Tag: Scientific Journals

AAAS: Bumble bees damage plant leaves and accelerate flower production when pollen is scarce

Bumble bee gardeners

Bumble bees rely heavily on pollen resources for essential nutrients as they build their summer colonies. Therefore, we might expect that annual differences in the availability of these resources must simply be tolerated, but Pashalidou et al. made observations suggesting that bees may have strategies to cope with irregular seasonal flowering (see the Perspective by Chittka). When faced with a shortage of pollen, bumble bees actively damaged plant leaves in a characteristic way, and this behavior resulted in earlier flowering by as much as 30 days. Experimenters were not able to fully replicate the results with their own damage, suggesting that there is a distinct method that the bees use to stimulate earlier flowering.

 

The Lancet: Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis

Background

Hydroxychloroquine or chloroquine, often in combination with a second-generation macrolide, are being widely used for treatment of COVID-19, despite no conclusive evidence of their benefit. Although generally safe when used for approved indications such as autoimmune disease or malaria, the safety and benefit of these treatment regimens are poorly evaluated in COVID-19.

Methods

We did a multinational registry analysis of the use of hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19. The registry comprised data from 671 hospitals in six continents. We included patients hospitalised between Dec 20, 2019, and April 14, 2020, with a positive laboratory finding for SARS-CoV-2. Patients who received one of the treatments of interest within 48 h of diagnosis were included in one of four treatment groups (chloroquine alone, chloroquine with a macrolide, hydroxychloroquine alone, or hydroxychloroquine with a macrolide), and patients who received none of these treatments formed the control group. Patients for whom one of the treatments of interest was initiated more than 48 h after diagnosis or while they were on mechanical ventilation, as well as patients who received remdesivir, were excluded. The main outcomes of interest were in-hospital mortality and the occurrence of de-novo ventricular arrhythmias (non-sustained or sustained ventricular tachycardia or ventricular fibrillation).

The Lancet Haematology: Attention should be paid to venous thromboembolism prophylaxis in the management of COVID-19

Since December, 2019, the coronavirus disease 2019 (COVID-19) has spread globally, infecting more than 1 million people and causing more than 70 000 deaths.

Among patients with COVID-19, especially those who are severely and critically ill, a variety of potential risk factors for venous thromboembolism exist, including infection, immobilisation, respiratory failure, mechanical ventilation, and central venous catheter use.

However, to the best of our knowledge, risk of venous thromboembolism in these patients has not yet been reported. Here we use a nationwide dataset from China to provide a delineation of venous thromboembolism risk in patients with COVID-19.

On behalf of the National Clinical Research Centre for Respiratory Disease, together with the National Health Commission of the People’s Republic of China, we collected data from 1099 patients with laboratory-confirmed COVID-19 in 31 provincial administrative regions throughout the country.

The study was supported by the National Health Commission, was designed by the investigators, and was approved by the institutional review board of the National Health Commission. Written informed consent from the patients was waived in light of the urgent need to collect data, and the fact that this was a retrospective analysis of deidentified data. Data were analysed and interpreted by the authors. Continuous variables were expressed as medians with IQR. Wilcoxon rank-sum tests were applied to continuous variables, and χ2 tests were used for categorical variables. To estimate the odds ratio (OR) associated with venous thromboembolism risk, variables including outcomes and laboratory findings that were adjusted by age (by use of logistic regression) were further analysed by logistic regression.

Research Square: COVID-19 presented with Deep Vein Thrombosis: An unusual case report

Background

On 31 December 2019, the World Health Organization (WHO) was informed of a cluster of cases of pneumonia of unknown cause detected in Wuhan City, Hubei Province, China. The pneumonia was caused by a virus called SARS-Cov-2, which was later named COVID-19. In this report, we present a patient with COVID-19 who developed deep vein thrombosis.

