NOTE: In the US, pasteurized milk (heated to 165F for a minute) and heat-treated colostrum (heated to 135F for one hour) are used in CAE prevention managements.
Maedi-visna (MV) and caprine-arthritis-encephalitis (CAE) virus. The lentiviruses cause persistent and progressive infection. The course of the disease is very slow, beginning in subclinical form and concluding with multiple organ degeneration, cachexia and death. In the concrete case of CAE, and although it is a lentivirus, newborn goats of infected mothers can develop encephalitis one month after birth.
BIOLOGY OF THE LENTIVIRUSES
|Fig. 1: Lentiviruses, like other viruses, are highly selective in terms of the infection target cells.|
Lentiviruses persist indefinitely within their hosts, and are species-specific. As with other viruses, they make use of the host cell machinery to produce their own proteins based on the information contained in the viral DNA. However, the target cell preferences of each family of viruses differ. In this sense, lentiviruses prefer cells that need to differentiate, as in the case of macrophages and lymphocytes. Ruminant lentiviruses are found in blood monocytes in latent form, and only express or multiply when the monocyte matures into a macrophage in the different body tissues (lungs, mammary glands, etc.), thereby causing lesions.
The intense viral tropism for these cells is the weak point of lentiviruses, since transmission of the infection requires the exchange of blood or body fluids among animals. This feature affords the only true opportunity for controlling the disease, by adopting adequate management protocols to avoid transmission between animals.
As has already been mentioned, lentiviruses produce disease progressively and very slowly. In many cases, however, the animal may be infected for life without developing any lesions — or the latter may be so mild as to elude detection.
Both MV and CAE produce multiorgan or multisystem disease, characterized by alterations of the lungs, mammary glands, joints and nervous structures. In a given animal there may be alterations in only one organ or in several at the same time. In ovine cattle the most frequent lesions are located at pulmonary level and in the mammary tissues, while in goats the prevalent locations are the joints and mammary glands.
At the start of the infectious process the manifestations are imprecise and very difficult to detect (thinning, slowed walking, delayed growth in young animals, etc.). As the disease progresses, cachexia, dyspnea (respiratory form), bilateral mammary hardening (mammary form of the disease), paralysis (neurological form) and lameness (articular form) develop.
The lesions are in turn characterized by the proliferation of macrophages and lymphocytes in the tissues, thus inducing alterations in tissue architecture and function.
Fig. 2: MV presents mammary, articular, respiratory and neurological variants.
- Airborne transmission (Pflüger's droplets): this form of transmission is intensified in situations of close contact among animals for prolonged periods of time (stables).
- Milk transmission: young animals become infected from the colostrum and milk.
- Through needles used for vaccination, etc. Although this route has been proposed, blood contains monocytes rather than macrophages; consequently, it is not considered to be a significant mechanism of transmission.
Fig. 3: Special attention should be given to the risk of airborne transmission.
A distinction must be made here between the diagnosis of the actual disease and the diagnosis of infection. Almost all animals respond to the virus by producing antibodies that are in turn detected by different laboratory techniques. However, only a part of these animals go on to develop the disease with symptoms and lesions.
At present, the diagnosis of MV and CAE is based on serological testing — mainly immune diffusion in agar gel, which detects the presence of antibodies against the virus.
As regards the incidence of infection, 80% of all goats in the western world are thought to be infected, while in developing countries this figure drops to only 10%. The reason for this seems to be the habit of feeding the young animals with mixed milk from the tank. On the other hand, the incidence of MV in Spain (specifically, in the Ebro valley) reaches 97% of all herds, and 47% of all animals.
Thus, infection is very widespread, though the frequency of the actual disease is very low, and relatively few animals become ill.
The lesions are characterized by the proliferation of macrophages and lymphocytes in the tissues, thus inducing alterations in tissue architecture and function. In addition to this primary disorder, it is important to take into account that the lentiviruses facilitate the appearance of secondary infections. In fact, we are encountering many cases of pasteurellosis (hemorrhagic septicemia) in farms with a high incidence of MV. These infections have been associated with a loss of T helper lymphocytes, with the consequent absence of an adequate immune response.
