlimbs. In the mild form" the rumen movements are reduced but

not entirely absent" the cattle are anorectic but bright and alert" and diarrhea is

common. The animals usually begin eating again


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parturient paresis.

Acute laminitis may be present and is most common in those animals that are not

severely affected! chronic laminitis may develop #ee's or months later. Anuria is a

common finding in acute cases" and diuresis after fluid therapy is a good prognostic

sign.

eath may occur in ()*2( hr" and rapid development of acute signs" particularly

recumbency" indicates a need for aggressive treatment. A reduction in heart rate"

rise in temperature" return of ruminal movement" and passage of large amounts of

soft feces are more favorable signs. %o#ever" some animals appear to improve

temporarily but become severely ill again


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microscopically if access to a laboratory is available! fluid from affected cattle #ill

have decreased numbers of proto$oa ,particularly large and medium si$ed

proto$oa. A Gram;s stain of ruminal fluid #ill reveal a change from predominantly

gram-negative bacteria ,normal to predominantly gram-positive bacteria in grain

overload" #ith a concomitant loss in bacterial diversity.

Increased blood d-lactate and l-lactate and inorganic phosphate concentrations"

mild hypocalcemia" and reduced urinary p% are also seen" but it is seldom

necessary to chec' such values to ma'e a firm diagnosis. The diagnostic problem

is to properly assess #hich animals require vigorous therapy ,or slaughter" #hich

require supportive therapy" #hich have only a mild indigestion that #ill correct itself

if #ater and grain inta'e are restricted and hay and exercise are provided" and

#hich need nothing beyond their routine care and ration. In an outbrea' of overload

involving several animals" it is necessary to identify those animals that need the

most intensive therapy and those that #ill recover #ith minimal medical therapy.

If the cattle are found #hile still eating" it is possible that some of the group #ill fall

into each category" and close monitoring is necessary to minimi$e losses. ?attle

found #hile engorging or shortly thereafter should be allo#ed no more concentrate

or #ater" but plenty of good hay for up to () hr" and should be forced to #al'

periodically. ?attle that appear normal at the end of the first day are probably in

good health" although if even one is ill" all should be monitored closely for )+ hr.

&ost of those that have eaten enough concentrate to be affected seriously sho#signs #ithin 0*+ hr.

Treatment

9or all cattle suspected of having eaten large quantities of concentrate" it is

believed that restricting #ater inta'e for the first =+*() hr is helpful" although this

has not been proven. If overload is serious" slaughter for salvage should be

considered! in feeders nearing the end of their feeding period" it may #ell be the

most economical choice. &ortality is high in severely affected animals unless

aggressive therapeutic measures are initiated early. In such animals" removal ofrumen contents and replacement #ith ingesta ta'en from healthy animals is

necessary. In animals that are still standing" rumenotomy is preferred to rumen

lavage" because animals may aspirate during the lavage procedure and only

rumenotomy ensures that all ingested grain has been removed. Rumen lavage may

be accomplished #ith a large stomach tube if sufficient #ater is available. A large-

bore tube ,(.4 cm inside diameter" < m long should be used" and enough #ater


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added to distend the left paralumbar fossa! gravity flo# is then allo#ed to empty out

#hat it #ill. Repeating this =4*(5 times achieves the same results ,and requires

about as much time as using rumenotomy to empty and #ash out the rumen #ith a

siphon.

mptying the rumen should be follo#ed by rumen inoculation ,see rugs for

Specific 7urposes in the Ruminant igestive System and" if not accomplished

before signs of severe illness are evident" by rigorous fluid therapy to correct the

metabolic acidosis and dehydration and to restore renal function. Initially" over a

period of ∼


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in quantities to #hich they are unaccustomed" should be avoided. 9eedlot cattle

should be introduced gradually to concentrate rations over a period of (*< #'"

beginning #ith a mixture of >45D concentrate in the milled feed containing

roughage.

6ast full revie#Crevision &arch (5=( by 7eter . ?onstable" @3Sc ,%ons" &S"7h" A?3I&

Subacute Ruminal Acidosis

(Chronic ruminal acidosis, Subclinical ruminal acidosis)

Ruminant animals are adapted to digest and metaboli$e

predominantly forage diets! ho#ever" gro#th rates and mil'

production are increased substantially #hen they consume high-

grain diets. ne consequence of feeding excessive amounts of

rapidly fermentable carbohydrates in conEunction #ith inadequate

fiber to ruminants is subacute ruminal acidosis" #hich is

characteri$ed by periods of lo# ruminal p%" depressed feed

inta'e" and subsequent health problems. ?hronic disease

conditions secondary to subacute ruminal acidosis can negate the

production gains accomplished by high grain feeding. airy cattle"

feedlot cattle" and feedlot sheep are all at high ris' for developing

this condition. Although dairy cattle are typically fed diets that are

higher in forage and fiber compared #ith feedlot animals" this

advantage is offset by their much higher dry-matter inta'es.

Etiology

Ruminal p% fluctuates considerably during a ()*hr period

,typically bet#een 5.4*=.5 p% units and is determined by the

dynamic balance bet#een the inta'e of fermentable

carbohydrates" buffering capacity of the rumen" and rate of acid


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absorption from the rumen. If ruminal p% drops belo# 4.4 ,the

normal physiologic nadir for more than a fe# hours a day in an

animal" it is considered to have subacute ruminal acidosis. @y

convention" ruminal acidosis is considered subacute #hen the lo#

ruminal p% is caused by excessive accumulation of volatile fatty

acids ,39A #ithout persistent lactic acid accumulation" and #hen

the lo# ruminal p% is restored to normal by the animal;s o#n

physiologic responses.

The ability of the rumen to rapidly absorb organic acids

contributes greatly to the stability of ruminal p%. It is rarely difficult

for peripheral tissues to utili$e 39A already absorbed from the

rumen! ho#ever" absorption of these 39A from the rumen can be

an important bottlenec'.

Ruminal 39A are absorbed passively across the rumen #all. This

passive absorption is enhanced by finger-li'e papillae" #hich

proEect a#ay from the rumen #all and provide massive surface

area for absorption. Ruminal papillae increase in length #hen

cattle are fed higher-grain diets! this presumably increases

ruminal surface area and absorptive capacity" #hich protects the

animal from acid accumulation in the rumen. If the absorptive

capacity of these cells is impaired ,eg" chronic rumenitis #ithfibrosis" it becomes much more difficult for the animal to maintain

a stable ruminal p% follo#ing a meal.

ne mechanism by #hich affected animals resolve ruminal

acidosis and return ruminal p% to normal is by selecting long

forage particles" either by choosing to preferentially consume long

dry hay or by sorting a mixed ration in favor of longer forage

particles. Another mechanism is by reducing overall feed inta'e.

epressed dry-matter inta'e becomes especially evident ifruminal p% falls belo# 4.4. Inta'e depression may be mediated

by p% receptors andCor osmolality receptors in the rumen.