Case presentation

A 57-year-old woman presented to the clinic’s infectious department with no underlying illness due to pain, redness, and leg swelling. According to a patient report, she had a mild dry cough for the past 3 days and had no other symptoms. The patient had no history of prone thrombosis conditions. Initially, CT angiography was performed to rule out pulmonary thromboembolism, which showed no evidence of thrombosis. Dilatation and thrombosis were seen in the examinations of the paired veins of the leg, popliteal, superficial and left femoral joints, and no evidence of vascular flow suggesting acute DVT. Because of fever and lymphopenia, nasal swabs were used for sampling and SARS-CoV-2 nucleic acid was detected by RT-PCR. Chest X-ray also revealed bilateral patchy ground-glass opacity. Other tests including ANA, Anti-dsDNA, RF test and ACA test was normal. Heparin at a dose of 80 units/kg IV bolus, chloroquine 400 mg single dose and lopinavir/ritonavir (Kaletra) 400 mg twice daily were prescribed to treat illness and relieve symptoms. On illness day 3, fever stopped and nasal swab sample turned undetectable for SARS-CoV-2 by RT-PCR as well as swelling and tenderness on her leg had been disappeared gradually. She is under regular follow-up with no new symptoms to date.

Conclusion

The mechanism of DVT formation due to COVID-19 is unknown despite thrombocytopenia, and has not been investigated but it resolved as COVID-19 symptoms, tenderness, and leg pain improved. Although COVID-19 presented with Deep Vein Thrombosis is a rare condition, in middle-aged people with sudden onset of manifestations, we should recognize it from other diseases as an important and treatable differential diagnosis. Rapid diagnostic assays, efficient treatment, and prudent use of CT-scan are important to control future COVID-19 spread.

The National Library of Medicine: Occurrence of Kawasaki disease after simultaneous immunization

A recent population‐based study has shown that vaccinations did not increase the risk of Kawasaki disease (KD).1 In contrast, various vaccines, including those against rotavirus, hepatitis B, and influenza, have been suggested to be triggers for KD occurrence.2 We report a pediatric case of KD that occurred after simultaneous immunization with measles/rubella, varicella, and pneumococcal vaccine, suggesting that the vaccination is associated with KD.

A healthy 14‐month‐old Japanese girl without any past or family histories had a fever the day after concomitant inoculation (day 1 of illness) with initial measles/rubella (MR), initial varicella, and fourth pneumococcal vaccination. On day 2 of illness, rash/redness appeared around the previous bacille Calmette–Guérin (BCG) inoculation site (Fig. 1a). On day 4 of illness, she had conjunctival congestion, rash on the trunk, oral‐mucosal inflammation, and reddening of palms with C‐reactive protein (CRP) 4.2 mg/dL and white blood cell count 18 200/μL. On day 5 of illness with persistent fever, she was diagnosed with definite KD on meeting five of the six KD criteria. Given that KD symptoms were resolving with decreasing serum CRP (3.2 mg/dL), aspirin was given on its own without i.v. immunoglobulin. Rash/redness around the BCG inoculation site was still evident, which became a crust on day 11 of illness (Fig. 1b). Echocardiography indicated neither coronary artery sequelae nor heart lesions throughout the clinical course. Antibody analysis on day 6 of illness was as follows: rubella (−), Varicella‐Zoster virus (VZV) (−), Epstein–Barr virus (−), and measles immunoglobulin (Ig)G (−)/IgM (+). Rubella, VZV, and measles seroconverted on antibody analysis 3 months after immunization. The parents of the patient provided informed consent for the publication of this report.

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Bacille Calmette–Guérin (BCG) inoculation site on (a) day 2 and (b) day 11. (a) Redness at the site of previous BCG inoculation is evident. (b) Formation of crust at the BCG inoculation site, which is pathognomonic for Kawasaki disease.

Kawasaki disease symptoms in this patient appeared after simultaneous inoculation with MR, varicella, and pneumococcal vaccine. We diagnosed KD based on clinical symptoms and considered that vaccinations might be associated with KD occurrence. We suggest two possibilities to explain this clinical manifestation: triggered by one of the vaccinations, possibly measles, or by a reaction to the simultaneous immunization itself.

First, KD may have been triggered by one of the vaccinations, possibly measles. Vaccination sometimes accompanies/causes “fever” or “infection‐like symptoms”; therefore, we must distinguish KD from short‐term accompanying events with vaccination. This patient had rash/redness around the BCG inoculation site. It appeared soon after vaccination and gradually became a crust, and these findings are pathognomonic for KD. Rash/redness followed by crust formation at the BCG inoculation site has been observed in 70% of KD patients aged 3–20 months.3 The presence of five of the six KD criteria and this change at the BCG inoculation site were strongly suggestive of KD. In addition, we need to consider that this patient developed measles after immunization. Six days after vaccination, her serum measles antibody titer was elevated: measles IgG (−)/IgM (+). This result, however, is consistent with the reaction caused by measles vaccination. Also, the occurrence of fever soon after vaccination may rule out the possibility of modified measles caused by live vaccination, because this always takes several days to cause fever.

