key: cord-0761194-dpfek3nj
authors: Njaa, Bradley L.; Panciera, Roger J.; Clark, Edward G.; Lamm, Catherine G.
title: Gross Lesions of Alimentary Disease in Adult Cattle
date: 2012-10-23
journal: Vet Clin North Am Food Anim Pract
DOI: 10.1016/j.cvfa.2012.07.009
sha: 1e5267a87d551bc5b6cf7ee31a9946314c34e505
doc_id: 761194
cord_uid: dpfek3nj

The purpose of the gross necropsy examination of the gastrointestinal tract is to recognize the presence of lesions, thus requiring a basic understanding of its normal appearance and anatomy. This article highlights gross changes to the gastrointestinal tract of adult cattle that help place the disease processes into broad categories. Although few gross lesions reach the zenith of pathognomonic, there are numerous lesions that, when considered in aggregate with history (eg, number of animals affected, environment, duration of signs, time of onset relative to management changes, previous management) and clinical signs, can help narrow the spectrum of causes, provide a basis for a strong presumptive diagnosis, and focus diagnostic test selection.

of controlled inflammation. Once the animal dies, these organisms continue to rapidly proliferate, are exothermic, and release destructive enzymes and gases that lead to rapid autolytic and putrefactive changes that can quickly obfuscate the superficial intestinal mucosa either obscuring lesions or creating pseudolesions. Timely examination of the GIT is essential for the best opportunity to contribute to the diagnostic process.

For ease of examination during necropsy, the gastrointestinal system is divided into three to four sections: the oral cavity and esophagus; the forestomachs and true stomach (abomasum); and the intestines, which can be divided into small and large intestines separately or examined as a continuum. Examination of the GIT begins with a thorough examination of the oral cavity, including the lips, gums, hard and soft palate, teeth, and tongue for erosions, ulceration, hemorrhage, and masses. Remember that many esophageal lesions tend to be in the distal one-third of the esophagus.

It is important to be thorough to detect subtle mucosal erosions or ulcers, find stray wire or lead particles in the reticulum, identify parts of toxic plants in all compartments, characterize the feed, or observe substances that are not miscible in water-based rumen contents. These changes can be easily overlooked or missed if this part of the necropsy is given a cursory glance or omitted all together. All four compartments must be thoroughly opened and their contents evacuated to better examine the mucosa.

Ideally, the small and large intestine should be stripped from its mesenteric attachments before or during removal from the peritoneal cavity allowing palpation for masses, recognition of any color variation, and localization of any areas of serosal inflammation or perforations. A good place to begin is where the ileum attaches to the cecum and begin stripping orally toward the duodenum. Identifying the ileum is also important because it is a common location for many intestinal diseases and ensures that Peyer's patches are located and collected. Resist the temptation to only "spot check" various segments of the intestine because subtle or regionally variable lesions could be easily missed.

While opening segments of intestine to assess contents, the mucosa can be more thoroughly evaluated. The often semifluid to pasty consistency of intestinal contents may obscure the mucosa beneath impairing its thorough examination. It is tempting to scrape this material off of the mucosa with the edge of the necropsy knife, but that damages the underlying epithelium if histopathology is desired. If that is the only means of assessment, then ensure that other segments with similar gross lesions are sampled for histopathology. Small amounts of water under low pressure or small amounts poured over the mucosa more gently clear the contents from the surface and allow more detailed examination. If a pathogen is suspected, representative sections of bowel should be collected for microbiologic testing before opening or flushing the segments. Ensure that segments of intestine collected for microbial testing are kept closed, using string to seal the ends of the segments. When submitting to the laboratory, it is imperative that segments of bowel are packaged separately from other fresh tissues.

The purpose of the gross necropsy examination of the GIT is to recognize the presence of lesions, thus requiring a basic understanding of its normal appearance and anatomy. This article highlights gross changes to the GIT of adult cattle that help place the disease process into broad categories. Although few gross lesions reach the zenith of pathognomonic, there are numerous lesions that when considered in aggregate with history (number of animals affected, environment, duration of signs, time of onset relative to management changes, previous management, and so forth) and clinical signs can help narrow the spectrum of causes, provide a basis for a strong presumptive diagnosis, and focus diagnostic test selection.

