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Chapter 9 Alterations in Body Weight or Size

John Maas, Meri Stratton-Phelps

MAJOR CLINICAL SIGNS OR PROBLEMS ENCOUNTERED

Decreased growth and decreased weight gain in growing animals, 147
Weight loss, 56
Obesity, 164
Pica, 169

Slowed growth and below-normal weight gain usually happen at the same time, although occasionally they develop separately. By definition a decrease in growth and weight gain is limited to the growing animal. Similar pathogenic mechanisms cause weight loss or an emaciated condition in an adult patient. This arbitrary age division allows the clinician to consider possible causes that are more or less common for a given age-group.

Potential growth and weight gain are genetically determined. They differ according to species, breed, and sex, and marked differences in potential growth exist within a breed. The potential for growth in ruminants is greater in the offspring of multiparous females than in those from primiparous females. The normal or minimum growth and weight gain rates for common breeds of the various large animal species are outlined in the section on assessment of growth and weight gains.

MECHANISMS OF DECREASED GROWTH AND DECREASED WEIGHT GAIN

Major pathogenic mechanisms that result in decreased growth and decreased weight gain include the following:

image Inadequate dietary intake of essential nutrients
image Infections or inflammation
image Parasitism
image Genetic errors in metabolism or physiologic function
image Concurrent toxicosis
image Environmental causes
image Multiple causes

Inadequate intake of one or more essential nutrients is an important cause of decreased growth. In many cases growing animals are not provided with a sufficient volume of feed to meet their nutrient requirements. Young animals rely on a highly digestible diet that provides energy and essential nutrients for growth. Even animals fed an appropriate volume of a poor-quality milk replacer could suffer from poor growth. Milk replacers formulated with sources of protein, fat, vitamins, and minerals that have limited nutrient digestibility may induce a state of energy, protein, vitamin, or mineral malnutrition. For some young animals, poor-quality forage is the only feed available. Weaned foals and ruminants rely on forages and cereal grains to provide essential nutrients. Hay that has been harvested at a late stage of growth usually has a lower nutrient digestibility compared with young forages. Diets low in digestible energy or protein or both reduce total daily intake in ruminants (Table 9-1) because of the increased turnover time (T½) in the gastrointestinal tract and subsequent decreased throughput. This compounds the problems caused by an inadequate intake of digestible nutrients. The digestibility of forages is even lower for horses than for ruminants.

Table 9-1 Maximum Dry Matter Intake (DMI) Related to Forage Quality for Cattle

Forage Quality Maximum DMI/Day (% Body Weight) Maximum DMI for 500 kg/Cow/ Day (kg)
Poor 1–1.5 5–7.5
Oat straw    
Corn stover    
Average 2 10
Meadow grass hay    
Excellent 2.5 12.5
Alfalfa hay (25% crude fiber)    
Corn silage    

From Maas J: Relationship between nutrition and reproduction in beef cattle, Vet Clin North Am, 3:634, 1987.

Protein-calorie malnutrition (PCM) is the most common clinical cause of decreased growth and decreased weight gain in young animals. It is characterized by smaller size and lower weight than the normal minimums for age, breed, and sex. Inadequate intake of digestible energy and protein (or essential fatty acids in the neonate primarily adapted to a milk diet) results in inadequate levels of amino acids, fats, and carbohydrates for normal metabolism and growth. Diets that lack any of the other essential nutrients (fatty acids, vitamins, macrominerals, or trace minerals) can also decrease growth. Deficiencies of calcium, phosphorus, and magnesium result in improper skeletal formation. Deficiencies in other macrominerals (e.g., sodium, chloride, potassium), trace minerals (e.g., copper, zinc, manganese, cobalt, iron), and vitamins (e.g., A, D, E, thiamin) cause biochemical dysfunctions that lead to inefficient metabolism and growth. Large animal patients that grow slowly as a result of inadequate diets often have normal or increased appetites until they are terminally ill. Physical findings and clinicopathologic data from animals with PCM often are within the normal range until the disease process is well advanced.

Infections or inflammatory processes are important causes of decreased growth and decreased weight gain in young horses and ruminants. The decrease in growth can be of short duration followed by recovery and compensatory gain (cryptosporidiosis) or can persist (chronic bronchopneumonia). Infections or inflammatory processes can also result in nutrient malabsorption (chronic salmonellosis, acute rotavirus diarrhea), anorexia (pharyngeal abscesses), increased nitrogen turnover, and direct protein losses (gastrointestinal disease). Energy or protein requirements may be increased as a result of infection and inflammation.

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Parasitism often affects young horses and ruminants and results in decreased growth and decreased weight gain by increasing nutrient requirements, increasing nutrient losses, and/or decreasing nutrient absorption. The animal’s metabolic rate and nutrient requirements may also increase as a result of inflammatory and immune reactions that arise secondary to parasitism.

Genetic diseases (α-mannosidosis, dwarfism) result in decreased growth through generalized errors in the genetic code or interference with strategic reactions in one or more metabolic pathways. Congenital cardiac malformations (tetralogy of Fallot, interventricular septal defect) create physiologic inefficiencies that require energy beyond the body’s ability to supply it. Congenital renal disease (agenesis, dysplasia, hypoplasia, polycystic kidney disease) affects homeostatic mechanisms that regulate electrolyte and acid-base balance, results in the production of uremic toxins, and often results in partial anorexia and PCM. Digestive tract malformations including cleft palate, megaesophagus, and brachygnathism can reduce nutrient ingestion and impair growth.

Toxicities, although rare in growing animals, result in decreased weight gain by interfering with metabolic pathways (e.g., ammonia toxicity, zinc-induced copper deficiency with abnormal skeletal development in foals), by causing loss of body reserves (e.g., thiamin deficiency in horses, bone marrow hypoplasia and associated bleeding diatheses in ruminants associated with bracken fern toxicity), by inducing anorexia, or by a combination of mechanisms. The pathogenic mechanisms of many toxins are not yet known.

Environmental factors including extreme heat or cold or high humidity result in decreased growth and decreased weight gain. Extremely cold conditions increase an animal’s daily energy requirements. During extremely hot weather feed intake often decreases, which may contribute to decreased growth. Often, environmental conditions influence the development of disease, resulting in a subsequent increase in nutrient requirements in a growing animal (e.g., calves with PCM housed in poorly ventilated or overly humid conditions become much more susceptible to infectious pneumonia).

In many cases a combination of these diverse factors may influence the growth and weight gain of young animals. A period of increased growth rate and weight gain, called compensatory gain, often occurs after a period of restricted growth. In growing foals, compensatory gain should be closely monitored to prevent excessively rapid growth and abnormal skeletal development.

Boxes 9-1 and 9-2 list many of the possible causes of decreased growth and decreased weight gain in horses and ruminants, respectively.

Box 9-1 Causes of Decreased Growth and Decreased Weight Gain in Horses

COMMON CAUSES

Protein-calorie malnutrition (PCM), inadequate nutrient intake
Extreme environmental factors
Parasitism (Parascaris equorum, small strongyles, large strongyles, tapeworms, bots)
Bacterial pneumonia (Rhodococcus equi, Streptococcus zooepidemicus), lung abscessation
Viral pneumonia (equine herpes virus, equine influenza)
Gastric ulcers
Lameness (e.g., physitis, osteochondritis dissecans, contracted tendons, osteomyelitis)
Prematurity, dysmaturity
Diarrhea (Clostridium, species, Salmonella, species, sand enteropathy, other causes)

LESS COMMON CAUSES

Esophageal stricture, megaesophagus (idiopathic, acquired)
Peritonitis
Congenital cardiac and great vessel anomalies
Endocarditis
Jaw pain (fracture, dental abnormality)
Cryptosporidiosis
Selenium deficiency
Copper deficiency
Vitamin A deficiency
Vitamin D deficiency
Thiamine deficiency
Phosphorus deficiency
Osteodystrophy
Lead toxicity
Goiter
Generalized steatitis
Rotavirus infection (foals)
Wound myiasis

UNCOMMON CAUSES

IgM-deficiency
Combined immunodeficiency disease in foals
Gonadal dysgenesis, intersex (XO, XXY)
Ammonia toxicity
Sarcocystosis
Fluorosis
Congenital renal abnormalities (hypoplasia, dysplasia, agenesis, polycystic kidney disease)
Hydrocephalus
Myeloproliferative disease
Biliary atresia
Hepatic portosystemic shunt

Box 9-2 Causes of Decreased Growth and Decreased Weight Gain in Ruminants

COMMON CAUSES

Protein-calorie malnutrition (PCM)
Mannheima, Pasteurella, Haemophilus, pneumonia
Ostertagiasis I and II
Coccidiosis
Parasitism (flukes, gastrointestinal worms, lungworms)
Salmonellosis
Bovine virus diarrhea
Hepatic abscessation, liver disease
Rotavirus infection
Diarrhea, undifferentiated
Lameness (sole abscess, foot rot, laminitis, foot warts, osteomyelitis)
Cryptosporidiosis
Enterotoxigenic Escherichia coli,
Coronavirus
Selenium deficiency
Copper deficiency (molybdenosis)
Sarcoptic mange

