What Does BVD Look Like? Symptoms and Herd Signs

Bovine viral diarrhea can look like almost anything, which is exactly what makes it so dangerous. In a single herd, BVD might show up as a wave of fever and runny noses in one group of calves, a string of unexplained abortions in the breeding cows, a handful of stunted “poor doers” that never seem to thrive, or no obvious signs at all while milk production quietly slips. The virus exists on a spectrum from subclinical to rapidly fatal, and the form it takes depends on the animal’s immune status, the viral strain involved, and whether the infection is acute or lifelong. Understanding what to watch for across that spectrum is the key to catching BVD before it hollows out a herd’s productivity.

Acute Infection in Otherwise Healthy Cattle

When BVD virus enters a naive herd for the first time, the initial wave of acute infections can be surprisingly easy to miss. Many immunocompetent adult cattle develop only mild, transient signs: a brief fever, some nasal discharge, a drop in appetite lasting a few days, and perhaps a short bout of loose stool. These animals recover on their own and develop antibodies, so the episode often gets chalked up to a minor respiratory bug or a dietary hiccup. The diarrhea that gives the disease its name is not always the most prominent feature, and in some outbreaks it barely appears at all.

Where acute BVD becomes more visible is in younger or immunologically naive stock. Calves and yearlings tend to develop higher fevers, more obvious depression, and more pronounced respiratory signs including coughing and mucopurulent nasal discharge. Oral ulcers can appear on the gums, tongue, and hard palate. Because BVD suppresses the immune system, secondary bacterial infections often pile on, turning what started as a viral fever into full-blown pneumonia or enteritis that responds poorly to antibiotics. If you are treating a pen of calves for respiratory disease and the antibiotics just are not working, BVD should be on the list of suspects.

Hemorrhagic and Severe Acute Forms

Not all BVD strains behave the same way. Beginning in the 1980s and 1990s, outbreaks caused by more virulent strains, particularly certain BVDV type 2 isolates, revealed a far more dramatic face of the disease. These strains can cause hemorrhagic syndrome, a rapidly progressing and often fatal condition characterized by severe drops in white blood cells and platelets.

In experimentally infected calves exposed to a virulent type 2 strain, all animals developed marked drops in white blood cell and platelet counts within six to ten days, and some progressed to bloody diarrhea and became moribund. Animals were killed for examination between six and eleven days after infection, and the internal damage resembled an accelerated version of mucosal disease, though without the classic oral erosions seen in that condition.¹ A German outbreak involving a type 2c strain painted a similar picture on farms: affected cattle first showed respiratory-like signs with fever up to 41°C, nasal and eye discharge, and exhaustion. Within hours to days they developed diarrhea that ranged from watery to bloody, and pinpoint hemorrhages appeared on the membranes of the eyes and mouth. The fever did not respond to antibiotics, and in severe cases the first deaths occurred just two to three days after signs began.²

Calves with hemorrhagic syndrome in another investigation showed moderate fever, dullness, nasal discharge, and widespread petechial and larger bruise-like hemorrhages across mucosal surfaces. Blood work confirmed severe thrombocytopenia and anemia, and all affected calves died within ten days of the first clinical signs.³ These hemorrhagic presentations are less common than the mild acute form, but when they strike a naive herd the mortality can be shocking.

What Persistently Infected Animals Look Like

The single most important thing to understand about BVD at the herd level is the role of persistently infected animals. When a pregnant cow is exposed to the virus during roughly the first four months of gestation, before the fetal immune system has matured, the calf can be born carrying the virus for life. The fetus’s immune system never learns to recognize the virus as foreign, so the animal sheds massive quantities of virus every day through nasal secretions, saliva, urine, feces, and other bodily fluids without ever mounting an immune response against it.⁴ Persistently infected cattle are far more efficient transmitters than animals with a short-term acute infection, and they are considered the primary reservoirs keeping BVD circulating in herds.⁵

Some persistently infected calves look perfectly normal at birth and may appear healthy for months or even years. Others, however, show telltale signs from the start. In one experimental study where pregnant cattle were deliberately infected, the resulting persistently infected calves were generally small, appeared unthrifty as typical “poor doers,” and some developed secondary infections with diarrhea and respiratory disease. One was weak at birth and died the following day.⁶ On a practical level, if you have a calf that is chronically undersized, repeatedly sick with respiratory or gut infections, and never quite catches up to its pen-mates despite adequate nutrition and treatment, persistent BVD infection should be considered.

The tricky part is that the normal-looking persistently infected animals are just as dangerous to the herd as the sickly ones. A healthy-appearing PI heifer that enters the breeding herd can quietly infect dozens of other cattle and generate the next generation of PI calves before anyone suspects a problem.

