by Dr. Michelle Arnold, DVM
Ovine progressive pneumonia (OPP) is one of the most economically important chronic diseases in sheep production worldwide. OPP is caused by a retrovirus of the genus Lentivirus known as Maedi-Visna virus (MVV), so named because ‘maedi’ means “breathlessness” and ‘visna’ means “wasting”. MVV is often referred to as OPP virus (OPPV), and together with Caprine Arthritis–Encephalitis virus (CAEV), they form the “Small Ruminant Lentivirus” (SRLV) group of viruses that primarily targets the lungs, mammary glands, joints, and brain. These are lifelong infections that cause slow development of lesions that often go unrecognized without good production records. During the 2011 NAHMS Sheep Study, only half of the sheep operations (representing 85% of the nation’s ewe inventory) interviewed were familiar with OPP and, of those, only 16% had a control program in place. In the same study, 54 flocks (1415 sheep) in Wyoming were tested with the ELISA OPP blood test, resulting in 18% of the individual animals were positive and 47.5% of the flocks.
The primary route of transmission for the OPP virus is through the air (by aerosol) or direct contact with virus-contaminated nasal secretions from infected to susceptible animals (known as ‘horizontal’ transmission), and viral transmission is most efficient when animals are housed indoors in close proximity to each other. The virus may also be transmitted from infected ewes to lambs (known as ‘vertical’ transmission) by infection either during pregnancy or through milk or colostrum. In contrast, lentiviruses are primarily transmitted in goats via colostrum and milk, but there is evidence close contact with infected animals will also transmit the virus. Accidental transmission of SRLV by people during milking or by re-using hypodermic needles on multiple animals is also possible. Sexual transmission is thought to be possible since SRLVs have been found in the male genital system and viral shedding in semen has been demonstrated. There is also a strong inherited genetic component of resistance or susceptibility to the lentiviruses. Dr. Holly Neaton, OPP Society, states, "The 2012 research from MARC in Clay Center, NE, found that weaning early (6-8 weeks) and testing about 60 days later revealed only 10-30% of the lambs were infected. Culling and repeated testing of the negative lambs along with distance from the infected flock gave the producer a negative ewe lamb group."
Animals infected with OPP or CAE are infected for life, but because of the long incubation period typical of these viruses, it generally takes years for recognizable signs of disease to develop. Of those infected individuals, approximately 30% develop disease while the remainder have subclinical infections that may be missed without examining production records. SRLVs affect an array of target organs, most importantly the lungs (primarily OPPV), central nervous system consisting of brain and spinal cord (both OPPV and CAEV), mammary gland (both OPPV and CAEV) and joints (primarily CAEV). The clinical disease that results depends on the viral strain, the species of animal affected (sheep or goat) and the genetic background of each breed or animal. In general, only one of the target organs is mainly affected, but it is not unusual to find several organs affected in the same animal, with varying degrees of severity. In both sheep and goats, only the respiratory and neurologic syndromes lead the animal to extreme weight loss and death, either by damaging lung function or by some alteration of the nervous system. Localization of the virus to the joints or the udder does not directly result in weight loss or death, although in the joints they can cause varying degrees of lameness (mostly seen in goats) or in the udder they cause decreased milk production leading to undernourished lambs or kids. Therefore, animals with joint and/or udder involvement are often prematurely culled due to poor production.
In sheep, the onset of clinical signs of OPP is variable and most are underlying, subclinical infections. Typically, clinical signs are observed in sheep over 2 years old and consist of progressive weight loss despite a normal appetite (“wasting”) and difficult breathing. Initially, labored breathing is detected only after physical exertion and is noticed when a flock is driven. Affected animals are described as having a rhythmic jerk of the head with each breath inhaled and lag behind the rest of the flock. As the severity of lung disease progresses, affected sheep (commonly referred to as ‘lungers’) may show open mouth breathing, coughing, flaring of nostrils, an increased respiratory rate, and forced expirations but without fever. These sheep frequently develop secondary bacterial infections and fever, which worsens the breathing difficulty. Over time, infected sheep may develop labored breathing at rest and spend most of their time lying down. Sheep with OPP-associated pneumonia may look similar to sheep with other forms of chronic respiratory disease such as caseous lymphadenitis abscesses, lung tumors, mycoplasma pneumonia, parasitic pneumonia, pulmonary adenomatosis, ovine adenovirus, and respiratory syncytial virus infections. If a necropsy is performed after death, the chronically affected lungs show a grey discoloration, are much larger and heavier than normal, and have tiny grey spots in a diffuse pattern on the lung surface. Besides the weight loss and labored breathing with the respiratory form of disease, other clinical signs associated with SRLV infection are possible depending on the target organ involved. The syndrome involving the joints occurs in both small ruminant species but it is much more commonly seen in goats. This form involves development of arthritis, joint swelling, pain and lameness, potentially affecting multiple joints although the carpal joints (front knees) are the ones most frequently affected (see Figure 1). Some virus strains prefer to attack the mammary gland causing a mastitis, often referred to as ‘hard bag’, resulting in an enlarged, symmetrically firm udder and marked reduction of milk production although the milk looks normal. Other viral strains may invade the central nervous system (brain and/or spinal cord) causing meningitis and encephalitis. This form results in various neurological signs, such as progressive staggering, hind limb weakness with stumbling gait, progressive incoordination, which can lead to total paralysis and a downer animal. The neurologic form of CAEV primarily affects kids 1-6 months of age while OPPV tends to affect mature sheep. OPP can be widespread in a flock before clinical cases are observed because of the insidious onset and slow disease progression. Unfortunately, once clinical signs are observed, the organ system or systems are often severely affected, and death is imminent. However, the economic losses associated with OPP are primarily due to infected animals with impaired production rather than those with obvious clinical signs. Compared with uninfected flocks, OPP-infected ewes have decreased milk production, lower conception rates, lambs with lower birth weight, retarded growth and lower weaning weights, and a higher proportion of animals culled prematurely. Many of those production losses go unnoticed, so the overall severity of OPP in a flock is often difficult to determine without excellent records.