Inflammation of the ruminal epithelium ,rumenitis could cause

pain and also contribute to inta'e depression during subacute

ruminal acidosis.


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Absorption of 39A inherently increases as ruminal p% drops.

These acids are absorbed only in the protonated state. @ecause

they have a pJa of about ).+" the proportion of these acids that

are protonated increases dramatically as ruminal p% decreases

belo# 4.4. Hnfortunately" ruminal carbohydrate fermentation shifts

to lactate production at lo#er ruminal p% ,mostly due

toStreptococcus bovis proliferating and shifting to lactate instead

of 39A production! this can offset gains from 39A absorption.

Ruminal lactate production is undesirable because lactate has a

much lo#er pJa than 39A ,


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bacteria and proto$oa are present" the ruminal microflora are less

stable and less able to maintain normal ruminal p% during periods

of sudden dietary change. Thus" periods of subacute ruminal

acidosis leave animals more susceptible to future episodes of

ruminal acidosis.

Pathogenesis

6o# ruminal p% may lead to rumenitis" erosion" and ulceration of

the ruminal epithelium. nce the ruminal epithelium is inflamed"

bacteria may coloni$e the papillae and lea' into the portal

circulation. These bacteria may cause liver abscesses" #hich may

eventually lead to peritonitis around the site of the abscess. If the

ruminal bacteria clear the liver ,or if bacteria from liver infections

are released into circulation" they may coloni$e the lungs" heart

valves" 'idneys" or Eoints. The resulting pneumonia" endocarditis"

pyelonephritis" and arthritis are often difficult to diagnose

antemortem. 7ostmortem evaluation of these conditions in

animals that are slaughtered" culled" or that died on the farm can

be very beneficial.

?audal vena cava syndrome is caused by the release of septic

emboli from liver abscesses! this septic material then travels via

the caudal vena cava to the lungs. These bacteria proliferate inlung tissue and may ultimately invade pulmonary vessels" causing

them to rupture. This is observed clinically as hemoptysis and

even peracute deaths due to massive pulmonary hemorrhage.

Subacute ruminal acidosis has also been associated #ith laminitis

and subsequent hoof overgro#th" sole abscesses" and sole

ulcers. The severity of laminitis depends on the duration and

frequency of metabolic insult. These foot problems generally do

not appear until #ee's or months after the initiating event. Themechanism by #hich subacute ruminal acidosis increases the ris'

of laminitis has not been fully characteri$ed.

Clinical Fin!ings

The maEor clinical manifestation of subacute ruminal acidosis is

reduced or cyclic feed inta'e" or both. ther associated signs


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include decreased efficiency of mil' production" reduced fat test"

poor body condition score despite adequate energy inta'e"

unexplained diarrhea" and episodes of laminitis. %igh rates of

culling or unexplained deaths may be noted in the herd. Sporadic

nosebleeds due to caudal vena cava syndrome may also be

observed. The clinical signs are delayed and insidious. Actual

episodes of lo# ruminal p% are not identified! in fact" by the time

an animal is observed to be off-feed" its ruminal p% has probably

been restored to normal. iarrhea may follo# periods of lo#

ruminal p%! ho#ever" this finding is inconsistent and may be

related to other dietary factors as #ell.

Diagnosis

Subacute ruminal acidosis is diagnosed on a group rather than

individual basis. &easurement of p% in the ruminal fluid of a

representative portion of apparently healthy animals in a group

has been used to assist in ma'ing the diagnosis of subacute

ruminal acidosis in dairy herds. Animal selection should be from

highest-ris' groupsK co#s bet#een =4*


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@ecause subacute ruminal acidosis is not detected at the time of

depressed ruminal p%" there is no specific treatment for it.

Secondary conditions may be treated as needed.

Pre)ention

The 'ey to prevention is reducing the amount of readily

fermentable carbohydrate consumed at each meal. This requires

both good diet formulation ,proper balance of fiber and nonfiber

carbohydrates and excellent feed bun' management. Animals

consuming #ell-formulated diets remain at high ris' for this

condition if they tend to eat large meals because of excessive

competition for bun' space or follo#ing periods of feed

deprivation.

9ield recommendations for feeding component-fed concentrates

to dairy cattle during the first < #' of lactation are usually

excessive. 9eeding excessive quantities of concentrate and

insufficient forage results in a fiber-deficient ration li'ely to cause

subacute ruminal acidosis. The same situation may be seen

during the last fe# days before parturition if the ration is fed in

separate components! as dry-matter inta'e drops before calving"

dry co#s preferentially consume concentrates instead of forage

and develop acidosis.

Subacute ruminal acidosis may also be caused by errors in

delivery of the rations or by formulation of rations that contain

excessive amounts of rapidly fermentable carbohydrates or a

deficiency of fiber. Recommendations for the fiber content of dairy

rations are available in the 8ational Research ?ouncil

report" Nutrient Requirements of Dairy Cattle ,see 8utritional

Requirements of airy ?attle. ry-matter content errors in total

mixed rations are commonly related to a lac' of adEustment forchanges in moisture content of forages.

Including long-fiber particles in the diet reduces the ris' of

subacute ruminal acidosis by encouraging saliva production

during che#ing and by increasing rumination after feeding. The

provision of adequate long-fiber particles reduces the ris' for

http://www.merckmanuals.com/vet/management_and_nutrition/nutrition_cattle/nutritional_requirements_of_dairy_cattle.htmlhttp://www.merckmanuals.com/vet/management_and_nutrition/nutrition_cattle/nutritional_requirements_of_dairy_cattle.htmlhttp://www.merckmanuals.com/vet/management_and_nutrition/nutrition_cattle/nutritional_requirements_of_dairy_cattle.htmlhttp://www.merckmanuals.com/vet/management_and_nutrition/nutrition_cattle/nutritional_requirements_of_dairy_cattle.html


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ruminal acidosis but cannot eliminate it. If a total mixed ration is

fed" it is important that the long-fiber particles not be easily sorted

a#ay from the rest of the diet! this could delay their consumption

until later in the day or cause them to be refused completely.

Sorting can be prevented by providing long-fiber particles that are

/∼4 cm in length" by having adequate ,∼45 to 44D moisture inthe mixed ration" and by including ingredients such as liquid

molasses that help ration ingredients stic' together.

Ruminant diets should also be formulated to provide adequate

buffering. This can be accomplished by feedstuff selection andCor

by the addition of dietary buffers such as sodium bicarbonate or

potassium carbonate. ietary cation-anion difference ,?A is

used to quantify the buffering capacity of a diet! diets for animals

at high ris' for ruminal acidosis should be formulated to provide a

?A of 1(45 mqC'g of diet dry matter" using the formula ,8a L

J * ,?I L S to calculate ?A.