LESS COMMON CAUSES

Johne’s disease
Cardiac or great vessel anomalies
Hydrocephalus
Myiasis
Ammonia (urea) toxicity
Goiter
Eperythrozoonosis
Arthrogryposis
Thiamine deficiency
Cobalt deficiency
Urachal or bladder abscess
Peritonitis
Pharyngeal abscess, injury
Giardiasis
Osteodystrophy, rickets
Neonatal isoerythrolysis
Immune-mediated anemia
Zinc deficiency
Vitamin A deficiency
Adenovirus infection
Tick infestation
Sarcocystosis
Abomasal ulcers
Severe bovine papular stomatitis

UNCOMMON CAUSES

Gonadal dysgenesis, intersex
Brisket disease
Epidermolysis bullosa
Phosphorus deficiency
Osteogenesis imperfecta in Friesians
Calf lymphosarcoma
Granulocytopathy
Congenital porphyria
Hypersensitivity to soy protein
Bacteroides fragilis, diarrhea
α-Mannosidosis
Generalized glycogenosis
Zygomycosis
Mucormycosis
Omental bursitis
Schistosomiasis (exotic)
Trypanosomiasis (exotic)
Hyena disease (exotic)
Lethal skin defects in Japanese black cattle (exotic)
Babesiosis (exotic)

TOXINS

Pyrrolizidine alkaloid toxicosis
Herbicide toxicity
Zinc toxicity
Fluorosis
Selenium toxicity
Aflatoxicosis
Ergotism
Iodine toxicity

PLANT TOXINS

Cassia, species
Bracken fern
Fescue toxicity
Leucaena leucocephala,
Oxalate toxicity
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Approach to the Diagnosis and Management of Decreased Growth and Decreased Weight Gain in Horses

1 Take a general history and a diet history.
a General history
i What is the patient’s age? Was the foal born prematurely? Were any congenital defects identified during the initial examination of the foal after birth? Did the foal have any complications from sepsis?
ii What is the stocking density of the herd? Is the foal exposed to a high parasite load in the environment? What is the foal’s deworming history? Have there been previous problems with gastrointestinal parasitism on the farm? What is the vaccination history of the mare and the foal? Does the farm have a history of infectious disease agents (Rhodococcus equi, Streptococcus equi, subsp. equi,)? Are there any sick horses on the same farm? Has the foal shown any evidence of systemic illness (diarrhea, nasal discharge, cough, pyrexia)?
iii What type of protection is provided from adverse weather conditions? Are there any toxins in the foal’s environment?
b Diet history
i If the foal is nursing, what is the weight condition of the mare? Is the mare producing a sufficient amount of milk for the foal? If the foal is an orphan, what type of milk replacer is the owner using? What is the daily energy and protein intake of the foal? Is the owner mixing the solution properly? Does the foal have access to a creep feed? What is the owner using as a creep feed? How much of the creep feed does the foal consume daily?
ii If the foal is a weanling, when was the foal weaned? Does the foal compete with other foals for feed? Has the owner changed the foal’s diet recently? If yes, what changes were made? Does the foal have a good appetite? Has the foal’s appetite changed recently?
(1) What type of forage is fed to the foal? What is the quality of the forage? Is there gross evidence of dirt, mold, or weed contamination in the forage? Has a hay analysis been performed on the forage? How much forage is offered to the foal (in weight)? How much forage (in weight) does the foal eat each day?
(2) What type of supplemental feed is fed to the foal? What is the nutrient composition of the supplemental feed? Is the supplemental feed of high quality? How much of the supplemental feed (in weight) does the foal eat each day?
(3) Is the foal offered a vitamin and mineral supplement? Is the vitamin and mineral supplement offered free choice? How much of the supplement (in weight) does the foal eat each day? Could any nutrients be consumed in a toxic amount? Has the owner provided any supplemental parenteral vitamins or minerals to the foal?
2 Perform a physical examination.
a What is the body weight of the foal (measured by using either a scale or weight tape)? What is the body condition score (BCS) of the foal (see Table 9-21)? Is the foal small, thin, or underweight according to growth charts (Table 9-2, Figs. 9-1 and 9-2)?
b Does the foal show any signs of infectious disease (current or resolved)?
c Does the foal have evidence of a congenital abnormality (cardiac, renal, gastrointestinal, oral)?
d Does the foal have any musculoskeletal abnormalities?
3 Examine the feces.

Table 9-21 Body Condition Scoring System for Horses

Score Description
1 Poor. Animal is extremely emaciated. Spinous processes, ribs, tailhead, tuber coxae, and tuber ischii project prominently. Bone structure of the withers, shoulders, and neck is noticeable. No fatty tissue can be felt.
2 Very thin. Animal is emaciated. There is a slight fat covering over the base of the spinous processes; the transverse processes of the lumbar vertebrae feel rounded. Spinous processes, ribs, tailhead, tuber coxae, and tuber ischii are prominent. Bone structure of the withers, shoulders, and neck is faintly discernible.
3 Thin. Fat buildup is present about halfway on the spinous processes; the transverse processes cannot be felt. There is a slight fat cover over the ribs. Spinous processes and ribs are easily discernible. Tailhead is prominent, but individual vertebrae cannot be visually identified. Tuber coxae appear rounded but are easily discernible; tuber ischii are not distinguishable. Bone structure of the withers, shoulders, and neck is accentuated.
4 Moderately thin. Negative crease can be seen along the back. Faint outline of ribs is discernible. Tailhead prominence depends on conformation; fat can be felt around tailhead. Tuber coxae are not discernible. Withers, shoulders, and neck are not obviously thin.
5 Moderate. Back is level. Ribs cannot be visually distinguished but can be felt easily. Fat around tailhead is somewhat spongy. Withers appear rounded over spinous processes, and shoulders and neck blend smoothly into the body.
6 Moderately fleshy. Slight crease may be seen down the back. Fat over ribs is spongy, and fat around tailhead is soft. Fat is beginning to be deposited along withers, behind shoulders, and along neck.
7 Fleshy. Crease may be seen down the back. Individual ribs can be felt, but there is noticeable filling of fat between ribs. Fat around tailhead is soft. Fat is deposited along withers, behind shoulders, and along neck.
8 Fat. Crease is seen down the back. Ribs are difficult to feel. Fat around tailhead is very soft. Areas along withers and behind shoulders are filled with fat, and neck is noticeably thickened. Fat is deposited along inner thighs.
9 Extremely fat. Obvious crease is seen down the back. Patchy fat appears over ribs. Bulging fat is seen around tailhead along withers, behind shoulders, and along neck. Fat along inner thighs may cause thighs to rub together. Flank is filled with fat.

From Henneke GD, Potter GD, Kreider JL, Yeates BF: Relationship between condition score, physical measurements and body fat percentage in mares, Equine Vet J, 15:371, 1983.

Table 9-2 Weight as a Percentage of Mature Body Weight in Horses

image
image

Fig. 9-1 Estimated weight gain of horses of various mature body weights.

Modified from National Research Council [NRC]: Nutrient requirements of horses, Washington, DC, 1978, National Academy of Sciences, NRC.

image

Fig. 9-2 A to C, Body weight as a percentage of mature body weight for horses at a given age.

A modified from Crampton WW: J Agric Hortic 26:172, 1923; B modified from Lewis LD: Feeding and care of the horse, Philadelphia, 1982, Lea & Febiger; C modified from Hintz HF: Factors affecting the growth rate of horses, Horse Short Course Proceedings, Texas A&M Animal Agriculture Conference, 1979, College Station, Texas.

What is the consistency of the feces? Refer to Chapter 20 for the diagnosis and management of neonatal diarrhea; refer to Chapter 7 if the foal is older and has evidence of diarrhea. Is there evidence of sand in the manure? Perform a fecal egg count. If the foal has a positive fecal egg count, follow the parasite control program recommendations in Chapter 49. If a negative fecal egg count is reported but parasitic infestation is still suspected, repeat the test in 2 to 3 weeks or follow the deworming protocols in Chapter 49. Evaluate the feces occult blood. If the foal has a positive fecal occult blood test, review the medical management for melena in Chapter 7.

