A Crimean-Congo haemorrhagic fever (CCHF) outbreak emerged from 2001 to 2003 in the Middle Anatolia region of Turkey. This study describes the clinical characteristics and outcome features of CCHF patients admitted to four tertiary care hospitals in Turkey. Definitive diagnosis was based on the detection of CCHF virus-specific IgM by ELISA or of genomic segments of the CCHF virus by RT-PCR. Related data were collected by a retrospective chart review. Hospital costs were extracted from the final discharge bills. Univariate and multivariate analyses were conducted to determine the independent predictors of mortality. CCHF virus-specific antibodies or genomic segments were detected in the sera of 99 cases. Seven cases that were treated with ribavirin were excluded from the study. Cases were mostly farmers (83 cases, 90 %), and 60 % had a tick-bite history before the onset of fever. Impaired consciousness and splenomegaly were independent predictors of a fatal outcome.

Thrombocytopenia of < or = 20 x 10(9)/l, a prolonged aPTT > or = 60s, the existence of melena, and somnolence were independent predictors of fatality.

Highlights Decrease in %LUC (Large unstained cells%) value predicts severe SARS-CoV-2 infection. Laboratory parameters associated with the severe illness in COVID-19 patients. The optimal cut-off values of relevant parameters to define risk of critical illness. The relevant coagulation abnormalities to predict severe patients with COVID-19.

To investigate Crimean-Congo hemorrhagic fever virus in Turkey, we conducted a seroepidemiologic survey during January–April 2009. Seroprevalence of infection was 10% in a sample from an outbreak region and increased with patient age, indicating that the virus had been previously present in Turkey. We also estimated that 88% of infections were subclinical.

Multisystem inflammatory syndrome in adults (MIS-A) is a new syndrome related with COVID-19. A case-based review was performed to present real-life experiences in terms of main findings and treatment options. We described two cases with the diagnosis of MIS and searched the literature to review all reported ≥ 18-year-old cases. The PubMed, Scopus, and Web of Science databases were searched. All relevant articles from January 2020 to February 2021 were reviewed. An adolescent and an adult patient (18 and 40 years-old, respectively) with the diagnosis of MIS were presented. Both had the consistent clinical findings with the case definition criteria. Although steroid, intravenous immunoglobulin (IVIG) and supportive care treatments have been suggested in the literature, there exists no treatment guideline for MIS-A. The clinical and laboratory findings of the patients progressively improved with the implementation of the IVIG and the pulse steroid treatments. A total of 51 cases (≥ 18 years-old) with MIS were analyzed. Mean age was 29.4 ± 10 years. Fever (80.4%), gastrointestinal (72.5%), and respiratory symptoms (54.9%) were the predominant symptoms. Cardiovascular abnormalities were the most frequent reported findings (82.4%, 42/51). The dermatological and conjunctival findings were reported in 39.2% and 35.3% of the patients, respectively. The increased level of inflammatory biomarkers was remarkable. Most of the patients were treated successfully with steroid and IVIG. Clinicians managing adult patients should keep in mind the development risk of MIS related with SARS-CoV-2 infection to perform necessary interventions properly without delay. IVIG and pulse steroid treatments are the effective options on clinical improvement.

Our results suggest that the nosocomial occurrence of IRAB is strongly related to an ICU stay and duration of hospital stay, and that IRAB occurrence may be favored by the selection pressure of previously used antibiotics.

Although Crimean-Congo hemorrhagic fever (CCHF) is a widespread tick-borne disease, little is known about its pathogenesis. The interaction of the virus with host cells is most likely responsible for the pathogenesis of CCHF. The main contributors are endothelial cells (ECs) and immune cells. There are 2 theories underlying the CCHF pathogenesis: One is that the virus interacts with the ECs directly and the other that it interacts indirectly via immune cells with subsequent release of soluble mediators. ECs are activated upon infection by the upregulation of soluble molecules and proinflammatory cytokines. Probably, in severe cases, deregulation and excessive release of the cytokines accompanied by endothelial activation have toxic effects, leading to increased vascular permeability, vasodilatation, and subsequently hypotension, multiple organ failure, shock, and death. Studies indicate that CCHF virus (CCHFV) also can impair the innate immune system and cause a delay in adaptive immune response, which is critical for the clearance of CCHFV. The virus has many different ways to block the immune response, leading to uncontrolled viral replication followed by systemic spread of the virus throughout the body. Partial activation of dendritic cells and macrophages, delayed induction of interferons, weak antibody response, apoptosis of lymphocytes, and hemophagocytosis are some of these tactics. However, there are many points waiting for clarification about the pathogenesis of CCHF. Although the high risk of contagiousness limits research, we need more studies to understand the CCHF pathogenesis better. Here we review the main characteristics of the pathogenesis of CCHF.

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