Supplementing the diet #ith direct-fed microbials that enhance

lactate utili$ation in the rumen may reduce the ris' of subacute

ruminal acidosis. Measts" propionobacteria" lactobacilli" and

enterococci have been used for this purpose. Ionophore ,eg"

monensin sodium supplementation may also reduce the ris' byselectively inhibiting ruminal lactate producers and by reducing

meal si$e.

6ast full revie#Crevision &arch (5=( by Garrett R. et$el" 3&"&S

@loat in Ruminants

,Ruminal tympany


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Bloat is an overdistention of the rumenoreticulum with the gases of

fermentation, either in the form of a persistent foam mied with the ruminal

contents, called primary or frothy bloat, or in the form of free gas separated

from the ingesta, called secondary or free!gas bloat" #t is predominantly a

disorder of cattle but may also be seen in sheep" $he susceptibility of

individual cattle to bloat varies and is genetically determined"

%eath rates as high as &' are recorded in cattle graing bloat!prone pasture,

and in pastoral areas, the annual mortality rate from bloat in dairy cows may

approach *" $here is also economic loss from depressed mil+ production in

nonfatal cases and from suboptimal use of bloat!prone pastures" Bloat can be

a significant cause of mortality in feedlot cattle"

Etiology and Pathogenesis

#n primary ruminal tympany, or frothy bloat, the cause is entrapment of the

normal gases of fermentation in a stable foam" Coalescence of the small gas

bubbles is inhibited, and intraruminal pressure increases because eructationcannot occur" Several factors, both animal and plant, influence the formation

of a stable foam" Soluble leaf proteins, saponins, and hemicelluloses are

believed to be the primary foaming agents and to form a monomolecular layer

around gas rumen bubbles that has its greatest stability at about p -"'"

Salivary mucin is antifoaming, but saliva production is reduced with

succulent forages" Bloat!producing pastures are more rapidly digested and

may release a greater amount of small chloroplast particles that trap gas

bubbles and prevent their coalescence" $he immediate effect of feeding is

probably to supply nutrients for a burst of microbial fermentation" owever,the ma.or factor that determines if bloat will occur is the nature of the ruminal

contents" /rotein content and rates of digestion and ruminal passage reflect

the forage0s potential for causing bloat" 1ver a &2!hr period, the bloat!causing

forage and un+nown animal factors combine to maintain an increased

concentration of small feed particles and enhance the susceptibility to bloat"


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Bloat is most common in animals graing legume or legume!dominant

pastures, particularly alfalfa, ladino, and red and white clovers, but also is

seen with graing of young green cereal crops, rape, +ale, turnips, and

legume vegetable crops" Legume forages such as alfalfa and clover have a

higher percentage of protein and are digested more 3uic+ly" 1ther legumes,

such as sainfoin, crown vetch, mil+ vetch, fenugree+, and birdsfoot trefoil, are

high in protein but do not cause bloat, probably because they contain

condensed tannins, which precipitate protein and are digested more slowly

than alfalfa or clover" Leguminous bloat is most common when cattle are

placed on lush pastures, particularly those dominated by rapidly growing

leguminous plants in the vegetative and early bud stages, but can also be

seen when high!3uality hay is fed"

4rothy bloat also is seen in feedlot cattle, and less commonly in dairy cattle,

on high!grain diets" $he cause of the foam in feedlot bloat is uncertain but is

thought to be either the production of insoluble slime by certain species of

rumen bacteria in cattle fed high!carbohydrate diets or the entrapment of the

gases of fermentation by the fine particle sie of ground feed" 4ine particulate

matter, such as in finely ground grain, can mar+edly affect foam stability as

can a low roughage inta+e" 4eedlot bloat is most common in cattle that have

been on a grain diet for *5& mo" $his timing may be due to the increase in the

level of grain feeding or to the time it ta+es for the slime!producing rumenbacteria to proliferate to large enough numbers"

#n secondary ruminal tympany, or free!gas bloat, physical obstruction of

eructation is caused by esophageal obstruction due to a foreign body (eg,

potatoes, apples, turnips, +iwifruit), stenosis, or pressure from enlargement

outside the esophagus (as from lymphadenopathy or sporadic .uvenile

thymic lymphoma)" #nterference with esophageal groove function in vagal

indigestion and diaphragmatic hernia may cause chronic ruminal tympany"

$his also occurs in tetanus" $umors and other lesions, such as those causedby infection with Actinomyces bovis, of the esophageal groove or the

reticular wall are less common causes of obstructive bloat" $here also may be

interference with the nerve pathways involved in the eructation refle"

Lesions of the wall of the reticulum (which contains tension receptors and

receptors that discriminate between gas, foam, and li3uid) may interrupt the


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normal refle that is essential for escape of gas from the rumen"

Ruminal tympany also can be secondary to the acute onset of ruminal atony

that occurs in anaphylais and in grain overload6 this causes a reduction inrumen p and possibly an esophagitis and rumenitis that can interfere with

eructation" Ruminal tympany also develops with hypocalcemia" Chronic

ruminal tympany is relatively fre3uent in calves up to - mo old without

apparent cause6 this form usually resolves spontaneously"

7nusual postures, particularly lateral recumbency, are commonly associated

with secondary tympany" Ruminants may die of bloat if they become

accidentally cast in dorsal recumbency or other restrictive positions in

handling facilities, crowded transportation vehicles, or irrigation ditches"

Clinical Findings

Bloat is a common cause of sudden death" Cattle not observed closely, such

as pastured and feedlot cattle and dry dairy cattle, usually are found dead" #n

lactating dairy cattle, which are observed regularly, bloat commonly begins

within * hr after being turned onto a bloat!producing pasture" Bloat may

develop on the first day after being placed on the pasture but more commonly

develops on the second or third day"

#n primary pasture bloat, the rumen becomes obviously distended suddenly,

and the left flan+ may be so distended that the contour of the paralumbar

fossa protrudes above the vertebral column6 the entire abdomen is enlarged"

8s the bloat progresses, the s+in over the left flan+ becomes progressively

more taut and, in severe cases, cannot be 9tented": %yspnea and grunting are

mar+ed and are accompanied by mouth breathing, protrusion of the tongue,

etension of the head, and fre3uent urination" 1ccasionally, vomiting occurs"

Rumen motility does not decrease until bloat is severe" #f the tympany

continues to worsen, the animal will collapse and die" %eath may occur within* hr after graing began but is more common ∼;52 hr after onset of clinical

signs" #n a group of affected cattle, there are usually several with clinical bloat

and some with mild to moderate abdominal distention"

#n secondary bloat, the ecess gas is usually free on top of the solid and fluid

ruminal contents, although frothy bloat may be seen in vagal indigestion


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when there is increased ruminal activity" Secondary bloat is seen

sporadically" $here is tympanic resonance over the dorsal abdomen left of the

midline" 4ree gas produces a higher pitched ping on percussion than frothy

bloat" $he distension of the rumen can be detected on rectal eamination" #n

free!gas bloat, the passage of a stomach tube or trocariation releases large

3uantities of gas and alleviates distention"