4 Perform blood analyses.
a Perform a complete blood count (CBC) and include a plasma protein and fibrinogen concentration. If the foal is anemic, determine the cause of the anemia following the guidelines in Chapter 24. If the foal’s CBC indicates inflammation, review Chapters 25 and 26 and select appropriate ancillary diagnostic tests to identify the source of the infection or inflammation.
b Perform a serum biochemical analysis. Evaluate the results for evidence of systemic disease. Serum albumin is usually within normal limits with PCM until the condition is terminal. Serum glucose is usually normal but it may be decreased in neonatal foals with sepsis. Serum glucose may be elevated in stressed animals. Serum urea nitrogen and creatinine concentrations are elevated in foals with renal disease. Serum urea nitrogen decreases in cases of chronic protein malnutrition.
c If the foal has evidence of systemic disease, perform ancillary diagnostic tests to identify the source of the illness, then manage the case with appropriate medical or surgical intervention.
5 Analyze the diet and improve the feeding program.
a Determine whether the energy, protein, mineral, and vitamin content of the diet meets the requirements of the growing foal (Table 9-3).
i Young horses require adequate levels of essential amino acids for growth. Lysine is the first and threonine is the second limiting amino acid in the equine. Growing foals should consume 4.3% of their crude protein requirement as lysine (multiply the crude protein requirement by 4.3%).6 Growing foals should also consume at least 0.5% threonine (DM) in their diet. Soybean meal and alfalfa hay contain approximately 3.3% and 0.9% lysine (DM), respectively, whereas cereal grains are poor sources of lysine.
ii Milk replacer

Table 9-3 Daily Nutrient Requirements for Growth in Equines of Various Mature Body Weights

image

If the foal is consuming a milk replacer, review the guaranteed analysis for the nutrient content of the product. Review the mixing instructions with the owner or farm manager. Develop a feeding program appropriate for the foal’s age.

iii Forage

The most accurate way to determine the nutrient content of forage or pasture is with an analysis. Forage sampling instructions and forage analysis companies are listed in Boxes 9-3 and 9-4. University Extension services often provide a forage analysis service. If the client does not purchase a large volume of hay, or if analysis cannot be performed, forage tables from the Nutrient Requirement Council reference books (www.nap.edu) or nutrient tables from the Equi-Analytical Laboratories forage laboratory database (www.equi-analytical.com) can be referenced to estimate the concentration of different nutrients in common forages and supplemental feeds. Use the daily nutrient requirement table (see Table 9-3) to recommend the type and amount of forage the foal should consume based on the nutrient content of the forage.

iv Commercial feeds and grain mixes

Box 9-3 Forage and Large Animal Feed Sampling Instructions

SAMPLING PASTURE

1 Collect pasture samples from a 1-foot-square area. Sample only the same type of forage that the horses are grazing. Sample 10 to 20 sites.
2 Using scissors, cut the pasture to within 1 inch of the ground. Do not collect soil-contaminated pasture. Cut all samples to a length of 1 inch, and place all samples into a clean bucket.
3 After sampling is complete, mix the samples well and place the forage into a plastic sealable bag (1-gallon Ziplock). Label the bag with the date of sampling, the collection site, and the owner’s name.
4 If the sugar and starch content of the sample is of special interest, the sample should be frozen and shipped on ice to the analysis company.

SAMPLING HAY USING A CORE HAY SAMPLER

1 Choose 10 to 20 bales randomly from the hay shipment. Only one type of forage should be submitted for analysis in the same container. If more than one type of hay is analyzed, each should be placed into a separate, labeled plastic bag.
2 Use the core hay sampler with a ratchet brace or drill to collect two samples from each bale. Square bales should be sampled from the long end of the bale. Round bales should be sampled along a horizontal line at the curve of the bale. Place all samples into a plastic sealable bag (1-gallon Ziplock), and label the bag with the date, type of hay, and owner’s name.

SAMPLING HAY BY HAND

1 Choose 10 to 20 bales randomly from the hay shipment. Only one type of forage should be submitted for analysis in the same container. If more than one type of hay is analyzed, each should be placed into a separate, labeled plastic bag.
2 Open the bale, and divide the bale in thirds. Collect a handful of hay from the center of the bale at each site (two samples per bale). Include everything that you have grabbed (including weeds and other plants) in the sample. Cut all samples to a length of 1 inch, and place all samples into a clean bucket. Thoroughly mix the cut hay samples, place the forage into a plastic sealable bag (1-gallon Ziplock), and label the bag with the date, type of hay, and owner’s name. Ensure that all parts of the sample (leaves and stems) are included in the final sample.

SAMPLING GRAIN OR PELLETED FEED

1 Analysis of two to four samples from 10 bags is recommended to obtain a representative sample of feed. Only one type of feed should be submitted for analysis in the same container. If more than one type of grain or pelleted feed is analyzed, each should be placed into a separate, labeled plastic bag.
2 Open a bag or a bin, and obtain a 2- to 4-ounce sample from two to four locations in the bag or bin. A sample should be obtained from the bottom of the bin or bag to ensure that a sample of the settled feed is analyzed. When multiple bags or bins are sampled, samples from each bin or bag should be placed into a clean plastic bucket. Once all sampling has been completed, the feed sample should be mixed well, and approximately 1 pound of the feed should be placed into a plastic sealable bag (1-gallon Ziplock). Label the bag with the date, type of feed, and owner’s name.

Box 9-4 Feed Analysis Companies

1 Equi-Analytical Laboratories/Dairy One
730 Warren Road
Ithaca, NY 14850
(877) 819–4110; (800) 496–3344
2 Cumberland Valley Analytical Services, Inc.
P.O. Box 669
Maugansville, MD 21767
UPS/FedEx: 14515 Industry Drive
Hagerstown, MD 21742
(800) 282-7522
3 Eurofins Scientific, Inc.
P.O. Box 1292
Des Moines, IA 50305
UPS/FedEx: 3507 Delaware Avenue
Des Moines, IA 50313
(800) 880-1038

The guaranteed analysis on the feed tag label provides the nutrient content of certain ingredients. Contact commercial feed companies for the energy content of their product. Make recommendations about the appropriate use of commercial equine feeds, grain, or grain mixes for young growing foals based on the clinical health of the foal.

v Vitamins and minerals

Ensure that the diet meets the vitamin and mineral requirements of the foal. Supplement the diet if necessary.

b If the foal or weanling has a nutrient deficiency, the problem should be corrected by a change in the diet or through appropriate parenteral supplementation.
c If the diet history indicates that nutrients for maintenance and growth have been steadily consumed, the search for another cause of decreased growth and decreased weight gain should continue.
6 Perform ancillary diagnostic tests.

If the cause of the decreased growth and/or poor weight gain has not been determined, additional diagnostic tests should be performed. Possible tests include, but are not limited to ultrasound, radiographs, serum or whole blood trace mineral analysis, and carbohydrate absorption tests (oral D-glucose, D-xylose).

Approach to the Diagnosis and Management of Decreased Growth and Decreased Weight Gain in Ruminants

1 Take a general history and a diet history.
a General History
i What is the age of the animal? When was a decrease in growth observed? How many animals in the herd are affected? What are the ages of the affected animals? Has the herd had historical problems with growth of the young?
ii Identify the problem as acute, subacute, or chronic.
iii Check for signs or history of previous infectious disease.
iv Determine the parasite control procedures for the animal or herd.
v Examine the environment, including feed preparation areas and equipment, for possible toxic substances (e.g., zinc from galvanized buckets).
b Diet history
i Obtain an accurate diet history, including diet information when a milk or milk replacer diet is being fed (birth to 2 or 3 months of age). Note the age and condition of the dam if patient was suckled before weaning. An accurate postweaning dietary history is essential. Suckled animals are developed ruminants at weaning, but hand-reared animals (dairy calves, bummer lambs, and dairy kids) are usually not fully developed ruminants at the time they are weaned from milk.
ii Inspect all forages and concentrates for quality, signs of spoilage, or abnormal color or odor. Has an analysis been performed on the forage? Is the feed formulated appropriately?
iii Because ruminants are often fed in groups, note whether all animals have adequate space to eat simultaneously.
2 Perform a physical examination.
a Determine the patient’s age and weight. Check the patient against age and weight charts (Figs. 9-3 to 9-6).
b Carefully note any signs of infectious or parasitic disease.
c Evaluate the animal for any signs of congenital abnormalities.
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3 Examine the feces.
image

Fig. 9-3 Minimum growth curve for dairy heifers.

From Sniffen CJ: Feed Manage 35:37, 1984.

image

Fig. 9-4 Estimated growth curves for beef cows of various breeds. AA, Angus; CC, Charolais; CA, Charolais × Angus; FA, Holstein × Angus.

Modified from Nadarajah K, Marlowe TJ, Notter DR: Growth patterns of Angus, Charolais, Charolais X Angus and Holstein X Angus cows from birth to maturity, J Anim Sci 59:957, 1984.

image

Fig. 9-5 Mean growth curves of Angus (A), and Hereford (H), males (image) and females (image).

Modified from Brown JE, Brown CJ, Butts WT: A discussion of the genetic aspects of weight, mature weight and rate of maturing in Hereford and Angus cattle, J Anim Sci 34:525, 1972.

image

Fig. 9-6 Growth curve for young goats.

Modified from Morand-Fehr P, Hervieu J, Bas P, Sauvant D: Proc Third Int Conf Goat Prod Dis 3:96, 1982.

Perform flotation, sedimentation, and Baermann’s procedures to detect patent parasitic infestation. Perform a fecal occult blood test; if the result is positive or if there is evidence of diarrhea, see the section on melena or diarrhea in Chapter 7. If diarrhea is noted in neonatal calves, refer to Chapter 20 for diagnostic and therapeutic management.

4 Perform blood analysis.
a Perform a CBC, including plasma protein and fibrinogen. Calculate the erythrocytic indices, and document and characterize the anemia if present. If a herd problem exists in a selenium-deficient region, measure the whole blood selenium concentration or glutathione peroxidase activity.
b Perform a serum biochemical analysis. Serum albumin is decreased late in PCM. Albumin is normally lower in neonates (approximately 1 g/dL less) than in adults. The blood urea nitrogen (BUN) level is often low in ruminants as a result of urea recycling through saliva. Total serum calcium may be decreased with hypoalbuminemia (ionized serum calcium remains normal), anorexia, or hypocalcemic syndromes (milk fever). Serum phosphorus may be increased during severe starvation or decreased with anorexia.

