Background
Colostrum‐derived antibodies are crucial for the protection of newborn lambs from infectious diseases. Several colostrum replacer products that contain bovine antibodies are on the market. We investigated the absorption and persistence of bovine antibodies from a powdered colostrum replacer in newborn lambs.
Methods
We tested a lamb colostrum replacer containing bovine serum in lambs that were separated from their dams at birth. Immunoglobulin G (IgG) uptake was analysed by ELISA, and the persistence of antigen‐specific antibodies was analysed by parainfluenza 3 virus (PI‐3) neutralisation assay.
Results
Serum antibody ELISA performed on days 1 and 14 revealed IgG levels of 17.9 ± 2.8 and 27.5 ± 2.5 mg/ml, respectively. PI‐3 antibodies derived from the colostrum replacer were present for 86.3 ± 10.6 days.
Conclusions
Antibodies derived from bovine serum protein delivered to lambs via a commercial colostrum replacer are readily absorbed and persist for months, suggesting that these products may offer adequate protection.
Mycoplasma ovipneumoniae (M. ovipneumoniae) is a respiratory pathogen associated with the development of mild to moderate respiratory disease in domestic lambs and severe pneumonia outbreaks in wild ruminants such as bighorn sheep. However, whether M. ovipneumoniae by itself causes clinical respiratory disease in domestic sheep in the absence of secondary bacterial pathogens is still a matter of debate. The goal of our study was to better understand the role of M. ovipneumoniae as a respiratory pathogen in domestic sheep and to explore potential antibiotic treatment approaches. Therefore, we inoculated four-month-old, specific-pathogen-free lambs with field isolates of M. ovipneumoniae and monitored the lambs for eight weeks for colonization with the bacteria, M. ovipneumoniae-specific antibodies, clinical symptoms, and cellular and molecular correlates of lung inflammation. After eight weeks, lambs were treated with the macrolide antibiotic gamithromycin and observed for an additional four weeks. Stable colonization of the upper respiratory tract with M. ovipneumoniae was established in all four M. ovipneumoniae-inoculated, but in none of the four mock-infected lambs. All M. ovipneumoniae-infected lambs developed a robust antibody response to M. ovipneumoniae within 2 weeks. However, we did not observe significant clinical symptoms or evidence of lung damage or inflammation in any of the infected lambs. Interestingly, treatment with gamithromycin failed to reduce M. ovipneumoniae colonization. These observations indicate that, in the absence of co-factors, M. ovipneumoniae causes asymptomatic colonization of the upper respiratory tract of that is resistant to clearance by the host immune response as well as by gamithromycin treatment in domestic lambs.
To understand protective immune responses against the onset of Group A
Streptococcus
respiratory infection, we investigated whether MyD88 KO mice were susceptible to acute infection through transmission. After commingling with mice that had intranasal GAS inoculation, MyD88
-/-
recipient mice had increased GAS loads in the nasal cavity and throat that reached a mean throat colonization of 6.3 x 10
6
cfu/swab and mean GAS load of 5.2 x 10
8
cfu in the nasal cavity on day 7. Beyond day 7, MyD88
-/-
recipient mice became moribund, with mean 1.6 x 10
7
cfu/swab and 2.5 x 10
9
cfu GAS in the throat and nasal cavity, respectively. Systemic GAS infection occurred a couple of days after the upper respiratory infection. GAS infects the lip, gingival sulcus of the incisor teeth, the lamina propria of the turbinate but not the nasal cavity and nasopharyngeal tract epithelia, and C57BL/6J recipient mice had no or low levels of GAS in the nasal cavity and throat. Direct nasal GAS inoculation of MyD88
-/-
mice caused GAS infection mainly in the lamina propria of the turbinate. In contrast, C57BL/6J mice with GAS inoculation had GAS bacteria in the nasal cavity but not in the lamina propria of the turbinates. Thus, MyD88
-/-
mice are highly susceptible to acute and lethal GAS infection through transmission, and MyD88 signaling is critical for protection of the respiratory tract lamina propria but not nasal and nasopharyngeal epithelia against GAS infection.
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