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Fig. 4 in Nematode-coccidia parasite co-infections in African buffalo: Epidemiology and associations with host condition and pregnancy

Fig. 4. Predicted mean and standard error body condition scores show associations with infection presence and season, with co-infected buffalo in much lower condition in the early wet season (Table S2). Coccidia infection status is represented with C– and C+; nematode infection status is represented with N– and N+.

Fig. 5 in Nematode-coccidia parasite co-infections in African buffalo: Epidemiology and associations with host condition and pregnancy

Fig. 5. Season and co-infection differences in nematode aggregation. (a) Aggregation patterns in calves (b) and non-calves. (c) In non-calves, the distribution of nematode parasites in the late wet season shows that k is not significantly different in coccidia positive vs. negative buffalo. (d) In the early wet season coccidia positive buffalo have a truncated distribution, resulting in significantly reduced aggregation. Arrows indicate nematode intensity values in the tail of the distribution of coccidia negative buffalo. Coccidia infection status is represented with C– and C+.

Fig. 3 in Nematode-coccidia parasite co-infections in African buffalo: Epidemiology and associations with host condition and pregnancy

Fig. 3. Patterns of parasite egg/oocyst counts with co-infection for (a) nematodes and (b) coccidia. (c), the mean nematode intensity in calves is higher in early wet season than in the late wet season independent of co-infection with coccidia. (d) Co-infection with coccidia alters the seasonal patterns of nematode intensity in non-calf buffalo (>1 year, juvenile through senescent). Calf vs. non-calf division is based on model paramters (Table 1).

Fig. 2 in Nematode-coccidia parasite co-infections in African buffalo: Epidemiology and associations with host condition and pregnancy

Fig. 2. Age specific patterns of parasite prevalence with co-infection. (a) Prevalence of nematodes is higher in buffalo co-infected with coccidia (C+) compared to coccidia negative buffalo (C–) in all age categories (N = 33, 318, 166, 272, 162 for calf, juvenile, subadult, adult and senescent C– buffalo; N = 58, 237, 55, 54, 20 for C+ buffalo). (b) Prevalence of coccidia is higher in buffalo co-infected with nematodes (N+) compared to nematode negative buffalo (N–) in calf, juvenile, subadult, and senescent buffalo but not adult buffalo (N = 13, 107, 92, 144, 56 for calf, juvenile, subadult, adult and senescent N– buffalo; N = 38, 448, 129, 208, 100 for N+ buffalo).

Fig. 1 in Nematode-coccidia parasite co-infections in African buffalo: Epidemiology and associations with host condition and pregnancy

Fig. 1. Age, sex and seasonal patterns of infection. Both parasites had the highest (a) prevalence (sample size for calf, juvenile, subadult, adult, and senescent respectively: N = 91, 555, 221, 326, 182) and (b) mean intensity in calves and juveniles (nematode N = 78, 448, 129, 208, 100; coccidia N = 58, 237, 55, 60, 14). (c) Males had lower estimated nematode prevalence and (d) higher estimated coccidia intensity compared to female buffalo. (e) The estimated nematode prevalence, coccidia prevalence, and (f) mean coccidia intensity were all increased in the early wet season compared to the late wet season. ‡Indicates significant differences at p <0.05.

Fig. 4. Maximum Likelihood phylogenetic tree generated using N in The African buffalo parasite Theileria. sp. (buffalo) can infect and immortalize cattle leukocytes and encodes divergent orthologues of Theileria parva antigen genes

Fig. 4. Maximum Likelihood phylogenetic tree generated using N-terminal sequences of T. sp. (buffalo) and T. parva PIM antigen genes. Maximum composite likelihood trees were constructed using 1000 bootstrap replicates as implemented in MEGA5; the optimal nucleotide substitution model was identified using data monkey. The tree constructed with RAxML (Stamatakis et al., 2014) using a GTR/G/I model with 100 bootstrap iterations.

Fig. 5 in The African buffalo parasite Theileria. sp. (buffalo) can infect and immortalize cattle leukocytes and encodes divergent orthologues of Theileria parva antigen genes

Fig. 5. Maximum Likelihood Phylogenetic trees illustrating the genetic relationships of T. parva CD8 T target antigen gene orthologues from T. sp. (buffalo). Panel (A) Tp6; Panel B Tp7: Panel C Tp8. Sequences were aligned and used to construct a maximum likelihood tree, at which the nodes were confirmed using 1000 bootstrap replications. The bootstrap values indicating the degree of support for each node are shown and also the GenBank accession numbers of the sequences. For Tp6, the tree was rooted using the prohibitin gene sequences present in Babesia bovis (XM001609045) and Theileria orientalis (AB161472). For Tp7, the tree was rooted using the putative Heat shock protein 90 gene sequences from Toxoplasma gondii (AY344115), Babesia bovis (AK442026) and Theileria annulata (XM_947380). For Tp8, the tree was rooted using an orthologue of Tp8 found in Theileria equi (CP001669).

