This study aimed to determine the seroprevalence of Toxoplasma gondii in pregnant women in the south western region of Saudi Arabia and to find out the possible risk factors that may lead to infection. This cross sectional hospital based study was carried out at three hospitals in the south western region of Saudi Arabia from January 2008 to August 2010. Blood samples from 487 pregnant women were collected and used to detect anti-T. gondii antibodies IgM and IgG by enzyme linked immunosorbent assay (ELISA). A questionnaire interview was carried out to ask about some risk factors of infection. Among the 487 studied pregnant women, 38.8 % were seropositive for anti T. gondii IgG while 6.2 % were positive for anti T. gondii IgM and 3.3 % were positive for both anti T. gondii IgG & IgM. The only risk factor associated with seropositive anti T. gondii IgM was the history of the intake of immunosuppressive drugs. Regarding anti T. gondii IgG seropositivity, it was found to increase significantly with increased age, number of gravida and parities, and previous history of toxoplasmosis. The seroprevalence of T. gondii IgG & IgM by ELISA among pregnant women in the south western region of Saudi Arabia is considerable with few identifiable significant risk factors reported.

Abstract. Two hundred and three Plasmodium falciparum isolates from Jazan area, southwest Saudi Arabia, were typed for Pfcrt, Pfmdr1, dhps, and dhfr mutations associated with resistance to chloroquine, mefloquine, halofantrine, artemisinin, sulfadoxine-pyrimethamine, and the neutral polymorphic gene Pfg377. A large proportion (

BACKGROUND AND OBJECTIVES:Chloroquine has been the drug of choice for the treatment of malaria for many decades. We aimed to examine the molecular basis of chloroquine resistance among Plasmodium falciparum isolates from the southwestern region of Saudi Arabia by analyzing the K76T and N86Y mutations in the PfCRT and PfMDR1 genes, respectively.PATIENTS AND METHODS:P falciparum-infected blood spot samples (n=121) were collected on filter papers. DNA was extracted and fragments from the above genes were amplified using nested PCR. The amplicons were digested by ApoI enzyme and sequenced.RESULTS:Of the 121 samples, 95 and 112 samples could be amplified for PfCRT K76T and PfMDR1 N86Y mutations, respectively. All of the samples amplified for the PfCRT K76T mutation were undigestible by ApoI, suggesting the presence of the K76T mutation. For the PfMDR1 N86Y mutation, 65/109 samples (59.6%) were digestible when treated with ApoI in a pattern, suggestive of the presence of the investigated wild allele (N86). However, 44/109 samples (40.4%) were digestible by ApoI, suggesting the presence of the mutated allele (Y) at position 86. DNA sequencing confirmed these results.CONCLUSION:Surprisingly, all isolates exhibited the mutated allele at codon 76 (K76T) of PfCRT. However, the mutated mutant allele at codon 86 (N86Y) of PfMDR1 was found in 40.4% of the samples studied. To our knowledge, this is the first study that has investigated the existence of the mutation in the PfMDR1 gene in the country. This study will contribute to the development of new strategies for therapeutic intervention against malaria in Saudi Arabia.

In this article, two strains of mice BALB/C and C57 were infected with Egyptian strain of Schistosoma mansoni. BALB/C mice appeared to harbor fewer parasites than did C57 mice. The hepatic and intestinal tissues of C57 mice were loaded with more eggs than that of BALB/C mice. Regardless the strain of mice, the number of eggs per gram of liver tissues was higher than in the intestinal tissues. Some biochemical parameters were measured in the liver of infected and non-infected mice; a significant decrease in the activities of alkaline phosphatase, catalase, glutathione-s-transferase, glutathione, and total lipids of infected mice compared to their matched control were observed. However, there was a significant increase in malondialdehyde level of infected mice compared to their matched group. Detailed discussion on the parasitological and biochemical differences between the two strains was presented.

This study was designed to assess the effect of green tea, an aqueous extract of Camellia sinensis, on the oxidative stress, antioxidant defense system and liver pathology of Schistosoma mansoni-infected mice. Green tea at concentration of 3% (w/v) was given orally to treated mice as sole source of drinking water from the end of the 4th week to the end of 10th week post-infection; untreated mice were allowed to drink normal water. The data of the studied S. mansoni-infected mice exhibited a suppression of hepatic total antioxidant capacity, superoxide dismutase (SOD), catalase (CAT) activity and glutathione content. The liver lipid peroxidation was deleteriously elevated in S. mansoni-infected mice. The hepatic total protein content, AST and ALT activities were profoundly decreased in the S. mansoni-infected mice. Most hepatocytes were damaged and showed abnormal microscopic appearance with aggressive necrosis. Both total protein and glycogen levels have been greatly reduced as indicated by histochemical examination. The treatment of S. mansoni-infected mice with green tea succeeded to suppress oxidative stress by decreasing the lipid peroxides but failed to significantly enhance the antioxidant defense system and deteriorated changes owing to liver damage and necrosis. In consistence with biochemical data, histopathological and histochemical data indicated that treatment of S. mansoni-infected mice with green tea could ameliorate hepatocytes thus reduce cellular necrosis and partially restore both total protein and glycogen levels. Thus, the study concluded that the green tea suppresses the oxidative stress through its constituent with free radicals scavenging properties rather than through the endogenous antioxidant defense system.