Lesions

cm in diameter) is necessary, but an incision through the s+in must be

made before it can be inserted through the muscle layers and into the rumen"

#f the cannula fails to reduce the bloat and the animal0s life is threatened, an

emergency rumenotomy should be performed" #f the cannula provides some


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relief, an antifoaming agent can be administered through the cannula, which

can remain in place until the animal has returned to normal, usually within

several hours"

4ig" *

Cannulation of rumen, cow"

#llustration by %r" ?heorghe

Constantinescu"

@hen the animal0s life is not immediately threatened, passing a stomach tube

of the largest bore possible is recommended" 8 few attempts should be made

to clear the tube by blowing and moving it bac+ and forth in an attempt to find

large poc+ets of rumen gas that can be released" #n frothy bloat, it may be

impossible to reduce the pressure with the tube, and an antifoaming agent

should be administered while the tube is in place" #f the bloat is not relieved

3uic+ly by the antifoaming agent, the animal must be observed carefully for

the net hour to determine if the treatment has been successful or if an

alternative therapy is necessary"


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8 variety of antifoaming agents are effective, including vegetable oils (eg,

peanut, corn, soybean) and mineral oils (paraffins), at doses of &>'5>'' mL"

%ioctyl sodium sulfosuccinate (docusate), a surfactant, is commonly

incorporated into one of the above oils and sold as a proprietary antibloat

remedy, which is effective if administered early" /oloalene (&>5>' g, /1) is

effective in treating legume bloat but not feedlot bloat" /lacement of a rumen

fistula provides short!term relief for cases of free!gas bloat associated with

eternal obstruction of the esophagus"

Control and Prevention

/revention of pasture bloat can be difficult" Management practices that have

been used to reduce the ris+ of bloat include feeding hay, particularlyorchardgrass, before turning cattle on pasture, maintaining grass dominance

in the sward, or using strip graing to restrict inta+e, with movement of

animals to a new strip in the afternoon, not the early morning" ay must

constitute at least one!third of the diet to effectively reduce ris+ of bloat"

4eeding hay or strip graing may be reliable when the pasture is only

moderately dangerous, but these methods are less reliable when the pasture

is in the pre!bloom stage and the bloat potential is high" Mature pastures are

less li+ely to cause bloat than immature or rapidly growing pastures"

$he only satisfactory method available to prevent pasture bloating is

continual administration of an antifoaming agent during the ris+ period" $his

is widely practiced in grassland countries such as 8ustralia and


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is a highly effective nonionic surfactant that can be given at *'5&' gheadday

and up to 2' gheadday in high!ris+ situations" #t is safe and economical to

use and is administered daily through the susceptible period by adding to

water, feed grain mitures, or molasses" 8 similar polymer (8lfasure) and a

water soluble miture of alcohol ethoylate and pluronic detergents (Blocare

2>**) also are effective but lac+ approval by the 4%8" #onophores are effective

in preventing bloat, and a sustained!release capsule that is administered into

the rumen and releases ;'' mg of monensin daily for a *''!day period

protects against pasture bloat and improves mil+ production on bloat!prone

pastures"

$he ultimate aim in control is development of a pasture that permits high

production, while +eeping incidence of bloat low" $he use of pastures ofclover and grasses in e3ual amounts comes closest to achieving this goal"

Bloat potential varies between cultivars of alfalfa, and low!ris+ L#R% (low

initial rate of digestion) cultivars are available commercially" $he addition of

legumes with high condensed tannins to the pasture seeding mi (*'

sainfoin) can reduce the ris+ of bloat where there is strip graing, as can the

feeding of sainfoin pellets"

$o prevent feedlot bloat, rations should contain D*'5*> cut or chopped

roughage mied into the complete feed" /referably, the roughage should be acereal, grain straw, grass hay, or e3uivalent" ?rains should be rolled or

crac+ed, not finely ground" /elleted rations made from finely ground grain

should be avoided" $he addition of tallow (;5> of the total ration) may be

successful occasionally, but it was not effective in controlled trials" $he

nonionic surfactants, such as poloalene, have been ineffective in preventing

feedlot bloat, but the ionophore lasalocid is effective in control"

Last full reviewrevision March &'*& by Clive C" ?ay, %EM, MESc, %ESc

(ons), 48CESc, %8C#M (ons)

Traumatic Reticuloperitonitis

(ardware disease, $raumatic gastritis)


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Traumatic reticuloperitonitis develops as a consequence of perforation of the

reticulum. It is important as differential diagnosis of other diseases mar'ed by stasis

of the GI tract because it causes similar signs. Traumatic reticuloperitonitis is most

common in mature dairy cattle" occasionally seen in beef cattle" and rarely reported

in other ruminants.

?attle commonly ingest foreign obEects because they do not discriminate against

metal materials in feed and do not completely masticate feed before s#allo#ing.

The disease is common #hen green chop" silage" and hay are made from fieldsthat contain old rusting fences or baling #ire" or #hen pastures are on areas or

sites #here buildings have recently been constructed" burned" or torn do#n. The

grain ration may also be a source due to accidental addition of metal.

Etiology

S#allo#ed metallic obEects" such as nails or pieces of #ire" fall directly into the

reticulum or pass into the rumen and are subsequently carried over the

ruminoreticular fold into the cranioventral part of the reticulum by ruminal

contractions. The reticulo-omasal orifice is elevated above the floor" #hich tends toretain heavy obEects in the reticulum" and the honeycomb-li'e reticular mucosa

traps sharp obEects. ?ontractions of the reticulum promote penetration of the #all by

the foreign obEect. ?ompression of the ruminoreticulum by the uterus in late

pregnancy and straining during parturition increase the li'elihood of an initial

penetration of the reticulum and may also disrupt adhesions caused by an earlier

penetration.

7erforation of the #all of the reticulum allo#s lea'age of ingesta and bacteria"

#hich contaminates the peritoneal cavity. The resulting peritonitis is generally

locali$ed and frequently results in adhesions. 6ess commonly" a more severe

diffuse peritonitis develops. The obEect can penetrate the diaphragm and enter the

thoracic cavity ,causing pleuritis and sometimes pulmonary abscessation and the

pericardial sac ,causing pericarditis" sometimes follo#ed by myocarditis.

ccasionally" the liver or spleen may be pierced and become infected" resulting in


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abscessation" or septicemia can develop.

4ig" &

The relationship bet#een thereticulum" diaphragm" andheartCpericardium in large ruminants.Illustration by r. Gheorghe?onstantinescu.

Clinical Fin!ings

The initial penetration of the reticulum is characteri$ed by the sudden onset of

ruminoreticular atony and a sharp fall in mil' production. 9ecal output is decreased.