Fig. 3 in The African buffalo parasite Theileria. sp. (buffalo) can infect and immortalize cattle leukocytes and encodes divergent orthologues of Theileria parva antigen genes

Fig. 3. PCR amplification of genes encoding Theileria parva antigens from Marula schizont-infected leukocyte cultures. Panel A, p104 primers; Panel B PIM, primers; Panel C p67 primers. The order of the schizont-infected lymphocyte samples is (1) N6; (2). N13; (3). N18; (4). N20; (5). N33; (6). N36; (7). N38; (8). N43; (9). N50; (10). N55; (11). N69; (12). N76; (13). N77, (14). N79; (15). N86, (16). N88; (17). N99; (18). N100; (19). N102; (20). N103; (21). N106; (22). N107.

Fig. 2 in The African buffalo parasite Theileria. sp. (buffalo) can infect and immortalize cattle leukocytes and encodes divergent orthologues of Theileria parva antigen genes

Fig. 2. Results of a semi-nested PCR assay used to amplify 18S ribosomal subunit DNA using primers specific for T. parva and T. sp. (buffalo). Samples are as follows: 1)N13 2)N18 3) N20 4)N33 5)N36 6) N43 7)N50 8)N55 9) N69 10)N76 11) N79 12) N86 13) N88 14) N99 15)N100 16) N102 17) N103 18)N107 19—21) T. parva clones 22—24) T. sp. (buffalo) clones (documented in Table 2).

Fig. 1 in The African buffalo parasite Theileria. sp. (buffalo) can infect and immortalize cattle leukocytes and encodes divergent orthologues of Theileria parva antigen genes

Fig. 1. Reverse line blot analysis of schizont cultures containing parasites isolated from Marula farm. The following species-specific oligonucleotide probes were used (a) T. annulata, (b) T. parva, (c) T. mutans, (d) T. velifera, (e) T. taurotragi, (f) T. buffeli, (g) T. sp. (buffalo). (h) B. bigemina, (i) B. bovis. The order of the experimental samples hybridized is DNA from cell culture isolates in lanes 1—22 was lane 1; (1) N6, (2) N13, (3) N18, (4) N20, (5) N33, (6) N36, (7) N38 (8) N43, (9) N50 (10) N55, (11) N69, (12) N76, (13) N77, (14) N79, (15) N88, (16) N99, (17) N100 (18) N103, (19) N106, (20) N107, (21) N86, (22) N102 and DNA extracted from whole cattle blood (23) N106 (24) N69 (25) N86.

opencc-by-4.0Aug 2023View details →

Fig. 2 in Epidemiology of Anaplasma marginale and Anaplasma centrale infections in African buffalo (Syncerus caffer) from Kruger National Park, South Africa

Fig. 2. Individual value plots showing the distribution of results for intensity of infection (log-transformed number of copies/reaction) with Anaplasma marginale (a) and Anaplasma centrale (b), using a real-time qPCR from a managed African buffalo (Syncerus caffer) herd from Kruger National Park, South Africa. Error bars represent one standard error, numbers at the top of figure represent sample size.

opencc-by-4.0Aug 2023View details →

Fig. 1 in Epidemiology of Anaplasma marginale and Anaplasma centrale infections in African buffalo (Syncerus caffer) from Kruger National Park, South Africa

Fig. 1. The proportion of animals infected with Anaplasma spp. from a managed African buffalo (Syncerus caffer) herd from Kruger National Park, South Africa. a) The mean prevalence of animals with A. marginale single infection, A. centrale single infection, or co-infections with each other over four age groups: calves (0–1 years old), sub-adults (1–5.5 years old), adults (5.5–15 years) and geriatrics (15 years plus); b) the mean prevalence of new infections with A. marginale or A. centrale for each capture event over the two-and-a-half-year study period. Numbers at the top of figure represent sample size.

opencc-by-4.0Aug 2023View details →

Fig. 3 in Epidemiology of Anaplasma marginale and Anaplasma centrale infections in African buffalo (Syncerus caffer) from Kruger National Park, South Africa

Fig. 3. Patterns of infection with Anaplasma spp. based on age and sex for a managed African buffalo (Syncerus caffer) herd from Kruger National Park, South Africa. a) The infection intensity (log-transformed number of copies/reaction) of A. marginale and A. centrale based on age (years); b) overall proportion of animals infected with A. marginale or A. centrale based on sex; c) infection intensity (log-transformed number of copies/reaction) results for A. marginale or A. centrale based on sex. * indicates statistical significance (p <0.05). Error bars are standard error.

opencc-zeroAug 2020View details →

Data from: A natural gene drive system influences bovine tuberculosis susceptibility in African buffalo: possible implications for disease management