Hypophosphatemia may be the result of dietary deficiency or Brassica, feeding, or it may be associated with copper deficiency. Measure serum (plasma) copper if a herd problem exists in a copper-deficient region (or a region with excess molybdenum or sulfate or both). Copper (serum or plasma) concentrations below 0.5 μg/mL (ppm) indicate deficiency. Liver copper levels are even more indicative of status. Serum glucose may be increased with stress or decreased or normal near death.

5 Analyze the diet and improve the feeding program.

Compare nutrient intake with the requirements for maintenance and growth of the various ruminant species (Tables 9-4 through 9-10). If the neonate is being fed a milk diet, evaluate the quality of the product and ensure that the animal’s intake meets the dietary requirements (see Tables 9-4 and 9-5). Ensure that the milk replacer is mixed properly. If the ruminant is consuming a grain mix or forage, ensure that the quantity and the quality of the feed are adequate to allow sufficient intake in developed ruminants (see Table 9-1). Forage sampling instructions are listed in Box 9-3. If anorexia is present, look for more specific signs of a primary disease process. If the diet supplies adequate nutrients for maintenance and growth, consider decreased growth and decreased weight gain to be caused by a primary disease condition.

Table 9-4 Daily Energy and Protein Requirements for 50-kg Calves on a Milk Diet

  Digestible Energy Requirements Digestible Protein Requirements
Maintenance 45–55 kcal/kg body weight 0.5 g/kg body weight
Gain 300 kcal/100 g gain in body weight* 22 g/100 g of weight gain
0.5 kg daily gain 1500 kcal  
1 kg daily gain 3000 kcal  

* A 50-kg calf gaining 0.75 kg/day would have a daily energy requirement of 5000 kcal of digestible energy (2750 kcal maintenance + 2250 kcal/0.75 kg of gain).

A 50-kg calf gaining 0.75 kg/day would have a daily protein requirement of 190 g of digestible protein (25 g of maintenance + 165 g of gain).

Table 9-5 Net Energy (NE) Requirements of Young Lambs on Milk-Replacer Diets*

image

Table 9-6 Net Energy (NE) Requirements for Growth of Beef Cattle (Mcal/day)

image

Table 9-7 Daily Nutrient Requirements for Growth of Dairy Calves

image

Table 9-8 Protein Requirements for Growth of Beef Cattle (Crude Protein g/day)

image

Table 9-9 Calcium (Ca) and Phosphorus (P) Requirements for Growth of Beef Cattle (g/day)

image

Table 9-10 Nutrient Requirements for Growth in Sheep of Various Mature Body Weights

image
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WEIGHT LOSS

The clinical problem of weight loss suggests that an individual large animal patient or a herd has lost weight over a known period of time. It may also suggest that the patient has reached a subnormal adult weight and size (see section on decreased growth and decreased weight gain, earlier). Late pregnancy, early lactation, and intense exercise are normal physiologic conditions commonly accompanied by mild to moderate weight loss. Late pregnancy can be associated with decreased body condition without actual weight loss, because weight is gained with the conceptus. During pregnancy and lactation the loss of body condition may be mild, resulting in a low normal BCS, or the loss may be severe and can threaten the health of both the dam and the neonate.

Weight loss in adult animals is most commonly associated with one or more of the following circumstances (other causes are listed in Boxes 9-5 and 9-6):

image Anorexia
image Increased nutrient demands
image PCM
image Micronutrient deficiencies
image Parasitism

Box 9-5 Causes of Weight Loss in Horses

COMMON CAUSES

Protein-calorie malnutrition (PCM)
Parasitism
Dental, jaw abnormalities
Sand enteropathy
Chronic colonic impaction
Gastric ulcers
Right dorsal colitis
Peritonitis
Internal abdominal abscess
Streptococcus equi, (lymph node abscessation, pulmonary or mesenteric abscessation)
Pneumonia (bacterial, viral)
Pleuritis, pleuropneumonia, pulmonary abscessation
Chronic obstructive pulmonary disease
Chronic renal failure
Acute renal failure
Pituitary pars intermedia dysfunction
Neoplasia (alimentary tract)

LESS COMMON CAUSES

Guttural pouch infection
Otitis media, interna
Paranasal sinus infection
Oral foreign body
Vesicular stomatitis
Esophageal abnormalities (esophagitis, diverticula)
Gastric squamous cell carcinoma
Duodenal ulcers
Gastric impaction
Lymphocytic-plasmacyte enterocolitis
Eosinophilic enterocolitis
Multisystemic eosinophilic epitheliotropic disease
Granulomatous enteritis
Proliferative enteropathy
Idiopathic diarrhea
Toxic hepatopathy
Chronic hepatitis
Cholelithiasis
Pyrrolizidine alkaloid hepatotoxicity
Amyloidosis
Urolithiasis
Renal tubular acidosis
Glomerulonephritis
Pyelonephritis
Renal neoplasia
Urinary bladder neoplasia
Osteomyelitis
Infectious arthritis
Atrial fibrillation
Cardiac or great vessel anomalies
Congestive heart failure
Endocarditis, pericarditis
Splenic rupture, abscess
Lymphoma, lymphosarcoma
Malignant melanoma
Granulosa cell tumor
Purpura hemorrhagica
Autoimmune anemia or thrombocytopenia
Cauda equina neuritis
Equine motor neuron disease
Nocardiosis
Coccidioidomycosis
Cryptococcosis
Agammaglobulinemia
Anhidrosis
Giardiasis
Aflatoxicosis
Equine adenovirus
Equine viral arteritis
Equine infectious anemia

UNCOMMON CAUSES

Rabies
Nigropallidal encephalomalacia
Botulism
Nutritional myodegeneration
Rectus capitus ventralis muscle rupture
Skeletal or vertebral neoplasia
Spinal abscessation
Micronema deletrix, infection of the central nervous system
Rhodococcus equi, infection
Tuberculosis
Pleural mesothelioma
Pneumocystis carinii, pneumonia
Pulmonary aspergillosis
Micropolyspora faeni, hypersensitivity pneumonitis
Testicular neoplasia
Mammary carcinoma
Ovarian adenoma
Pancreatic neoplasia
Malignant mesothelioma
Pulmonary neoplasia
Strongylus vulgaris, thromboembolism
Portal vein shunt
Liver fluke
Theiler’s disease
Basophilic enterocolitis
Ileal hypertrophy
Myeloproliferative disease
Pyloric stenosis
Colonic fistula
Prognathia, brachygnathia
Aortic aneurysm
Enzootic cystitis
Polycystic disease
Pheochromocytoma
Hyperparathyroidism
Diabetes mellitus
Systemic granulomatous inflammation
Seborrhea
Bullous pemphigoid
Panniculitis
Lupus erythematosus
Pemphigus foliaceous
Eosinophilic dermatitis
Horsefly-deerfly infestation
Wound myiasis
Steatitis
Goiter
Erythrocytosis
Histoplasmosis
Phycomycosis
Fungal granuloma
Tularemia
Babesiosis
Brucellosis
Phosphorus deficiency
Vitamin A deficiency
Multiple cartilaginous exostoses
Trypanosoma evansi, infection (exotic)
Trombiculiasis (exotic)
Nagana (exotic)
Pseudomonas pseudomallei, infection (exotic)
Uasin Gishu skin disease (exotic)
Besnoitiosis (exotic)
Dourine (exotic)
Glanders (exotic)
Grass sickness (exotic)
Louping ill (exotic)
Trypanosoma equinum, infection (exotic)
Trypanosoma hippicum, infection (exotic)
Stachybotryotoxicosis (exotic)

TOXINS

Phenylbutazone, flunixin, and other nonsteroidal antiinflammatory drugs
Vitamin D calcinosis
Zinc
Selenium
Fluoride
Arsenic
Mercury
Vitamin K3
4-Aminopyridine
Pentachlorophenol
Dioxin
Aflatoxicosis

PLANT TOXINS

Yellow star thistle
Red maple leaf
White snakeroot (tremetol)
Plant calcinosis
Thornapple
Crofton weed
Pimela, (exotic)
Swainsonia (exotic)
Birdsville disease (exotic)
Pachysandra paralysis (exotic)