The rectal temperature is often mildly increased. The heart rate is normal or slightly

increased" and respiration is usually shallo# and rapid. Initially" the co# exhibits an

arched bac'! an anxious expression! a reluctance to move! and an uneasy" careful

gait. 9orced sudden movements as #ell as defecating" urinating" lying do#n" getting

up" and stepping over barriers may be accompanied by groaning. A grunt may be

elicited by applying pressure to the xiphoid or by firmly pinching the #ithers" #hich

causes extension of the thorax and lo#er abdomen. The grunt can be detected by

placing a stethoscope over the trachea and applying pressure or pinching the

#ithers at the end of an inspiration. Tremor of the triceps and abduction of the

elbo# may be seen.

In chronic cases" feed inta'e and fecal output are reduced" and mil' production

remains lo#. Signs of cranial abdominal pain become less apparent" and the rectal


35/233

temperature usually returns to normal as the acute inflammation subsides and

peritoneal contamination is #alled off. Some cattle develop vagal indigestion

syndrome ,see belo# due to the adhesions that form after foreign body perforation"

particularly those on the ventromedial reticulum.

?o#s #ith pleuritis or pericarditis due to foreign body perforation usually are

depressed" tachycardic ,15 bpm" and pyrexic ,=5)B9 N)5B?O. 7leuritis is manifest

by fast" shallo# respiration! muffled lung sounds! and possibly pleuritic friction rubs.

Thoracentesis may yield several liters of septic fluid. Traumatic pericarditis is most

commonly characteri$ed by muffled heart sounds! ho#ever" early in the disease

process pericardial friction rubs or gas and fluid splashing sounds ,#ashing

machine murmur can be heard on auscultation. Pugular vein distention and

congestive heart failure #ith mar'ed submandibular and bris'et edema is a

frequent sequela of traumatic reticulopericarditis. 7rognosis is grave #ith these

complications. 7enetration through the pericardium into the myocardium usually

results in extensive hemorrhage into the pericardial sac or ventricular arrhythmias

and sudden death.

Diagnosis

This can be based on history ,#hen available and clinical findings if the co# is

examined #hen signs initially appear. :ithout an accurate history and #hen the

condition has been present for several days or longer" diagnosis is more difficult.

ther causes of peritonitis" particularly perforated abomasal ulcers" can be difficultto distinguish from traumatic reticuloperitonitis. ifferential diagnoses should include

conditions that can produce variable or nonspecific GI signs" eg" indigestion"

lymphosarcoma" or intestinal obstruction. Abomasal displacement or volvulus

should be ruled out by simultaneous auscultation and percussion. 7leuritis or

pericarditis of nontraumatic origin produces signs similar to those associated #ith

foreign body perforation.

Although not al#ays necessary" laboratory tests may be helpful. In many cases"

there is a neutrophilia #ith a left shift. Serum haptoglobin" amyloid-A" and totalplasma protein concentrations may be mar'edly increased" and plasma fibrinogen

concentrations may be elevated. Affected cattle may have coagulation

abnormalities" as evidenced by prolonged prothrombin time" thrombin time" and

activated partial thromboplastin time. The acid-base status and serum electrolyte

levels are typically normal because abomasal and small-intestinal absorption can

remain normal. %o#ever" mar'ed hypo'alemic" hypochloremic metabolic al'alosis


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can be seen" presumably because adynamic ileus from peritonitis can affect

abomasal and GI motility and resorption of abomasal secretions. The metabolic

al'alosis can be created or exacerbated by treatment #ith al'alini$ing agents such

as magnesium hydroxide used as a laxative. 7eritoneal fluid analysis can be helpful

in determining if peritonitis is present" particularly the concentration of -dimer and

the neutrophil percentage in the peritoneal fluid. %o#ever" the peritonitis frequently

becomes #alled off" and in these cases peritoneal fluid may be #ithin the reference

range unless obtained from #ithin the lesion. The presence of a magnet in the

reticulum can be determined by movement of a magnetic compass in the region of

the cranioventral abdomen! the presence of a magnet in the reticulum ma'es

traumatic reticuloperitonitis very unli'ely unless the penetrating obEect is not

magnetic.

Hltrasonography of the ventral abdomen is the most accurate means of diagnosing

locali$ed peritonitis near the reticulum and characteri$ing the reticular contraction

frequency. It rarely identifies the presence of a penetrating obEect. Hltrasonography

of the heart and thorax is very useful in the diagnosis of pleuritis and pericarditis as

a sequelae to traumatic reticuloperitonitis.

6ateral radiographs of the cranioventral abdomen can detect metallic material in the

reticulum but should only be ta'en after oral administration of a magnet. To

determine #hether the reticulum is currently perforated" the foreign body must be

visible beyond the border of the reticulum" unattached to the magnet in thereticulum" or positioned off the floor of the reticulum. A depression in the

cranioventral aspect of the reticulum or identification of an abscess ,by gas

accumulation outside a viscus" soft-tissue masses" or a fluid line in the cranial

abdomen are also reliable radiographic findings of penetration. 7ortable

radiographic units cannot penetrate the reticular area of standing adult cattle" and

the co# may need to be transported to #here there is equipment #ith sufficient

po#er. The co# should not be placed in dorsal recumbency in order to obtain

radiographs because such manipulation places stress on adhesions and may lead

to a locali$ed peritonitis becoming a diffuse peritonitis due to gravitational spread ofinfection.

lectronic metal detectors can identify metal in the reticulum but do not distinguish

bet#een perforating and nonperforating foreign bodies.

Treatment


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Treatment of the typical case seen early in its course may be surgical or medical.

ither approach improves the chances of recovery from ∼05D in untreated casesto +5*5D. Surgery involves rumenotomy #ith manual removal of the obEect,s

from the reticulum! if an abscess is adhered to the reticulum" it should be aspirated

,to confirm that it is an abscess and then drained into the reticulum. Antimicrobials

should be administered perioperatively. &edical treatment involves administration of

antimicrobials to control the peritonitis and a magnet to prevent recurrence.

@ecause of the mixed bacterial flora in the lesion" a broad-spectrum antimicrobial

agent such as oxytetracycline ,=0 mgC'g" I3" sid should be used. 7enicillin ,(("555

IHC'g" I&" bid is used #idely and is effective in many cases despite its limited

spectrum. Affected co#s should be confined for =*( #'! placing them on an inclined

plane ,elevated in front is believed by some to limit further penetration of the

foreign obEect" but supporting studies are lac'ing. Supportive therapy" such as oral

or occasionally I3 fluids and S? calcium borogluconate" should be administered as

needed. Rumen inoculation is beneficial in some cases #ith prolonged ruminal

stasis and loss of normal flora.

&ore advanced cases" those #ith obvious secondary complications" or those that

do not respond to initial medical or surgical therapy should be evaluated from an

economic perspective! if the co# is of limited value" slaughter should be considered

if the carcass is li'ely to pass inspection.

