Immunotherapy IT ; and skin testing ST ; . J Allergy Clin Immunol 1987; 79: 660-77. Bousquet J, Michel FB. Safety considerations in assessing the role of immunotherapy in allergic disorders. Drug Saf 1994; 10: 5-17. Hejjaoui A, Dhivert H, Michel FB, Bousquet J. Immunotherapy with a standardized Dermatophagoides pteronyssinus extract. IV. Systemic reactions according to the immunotherapy schedule. J Allergy Clin Immunol 1990; 85: 473-9. Hejjaoui A, Ferrando R, Dhivert H, Michel FB, Bousquet J. Systemic reactions occurring during immunotherapy with standardized pollen extracts. J Allergy Clin Immunol 1992; 89: 925-33. Vourdas D, Syrigou E, Potamianou P, Carat F, Batard T, Andre C, et al. Double-blind, placebo-controlled evaluation of sublingual immunotherapy with standardized olive pollen extract in pediatric patients with allergic rhinoconjunctivitis and mild asthma due to olive pollen sensitization. Allergy 1998; 53: 662-72. Di Rienzo V, Pagani A, Parmiani S, Passalacqua G, Canonica GW. Post-marketing surveillance study on the safety of sublingual immunotherapy in pediatric patients. Allergy 1999; 54: 1110-3. Grammer LC, Shaughnessy MA, Suszko IM, Shaughnessy JJ, Patterson R. Persistence of efficacy after a brief course of polymerized ragweed allergen: a controlled study. J Allergy Clin Immunol 1984; 73: 484-9. Mosbech H, Osterballe O. Does the effect of immunotherapy last after termination of treatment? Follow-up study in patients with grass pollen rhinitis. Allergy 1988; 43: 523-9. Des-Roches A, paradis L, Knani J, Hejjaoui A, Dhivert H, Chanez P, et al. Immunotherapy with a standardized Dermatophagoides pteronyssinus extract. V- Duration of efficacy of immunotherapy after its cessation. Allergy 1996; 51: 430-3. Naclerio RM, Proud D, Moylan B, Balcer S, Freidhoff L, KageySobotka A, et al. A double-blind study of the discontinuation of ragweed immunotherapy. J Allergy Clin Immunol 1997; 100: 293-300. Durham SR, Walker SM, Varga EM, Jacobson MR, O'Brien F, Noble W, et al. Long-term clinical efficacy of grass-pollen immunotherapy . N Engl J Med 1999; 341: 468-75. Filiaci F, Zambetti G, Romeo R, Ciofalo A, Luce M, Germano F. Nonspecific hyperreactivity before and after nasal specific immunotherapy. Allergol Immunopathol 1999; 27: 24-8. Bousquet J, Hejjaoui A, Clauzel AM, Guerin B, Dhivert H, SkassaBrociek W, et al. Specific immunotherapy with a standardized Dermatophagoides pteronyssinus extract. II. Prediction of efficacy of immunotherapy. J Allergy Clin Immunol 1988; 82: 971-7. Des-Roches A, Paradis L, Mnardo J-L, Bouges S, Daurs J-P, Bousquet J. Immunotherapy with a standardized Dermatophagoides pteronyssinus extract. VI. Specific immunotherapy prevents the onset of new sensitizations in children. J Allergy Clin Immunol 1997; 99: 450-3. Johnstone DE. Immunotherapy in children: past, present, and future. Part I ; . Ann Allergy 1981; 46: 1-7. Jacobsen L. The benefit of specific allergy treatment. In: Basomba A, Sastre J, editors. Proceedings of the XVI European Congress of Allergology and Clinical Immunology. Bologna, Italy: Monduzzi Editore; 1995. p. 745-50. Jacobsen L, Dreborg S, Mller C, Valovirta E, Wahn U, Niggemann B, et al. Immunotherapy as a preventive treatment. J Allergy Clin Immunol 1996; 97: 232 abstract ; . Norman P. Is there a role for immunotherapy in the treatment of asthma? Yes. J Respir Crit Care Med 1996; 154: 1225-8. Barnes P. Is there a role for immunotherapy in the treatment of asthma? No. J Respir Crit Care Med 1996; 154: 1227-8. Barnes PJ. Therapeutic strategies for allergic diseases. Nature 1999; 402 6760 Suppl ; : B31-8. Presta LG, Lahr SJ, Shields RL, Porter JP, Gorman CM, Fendly BM, et al. Humanization of an antibody directed against IgE. J Immunol 1993; 151: 2623-32. Saban R, Haak-Frendscho M, Zine M, Ridgway J, Gorman C, Presta LG, et al. Human FcERI-IgG and humanized anti-IgE monoclonal antibody MaE11 block passive sensitization of human and rhesus monkey lung. J Allergy Clin Immunol 1994; 94: 836-43. Winter G, Harris WJ. Humanized antibodies. Immunol Today 1993; 14: 243-6. MacGlashan D, Jr., Bochner BS, Adelman DC, Jardieu PM, Togias A, for instance, paxil interaction. 