Background: Leishmaniasis, a disease caused by a protozoan, causes numerous deaths in humans each year. After malaria, leishmaniasis is known to be the deadliest parasitic disease globally. Direct visual detection of leishmania parasite through microscopy is the frequent method for diagnosis of this disease. However, this method is time-consuming and subject to errors. This study was aimed to develop an artificial intelligence-based algorithm for automatic diagnosis of leishmaniasis. Methods: We used the Viola-Jones algorithm to develop a leishmania parasite detection system. The algorithm includes three procedures: feature extraction, integral image creation, and classification. Haar-like features are used as features. An integral image was used to represent an abstract of the image that significantly speeds up the algorithm. The adaBoost technique was used to select the discriminate features and to train the classifier. Results: A 65% recall and 50% precision was concluded in the detection of macrophages infected with the leishmania parasite. Also, these numbers were 52% and 71%, respectively, related to amastigotes outside of macrophages. Conclusion: The developed system is accurate, fast, easy to use, and cost-effective. Therefore, artificial intelligence might be used as an alternative for the current leishmanial diagnosis methods.

Toxoplasma gondii is a pathogenic protozoan parasite that infects the nucleated cells of warm-blooded hosts leading to an infectious zoonotic disease known as toxoplasmosis. The infection outcomes might be severe and fatal in patients with immunodeficiency, diabetes, and pregnant women and infants. The One Health approach to toxoplasmosis highlights that the health of humans is closely related to the health of animals and our common environment. The presence of drug resistance and side effects, the further improvement of sensitivity and specificity of serodiagnostic tools and the potentiality of vaccine candidates to induce the host immune response are considered as justifiable reasons for the identification of novel targets for the better management of toxoplasmosis. Thus, the identification of new critical proteins in the proteome of Toxoplasma parasites can also be helpful in designing and test more effective drugs, vaccines, and diagnostic tools. Accordingly, in this study we present important proteins found in the proteome of the life cycle-specific stages of Toxoplasma parasites that are potential diagnostic or vaccine candidates. The current study might help to understand the complexity of these parasites and provide a possible source of strategies and biomolecules that can be further evaluated in the pathobiology of Toxoplasma parasites and for diagnostics and vaccine trials against this disease.

Toxoplasmosis is a parasitic disease with worldwide prevalence. Despite the relatively similar effects of toxoplasmosis and smoking on alteration in neurotransmitters, especially dopamine, little is known about the relation of Toxoplasma gondii infection and addiction to cigarette smoking. Therefore, the main objective of this study was to assess the relationship between latent toxoplasmosis and smoking. Through a case-control study, 216 regular cigarette smokers and 324 nonsmoker age- and gender-matched subjects were evaluated for anti-T.gondii IgG antibodies with enzyme-linked immunosorbent assay (ELISA). During the sampling, a structured questionnaire was used to obtain the demographic information of participants and the risk factors of acquired Toxoplasma. The median ages of case and control groups were 51.04 ± 18.1 (22–97 years) and 51.03 ± 16.5 (21–89 years), respectively (p = 0.99). Anti-T.gondii IgG antibodies were detected in 44 (20.37%) cases and in 135 (41.67%) controls. There was a statistically significant difference for the positivity rate between the smokers and the control group (OR = 0.35; 95%CI: 0.19–0.65; and p = 0.001). The overall prevalence was 33.14%. This study indicated the inverse association between seropositivity to Toxoplasma infection and cigarette smoking. This relationship could be due to the changes that latent toxoplasmosis has on the neurotransmitters, especially dopamine, which needs more research.

Background. Toxoplasma parasite alters the transduction of neurotransmitter signals and leads to changes in the level of brain neurotransmitters including tyrosine and dopamine, so behavior changes can occur in infected hosts. Based on this concept, this study was conducted for evaluation of the tyrosine and dopamine serum levels in infected mice with chronic toxoplasmosis. Materials and Methods. Toxoplasma gondii (Prugniaud strain II) was injected intraperitoneally into BALB/c mice to induce chronic toxoplasmosis. Modified agglutination test (MAT), polymerase chain reaction (PCR), and microscopic methods were conducted to confirm the induction of chronic toxoplasmosis. The infected mouse sera were separated at days 40, 50, 60, 70, and 80 for evaluation of tyrosine and dopamine serum levels using high-performance liquid chromatography (HPLC). Results. Microscopic methods confirmed the formation of the Toxoplasma cysts in mouse tissues. Inducing chronic toxoplasmosis is also confirmed by MAT, PCR, and histological methods. HPLC results indicated a decrease in serum tyrosine level at day 40 in infected mice in comparison to control, and the levels were too low to be measured at other times. However, a significantly high serum dopamine level was observed that gradually increased after parasite inoculation. Conclusions. No detection of tyrosine level in most of the sample groups is probably related to the very low concentration of tyrosine in sera. However, low concentration of tyrosine at day 40 and increase of dopamine in most of the sample groups suggest the production of dopamine from tyrosine due to the presence of Toxoplasma in infected mice.

Background: Few investigations of genotype II of Toxoplasma gondii, the most prevalent form of the Toxoplasma parasite in humans, have been carried out on due to the rapid conversion of tachyzoites to bradyzoites in its life cycle. The current study aimed to create animal and in vitro models for production of the tachyzoites of the Prugniaud (PRU) genotype II strain.Methods: To develop an immunocompromised model and obtain tachyzoites of the PRU strain, BALB/c mice were orally treated with dexamethasone (10 mg/kg), cyclophosphamide (36 mg/kg), and cyclosporine (18 mg/kg) from 5 days prior to inoculation. Then, 10‐15 tissue cysts of PRU strain were inoculated intraperitoneally into the mice. The tachyzoites obtained from mice were then cultivated in a HeLa cell culture. The resulting yield of tachyzoites was cryopreserved in 92% fetal calf serum, 8% dimethyl sulfoxide. The infectivity of these tachyzoites was evaluated using in vivo and in vitro examinations.Results: Numerous tachyzoites were observed in the peritoneal fluid of the immunosuppressed mice within 10‐15 days after inoculation, and many tachyzoites were harvested from the HeLa cell culture. Trypan Blue staining showed 80% viability of the tachyzoites recovered from cryopreservation and this was confirmed by HeLa cell culture. In addition, mice infected intraperitoneally with the recovered tachyzoites presented with cysts in the brain after 2 months.Conclusion: We have developed an animal model for mass production of T. gondii tachyzoites of the PRU strain. This method can provide fresh viable tachyzoites of Toxoplasma gondii for use as and when required in future investigations.