Category: Diseases, Syndromes and Conditions

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NICD Warns of Malaria Being Misdiagnosed as COVID

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Mosquito
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The National Institute for Communicable Diseases has warned that, as South Africa enters its peak malaria season, cases of malaria are being misdiagnosed as COVID. Both malaria and COVID have similar non-specific early symptoms such as fever, chills, headaches, fatigue and muscle pain. Undiagnosed and untreated malaria rapidly progresses to severe illness and can be fatal.

Speaking at a media briefing on Wednesday, principal NICD medical scientist Dr Jaishree Raman said that Gauteng has seen a slight increase of malaria cases recently. 

Dr Raman noted that COVID “has pulled resources from the malaria programmes, reducing active surveillance and case investigation, which is reducing the ability [to] classify cases accurately.”

However, the NICD does not know the exact source of the malaria. “Data cleaning and case classification is ongoing, so at the moment, we cannot say whether the uptick in cases is due to locally-acquired or imported malaria,” she said.

The NICD advises that any individual that prevents with fever or ‘flu-like illness, if they reside in a malaria-risk area in Limpopo, KwaZulu-Natal and Mpumalanga or have travelled to a malaria-risk area, especially Mozambique, in the past six weeks, must be tested for malaria by blood smear microscopy or malaria rapid diagnostic test. If they test positive for malaria, the patient must be started on malaria treatment, immediately.

The NICD also advises patients to remember to inform their healthcare provider of their recent travel, especially to neighbouring countries and malaria risk areas in South Africa.  

‘Taxi malaria’, transmitted by hitch-hiking mosquitoes, should be considered in a patient with unexplained fever who has not travelled to a malaria-endemic area, but is getting progressively sicker, with a low platelet count.

Source: NICD

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Ozone Therapy in a Complex Periodontal Inflammation Case

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A new treatment approach for tissue inflammation around the dental root and root canal has been implemented, which uses ozone therapy. When used in a complex clinical case, the method helped save a patient’s tooth. 

Inflammation of the dental pulp and the periodontium, if not localised only on the inside or the outside but affects both areas, can be extremely difficult to completely cure a tooth. Such cases are difficult to diagnose, therefore, professional literature contains only a few descriptions of them, and there are no general treatment recommendations. Some dentists prefer to focus on the internal canals first, while others suggest treating the pulp and the periodontium simultaneously. A dentist from RUDN University implemented a single protocol for comprehensive pulp and periodontium treatment.

Explaining the problem, RUDN Associate Professor Maria Makeeva, PhD, said: “Inflammation of periodontal tissues often leads to tooth loss. In some cases, a lost tooth cannot be replaced with an implant, because the consequences of the infection worsen the implantation prognosis. Therefore, keeping the tooth is a more desirable outcome in this scenario.”

As described in described in Clinical, Cosmetic and Investigational Dentistry, the new approach was carried out in a patient (aged 44) with significant inflammation of the right mandibular canine. The patient was initially diagnosed with periodontium inflammation; the tooth was loose, and a flow of pus was seen. The first steps were typical for a periodontal inflammation treatment protocol: the patient was administered an antibiotic and then was instructed to rinse the tooth with chlorhexidine. The dentist also scaled the tooth. After that, the patient remained under observation for six months. Although the bleeding and pyorrhoea stopped, the dentist discovered tissue injury around the root of the tooth, which had caused bone destruction. It turned out that one narrow area had an 8mm deep periodontal pocket, and that the initial inflammation transferred to the internal tissues of the tooth.

A periodontologist and an endodontist together implemented a comprehensive treatment approach. After removing the dead pulp from the dental canals, which were then dried and treated with ozone for 24 seconds for better disinfection. After a week of dressing, the treatment was repeated, and the cavity was covered with a permanent filling made of a light-cured composite material. After cleaning, the periodontal pocket was rinsed, dried, and treated with ozone for 18 seconds. A recall examination in six months showed no inflammation of the tooth. Additionally, the bone tissue was recovering, and the periodontal pocket reduced to 4mm.

“Simultaneous inflammation of the pulp and periodontium tissues is very difficult to treat. It can be caused by several types of pathogens at the same time that migrate between tissues and worsen the prognosis. Our experience shows that such an infected tooth can be saved, but it requires close collaboration of a periodontologist and an endodontist, as well as a patient’s complete compliance with oral hygiene recommendations. One should also take into consideration possible bacterial resistance to antibiotics and therefore use additional antibacterial treatment, such as ozone,” explained Dr Makeeva.

