With the progression of the COVID-19 pandemic, there have been different reports about the development of autoimmune diseases once the infection is controlled. After entering the respiratory ...epithelial cells, SARS-CoV-2—the virus that causes the disease—triggers a severe inflammatory state in some patients known as “cytokine storm” and the development of thrombotic phenomena—both conditions being associated with high mortality. Patients additionally present severe lymphopenia and, in some cases, complement consumption and autoantibody development. There is a normalization of lymphocytes once the infection is controlled. After this, autoimmune conditions of unknown etiology may occur. A hypothesis for the development of post-COVID-19 autoimmunity is proposed based on the consequences of both a transient immunosuppression (both of innate and acquired immunity) in which self-tolerance is lost and an inappropriate form of immune reconstitution that amplifies the process.
In December 2019, a new and highly contagious infectious disease emerged in Wuhan, China. The etiologic agent was identified as a novel coronavirus, now known as Severe Acute Syndrome Coronavirus-2 ...(SARS-CoV-2). Recent research has revealed that virus entry takes place upon the union of the virus S surface protein with the type I transmembrane metallo-carboxypeptidase, angiotensin converting enzyme 2 (ACE-2) identified on epithelial cells of the host respiratory tract. Virus triggers the synthesis and release of pro-inflammatory cytokines, including IL-6 and TNF-α and also promotes downregulation of ACE-2, which promotes a concomitant increase in levels of angiotensin II (AT-II). Both TNF-α and AT-II have been implicated in promoting overexpression of tissue factor (TF) in platelets and macrophages. Additionally, the generation of antiphospholipid antibodies associated with COVID-19 may also promote an increase in TF. TF may be a critical mediator associated with the development of thrombotic phenomena in COVID-19, and should be a target for future study.
In Colombia, South America, there is a subspecies of the South American rattlesnake
,
, a snake of the Viperidae family, whose presence has been reduced due to the destruction of its habitat. It is ...an enigmatic snake from the group of pit vipers, venomous, with large articulated front fangs, special designs on its body, and a characteristic rattle on its tail. Unlike in Brazil, the occurrence of human envenomation by
in Colombia is very rare and contributes to less than 1% of envenomation caused by snakes. Its venom is a complex cocktail of proteins with different biological effects, which evolved with the purpose of paralyzing the prey, killing it, and starting its digestive process, as well as having defense functions. When its venom is injected into humans as the result of a bite, the victim presents with both local tissue damage and with systemic involvement, including a diverse degree of neurotoxic, myotoxic, nephrotoxic, and coagulopathic effects, among others. Its biological effects are being studied for use in human health, including the possible development of analgesic, muscle relaxant, anti-inflammatory, immunosuppressive, anti-infection, and antineoplastic drugs. Several groups of researchers in Brazil are very active in their contributions in this regard. In this work, a review is made of the most relevant biological and medical aspects related to the South American rattlesnake and of what may be of importance for a better understanding of the snake
, present in Colombia and Venezuela.
In Colombia, there are two species of bushmaster snakes, Lachesis acrochorda, which is distributed mainly in the west of the country (in the Choco region), and Lachesis muta in the southeast (in the ...Amazon and Orinoquia region), whose presence has been reduced due to the destruction of their habitats. Captive maintenance is challenging, making it difficult to obtain their venom for study and antivenom manufacturing. They are the largest vipers in the world. The occurrence of human envenomation is quite rare, but when it occurs, it is associated with high mortality. Bushmaster venom is necrotizing, hemorrhagic, myotoxic, hemolytic, and cardiovascular depressant. Due to the presence of bradycardia, hypotension, emesis, and diarrhea in some patients (Lachesis syndrome), the possibility of a vagal or cholinergic effect is raised. The treatment of envenomation is hindered by the scarcity of antivenom and the need to use high doses.
A review of the most relevant biological and medical aspects of bushmaster snakes is presented, mainly for those occurring in Colombia, to facilitate their recognition and raise awareness about the need for special attention to improve their conservation and advance scientific knowledge, in particular, about their venom.
