Gi Exam 1

Front 1

Piglets-Clostridium perfringens Types A and C; C. difficile

Back 1

Age affected: C. perfringens (both) 1-14 days old, can occur within 12 hours; C. difficile 1-7 days
Hallmarks: Tends to occur in non-immune herds. Type A is very non-distinct; Type C only hemorrhagic diarrhea of neonatal piglets; C. difficile often accompanied by edema.
Treatment: Antibiotics for mildly sick or clinically unaffected to prevent further losses, penicillin or ampicillin; fluids with dextrose; antitoxin for C. perfingens type C may be used in show or pet pigs but not common in commercial operations.
Prognosis: Type A-fair to guarded; Type C-grave; C. difficile-death usually very low.
Prevention: Type C-immunize sows 2-3 weeks prior to farrowing. Type A-vaccine available. Good sterilization/disinfection of farrowing cages.

Front 2

Piglets-E. coli (enterotoxigenic)

Back 2

Age affected: 1 day to post weaning, most commonly 0-4 days of age.
Hallmark: may appear as early as 2-3 hours after birth. May cause vomiting, litters born to gilts more likely affected than sows.
Diagnosis: Necropsy culture, gram-neg rods adhered to gut, alkaline pH of diarrhea suggests bacteria.
Treatment: Antibiotics according to sensitivity, start with broad spectrum such as ceftiofur. Fluid therapy
Prognosis: good to guarded.
Prevention: vaccination of sows and gilts, ensure that piglets ingest colostrum. Keep ambient temperature 86-93 degrees F. Proper sanitation.
Other: By one week of age, piglets make their own specific antibodies and develop immunity.

Front 3

Piglets (and all)-Coronavirus/TGE

Back 3

Age affected: 1 day to adult
Hallmarks: transient vomiting followed rapidly by watery diarrhea. More of a problem in herds that have never been exposed. Most common in the winter, seems to inactivate during the summer.
Diagnosis: necropsy, villous atrophy of small intestine, stomach distended with curdled milk, congestion of the stomach. Detection of viral antigen in small intestine.
Treatment: fluids with electrolytes and glucose. Warm dry environment (corona likes it cold), antibiotics for secondary bacterial infections, cross-suckling.
Prognosis: Grave for piglets, improves with age.
Reservoirs: carrier pigs, subclinical infections, non-swine hosts.
Prevention: maintain closed herd, strict biosecurity measures, quarantine new animals for at least 1 month, keep herd in enclosed buildings. Vaccinate.
Other: Not to be confused with other corona virus that causes resp. infection.

Front 4

Piglets-Rotavirus

Back 4

Age affected: 2-7 wks, avg. age 19 days (maternal antibodies wane after 2 wks).
Hallmarks: Mild diarrhea and dehydration, 2-3 days duration. Comes from fecal-oral contamination; piglets shed virus in large amounts during infection.
Diagnosis: Necropsy, ELISA test on feces or gut.
Treatment: fluids, electrolytes, and glucose, abx for secondary infection, proper temperature.
Prognosis: fair to good, mortality low (esp. compared to TGE).
Prevention: Sanitation and disinfection of farrowing crates. Vaccination of sows and gilts during gestation, and neonatal piglets.

Front 5

Piglets-Cryptosporidiosis

Back 5

Age affected: 3 days to weaning, up to 12 wks of age.
Hallmarks: suspect only if no bacterial or viral cause identified.
Diagnosis: Fecal floatation
Treatment: Fluids, no practical medicine treatment.
Prognosis: good to fair
Prevention: sanitation.

Front 6

Piglets-Coccidiosis

Back 6

Age affected: 5-15 days, 7-11 days most common.
Hallmarks: suspect when diarrhea does not respond to antibiotics. Endemic on most farms.
Diagnosis: oocysts in feces, lesions occur in jejunum and ileum.
Treatment: No effective coccidiostats currently on the market, Baycox/toltrazuril in Canada.
Prognosis: Guarded
Prevention: sanitation

Front 7

Grower/finisher pigs-swine dysentery

Back 7

Age affected: 5-30 weeks, or 30-150 lbs.
Hallmarks: watery diarrhea with blood, mucus, and shreds of white exudate (sloughed mucosa). Severely affected pigs may become weak, uncoordinated, emaciated, and will die. Scarring of intestine causes pig to become a poor-doer.
Diagnosis: Dark field microscopy detection of BRACHYSPIRA HYODYSENTERIAE on mucosal scraping. Lesions only in the large intestine.
Treatment: Lincomycine added to feed or water. IM injection may be used in a single affected pig.
Prognosis: varies based on severity, individual resistance/response, and rapid/delayed treatment.
Prevention: Strict biosecurity measures, Quarantine new or returning animals.

