A number of routes of transmission of Map infection have been proposed. The relative effectiveness of each route can vary with age and management practices.

The primary route of Map transmission in all species is thought to be fecal-oral (Clarke, 1997; Stehman, 1996). Excretion (shedding) of variable numbers of Map in the feces of most affected animal species has been documented (Clarke, 1997; Chiodini et al., 1984; Stehman, 1996; Sweeney, 1996), as has the relative ease of experimental oral transmission in young cattle and sheep (Clarke, 1997). Age-related resistance has been clearly demonstrated only in cattle, but young animals are assumed to be most susceptible in all species (Stehman, 1996). Fecal contamination of the udder or calving environment is therefore thought to be the primary risk factor for neonatal infection. This conclusion is supported by epidemiologic evidence that removal of newborn calves from dams at birth (before suckling) was associated with lower within-herd prevalence of Map infection (Collins, 1994).

The possibility of prenatal transmission in cattle has long been suspected: Map has been recovered from bovine testes (Tunkl and Aleraj, 1965), semen (Larsen and Kopecky, 1970; Larsen et al., 1981; Lukashaw et al., 1962; Tunkl and Aleraj, 1965), bulbourethral gland (Larsen and Kopecky, 1970), prostate and seminal vesicles (Larsen and Kopecky, 1970; Larsen et al., 1981), uterus or uterine flushes (Goudswaard, 1970; Kopecky et al., 1967; Lawrence, 1956; Pearson and McCelland, 1955; Rohde and Shulaw, 1990), and fetal tissue (Doyle, 1958; Lawrence, 1956; Muhammed and Eliasson, 1979; Pearson and McCelland, 1955; Seitz et al., 1989; Sweeney et al., 1992c). The estimated risk of fetal infection from culture-positive dams is reported to be 26.4 percent with a 95 percent confidence interval (CI) of 11.3–40.7 percent (Seitz et al., 1989). In another study, only 8.6 percent of fetuses from asymptomatic infected cows were Map-culture positive (compared with 20–40 percent reported for symptomatic cows), suggesting that risk of fetal infection in “light shedders” (less than 3000 colony-forming-units per gram [cfu/g] of feces) is low (Sweeney et al., 1992a). Despite evidence of fetal infections, the prevalence of prenatal modes of transmission is unknown.

In dairy cows, Map has been isolated from mammary gland (Doyle, 1954; Goudswaard, 1970; Taylor et al., 1981), and up to 35 percent of infected cows with clinical signs shed the organism in milk (Hole, 1958; Goudswaard, 1970; Taylor et al., 1981). In more recent studies, 19 percent of asymptomatic

Front Matter (R1-R14)

Executive Summary (1-12)

1. Introduction (13-15)

2. Johne's Disease in Domesticated and Wild Animals (16-44)

3. Diagnostics (45-65)

4. Control Principles and Programs (66-98)

5. Economic Implications of Johne's Disease (99-103)

6. Johne's Disease and Crohn's Disease (104-120)

7. Conclusions and Recommendations (121-132)

References (133-174)

Appendix A: Interpretation of Diagnostic Results (175-178)

Appendix B: USAHA Voluntary Johne's Disease Herd Status Program for Cattle (179-193)

Appendix C: USDA/APHIS Draft Johne's Disease Control Program (194-220)

About the Authors (221-225)

Board on Agriculture and Natural Resources Publications (226-229)