Box 9-6 Causes of Weight Loss in Ruminants

COMMON CAUSES

Protein-calorie malnutrition (PCM)
Bacterial pneumonia, pulmonary abscessation
Parasitism (lungworms, gastrointestinal parasites)
Johne’s disease (paratuberculosis)
Bovine leukosis
Peritonitis
Ruminal lactic acidosis
Urolithiasis
Pyrrolizidine alkaloid toxicity
Displaced abomasum
Hepatic abscess
Abomasal ulcer
Rotavirus diarrhea
Coronavirus diarrhea
Sarcoptic mange
Foot rot
Pedal osteomyelitis
Sole abscess
Traumatic reticuloperitonitis, pericarditis
Ketosis
Vagal indigestion
Winter dysentery (B)
Salmonellosis
Fat necrosis (B)
Actinobacillosis
Actinomycosis
Pharyngeal, retropharyngeal abscess
Pyelonephritis, cystitis
Selenium deficiency
Bovine virus diarrhea (B)
Coccidiosis
Copper deficiency
Dental abnormalities
Enterotoxigenic colibacillosis
Agammaglobulinemia (failure of passive transfer) in neonates
Fescue toxicity (B)
Anaplasmosis (B)
Septic arthritis
Infectious bovine rhinotracheitis (B)
Intussusception
Leptospirosis
Mastitis, coliform or staphylococcal
Lice or ked infestation
Hepatic abscess
Liver fluke infestation
Pasteurellosis, septicemic
Pregnancy toxemia
Bluetongue (O)
Cryptosporidiosis
Mammary abscess
Wound myiasis
Diarrhea, unknown cause

LESS COMMON CAUSES

Rabies
Sarcocystosis (B)
Sodium chloride deficiency
Cardiac or great vessel anomalies
Thymic lymphosarcoma (B)
Tuberculosis
Ulcerative stomatitis
Vesicular stomatitis
Salt toxicity, water deprivation
Psoroptic mange
Postparturient hemoglobinuria
Malignant catarrhal fever
Aspiration pneumonia
Brisket disease
Neoplasia
Omasal impaction
Abomasal impaction
Listeriosis
Pleuritis
Renal amyloidosis
Acute renal failure
Hydronephrosis, urachal abscess, bladder abscess
Dermatophilosis
Glomerulonephritis
Thiamine deficiency
Fluorosis
Esophageal malfunctions
Cobalt deficiency
Coenurosis (gid)
Congenital porphyria
Endocarditis
Aflatoxicosis
Eperythrozoonosis
Mandible, maxilla fracture
Goiter
Lingual injury, abscess
Vena caval thrombosis
Colonic obstruction
Otitis media, externa
Papular stomatitis (B)
Micropolyspora faeni, hypersensitivity pneumonitis
Loss of teeth, periodontal disease
Sinusitis

UNCOMMON CAUSES

Buss disease (transmissible serositis) (B)
Neoplasia (other than bovine leukemia virus)
Systemic candidiasis
Local and systemic mycoses
Mycoplasma, arthritis
Ulcerative posthitis, vulvitis (B)
Polycythemia (B)
Phosphorus deficiency
Vitamin A deficiency
Zinc deficiency
Bovine spongiform encephalopathy
Meuse-Rhine-Yssel muscular dystrophy (B)
Epidermolysis bullosa (B, O)
Familial acantholysis
Portal vein anomaly
Granulocytopathy
Pulmonary listeriosis
Cholelithiasis
Bronchobiliary fistula (B)
Hypersensitivity to soy or milk replacer
Diabetes mellitus
Idiopathic granulocytopenia or thrombocytopenia
Endocardial fibroelastosis (B)
α-Mannosidosis (B)
Fungal granuloma
Generalized glycogenosis (B)
GMI gangliosidosis
Hereditary zinc deficiency (B)
Lethal trait A-46, keratogenesis imperfecta (B)
Omental bursitis (B)
East Coast fever (theileriosis) (exotic)
Tick-borne fever (exotic)
Idiopathic sporadic bovine encephalomyelitis (exotic) (B)
Surra (exotic) (B)
Trypanosomiasis (exotic)
Melioidosis, Pseudomonas pseudomallei, (exotic)
Petechial fever (exotic) (B)
Besnoitiosis (exotic)
Ibaraki disease (exotic) (B)
Turning sickness (exotic) (B)
Contagious pleuropneumonia (exotic) (B)
Schistosomiasis (exotic)
Louping ill (exotic)
Foot-and-mouth disease (exotic)
Lethal skin defects in Japanese black cattle (exotic)
Echinococcosis (exotic)
Endemic ethmoid carcinoma (exotic)
African bovine malignant catarrhal fever (exotic)
Idiopathic storage disease in cattle (exotic)
Babesiosis (exotic)

TOXINS

Selenium
Trichothecene (T-2)
Vitamin D3
Diesel fuel
Polybrominated biphenyls
Cobalt
Herbicides
Zinc
Furazolidone
4-Aminopyridine
Chlorpyrifos
Toxins associated with crude oil, kerosene
Ergotism
Arsenic
Lead
Mercury
Ethylene glycol
Stachybotryotoxicosis (exotic)

PLANT TOXINS

Gossypol (cottonseed)
Helenium, sneezeweed
Acorn, oak
Bracken fern
Perennial broomweed (Gutierrezia),
Cocklebur
Hairy vetch (Vicia villosa),
White snakeroot (tremetol)
Mushroom
Tung tree
Fireweed (Kochia scoparia),
Locoweed (Oxytropis, Astragalus),
Phalaris, species
Bermuda grass
Pimela, species (exotic)
Geigeria, species (exotic)
Cestrum, species (exotic)
Yellow wood (exotic)
Leucaena leucocephala, species (exotic)

B, Bovine; O, ovine.

Anorexia usually occurs secondary to a primary disease. Increased nutrient requirements are associated with normal physiologic conditions (e.g., pregnancy, lactation, exercise, cold weather) and with pathologic processes (e.g., sepsis, trauma, parasitism, burns). Mild to severe PCM is often associated with inadequate feed quality (see Table 9-1) or quantity but can also be caused by increased energy requirements resulting from adverse environmental conditions. Weight loss can also occur with a deficiency of essential micronutrients such as copper, cobalt (vitamin B12), or vitamin A. Parasitism should always be on the differential list in an animal that has lost weight.

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Mechanisms of Weight Loss

Anorexia is the loss of appetite or lack of desire for food; it may be complete or partial. It is a primary mechanism for weight loss of short or intermediate duration. Weight loss results from decreased nutrient intake. When partial anorexia occurs over a long period, the weight loss may be subtle and go unrecognized. Acute, complete anorexia results in more dramatic weight loss.

In domestic species, anorexia is usually associated with a primary disease condition and is regulated by cytokines, including interleukin (IL)-1 and tumor necrosis factor alpha (TNF-α), released during an inflammatory response. Resolution of the primary disease process usually results in a return to voluntary food consumption. Anorexia must be differentiated from dysphagia by observation. The distinction between the conditions that cause anorexia and those that control hunger and satiety is not clear; however, many diseases that cause anorexia also result in dehydration, electrolyte imbalances, and/or acid-base disorders.

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In addition to causing anorexia, many disease processes cause an increase in the nutrient requirements for basal metabolism. Nutrient requirements for maintenance, growth, pregnancy, lactation, and exercise have been well defined for many large animal species. Nutrient requirements in disease have not been adequately evaluated in large animals, and most information is currently extrapolated from humans, laboratory animals, and small animal species. In human patients, published estimates indicate that requirements for energy and protein increase approximately 10% after elective surgery, 20% with fractures, 30% to 60% with severe infection or sepsis, 40% with peritonitis, and 50% to 110% with major burns.7,8 In humans, the resting energy expenditure is estimated to increase by 14% for each degree Celsius increase in body temperature.9 Extrapolation of these data directly to equine and ruminant patients is probably not possible; however, the figures do indicate the degree of change in nutrient requirements as a result of disease. The stress of many disease processes results in an increase in serum cortisol and in glucagon. The decreased insulin/glucagon ratio alters the production of glucose and results in hyperglycemia because of enhanced hepatic gluconeogenesis. An increase in sympathetic activity appears to regulate fat oxidation, the increased release of fatty acids from cellular lipid stores, and the development of hypertriglyceridemia in many patients with sepsis. Protein degradation and a negative nitrogen balance are also hallmarks of the acute response to infection. Weight loss resulting from protein and lipid catabolism is often observed in large animal patients with sepsis, owing to altered metabolic activity and nutrient requirements.

In conditions such as burns, peritonitis, pleuritis, colitis, and granulomatous bowel disease, nutrients (particularly proteins) are lost. In many disease conditions, concurrent anorexia and increased nutrient requirements greatly increase the risk of PCM and weight loss. Certain conditions, such as Johne’s disease in ruminants and granulomatous enteritis in horses, are also associated with a malabsorption or malassimilation syndrome. In these types of diseases, nutrients are not efficiently digested and absorbed; anorexia may be absent, and dietary intake may appear normal, but weight loss still occurs.

PCM continues to be a persistent problem in domestic animals. Inadequate ingestion of energy and protein obviously results in weight loss, but PCM and associated weight loss can occur through several other mechanisms. The most direct cause is that the animal receives an inadequate volume of feed to meet their dietary requirements. This can occur as frank underfeeding of all animals or as a consequence of inadequate feeding facilities that create competition among animals for available feed. The latter circumstance occurs most dramatically when animals of varying ages are mixed; the younger animals with the highest requirements are often pushed away by older, dominant individuals.