Front 8

Grower/finisher pigs-proliferative enteropaty/ileitis

Back 8

Age affected: any, typically occurs 2 weeks after a stressful event.
Hallmarks: three "types"-diarrhea syndrome, wasting syndrome, and acute hemorrhagic enteropthy that leads to death. This is the "Johne's" of pigs.
Diagnosis: Caused by LAWSONIA INTRACELLULARIS, this is notoriously difficult to culture. Lesions in the ileum and colon. Diarrhea and wasting forms, bowel will be thickened and necrotic. Acute, hemorrhagic form, bowel will be hemorrhagic.
Treatment: can be self limiting. Tylan or other antimicrobials can be added to feed or water.
Prevention: vaccination. Avoid risk factors (commingling, moving, weather stress, humid environments, disruption in feed intake), good sanitation, addition of effective antimicrobials prophylactically in food.

Front 9

Grower/finisher pigs-whipworms

Back 9

Age affected: 1-6 months
Hallmarks: not much of a problem in confinement-raised herds. Mucohemorrhagic diarrhea similar to swine dysentary but without the shreds of mucosa.
Diagnosis: Fecal flotation. Necropsy lesions and visible worms can be found in the cecum and colon.
Treatment: Dewormer-Tramisol, Atgard, and Safeguard (fenbendazole).

Front 10

Grower/finisher pigs-Salmonellosis

Back 10

Age affected: 3-30 wks.
Hallmarks: Two forms. Septicemic form (S. choleraesuis) is sudden onset, causes red to purple discoloration of the skin, and often leads to death before diarrhea develops. Enterocolonic form (S. typhimurium causes bloody mucoid diarrhea with a foul necrotic smell, can cause rectal strictures, recovered animals are often chronic poor-doers. Classic appearance of pigs with enteric form is immaciation with extremely distended belly.
Diagnosis: Culture. Enterocolonic form causes "volcanic eruptions" (lesion) in the small and large intestines.
Treatment: antibiotics with gram negative activity. eg. Ceftiofur. Be careful with drugs that have excessive withdrawal times due to how rapid pigs go to market.
Prognosis: Varies, but septicemic form has very poor prognosis.
Control: Sanitation is key. Remove diseased stock. Early weaning of piglets. Vaccination is moderately successful. Prophylactic antibiotics added to feed.

Front 11

Pigs-Gastric ulcers

Back 11

Age affected: Any. Almost all 10-12 wk old pigs have some gastric ulceration.
Hallmarks: Reduced feed intake, vomiting shortly after eating, sudden death, black tarry feces, "gothic pig syndrome".
Diagnosis: Occult blood test of feces is suggestive, endoscopy (show/pet pigs), necropsy.
Treatment: Antacids, H2 blockers, proton pump inhibitors-only practical for show or pet pigs.
Prognosis: good with treatment, guarded without.
Prevention: Avoid finely ground feed, overcrowding, unsanitary environments, being off feed, high humidity, and other stresses.
Other: Barrows have higher mortality.

Front 12

Pigs-Rectal prolapse

Back 12

Occurs due to pig piling during cold weather, coughing, and sometimes with diarrhea.
Imperative to isolate prolapsed pig to avoid being chewed on by other bored pigs.
Repair: If fresh and undamaged, the prolapse can be lubed and replaced, then prevented from recurring with a "purse string" tie around the anus for 2 weeks. If old or damaged, a prolapse ring is placed in the anus and fixed in place with an emasculator band. The prolapsed portion and ring are allowed to slough off (4-5 days).
The sooner a prolapse is dealt with the easier it is to fix!

Front 13

Stomatitis of cattle: Vesicular stomatitis

Back 13

Affects cattle, pigs, horses, and occasionally sheep.
Incubation of 3-14 days, duration of 2-21 days.
Typically starts in Mexico, spreads at shows.
Vesicles that progress to ulcers.
High morbidity, low mortality. Leads to loss of milk production or rate of gain.
Treatment is symptomatic-viral infection.
This disease is reportable to the state vet.
Note: infection of horses is what differentiates vesicular stomatitis from foot and mouth disease.

