NORMAL GASTROINTESTINAL MOTILITY

The form and function of the small intestine of farm animals is similar between species but the stomachs and large intestines vary considerably.¹ The motility patterns in both the small and large intestine are similar among the species. In the small intestine, the fundamental unit of electrical activity is the slow wave, which is a subthreshold fluctuation in membrane potential. Slow waves are constantly propagated from the stomach to the rectum. When an additional stimulus causes the membrane potential to exceed the excitation threshold, a spike or electrical response activity occurs, which is usually accompanied by contraction. Almost all spike activity in the intestine is superimposed on slow waves, which are important in controlling frequency and velocity at which spiking events occur. The spiking activity, also known as the migrating myoelectric complex, is the myoelectric pattern in the stomach and small intestine of fasted nonruminants, fed and fasted ruminants, and pigs and horses fed ad libitum.² There are three phases of the migrating myoelectric complex:

There is very little muscle contraction or transit of gut contents during the quiescent phase. During the irregular phase, contractions mix the intestinal contents and propel them in an aboral direction. The activity front is accompanied by intense muscular contraction that obliterates the lumen, preventing backflow of content as it propagates, or migrates, down the intestine. In nonruminants, and pigs and horses fed periodically, feeding abolishes the migrating myoelectric complex for several hours. It is replaced by the fed pattern, characterized by intermittent spike activity resembling the irregular phase.

Normal cecal and colonic myoelectric activities, like those of the small intestine, are characterized by slow waves and spikes. However, unlike the small intestine, the patterns of spikes vary greatly with the species and the area of the large intestine.²

Abnormalities of stomach and intestinal motility represent the most common consequence of gastrointestinal tract disease. Disruption in gastrointestinal tract motility can result in:

HYPERMOTILITY AND HYPOMOTILITY

The most important functions of alimentary tract motility are the peristaltic movements that move ingesta from the esophagus to the rectum, the segmentation movements that churn and mix the ingesta, and the tone of the sphincters. In ruminants these movements are of major importance in the forestomach. Prehension, mastication and swallowing are other functions of alimentary tract motility that are essential for normal function. Eructation of ruminal gases is an additional crucial function of motility in ruminants.

Abnormal motor function may take the form of increased or decreased motility. Peristalsis and segmenting movements are usually affected equally and in the same manner. Motility depends upon stimulation via the sympathetic and parasympathetic nervous systems and is thus dependent upon the activity of the central and peripheral parts of these systems, and upon the intestinal musculature and its intrinsic nervous plexuses. Autonomic imbalance, resulting in a relative dominance of one or other system, is manifested by hypermotility or hypomotility, and can arise as a result of stimulation or destruction of hypothalamic centers, the ganglia, or the efferent or afferent peripheral branches of the system. Debility, accompanied by weakness of the musculature, or severe inflammation, such as occurs in acute peritonitis or after trauma, or infarction, results in atony of the intestinal wall. Less severe inflammation, such as occurs in mild gastritis and enteritis, may result in an increase in muscular activity and increased propulsive activity. Increased motility causes diarrhea, decreased motility causes constipation, and both have deleterious effects on digestion and absorption.

Increased irritability at a particular intestinal segment increases its activity and disturbs the normal downward gradient of activity that insures that the ingesta is passed from the esophagus to the rectum. Not only is the gradient towards the rectum made steeper, thus increasing the rate of passage of ingesta in that direction, but the increased potential activity of an irritated segment may be sufficiently high to produce a reverse gradient to the oral segments so that the direction of the peristaltic waves is reversed orally to the irritated segments.

DISTENSION

One of the major results of abnormality of motility is distension of the tract. This occurs in a number of disturbances, including the rapid accumulation or inefficient expulsion of gas, complete occlusion of the lumen by intestinal accident or pyloric or ileocecal valve obstruction, and engorgement on solid or liquid feeds. Fluids, and to a lesser extent gas, accumulate because of their failure to pass along the tract. Much of the accumulated fluid represents saliva and gastric and intestinal juices secreted during normal digestion. Distension causes pain and, reflexly, increased spasm and motility of adjoining gut segments. Distension also stimulates further secretion of fluid into the lumen of the intestine and this exaggerates the distension. When the distension passes a critical point, the ability of the musculature of the wall to respond diminishes, the initial pain disappears, and a state of paralytic ileus develops in which all muscle tone is lost.

ABDOMINAL PAIN

Visceral pain may arise in any abdominal viscus or organ but the mode of its development is always the same and alimentary tract disease is the major cause of visceral and, more specifically, of abdominal pain. The most important mechanism is stretching of the wall of the viscus, which stimulates free pain endings of the autonomic nerves in the wall. Contraction does not of itself cause pain but does so by causing direct and reflex distension of neighboring segments. Thus spasm, an exaggerated segmenting contraction of one section of intestine, will result in distension of the immediately oral segment of intestine when a peristaltic wave arrives. When there is increased motility for any reason, excessive segmentation and peristalsis cause abdominal pain, and the frequent occurrence of intermittent bouts of pain depends upon the periodic increases in muscle tone that are typical of alimentary tract wall. Other factors that have some stimulating effect on the pain end organs are edema and failure of local blood supply, such as occurs in local embolism or in intestinal accidents accompanied by twisting of the mesentery. A secondary mechanism in the production of abdominal pain is the stretching and inflammation of serous membranes.

Clinically, abdominal pain can be detected by palpation and the eliciting of pain responses. However, it is unknown if the response elicited is due to involvement of underlying organs or to referred pain. It is difficult to decide if referred pain occurs in animals. In humans it is largely a subjective sensation, although often accompanied by local hyperalgesia. There are no known examples of referred pain that are of diagnostic importance in animals and a local pain response on palpation of the abdomen is accepted as evidence of pain in the serous membranes or viscera that underlie the point of palpation.

DEHYDRATION AND SHOCK

An immediate effect of distension of the stomach or small intestine by the accumulation of saliva and normal gastric and intestinal secretions is the stimulation of further secretion of fluid and electrolytes in the oral segments. The stimulation is self-perpetuating and creates a vicious cycle resulting in loss of fluid and electrolytes to the point where fatal dehydration can occur. The dehydration is accompanied by acidosis or alkalosis depending on whether the obstruction is in the intestine and accompanied by loss of alkali, or in the stomach and accompanied by a large loss of acid radicals. The net effect is the same whether the fluid is lost by vomiting or is retained in the gut.

The same cycle of events occurs in ruminants that gorge on grain but here the precipitating mechanism is not distension but a gross increase in osmotic pressure of the ingesta due to the accumulation of lactic acid. Dehydration is also of major importance in diarrhea, irrespective of the cause. An important additional factor in the production of shock, when there is distension of alimentary segments, is a marked reflex depression of vasomotor, cardiovascular and respiratory functions. In diarrhea in calves in which there is no septicemia nor toxemia associated with bacteria, the end-point in the phase of dehydration can be cardiac failure due to severe metabolic acidosis. Renal ischemia leading to uremia may result from decreased circulating blood volume and also contribute to a fatal outcome. These matters are discussed in detail in the section in Chapter 2 on disturbances of body fluids, electrolytes and acid–base balance.