Mucosal Disease

Mucosal disease is the most dramatic and invariably fatal outcome of BVD, but it only occurs in persistently infected animals. It develops when a second form of the virus, called the cytopathic biotype, emerges through mutation within a PI animal that already carries the non-cytopathic form.⁷ The cytopathic virus replicates without restraint, and the PI animal’s tolerant immune system has no way to fight back.

Clinically, mucosal disease is recognizable by severe, widespread erosions and ulcers throughout the digestive tract, from the mouth all the way through the intestines. Affected cattle develop profuse, often bloody diarrhea, stop eating, drool excessively due to oral pain, and deteriorate rapidly. The erosions in the mouth, on the tongue, and along the esophagus and rumen are among the most characteristic pathological findings in all of cattle medicine. Research into the mechanism has shown that the intrinsic apoptosis pathway, essentially a program of cell self-destruction, is the key driver of the tissue damage seen in mucosal disease lesions.⁸ There is no effective treatment. An animal diagnosed with mucosal disease will die, usually within days to a couple of weeks.

Mucosal disease tends to strike animals between six months and two years of age, though it can occur at any age in PI cattle. On the herd level, a case of mucosal disease should raise an immediate red flag: if one animal developed it, there is almost certainly at least one persistently infected animal in or recently removed from the herd.

Reproductive Signs and Congenital Defects

For many herds, BVD’s biggest damage is not the sick animals you can see but the pregnancies you lose. The reproductive impact depends heavily on when during gestation the dam is infected.

Early pregnancy: Infection in the first month or so often causes embryonic death and resorption. The cow simply comes back into heat, and no one realizes a pregnancy was lost. In experimental work where heifers were infected between days 29 and 41 of pregnancy, all four animals experienced fetal death; two aborted and two resorbed the fetus entirely.⁹
Mid-gestation (roughly days 60 to 180): This is the window for congenital defects. The virus can damage the developing brain, producing calves born with cerebellar hypoplasia (an underdeveloped cerebellum), hydranencephaly, hydrocephalus, or other brain malformations.¹⁰ In a study examining congenital brain anomalies in newborn calves, cerebellar hypoplasia was the most common lesion, and BVD was the single most important cause identified.¹¹ These calves may be born alive but show incoordination, tremors, an inability to stand, or blindness.
Before immune maturity (roughly before day 125): This is the critical window for creating persistently infected calves. The fetus survives but becomes immunotolerant to the virus and will carry it for life.
Late gestation: The fetal immune system is now functional enough to mount a response, so infection at this stage usually results in a normal, seropositive calf or, in some cases, a weak or premature calf.

At the herd level, a BVD-related reproductive problem often shows up as a vague decline in conception rates, a cluster of returns to service, a few abortions spread over weeks or months, or an uptick in weak or deformed calves at calving time. Because the losses are scattered and diverse, they rarely point obviously at a single cause unless someone is looking for it.

Herd-Level Signs That Are Easy to Miss

One of BVD’s most frustrating characteristics is that in herds where the virus has been circulating for a while, the most common presentation is no dramatic illness at all. Instead, you see an erosion of overall herd performance that is difficult to pin on any one thing. Conception rates drift downward. Calves grow a little more slowly. Pneumonia and scours treatments climb but no single pathogen dominates the diagnostic workups. Milk production dips.

A study of Flemish dairy herds found that herds with higher BVD antibody levels, indicating more virus exposure, had significantly higher bulk milk somatic cell counts compared to essentially BVD-naive herds, suggesting a subtle but measurable impact on udder health across the herd.¹² Economically, the reported impact of BVD ranges widely depending on the situation. A systematic review found costs from essentially zero in some stable, endemic situations up to £552 per cow per year in severe acute outbreaks of naive herds.¹³ Modeling of New Zealand pastoral herds estimated direct losses of about NZ$22 per cow per year in dairy and NZ$41 per cow per year in beef for a naive herd experiencing an outbreak, with the biggest dairy losses coming when PI replacement heifers joined the milking herd and the biggest beef losses coming from reduced pregnancy rates.¹⁴

The pattern worth watching for is a combination of problems rather than a single dramatic one: declining fertility, increased calf mortality, higher treatment costs for secondary infections, and occasional congenital abnormalities or mucosal disease cases. Individually, each problem has a dozen possible explanations. Together, they paint a picture that should prompt BVD investigation.