There are numerous ways to codify gastrointestinal gross pathology. One of the most practical methods is to classify lesions using the following broad categories: color variation, mucosal surface integrity, size variation, and luminal content features. Each category is briefly introduced in general broad terms. For each functional and anatomic division, normal is defined followed by application of the method to each segment. The GIT is divided into the oropharynx, esophagus, forestomachs, abomasum, and intestines.

Red mucosa in the abomasum and intestines is often normal or uninterpretable as it relates to disease or inflammation but is commonly misdiagnosed as hemorrhage and inflammation (Fig. 2) . Many dead cattle can have segments of quite red intestine, even with bloody contents, that histologically do not translate into hemorrhage or inflammation. Smudgy red to pink discoloration of gastrointestinal serosa is frequently encountered in adult cattle with prolonged postmortem intervals caused by lysis of red cells with leakage or imbibition of hemoglobin into the tissue interstitium. With time and proliferation of bacteria, imbibed hemoglobin can react with bacteria-derived hydrogen sulfide to produce iron-containing compounds that impart a dark green to black tissue discoloration, referred to as "pseudomelanosis."

Serosal surfaces of the forestomachs, abomasum, and intestines tend to be highly variable, ranging from pale tan to pink to medium purple, dependent largely on the postmortem interval. Never judge an animal as pale based solely on serosal surface pallor. Serosa may be helpful along with subcutaneous tissues in detecting and confirming icterus.

In general, mucosal surfaces have a glistening sheen that is best mimicked by visual appearance of "semigloss" to "glossy" finish house paints. When mucous membranes have a texture that is analogous to "matte" or "eggshell" paint finishes, that is strongly suggestive of erosion or shallow ulcers. When the center of defects is brighter or Gross Lesions of Alimentary Disease darker red compared with the surrounding glistening mucosa, that is strongly suggestive of ulceration. Adherent feed or fibrin to the mucosal surface is a strong indication of local necrosis and inflammation.

Variation in the size of segments of the GIT tends to be the result of changes in wall thickness and luminal diameter. In general, increases in mural thickness can be caused by physiologic hypertrophy to the tunica muscularis or mucosal epithelium or by expansion of selected lamina or all layers of the wall because of accumulation of excess fluid or gas, infiltration by inflammatory cells, neoplasia, or a combination. Mural thickness may be decreased in cases where the luminal diameter is greatly expanded causing mural stretching or in cases where there is mural necrosis.

Excess fluid collected in tissues can be an antemortem physiologic response to hypoproteinemia leading to edema; it can result from localized or systemic inflammation, or possibly a response to excessive intravenous administration of fluid. Postmortem fluid accumulation can occur if the postmortem interval to necropsy is prolonged or if the carcass remains in an environment with high ambient temperatures and relative humidity. Similarly, excessive expansion by gas may be caused by antemortem proliferation of gas-producing bacteria, complications related to previous surgery, or disease. More commonly, excess gas accumulation in a carcass occurs postmortem related to proliferation of gas-producing anaerobic bacteria, such as Clostridium spp.

Luminal diameter is dependent on the muscular and neural integrity of the viscus wall, the transit time of the luminal contents, and the balance between absorption and secretion in the various segments of the GIT. Any alteration to one or more of these components can dramatically affect the size of the GIT, especially the intestines. For example, a focal intestinal obstruction can lead to proximal accumulation of fluid and resultant distention along with collapse or narrowing of the distal bowel (Fig. 3) .

Luminal contents are normally variable depending on the segment being examined in terms of odor, consistency, and color. Factors that contribute to this include type of diet (pasture vs dry lot vs feedlot rations); amount and type of water consumption; and concurrent stressors, such as animal density, environmental stressors, and disease. Ruminal contents tend to have a sweet aromatic scent when cattle are on pasture or fed silage but become more sour and acidic in the face of high-grain diets or in cases of acidosis. Intestinal contents tend to move from coarse to liquid to pasty to semisolid when moving from oral to anal. Deviation from this often correlates with various disease states. Finally, color is extremely variable throughout the bowel and only in few circumstances is it diagnostically useful.

Oropharyngeal mucosa tends to be highly variable in terms of melanin pigmentation depending on the breed and color variations within particular breeds. Dorsally, the dental pad is a thickened, often fissured area that apposes the lower incisor teeth. Teeth tend to have white enamel with darker green to brown to black staining of the opposing surface of upper and lower arcades.