CAUSES OF DYSPHAGIA AND INABILITY TO SWALLOW

LOCAL CAUSES OF DROOLING

SYSTEMIC CAUSES OF EXCESSIVE SALIVATION

VOMITING

Vomiting is the forceful ejection of contents of the stomach and the proximal small intestine through the mouth and is a complex motor disturbance of the alimentary tract. It is a vigorously active motion signaled by hypersalivation, retching and forceful contractions of the abdominal muscles and diaphragm. Vomiting is essentially a protective mechanism with the function of removing excessive quantities of ingesta or toxic materials from the stomach. It occurs in two forms: projectile and true vomiting.

REGURGITATION

Regurgitation is the expulsion through the mouth or nasal cavities of feed, saliva and other substances that have not yet reached the stomach. In most cases it is due to abnormalities of the esophagus that interfere with swallowing. A common example in large animals is the regurgitation of feed, saliva, and perhaps blood-stained fluid from the esophagus of the horse with esophageal obstruction. Esophagitis is also a common cause of regurgitation.

Ruminants regurgitate rumen contents as part of rumination but the material is not expelled from the mouth nor into the nasal cavities. The regurgitation of rumen contents through the mouth does occur in cattle occasionally, is abnormal, and is a dramatic event. It is most commonly associated with loss of tone of the cardia or inflammation of the cardia (see examples below).

Nasogastric regurgitation or gastric reflux occurs in the horse. Stomach contents flow into the esophagus, and usually into the nasopharynx and nasal cavities, as a result of distension of the stomach with fluid (which usually originates in the small intestine). This involuntary process is usually slow and gradual, unlike true vomiting. Gastric reflux in the horse can be elicited by nasogastric intubation. Spontaneous efflux of stomach contents is indicative of high-volume and high-pressure fluid distension of the stomach. On other occasions the presence of sequestrated gastric fluids can be confirmed only by the creation of a siphon, using the nasogastric tube to infuse a volume of fluid then disconnecting its supply in order to retrieve the nasogastric reflux.

Causes of vomiting and regurgitation include:

DIARRHEA

Diarrhea is the increased frequency of defecation accompanied by feces that contain an increased concentration of water and decrease in dry matter content. The consistency of the feces varies from soft to liquid.

Abnormalities of peristalsis and segmentation usually occur together and when there is a general increase in peristaltic activity there is increased caudal flow, resulting in a decrease in intestinal transit time and diarrhea. Because of a lack of absorption of fluid the feces are usually softer than normal, the dry matter content is below the normal range, and the total amount of feces passed per day is increased. The frequency of defecation is usually also increased. Common causes of diarrhea are:

CONSTIPATION

Constipation is the decreased frequency of defecation accompanied by feces that contain a decreased concentration of water. The feces vary in consistency from being hard to dry and of small bulk. True constipation as it occurs in humans is usually characterized by failure to defecate and impaction of the rectum with feces. When the motility of the intestine is reduced, the alimentary transit time is prolonged and constipation or scant feces occurs. Because of the increased time afforded for fluid absorption, the feces are dry, hard and of small bulk and are passed at infrequent intervals. Constipation may also occur when defecation is painful, as in cattle with acute traumatic reticuloperitonitis.

SCANT FECES

Scant feces are small quantities of feces, which may be dry or soft. Scant feces occur most commonly in cattle with abnormalities of the forestomach or abomasum resulting in the movement of only small quantities of ingesta into the small and large intestines (an outflow abnormality). The details are available in Chapter 6. When there is complete intestinal stasis the rectum may be empty except for blood-tinged, thick, pasty material.

Common causes of constipation or scant feces are:

COMMON CAUSES OF ALIMENTARY TRACT PAIN

RUMEN OF CATTLE

Examination of the rumen contents is often essential to assist in determination of the state of the rumen environment and digesta. Passage of a stomach tube into the rumen will determine the patency of the esophagus and if there is increased intraruminal pressure associated with a frothy or free-gas bloat. In a free-gas bloat, large quantities of gas are usually released within a minute. In a frothy bloat, the ruminal end of the tube may become occluded by the froth and very little if any gas is released. Moving the tube back and forth within the rumen and blowing air into the tube to clear the ruminal end may result in the release of some gas.

When the tube is in the rumen, some rumen juice can be siphoned or pumped out and collected in an open beaker for field and laboratory analysis. The color, depending on the feed to a limited extent, will be green, olive-green or brown-green. In cattle on pasture or being fed good quality hay, the color is dark green. When silage or straw is the diet the color is yellow-brown. In grain overload the color is milky-gray, and in rumen stasis of long duration with putrefaction, the color is greenish-black. The consistency of the rumen contents is normally slightly viscid, and watery rumen content is indicative of inactive bacteria and protozoa. Excess froth is associated with frothy bloat as in primary ruminal tympany or vagus indigestion. The odor of the rumen contents is normally aromatic and, although somewhat pungent, not objectionable to the nose. A moldy, rotting odor usually indicates protein putrefaction, and an intensely sour odor indicates an excess of lactic acid formation, due to grain or carbohydrate engorgement. The pH of the rumen juice varies according to the type of feed and the time interval between the last feeding and taking a sample for pH examination. The normal range, however, is between 6.2 and 7.2. The pH of rumen juice should be examined immediately after the sample is obtained, using a wide range pH (1–11) paper. High pH values (8–10) will be observed when putrefaction of protein is occurring in the rumen or if the sample is mixed with saliva. Low pH values (4–5) are found after the feeding of carbohydrates. In general, a pH below 5 indicates carbohydrate engorgement; this pH level will be maintained for between 6–24 hours after the animal has actually consumed the carbohydrate diet. Microscopic examination of a few drops of rumen fluid on a glass slide with a low-power field will reveal the level of protozoon activity. Normally 5–7 protozoons are active per low-power field. In lactic acidosis the protozoa are usually absent or a few dead ones are visible.

DECOMPRESSION OF DISTENDED RUMEN

In adult cattle with severe abdominal distension due to gross distension of the rumen it is difficult, if not impossible, to assess the status of the abdomen. To determine if the rumen is distended and/or to relieve the pressure a large-bore stomach tube should be passed (Colorado Kingman Tube: 2 m long and 3 cm inside diameter). In vagus indigestion, the rumen may be grossly distended with fluid contents, which will gush out through a large-bore tube. In some cases 100–150 L of rumen contents may be released. If no contents are released the contents may be frothy or mushy and the rumen end of the tube will plug almost instantly. Rumen lavage may then be attempted using a water hose to deliver 20–40 L of water at a time followed by back drainage using gravity flow. After the rumen is partially emptied it is usually possible to more accurately assess the rumen and the abdomen.

DECOMPRESSION OF THE HORSE’S STOMACH

Attempts to pass a nasogastric tube in the horse will usually detect complete or partial obstruction of the esophagus. In gross distension of the stomach in the horse, there is an immediate rush of fluid contents as soon as the cardia is passed (gastric reflux). The technique of gastric decompression is therapeutic and diagnostic. Gastric distension is a highly distressing feature of some colic cases and the mere pain relief of gastric decompression facilitates the clinical examination. The retrieval of significant volumes (2 L or more) of sequestrated gastric fluid is also an extremely specific indicator of intestinal obstruction, especially small intestinal obstruction, and a reasonably specific indicator that surgical intervention is necessary.

