The aim of the present study was to infer phenotypic responses and genetic parameters of the F1 calf diseases diarrhoea (DIAR) and pneumonia (PNEU) in dependency of the prenatal maternal health status (PMHS) of the dam and of the herd-calving year. The PMHS considered diagnoses for the cow disease mastitis (MAST) and claw disorders (CD) during gestation of F0 dams. Furthermore, 305-d milk production traits of F1 offspring from either healthy or diseased dam groups were compared. The study comprised 20,045 female calves (F1 = generation 1) and their corresponding dams (F0 = parental generation 0), kept in 41 large-scale herds. All F1 calves were from their dams' 2nd parity, implying that all dam (maternal) diseases were recorded during the first lactation and dry period of the dams. The F1 calves were phenotyped for DIAR up to 30 days post-partum, and for PNEU up to 180 days of age. At least one entry for the respective disease implied a score = 1 = sick, otherwise, a score = 0 = healthy, was assigned. Production records of the 10,129 F1 cows comprised 305-d records in first lactation for milk yield (MY), protein yield (PY) and fat yield (FY). Linear and generalised linear mixed models were applied to infer phenotypic responses of F1 traits in dependency of the PMHS for CD and MAST. A diagnosis for MAST or CD in F0 cows during gestation was significantly (p ≤ 0.05) associated with an increased prevalence for DIAR and PNEU, with pairwise differences of least-squares-means between calves from healthy and diseased cow groups up to 3.61%. The effects of PMHS on 305-d production traits in offspring were non-significant (p > 0.05). In bivariate genetic analyses, DIAR and PNEU were defined as different traits according to the PMHS, i.e., DIAR-MASThealthy and DIAR-MASTdiseased, DIAR-CDhealthy and DIAR-CDdiseased, PNEU-MASThealthy and PNEU-MASTdiseased, and PNEU-CDhealthy and PNEU-CDdiseased. The direct heritabilities for DIAR and PNEU were quite similar in the healthy and respective diseased dam group. Slightly larger direct heritabilities in the diseased dam groups were due to increased genetic variances. Maternal heritabilities were quite stable and smaller than the direct heritabilities. In random regression models, genetic parameters for DIAR and PNEU were estimated along the continuous herd-calving-year prevalence scale, considering a prevalence for MAST and CD (based on the 20,045 dam records plus 16,193 herd contemporary records) in the range from 0% to 30%. Direct heritabilities for PNEU were quite stable along the herd-calving-year gradient for MAST and CD. For DIAR, we observed stronger estimate fluctuations, especially increasing direct heritabilities in dependency of the herd-calving-year prevalence for MAST from 0.13 (at a MAST prevalence of 0%) to 0.30 (at a MAST prevalence of 30%). Consequently, obvious genotype x herd-calving-year PMHS interactions were observed for DIAR on the prenatal MAST scale, with a minimal correlation of 0.48 between direct genetic effects at 0% MAST prevalence and at 30% MAST prevalence. The correlations between direct genetic and maternal genetic effects were antagonistic at all herd-calving-year prevalence levels, displaying strongest fluctuations for "DIAR-MAST." The genotype x herd-calving-year PMHS interactions for DIAR suggest consideration of specific sires according to the herd health status for CD and for MAST.