Oral mucosa typically has a bright, slightly moist sheen. The hard palate has transverse ridges from which caudally project papillae that help guide food in an aboral direction. The soft palate is continuous with the hard palate and tends to have a smooth surface. The cheek mucosa has long, broad, aborally directed papillae that are sharply pointed in health (Fig. 4) . Tongues are their principle organ of prehension in cattle. Overlying the dorsal surface of the tongue are small, fine, sharp papillae, many of which play a sensory role. Approximately three-fifths caudal to the rostral tip is the lingual fossa demarcating the rostral edge of a large dorsal prominence called the torus linguae. 2 Brown to blackened teeth with hypoplastic enamel is likely caused by chronic fluorosis (Fig. 5) . Alternatively, hypoplastic or dysplastic enamel can be the result of in utero bovine viral diarrhea virus (BVDV) infections (Fig. 6) . Oropharyngeal mucous membranes can become pale because of anemia or severe blood loss. Alternatively, they can become cyanotic because of cardiovascular compromise and collapse. When a cow is exposed to high nitrate-containing plants (frost-damaged cereal crops, Brassicaceae spp, and Sorghum spp) or fertilizers, the nitrate is converted to nitrite and when it is absorbed converts hemoglobin to methemoglobin, imparting a light brown or "muddy" tincture to blood and tissues (Fig. 7) .

Localized and systemic diseases with inherent epitheliotropism may first be visualized when examining the oropharynx but are rarely limited to this location. Shallow erosions tend to be slightly different from the surrounding tissue because of pigmentation changes and loss of the typical sheen ( Fig. 8) . Similar lesions may be seen in the lingual mucosa ( Fig. 9 ). Causes frequently associated with this lesion include BVDV, bluetongue virus (BTV), herpes viruses that cause malignant catarrhal fever (MCF), rinderpest, and rupture of epithelial vesicles.

Vesicular disease is a category of disease that typically involves a certain degree of alarm and investigation and confirmatory testing by federal veterinarians. In North America, these most often are categorized as foreign animal diseases or transboundary animal diseases. Commonly, intact vesicles or erosions, the result of ruptured vesicles, are the first sign of concern, initially observed on the muzzle and in the oral cavity. Ruptured vesicles and erosions when secondarily infected, can become deep, inflamed, painful, mucosal ulcers. Possible causes include foot-and-mouth disease, vesicular stomatitis, chronic BVD, BTV, and MCF ( Fig. 10) . 3 Other causes that tend to lead to severe erosion or ulceration include blister beetle (cantharidin) toxicosis; traumatic injury secondary to coarse feeds or caustic chemicals; and uremia. In extreme cases, plant awns or hair may embed themselves in the ulcerated lingual mucosa, especially in the lingual fossa, giving the appearance of lingual "hair" (Fig. 11 ). Two of the more commonly referred to ailments of the oropharynx that lead to swelling and variation in size are "lumpy jaw" and "wooden tongue." The former is also referred to as "actinomycosis," denoting a severe osteomyelitis that results from Actinomyces bovis penetration through the oropharyngeal mucosa with subsequent penetration of the periosteum of the mandible and eventual mandibular osteomyelitis. 4 This results in a severely disfiguring disease (Fig. 12) . Wooden tongue, also called "actinobacillosis," is a lingual infection by Actinobacillus lignieresii. The tongue becomes markedly enlarged and painful and may develop ulceration because of its obstructive size and susceptibility to trauma (Fig. 13) . 5 Animals repeatedly exposed to bracken fern forage run the risk of developing squamous cell carcinoma of the upper GIT (Fig. 14) . 6 Rarely, other neoplasms may affect the oropharynx leading to cachexia either through obstruction or because of impaired ability to masticate food.

Once opened and laid flat, the esophageal mucosa tends to be normally quite pale, with a smooth texture, lacking surface folds. The underlying submucosa is normally loosely attached to the overlying mucosa allowing for a moderate amount of laxity when the mucosa is torqued relative to the muscle layer.