RADIOGRAPHY

Because of their large size, and the presence of substantial amounts of gas in the large intestine, abdominal radiography has not been used routinely as a diagnostic aid in mature horses with abdominal pain. Similarly, in mature cattle the sheer size of the abdomen and the gas in the rumen has not favored abdominal radiography except for identifying the presence of metal objects in the reticulum. Esophageal radiography is, however, useful for the diagnosis of disorders of swallowing in horses.

Foals, calves and small horses are too small to be palpated per rectum, and abdominal radiography, with and without contrast media, has been used diagnostically in colic of foals. A standard lateral abdominal radiography is a valuable diagnostic aid in the foal with colic.⁴ The site of the lesion, whether gastric, small or large intestinal, or a combination of all three, can be determined from the radiographs. The sensitivity of radiography in detecting gastrointestinal lesions in neonatal foals was found to be 96%; the specificity was 71%.⁴

Knowledge of the radiographic appearance of the normal neonatal abdomen is important before lesions can be reliably detected. The standing lateral radiographic of the normal abdomen of the neonatal foal is characterized by:

Abdominal radiography has also been used for the diagnosis of enterolithiasis and sand accumulation as causes of colic.³ The technique provides a high positive-predictive value and is cost-effective in high-prevalence areas.

ABDOMINAL ULTRASONOGRAPHY

Abdominal ultrasonography has been used to identify small intestine intussusceptions, large colon displacements, abdominal viscera and neoplasms. The technique may require only several minutes in the hands of an experienced clinician.

GASTROENTEROSCOPY

Fiberoptic gastroduodenoscopy is a practicable procedure in a sedated horse that has had no feed for 12–24 hours. A 275 × 13.5 cm fiberoptic instrument is passed via a nostril to the stomach, which is then distended with air. The control of the objective of the endoscope is quite difficult and entry into the pylorus particularly so, so that examination of the duodenum is not possible in all horses.

LAPAROSCOPY

In this procedure a laparoscope is passed through an incision in the abdominal wall of either the left or right paralumbar fossa.¹⁴ Feed must be withheld for 36 hours, analgesia is provided during the procedure, and abdominal insufflation with carbon dioxide is required in order to separate the viscera for viewing. Laparoscopy in standing horses is a valuable diagnostic aid for examination of the structures in the dorsal regions of the abdomen. In the standing horse, the anatomic structures of importance that can be viewed in the left half of abdomen are the hepatic duct, left lateral and quadrate lobes of the liver, stomach, left kidney with associated nephrosplenic ligament, segments of the jejunum, descending colon and ascending colon, left side of the male and female reproductive tracts, urinary bladder, vaginal ring and mesorchium. The important structures observable in the right side of the abdomen are the common hepatic duct, left lateral, quadrate and right lobes of the liver, caudate process of the liver, stomach, duodenum, right dorsal colon, epiploic foramen, omental bursa, right kidney, base of the cecum, segments of jejunum, descending colon and ascending colon, urinary bladder, right half of the male and female reproductive tracts, and rectum.¹⁴

In the dorsally recumbent horse under general anesthesia, with laparoscopy the main structures of diagnostic relevance in the caudal region of the abdomen are the urinary bladder, mesorchium, ductus deferens (left and right), left and right vaginal rings, insertion of the prepubic tendon, random segments of jejunum and descending colon, the pelvic flexure of the ascending colon, body of the cecum and cecocolic fold. The main structures observed in the cranial region of the abdomen are the ventral surface of the diaphragm, falciform ligament and round ligaments of the liver, ventral portion of the left lateral, left medial, quadrate and right lateral lobes of the liver, spleen, right and left ventral colons, sternal flexure of the ascending colon, apex of the cecum, and stomach.¹⁵ Alterations in cardiovascular and respiratory functions in response to the pneumoperitoneum and various positional changes indicated a need for continuous and thorough anesthetic monitoring and support.

GLUCOSE ABSORPTION TEST

The oral glucose tolerance test is one of the simplest tests of small intestinal absorptive capacity to perform. However, because of the many factors that affect blood glucose concentration, including factors not related to small-intestinal absorptive capacity, results of the test can on occasion be difficult to interpret.¹⁶ Oral glucose tolerance testing can produce abnormal results in horses with diseases that do not involve the small intestine, such as lower motor neurone disease or polysaccharide storage myopathy. On the other hand, the oral glucose tolerance test is often used because of the ready availability of glucose for oral administration and routine nature of measurement of blood glucose concentrations.

The main indications for performing oral glucose tolerance testing include unexplained weight loss believed to be associated with gastrointestinal disease, and suspected protein-losing enteropathy. Contraindications are those listed above. In addition, care should be exercised in performing the test in horses at increased risk of laminitis, as rapid passage of unabsorbed glucose into the large colon and cecum can cause laminitis.

Horses for oral glucose tolerance testing are first fasted for 12–18 hours. Access to water should be provided. Glucose is given by stomach tube at 1 g/kg body weight (BW) of anhydrous glucose (or comparable) as a 10–20% solution in water. Blood for measurement of glucose concentration is collected immediately before, and every 30 minutes for 4–6 hours after glucose administration. Some protocols involve less frequent (hourly) collection of blood. One protocol requires collection of blood samples before and 120 minutes after administration of glucose. This last protocol is not recommended as early or delayed peaks in blood concentration are not detected. The blood glucose concentration in the normal horse increases by at least 85% (from 90 up to 180 mg/dL (5.0 to 10.0 mmol/L)) with peak blood concentrations attained 90–150 minutes after administration of glucose. Horses with partial malabsorption have increases in blood glucose concentration of 15–85% of baseline values, and horses with complete malabsorption have no increase or less than 15% increase in blood glucose concentration by 2 hours.¹⁷ Blood concentrations of glucose in normal horses return to resting values in approximately 6 hours. The shape of the curve is affected by the horse’s previous diet, the curve being much lower in horses fed on stored feeds such as hay and grain compared to horses eating pasture of clover and grass.

Horses with weight loss and complete failure of absorption of glucose are likely to have extensive infiltrative disease of the small intestine such as lymphosarcoma or granulomatous enteritis.¹⁷ Of 25 horses with partial failure of glucose absorption, 18 (62%) had structural abnormalities of the small intestine. Clearly abnormal results of the oral glucose tolerance test therefore appear to be fairly specific for severe and widespread small-intestinal disease. Care should be taken when interpreting results that deviate only marginally from normal values.

STARCH DIGESTION TEST

A suitable test for the evaluation of gastric, small-intestinal and pancreatic function is the starch digestion test. The test relies on the presence of amylase in the small intestine with subsequent cleavage of starch into glucose, which is then absorbed into the blood. The horse is fasted for 18 hours and then given corn starch (1 kg in 4 L of water or 2 g/kg BW) by stomach tube. A pretreatment blood sample is matched with others taken at 15, 30, 60, 90 and 120 minutes and then hourly to 6 hours.

In the normal horse there is an increase in blood glucose levels of about 30 mg/dL (1.7 mmol/L) (from 90 up to 120 mg/dL (5.0–6.7 mmol/L)), with the peak occurring at 1–2 hours and the curve returned to pretreatment level at 3 hours.¹⁸ The test can be affected by the diet of the horse prior to testing.