Front 14

Stomatitis of cattle: Bovine viral diarrhea virus

Back 14

Multisystemic viral disease of cattle.
Two forms: cytopathic and non-cytopathic. Can seroconvert from one to the other.
Acute infection of immunocompetent naive cattle: 1. systemic infection with mild signs, or 2. acute gastroenteritis with fever, salivation, erosions, and diarrhea.
Persistent infection: occurs when cattle are exposed in utero to non-cytopathic form. Results in "mucosal disease" when cytopathic form is encountered; rapidly results in death. PI cattle shed virus constantly, are poor doers, and tend to get other infections due to immunocompromise.
Average age <2 years.
Diagnosis: Serology and virus isolation. Ear punch biopsy and immunohistochemistry is used to detect PIs.
Treatment: Symptomatic.
Prognosis: If erosions do not get worse, prognosis is good. Cattle with mucosal disease always die.
Prevention: Vaccination, identify and cull PI cattle.

Front 15

Stomatitis of cattle: Caustic substances

Back 15

Typically occurs when calcium chloride supplement is given to a cow with pre-existing toxemia or renal disease. Chloride is highly causting to the oral mucosa and GI.

Front 16

Stomatitis of cattle: Foot and mouth disease, rinderpest, vesicular exanthema

Back 16

These are foreign diseases, and all of them are reportable.

Front 17

Stomatitis of cattle: Malignant Catarrhal Fever

Back 17

Highly fatal virus of cattle, sheep, and wild ungulates.
Severe keratoconjunctivitis, mucopurulent nasal and lacrimal discharge, high fever. Lesions in the mouth can affect the papilla; if bright red, indicates active viremia.
Sheep are carriers, and seem to shed virus heaviest at lambing.
Mainly controlled by isolating sick animals and avoiding sheep/cattle contact.

Front 18

Stomatitis of cattle: Bluetongue

Back 18

Mild disease in cattle, more severe in sheep.
Causes a burnt appearing muzzle.
In sheep: edematous swelling of the face, tongue may become cyanotic.
Diagnosed by serology and virus isolation.
Treatment is supportive.

Front 19

Stomatitis of cattle: Bovine Papular Stomatitis

Back 19

The "chicken pox" of cattle. Mostly occurs in young, and causes little damage or problems.
Afterwards leaves freckle like marks on the nose.
No reason to treat.
May reach 100% morbidity by mortality is rare.
Potentially zoonotic.

Front 20

Stomatitis of cattle: Uremia

Back 20

Salivary glands of cattle recycle ammonia. If severe renal disease, too much is secreted and causes necrosis and inflammation of the oral mucosa.

Front 21

Stomatitis of cattle: Contagious Ecthyma (ORF)

Back 21

Most common in sheep and goats.
Causes large lumpy lesions on the nose and lips, can occur on the teats.
Does not typically cause much problem, unless lesions on the teats prevent the mother from allowing young to nurse; then supportive care for the young will be required.
Zoonotic.

Front 22

Principles of diagnosing stomatitis diseases of cattle/ruminants

Back 22

1. Inspection of oral cavity is a must.
2. ALWAYS KEEP RABIES IN MIND.
3. Serology, culture, virus isolation.
4. Based on typical symptoms and history.

Front 23

Principles of treating stomatitis diseases of cattle/ruminants

Back 23

1. Most causes are viral, so treatment is symptomatic.
2. Provide good quality, easily digestable ration (soft grass is best)
3. Antibiotics as needed to prevent secondary infections.
4. Antiseptic mouthwasyes can be used.

Front 24

Prognosis of stomatitis in cattle/ruminants

Back 24

Grave for BVD/Mucosal disease, Foot and mouth disease, rinderpest, and malignant catarrhal fever.
Fair to good for the vesicular diseases and caustic substances.
No Problem with bovine papular stomatitis.

Front 25

Foreign bodies of cattle/ruminants

Back 25

General symptoms: difficulty eating/drinking, abnormal chewing, slobbers, necrotic breath.
Etiologies: Grass awns are most common; also sticks, bones, wood, cans, wire, etc.
Diagnosis: examination of the oral cavity, pass a stomach tube, endoscopy
Treatment: Remove object, prophylactic antibiotics. Consider slaughter if really bad.