At the level of the thoracic inlet is where a clearly demarcated line of congestion abruptly ends in pallor forming what is most commonly referred to as a "bloat line" (Fig. 15 ). This lesion occurs in cattle that develop markedly increased intraabdominal pressure as ruminal pressure increases because of excess uneructated gas accumulation. This increased abdominal pressure compresses the thorax and blanches the intrathoracic portion of the esophagus, whereas the esophagus cranial

Erosive lesions in the alimentary mucosa are strongly suggestive of BVDV infections, whereas ulcerative lesions have a much broader spectrum of potential etiologies 13 to the thoracic inlet tends to be markedly congested. 7 Any reason to prevent eructation of gas can lead to the formation of a bloat line.

Serpentine, pale white to orange red spirurid parasites are commonly found burrowed in the epithelium of the esophagus, and occasionally the lingual mucosa. This is the typical presentation of Gongylonema pulchrum infestations. 8 When present in the ruminal submucosa, they are Gongylonema verrucosum. 9 They are clinically inconsequential (Fig. 16) .

Papules that form in the esophageal mucosa and oral mucosa (see Fig. 4 ) are very common in younger cattle, most often the result of bovine papular stomatitis virus, a member of the genus Parapoxvirus. Transmission probably occurs through direct contact and stress or immunosuppression may precipitate disease. 10 These lesions are variable in size, typically very round to oval, and can be subtle raised foci or very prominent papules with raised rims and eroded centers and have adherent fibrin and feed material (Fig. 17) . Erosions can affect the esophagus with causes similar to those described for the oropharynx (BVD, MCF, BTV) (Fig. 18) . Deeper ulcerated lesions may be the result of secondarily infected BVD erosions, mucosal disease, MCF, infectious bovine rhinotracheitis, ruptured vesicles, or mucosal trauma (Fig. 19 ). 3 Mucosal injury to the esophagus tends to heal by fibrosis and scarring resulting in luminal narrowing and stricture formation near the site of injury (Fig. 20) . Injury may be caused by luminal foreign bodies that become lodged or any of the other infectious causes. Proximal to the stricture, the esophagus may become dilated because of slowed or impaired passage of ingesta into the forestomachs. Periesophageal fasciitis that can result from "balling gun" injuries can cause esophageal luminal narrowing (Fig. 21) . Traumatic injury from boluses forcibly ejected into the surrounding periesophageal tissue results in localized tissue damage, edema, and inflammation. In addition, pharyngeal trauma associated with this type of injury can result in acquired megaesophagus presumably caused by vagal nerve injury. 11 Rarely, intraluminal, mural, or periesophageal neoplasia can result in obstruction, luminal narrowing or dilation, dependent on either direct or indirect effects on esophageal function (Fig. 22) .

Forestomachs represent large, mucosal-lined, fluid-filled, and microbe-laden fermentation vats that are necessary for ruminants to convert the complex carbohydrates of plants into absorbable fatty acids. During the course of the digestion and fermentation 

The reticulum or "honeycomb" is the most cranial, small, relative to the other forestomachs, sac comprising a mucosal web of interconnected, irregularly square, pentagonal or hexagonal, cells that are further divided into even smaller divisions. 12 Coarse, large, and heavy materials or objects tend to collect in the reticulum. Sharp objects indiscriminately ingested can accumulate in the reticulum resulting in an increased risk of mural penetration with consequences ranging from focal abscessation to peritonitis to diaphragmatic and pericardial perforation leading to a condition known as "traumatic reticulopericarditis" (Fig. 23) . Ingestion of heavy material, such as lead, tends to collect in the mucosal-lined, ridged cells making this an important forestomach compartment to thoroughly examine (Fig. 24) . Mucosal changes previously discussed can result in similar changes in the reticulum but are often missed because they are typically too subtle or the diagnosis is made based on lesions in other portions of the GIT (Fig. 25) .