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Fda paxil recall Infection of the dam as with Mandy ; , but after many months. The alpacas at Farm C aborted in April 2003, and the stillbirths at Farm D were also in 2003. VF likely had her acute infection with BVD in August or September of 2002 at one of those farms, and if the other alpacas were infected at the same time, there was also quite a delay before they aborted or had the stillbirths. Up to what point in gestation can infection with BVD produce a PI cria? Can an alpaca be infected with BVD during the crucial phase of gestation and still produce a normal cria? Can BVD cause congenital abnormalities in cria if exposure is later in pregnancy, as it does in cattle? All of my cria that were in later gestation when their moms were exposed to BVD virus turned out normally. Can some PI alpacas stay appearing healthy for an extended length of time? At this point the only clinical information is on Gabriel and MC. Both had very low birth weights; both had large umbilical hernias. Other than unformed stool, Gabriel was fine, had gained weight well, and had had no illnesses at the time of his euthanization. MC did well for the first 6 weeks of his life, and then had pneumonia; his next episode of pneumonia was not until he was 5 months old. Only time and testing will tell just how common BVD is in alpacas. I believe it is much more prevalent than any one has thought. Alpacas certainly have a reputation for being easy aborters and it is not unusual to hear of poor doing cria both of these could be from BVD. The article Communicable Disease Risks to Wildlife from Camelids in British Columbia by Dr. Schwantje and Dr. Stephen, cited in the previous article on BVD, shows 6% of llamas sampled had antibodies to BVD, that camelid owners reported the most common cause of death being neonatal failure to thrive or stillbirths, and that 9% of camelid submissions to the provincial lab had the diagnosis of idiopathic no cause found ; abortion. No one has ever seen a connection between these. There were no pathological findings to suggest BVD in Mandy's aborted fetus or in Gabriel only testing specifically for the virus showed it to be present. It is quite possible that many of the alpaca abortions sent for testing where no cause has been found could be from BVD it has never been considered one of the routine tests. Poor doing cria who died would have autopsy findings in keeping with their final illness such as pneumonia, with no indication that their underlying problem may have been that they were PI. I think it likely that BVD has been around in herds for quite a while, and that it has been spread by unrecognized PI animals. Many females with cria at side go to other farms for breeding; if it was a PI cria it would be infecting all the alpacas at that farm. If there was a PI alpaca on a farm, a female going there for breeding could return carrying a PI fetus. The first BVD cases may have been contracted from cattle, or, considering that a study from Peru showed an 11.5% incidence of antibodies to BVD, some imported alpacas could have been carrying PI fetuses. The experiences at Farm C, with many abortions, are probably the exception. Just having a few abortions, or the experience at Farm D, with a couple of stillbirths, or Farm B, with only one mild illness, may be more typical. The whole concept of persistent infection will be hard for some people to grasp. I expect that many people will not want to know about or deal with this. Alpaca owners have a reputation for being secretive about any illnesses or deaths in heir herd; I doubt that many will broadcast that they have discovered BVD cases in their herd. I also know that some people will not have enough scientific understanding to realize that I do not. 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