Diagnosis of OPP or CAE is most often accomplished with a blood test to detect specific antibodies in infected animals. The lentiviruses produce persistent infections that can normally be detected after the first 2-3 weeks. Published data show nearly a 95% accuracy rate for antibody detection in today’s commercial test kits. However, there is no one-time perfect test and test results must be interpreted in light of the herd-level prevalence of infection. For example, the likelihood a negative test result is correct is enhanced if all herd mates also test negative. False positive results can also occur for no apparent reason. Antibody levels can wax and wane, and an infected animal can test negative although this is rare. Therefore, if the test result is unexpected, further testing by PCR is recommended. Flocks/herds should be tested for SRLV twice a year initially, followed by annual testing for herds/flocks that are primarily negative, with testing performed prior to lambing/kidding. If working to become virus-free quickly, institute repeated testing at 2–3-month intervals until 2-3 consecutive, whole-group negative tests have occurred. Any new animals or those returning from shows should be quarantined and tested twice (at least 60 days apart) before introduction to other negative animals. Animals younger than 6 months of age generally should not be tested, but if a young animal is test-positive, it should be re-tested after 6 months of age because of the potential for detection of colostral antibodies passed from the dam to offspring or use another test method for virus detection such as a PCR assay.
Although there are currently no vaccines available for OPP, management practices can be implemented to prevent the introduction or reduce the presence of the disease within a flock. Isolation of negative sheep flocks from known positive animals is important for preventing virus transmission. This includes keeping sheep away from goats infected with the CAE virus because some strains of CAE virus can infect sheep and vice versa. Additionally, OPP-infected ewes can shed the virus in colostrum and milk; therefore, in OPP-infected flocks, lambs should be removed from infected dams at birth and fed colostrum and milk from OPP test-negative ewes or fed heat-treated colostrum and pasteurized milk. Replacement lambs should be segregated away from any infected animals to prevent transmission through the air or contact.
Before any control practices are implemented, the number of animals with OPP and the goals (control vs eradication of OPP) of the producer should be carefully considered. Results of the NAHMS 2011 sheep study indicate that 46.5% of sheep producers in the United States do not know the OPP status of their flocks. Flocks with a high number of OPP-infected animals may consider depopulation, but that option may not be necessary since testing and removing test-positive animals can be effective. Simply culling animals with clinical signs of OPP is not an effective strategy due to the long incubation period during which animals with an underlying infection can transmit the virus to susceptible flock mates. If immediate culling is not possible, separation of positive and negative ewes into two different flocks will significantly reduce horizontal spread. One of the most effective control programs focuses on culling both infected ewes and their offspring. This reduces the presence of the virus progressively by selectively culling positive sheep and replacing them with offspring from negative ewes. This strategy has two important advantages, namely, avoiding virus transfer through milk or colostrum from dam to offspring, and there is good evidence the offspring of negative ewes are more resistant to infection over the course of their lifetimes. Ultimately, the decision about which testing and management strategies to implement for the control and prevention of OPP should be made on a flock-by-flock basis with a veterinarian, taking into account market prices and the prevalence of infected animals in the flock. For artificial insemination in genetic selection programs, only certified small ruminant lentivirus-free males should be used as semen donors to avoid transmission of the virus. Heat-treating colostrum will inactivate the SRLVs and should help prevent this method of transmission from the dam to her offspring. Colostrum from any dam may be heated to between 133⁰ and 138⁰ F (56⁰ to 59⁰ C) and held at that temperature for one hour to inactivate the virus. An accurate thermometer is important. It is recommended to use a water bath or double boiler to regulate the temperature more closely. A large batch may be heat-treated and frozen in small feeding-size portions for later use. If heated higher than 140⁰ F, the usefulness of the colostrum will be greatly reduced due to denaturing of beneficial proteins, including the antibodies needed to fight other infectious microorganisms.
OPP is an underdiagnosed and sometimes fatal disease of sheep that primarily causes underlying economic losses. The infection has a slow yet steady impact on sheep health and production and negatively affects many relevant economic parameters including ewe fertility, lamb weight at weaning and adult culling age. Having OPP antibodies (and therefore a positive result on a blood test) implies chronic, lifelong infection and may restrict animal access and trade in fairs, shows and exports. However, OPP-free flocks may have added value as breeding and replacement stock. Detection of infection is performed by an inexpensive, highly accurate but imperfect, blood test. Testing sheep for antibodies against SRLVs allows producers to know the OPP status of their flocks and will help them make informed decisions regarding the implementation of management practices to minimize virus transmission and to work towards a negative flock status. The future of OPP control is genetic selection for sheep that are resistant to SRLVs, making it much easier to maintain OPP-free flocks and prevent disease. The best way for an OPP-infected flock to eradicate the disease is to test all animals and cull those with positive test results. For flocks not infected with OPP, the best way to prevent introduction of the disease is to quarantine and frequently test all potential flock additions before allowing them to commingle with the negative flock.
Michelle Arnold, DVM is an Associate Professor at the University of Kentucky in the Clinical Title Series. She is housed in the UK Veterinary Diagnostic Laboratory in Lexington, KY and has served as the Ruminant Extension Veterinarian since 2010. Previous to returning to her roots in KY, she was in private veterinary practice for 20 years and was a partner in a Holstein dairy then a commercial cow/calf and stocker operation in TN. She has two sons, Briscoe and Brody, both of whom graduated from the University of KY.