Forestomach mucosae tend to be greenish black because of staining by chlorophyllcontaining feed. This staining tends to be relatively uniform throughout these compartments with the exception of the broad rumen pillars, which often are pale, lack papillae, and tend to have a thickened squamous mucosa. When the stained superficial layers of stratified squamous epithelium become blotchy, it is often an indication of disease processes that cause superficial erosions, such as BVD, MCF, or chemical rumenitis (Fig. 26) . Similar blotchiness of the omasal mucosa is also typically seen. Any type of hemorrhagic diathesis can result in mural hemorrhages to any tissue or organ system. One cause to keep in mind is the acute hemorrhagic and thrombocytopenic form of acute BVD (Fig. 27) . 13 Ulceration and mural necrosis can be seen in cases of necrobacillosis and mycotic infections. Both conditions are typically secondary invasion of the forestomach mucosa by Fusobacterium necrophurm or fungal organisms after primary traumatic or chemically (acidosis) induced mucosal injury (Fig. 28) . Necrobacillosis invades through the mucosa into the wall but rarely penetrates to the serosal surfaces (Fig. 29) . However, mycotic infections can either be superficial mucosal proliferation caused by infections with Candida albicans (Fig. 30) or deep and transmural involving the ruminal serosa because of the propensity of many fungi (ie, Aspergillus spp, Mucor spp, Absidia spp, Rhizoporus spp) to not only proliferate in squamous epithelium but also in the walls of blood vessels causing deep inflammation and infarction (Fig. 31) . 11 Ruminal mucosa varies from lacking papilla along the pillars to being densely covered by rumen papilla that range in length and size depending on the predominant feed-associated volatile fatty acids produced in the rumen fluid. Physiologic thickening and lengthening of the ruminal villi tends to occur with feeds that result in higher levels of propionate and butyrate. Conversely, as the percent of dietary roughage increases, production of propionic and butyric acid decreases while ruminal acetic acid levels tend to increase, and ruminal mucosal papillar hypertrophy and hyperplasia does not occur. 11 During necropsy examination of a normal adult bovid, the oral and esophageal mucosa remain firmly and tenaciously attached to the underlying submucosa, whereas the forestomach mucosa tends to normally lift off and away from the underlying, typically reddened submucosa within a few hours of death (Fig. 32) . 3 Conversely, easily sloughed oral and esophageal mucosa and firmly adherent forestomach mucosa are indications of disease.

Parasitism of the ruminal mucosa can be challenging to observe and confirm without close inspection. Adult flukes that affect forestomachs of cattle from numerous genera are commonly grouped as paramphistome infections (Fig. 33) . Adult parasites are red, pear-shaped, and tend to easily blend in with the rumen papillae but are typically incidental gross findings. 9 Long, keratinized, papillary mucosal projections as the omasum opens into the reticulum and gastric groove are normal and referred to as unguiculliform papillae (Fig. 34) . 14 However, proliferative lesions affecting the forestomachs can include papular stomatitis lesions (Fig. 35) and neoplasms, such as mural lymphoma, or mucosal epithelial neoplasms, such as fibropapillomas (Fig. 36) .

Representing the true stomach of ruminants, this viscus is located caudal, ventral, and to the right of the rumen. It is typically slightly more purple than the forestomachs on its serosal surface and typically has a mucosa that is more red to reddish purple. The mucosal surface has much more of a wet, glistening sheen, lining a series of rugal folds. Red, multifocal to confluent areas of hemorrhage in the abomasal mucosa are most often an indication of an ulcerative or infarction process (Fig. 37) . Causes for such changes include various hemorrhagic diatheses including toxins (arsenic); corticosteroids (exogenous and endogenous); and infectious diseases (acute, thrombocytopenic, hemorrhagic BVD) (see Fig. 27 ). Perforating abomasal ulcers tend to affect young cattle. Less commonly, older animals may develop ulcerative lesions that eventually perforate and cause severe peritonitis (Fig. 38) . Abomasal displacement and volvulus is a common condition affecting dairy cattle usually around the time of parturition. With the highest incidence in intensively managed herds, the abomasum typically displaces ventrally and to the left of the rumen. Less commonly, the abomasum displaces to the right increasing the chance for abomasal volvulus. The omasum is often involved in abomasal torsions. When severe, blood vessels in the neck of the omasum become obstructed resulting in not only organ distention but also severe congestion and hemorrhage (Fig. 39) . 15 Focal to diffuse mucosal thickening of abomasal rugal folds is characteristic of parasitism (Fig. 40) . The lesion is a combination of mucous metaplasia and hyperplasia with associated chronic inflammation. The causes for this lesion include either Ostertagia spp or Trichostrongylus axei. 11 The most common neoplasm that affects cattle is lymphoma. The abomasal wall is a predilection site (Fig. 41) . Infiltration may be diffuse imparting a pale tan tincture to the entire affected area or multifocal, nodular infiltration of neoplastic lymphocytes. Other common sites for infiltration by neoplastic lymphocytes include forestomachs, heart, lymphoid organs, liver, reproductive tract, and spinal canal. 16 