Source: News-Medical.Net

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A New Method to Block Listeria Infections

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University of Queensland researchers have unlocked a way of fighting Listeria infections, which can cause severe and potentially illness in pregnant women and immunocompromised individuals.

Listeria infection does not cause disease in most people, but can be deadly for the immunocompromised and is also a major health concern during pregnancy and can lead to miscarriage, stillbirth and premature birth.

From 2017 to 2018, South Africa suffered the world’s largest listeriosis outbreak, in which there were 216 deaths out of 1060 recorded cases.

During the study, published in the journal PLOS Pathogens, researchers discovered a way to block Listeria from making the proteins that allow bacteria to survive and multiply in immune cells. University of Queensland’s Professor Antje Blumenthal said using a small, drug-like inhibitor has improved their understanding of Listeria’s weak spot.

“Listeria is found in the soil and sometimes in raw foods. Once ingested it can hide from the immune system and multiply inside immune cells,” Prof Blumenthal said.

“Instead of killing the bacteria, the immune cells are used by the bacteria to multiply and are often killed by Listeria growing inside them.

“Our study showed the bacteria could be cleared with a small drug-like inhibitor that targets the ‘master regulator’ of the proteins that help Listeria grow in immune cells. The inhibitor helped the immune cells survive infection and kill the bacteria.”

Previously, studies into Listeria’s ‘master regulator’, which controls critical proteins that make the bacteria virulent, have mostly been based on engineered bacteria, or mutated versions of these proteins.

“By using a drug-like inhibitor, we were able to use molecular imaging and infections studies to better understand what happens to Listeria when the bacteria cannot effectively grow inside immune cells and hide from immune defence mechanisms,” Prof Blumenthal said.

“We hope that our discovery, together with recent research into the master proteins’ molecular structure and functions, could guide the development of inhibitors and new drugs to treat Listeria infection.”

“Our findings could also inform design of inhibitors against related proteins that are found in different bacteria,” Prof Blumenthal said.

Source: University of Queensland

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New AIRD Therapies Could Cut Side-effects

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New therapies for autoimmune rheumatic diseases (AIRDs) that are designed to better regulate lipid metabolism could significantly reduce the harmful side-effects caused by conventional treatments, researchers found in a new large-scale review.

AIRDs include rheumatoid arthritis, lupus and Sjögren’s syndrome – conditions which affect millions and all with high rates of morbidity. The pathogenesis of autoimmune conditions is still ill-defined and delivering targeted therapeutic strategies is challenging.

As a result, current treatments for AIRDs are primarily designed to suppress the symptoms (inflammation), but are ‘low target’, ie may also have unintended side-effects. In this regard, AIRDs drugs often cause changes to cell metabolism (such as lipid metabolism) and function, putting patients at greater risk of co-morbidities such as cardiovascular disease (CVD).

Lead author Dr George Robinson (Centre for Rheumatology Research, UCL Division of Medicine) said: “While the mechanisms that cause rheumatic diseases are ill-defined, some recent research indicates cell metabolism may play an important role in triggering or worsening their onset or affect.

“In this review we therefore sought to understand the effect of both conventional and emerging therapies on lipid metabolism in patients with AIRDs.”

For the study, published in the Journal of Clinical Investigation, researchers reviewed more than 200 studies to assess and interpret what is known regarding the on-target/off-target adverse effects and mechanisms of action of current AIRD therapies on lipid metabolism, immune cell function and CVD risk.

Explaining the findings, Dr Robinson said: “Our review found that current AIRD therapies can both improve or worsen lipid metabolism, and either of these changes could cause inflammation and increased CVD risk.

“Many conventional drugs also require cell metabolism for their conversion into therapeutically beneficial products; however drug metabolism often involves the additional formation of toxic by-products, and rates of drug metabolism can be different between patients.”

The review noted that optimal combinations of immunosuppressive treatments to better control inflammation could lead to an improved metabolic/lipid profile in AIRDs.

However, many studies also showed that lipid lowering drugs such as statins do not sufficiently lower CVD risk in some AIRDs, possibly because they cannot completely restore the anti-inflammatory properties

Dr Robinson added: “The unfavourable off-target adverse effects of current therapies used to treat AIRDs provides an opportunity for optimal combination co-therapies targeting lipid metabolism that could reduce immune complications and potential increased CVD risk in patients.

“New therapeutic technologies and research have also highlighted alternative metabolic pathways that can be more specifically targeted to reduce inflammation but also to prevent undesirable off-target metabolic consequences of conventional anti-inflammatory therapies.”