How BVD Is Confirmed

Because BVD’s clinical signs overlap with so many other conditions, diagnosis always requires laboratory testing. The gold standard approach involves testing ear notch tissue samples or blood for viral antigen or viral RNA. Ear notch samples can be screened using antigen-capture ELISA, immunohistochemistry, RT-PCR, or immunofluorescence methods.¹⁵ An international proficiency trial across 40 veterinary diagnostic laboratories tested these methods side by side on standardized panels of ear notch and serum samples.¹⁶

Identifying persistently infected animals is the cornerstone of any control program, but it comes with a diagnostic wrinkle that trips up many producers. Newborn PI calves that receive colostrum from vaccinated or previously exposed dams absorb maternal antibodies that can temporarily mask the virus. In PI calves, infected white blood cells disappeared from circulation for three to eight weeks after colostrum intake, and antigen levels in tissue samples dropped dramatically, with one commonly used antigen test failing to detect the virus until 90 to 158 days after birth.¹⁷ This means a PI calf tested too early in life can come back negative, get a clean bill of health, and then start shedding virus again once the maternal antibodies wane.

RT-PCR-based tests using primers from the conserved 5’UTR region of the viral genome have proven more reliable in the face of maternal antibodies than antigen-capture ELISAs. Serum samples with high viral RNA loads identified PI animals with complete accuracy, while lower loads indicated transient infection, and intermediate values flagged animals for retesting.¹⁸ For practical purposes, many eradication programs recommend testing calves at or after about five weeks of age, or retesting any young animal that initially tests negative if the herd has known BVD exposure. One large-scale study collected ear notches from over 1,000 calves at roughly 3, 10, 24, and 38 days of age and compared test performance across those time points, finding that the window of maternal antibody interference is a real concern for early sampling.¹⁹

An Emerging Third Genotype

Most producers and veterinarians think of BVD as a two-genotype problem: BVDV-1 and BVDV-2. But a third group, sometimes called HoBi-like pestivirus or BVDV-3, has been turning up in cattle and small ruminants in parts of South America, Asia, and Europe. Its clinical signs look much the same as classical BVD infection.²⁰ The concern is that while some commercial BVD diagnostic tests can detect HoBi-like viruses, they cannot reliably distinguish them from BVDV-1 or BVDV-2, and some tests may miss them altogether.²¹ Newer multiplex RT-qPCR assays have been developed that can specifically detect and differentiate all three genotypes without cross-reactivity.²² For herds in regions where BVDV-3 has been reported, or herds importing animals from those regions, this is worth discussing with your veterinarian and diagnostic lab.

BVD in Species Other Than Cattle

BVD is not exclusively a cattle problem. The virus has a broader host range than many producers realize, and this matters both for diagnosis and for biosecurity.

White-tailed deer, the most abundant free-ranging ruminant in North America, are susceptible to BVD and can become persistently infected. Research has demonstrated that PI deer shed the virus in a pattern similar to PI cattle, and in one study, contact between a PI deer and susceptible deer resulted in the birth of a PI fawn, proving that the virus can be maintained within deer populations through congenital infection.²³ For a deer population to serve as a true wildlife reservoir, animals need to be susceptible, capable of shedding virus, able to maintain it in the population, and have enough contact with cattle for spillback to occur.²⁴ Whether all four conditions are routinely met in the wild remains an open question, but the possibility complicates eradication efforts in areas with dense deer populations.

South American camelids, including alpacas and llamas, are also susceptible and can become persistently infected. In alpacas, transient BVD infection from contact with PI alpacas produced only mild signs.²⁵ But persistently infected camelids tell a grimmer story. The chronic form is most common, featuring poor weight gain, intermittent illness, chronic diarrhea, joint swelling, and recurrent respiratory disease despite antibiotic treatment. Diarrhea is not always a consistent finding. The mortality rate in persistently infected New World camelids appears to approach 100%.²⁶ Operations that run cattle alongside alpacas or llamas, or that share pastures and equipment between species, should factor this cross-species risk into their BVD control plans.

Why the Two Biotypes Matter for What You See in the Field

You will sometimes hear BVD discussed in terms of “cytopathic” and “non-cytopathic” biotypes. This distinction is not just academic jargon. It underpins the entire disease picture. The non-cytopathic form is the one circulating in the real world. It is responsible for acute infections, for establishing persistent infections in fetuses, and for the immune suppression that makes BVD-exposed cattle vulnerable to secondary disease. The cytopathic form arises through spontaneous mutations within a PI animal and essentially cannot survive on its own in the field; it fails to establish chains of infection and cannot create new persistent infections.⁴

What this means practically is that the non-cytopathic biotype is the one you are fighting at the herd level through biosecurity, vaccination, and PI removal. The cytopathic biotype matters only insofar as it triggers mucosal disease in individual PI animals. You cannot “catch” mucosal disease from another animal; it develops internally when the PI animal’s own virus mutates. That is why mucosal disease is always a sporadic event in individual PI animals rather than an outbreak that sweeps through a group.⁷ If you see two or three mucosal disease cases in the same year, it does not mean the disease is spreading between them. It means you have multiple PI animals in the herd, each undergoing its own internal mutation event.