Front 26

Woody tongue-cattle

Back 26

Symptoms: enlarged, stiff tongue, may protrude from mouth; difficulty eating, slobbers, abnormal chewing, lesions contain characteristic "sulfur" granules
Etiology: Granulomatous lesion caused by Actinobacillus lignieresii
Diagnosis: Culture, examination of the oral cavity.
Treatment: Sodium iodine. (possible this causes abortion, but not proven). Sulfonamides, tetracycline, NSAIDs-don't work as well as sodium iodine. Provide soft feed
Prognosis: Treatment is usually successful, and prognosis is good if only tongue is involved. Prognosis fair if other organs or lymphnodes are involved.

Front 27

Lumpy jaw-cattle

Back 27

Clinical signs: hard swollen jaw, may have fistulous tracts, lesions contain characteristic "sulfer" granules.
Etiology: Caused by Actinomyces bovis (normal oral flora) that penetrates tissue after oral trauma.
Diagnosis: PE-hard, immovable, non-painful mass on jaw. Radiographs, culture, biopsy.
Treatment: Sodium iodine is best. Penicillin or streptomycin may be given but does not work as well. Surgical removal if little bone involvement.
Prognosis: starts out fair, decreases as bony involvement increases and fistulous tracts appear.

Front 28

Traumatic Pharyngitis-cattle

Back 28

Caused by forceful use of balling guns, frick speculums, or other equipment that is inserted into the pharyngeal region.
Symptoms: swelling of the throat-latch area, dyspnea, will hold head up and out.
Diagnosis: based on history and physical.
Treatment: FANO, slaughter (survival is rare)
Before treating or slaughtering, consider what medications were given if caused by a balling gun, that may prevent the animal from going to slaughter (withdrawal times).

Front 29

Choke-cattle/ruminants

Back 29

Symptoms: palpable/visible mass on the LEFT side of the neck. Reflux, slobbers, bloat.
Etiology: Occurs in summer and fall when apples, pears and other fruit are available. Sheep and goats may choke on grain or pellets, but this is rare in cattle. May also be caused by swelling from a sting, if a bee or wasp is swallowed with the fruit.
Diagnosis: palpation of the oral cavity and neck, pass a stomach tube ("choke" may also be caused by extra-luminal masses), endoscopy
Treatment: Relieve bloat 1st! Removal of blockage-"milk" up the esophagus if close to the mouth, push down into the rumen with a kingman tube if close to the rumen (esophagus enters at 8th intercostal space), rumenotomy and pass a tube retrograde, wire hook or Probang to "spear" the object and pull it up, shop vac (??). Also consider immediate slaughter if animal is low value. Post removal NSAIDs and antibiotics as needed.
Prognosis: good unless esophageal mucosa has been damaged. Guarded for first 24 hours.

Front 30

Calf Diphtheria-cattle

Back 30

Caused by Fusobacterium necrophorum. Occurs only in calves.
Causes foul breath and "choke"-like symptoms.

Front 31

Ruminant liver disease-Liver abscess

Back 31

Clinical signs: Usually subclinical, differential for poor-doers. Bilateral epistaxis-caused by abscess that penetrates into major liver vessels and causes thrombosis in the caudal vena cava.
Etiology: Most cases are caused by Fusobacterium necrophorum. Often a sequela to grain overload in cattle, or caseous lymphadenitis in sheep/goats. Occasionally associated with omphalitis or hardware disease.
Diagnosis: May have inflammatory leukogram, anemia of chronic inflammation, and increased liver enzymes with very active infections. Ultrasound +/-aspiration and culture. Chest radiographs may show "embolic pattern" in the lungs.
Treatment: Consider immediate slaughter. Long term antibiotic therapy can be used in pet/show/high value cattle.
Prognosis: poor
Control: Proper feed management (avoid overfeeding, properly secure feed, change feeds gradually, consider abx additives). Vaccines are available. Prevent caseous lymphadenitis from entering sheep/goat herds.

