Table 1.
Animal Identification, Infection, Treatment and Outcome.
Table 2.
Antibodies used for IHC and Fluorescent Co-Labeling IHC.
Fig 1.
Histologic Lesions in Holstein and Boran cattle.
Representative photomicrographs of H&E stained sections of lymph node medulla in uninfected control and infected Boran (day 12) and Holstein calves, and lung from uninfected control and infected Holstein calves. Note: Severe disruption of vessel walls by mononuclear cells and fibrinoid degeneration (lung and lymph node), and lymphohistiocytic interstitial pneumonia with edema (lung). Scale bar: 200 μm.
Fig 2.
Shown are the results of immunohistochemical labeling of the T. parva antigen, PIM, in the spleen. A. The spleen of the control calf lacks PIM immunoreactivity. B. In a representative infected Holstein calf, there is abundant PIM immunoreactivity within lymphocytes of the red and white pulp. Scale bar: 200 μm.
Fig 3.
Immunohistochemical Labeling of Leukocytes in the Lungs.
Shown are the results of IHC labeling for CD3-like immunoreactivity (CD3-li), CD163-li, IBA-1-li, and IL-17-li in the lung of uninfected control and representative infected Holstein calves. Note: CD3-li, CD163-li, and IL-17-li is significantly increased in the lungs of the infected calf. Furthermore, CD3+, CD163+, IBA-1+ and IL-17+ mononuclear cells are components of vasculitis lesions. Vascular endothelial cells consistently exhibit pronounced IL-17-li in the infected calf, but endothelial IL-17-li is rare in the control calf. Scale bar: 200 μm.
Table 3.
Mean Sectional Area Positive for CD163, IBA-1, and IL-17.
Fig 4.
Dual Fluorescence Labeling of Leukocytes in Lymph Nodes.
Shown are the results of dual fluorescence labeling for IL-17-li (pseudocolored cyan) and either CD3-, IBA-1-, or CD163-li (pseudocolored magenta) in the medulla of a lymph node from a control calf and representative infected calves. Note: IL-17-li was infrequent in the medulla of control calf lymph node but was widespread throughout the medulla of infected calves. Where it occurred within the non-vascular elements, IL-17-li was generally punctate and appeared intracellular. The cell-associated, punctate IL-17-li was considerably weaker in intensity and less dense as compared to the infected calves. In both the infected calves and, where present, in the control calf, intracellular punctate IL-17-li was most frequently co-localized with IBA-1-li cells and CD163-li cells but not with CD3-li cells. Scale bar: 20 μm.
Fig 5.
CD163 and IBA-1 Dual Fluorescence Labeling.
Shown are the results of dual fluorescence labeling for CD163-li (pseudocolored cyan) and IBA-1-li (pseudocolored magenta) in a lymph node cortical follicle and medulla from the control calf and representative infected calves. In both calves, most CD163-li cells were co-labeled by IBA-1-li but not all IBA-li cells were co-labeled with CD163-li. IBA-1-li cells without definitive CD163-li were most frequent in the control calf lymph parafollicular regions. Scale bar: 20 μm.