Plasmodium gallinaceum and Plasmodium juxtanucleare are the most common species of
Plasmodium causing avian malaria in domestic and wild chickens. In Thailand, P.
gallinaceum infection in poultry has been reported since 1996, but P. juxtanucleare infection
has never been reported. The objective of this study was to identify and characterize the
Plasmodium species infecting Burmese red junglefowls (Gallus gallus spadiceus) in Thailand
using molecular techniques. Seventeen Burmese red junglefowls from a farm in western
Thailand were suspected of being infected with blood parasite. Blood samples of all
seventeen Burmese red junglefowls were collected and examined. Microscopic examination
revealed the presence of Plasmodium trophozoites in 5 out of 17 samples. In comparison,
nested PCR detected 12 samples to be positive for Plasmodium spp. Molecular
characterization, based on partial sequence of mitochondrial cytochrome b gene, revealed 7
PCR-positive samples as P. juxtanucleare. Nucleotide sequence comparison and
phylogenetic analyses grouped these 7 P. juxtanucleare into 2 distinct groups. The first group
was identical to P. juxtanucleare previously reported from Brazil, Malaysia and Taiwan,
whereas the second group was identical to P. juxtanucleare from Japan. This is the first
report on molecular confirmation and characterization of P. juxtanucleare in Burmese red
junglefowls in Thailand.
Encephalitozoonosis is a common infectious disease caused by Encephalitozoon cuniculi in rabbits. The purpose of this study was to examine the levels of antibody in urines of experimentally E. cuniculi-infected rabbits. Humoral immune response and spore excretion in urines were also examined. Rabbits were orally infected with E. cuniculi, and sera and urines were collected. Levels of serum IgG, IgM, IgA and urinary IgG were examined. The presences of spores in urines were examined by quantitative PCR. Specific IgG in sera started to be detected at day 20 after infection and kept high level during the course of experiment. Serum IgM started to be detected 1 week earlier than that of serum IgG and decreased to almost undetectable level by day 100 after infection. However, the level of IgM increased gradually again thereafter. Serum IgA was transiently detected between 20 and 70 days after infection and kept undetectable level thereafter. Specific IgG in urines started to be detected from 60 days after infection. The amount of spore DNA was correlated with the amount of IgG in urine. In conclusion, the detections of serum and urinary antibodies were useful for the prediction of stage of latent infection in encephalitozoonosis.
The current study investigated the impact of the CCR5, TLR2 and TLR11 on production of nitric oxide (NO), IL-6 and IL-12 and growth of T. gondii, high virulent RH strain and avirulent PLK strain. All examined knockout macrophages infected with PLK strain produced significant lower levels of IL-12. On the other hand, TLR2- /- and TLR11-/- macrophages infected with RH strain produced significantly reduced levels of IL-12 as compared to wild-type macrophages. TLR2-/- and TLR11-/- macrophages infected with PLK strain significantly inhibited the production of IL-6 when compared to wild-type macrophages. Interestingly, significant reduction in the IL-6 and NO production was observed in TLR2-/- macrophages infected with PLK strain as compared to wild-type macrophages or to the other examined knockout macrophages. On contrary, significant increase in the NO levels was demonstrated in TLR11-/- macrophages infected with the RH strain. The growth of RH strain was significantly enhanced in CCR5-/- , TLR2-/- and TLR11-/- macrophages as compared to wild-type macrophages. The highest parasite growth of both RH and PLK strains was achieved in TLR2-/- macrophages. In conclusion, the current study suggests that TLR2 is the most critical receptor in the host defense against T. gondii infection.
A gene encoding Babesia gibsoni thrombospondin-related adhesive protein (BgTRAP),
known as a vaccine candidate, was stably expressed in Toxoplasma gondii
(Tg/BgTRAP). The molecular weight and the antigenic reaction of recombinant
BgTRAP expressed by the Tg/BgTRAP were similar to the original ones expressed by
B. gibsoni. To evaluate the antigenicity of the recombinant BgTRAP expressed by T.
gondii, the lysates of the recombinant parasite tachyzoites were intraperitoneally
injected into mice. The serum collected from Tg/BgTRAP-immunized mouse could
react to B. gibsoni parasites, while the serum collected from wild-type T. gondii
tachyzoites (Tg/wt)-immunized mice did not. These results indicate that T. gondii could
provide a new tool to produce foreign antigens from other protozoan parasites and the
recombinant BgTRAP expressed by T. gondii might be a useful antigen for developing
a diagnostic reagent and vaccine to control canine babesiosis.
Dipyridamole, an antiplatelet drug used for the secondary prevention and treatment of stroke, also has antiplasmodial activity and enhances the activity of chloroquine. We evaluated the inhibitory effects of dipyridamole on the growths of Babesia and Theileria parasites. The growth of B. bovis and T. equi was significantly inhibited at a 25 μM concentration of dipyridamole, while B. bigemina and B. caballi were significantly inhibited at 50 μM and 1 μM concentrations of dipyridamole, respectively, on day 3 of cultivation. The half maximal inhibitory concentration (IC50) of dipyridamole was calculated at 39.5±4.5, 26.3±10.9, 13.2±3.6, and 23.5±0.5 μM on the growth of B. bovis, B. bigemina, B. caballi, and T. equi, respectively. In a viability assay, B. bovis, B. bigemina, and T. equi failed to grow at the previous treatment concentration of 100 μM of dipyridamole, while B. caballi had not grown at the previous treatment concentration of 50 μM of dipyridamole. As for in vivo inhibitory assay, treatment with 100 mg/kg of body weight dose of dipyridamole could not inhibit the in vivo growth of B. microti. In conclusion, dipyridamole might be used as a chemotherapeutic agent against bovine and equine piroplasm parasites. However, dipyridamole could not orally treat against B. microti infection.