Visceral leishmaniasis-human immunodeficiency virus coinfection in a 52-year-old male in southwest Iran: a case report.

BACKGROUND: Leishmaniasis is a rare infectious disease observed in subtropical and tropical areas. This disease that demonstrates different clinical characteristics is caused by intracellular Leishmania protozoan. One of the important countries facing the incidence of this infectious disease is Iran. Recently, human immunodeficiency virus-Leishmania coinfection has been indicated in Iran. CASE PRESENTATION: In the present case report, we show an atypical case of severe visceral leishmaniasis in a 52-year-old Iranian-Arab male with positive human immunodeficiency virus status. Leishmaniasis was detected by node biopsy and subsequently histopathology evaluations and confirmed by molecular methods. CONCLUSIONS: The current study was the first report of an atypical case of a patient with Leishmania-human immunodeficiency virus coinfection in southwestern Iran, which was not responsive to the treatment. Therefore, the health authorities should be aware of these reports, which require permanent clinical follow-up of the patients as well as effective treatments.

Can Echinococcus granulosus-Derived MicroRNAs be Biomarkers for Diagnosis and Follow-up of Cystic Echinococcosis Patients?

INTRODUCTION: Cystic echinococcosis (CE) is a neglected tropical disease caused by the larval stages of Echinococcus granulosus (E. granulosus). MicroRNAs (miRNAs) are small noncoding RNAs acting as mediators in host-parasite interaction. Recently, numerous studies have been conducted on miRNAs in infectious diseases; however, little data are available about the role of miRNAs in pathogenesis and early diagnosis of CE. METHODS: The current study evaluated the expression of four E. granulosus-derived miRNAs, including egr-miR-125,5p, egr-let-7,5p, egr-miR-2, and egr-miR-71 in fibrotic and healthy liver tissues of 31 CE patients with active and inactive hydatid cysts by qRT-PCR. RESULTS: Of the 31 patients, 48.4% had active cysts (CE1 and CE2), while the remainder had transitional (16.1%) and inactive (35.5%) CE types cysts. The qRT-PCR analysis revealed a significant increase of 11.2, 9.91, 6.2, and 13.1-fold in the fibrotic tissue group for egr-miR-125,5p, egr-let-7,5p, egr-miR-2, and egr-miR-71, respectively. Among these miRNAs, egr-miR-125-5p exhibited the highest area under the curve (AUC) value of 0.8050 for predicting liver fibrosis. CONCLUSIONS: Our findings provide new data about the role of E. granulosus-derived miRNAs in pathogenesis of CE. The high AUC of egr-miR125,5p reflecting the possibility of using egr-miR125,5p as biomarker in CE diagnosis. Further studies on serum of CE patients are needed to confirm the potential role of circulating egr-miR-2a-3p and egr-miR-125-5p in the early diagnosis of CE.

Primary disseminated intraabdominal hydatidosis: a case report.

BACKGROUND: Hydatidosis, a zoonotic disease caused by the larvae of Echinococcus granulosus sensu lato (E. granulosus s.l.), can be primary or secondary. However, primary disseminated intraabdominal hydatidosis is a rare form of the disease, accounting for about 2% of all intraabdominal cysts. CASE PRESENTATION: We report herein a case of primary disseminated intraabdominal hydatidosis with multiple organ involvement in a 51-year-old Iranian man presenting to a healthcare facility with abdominal pain. During the physical examination, two abdominal masses were palpated. Ultrasound and computed tomography revealed six cystic lesions in the patient's liver, subhepatic region, pelvic, and omentum. Afterward, he underwent surgery, during which the cystic lesions were completely removed. The patient received albendazole (400 mg/kg/day) postoperatively and was recommended to continue the treatment for 4 months. CONCLUSIONS: Although primary disseminated intraabdominal hydatidosis is rare, this problem is of great importance due to the fertility of cysts and the high risk of recurrence. Therefore, it is recommended to follow such patients with imaging modalities and enzyme-linked immunosorbent assay for native antigen B (AgB). In addition, patients should undergo albendazole therapy postoperatively for 4 months.