Detection and genotyping of Giardia duodenalis from cattle and pigs in Hualien country, Eastern Taiwan.

BACKGROUND: Giardia duodenalis is a zoonotic protozoan parasite causing diarrhea through waterborne or fecal-oral infection. The cysts can live in the drinking water and cause pandemic diseases. In Taiwan, very little information is available regarding the epidemiology of G. duodenalis in domestic animals. METHODS: Fecal samples were collected from cattle (n = 156) and pigs (n = 141) in Hualien country, eastern Taiwan. Detection and genotyping were done by microscopy examination of fecal samples and amplification of the ß-giardin gene using nested PCR. RESULTS: The prevalence of G. duodenalis infection was 19.87% for cattle (31/156) and 4.26% for pigs (6/141). Using nested PCR, 30 infected samples found in cattle belonged to Assemblage E, and one sample belonged to Assemblage D. For pigs, four samples belonged to Assemblage E, one belonged to Assemblage D, and another one belonged to Assemblage A. In addition, these results showed that G. duodenalis Assemblage A was detected in pigs and may cause zoonotic transmission. CONCLUSION: This is the first epidemiological investigation of G. duodenalis infection in animals in Hualien, Taiwan. These results could provide epidemiological information for disease control and public health protection.

Mitochondrial dynamics in Angiostrongylus cantonensis-infected mouse brain.

Angiostrongylus cantonensis is one of the most widespread parasites causing central nervous system (CNS) diseases in mammals. Since the mitochondrion is an essential cell organelle responsible for both physiological and pathological processes, its dysfunction might lead to inflammation and multiple disorders. In this study we aimed to investigate the changes in mitochondrial dynamics that occur in the mouse brain upon infection with A. cantonensis, using molecular biology techniques such as polymerase chain reaction (PCR), western blot analysis, transmission electron microscopy (TEM), and different staining methods. Here, we show that mouse brain infected with A. cantonensis exhibits altered mitochondrial dynamics, including fission, fusion, and biogenesis. Additionally, we demonstrate that caspases and B-cell lymphoma 2 (BCL-2) were significantly upregulated in A. cantonensis-infected brain. These results are indicative of the occurrence of apoptosis during A. cantonensis infection, which was further confirmed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. These findings suggest the change in mitochondrial dynamics in A. cantonensis-infected brain, providing another point of view on the pathogenesis of meningoencephalitis caused by A. cantonensis infection.

Angiostrongylus cantonensis activates inflammasomes in meningoencephalitic BALB/c mice.

Angiostrongylus cantonensis is a metastrongyloid nematode that causes eosinophilic meningoencephalitis in humans. A high infestation of A. cantonensis can cause permanent brain damage or even death. The inflammasome is an oligomeric molecular platform that can detect microbial pathogens and activate inflammatory cytokines. The recognition of larval surface antigens by pattern recognition receptors (PRRs) can cause oligomerization of the NOD-like receptor (NLR) or absent in melanoma 2 (AIM2) with the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) to form a caspase-1-activating scaffold. Activated caspase-1 converts pro-inflammatory cytokines into their mature, active forms. Helminths infection has been shown to activate NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasomes. In this study, we aimed to investigate the mechanism of inflammasome activation upon A. cantonensis infection in a mouse model. This study provides evidence that A. cantonensis infection can activate NLRP1B and NLRC4 inflammasomes and promote pyroptosis to cause meningoencephalitis.

Mitochondrial dynamics in the mouse liver infected by Schistosoma mansoni.

Mitochondrial dynamics is crucial for regulation of cell homeostasis. Schistosoma mansoni is one of the most common parasites known to cause liver disease. Mice infected by S. mansoni show acute symptoms of schistosomiasis after 8 weeks. Hence, in this study, we attempted to assess the direct effects of S. mansoni infection on mice liver, and to explore the expression of mitochondrial morphology, dynamics, and function. Our recent findings show that S. mansoni infection changes mitochondrial morphology and affects mitochondrial functions, which attenuates mitochondrial membrane potential and ATP generation. S. mansoni-infected mice increases mitochondrial numbers by upregulating of genes involved in mitochondrial biogenesis, including peroxisome proliferator-activated receptor c co-activator 1α (PGC1α) and mitochondrial transcription factor A (Tfam). This may promote mitochondria generation for accelerating the recovery of mitochondrial functions. Moreover, S. mansoni would disrupt mitochondrial dynamics including induced mitochondrial fission and promoted mitochondrial fragmentation in mice liver. More importantly, S. mansoni further stimulated upregulation both extrinsic and intrinsic apoptosis pathway in infected mice liver. The intrinsic pathway was triggered by cytochrome c release. Additionally, NFκB (nuclear factor-kappa B, p65) could play a protective role to inhibit apoptosis through reducing active caspase-3 expression. Therefore, our results confirmed the liver damage mechanism of experimental schistosomiasis in mice model.

Interferon gamma polymorphisms associated with susceptibility to tuberculosis in a Han Taiwanese population.

BACKGROUND: Polymorphisms of the interferon gamma (IFN-γ) gene are associated with the risk of tuberculosis (TB) in different populations. However, the genetic susceptibility to TB in Han Chinese living in Taiwan is still unknown. The purpose of this study is to evaluate whether the polymorphisms of the IFN-γ gene are associated with TB in Han Taiwanese. METHODS: A total of 200 TB patients and 202 age-matched non-TB individuals were enrolled. Five tag single nucleotide polymorphisms (tSNPs) and rs2430561 (+874) of IFN-γ were selected from a public database. The genotypes were determined using polymerase chain reaction assays. RESULTS: Three IFN-γ polymorphisms in intron 3, rs1861494 and rs2069718, and rs2430561 in interon 1 were strongly associated with TB. The C carrier (CT+TT) of rs1861494, TT homozygous of rs2069718, and AA homozygous of rs2430561 were risk genotypes for susceptibility to TB. CONCLUSION: The IFN-γ polymorphisms, rs1861494, rs2069718, and rs2430561, may confer the risk of TB in Han Taiwanese.

Prevalence and species identification of Cryptosporidium from fecal samples of horses in Taiwan.

Cryptosporidiosis is a zoonotic disease caused by the protozoan parasite Cryptosporidium. A total of 436 horse fecal samples were collected from 19 farms, and acid-fast staining method was used for primary screening. Cryptosporidium oocysts were found in 161 samples, among which 33 positive sample were selected for nested PCR, restriction fragment length polymorphism analysis and DNA sequencing of 18 S rDNA, showing 31 samples to be bovine C. parvum and 2 C. felis. The methods employed in this study should be useful as tools to identify cryptosporidiosis genotypes and species of livestock.