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•Colombian bushmasters; species that require special attention to ensure their survival and the proper study of their venoms.•Envenomation by Lachesis species are rare but considered serious.•The development of more potent and specific antivenoms for the management of their envenomation is urgently needed.
Andes-to-Amazon river connectivity controls numerous natural and human systems in the greater Amazon. However, it is being rapidly altered by a wave of new hydropower development, the impacts of ...which have been previously underestimated. We document 142 dams existing or under construction and 160 proposed dams for rivers draining the Andean headwaters of the Amazon. Existing dams have fragmented the tributary networks of six of eight major Andean Amazon river basins. Proposed dams could result in significant losses in river connectivity in river mainstems of five of eight major systems-the Napo, Marañón, Ucayali, Beni, and Mamoré. With a newly reported 671 freshwater fish species inhabiting the Andean headwaters of the Amazon (>500 m), dams threaten previously unrecognized biodiversity, particularly among endemic and migratory species. Because Andean rivers contribute most of the sediment in the mainstem Amazon, losses in river connectivity translate to drastic alteration of river channel and floodplain geomorphology and associated ecosystem services.
COVID-19 (Coronavirus Disease 2019) is a highly contagious infection and associated with high mortality rates, primarily in elderly; patients with heart failure; high blood pressure; diabetes ...mellitus; and those who are smokers. These conditions are associated to increase in the level of the pulmonary epithelium expression of angiotensin-converting enzyme 2 (ACE-2), which is a recognized receptor of the S protein of the causative agent SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2). Severe cases are manifested by parenchymal lung involvement with a significant inflammatory response and the development of microvascular thrombosis. Several factors have been involved in developing this prothrombotic state, including the inflammatory reaction itself with the participation of proinflammatory cytokines, endothelial dysfunction/endotheliitis, the presence of antiphospholipid antibodies, and possibly the tissue factor (TF) overexpression. ARS-Cov-19 ACE-2 down-regulation has been associated with an increase in angiotensin 2 (AT2). The action of proinflammatory cytokines, the increase in AT2 and the presence of antiphospholipid antibodies are known factors for TF activation and overexpression. It is very likely that the overexpression of TF in COVID-19 may be related to the pathogenesis of the disease, hence the importance of knowing the aspects related to this protein and the therapeutic strategies that can be derived. Different therapeutic strategies are being built to curb the expression of TF as a therapeutic target for various prothrombotic events; therefore, analyzing this treatment strategy for COVID-19-associated coagulopathy is rational. Medications such as celecoxib, cyclosporine or colchicine can impact on COVID-19, in addition to its anti-inflammatory effect, through inhibition of TF.
Cutaneous lupus erythematosus (CLE) is a common disease that may appear as a separate entity from systemic lupus erythematosus (SLE), precede SLE development, or occur as a manifestation of this ...systemic disease. It has a complex pathophysiology that involves genetic, environmental, and immune-mediated factors creating a self-amplification pro-inflammatory cycle. CLE is characterized by prominent type I interferons (IFNs) inflammation which are considered as the first precursors of the inflammatory cascade generated within the pathophysiology of CLE. TNF-α enhances the production of antibodies through the activation of B cells, and favors the expression of surface nuclear antigens on keratinocytes. UV light exposure favors keratinocyte apoptosis or necroptosis, which results in the release of multiple proinflammatory cytokines, including IL-6, IL-1α, IL-1β, TNF-α, IFNs, and CXCL10. Serum levels of IL-17 are elevated in patients with ACLE, SCLE, and DLE. Evidence suggests IL-22 plays a role primarily in tissue repair rather than in inflammation. High expression of BAFF and its receptors have been found in lesioned keratinocytes of patients with CLE, and patients with CLE have lower serum levels of the regulatory cytokines TGF-β and IL-10. The chemokines CXCL9 and CXCL10 (CXCR3 ligands) have an increased expression among these patients, and their expression is correlated with IFNs levels. CXCR3 ligands recruit cytotoxic type I cells through this receptor, further supporting the death of keratinocytes via necroptosis with the subsequent release of eNAs perpetuating the inflammatory cycle. Interface dermatitis is characterized by the presence of CXCR3-positive lymphocytes. This review describes the leading cytokines and chemokines present in the circulation and skin that play a fundamental role in the pathogenesis of CLE.