The only possible prophylactic measure is to create new herds with animals that are entirely seronegative. Of course, individuals of doubtful origin should not be introduced to the healthy herd. In this sense, it should be remembered that seronegative status in a given animal is only sufficient guarantee of health if the entire herd of origin is free from infection.
- Healthy herds should be created from non-infected young animals. To this effect, it is advisable to use colostrum and cow milks, a practice that could be particularly interesting in milk producing herds, considering the high value of sheep milk. Colostrum or mixed ovine or caprine milk should be avoided. The young animals should of course be separated immediately after birth. This practice is also very useful if Mycoplasmas are present on the farm.
- The farm should be adequately ventilated, separating the presumed sick herd from the healthy animals.
- A serological follow-up should be made to study the progress obtained in the herd. In any case, antibody detection is rather subjective, and the reading of results is not the same in all laboratories. It should be remembered that the definition of a healthy herd requires all its constituting animals to be negative.
- Seropositive animals should be sacrificed. However, considering the current prevalence of infection, this practice is clearly not feasible.
BREEDING OF NON-INFECTED ANIMALS
The proposed methodology can be used in ovine and caprine cattle to eradicate problems associated with lentiviruses and Mycoplasmas. In the latter case, the bovine farm from which the milk is obtained must be free of Mycoplasmas (prior trimestrial analysis of the milk tank).
- Immediately after birth, the newborn animals should be moved to another area.
- For the first 24 hours, the newborn animals should be fed bovine colostrum (200-400 ml/animal/day). For preparation purposes, it is advisable to freeze store the colostrum (-20ºC) in 250-500 ml containers, allowing it to thaw at room temperature. The amount required for the entire herd should be freeze stored. The males and females not destined for growth do not require such measures, provided they are kept separated from the other animals.
- The young animals should be grouped in batches of no more than 10-15 individuals, with access to milk ad libitum. If this procedure is not carried out correctly, many diarrhea problems may result. If you are inexperienced with these systems, an advisable approach is to initially try with small batches. One teat should be provided for every two animals, supplying hay and concentrate after day 14.
- Weaning after 6 weeks, with an abrupt change from milk to water.
- These newborn animals should be separated from the rest of the herd by a physical space of at least two meters.
- Of course, care must be taken to prevent newborn animals from suckling upon sheep.
- After six months, periodic examinations of all animals are required, sacrificing all seropositive individuals.
- It should be remembered that some males must also be preserved.
- Before starting these protocols, it should be taken into account that the task is hard, and that it must be followed for at least 3-4 years. For this reason, and at least under certain circumstances, a good alternative may be to replace the entire herd with another known to be free of such processes.
In herds in Zaragoza, replacements have been made from seronegative sheep. This simple practice has allowed very substantial reductions in percentage seropositivity, particularly among younger animals.
This working option is simple and very adequate. However, before proceeding, it should be taken into account that the protocol requires yearly sampling of the entire herd (with the exception of those animals that already yielded positive tests in previous years), and all individuals must be duly branded.
NEW ZEALAND SCHEME FOR CERTIFYING HERDS AS CAE-FREE
In New Zealand an ELISA test is used instead of immune diffusion to test for antibodies. Moreover, in that country it is taken into account that an infected animal may take several months in presenting antibodies. For this reason those farmers who voluntarily enroll in this scheme must sample their animals at least twice the first year, and then once more on a yearly basis.
In order to be included in the official registry of certified herds, the farmer is required to sacrifice all seropositive animals (or sell them for sacrifice), after which the entire herd must be retested at 6-12 months. In order to retain certification, the entire herd must be retested and of course be found to be 100% negative.
In Spain, the high prevalence of the infection (at least in the case of MV) and the high cost of the immune diffusion test make it difficult to apply these protocols individually. However, in the case of agalactia, it may indeed be useful to detect the Mycoplasma-free herds by means of a prevalence study based on the milk tank.