LACTOSE DIGESTION TEST

Newborn animals rely on ingestion of milk sugar (lactose) as an important source of energy until weaning. Lactose is digested in the proximal small intestine by lactase, a disaccharidase present in the brush border of intestinal epithelial cells that cleaves lactose into glucose and galactose. Loss of small-intestinal production of lactase, such as occurs in some bacterial and viral enteritides including rotavirus infection, results in failure to cleave lactose and passage of the sugar to the hind gut. Fermentation of lactose in the hind gut causes acute and sometimes severe osmotic diarrhea. A prime indication for the oral lactose tolerance test is therefore acute diarrhea in neonates being fed milk. The test not only has diagnostic usefulness because a positive test (i.e. demonstration of lactose intolerance) provides a clear indication for feeding lactose-free milk or providing supplemental lactase in the animal’s diet.

An oral lactose digestion test has been devised for foals. Lactose (1 g/kg BW) is given by stomach tube in a 20% solution to a foal that has been fasted for 2–4 hours. In foals and young horses up to 3 years of age there is a rise in blood glucose levels from 86 ± 11 mg/dL (4.8 ± 0.1 mmol/L) up to 153 ± 24 mg/dL (8.5 ± 1.3 mmol/L), with a peak achieved in 90 minutes, and the level returns to pretreatment levels in 5 hours. In foals of 1–12 weeks of age the plasma glucose concentration should rise by at least 35 mg/dL (1.9 mmol/L) and peak within 40 minutes of the administration of the lactose. With this test no changes in blood sugar levels occur in horses over 4 years of age. Instead there is abdominal discomfort followed by diarrhea, with feces the consistency of cow feces for the next 24 hours. Sucrose and maltose are readily digested by the intestine of the adult horse, but not by newborn foals. Maximum levels of the relevant intestinal disaccharidases (sucrase and maltase) are not achieved until 7 months of age. The oral lactose digestion test is likely to be of value as a monitor of epithelial damage in young horses. In humans the ability to hydrolyze lactose is one of the first functions of the intestinal mucosa to be lost where there is epithelial damage in the gut. It is also one of the last functions to return in the recovering patient. The loss of intestinal lactase may be the pathogenetic basis of the diarrhea that occurs in rotavirus infections in neonates. Lactase digestion is impaired in calves with mild diarrhea.¹⁹ Calves with acute diarrhea are in a catabolic state and respond with a larger increase in plasma glucose concentration to a given amount of glucose than do healthy calves.

A modification of the oral lactose tolerance test in foals includes a second evaluation in foals in which there is failure of blood glucose concentrations to increase by the appropriate amount after oral administration of lactose. At least 8 hours after the first test, foals are fed a meal of lactose-free milk, or of milk to which lactase has been added. Blood glucose concentrations are measured and an increase of at least 35 mg/dL (1.9 mmol/l) is interpreted as evidence of lactase deficiency. Such animals can then be maintained on a diet of lactose-free milk. Diarrhea usually resolves in 24 hours, but returns within hours of feeding milk containing lactose.

XYLOSE ABSORPTION TEST

D-xylose is used to evaluate small intestinal absorptive function because it is not metabolized by tissues, which is an advantage over the oral glucose tolerance test. d-xylose absorbed from the intestinal tract is excreted unchanged in the urine within 15 hours of dosing.²⁰ Concentrations of d-xylose in blood are therefore dependent only upon the rate of absorption from the intestine and rate of excretion into the urine. However, the compound is more expensive than glucose and measurement of d-xylose in blood requires a particular analysis that might not be readily available. Indications for the test are the same as those for the oral glucose tolerance test described above.

D-xylose, at a dose rate of 0.5 g/kg BW as a 10% solution, is administered by stomach tube after a starve of 18 hours.²¹ A maximum blood xylose level of 30 mg/dL (2.0 mmol/L) at 1.5 hours is a normal result in adult horses. In normal foals the peak blood concentration of xylose is reached in 30–60 minutes and the level attained varies with age, being highest (47 mg/dL (3.14 mmol/L)) at 1 month of age and lowest (19 mg/dL (1.25 mmol/L)) at 3 months (the pretreatment reading should be zero). In abnormal horses the xylose curve is flat (a peak of 7–13 mg/dL (0.5 mmol/L) at 60–210 minutes) contrasted with a peak of 20 mg/dL (1.3 mmol/L) at 60 minutes in normal horses. As an initial checking test, one postdosing sample at 2 hours is recommended.

Interpretation of the test is influenced by the customary diet of tested animals and feed deprivation. Horses receiving a high energy diet have a lower absorption curve than horses on a low energy diet. The test is also affected by the duration of deprivation of feed.²⁰ In mares deprived of feed for 72 and 96 hours, the rate of d-xylose absorption and the maximum concentrations of d-xylose in plasma were reduced.²² For example, apparent low absorption can be caused by increased transit time through the gut, due perhaps to excitement.

Low blood concentrations of xylose occur in horses with small intestinal infiltrative disease, such as lymphosarcoma or granulomatous enteritis.²⁰ The test appears to be quite specific (low false-positive rate) for small intestinal disease, but the sensitivity (false-negative rate) is unknown.

A d-xylose absorption curve has been determined for cattle. The xylose (0.5 g/kg BW) is deposited in the abomasum by abomasocentesis, and a peak of blood glucose is attained in about 90 minutes.

SUCROSE ABSORPTION TEST

The sucrose absorption test differs from the other tests in this section in that abnormal results are associated with detection of sucrose in blood or urine of horses. Sucrose is not normally absorbed intact – it is usually cleaved by disaccharidases in the small intestine into glucose and fructose, which are then absorbed. Intact sucrose is absorbed across compromised gastric mucosa and detection of sucrose in blood or urine indicates the presence of gastric ulceration, as mammals neither synthesize nor metabolize sucrose.^23,24 The sucrose absorption test involves administration of 250 g of sucrose to an adult horse that has been fasted overnight. Blood samples for measurement of serum sucrose concentration are collected at 0, 15, 30, 45, 60 and 90 minutes after dosing. Alternatively, a urine sample is collected 2 hours after dosing (the bladder must be emptied immediately before dosing). Peak serum sucrose concentrations occur 45 minutes after administration and peak values correlate with the severity of gastric ulceration. Horses with minimal lesions have serum sucrose concentrations of 103 pg/μL, whereas horses with the most severe lesions have concentrations of 3400 pg/μL.²⁴

RADIOACTIVE ISOTOPES

A technique used for determining whether a protein-losing enteropathy is present is based on the examination of feces for radioactivity after the intravenous administration of a radioactive agent. ⁵¹Cr¹³C-labeled plasma protein has been used for this purpose. Similarly, administration of radioactively labeled leukocytes reveals the presence of small-intestinal inflammatory disease in horses.^4,25 The test is quite specific, in that false-positive tests are uncommon, but not very sensitive.

