Ulceration results when necrosis occurs on or near the surface of a tissue and the necrotic cells slough away. Ulcers are common in disorders of the oral, esophageal, gastric, and intestinal mucosae. These locations all have thin and relatively fragile exposed tissue; infection usually occurs when something breaks through the mucosa. The resulting necrosis near the surface may be severe enough to erode the epithelium completly in the injured area, exposing the underlying CT.

The early events of ulcer formation are the same as those for any other acute inflammation: infiltration by neutrophils, alterations in vascular permeability, and edema. As the inflammatory response continues, underlying tissue becomes necrotic, decompensating the tissue above. The result is a region of focal necrosis that sloughs off from the healthy tissue.

Ulcers vary in severity, depending on how far into the tissue they descend. Gastric ulcers can be rather mild, occupying only the mucosa of the stomach, but given time and continued inflammation in the site, they can become severe enough to descend into the muscularis. They may be deep enough to perforate the wall, releasing gut contents into the peritoneal cavity, with potentially fatal results.

You've been called out to a small dairy operation to examine several Jersey cows that have been experiencing severe and sometimes bloddy diarrhea for the past two days. The producer tells you that they went off feed about three days ago and the diarrhea started about a day and a half afterwards.

Five cows are penned away from the others: they're all approximately 11 to 12 months of age and up to date on their vaccinations. All five are drooling profusely and standing against the gate or the walls with their heads drooping. All five defecate frequently and the diarrhea is bloody and foul-smelling. The producer mentions that two of his cows aborted recently. Another cow gave birth but the calf was very weak and died soon after birth. He wonders if the disease you see in the cows is related to the abortions and the death of the calf.

When you halter one's head you immediately discover multiple scabby erosions on her muzzle. Once she's in a head gate, you prop her mouth open with a speculum: the tongue is ulcerated and swollen with a large coalescing lesion on the dorsal surface. It looks very painful which might explain why she's off feed.

You have a pretty good suspicion of what this is, so you draw blood from the sick cows and send it off to the lab for testing. You also take nasal and oral mucosal swabs. You warn the dairyman to keep this group isolated from the rest until he hears from you. When the labs come back, your guess is confirmed.


As you suspected it would be, the diagnosis is bovine viral diarrhea, BVD, confirmed by viral isolation and culture. BVD is caused by infection with bovine pestivirus, a member of the Togaviridae family. Pestivirus infection can cause a variety of disease signs in cattle. Bovine viral diarrhea (BVD) is simply the name given to one of those disease complexes. Other syndromes attributed to pestivirus include persistent infection and shedding of virus without clinical signs, mucosal disease of calves, and congenital abnormalities due to infection in utero.

These are two biotypes of the bovine diarrhea virus, a cytopathic and a non-cytopathic strain. Infection with the cytopathic strain results in either a subclinical infection or classic BVD. The subclinical infection is the more prevalent of the two and signs consist of anorexia, fever, serous nasal discharge, and leukopenia. Most cases resolve within 10 days and the resulting antibodies generated in response to the infection may confer a lifelong immunity to further infection.

Classic BVD, while less common, is a memorable disease. Affected cattle experience acute gastroenteritis and respiratory signs. Typical BVD cases experience a high fever, acute watery diarrhea (often hemorrhagic), decreased or absent rumen motility, and ulcerative lesions of the oral mucosa. Examination of the buccal papillae shows they have been blunted. This is due to replication of the virus within the papillae and subsequent cell destruction as the virus spreads.

With prompt treatment and careful management, classic BVD will resolve within 10 days unless secondary infection occurs. Bacterial infection is a common sequela of BVD since the mucosal barrier is damaged, allowing easier entry for the bacteria, and the virus induces acute immunosuppression. In order to avoid the complication of secondary bacterial infection, prophylactic doses of antibiotics are recommended.

BVD can also cause disease in naïve pregnant cattle (usually first calf heifers, since they haven't been exposed to as many pathogens as their older sisters) and the fetuses they are carrying. First trimester infection of pregnant cattle can result in conception failure and abortion. Later infection can result in fetal abnormalities, including cerebellar hypoplasia, lenticular cataracts, and hyrocephalus. If the virus is of the non-cytopathic variety, infection of a fetus between day 80 and 120 can result in a calf that becomes an immunotolerant carrier predisposed to development of mucosal disease. The likelihood of an asymptomatic carrier being present in this herd mandates that the entire herd be tested for the presence of virus.


These cattle have the classic form of BVD , with ulcerations of the esophageal mucosa. A low magnification view shows the extensive erosion of the surface mucosa that's taken place. There's normal esophageal epithelium on either side: the ulcer is a well-defined lesion with a sloughing surface and deep-seated inflammation of the underlying submucosa. This is the reason the cows aren't eating: it hurts like hell to swallow when you have something like this in your throat! It's very likely, given the bloody stools, that they also have some pretty serious gastric and intestinal erosions as well.

At the edge of the lesion the extent of the epithelial disruption is obvious. The epithelium is very friable. The lamina propria/submucosa is infiltrated with inflammatory cells and damage is to the full thickness. The bed of the ulcer shows clearly that there's been a complete removal of epithelium, hence this is an "ulceration," not an "erosion," which would only involve the epithelium.

This ulcer is caused by a ruptured vesicle that's been formed by the BVD virus. Once the vesicle ruptures, the underlying tissue is exposed to bacteria and other pathogens and secondary infection sets in. The influx of neutrophils is not caused by the virus itself, but by the tissue irritation from the ruptured vesicle and from secondary invaders.



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