Porcine Cytomegalovirus

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Inclusion Body Rhinitis (Porcine Cytomegalovirus Infection)


A viral infection usually manifested in nursing or newly-weaned piglets as a rhinitis and conjunctivitis accompanied by sneezing and nasal discharge. Infection of pregnant, naïve sows may lead to delivery of dead, mummified, stillborn or weak piglets.


Porcine cytomegalovirus (PCMV), also known as inclusion body rhinitis (IBR) occurs in all age groups of previously uninfected swine, including developing fetuses. PCMV occurs only in pigs although similar infections with related viruses occur in many other species, including people. PCMV occurs worldwide in the major swine-raising countries. Infection is common but often is inapparent when herd immunity is present or in pigs over six weeks old.

Historical information

A rhinitis of pigs accompanied by inclusion bodies was described in 1955. In 1961 the disease was identified as a transplacental infection of fetal pigs. Beginning in the early 1960s and extending into the late 1980s, research reports provided details on the disease and its manifestations in all ages of swine as well as characteristics of the virus that causes the disease. There has been interest in a possible relationship of PCMV to reproductive failure in dams and early neonatal losses. It has been suspected of predisposing swine to other respiratory diseases, especially atrophic rhinitis. Losses from PCMV are small. The disease and infection are largely ignored by swine raisers.


Porcine cytomegalovirus causes inclusion body rhinitis. The cytomegaloviruses are a subgroup of the herpesviruses. They have many of the characteristics of herpesviruses, including the ability to induce latent infection in carriers that can later be reactivated by stress. PCMV can be propagated in cell culture. In several epithelial type cells of swine the virus causes marked cell enlargement and formation of large intranuclear inclusion bodies.


Serologic testing has shown that many herds are serologically positive to PCMV. The presence of the virus within a herd often is unrecognized because many sows are immune, show no signs of infection, and colostral antibodies protect their young piglets from lesions as they are infected.

Virus is shed during and for some time after infection. Many infected piglets three to eight weeks old shed virus. Virus is shed in nasal and ocular secretions, urine and the aerosol created by sneezing and coughing. Transmission of virus is, presumably, through inhalation or ingestion of virus. Many recovered animals have virus sequestered as a latent infection and can then become shedders if severely stressed. These carriers then disseminate virus while mixed with susceptible swine.

Experimentally, and probably naturally, the virus sometimes crosses the placenta to infect developing fetuses. Infected fetuses may be killed, mummified, stillborn or born alive as infected, weak piglets. Infected piglets then spread virus to susceptible piglets.


The primary site of virus replication is believed to be in the nasal mucous glands or the lachrymal or Harderian glands. Destruction of their cells results in a marked rhinitis and conjunctivitis.

Viremia follows replication. The virus localizes in epithelial and endothelial cells at many sites as well as within macrophages and reticuloendothelial cells. The intracellular virus causes marked enlargement and destruction of many infected cells but persists and is tolerated by other cells. Regeneration can occur in some simple glands by proliferation and differentiation of ductal cells. Endothelial cell damage and necrosis is believed to be responsible for the petechial hemorrhages and edema that accompany IBR. Bone marrow damage is suspected of causing anemia in neonates. Widespread damage caused by the virus or secondary infections can lead to death.

Clinical signs

The disease usually is observed in one to five week old pigs. In suckling pigs, especially pigs less than three weeks old, signs include mucopurulent rhinitis accompanied by violent sneezing, respiratory distress, conjunctivitis, shivering, perhaps mouth breathing, and a variable death loss. Although unusual, mortality can be high in pigs born to naïve gilts or sows, or if PCMV is complicated by other diseases.

Infected neonatal piglets appear weak, anemic or stunted and there may be edema around the throat and tarsal joints. Signs in older pigs or dams with viremia may include listlessness and mild anorexia or may be inapparent.

Fetal mummification, stillbirths, neonatal deaths and failure of piglets to thrive have been associated with infection of naïve, pregnant sows. Evidence that IBR caused these has been accumulated through field observations and is supported by related research.


In nursing piglets, the most commonly recognized gross lesion is mucopurulent exudate in, and perhaps obstructing, nasal passages. Complications sometimes include sinusitis, otitis media or pneumonia. In neonatal pigs, petechial hemorrhages and subcutaneous edema can occur. Effusions in the thorax, abdomen and pericardial sac and edema of the lungs often are present. Microscopically, intranuclear inclusions usually can be found in nasal mucous glands, Harderian glands and lachrymal glands of nursing pigs. They may be present in renal glomeruli and tubular epithelium, liver, capillary endothelium, choroid plexus, glial cells and in various epithelial type cells. Focal gliosis is common throughout the central nervous system (CNS). Inclusions sometimes can be found at several sites in fetuses.


The disease usually is diagnosed after finding microscopic, basophilic intranuclear inclusions in tissues of a typical, infected piglet. Where available, an enzyme linked immunosorbent assay (ELISA) or an indirect immunofluorescent (IF) test on serum samples can be used to confirm the presence of PCMV in a herd. If reproductive problems have occurred in a herd, PCMV will need to be differentiated from other reproductive diseases, especially parvoviral infection, pseudorabies (PRV) and porcine reproductive and respiratory syndrome (PRRS).


Because the disease seldom is recognized as a cause of severe loss, control measures often are ignored. Growing pigs usually are protected from large losses by antibodies provided by their immune dams. As piglets grow, they are exposed to virus in the environment and respond by producing their own antibodies.

Environmental conditions, if poor, should be improved. Herd immunity via acclimatization of breeding stock is commonly practiced. There is no known effective treatment or medication. Antibiotics may be useful to control concurrent diseases or secondary bacterial infections.