Front 32

Cattle: Bloat

Back 32

Two types-gas bloat and frothy bloat
Clinical signs: Acute onset, bulging of the left paralumbar fossa, dyspnea, may appear uncomfortable but happy, may be found dead.
Etiology: 1. Frothy bloat-diets high in soluble protein such as alfalfa, clover (legumes), and winter wheat. Also, grain diets increase slime forming bacteria. Any rapid change in diet may trigger frothy bloat, and lush pastures are associated with frothy bloat.
2. Free gas bloat-grain/carb heavy diets lead to excessive gas production. Failure to eructate due to a large variety of causes will lead to gas bloat. Gas bloat can be positional; esophageal opening is pinched off, or covered with rumen content.
3. Gas bloat tends to occur sporatically, while frothy bloat will occur in groups.
Diagnosis: Based on typical history. Passing a tube or trocarizing the rumen can distinguish between frothy bloat and gas bloat (providing an opening will relieve gas bloat rapidly).
Treatment: Keep animal moving to mix rumen content, position animal up an incline to reduce pressure on the diaphragm, improve saliva flow, pass a tube to relieve free gas; Therabloat or home mixture of veg oil, water, and detergent will eliminate frothy bloat. Rumenostomy may provide relief from chronic bloat until slaughter. Correct the underlying problem! Transfaunation may help in cases where rumen flora has been disturbed.
Control: Control access to legumes, administer monensin prior to exposure to bloat causing agents, daily BloatGuard, avoid rapid changes in diet, provide adequate roughage, avoid fine grains, avoid over feeding.

Front 33

Cattle: Hardware disease

Back 33

Clinical signs: Anorexic, depressed, decreased milk production/weight gain, grunting, distended jugulars, "washing machine" sound of heart ascultation.
Etiology: Wire, nails, and other heavy metal objects will fall into the reticulum when eaten. During rumenal contractions they penetrate the reticulum wall, and migrate, causing peritonitis. Can cause pericarditis if the pericardial sac is penetrated. Usually seen in adult cattle. Dairy cattle tend to have a higher incidence than beef cattle.
Diagnosis: "Grunt" test (not very specific); neutrophilia, hyperfibrinogenemia, and total protein above 10; exploratory sx; radiographs; "washing machine" heart sounds and distended jugulars suggestive of traumatic pericarditis.
Treatment: Magnets! Antibiotics and NSAIDs (start with ceftiofur and banamine, short withdrawal time if no response); surgery; consider slaughter.
Control: Give magnets to all heifers prior to first parturition. Use magnets on feed mixing equipment to reduce potential. Avoid grazing cattle where buildings have been torn down.

Front 34

Cattle: Simple Indigestion

Back 34

Disturbance of normal rumen flora.
Clinical signs: Anorexia, increase or decrease in rumen motility, gassy pings over upper right rib of paralumbar fossa, diarrhea, bloat, dehydration.
Etiology: Over consumption of indigestible feeds, overconsumption of regular feeds, damaged feeds (eg. moldy), sudden changes in feed. Typically occurs sporadically, but can occur in outbreaks. Suspect feeds: new silage, bottom of the silo feeds, and moldy feeds.
Diagnosis: Based on history and lack of severe signs. Check rumen pH and microflora to rule out more serious ruminal acidosis. Diagnosis by exclusion or response to treatment.
Treatment: Laxatives and transfaunation if necessary. Most animals return to normal in 2-3 days without treatment. Give fluids if dehydrated from diarrhea.
Control: Maintain good quality feed and change feeds gradually.

Front 35

Cattle: Ruminal acidosis

Back 35

Clinical signs: Depression, hypertonic rumen followed by atonic rumen, acute death, anorexia, fluid filled rumen, diarrhea, dehydration, staggering.
Etiology: Overconsumption of carbohydrates favors gram positive bacteria, which overproduce lactic acid, lowering rumen pH. Protozoa and other normal flora die. Lactic acid is absorbed into circulation causing systemic acidosis, and what is left in the rumen cause water to be pulled into the rumen. Lactic acid damage to the rumen mucosa leads to bacterial or mycotic rumenitis (and possibly liver abcess/vena cava syndrome)
Diagnosis: History, and check rumen pH and rumen flora (protozoa will be dead).
Treatment: Alkalizing fluids IV, empty rumen if possible, ruminal penicillin and systemic penicillin, magnesium hydroxide will help neutralize rumen acid, mineral oil, NSAIDs, B vitamins, TRANSFAUNATE!
Control: Control access to carbohydrate rich feeds.