Pre)ention7reventive measures include avoiding the use of baling #ire" passing feed over

magnets to remove metallic obEects" 'eeping cattle a#ay from sites of ne#

construction" and completely removing old buildings and fences. Additionally" bar

magnets may be administered 7" preferably after fasting for =+*() hr. Hsually" the

magnet remains in the reticulum and holds any ferromagnetic obEects on its surface.

There is good evidence that giving magnets to all herd replacement heifers and

bulls at ∼= yr of age minimi$es the incidence of traumatic reticuloperitonitis.

3agal Indigestion Syndrome in Ruminants

(Chronic indigestion)


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3agal indigestion syndrome is characteri$ed by the gradual development of

abdominal distention secondary to rumenoreticular distention. The distention #as

originally thought to be the result of lesions affecting the ventral vagus nerve. 3agal

indigestion syndrome is seen most commonly in cattle but has been reported in

sheep.

Etiology an! Pathogenesis

iseases that result in inEury" inflammation" or pressure on the vagus nerve can

result in clinical signs of vagal indigestion syndrome. %o#ever" vagal nerve damage

is not present in most cases of vagus indigestion" and the most common cause istraumatic reticuloperitonitis ,see Traumatic Reticuloperitonitis. ?onditions resulting

in mechanical obstruction of the cardia or reticulo-omasal orifice ,eg" papillomas or

ingested placenta can also result in vagal indigestion if ruminoreticular distention is

present and the condition is subacute to chronic.

%istorically" there #ere ) types of vagal indigestion described based on the

purported site of the functional obstruction. Type I #as failure of eructation or free-

gas bloat" type II #as a failure of omasal transport" type III #as secondary abomasal

impaction" and type I3 #as indigestion of late gestation. Type I and I3 are rare.

Type I vagal indigestion" or failure of eructation" results in free-gas bloat and has

been attributed to inflammatory lesions in the vicinity of the vagus nerve" such as

locali$ed peritonitis" adhesions ,usually after an episode of traumatic

reticuloperitonitis" or chronic pneumonia #ith anterior mediastinitis. ther potential

causes for type I vagal indigestion include pharyngeal trauma" #hich affects a more

proximal part of the vagus nerve" and esophageal compression by abscesses or

neoplasia" such as lymphosarcoma. 3agal indigestion can develop in cattle after

abomasal volvulus #ithout abomasal impaction. These cases #ould presumably fall

into the category of type I vagal indigestion #ith damage to the vagal nerve near the

reticulum and omasum.

Type II vagal indigestion" more correctly termed failure of omasal transport"

develops as a result of any condition that prevents ingesta from passing through the

omasal canal into the abomasum. Adhesions and abscesses ,reticular or single liver

http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_ruminant_forestomach/traumatic_reticuloperitonitis.htmlhttp://www.merckmanuals.com/vet/digestive_system/diseases_of_the_ruminant_forestomach/traumatic_reticuloperitonitis.html


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abscesses are the most common cause of failure of omasal transport and are

usually located on the right or medial #all of the reticulum near the route of the

vagus nerve. Reticular abscesses and adhesions are almost invariably the result of

traumatic reticuloperitonitis. &echanical obstruction of the omasal canal by ingested

material ,eg" plastic bags" rope" placenta or masses ,eg" lymphosarcoma"

squamous cell carcinoma" granulomas" or papillomas can also cause chronic

ruminoreticular distention due to failure of omasal transport.

Type III vagal indigestion is a secondary abomasal impaction. 7rimary abomasal

impaction develops due to feeding of dry" course roughage" such as stra#" in a

chopped or ground form #ith restricted access to #ater and usually during

extremely cold temperatures ,see ietary Abomasal Impaction. Secondary

abomasal impaction is seen most commonly after an episode of traumatic

reticuloperitonitis or occasionally as a sequela to abomasal volvulus. &echanical

fixation of the reticulum to the ventral abdominal floor in co#s #ith reticuloperitonitis

interferes #ith the normal sieving action of the reticulum" #ith passage of large fiber

particles ,1( mm length into the abomasum. The abomasum has difficulty in

emptying the larger particles of food because of the increased viscosity" and they

accumulate in the abomasum" resulting in abomasal impaction.

Type I3 vagal indigestion" or partial forestomach obstruction" is poorly defined. It

typically develops in cattle during gestation and is more appropriately termed

indigestion of late gestation. The condition is thought to be related to the enlarginguterus shifting the abomasum to a more cranial position" #hich inhibits normal

abomasal emptying.

Clinical Fin!ings

The clinical signs vary to some extent #ith the location of the obstruction. In all

cases" there is a gradual development ,over days to #ee's of abdominal distention

secondary to ruminoreticular distention. istention of the dorsal and ventral sacs of

the rumen results in an Q6-shaped rumen on rectal examination. 6eft dorsal and left

and right ventral distention of the abdomen causes a Qpapple ,pear plus appleshape as vie#ed from behind.

?attle #ith vagal indigestion syndrome have a diminished appetite" #hich typically

improves temporarily if distention is relieved. &il' production gradually decreases"

fecal output is reduced" and the rumen develops a Qsplashy fluid consistency. The

feces are characteristically very scant and stic'y and may contain longer than

http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_abomasum/dietary_abomasal_impaction.htmlhttp://www.merckmanuals.com/vet/digestive_system/diseases_of_the_abomasum/dietary_abomasal_impaction.html


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normal particles. The strength of rumen contractions is decreased! ho#ever" rumen

motility is often increased ,


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concentration is usually lo# due to decreased potassium inta'e in the feed. Serum

calcium concentration is often moderately decreased because of ongoing mil'

production" but it is rarely lo# enough to cause recumbency. Serum urea and

creatinine concentrations increase #ith dehydration due to prerenal a$otemia.

Diagnosis

iagnosis is based on the presence of subacute to chronic ruminoreticular and

abdominal distention. @ecause vagal indigestion is by definition a subacute to

chronic disease" this diagnosis should not be made in cattle that have not been sic'

for at least several days" #hich rules out acute rumen tympany and acute frothy

bloat. ther causes of abdominal distention" such as ascites and uterine

enlargement" are included in the differential diagnosis and can almost invariably be

ruled out by rectal palpation due to the absence of ruminoreticular distention.

ccasional cases of longstanding obstruction of the cecum or small intestine can

cause severe ruminoreticular and abdominal distention! ho#ever" palpable cecal or

small-intestinal distention is also palpable rectally. In addition" the rumen is

distended but not 6-shaped" and a characteristic ping is present in the case of

cecocolic volvulus.

iagnosing the specific cause of vagal indigestion is more difficult but is important

because of differences in treatment and prognosis. 7hysical examination" rectal

examination" ?@?" blood acid-base determination" and serum biochemical values

are often useful. 7eritoneal fluid analysis can support the diagnosis of peritonitis iftotal protein or nucleated cells are increased. 6ateral radiographs of the reticulum

should be ta'en to identify an opaque linear foreign body ,eg" #ire or reticular

abscess. Hltrasonography of the cranioventral abdomen can indicate the presence

of focal peritonitis and the reticular contraction rate. efinitive diagnosis often

requires exploratory surgery ,left paralumbar fossa laparotomy and rumenotomy.