The quality of the diet, particularly dietary forages such as hay and pasture, is an important factor in the development of PCM and total nutrient intake. Table 9-1 lists guidelines for estimating the maximum daily intake by cattle. It is evident that as forage quality (digestibility) decreases, maximum daily intake decreases because poor-quality feed must remain in the rumen for an increased period of time before it is sufficiently digested to allow passage through the reticuloomasal orifice. Maximum dry matter intake (DMI) as a percentage of body weight is somewhat higher in small ruminants than in cattle. However, the energy requirement per kilogram of body weight is higher in small ruminants than in cattle. Similar estimates for maximum DMI in horses related to forage quality are not available. Horses do not have a pregastric fermentation organ (rumen) and can ingest slightly more of the same quality forage than cattle. Low-quality forages are often the cause of PCM, even when an unlimited quantity is available. The best way to determine the nutrient content of forage, grain, and pelleted feeds is to have the feed analyzed by a forage laboratory. Feed analysis instructions are provided in Box 9-3. Feed tag labels or forage databases can be referenced if a forage analysis is not performed.

Environmental factors can have a major influence on nutrient requirements and can increase the subsequent risk for PCM and weight loss. The most important environmental factor is the ambient temperature. Nutrient requirements for maintenance change with a decreasing ambient temperature as follows:

image Adult horses:, Estimated increase in digestible energy (DE) requirements by 2.5% for every degree Celsius below the lower critical temperature (LCT). The LCT for adult horses ranges from 5° C to −15° C, depending on the horse’s adaptation to the environment. In cold temperatures, when the hair coat is wet, the maintenance DE requirement may be increased by as much as 50%.10
image Beef cattle:, 1% increase in maintenance energy requirements (total digestible nutrients [TDN], net energy of maintenance [NEm], digestible energy [DE], and metabolizable energy [ME]) for each 1° C drop below 20° C (68° F).
image Dairy cattle (lactating):, 25% increase in energy requirements (TDN, net energy of lactation [NEL]) as ambient temperature drops from 20° C (68° F) to −10° C (14° F).
image Sheep with 10-cm wool:, 1% increase in energy requirements (TDN, ME, DE) for each 1° C drop below lower critical temperature (approximately −10° C).

There are also additive effects of wind and rain that increase energy requirements in large animal species. As nutrient requirements increase, the dietary intake must also increase to prevent weight loss associated with PCM. Horses in inclement weather may not be able to consume enough forage to meet their increased energy requirements, and for these animals, dietary fat and limited grain supplementation may be required.

Deficiencies of micronutrients (trace minerals, B vitamins) often result in inefficiencies in basic biochemical pathways. These inefficiencies, if marked, can be associated with weight loss. Genetic errors in metabolism can cause similar disturbances, but these usually manifest as decreased growth and even death in young animals.

Parasitism is a common cause of weight loss in adult domestic animals. The mechanisms by which parasite infestation can result in weight loss include a loss of body fluid and tissues resulting in increased nutrient requirements, competition for nutrients in the gastrointestinal tract, malassimilation and malabsorption, inflammation resulting in increased nutrient requirements, micronutrient deficiencies, and organ or vascular damage from migrating parasite larvae. Anorexia may also develop in the advanced stages of severe parasitism.

Approach to the Diagnosis and Management of Weight Loss in Adult Horses

Use the flow sheet in Fig. 9-7 to aid in decision making.

image

Fig. 9-7 Flow sheet for classifying conditions associated with weight loss.

1 Take a general history and a diet history.
a General history
i Is the weight loss affecting one animal, or many animals? If many horses are affected, what is the age range of the affected animals? How long has the caretaker noticed weight loss in the horse? How much weight has been lost? Is this an estimate of weight loss, or have the horse(s) been monitored on a scale or with a weight tape? What is the change in BCS of the horse(s)? Has the diet been changed to manage the weight loss? Weight loss is often suspected but not documented in the initial complaint or history. Acute weight loss of 5% to 10% is significant. Quantitation of weight loss and BCS changes is important.

If a weight tape will not fit around the girth of the horse, or if the horse has a BCS of 1 to 3, a body weight estimate is made using measurements of the length and girth of the horse.11-12 Length is measured from the tuber ischium to the point of the shoulder, and girth is measured at the withers, behind the elbows, at the end of expiration.


image


The weight of miniature horses should be obtained using a small animal clinic scale. If a scale is not available to weigh a miniature horse, then the following equation can be used to estimate the weight of the miniature horse.13


image


ii Is there any past or current clinical disease in the horse or herd? If so, when was the disease first diagnosed? How many animals were affected? What type of treatment was administered? Was the diet changed during this period of time? Question the caretaker closely about any clinical signs of diarrhea, coughing, dysphagia or polyuria. What is the deworming history of the horse and herd? Has the deworming protocol been changed lately?
b Diet history
i Obtain an accurate, dietary history including the type and amount of feed offered (in pounds, ounces) and the amount of feed refused by the horse(s). It is essential that feeds are weighed accurately. Nutrient requirements of adult ponies and horses are listed in Table 9-11. For how long does the horse have access to pasture? What type of grass is available in the pasture? Is the pasture overgrazed? Are any diet supplements fed to the horse? If so, what amount is fed? Does the horse have access to a salt or trace mineral block? How long has this diet been fed? Have there been any changes in the forage offered to the animals? Forage quality is often not consistent between hay shipments. Has a forage analysis been performed on the pasture or hay? If yes, obtain a copy of the analysis for the patient record. Inspect the pasture and all feeds for gross quality, evidence of spoilage, abnormal color or odor, presence of weeds and mold, and quantity of feed the owner has at the facility.
ii How are the horses fed? What type of feeder is used? Are mats placed under the feeders to reduce sand and dirt ingestion? Is there competition among the horses for food? Are there any toxic substances in the horse’s environment? What is the water source for the horses? Is the water clean?
2 Perform a physical examination.
a Observe the horse while it is eating forage. Can the horse prehend, masticate, and swallow food normally? Is the horse dysphagic? Does the horse have a good appetite? Is the horse hungry? Are there any signs of neurologic disease?
b Examine the patient closely to identify signs of concurrent disease (e.g., pyrexia, diarrhea, melena, dysphagia, abnormal dentition, icterus, nasal discharge, cough, dyspnea, tachycardia, cardiac murmur, dysuria).
c What are the horse’s body weight (scale or weight tape) and BCS (see Table 9-21)?
3 Examine the feces.

Table 9-11 Daily Nutrient Requirements of Ponies and Horses of Mature Body Weight

image

What is the consistency of the feces? If the horse has evidence of diarrhea, review the section on diarrhea in Chapter 7. How long are the fibers in the feces? Perform a glove test. Is there evidence of sand in the feces? Horses can have a significant volume of sand in the large intestine while having negative fecal sand test results. Perform a fecal egg count. An enzyme-linked immunosorbent assay (ELISA) may be useful in diagnosing a tapeworm infection. Follow the parasite control program in Chapter 49 if the horse has evidence of fecal parasites or if a parasite infection is suspected despite a negative fecal egg count. Perform a fecal occult blood test; if the result is positive, see the section on melena in Chapter 7.

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4 Perform blood analyses.
a Perform a CBC, including plasma protein and fibrinogen. Examine the results closely for indication of an inflammatory process (e.g., leukocytosis, neutrophilia, leukopenia, neutropenia, hyperfibrinogenemia, decreased plasma protein/fibrinogen ratio [below 10]). Calculate the erythrocytic indices, and characterize anemia, if present.
b Perform a serum biochemical analysis. The serum albumin half-life is approximately 19 days in horses. Hypoalbuminemia may be associated with colitis, internal abscessation, PCM, liver disease, renal disease, and granulomatous bowel disease, among other conditions. Albumin is often within normal limits in PCM until the patient is near death. Globulin (particularly γ-globulins) may be increased with inflammation, and the albumin/globulin ratio may be decreased. The glucose concentration is usually normal or elevated as a result of stress and may also be elevated in horses with pituitary pars intermedia dysfunction (PPID) and equine metabolic syndrome. Hyperlipidemia (serum triglyceride between 100 and 500 mg/dL) is commonly associated with early anorexia and can be present in horses with PPID. Hyperlipemia (serum triglyceride above 500 mg/dL) is a serious condition associated with prolonged anorexia and hepatic lipidosis and is often found in miniature horses, ponies, and donkeys under severe physiologic stress (PCM and lactation). Unconjugated bilirubin levels can rise to 6 or 7 mg/dL with anorexia or decreased food intake. An elevated γ-glutamyltransferase (GGT) (above 25 IU/L) may indicate hepatic disease. Horses with PCM may have a low serum urea nitrogen if the protein malnutrition is prolonged and severe.
5 Analyze the diet and improve the feeding program.
a Determine if the energy, protein, mineral, and vitamin content of the diet meets the nutrient requirements of the horse at their current metabolic state and activity level (see Table 9-11). Include pertinent environmental and management factors in the nutrient requirement calculations. The quality of the feeds should be assessed.
i Forage

The most accurate way to determine the nutrient content of forage or pasture is with an analysis. See Box 9-3 for instructions on how to sample feeds for analysis. Contact a university extension service for forage analysis. If the client does not purchase a large volume of hay, or if analysis cannot be performed, forage tables from the Nutrient Requirement Council reference books (www.nap.edu), or nutrient tables from the Equi-Analytical Laboratories forage laboratory database (www.equi-analytical.com) can be used to estimate the concentration of different nutrients in common forages and supplemental feeds.

ii Commercial Feeds

The guaranteed analysis on feed tag labels provides the nutrient content of certain ingredients. Contact commercial feed companies for the energy content of their products.

