This is the first study investigating associations between C. burnetii
antibody levels and perinatal death in cattle herds. The association was assessed as concurrent measures, as outcomes occurring later that the BMT measure, and as the "outcome" occurring prior to the BTM measure. The rationale behind this strategy was that the pathogenesis and time relationship between BTM S/P levels and stillbirth and perinatal calf mortality is still not known, i.e. does BTM S/P raise before or after or concurrent with stillbirth and perinatal death. The risk of perinatal death was two-fold higher in herds with very high levels of BTM antibodies compared to those with no antibodies (Figure ), but only when the antibody level was high 8 to 9 months after parturition. A more persistent effect could have been expected, because all our INCREASE analyses were non-significant and the between sample correlation was very high. Although not statistically significant, increases in BTM antibody levels seemed to be associated with increased risk of perinatal death (data not shown). This suggests that the statistical power was insufficient rather than indicating a lack of effect. But also that effects of C. burnetii
infection on perinatal deaths is limited and associated with some variation similar to human coxiellosis [8
] if present at all. However, BTM analyses are herd samples and the association between individual animal antibody levels and calving results were not included. Such analysis may reveal associations.
The three modelled slopes representing the three parity groups (Figure ) are comparable, but baseline values (S/P ratio = 0) differ with parity = 1 having the highest baseline risk. The higher baseline risk in the parity = 1 group reflects a higher risk of dystocia in 1st
parity cows and supports the validity of our model. The reason that parity > 2 baseline has higher risk than parity = 2 is that the parity > 2 group includes the oldest cows with high risk of dystocia and associated risk of perinatal death [10
The study depended on specific antibody recordings in BTM. C. burnetii
antibodies can be excreted in milk, but it is uncertain if all infected animals excrete antibodies and if so, at which level. C. burnetii
phase II antibodies have been associated with occurrence of C. burnetii
in placentas, whereas phase I antibodies have not [11
]. Moreover, sero-negative animals can harbour C. burnetii
in the placenta [7
]. The finding of an association between herd level antibodies occurring 8 to 9 month after calving questions the pathogenesis. The correlation between infection and antibody excretion is still poorly understood. A possible explanation may be that detectable antibodies are only present in the lactation following the calving where infection occurred, whereas the calving coinciding with infection results in higher perinatal mortality but with delayed production of antibodies. However, this hypothesis is at present highly speculative. Although not significant it should be mentioned that results in Table show a borderline significant association (p = 0.07) between perinatal death and increased antibody level 7 months later. Presence of antibodies may just indicate past exposure to C. burnetii
in the herd and therefore not the actual bacterial load at actual pregnancy and parturition. The specific state of infection in the herd or in individual animals could thus not be assessed while using antibodies in BTM. Furthermore, as not all animals in a herd are infected, the BTM level would be affected by the within-herd prevalence and by the individual milk yield, since BTM antibody level is an aggregated score for the entire herd. A recent German study suggested that among the majority of infected herds, the within-herd prevalences were below 10% [11
]. This indicates that many herds have antibodies in BTM, but only few animals contribute to the status. Thus, results based on BTM measurements might be misinterpreted because antibodies in the BTM most likely are produced by a few animals in the herd, and perinatal mortality has other causes than coxiellosis as well. BTM data most likely underestimate the effect or leave it unnoticed. Therefore, to elucidate the pathogenesis, it would be necessary to test individual animals for further knowledge about the influence of infection status on stillbirth and perinatal death.