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SummaryWe studied experimental lagochilascariosis in male and female mice of four strains. The survival ratio and number of larvae recovered varied: B10.A and C57BL/6 mice had the highest number of larvae 90 days after infection and the lowest survival ratio at 345 days of infection. BALB/c mice had an intermediate survival ratio and number of larvae. A/J mice had the lowest number of larvae and the highest survival ratio. Our findings suggest that resistance to Lagochilascaris minor is not linked to the H-2 a region because both susceptible B10.A and resistant A/J mice express the H-2 a haplotype. However, the pattern of mortality and larvae recovered that we observed in C57BL/6 mice, which possess the same genetic background as B10.A, indicates that the background genotype does affect the outcome of lagochilascariosis in mice. This study demonstrates that the genetic background, but not H-2 a or sex, determine the outcome of lagochilascariosis in mice.
Lagochilascaris minor is the etiological agent of lagochilascariosis, a disease that affects the neck region and causes exudative abscesses, with eggs, adult parasites and L3/L4 larvae in the purulent exudates. Mice are now considered to be intermediate hosts for the parasite. To determine the pattern of infection in B1 cell-deficient mice, experimental lagochilascariosis was studied in BALB/c and X-chromosome-linked immunodeficient (xid) mice. BALB.xid-infected mice showed lower numbers of larvae. Third-stage larvae, fourth-stage larvae and adult parasites were found in both strains. BALB/c mice produced IgM, IgG, IgA and IgE against the crude extract and secreted/excreted antigens of the parasite. On the other hand, BALB.xid mice did not produce IgM and produced lower levels of IgG and IgA, and similar quantities of IgE.
Lagochilascaris minor is the causative agent of lagochilascariosis, a disease that affects the neck region and causes festering abscesses, with eggs, adult parasites and L3/L4 larvae within the purulent exudates. Today, mice are considered to be intermediate hosts for the parasite. C57BL/6 mice produce immunoglobulin IgM, IgA and IgG against the crude extract of the parasite; on the other hand, antibodies produced against the secreted/excreted antigens of Lagochilascaris minor present lower levels of IgM, IgA and IgG. This is the first description of antibody detection against different antigens of Lagochilascaris minor.
Recently, we demonstrated that C57BL/6 mice are more susceptible to experimental lagochilascariosis than BALB/c mice. To investigate the pattern of infection and the role of the genetic background on susceptibility to infection, we studied experimental lagochilascariosis in H-2a identical B10.A and A/J mice. Infected B10.A mice had a lower survival ratio and more severe lesions in the lungs than did A/J mice. Splenocytes of A/J mice immunized with the crude extract of the parasite showed increased proliferation and produced a higher level of interleukin 10 and interferon-γ in the presence of CE or concanavalin A when compared to B10.A mice. This suggests that resistance of A/J mice may be due to less severe lesions in lungs and other organs and a better immune response to parasite antigens. This paper provides evidence that major histocompatibility complex haplotype does not influence the survival to experimental infection with L. minor.
Lagochilascaris minor is the causative agent of lagochilascariosis, a disease that affects the neck region causing exudative abscesses with eggs, adult parasites and L3/L4 larvae within purulent exudates. Nowadays, mice are considered intermediate hosts for the parasite. To determine the pattern of infection in B1 cell-defective mice, experimental lagochilascariosis was studied in BALB/c and X-chromosome-linked immunodeficient (Xid) mice. BALB.xid infected mice showed higher survival ratios and less intense lung lesions than BALB/c mice. Serum levels of IL-10 was higher in BALB/c infected mice when compared to BALB.xid animals; however, serum levels of IFNγ, in control and infected BALB.xid mice, were statistically different from that seen in BALB/c mice. We discuss the participation of B1 cells and their cytokines in the resistance to infection.
The present study evaluated the hemogram, different proteins, plasma enzymes, serum enzymes and specific antibody production of Felis domesticus experimentally infected by Lagochilascaris minor. The infected animals were seen to present increased total leukocytes (particularly eosinophils), decreased platelet counts, increased aspartate-aminotransferase and alanine-aminotransferase and, especially, the presence of specific IgG antibodies against antigens of the parasite. The reaction with crude extract of adult parasites was shown to be more specific, thereby enabling serum discrimination between the animals: non-infected, infected with other parasites and infected with lagochilascariosis. This is the first description of the standardization of a serological reaction for diagnosing lagochilascariosis in Felis domesticus.
SummaryLagochilascaris minor is the causative agent of human lagochilascariosis, a disease that affects the neck region causing abscesses with eggs, adult parasites and L3/L4 larvae within purulent exudates. Nowadays, mice are considered intermediary hosts for the parasite. In previous study we observed that A/J mice experimentally infected with Lagochilascaris minor showed higher survival ratios than B10.A mice. Now, we denoted that A/J mice (resistant to experimental infection) produced higher levels of IgM, IgG and IgA against the crude extract (excepted for IgM) and secreted/excreted antigens of the parasite; on the other hand, B10.A mice (susceptible to experimental infection) produced higher levels of IgE in the later period of the experimental infection than A/J infected mice.
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