EQUINE AND BOVINE PERITONEAL FLUID

Normal peritoneal fluid is a transudate with properties as summarized in Tables 5.1 and 5.2. It has functions similar to those of other tissue fluids. It contains mesothelial cells, lymphocytes, neutrophils, a few erythrocytes and occasional monocytes and eosinophils. The following general comments apply:

Abdominocentesis in cattle

The choice of sites for paracentesis is a problem because the rumen covers such a large portion of the ventral abdominal wall and avoiding penetration of it is difficult. Cattle have a low volume of peritoneal fluid, and failure to obtain a sample is not unusual.²⁷ The most profitable sites are those that, on an anatomical basis, consist of recesses between the forestomachs, abomasum, diaphragm and liver. These are usually caudal to the xiphoid sternum and 4–10 cm lateral to the midline. Another recommended site is left of the midline, 3–4 cm medial and 5–7 cm cranial to the foramen for the left subcutaneous abdominal vein. A teat cannula similar to the one described for use in the horse is recommended but, with care and caution, a 16-gauge 5 cm hypodermic needle may also be used. The needle or cannula is pushed carefully and slowly through the abdominal wall, which will twitch when the peritoneum is punctured. When this happens the fluid will usually run out into a vial without the aid of a vacuum. However, if it does not, a syringe may be used and the needle may be moved backwards and forwards in a search for fluid, with the piston of the syringe withdrawn. A further site is the right caudoventral abdominal wall medial to the fold of the flank, using a 3.8 cm, 15-gauge needle.²⁷

In calves, a reliable technique includes the use of sedation with intravenous xylazine hydrochloride and diazepam. The animal is placed in left lateral recumbency with the right hind limb pulled dorsally and caudally. One site slightly dorsal and caudal to the umbilicus is prepared together with another site in the center of the inguinal region. The site is prepared with local anesthetic and a 14-gauge needle is introduced and directed slightly caudally and toward the midline while keeping it parallel to the inner abdominal wall once the peritoneal cavity is entered.³³ A 3.5 gauge urinary catheter (1.2 mm × 56 cm sterile feeding tube) is inserted through the needle and a 3 mL sterile syringe is attached to the catheter. Gentle suction is applied. The fluid is placed in a 2 mL tube containing tri-potassium EDTA. A 14-gauge over-the-needle catheter can also be used, followed by insertion of a 3.5 French feeding tube. If fluid cannot be obtained from the first site, the inguinal site is used using the same basic technique and with the catheter directed slightly cranially toward the midline.

Failure to obtain a sample does not preclude the possibility that peritonitis may be present: the exudate may be very thick and contain large masses of fibrin, or the peritonitis may be localized. Also, animals that are dehydrated may have less peritoneal fluid than normal. Most animals from which samples cannot be obtained, however, are in fact normal. In animals in which peritonitis is strongly suspected for clinical reasons, up to four attempts at paracentesis should be made before aborting the procedure. The fluid should be collected into an anticoagulant, preferably EDTA, to avoid clotting.

Abnormal peritoneal fluid in cattle is a highly sensitive indicator of peritoneal disease, but not a good indicator of the nature of the disease. The most pronounced abnormalities occur in acute diseases of the peritoneum; chronic peritonitis may be accompanied by peritoneal fluid which is almost normal.

Examination of the fluid should take into account the following characteristics:

• Large amounts (10–20 mL) of serosanguineous fluid suggests infarction or necrosis of the gut wall

• Heavily bloodstained fluid, whole blood or fluid with streaks of blood through it are more likely to result from puncture of a blood vessel or from bleeding into the cavity, as in dicoumarol poisoning or with a neoplasm of the vascular system

• The same sort of bloodstained fluid as above may accompany a ruptured uterus or bladder or severe congestive heart failure

• Large quantities of yellowish-colored turbid fluid suggests acute diffuse peritonitis. The degree of turbidity depends on the number of cells and the amount of fibrin present

• Particulate food material in the sample indicates perforation or rupture of the gut, except that penetration of the gut with the instrument during collection may be misleading. Such samples are usually heavily fecal in appearance and contain no mesothelial cells

• Laboratory examination is necessary to derive full benefit from the sample. This will include assessment of: the number and type of leukocytes present – the number is increased in peritonitis, neutrophils predominating in acute peritonitis and monocytes in chronic forms; the number of erythrocytes present; whether bacteria are present inside or outside the neutrophils; and total protein content.

The significant values for these items are included in Table 5.1.

Table 5.1 Guidelines for the classification and interpretation of bovine peritoneal fluid

Reference values for peritoneal fluid constituents of normal adult cattle may be inappropriate for interpretation of peritoneal fluid analysis in calves of up to 8 weeks of age.³⁴ The peritoneal fluid nucleated cell count and mononuclear cell counts are higher in calves, and the eosinophil counts are lower than in adult cows.

INCREASED MOTILITY

When motility is increased, the administration of atropine or other spasmolytics such as dipyrone or proquamezine is usually followed by disappearance of the abdominal pain and a diminution of fluid loss. Meperidine, butorphanol and pentazocine inhibit regular cyclic myoelectric activity in the jejunum.³⁶ There is a need for some scientific clinical investigation into the desirability of treating intestinal hypermotility, if it does exist in enteritis for example, and the efficacy of anticholinergics. Loperamide has an antidiarrheal effect in experimentally induced diarrhea in calves but the mechanism of action does not involve changes in intestinal motility.

DECREASED MOTILITY

When gastrointestinal motility is decreased, the usual practice is to administer parasympathomimetic drugs or purgatives, usually combined with an analgesic. Prokinetic drugs such as metoclopramide hydrochloride and cisapride monohydrate increase the movement of ingesta through the gastrointestinal tract.³⁷ They are useful because they induce coordinated motility patterns.

ETIOLOGY

Stomatitis may be caused by physical, chemical or infectious agents, the last being the largest group of causes. The agents are listed under these group headings below.

PATHOGENESIS

The lesions of stomatitis are produced by the causative agents being applied directly to the mucosa, or gaining entrance to it by way of minor abrasions, or by localization in the mucosa from a viremia. In the first two instances, the stomatitis is designated as primary. In the third, it is usually described as secondary because of the common occurrence of similar lesions in other organs or on other parts of the body, and the presence of a systemic disease. The clinical signs of stomatitis are caused by the inflammation or erosion of the mucosa and the signs vary in severity with the degree of inflammation.

CLINICAL FINDINGS

There is partial or complete anorexia and slow, painful mastication. Chewing movements and smacking of the lips are accompanied by salivation, either frothy and in small amounts, or profuse and drooling if the animal does not swallow normally. The saliva may contain pus or shreds of epithelial tissue. A fetid odor is present on the breath only if bacterial invasion of the lesion has occurred. Enlargement of local lymph nodes may also occur if bacteria invade the lesions. Swelling of the face is observed only in cases where a cellulitis or phlegmon has extended to involve the soft tissues. An increased desire for water is apparent and the animal resents manipulation and examination of the mouth.

Toxemia may be present when the stomatitis is secondary to a systemic disease or where tissue necrosis occurs. This is a feature of oral necrobacillosis and many of the systemic viremias. In some of the specific diseases, lesions may be present on other parts of the body, especially at the coronets and mucocutaneous junctions.

Several different lesions of the oral cavity may be present and their characteristic appearances are as follows. The importance of vesicular diseases such as foot-and-mouth disease means that the recognition and differentiation of these lesions assumes major importance.

Erosions are shallow, usually discrete, areas of necrosis, which are not readily seen in the early stages. They tend to occur most commonly on the lingual mucosa and at the commissures of the mouth. The necrotic tissue may remain in situ but is usually shed, leaving a very shallow discontinuity of the mucosa with a dark red base that is more readily seen. If recovery occurs, these lesions heal very quickly.