In health, intestines vary from pale pink to purple when viewed from the serosal surface and pink-purple to red when the mucosal surface is examined. The mucosal surface has a moist to very wet, velvety, glistening sheen, analogous to a glossy paint finish. Throughout its length, there are mucosal folds designed to increase surface area. Moving aborally, villi tend to decrease in length with no villi present in the large intestine, whereas goblet cell numbers increase such that they are maximal in the distal large intestine.

In general, enteritis is a relatively pedestrian diagnosis histologically but can be very confusing grossly. Redness is only one feature to consider when determining if an animal has enteritis, given that in many cases mucosal redness is a variation of normal. Gross evidence of enteritis is reliably identifiable when there is adherent ingesta mixed with fibrin, erosions, ulcers, and mural necrosis (Fig. 42) . Other features include luminal casts of necrotic material and mucosal thickening without loss of the mucosal sheen. Serosal changes to look for include mural edema, serosal congestion or multifocal hemorrhage (Fig. 43) , loss of the normal serosal glistening surface, and adherent fibrin. If serosal fibrin is mixed with feed material a perforation must be suspected. Finally, enteritis typically results in abnormal fluid contents downstream in the large intestine.

Bright red intestinal mucosa caused by hemorrhage with luminal necrotic debris or clotted blood is in indication of enteritis (Fig. 44) . In general, causes to consider include Eimeria spp; coronavirus (winter dysentery); BVDV; MCF; Clostridium spp; heavy metal intoxication; Salmonella spp; bowel strangulations; and Trichuris spp (whipworms). 3, 11 When large amounts of fibrin are present overlying the mucosal surface, causes to consider include Salmonella spp or Clostridium spp (Fig. 45) . If there is hemorrhage and necrosis of the Peyer's patches or regional lymphoid tissue, BVD, Salmonella spp, or both should be strongly considered as possible causes for this lesion (Fig. 46) . 11 Chronically, salmonellosis can manifest as focal areas of necrosis rimmed by fibrosis, commonly referred to a "button ulcers" (Fig. 47) . 11 Intestinal contents tend to have a more putrid, pungent odor caused by the amount of miasma present in cases of some bacterial enteritis, such as salmonellosis.

Mycobacterium avium subspecies paratuberculosis, the causative organism for Johne's disease, is a resilient intracellular organism that induces a prominent granulomatous reaction. Large numbers of macrophages are attracted to the lamina propria and submucosa of the affected intestine resulting in distinctive corrugation of the mucosa (Fig. 48) with a subsequent reduction in luminal diameter and functional absorptive surface area. In addition, a distinctive serosal and mesenteric response to this organism is granulomatous lymphangitis (see Fig. 48B ). Jejunal hemorrhagic syndrome (or hemorrhagic bowel syndrome) is a relatively poorly understood entity of cattle resulting from chronic and ongoing intraluminal small intestinal hemorrhage without any evidence of concurrent enteritis (Fig. 49) . Typically, affected animals present with signs of obstruction or possibly sudden death. The lesion can be segmental with variably sized collections of clotted blood that tend to minimally distend affected loops and yet have an underlying mucosa that is typically grossly normal. Isolation of Clostridium perfringens type A from cattle with this condition has been reported but likely does not represent a definitive cause. 17 Others have reported in dairy cattle that intensive management procedures and minimal exposure to pasture in high producing herds are predisposing factors to the development of this syndrome. 18 Mesenteric and omental fat and other fat stores can become massively necrotic with areas of saponification in cattle (Fig. 50) . Typically, affected animals are overconditioned, 2 years of age or older, and frequently of Channel Island lineage. The areas of necrosis and saponification are palpably hard and potentially obstructive. These lesions can vary from incidental findings to a cause of intestinal obstruction. 11 

Gastrointestinal tissues autolyze rapidly after death. Therefore, a short postmortem interval is paramount and samples should be collected early in the necropsy procedure 

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Gross Lesions of Alimentary Disease