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b If the horse has a dietary deficiency, the problem should be corrected by a change in the diet or through appropriate supplementation. Contact an equine clinical nutritionist for guidance on ration formulation.
c If the dietary history indicates that adequate nutrients for maintenance and performance have been steadily consumed, continue to search for another cause of the weight loss.
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6 Perform ancillary diagnostic tests.

If the weight loss is not caused by inadequate or poor-quality feed, additional diagnostic tests should be performed. Possible tests include but are not limited to ultrasound, gastric endoscopy, radiographs, serum or whole blood trace mineral analysis, serum insulin concentration, carbohydrate absorption tests (oral D-glucose, D-xylose [see Chapter 32]), and appropriate organ biopsy.

Approach to the Diagnosis and Management of Weight Loss in Adult Ruminants

1 Take a general history and a diet history.
a General history

Question the caretaker closely about any clinical signs that might indicate a primary disease (e.g., diarrhea, coughing, dysphagia, polyuria, depression, agalactia). Note if body condition is less than desired. Quantitate the weight loss or BCS if possible. Acute weight loss of 5% to 10% is quite significant. Carefully note the production level of the animal or herd (e.g., pregnancy [single, twins, triplets], lactation [level of milk production]). Evaluate the parasite control program. Does the herd have a history of chronic or recurrent disease (Johne’s disease, bovine virus diarrhea, ruminal lactic acidosis, laminitis, mastitis, pneumonia)?

b Diet history

Obtain an accurate, dietary history, particularly when signs of a primary disease are absent. Inspect all forages, concentrates, and feed additives for quality, signs of spoilage, abnormal color or odor, and quantity on hand. Be sure the feeding system allows for adequate consumption by all animals and that competition for feedstuffs does not occur. Check to see if the feeding program was changed before the onset of observed weight loss or loss of body condition. The history should include the weight, of each feedstuff and supplement fed and consumed per day. The maximum DMI can be estimated according to feed quality for cattle (see Table 9-1). Determine or estimate the nutrient analysis of the feedstuffs being fed. Examine the environment for possible toxic plants or substances.

2 Perform a physical examination.

Examine patients carefully for signs of concurrent disease (e.g., diarrhea, decreased ruminal motility, pyrexia, dysphagia, abnormal dentition, melena, icterus, mastitis, metritis, dyspnea, tachycardia). Is the patient hungry? Weigh the patient (or use a heart-girth measurement) and note the BCS (see Tables 9-18 through 9-20). Observe the patient for signs of muscle wasting and the presence or absence of subcutaneous fat. Test the milk with nitroprusside powder (a positive reaction indicates an acetoacetate concentrate above 5 mg/dL and is diagnostic of ketonlactia and ketonemia), or measure the ketone concentration in the urine. Measure the ruminal pH (pH above 7 is indicative of anorexia). Examine the skin for evidence of lice or keds.

3 Examine the feces.

Table 9-18 Body Conditioning Scoring System for Beef Cattle

image

Table 9-19 Body Conditioning Scoring System for Dairy Cattle

Score Description
1 Individual spinous processes have limited flesh covering and are prominent; the ends are sharp to the touch, and together the processes form a definite overhanging shelf effect to the loin region. Individual vertebrae of the chine, loin, and rump regions are prominent and distinct. Hooks and pin bones are sharp with negligible flesh covering, and severe depressions between hooks and pin bones are noted. The area below the tailhead and between the pin bones is severely depressed, causing the bone structure of the area to appear extremely sharp. (Body fat = 3.77%)
2 Individual spinous processes are visually discernible but not prominent. The ends of processes are sharp to the touch, although they have greater flesh covering, and the processes do not have a distinct overhanging shelf effect. Individual vertebrae of chine, loin, and rump regions are not visually distinct but are readily distinguishable by palpation. Hooks and pin bones are prominent, but the depression between them is less severe. The area below the tailhead and between the pin bones is depressed, but the bone structure is not devoid of flesh covering. (Body fat = 11.3%)
3 Spinous processes are discernible by applying slight pressure. Together the processes appear smooth, and the overhanging shelf effect is not noticeable. Vertebrae of the chine, loin, and rump regions appear as rounded ridges, and hooks and pin bones are rounded and smooth. The area between the pin bones and around the tailhead appears smooth, with no sign of fat deposition. (Body fat = 18.84%)
4 Individual spinous processes can be distinguished only by firm palpation, and together the processes appear flat or rounded with no overhanging shelf effect. The ridge formed by the vertebral column of the chine region is rounded and smooth, but loin and rump regions appear flat. Hooks are rounded, and the span between the hooks is flat. The area around the tailhead and pin bones is rounded, with evidence of subcutaneous fat deposition. (Body fat = 26.38%)
5 Bone structure of the vertebral column, spinous processes, hooks, and pin bones is not visually apparent, and evidence of subcutaneous fat deposition is prominent. The tailhead appears to be buried in fatty tissue. (Body fat = 33.9%)

From Wildman EE et al: J Dairy Sci, 65:495–501, 1982; and modified from National Research Council (NRC): Nutrient requirements of dairy cattle, Washington, DC, 2001, National Academy of Sciences, NRC.

Table 9-20 Body Condition Scoring System for Sheep

Score Description
0 Animal is extremely emaciated and at the point of death. No muscular or fatty tissue can be detected between the skin and the bone.
1 The spinous processes are prominent and sharp. The transverse processes are also sharp; the fingers pass easily under the ends, and it is possible to feel between each process. The eye muscle areas are shallow with no fat cover.
2 The spinous processes still feel prominent but also smooth, and individual processes can be felt only as fine corrugations. The transverse processes are smooth and rounded, and the fingers can be passed under the ends with a little pressure. The eye muscle areas are of moderate depth but have little fat cover.
3 The spinous processes are detected only as small elevations; they are smooth and rounded, and individual bones can be felt only with pressure. The transverse processes are smooth and well covered, and firm pressure is required to feel over the ends. The eye muscle areas are full and have a moderate degree of fat cover.
4 With pressure the spinous processes can just be detected as a hard line between the fat-covered muscle areas. The ends of the transverse processes cannot be felt. The eye muscle areas are full and have a thick covering of fat.
5 The spinous processes cannot be detected even with firm pressure, and there is a depression between the layers of fat where the spinous processes would normally be felt. The transverse processes cannot be detected. The eye muscle areas are very full and have a very thick fat cover. Large deposits of fat may be seen over the rump and tail.

From Russel A: Body condition scoring of sheep, In Pract, 6:91, 1984.

Perform flotation, sedimentation, and Baermann’s procedures to detect patent parasitic infestations. If the feces test positive for occult blood or are very dark, see the section on melena in Chapter 7. If there is evidence of or apparent diarrhea, see the section on diarrhea in Chapter 7.

4 Perform blood analysis.
a Perform a CBC, including plasma protein and fibrinogen. Interpret for evidence of inflammation. Calculate the erythrocytic indices, and characterize the anemia if present. Analyze for blood selenium concentration or glutathione peroxidase activity if a herd problem of weight loss exists in a selenium-deficient region.
b Perform a serum chemistry analysis. The serum albumin half-life is approximately 16½ days in cattle and 14 days in sheep and goats. Hypoalbuminemia is associated with internal abscessation, PCM, liver disease, renal disease, and Johne’s disease, among other conditions. In the first two of these conditions, albumin is often normal until the patient is near death, whereas with protein-losing renal or gastrointestinal disease or with failure to make albumin in severe hepatic disease, hypoalbuminemia is often seen by the time noticeable weight loss occurs. Globulins, particularly γ-globulins, may be increased with inflammation, and the albumin/globulin ratio may be decreased. The serum glucose concentration is usually not helpful in determining the cause or causes of weight loss. An elevated serum GGT (above 25 IU/L) may indicate hepatic disease or, in rare cases, pancreatic disease. Serum BUN is often low with PCM in ruminants because of salivary urea recycling. Serum (total) calcium may be decreased with hypoalbuminemia, anorexia, or hypocalcemic syndromes. Serum phosphorus may be increased during severe starvation or Johne’s disease or decreased with anorexia. The serum (plasma) copper concentration may be decreased if a herd problem of copper deficiency exists. Weight loss is particularly associated with copper deficiency when diarrhea is present in a region known to be copper deficient or in a region with excess dietary molybdenum or sulfates or both. A low serum copper concentration (below 0.5 μg/mL or ppm) indicates deficiency. Ketonlactia (above 5 mg/dL), indicated by a positive reaction (blue or purple) of milk with nitroprusside, may be associated with anorexia in ketosis or other conditions. Plasma β-hydroxybutyrate (BHB) concentrations have been reported to be a useful tool in diagnosing inadequate caloric intake, in pregnant sheep.14 Plasma BHB concentrations should be less than 0.8 mmol/L in pregnant ewes consuming adequate energy.14
5 Analyze the diet and improve the feeding program.