Vesicles are thin-walled swellings 1–2 cm in diameter filled with clear serous fluid. They are very painful and rupture readily to leave sharp-edged, shallow ulcers.

Ulcerative lesions penetrate more deeply to the lamina propria and are painful, as in necrotic stomatitis in calves associated with F. necrophorus. In lambs the tongue may be swollen and contain many microabscesses infected with Actinomyces (Corynebacterium) pyogenes. There is an accompanying abscessation of the pharyngeal lymph nodes.²

Proliferative lesions are characterized by an abnormality raised above the surface of the mucous membrane as in oral papillomatosis. Traumatic lesions are usually solitary and characterized by a discontinuity in the mucous membrane often with evidence of healing and the presence of granulation tissue.

Catarrhal stomatitis is manifested by a diffuse inflammation of the buccal mucosa and is commonly the result of direct injury by chemical or physical agents. Mycotic stomatitis is characterized by a heavy, white, velvety deposit with little obvious inflammation or damage to the mucosa.

Deformity of or loss of tissue at the tip of the tongue may result in a chronic syndrome of chewing and swallowing food in such a way that food is always oozing from between the lips. In sheep this may cause permanent staining of the hair around the mouth, creating an appearance similar to that of a tobacco-chewer. Loss of the tip is usually the result of predator attack on a newborn or sick lamb.

Laceration of the tongue can result in complete or partial severance of the organ, with the severed portion protruding from the oral cavity. In cattle, glossectomy interferes with prehension and the animal is unable to eat. Excessive loss of saliva is common because of interference with swallowing.

Ulceration of the soft palate of horses may occur in 16% of horses with dorsal displacement of the soft palate and is characterized clinically by reduced exercise tolerance, respiratory noise during light exercise or racing, dysphagia and coughing after exercising.⁴ The ulcers can be viewed by upper respiratory airway video-endoscopy. Bullous stomatitis in the horse is characterized by intact or ruptured vesicles on the peripheral margin of the tongue, the sublingual region and the mucosa of the oral cavity and lips.

CLINICAL PATHOLOGY

Material collected from lesions of stomatitis should be examined for the presence of pathogenic bacteria and fungi. Transmission experiments may be undertaken with filtrates of swabs or scrapings if the disease is thought to be due to a viral agent.

NECROPSY FINDINGS

The oral lesions are easily observed but complete necropsy examinations should be carried out on all fatally affected animals to determine whether the oral lesions are primary or are local manifestations of a systemic disease.

TREATMENT

Affected animals should be isolated and fed and watered from separate utensils if an infectious agent is suspected. Specific treatments are described under the headings of the individual diseases. Nonspecific treatment includes frequent application of a mild antiseptic collutory such as a 2% solution of copper sulfate, a 2% suspension of borax or a 1% suspension of a sulfonamide in glycerin. Indolent ulcers require more vigorous treatment and respond well to curettage or cauterization with a silver nitrate stick or tincture of iodine.

In stomatitis due to trauma, the teeth may need attention. In all cases, soft, appetizing food should be offered and feeding by stomach tube or intravenous alimentation may be resorted to in severe, prolonged cases. If the disease is infectious, care should be exercised to insure that it is not transmitted by the hands or dosing implements.

ETIOLOGY

The causes may be congenital or acquired.

PATHOGENESIS

There are some limitations to the use of number of incisors for determining age in sheep.¹⁶ In mixed-age female sheep flocks, the median age when two, four, six and eight incisors come into wear is 15, 23, 30 and 42 months of age, respectively.¹⁶ Errors will be made by assuming that all sheep gain a pair of permanent incisors at annual intervals between 1.5 and 4.5 years of age.

In periodontal disease or broken-mouth disease of sheep the primary lesion is an acute gingivitis around permanent incisors and premolars at the time of their eruption. This subsides leaving a chronic gingivitis and an accumulation of subgingival plaque. On some farms, for reasons not understood, this gingivitis penetrates down into the alveoli, causing a severe periodontitis and eventual shedding of the teeth.¹⁷ The severity of the gingivitis can vary between farms.¹⁸ The disease is episodic in nature, with discrete acute inflammatory incidents leading to periodontal injury that may resolve by healing.⁸ The balance between repair and the various short- and long-term acute episodes probably accounts for the large variation in incidence and age onset of tooth loss both within and between flocks.⁴ The inflammatory periodontal disease markedly affects the tooth’s mobility.¹⁹ Collagen fibrils supporting the tooth become abnormal. The deepened periodontal pocket resulting from inflammation removes the major area of support for the tooth and abnormal loads are applied to fibers deeper within the tissue.²⁰ While the incisor teeth are usually most severely affected, the cheek teeth are also involved.⁵ In some unusual circumstances the gingivitis appears to arise from heavy deposits of dental calculus.²¹ In the Scottish disease there is local alveolar bone loss but no accompanying general skeletal deficiency.⁶

CLINICAL FINDINGS

The most obvious evidence of broken-mouth disease is incisor tooth loss, which usually occurs when sheep are between 3.5 and 6.6 years; normal sheep without broken mouth will retain their teeth beyond 7 years of age. Several dental health indices can assist to assess the amount of gingivitis, tooth movement, gum recession and pocketing.⁵ Gingivitis is characterized by redness and edema of the attached gingiva. Bleeding from the gingivae is also a feature. Clinical gingivitis is evident as soon as the permanent teeth erupt. Chronic gingivitis results in a downward retreat of the gum margin, loss of its normal, scalloped shape and fibrosis of the gingiva. Within a year prior to tooth loss, tissue damage around the incisors leads to deepening of the gingival sulcus and the formation of pockets which are readily detected by the use of graduated dental measuring probes. The normal sulcus is 0.5–1.0 mm deep labially and up to 4 mm deep lingually; pockets may be over 1.0 cm in depth prior to tooth loss. Crown lengthening, protrusion, hemorrhages, loosening and lingual periodontitis are characteristic. If sheep affected with broken mouth periodontal disease are examined over a 12-month period, only a few animals undergo clinically significant destruction.⁸ The relationship between periodontal disease and body condition score in sheep is variable.¹⁴

Secondary starvation occurs even with a plentiful feed supply. Inspection of the mouth may reveal the worn or damaged incisor teeth but the molar teeth are not easily inspected in the living animal and tooth lesions can be missed. Since it is common to find that both incisors and molars are all affected, damage to incisors should lead the clinician to suspect that molar disease is also present.

Cattle fed sweetpotato cannery waste develop black, stained teeth with severe enamel erosion.³

An abattoir survey of dental defects in cull cows, all over 30 months of age found that 14.6% had one or more missing incisors, most of which were acquired losses.²² Rotation and overlapping of rostral teeth were common, as was attrition. Congenitally absent first lower premolars, other missing teeth, large and often multiple interdental spaces and a few cases of macrodontia, cavitation, multiple defects and fractures were observed in cheek tooth arcades. There were also some unusual patterns of premolar and molar attrition, often attributable to malocclusion, one result of which was the formation of a hook at the posterior extremity of the third maxillary molar.

CLINICAL PATHOLOGY

On bacteriological examination spirochetes and Fusobacterium spp. are present.

