Identification of transmission chains and clusters associated with COVID-19 in Tunisia.

BACKGROUND: The aim of this study was to characterize the transmission chains and clusters of COVID-19 infection in Tunisia. METHODS: All cases were confirmed by Reverse Transcriptase Polymerase Chain Reaction of a nasopharyngeal specimen. Contact tracing is undertaken for all confirmed cases in order to identify close contacts that will be systematically screened and quarantined. Transmission chains were identified based on field investigation, contact tracing, results of screening tests and by assessing all probable mode of transmission and interactions. RESULTS: As of May 18, 2020, 656 cases out of a total of 1043 confirmed cases of Coronavirus disease 2019 belong to 127 transmission chains identified during the epidemic (mean age 42.36 years, Standard deviation 19.56 and sex ratio 0.86). The virus transmission is the most concentrated in the governorate of Tunis (31.5%), Ariana (10.2%) and Ben Arous (10.2%). Virus transmission occurred 50 times (9.72% of secondary transmission events) between two different governorates. A maximum of seven generations of secondary infection was identified, whereas 62% of these secondary infections belong the first generation. A total of 11 "super spreader" cases were identified in this investigation. Four large clusters have been identified. The evolution of secondary cases highlighted two peaks: one in 2nd April and a second in 16 th April whereas imported cases caused local transmission of virus during the early phase of the epidemic. CONCLUSION: Correct contact tracing and early active case finding is useful to identify transmission chains and source of infection in order to contain the widespread transmission in the community.

Clinical Presentation of Cutaneous Leishmaniasis caused by Leishmania major.

BACKGROUND/AIMS: The diagnosis of cutaneous leishmaniasis (CL) is based on the microscopic detection of amastigote, isolation of the parasite, or the detection of Leishmania DNA. Nevertheless, since these techniques are time consuming and not usually available in many endemic countries, the diagnosis remains clinical. Consequently, such disease may be overlooked because of its similarity to other skin diseases. The aim of this study is to describe the clinical polymorphism of CL caused by Leishmaniamajor. METHODS: A cross-sectional survey was carried out on 166 patients. Diagnoses were made by both microscopic examination of stained tissue-scraping smears and PCR. The Leishmania species was identified by restriction enzyme analysis of the ribosomal internal transcribed spacer 1 region. The clinical polymorphism was analyzed only for patients with a positive diagnosis for CL and L. major as the identified species. RESULTS AND CONCLUSION: Of the 166 patients, 75 patients fit the inclusion criteria. Twelve different types of CL caused by L. major were defined. The most common type was the ulcero-crusted form followed by the papulonodular form and the impetigenous form. The ulcerated, mucocutaneous, lupoid, and sporotricoid forms were less common. The eczematiform, erysipeloid, verrucous, psoriasiform, and pseudotumoral types were represented by a single case. Zoonotic CL caused by L. major can simulate many other skin diseases, which may lead to a significant spread of this disease and increases in morbidity and drug resistance. This large polymorphism may be the result of a complex association between the genetics of the parasite and the immune response of the host.

Unexpected co-detection of promastigote and amastigote Leishmania forms in a human cutaneous lesion: implications for leishmaniasis physiopathology and treatment.

Cutaneous leishmaniasis pathogenicity depends on the survival and replication of the parasitic protozoa in the form of non-motile amastigotes inside macrophages. Here, we report the unprecedented observation of both Leishmania major amastigote and promastigote forms (the latter is normally detected only in the mid gut of the insect vector or in vitro culture) in a cutaneous lesion of a 6-year-old boy. This finding suggests that modifications of the skin lesion environment, such as maceration and changes in pH or temperature, could promote the in situ transformation of Leishmania amastigotes into promastigotes. This observation raises questions about the physiopathology of cutaneous leishmaniasis and the influence of micro-environmental changes on the efficiency of topical treatments.