Front 36

Cattle: Vagal indigestion

Back 36

Clinical signs: Hypermotile rumen, "papple" shape, bradycardia, weight loss, decreased fecal output.
Etiology: Due to vagal nerve over or understimulation from a variety of causes. Four types: 1. Bloat, 2. Omasal transport failure, 3. Abomasal transport failure, 4. Abomasal transport failure due to large calf.
Diagnosis: History and signs; exploratory ruling out other causes, adhesions around reticulum or abomasum are suggestive; plasma/rumen Cl levels-dec plasma Cl and inc. rumen Cl suggests abomasal transport failure.
Treatment: Consider slaughter; Supportive therapy, specific therapy if causative lesion can be identified, relieve forestomach distention, transfaunate.
Control: Varies based on the causative lesion.

Front 37

Cattle: Rumen drinker (reticulorumenal milk accumulation)

Back 37

Clinical signs: Poor doer, poor hair coat, poor rumen motility, recurrent bloat
Etiology: Only occurs in nursing calves. Frequent feeding with a stomach tube or esophageal feeder allows fluid feed to spill into the rumen where it ferments and putrefies.
Diagnosis: History, alkaline rumen pH, putrid odor to rumen fluid.
Treatment: Empty rumen of putrid fluid, wean from liquid diet or switch to a higher quality milk replacer. If calf is being tube fed, withholding food until the calf is hungry will often stimulate them to start nursing a bottle on their own.
Control: None specifically

Front 38

Cattle: Left displaced abomasum

Back 38

Abomasum becomes trapped to the left of the rumen with the greater curvature directed dorsally.
Clinical Signs: Anorexia, dehydration, decreased production, TPR normal to increased, ketotic.
Etiology: High association with calving, occurs more often in dairy cattle, associated with rapid switch to a high concentrate diet; often concurrent with metritis or mastitis.
Diagnosis: Left paralumbar fossa may appear shrunken (rumen is pushed away from the body wall), "ping" detected in the left paralumbar fossa, liptak test (test pH of fluid just below ping, 2-4=abomasum, 5.5-8=rumen).
Treatment: Fluids, NSAIDs, IV dextrose SID if ketotic; Correction of displacement by rolling, roll and tack/toggle, left flank abomasopexy, or right flank omentopexy. When doing a tack/toggle or abomasopexy, sutures should be placed a hands breath right of midline, and a hands breath caudal to the xyphoid.
Control: avoid rapid switch over to a high concentrate diet (use "transition" rations), provide appropriate amounts of roughage and avoid excess carbohydrates.
Prognosis: Good if not long-standing and other concurrent diseases are not severe.

Front 39

Cattle: Right displaced abomasum or Right torsed abomasum

Back 39

Abomasum becomes trapped against the right body wall with the greater curvature directed dorsally; becomes twisted during RTA. THESE TWO CANNOT BE EASILY DIFFERENTIATED AND RIGHT DISPLACEMENT SHOULD ALWAYS BE TREATED AS AN EMERGENCY.
Clinical Signs: Anorexia, dehydration, decreased production, TPR normal to increased, ketotic. Signs will be exacerbated if RTA.
Etiology: High association with calving, occurs more often in dairy cattle, associated with rapid switch to a high concentrate diet; often concurrent with metritis or mastitis.
Diagnosis: Consistent "ping" detected in the right paralumbar fossa (will be transient if just indigestion), liptak test (test pH of fluid just below ping, 2-4=abomasum, 5.5-8=rumen), can sometimes be felt by rectal palpation.
Treatment: Fluids, NSAIDs, IV dextrose SID if ketotic; Correction of displacement by rolling, roll and tack/toggle, right flank abomasopexy, or right flank omentopexy. When doing a tack/toggle or abomasopexy, sutures should be placed a hands breath right of midline, and a hands breath caudal to the xyphoid.
Control: avoid rapid switch over to a high concentrate diet (use "transition" rations), provide appropriate amounts of roughage and avoid excess carbohydrates.
Prognosis: Good for RDA if not long-standing and other concurrent diseases are not severe. Poorer for RTA but still good prognosis if treated quickly.