TREATMENT AND CONTROL

There is no reliable treatment and control for broken mouth in sheep. The use of dental prosthetics glued to the incisors when the ewe has three pairs of incisors in place is being investigated. The use of antimicrobials has been proposed to control the gingivitis but there is no apparent effect on the periodontal disease. Cutting the incisor teeth of ewes to control premature tooth loss has been explored but the practice has been banned in the UK.²³

ETIOLOGY

Parotitis may be parenchymatous, when the glandular tissue is diffusely inflamed, or it may be a local suppurative process. There are no specific causes in farm animals, cases occurring only sporadically and due usually to localization of a blood-borne infection, invasion up the salivary ducts associated with stomatitis, irritation by grass awns in the duct, or salivary calculi.¹ Avitaminosis A often appears to be a predisposing cause.

Local suppurative lesions are caused usually by penetrating wounds or extension from a retropharyngeal cellulitis or lymph node abscess. Neoplasia of the parotid glands of cattle examined at slaughter has been described.²

PATHOGENESIS

In most cases only one gland is involved. There is no loss of salivary function and the signs are restricted to those of inflammation of the gland.

CLINICAL FINDINGS

In the early stages, there is diffuse enlargement of the gland accompanied by warmth and pain on palpation. The pain may interfere with mastication and swallowing and induce abnormal carriage of the head and resentment when attempts are made to move the head. There may be marked local edema in severe cases. Diffuse parenchymatous parotitis usually subsides with systemic and local treatment within a few days, but suppurative lesions may discharge externally and form permanent salivary fistulae.

CLINICAL PATHOLOGY

Bacteriological examination of pus from discharging abscesses may aid the choice of a suitable antibacterial treatment.

NECROPSY FINDINGS

Death occurs rarely and necropsy findings are restricted to local involvement of the gland or to primary lesions elsewhere in the case of secondary parotitis.

TREATMENT

Systemic treatment with sulfonamides or antibiotics is required in acute cases, especially if there is a systemic reaction. Abscesses may require draining and, if discharge persists, the administration of enzymes either parenterally or locally. A salivary fistula is a common sequel.

ETIOLOGY

Pharyngitis in farm animals is usually traumatic. Infectious pharyngitis is often part of a syndrome with other more obvious signs.

PATHOGENESIS

Inflammation of the pharynx is attended by painful swallowing and disinclination to eat. If the swelling of the mucosa and wall is severe, there may be virtual obstruction of the pharynx. This is especially so if the retropharyngeal lymph node is enlarged, as it is likely to be in equine viral infections such as rhinovirus.

In balling-gun-induced trauma of feedlot cattle treated for respiratory disease with boluses of sulfonamides, perforations of the pharynx and esophagus may occur with the development of periesophageal diverticulations with accumulations of ruminal ingesta, and cellulitis.¹ Improper administration of a magnet to a mature cow can result in a retropharyngeal abscess.⁴

Pharyngeal lymphoid hyperplasia in horses can be graded into four grades (I–IV) of severity based on the size of the lymphoid follicles and their distribution over the pharyngeal wall.

CLINICAL FINDINGS

The animal may refuse to eat or drink or it may swallow reluctantly and with evident pain. Opening of the jaws to examine the mouth is resented and manual compression of the throat from the exterior causes paroxysmal coughing. There may be a mucopurulent nasal discharge, sometimes containing blood, spontaneous cough and, in severe cases, regurgitation of fluid and food through the nostrils. Oral medication in such cases may be impossible. Affected animals often stand with the head extended, drool saliva and make frequent, tentative jaw movements. Severe toxemia may accompany the local lesions, especially in oral necrobacillosis and, to a less extent, in strangles. Empyema of the guttural pouches may occur in horses. If the local swelling is severe, there may be obstruction of respiration and visible swelling of the throat. The retropharyngeal and parotid lymph nodes are commonly enlarged. In ‘pharyngeal phlegmon’ in cattle there is an acute onset with high fever (41–41.5°C, 106–107°F), rapid heart rate, profound depression and severe swelling of the soft tissues within and posterior to the mandible to the point where dyspnea is pronounced. Death usually occurs 36–48 hours after the first signs of illness.

In traumatic pharyngitis in cattle, visual examination of the pharynx through the oral cavity reveals hyperemia, lymphoid hyperplasia and erosions covered by diphtheritic membranes. Pharyngeal lacerations are visible, and palpation of these reveals the presence of accumulated ruminal ingesta in diverticulae on either side of the glottis.¹ External palpation of the most proximal aspect of the neck reveals firm swellings, which represent the diverticula containing rumen contents. A retropharyngeal abscess secondary to an improperly administered magnet can result in marked diffuse painful swelling of the cranial cervical region.⁴ Ultrasonographic examination of the swelling may reveal the magnet within the abscess.⁴

Palpation of the pharynx may be performed in cattle with the use of a gag if a foreign body is suspected, and endoscopic examination through the nasal cavity is possible in the horse.

Most acute cases recover in several days but chronic cases may persist for many weeks, especially if there is ulceration, a persistent foreign body or abscess formation. Pharyngitis has become one of the most commonly recognized diseases of the upper respiratory tract of the horse. Chronic pharyngitis after viral infections is relatively common and results in a break in training, which is inconvenient and costly. On endoscopic examination there may be edema in early and relatively acute cases. In long-standing cases there is lymphoid infiltration and follicular hyperplasia. This is more common and more severe in young horses, who also suffer more attacks of upper respiratory tract disease. The condition does not appear to diminish racing performance or respiratory efficiency. If secondary bacterial infection is present a purulent exudate is seen on the pharyngeal mucosa and in the nostrils. Affected horses cough persistently, especially during exercise, are dyspneic and tire easily. Guttural pouch infections may occur secondarily. An occasional sequel is aspiration pneumonia.

CLINICAL PATHOLOGY

Nasal discharge or swabs taken from accompanying oral lesions may assist in the identification of the causative agent. Moraxella spp. and Streptococcus zooepidemicus can be isolated in large numbers from horses with lymphoid follicular hyperplasia grades III and IV.

NECROPSY FINDINGS

Deaths are rare in primary pharyngitis and necropsy examinations are usually undertaken only in those animals dying of specific diseases. In ‘pharyngeal phlegmon’ there is edema, hemorrhage and abscessation of the affected area and on incision of the area a foul-smelling liquid and some gas usually escape.

TREATMENT

The primary disease must be treated, usually parenterally, by the use of antimicrobials. ‘Pharyngeal phlegmon’ in cattle is frequently fatal and early treatment, repeated at short intervals, with a broad-spectrum antimicrobial is necessary.

Pharyngeal lymphoid hyperplasia is not generally susceptible to antimicrobials or medical therapy. Surgical therapy including electrical and chemical cautery is indicated and has been successfully applied.

ETIOLOGY

Foreign bodies or tissue swellings are the usual causes.

PATHOGENESIS

Reduction in caliber of the pharyngeal lumen interferes with swallowing and respiration.

CLINICAL FINDINGS

There is difficulty in swallowing and animals may be hungry enough to eat but, when they attempt to swallow, cannot do so and the food is coughed up through the mouth. Drinking is usually managed successfully. There is no dilatation of the esophagus and usually little or no regurgitation through the nostrils. An obvious sign is a snoring inspiration, often loud enough to be heard some yards away. The inspiration is prolonged and accompanied by marked abdominal effort. Auscultation over the pharynx reveals loud inspiratory stertor. Manual examination of the pharynx may reveal the nature of the lesion but an examination with a fiberoptic endoscope is likely to be much more informative. When the disease runs a long course, emaciation usually follows. Rupture of abscessed lymph nodes may occur when a nasal tube is passed, and can result in aspiration pneumonia.