•CLE has a complex pathophysiology that involves genetic, environmental, and immune-mediated factors.•Its pathophysiology involves a complex interaction between the innate and adaptive responses.•CLE is considered an interferonopathy, as IFNs are the most critical cytokines contributing to the disease's pathogenesis.
We report case of a 48 years old woman bitten on her right foot by a Bothrops atrox viper. As a result, she developed a severe coagulopathy which improved with application of polyvalent antivenom. ...Four days after bite she suffered a devastating brainstem ischemic stroke. Possible pathogenetic mechanisms are discussed.
•Bothrops atrox envenomation rarely cause cerebral arterial thrombosis.•Basal and posterior brain arteries are particularly susceptible.•The endothelial damage is one of the most probable pathogenic mechanisms.
In southwestern Colombia there is a notable variety of snakes that belong to the Viperidae family (vipers). The particular clinical manifestation related to species is poorly reported.
Based on a ...prospective study about envenomation caused by vipers from 2011 to 2019 at the Fundación Valle del Lili Hospital, Cali, in southwest Colombia, we selected cases of admitted patients in which the snakes responsible were fully identified. They were cataloged by clinical syndrome according to prevalent signs (edema-inducing, necrotizing, blister-inducing, procoagulant, anticoagulant or myotoxic) and were related to the species that caused the envenomation.
From a cohort of 53 patients, 21 patients (16 males 72.7%) with an average age of 35 (3-69) y were included. The syndromes associated with envenomation were anticoagulant and necrotizing effects of Bothrops asper (five patients 22.7%), blister-inducing and anticoagulant effects of Bothrops rhombeatus (five 22.7%), anticoagulant effects of Bothrops punctatus (three patients 13.6%), edema-inducing and anticoagulant effects of Bothriechis schlegelii (five 22.7%), edema-inducing and myotoxic effects of Bothrocophias colombianus (one 4.5%), edema-inducing and myotoxic effects of Bothrocophias myersi (one 4.5%) and edema-inducing effects of Porthidium nasutum (one 4.5%).
In southwestern Colombia there is notable variety in species of snakes belonging to the family Viperidae (vipers) whose envenomation causes various clinical syndromes.
The aim of this study is to describe both clinical and treatment needs in six patients who had a previous diagnosis of rheumatoid arthritis (RA) and were infected with Chikungunya virus (CHIKV). We ...report RA patients who acquired CHIKV infection, treated from the Fundación Valle del Lili Hospital, Cali, Colombia, between August 2014 and September 2015. Data of demographic information, clinical and laboratory findings, DAS28 score, dose of glucocorticoids (GC), or conventional or DMARD use was collected before, during CHIKV infection, and 6 months of follow-up. Five women and one man were analyzed, with an average age of 66 years, who had been receiving low doses of GC (4 mg of prednisolone/day on average). Two patients were being treated with methotrexate (MTX) and etanercept, one with MTX and other with etanercept, with an average DAS28 of 2.00 at the last control consultation. At the time of CHIKV infection, they presented an average DAS28 of 3.98, requiring more than double their usual dose of GC (average dose 8.75 mg/day of prednisolone). One patient required a change from etanercept to adalimumab and three others started rituximab, tocilizumab, and tofacitinib as second-line medication. A case series of patients with RA in remission are presented, who when contracting CHIKV infection developed exacerbation of their underlying disease, which in general was difficult to control. An increase in the doses of GC and change or induction to the use of second-line medications (anti-TNF, anti-CD20, or Janus kinase inhibitor) were required.
Key Points
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The clinical outcome of RA patients with CHIKV infections is not well known.
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A group of RA patients, who were in clinical remission, were affected during the 2014–2015 CHIKV epidemic and treated in a hospital in southwestern Colombia, and had severe reactivation of their RA.
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Some patients with RA in remission and who had CHIKV infection required an increase in the glucocorticoid, in addition to starting second-line medications (anti-TNF, anti-CD20, or Janus kinase inhibitor) or their modification.
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