Front 40

Cattle: Abomasal Impaction

Back 40

Clinical Signs: Anorexia, depression, weight loss, decreased fecal output, abdominal distention in lower right abdomen.
Etiology: Vagal indigestion (type III), late digestion heifers on poor quality roughage, functional obstruction, or mechanical obstruction.
Diagnosis: Large firm mass blottable in right cranial abdomen. Rumen chloride >30 mEq/L. Confirm by exploratory.
Treatment: Cathartics and lubricants, supportive therapy. Surgery often unrewarding. Slaughter
Control: None specific
Prognosis: Guarded to poor

Front 41

Ruminants: Abomasal dilation and emptying defect of Suffolk sheep

Back 41

Clinical Signs: anorexia, weight loss, depression, decreased fecal output, distention of lower right abdomen.
Etiology: Mechanism unknown. Mostly occurs in Suffolk and Suffolk crosses, but has occurred in other black faced sheep.
Diagnosis: Rumen chloride >30. Confirm by exploratory/necropsy.
Treatment: Cathartics and laxatives, supportive therapy. Surgery unrewarding. Slaughter.
Control: None specific
Prognosis: Poor to grave, high mortality.

Front 42

Cattle: Abomasal ulcer

Back 42

Clinical Signs: Dark tarry feces; colic with perforating ulcers. Sudden death if ulcer ruptures abomasal vessels.
Etiology: Associated with high concentrate diets, specifically the switch to a higher concentrate diet @ parturition. More common in high producing dairy cattle. 4 forms: slight bleeding, major bleeding, perforated with local peritonitis, perforated with diffuse peritonitis. Occur in adults and calves.
Diagnosis: Occult fecal blood is suggestive. Abdominocentesis can reveal perforated ulcer. Exploratory or necropsy to confirm.
Treatment: Change diet-more roughage, protectants, antiacids, blood transfusion if lots of bleeding, do not use NSAIDs.
Control: Use transition diet prior to parturition.
Prognosis: None given

Front 43

Cattle: Lymphosarcoma

Back 43

The pyloric portion of the abomasum is one of the most common locations in cattle for lymphosarcoma.

Front 44

Cattle: Intussusception

Back 44

Clinical Signs: Sudden onset colic, abdomen slowly distends bilaterally symmetrical, dehydration.
Etiology: Sporadic, often caused by intramural lesion, most cases are jejunal.
Diagnosis: Exploratory, ultrasound, rectal palpation.
Treatment: Surgical correction, supportive care, lidocaine to get GI moving again. Slaughter.
Control: None specific
Prognosis: Good if treated early; poor if ileus, continued abdominal distention post-op, or if long duration before treatment.

Front 45

Cattle: Hemorrhagic Bowel Syndrome

Back 45

Clinical Signs: Acute onset, pain/colic, abdominal enlargement, black tarry feces. Can be sudden death with no other signs.
Etiology: Sporadic cases or "mini outbreaks", predominant in mature dairy cattle. Proposed cause: Clostridium perfringens type A, and Aspergillus fumigatus.
Diagnosis: History of black tarry feces is suggestive. Exploratory/necropsy, ultrasound. Test for Clostridium and Aspergillus may support diagnosis, but can be found in normal animals.
Treatment: "Surgical kneeding" to break down clot and allow it to pass; surgical resection is not very successful. Abx and symptomatic treatment may be effective early on.
Control: Ration balance, forage quality, and feed management; antifungal feed additive; Vaccinate for C. perfringens.
Prognosis: Guarded to grave.

Front 46

Cattle: Torsion of the root of the mesentary

Back 46

Clinical Signs: Acute onset colic, with rapid abdominal enlargement.
Etiology: Sporatic, no specific predisposing factors. Can be a post-op complication. Typically involves the spiral colon.
Diagnosis: Pings over the right paralumbar fossa. Rectal palpation of distended viscus.
Treatment: Surgical correction. Slaughter.
Control: None specific
Prognosis: Fair if treated early, overall poor.

Front 47

Cattle: Cecal dilation/torsion

Back 47

Clinical Signs: Colic, scant feces, anorexia. Signs will be more pronounced with torsion.
Etiology: Sporadic. High concentrate diets->inc. VFAs->cecal atony, dilation, and torsion.
Diagnosis: Rectal palpation of distended cecum in pelvic canal. Pings high on the right side.
Treatment: Antacids, laxatives, fluids, switch to course high fiber diet. Immediate surgery required for torsions. Slaughter.
Control: None specific
Prognosis: Fair if treated early (80% for dilation, 75% for torsion)

Front 48

Cattle: Atresia coli, recti, or ani

Back 48

Clinical Signs: Normal until 2-4 days after birth, then colic/pain, depression. No feces!
Etiology: Congenital anomaly
Diagnosis: Rectal palpation, exploratory. History of no feces.
Treatment: Slaugher. Surgical correction may be pursued, but is really only successful for atresia ani.
Control: Do not breed animals that have undergone successful surgical correction, may be hereditary.
Prognosis: Atresia ani-good, others-guarded.