An association between measles or measles vaccination and KD occurrence has been previously reported. In a 6‐month‐old infant, KD occurred 2 weeks after measles. This suggests that measles triggered the KD through immunoreaction against measles infection.4 An earlier report described the isolation of measles virus from a pediatric patient with KD a few weeks after measles vaccination.5 Taken together, a possible association between vaccinations (especially measles) and KD occurrence is suggested, although it is still possible, however, that the timing of vaccinations just before the onset of Kawasaki disease was coincidental.

Second, vaccinations other than measles, that is, rubella, varicella, and pneumococcal vaccine, may have been associated with KD occurrence in this case. In particular, simultaneous inoculation may also be a cause of KD. Fever just after vaccination is possibly related to concomitant inoculation. Although simultaneous inoculation was shown not to increase side‐effects, it may trigger a stronger immunoreaction, causing fever and KD in this case.

Another point may be noteworthy. The present patient had the onset of KD only 1 day after the immunization: this rapidity/temporality is very limited. According to the review by Chang and Islam, only four cases were reported in which KD manifested ≤1 day after immunization, or KD symptoms appeared ≤12 h after the second shot of various vaccines.2 They speculated that this rapidity of symptom occurrence reflects “antigen sensitization” due to previous exposure to antigens, and is an immune‐mediated phenomenon. In the present case, however, only pneumococcal vaccination was the fourth shot, with the remaining vaccines (MR and varicella) being given for the first time.

In conclusion, the present single case supports the suggestion that vaccination triggers KD. Information on cases of KD associated with vaccination should be accumulated to clarify the pathophysiology or etiology of KD.

Disclosure

The authors declare no conflict of interests.

American Journal of Respiratory and Critical Care Medicine: Severe Acute Respiratory Syndrome and Venous Thromboembolism in Multiple Organs

Severe acute respiratory syndrome (SARS) is now known to be caused by a novel coronavirus, the SARS-associated coronavirus (SARS-CoV) (1). It is characterized by severe systemic symptoms in multiple organs, such as lung, immune system, and small vessels, and finally becomes respiratory failure. Initial autopsies reported the predominant pathological findings to be diffuse lung injury, injured immune organs, inflammatory response in systemic small vessels, and general toxic reaction (2).

Changes in coagulation and the development of thrombi have been reported in patients with SARS, but the extent of the effects of the SARS-associated coronavirus on the systemic circulation has yet to be established. Limited data are available on the extent of the damage to the systemic vasculature and circulation in patients with SARS. In the present study, an autopsy was performed on a 57-year-old man diagnosed with SARS and specimens from multiple organs were analyzed to assess pathological changes in the vasculature. Specimens from multiple organs, including the lungs, heart, liver, kidneys, adrenal glands, spleen, esophagus, stomach, intestine, vermiform appendix, pancreas, brain, cerebellum, brainstem, hilus of lung, mesenteric lymph node, and muscle tissues, were analyzed by light microscopy. Examination of all of the specimens revealed systemic circulatory disturbance and polyangiitis. Proliferation, swelling, and apoptosis of endothelial cells, and edema, inflammatory cell infiltration, and fibrinoid necrosis were observed in the walls of small blood vessels in specimens from the lungs, heart, liver, kidneys, adrenal glands, brain, gastrointestinal tract, and muscle tissues. In addition, thrombi were evident in the veins and microcirculation of the soft tissues surrounding the lungs, spleen, pancreas, kidneys, adrenal glands, and mesenteric lymph nodes (Figure 1A–1F).

This autopsy case report has demonstrated that in addition to the well-established diffuse alveolar damage and damage to the immune system, SARS is associated with systemic circulatory disturbance and polyangiitis, in particular thrombosis in the veins and microcirculation in multiple organs and tissues. To our knowledge, this is the first study to show the extent of the damage to the vasculature and circulation that can occur in patients with SARS.

Deep vein thrombosis and/or pulmonary embolism have been reported in patients with SARS previously (34). However, the pathogenesis of deep vein thrombosis in patients with SARS remains unknown. Emerging evidence suggests that viral infection may have a role in the onset of venous thromboembolism (56). The present study adds to this evidence by demonstrating widespread thrombosis associated with SARS.