Bovine tuberculosis (BTB) is endemic to the African buffalo (Syncerus caffer) of Hluhluwe-iMfolozi Park (HiP) and Kruger National Park, South Africa. In HiP, the disease has been actively managed since 1999 through a test-and-cull procedure targeting BTB-positive buffalo. Prior studies in Kruger showed associations between microsatellite alleles, BTB and body condition. A sex chromosomal meiotic drive, a form of natural gene drive, was hypothesized to be ultimately responsible. These associations indicate high-frequency occurrence of two types of male-deleterious alleles (or multiple-allele haplotypes). One type negatively affects body condition and BTB resistance in both sexes. The other type has sexually antagonistic effects: negative in males but positive in females. Here, we investigate whether a similar gene drive system is present in HiP buffalo, using 17 autosomal microsatellites and microsatellite-derived Y-chromosomal haplotypes from 401 individuals, culled in 2002-2004. We show that the association between autosomal microsatellite alleles and BTB susceptibility detected in Kruger, is also present in HiP. Further, Y-haplotype frequency dynamics indicated that a sex chromosomal meiotic drive also occurred in HiP. BTB was associated with negative selection of male-deleterious alleles in HiP, unlike positive selection in Kruger. Birth sex ratios were female-biased. We attribute negative selection and female-biased sex ratios in HiP to the absence of a Y-chromosomal sex-ratio distorter. This distorter has been hypothesized to contribute to positive selection of male-deleterious alleles and male-biased birth sex ratios in Kruger. As previously shown in Kruger, microsatellite alleles were only associated with male-deleterious effects in individuals born after wet pre-birth years; a phenomenon attributed to epigenetic modification. We identified two additional allele types: male-specific deleterious and beneficial alleles, with no discernible effect on females. Finally, we discuss how our findings may be used for breeding disease-free buffalo and implementing BTB test-and-cull programs.

opencc-zeroDec 2017View details →

Data from: Genetic responsiveness of African buffalo to environmental stressors: a role for epigenetics in balancing autosomal and sex chromosome interactions?

In the African buffalo (Syncerus caffer) population of the Kruger National Park (South Africa) a primary sex-ratio distorter and a primary sex-ratio suppressor have been shown to occur on the Y chromosome. A subsequent autosomal microsatellite study indicated that two types of deleterious alleles with a negative effect on male body condition, but a positive effect on relative fitness when averaged across sexes and generations, occur genome-wide and at high frequencies in the same population. One type negatively affects body condition of both sexes, while the other acts antagonistically: it negatively affects male but positively affects female body condition. Here we show that high frequencies of male-deleterious alleles are attributable to Y-chromosomal distorter-suppressor pair activity and that these alleles are suppressed in individuals born after three dry pre-birth years, likely through epigenetic modification. Epigenetic suppression was indicated by statistical interactions between pre-birth rainfall, a proxy for parental body condition, and the phenotypic effect of homozygosity/heterozygosity status of microsatellites linked to male-deleterious alleles, while a role for the Y-chromosomal distorter-suppressor pair was indicated by between-sex genetic differences among pre-dispersal calves. We argue that suppression of male-deleterious alleles results in negative frequency-dependent selection of the Y distorter and suppressor; a prerequisite for a stable polymorphism of the Y distorter-suppressor pair. The Y distorter seems to be responsible for positive selection of male-deleterious alleles during resource-rich periods and the Y suppressor for positive selection of these alleles during resource-poor periods. Male-deleterious alleles were also associated with susceptibility to bovine tuberculosis, indicating that Kruger buffalo are sensitive to stressors such as diseases and droughts. We anticipate that future genetic studies on African buffalo will provide important new insights into gene fitness and epigenetic modification in the context of sex-ratio distortion and infectious disease dynamics.

opencc-zeroDec 2019View details →

Microsatellite data from various African buffalo (Syncerus caffer) populations throughout Africa

1280 African buffalo (Syncerus caffer) samples genotyped with up to 19 microsatellites. 1275 samples are from East (12 populations) and southern Africa (4 populations). 5 samples are from central Africa (2 populations).

opencc-zeroDec 2022View details →

African buffalo helminth β-diversity

Concepts of β-diversity originally developed for use in free-living communities have been widely applied to parasite communities to gain insight into how infection risk changes with local conditions by comparing parasite communities across abiotic and biotic gradients. Factors shaping β-diversity in communities of immature parasites, such as larvae, are largely unknown. This is a key knowledge gap as larvae are frequently the infective life stage and understanding variation in these larval communities is thus key for disease prevention. Our goal was to uncover links between β-diversity of parasite communities at different life stages; therefore, we used gastrointestinal nematodes infecting African buffalo in Kruger National Park, South Africa to investigate within-host and extra-host drivers of adult and larval parasite community similarity.

publicDec 2022View details →

African buffalo helminth β-diversity

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publicAug 2020View details →

Data from: A natural gene drive system influences bovine tuberculosis susceptibility in African buffalo: possible implications for disease management

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