Front 49

Cattle: Rectal prolapse

Back 49

Clinical Signs: Rectum protrudes visibly from the anus, tenesmus.
Etiology: Predisposing factors: Increased abdominal pressure, excessive coughing, decreased anal tone, colitis, vaginal/uterine prolapse.
Diagnosis: Obvious
Treatment: Slaughter, replacement and purse-string, amputation. +/- antibiotic therapy after correction.
Control: Avoid predisposing factors
Prognosis: Good, depends on duration and condition of prolapse.

Front 50

Cattle: Fat necrosis

Back 50

Clinical Signs: Weight loss, anorexia, diarrhea, bloody stool, abdominal enlargement, treading back legs, kicking at abdomen.
Etiology: Most common in Channel Island breeds (Jersey and Guernsey). Fat cattle at higher risk.
Diagnosis: Rectal palpation of hard masses in the abdomen is suggestive.
Treatment: Slaughter
Control: Body condition score management.
Prognosis: Poor

Front 51

Cattle: Calf diarrhea

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Clinical Signs: Diarrhea, dehydration, depression.
Etiology: 6 major agents-E. coli(<5 days), Rotavirus(5-21d), Coronavirus(5-21d), Crypto(5-21d), Coccidia(21d-2yr), and Salmonella(21d-adult). Intestinal parasites may also cause diarrhea, but rarely seen due to ivomec use.
Diagnosis: Because all types are treated the same, specific diagnosis of causative agent is typically not done.
Treatment: Correct dehydration, give adequate milk and water. Supportive care.
Control: Ensuring successful passive transfer is key! Dairy calves often must be bottle fed colostrum to ensure enough is ingested. Vaccination for E. coli, roatvirus, coronavirus, salmoneall, and clostridium. Management practices: house dairy calves in hutches from within 1 day of birth until weaning. After weaning, group by age. Always care for youngest calves first. Properly clean and sanitize all equipment between uses (soak in soap/water first, then scrub, then spray with disinfectant and air dry).
Prognosis: Multivariate. If good passive transfer and management practices, prognosis is good.

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Cattle: Johne's Disease

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Clinical signs: Intermittent watery diarrhea and chronic weight loss. Cow will continue to eat well, but does not absorb nutrients properly. Stressful situations will trigger episode of diarrhea.
Etiology: Mycobacterium paratuberculosis. Majority of infections from ingesting feces or from milk. Symptoms occur between 2-6 years of age.
Diagnosis: Necropsy/biopsy-thickened gut wall. Serology, fecal culture. Must be 18 months or older to detect serology.
Treatment: None specific
Control: 1. Live with it. 2. Pull newborns from mom immediately and raise in clean environment with milk free from M. paratuberculosis. Calve only on clean pasture. Keep calves away from potentially infected animals for 6 months. Identify and remove infected cattle from the herd every 6 months. +/- Vaccination. 3. Sell out and start over.

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Cattle: Winter dysentery

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Clinical signs: Diarrhea, decreased milk production.
Etiology: Coronavirus. Occurs in mature dairy cattle during the winter, associated with increased confinement. High morbidity, low mortality.
Diagnosis: None
Treatment: Supportive care.
Control: Avoid crowding in the winter.

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Cattle: Salmonella

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Clinical signs: Bloody, foul smelling diarrhea; fever, anorexia.
Etiology: Cattle adapted strain is S. dublin. Survives in the environment for months. Zoonotic potential.
Diagnosis: None.
Treatment: Abx if infection is systemic. Supportive care.
Control: Good management practices prevent most cases. Vaccine is effective.

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Cattle: Green Grass Diarrhea

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Clinical signs: watery diarrhea
Etiology: Associated with lush pasture in the spring time.
Note: The change to a higher water content diet causes diarrhea, these cows are not sick.

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Small Ruminant Diarrhea

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Number one differential is internal parasites.
If very young, coccidia is a close second; treat with sulfa drugs.