Treatment an! Prognosis

If the value of the animal Eustifies treatment" surgery is almost al#ays needed to

identify and potentially correct the underlying cause. &edical management alone isusually ineffective. A left paralumbar fossa laparotomy and rumenotomy provides

the opportunity for definitive treatment in some cases. mptying the rumen at the

time of surgery may help restore normal rumen motility. Stimulation of lo#-threshold

tension receptors in the reticulum occurs under normal circumstances and causes

reflex reticuloruminal contractions. %o#ever" severe distention causes stimulation of


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high-threshold receptors that have the opposite effect and inhibit contractions.

Supportive or symptomatic therapy should be provided in all cases" #hich typically

involves correcting dehydration as #ell as calcium and electrolyte deficits"

commonly #ith oral fluids and electrolytes. Severely dehydrated animals and those

#ith longstanding disease require I3 fluids. 9resh #ater and normal feed should be

available. Transfaunation at surgery or via oroesophageal intubation may help

reestablish normal rumen flora in cattle #ith chronic anorexia. Antimicrobials

,procaine penicillin or oxytetracycline should be given if the underlying cause is

infectious or if a rumen fistula is created.

Treatment of type I vagal indigestion ,failure of eructation also typically involves

creating a rumen fistula to allo# free gas to escape. If surgery is not economically

feasible and the underlying cause of vagal indigestion has been identified andtreated" a rumen trocar can be placed temporarily. Such trocars are commercially

available and must be secure and self-retaining to prevent potentially fatal lea'age

of rumen contents into the peritoneal cavity. The trocar should not be removed for at

least ( #' to allo# firm adhesions to form bet#een the rumen and body #all.

The prognosis for animals #ith type I vagal indigestion is usually favorable. After

creation of a rumen fistula" the signs of vagal indigestion resolve in nearly all cases.

%o#ever" animals #ith chronic respiratory disease or pharyngeal trauma may not

recover from the underlying condition. 6ea'age of ingesta from fistulas can causeoff-flavored mil'. 7eritonitis can develop from lea'age around the fistula or follo#ing

rumenotomy! ho#ever" this should not happen #ith good surgical technique.

Type II vagal indigestion ,failure of omasal transport rarely responds to supportive

or symptomatic therapy #ithout surgical intervention. 6eft paralumbar fossa

laparotomy and rumenotomy can be used to identify adhesions in the vicinity of the

reticulum" reticular or hepatic abscesses" or obstruction of the omasal canal.

Removal of foreign bodies" #ires" and some masses at surgery and lancing of

perireticular abscesses into the reticulum affords a fair to good prognosis. A

diagnosis of lymphosarcoma at surgery #arrants a grave prognosis. Reticular

abscesses identified at surgery should be cautiously drained into the reticulum" and

antibiotics given for =5*=) days. Reportedly" +


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surgery. 6arge-bore cannulas placed through the body #all" through the adhesions"

and into the abscess #ill drain the purulent material. %o#ever" recurrence is more of

a problem #ith hepatic abscesses than #ith reticular abscesses.

Animals #ith type III vagal indigestion ,secondary abomasal impaction diagnosed

#ithout surgery usually do not receive further treatment because of the poor

prognosis" particularly if there is a history of traumatic reticuloperitonitis or abomasal

volvulus. If the diagnosis is made at surgery or if the abomasal impaction is thought

to be dietary" dioctyl sodium sulfosuccinate can be infused directly into the

abomasum via the reticulo-omasal orifice after emptying the rumen. A nasogastric

tube can be passed into the abomasum via the reticulo-omasal orifice at surgery

and left in place for continued treatment ,= gal of mineral oil daily for


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reticular motility and the appropriate stratification of feed particles for passage

through the abomasum. Therefore" prevention of traumatic reticuloperitonitis is

important. Good management practices may prevent some cases of vagal

indigestion associated #ith chronic pneumonia. arly diagnosis of abomasal

volvulus" #ith same-day surgical correction" may prevent some cases.

Ruminal rin'ing

QRuminal drin'ing is caused by failure of the reticular groove reflex and results in

ruminal acidosis in calves on a liquid diet. The disorder presents as primary chronic

disease ,ruminal drin'ing syndrome in veal calves" and in its acute form as acomplication secondary to different neonatal diseases" most commonly neonatal

diarrhea. It has also been described in artificially fed lambs.

The reticular groove is a muscular structure extending from the cardia to the

reticulo-omasal orifice. Its correct closure is a precondition for the direct passage of

ingested mil' or mil' replacer into the abomasum. :hen partial or total failure of the

reticular groove to close occurs" mil' spills into the reticulorumen and is fermented

to short-chain fatty acids andCor lactic acid. The subsequent drop in the p% of the

ruminal contents to values that occasionally fall belo# ) leads to variable degreesof inflammation of the mucosa of the forestomachs and the abomasum. In chronic

cases" hyper'eratosis or para'eratosis of the ruminal mucosa can lead to

impairment of ruminal motility #ith chronic or recurrent tympany. Additionally"

atrophy of the intestinal villi and a decrease in brush border en$yme activity #ith

maldigestion and malabsorption have been observed.


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Systemic consequences of acute ruminal drin'ing are mainly due to absorption of

organic acids from the digestive tract. In particular" the 6- and -isomers of lactic

acid may lead to metabolic acidosis #ith the accumulation of -lactate because of

an absence of a specific en$yme for its metabolism in mammals. This accumulation

of d-lactate has recently been found to be responsible for clinical signs such as

depression" ataxia" and general #ea'ness.

7rimary dysfunction of the reticular groove occurs as a result of stressful situations

,prolonged transport" grouping" change in feeding techniques especially in buc'et-

fed veal calves. ?linical signs usually appear some #ee's after the arrival of the

calves at the fattening units and are characteri$ed by inappetence" depression"

poor gro#th" hair loss" recurrent tympany" ventral abdominal distention" and passing

of clay-li'e feces. 9luid-splashing sounds can be heard on succussion of the left

flan'. Recovery of fermented ruminal contents via stomach tube is diagnostic. In

these advanced" chronic cases the prognosis is poor. If the disease is detected

early enough" feeding small volumes of mil' from a nipple-bottle or buc'et may be

successful. Additionally" the closure of the reticular groove can be triggered by

allo#ing the calf to suc' a finger before the mil' feed is offered.