Is the feed quantity and quality adequate to allow sufficient intake of nutrients (see Table 9-1)? Compare the nutrient intake from the diet with the requirements for the appropriate species (Tables 9-12 through 9-17). Consider any important environmental and management factors in the daily nutrient requirements. Review nutrient analysis profiles on the feeds and total mixed ration (TMR) ingredients. Is the TMR mixed properly? Are grain rations mixed properly? Is too much grain being fed to the animal or herd? Analyze the pasture, forage, or concentrate rations (see Box 9-3). Make appropriate recommendations to optimize the ration. Determine if the patient or patients have a normal appetite. Is anorexia present? If the dietary history and analysis indicate that adequate nutrients have been steadily consumed, the search for a primary cause for the weight loss should be resumed.

6 Perform ancillary diagnostic tests.
a If the weight loss is not related to the diet, additional diagnostic tests should be performed on the animal or on a number of animals in the herd. Possible tests include but are not limited to trace mineral analyses, ultrasound, and appropriate organ biopsy.
b Pathologic findings of affected ruminants often provide evidence of the effects of a systemic disease or of chronic malnutrition. Ruminants with PCM exhibit serous atrophy of fat in the coronary grooves of the heart and bone marrow at necropsy. Subcutaneous, abdominal, and perirenal fat are not present.

Table 9-12 Daily Nutrient Requirements for Dairy Cattle

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Table 9-13 Daily Nutrient Requirements for Lactating Dairy Cows at Various Production Levels

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Table 9-14 Daily Nutrient Requirements for Mature Beef Cows

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Table 9-15 Daily Nutrient Requirements for Bulls: Maintenance and Regaining Body Condition

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Table 9-16 Daily Nutrient Requirements of Sheep

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Table 9-17 Daily Nutrient Requirements of Goats

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OBESITY

Mechanisms of Obesity

Obesity is a common problem in domestic species. The prevalence of obesity is increasing in the domestic horse population, and obesity is a significant problem in many ruminant species raised as companion animals. Obese patients (especially ruminants) are at particular risk for reproductive failure or metabolic disease late in pregnancy or during lactation. The risk of obstructive urolithiasis increases in overweight goats and sheep. In horses, obesity may be related to a variety of diseases including equine metabolic syndrome, laminitis, and colic associated with strangulating lipomas. Obese horses and ponies that are rapidly losing weight or that are anorexic are particularly susceptible to hyperlipidemia and hyperlipemia.

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The mechanism of obesity is invariably a prolonged intake of total dietary energy above that needed for maintenance and either production or exercise. Obesity occurs most commonly in stabled horses fed high-energy feeds such as grain or high-fat supplemental feeds and in horses and ponies on lush pasture. Even horses that are fed a forage diet but have limited access to exercise may gain weight if they consume an excess amount of energy for their body size. Purebred or pet sheep and goats (particularly wethers) tend to be overfed. In dairy cattle, obesity occurs when cattle are fed well above requirements for maintenance and milk production. Poor reproductive performance is often associated with the initiation of obesity and is also a common sequela to obesity. Feeding for high milk production for lengthy periods in production groups predisposes infertile cows to become fat cows. Dry cows with access to high-energy diets are also predisposed to fat cow syndrome. The systemic complications associated with fat cow syndrome (fatty liver), and its diagnosis and treatment, are described in Chapter 33.

Diagnosis of Obesity in Horses and Ruminants

Diagnosis is obvious; it is made by physical examination. Overweight and obese animals have an elevated BCS (7 to 9/9 for horses; 8 to 9/9 for beef cattle; 4 to 5/5 for dairy cattle, sheep, and goats). Palpation of the back, gluteal area, and ribs should be included in the physical examination of sheep and camelids with long wool or fiber and of horses with a long winter hair coat so that a BCS can be accurately assigned. In some animals, external signs of fat deposition may be subtle. In these cases, ultrasonography can be used to identify the extent of deposition of intraabdominal fat in horses and of back fat in cattle. Clinical descriptions of obesity provided by the body condition scoring system are straightforward (Tables 9-18 to 9-21) and require minimal interpretation.

In some animals, obesity can be mistaken for the normal physiologic condition of pregnancy. In other cases, obesity could be mistaken for a distended abdomen from acute pathologic disease conditions including uroabdomen and peritonitis. A full physical examination should always be performed on a large animal patient before a weight loss ration is fed.

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Treatment of Obesity

Overweight and obese horses and ruminants should lose weight to extend life span and to improve production efficiency. In many cases a reduction in energy intake can be achieved by simply eliminating excess calories from grain or supplemental feeds. Animals that fail to lose weight after 1 to 2 months after a reduction in calories require a more aggressive weight loss program, which may include reformulation of their ration and the gradual implementation of an exercise program. Voluntary activity in animals that are turned out in pasture is rarely high enough to promote weight loss. Obese laminitic horses present a difficult challenge because exercise may not be practical, and weight loss must rely solely on dietary energy restriction.

Horses and companion ruminants that require a managed weight loss program should have the energy content of their diet evaluated by the veterinarian. The actual energy intake should be compared against the energy requirement for the animal’s current lifestage (see Tables 9-11 to 9-17). The animal’s current calorie intake should be reduced by 10% to 20% at the start of the weight loss program. Dietary protein should not be restricted. Supplemental feeds and treats should be reduced or eliminated from the diet, and only high-quality forage should be fed.

Feeding straw should be avoided because gastrointestinal complications including impaction colic could develop. A vitamin and mineral supplement should be fed during a weight loss program to ensure that the diet meets nutrient requirements. To prevent boredom, small amounts of forage should be fed frequently. When horses are being fed, hay can be placed in a double hay net or hay bag, or a restricted feeder (The Grazer Hay Feeding Machine) can be used to decrease the rate of intake. The target weight loss goal is between 0.5% and 2% of the original body weight each week. A weight tape should be used to assess the horse’s weight if a scale is not available. A BCS should be assigned to the animal at the start of the weight loss program. The body weight and BCS should be assessed every month to track changes in the animal’s weight.

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Owner compliance is essential during a weight loss program for horses and companion large animals. Owners should be encouraged to keep a weight loss journal and to include digital pictures to assess the animal’s BCS during the program. Excessive, rapid weight loss should be avoided. Weight loss programs should be approached with caution in animals that are either pregnant or lactating. Once the animal has achieved the ideal body weight and BCS, it should be placed on a maintenance ration and exercise program that will ensure that the ideal weight is maintained.

In a production management setting the ration should be evaluated and revised to reduce calories while maintaining sufficient energy intake to maximize reproduction or milk production. Care should be taken to ensure the animals consume an adequate concentration of vitamins and minerals to meet their requirements when they are fed an energy-restricted ration.

PICA

Pica (geophagia) is defined as a depraved or abnormal appetite. It is usually associated with animals that chew or eat wood (fences, trees, buildings), dirt, bones, or other inanimate objects not usually considered feedstuffs. The mechanism or mechanisms of pica are not yet understood. Pica has been associated with PCM, parasitism, obesity, and deficiencies of phosphorus, salt, protein (kwashiorkor), and micronutrients. Diagnosis is by observation or history or both. The main emphasis must be placed on identification and resolution of the primary problem. Pica must be differentiated from abnormal behavior associated with central nervous system diseases, bovine ketosis, and equine behavioral abnormalities associated with boredom.

References

1 Budzynski M, et al. Growth in halfbred horses. Roczniki Nauk Roln B. 1961;93:21.

2 Cunningham K, Fowler S. A study of growth in quarter horses. La Agric Exp Stn Bull. 1961:546.

3 Hintz HF. A review of recent studies on the growth of horses. Calif Vet. 1979:17. March

4 Jordan RM. Growth pattern in ponies. Proc Fifth Equine Nutr Physiol Symp. 1977;5:63.

5 Reed KF, Dunn NK. Growth of the Arabian horse. Proc Fifth Equine Nutr Physiol Symp. 1977;5:99.

6 National Research Council. Nutrient requirements of horses, ed 6 revised, Washington, DC: National Academies Press; 2007:54-68. 294–303

7 Kinney JM. The application of indirect calorimetry to clinical studies. In: Kinney JM, editor. Assessment of energy metabolism in health and disease. Columbus, Ohio: Ross Laboratories, 1980.

8 Long CL, Schaffel N, Geiger JW, et al. Metabolic response to injury and illness: estimation of energy and protein needs from indirect calorimetry and nitrogen balance. JPEN J Parenter Enteral Nutr. 1979;3:452.

9 Trujillo EB, Chertow GM, Jacobs DO. Metabolic assessment. In: Rombeau JL, Rolandelli RH, editors. Clinical nutrition: parenteral nutrition. ed 3. Philadelphia: Saunders; 2001:80.

10 National Research Council:. Nutrient requirements of horses, ed 6 revised, Washington, DC: National Academies Press; 2007:3.

11 Carroll CL, Huntington PJ. Body condition scoring and weight estimation of horses. Equine Vet J. 1988;20:41.

12 Reavell DG. Measuring and estimating the weight of horses with tapes, formulae and by visual assessment. Equine Vet Educ. 1999:188. December

13 Kentucky Equine Research: Feeding the miniature horse, Kentucky Equine Research Equine Review,

14 Russel A. Nutrition of the pregnant ewe. Vet Rec,(In Pract, 7:23, suppl). 1985;116:29.