In horses with metallic foreign bodies in the oral cavity or pharynx, the clinical findings include purulent nasal discharge, dysphagia, halitosis, changes in phonation, laceration of the tongue and stertorous breathing.¹ In case studies, most horses were affected with clinical signs for more than 2 weeks and had been treated with antimicrobials with only temporary improvement.¹

CLINICAL PATHOLOGY

A tuberculin test may be advisable in bovine cases. Nasal swabs may contain S. equi when there is streptococcal lymphadenitis in horses.

NECROPSY FINDINGS

Death occurs rarely and in fatal cases the physical lesion is apparent.

TREATMENT

Removal of a foreign body may be accomplished through the mouth. Treatment of actinobacillary lymphadenitis with iodides is usually successful and some reduction in size often occurs in tuberculous enlargement of the glands but complete recovery is unlikely to occur. Parenteral treatment of strangles abscesses with penicillin may effect a cure. Surgical treatment has been highly successful in cases caused by medial retropharyngeal abscess.

ETIOLOGY

Pharyngeal paralysis occurs sporadically, due to peripheral nerve injury, and in some encephalitides with central lesions.

PATHOGENESIS

Inability to swallow and regurgitation are the major manifestations of the disease. There may be an associated laryngeal paralysis, accompanied by ‘roaring’. The condition known as ‘cud-dropping’ in cattle may be a partial pharyngeal paralysis as there is difficulty in controlling the regurgitated bolus, which is often dropped from the mouth. In these circumstances, aspiration pneumonia is likely to develop.

CLINICAL FINDINGS

The animal is usually hungry but, on prehension of food or water, attempts at swallowing are followed by dropping of the food from the mouth, coughing and the expulsion of food or regurgitation through the nostrils. Salivation occurs constantly and swallowing cannot be stimulated by external compression of the pharynx. The swallowing reflex is a complex one controlled by a number of nerves and the signs can be expected to vary greatly depending on which nerves are involved and to what degree. There is rapid loss of condition and dehydration. Clinical signs of the primary disease may be evident but, in cases of primary pharyngeal paralysis, there is no systemic reaction. Pneumonia may follow aspiration of food material into the lungs and produces loud gurgling sounds on auscultation.

In ‘cud-dropping’ in cattle, the animals are normal except that regurgitated boluses are dropped from the mouth, usually in the form of flattened disks of fibrous food material. Affected animals may lose weight but the condition is usually transient, lasting for only a few days. On the other hand, complete pharyngeal paralysis is usually permanent and fatal.

CLINICAL PATHOLOGY

The use of clinicopathological examinations is restricted to the identification of the primary specific diseases.

NECROPSY FINDINGS

If the primary lesion is physical, it may be detected on gross examination.

TREATMENT

Treatment is unlikely to have any effect. The local application of heat may be attempted. Feeding by nasal tube or intravenous alimentation may be tried if disappearance of the paralysis seems probable.

ETIOLOGY

Primary esophagitis caused by the ingestion of chemical or physical irritants is usually accompanied by stomatitis and pharyngitis. Laceration of the mucosa by a foreign body or complications of nasogastric intubation may occur.¹ Nasogastric intubation is associated with a higher risk of pharyngeal and esophageal injury when performed in horses examined for colic.¹ This may be related to the use of larger-diameter nasogastric tubes to provide more effective gastric decompression, the longer duration of intubation in some horses, or the presence of gastric distension resulting in increased resistance to tube passage at the cardia.¹ In a series of six horses with esophageal trauma the lesions were detected 5 and 20 cm from the cranial esophageal opening.¹

The administration of sustained-release anthelmintic boluses to young calves that are not large enough for the size of the bolus used may cause esophageal injury and perforation.^2,3 The boluses are 8.5 cm in length and 2.5 cm in diameter and the calves 100–150 kg. The minimum body weight for these boluses is 100 kg but in the study some calves were younger than the recommended age and were also fractious when handled, which may have contributed to the injury.² Death of Hypoderma lineatum larvae in the submucosa of the esophagus of cattle may cause acute local inflammation and subsequent gangrene.

Inflammation of the esophagus occurs commonly in many specific diseases, particularly those that cause stomatitis, but the other clinical signs of these diseases dominate those of esophagitis.

PATHOGENESIS

Inflammation of the esophagus combined with local edema and swelling results in a functional obstruction and difficulty in swallowing. Traumatic injury to the esophagus results in edema, hemorrhage, laceration of the mucosa and possible perforation of the esophagus, resulting in periesophageal cellulitis, which spreads proximally and distally along the esophagus in fascial planes from the site of perforation. Perforation of the thoracic esophagus can result in severe and fatal pleuritis. There is extensive edema and accumulation of swallowed or regurgitated ingesta along with gas. The extensive cellulitis and the presence of ingesta results in severe toxemia, and dysphagia may cause aspiration pneumonia.

CLINICAL FINDINGS

In the acute injury of the esophagus, there is salivation and attempts to swallow, which cause severe pain, particularly in horses. In some cases, attempts at swallowing are followed by regurgitation and coughing, pain, retching activities and vigorous contractions of the cervical and abdominal muscles. Marked drooling of saliva, grinding of the teeth, coughing and profuse nasal discharge are common in the horse with esophageal trauma with complications following nasogastric intubation.¹ Regurgitation may occur and the regurgitus contains mucus and some fresh blood. If the esophagitis is in the cervical region, palpation in the jugular furrow causes pain and edematous tissues around the esophagus may be palpable. If perforation has occurred, there is local pain and swelling and often crepitus. Local cervical cellulitis may cause rupture to the exterior and development of an esophageal fistula, or infiltration along fascial planes with resulting compression obstruction of the esophagus, and toxemia. Perforation of the thoracic esophagus may lead to fatal pleurisy. Animals that recover from esophageal traumatic injury are commonly affected by chronic esophageal stenosis with distension above the stenosis. Fistulae are usually persistent but spontaneous healing may occur. In specific diseases such as mucosal disease and bovine malignant catarrh, there are no obvious clinical findings of esophagitis, the lesions being mainly erosive.

Endoscopy of the esophagus will usually reveal the location and severity of the lesion. Lateral cervical radiographs may reveal foreign bodies and extensive soft tissue swelling with pockets of gas.

CLINICAL PATHOLOGY

In severe esophagitis of traumatic origin a marked neutrophilia may occur, suggesting active inflammation.

NECROPSY FINDINGS

Pathological findings are restricted to those pertaining to the various specific diseases in which esophagitis occurs. In traumatic lesions or those caused by irritant substances, there is gross edema, inflammation and, in some cases, perforation.

TREATMENT

Feed should be withheld for 2–3 days and fluid and electrolyte therapy may be necessary for several days. Parenteral antimicrobials are indicated, especially if laceration or perforation has occurred. Reintroduction to feed should be monitored carefully and all feed should be moistened to avoid the possible accumulation of dry feed in the esophagus, which may not be fully functional.