Acute ruminal acidosis secondary to other disorders is most commonly seen in

calves #ith neonatal diarrhea but occurs also in other painful or #ea'ening

diseases. In these cases the clinical picture is usually dominated by the underlying

disease. In cases of severe rumenitis" calves may exhibit teeth grinding" arching ofthe bac'" and slight abdominal distention. 9orce-feeding of inappetent or primarily

anorectic calves can also cause ruminal acidosis or #orsen the situation by

providing substrate for further fermentation.

The prognosis for secondary ruminal drin'ing depends mainly on the success of

treatment of the underlying disease. ?alves #ith metabolic acidosis and

dehydration due to neonatal diarrhea #ill usually recover spontaneously from

ruminal drin'ing after adequate treatment" and the condition #ill in general remain

unrecogni$ed. In calves that #ere force-fed or that do not respond to treatment asexpected" ruminal drin'ing should be considered" and an examination of the ruminal

fluid should be performed. Removal of the contents and lavage #ith #arm #ater via

stomach tube may be beneficial" especially after prolonged force-feeding.

7rophylaxis of ruminal drin'ing consists of early treatment of diseased calves"

adequate feeding techniques" and minimi$ing stress in purchased calves.


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Ruminal 7ara'eratosis

Ruminal para'eratosis is a disease of cattle and sheep characteri$ed by hardening

and enlargement of the papillae of the rumen. It is most common in animals fed a

high-concentrate ration during the finishing period. It also is seen in cattle fed

rations of heat-treated alfalfa pellets" as #ell as in calves #ith prolonged ruminal

acidosis due to ruminal drin'ing. It does not appear to be related to the feeding of

antibiotics or protein concentrates. Incidence in a group may be as high as )5D.

The lesions are thought to be caused by the lo#ered p% and the increased

concentration of volatile fatty acids ,39A in the ruminal fluid" and do not usually

develop in cattle fed unprocessed #hole grain ,on #hich animals gain #eight as

readily. This may be related to the higher p% and higher concentration of acetic

acid compared #ith the longer chain 39A in the ruminal contents.

&any of the papillae are enlarged and hardened" and several may adhere togetherto form bundles. The papillae of the anterior ventral sac are commonly affected. In

cattle" the roof of the dorsal sac may sho# multiple foci ,each (*< cm ( of

para'eratosis. In sheep" abnormal papillae may be visible and palpable through the

#all of the intact rumen. Affected papillae contain excessive layers of 'eratini$ed

epithelial cells" particles of food" and bacteria. The rumens of affected cattle are

difficult to clean in the preparation of tripe. The abnormal epithelium" by interfering

#ith absorption" may reduce efficiency of feed utili$ation and rate of gain" although

there is little evidence to support this theory.

Ruminal para'eratosis may be prevented by finishing animals on rations that

contain unground ingredients in the proportion of = part roughage to < parts

concentrate. The necessity and economics of prevention are not #ell defined.


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Peritonitis

Peritonitis is an infammatory process that involves the peritoneal

cavity and its serosal surace, the peritoneum. This may result rom

trauma, surgery or vascular damage associated with an intestinalostruction and or accident or rom gastrointestinal ulceration.

Peritonitis is a serious and complex process that is oftenaccompanied by various degrees of abdominal pain,progressive signs of hypovolemia and septicemia and orenterotoxemia

Peritonitis may be primary or secondary disease. As aprimary disease it results commonly by rupture of or spread

of infection from a site less commonly by perforation of theabdominal wall from the exterior. Individual causes are asfollows:

Etiology

Cattle !u"alo:

#raumatic $eticulo peritonitis

Perforation or lea%age of abomasal ulcer

$upture of abomasums after torsion

$uminitis of cattle due to acute C&' indigestion

&epatic abscess of blac% disease in cattle and horses

$upture of vagina in young heifers during violate coitus

(eposition of semen in the peritoneal cavity

In)ection of hypertonic solution i.e calcium preparation inmil% fever.


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Intraperitoneal in)ection of non sterile solutions.

*pontaneous uterine rupture during parturation due todysto%ia.

*pontaneous rupture of rectum at calving.

*peci+c disease including tuberculosis and sporadic bovineencephalomyelitis.

&orses

$upture of dorsal sac of caecum or colon at foaling

Administration of nonsteroidal antiin-ammatory drugs causing caecalstasis and dilation and eventually perforation.

$ectal rupture or tar during rectal examination

After the attac% of strangle due to %treptococcus e/ui or Corynebacteriume/ui infection.

astric erosion and rupture related to ulceration caused by larva of

$astrophillus or (abronema spp.

• /ea%age from a caecal perforation caused by a heavy infestation of )noplocephala peroliata tapeworms.

)ctinobacillus e/uuili infection

*heep

Infestation with "esophagostomum sps larvae

*erositis or arthritis caused by 0ycoplasma sps.

oat


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• *erositisarthritis caused by 0ycoplasma sps.

Pathogenesis

a0 #oxemia

1icrobial population

#issue degradation2decomposition

#oxin elaboration

#oxin absorption via peritoneum

#oxemia

(eath within 34 5 46 hours.

b0 *hoc% and haemorrhages

(eposition of gut contents, infected uterine contents into peritonealcavity and haemorrhage resulting from the rupture

&ypovolemia

Peripheral circulatory failure, shoc% and haemorrhage.

c0 Paralytic ileus

#ransient hypermotility of the gut

$e-ex sympathetic stimulation

Inhibition of gut motility

Paralysis of intestinal musculature

Paralytic ileus.

d0Abdominal pain


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Irritation of the nerve endings

Persistent pain

#ransmission through spinal cord

$igidity of the abdominal wall

Arched bac% posture

7vidence of pain on palpation of abdominal wall.

e0 1uscle wea%ness

Peritoneal infection

Increased adrenocortical activities

Increased production of glucocorticoides aldosterone

8a ion retention and potassium ion loss

1uscle wea%ness

f0 Adhesions

Adhesion causes partial and complete obstruction of the intestine orstomach

Interfere with normal gut motility.

9agus indigestion in cattle and intestinal obstruction in horses.

!ymptoms

".Peracute di#use peritonitis

*evere wea%ness, depression and circulatory failure.

Animal is recumbent and often unable to rise, depressed almost to thepoint of coma.

*ubnormal temperature ;.


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&igh pulse rate?;;aeces have thic% sludge li%e consistency and be tenacious and dicult toremove from the rubber, gloves and have foul smell.

In cows with acute peritonitis, ruminal contents are reduced or absent.

In horse, gut stasis is evidenced by an absence or reduction of gut soundson auscultation.

In cattle, abdominal pain is evidenced by disinclination to move and liedown

/ying down with great care and grunting with pain. Arched bac% conditionand lowering of the head .

In horse, abdominal pain is evidenced by -an% watcing, %ic%ing at the

belly going down and rolling.

B. Chronic peritonitis

Indigestion and toxemiadue to adhesion

8/17/2019 Veterina

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