Source: University College London

Categories : Antibiotics Diseases, Syndromes and ConditionsTags : 1 Comment

AMR Caused Over 1.2 Million Deaths Globally in 2019

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Methicillin-resistant Staphylococcus aureus (MRSA) bacteria. Credit: CDC

Globally, infections by antimicrobial-resistant (AMR) bacteria caused more than 1.2 million deaths worldwide in 2019, according to a study published in The Lancet. It is the largest and most comprehensive one to date of this critical issue.

Lower-income countries are worst affected but antimicrobial resistance remains a global threat, the researchers wrote.

The researchers emphasised that investment in new drugs is urgently needed, as well as vaccination and better antimicrobial stewardship.

The estimate of global deaths from AMR, is based on the researchers’ analysis of 204 countries, assuming the counterfactual that the bacteria responsible would be antibiotic-susceptible.

Of the 4.95 million deaths in which AMR played a role, 1.27 million were directly attributable to it. In 2019, 860 000 deaths were estimated from HIV and 640 000 from malaria.

Most of the AMR-related deaths resulted from lower respiratory infections, such as pneumonia, and bloodstream infections, which can lead to sepsis.

Deaths from AMR were estimated to be highest in sub-Saharan Africa at 23.7 deaths per 100 000, and lowest in North Africa and the Middle East at 11.2 per 100 000. Young children are at most risk, with about one in five deaths linked to AMR being among the under-fives.

The researchers also noted that “resistance is high for multiple classes of essential agents, including beta-lactams and fluoroquinolones.”

MRSA (methicillin-resistant Staphylococcus aureus) was particularly deadly, while E. coli, K. pneumoniae, S. pneumoniae, A. baumannii, and P. aeruginosa were associated with high levels of resistance. The researchers wrote that “each of these leading pathogens is a major global health threat that warrants more attention, funding, capacity building, research and development, and pathogen-specific priority setting from the broader global health community.”

They also recommend that immunity to these pathogens be built up by vaccination, and since currently only S. pneumoniae has a vaccine readily available, these will need to be developed and deployed as a matter of urgency. They noted several limitations to their study, the first being the sparsity of data drawn from low- and middle-income countries, which may in fact lead to an underestimate of the prevalence of AMR. Secondly, there is the possibility of multiple sources of bias inherent in combining datasets from different providers. Finally, there may be bias in surveillance, eg if cultures are drawn only if a patient is unresponsive to antibiotics, leading to an overestimate.

Source: The Lancet

Categories : Diseases, Syndromes and Conditions Injury & TraumaTags :

A New Treatment for Chronic Tendon Disease

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The Achilles tendon can endure a load nearly 8 times body weight during exercise, rendering it vulnerable to injury despite its strength, which can be worsened by a failure to properly heal, forming bone instead of new tendon. A new study found that by inhibiting blood vessel formation, the anomalous bone growth can be prevented.

Due to the unique nature of tendons, failing to consult a doctor soon after an injury can lead to chronic tendon disease, which is characterised by pain, swelling, and movement problems. Tendon heterotopic ossification (HO) is a rare type of chronic tendon disease where new bone grows the tendon, causing even more damage. Famous athletes have had to retire early from sports due to a lack of a radical solution for Achilles tendon injuries.

Using single-cell sequencing technology, a team led by Professor Ouyang Hongwei found that changes in the tissue microenvironment of tendon HO alterations in gene expression and in tendon stem progenitor cells. These findings were published in Bone Research, providing a novel treatment for tendon heterotopic ossification.

The researchers firstly found that the tendon specific transcription factor MKX decreased significantly in heterotopic ossified human tendon, and deletion of MKX led to spontaneous ossification of mouse tendon, suggesting that MKX plays a critical role in tendon HO.

Further studies revealed that MKX knockout mouse tendon cells expressed high levels of genes related to blood vessel formation, resulting in vascular invasion and remodelling of the tendon extracellular matrix. This also resulted in abnormal activation of genes related to bone and cartilage in tendon stem cells. These data indicated that inhibition of blood vessel formation may improve the tendon tissue microenvironment and prevent HO progression.

Armed with this knowledge, Prof Ouyang and his colleagues searched for drugs that can inhibit the angiogenesis process. They found that local injection of a small molecule inhibitor known as BIBF1120 significantly inhibited the neovascularisation of tendon after injury, thus alleviating the progression of tendon HO.

Source: MedicalXpress

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Study Shows New Possibilities of Treating Rare Ossifying Disease

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Fibrodysplasia ossificans progressiva (FOP) is a rare disease characterised by anomalous bone growth at the site of even minor injuries. It results in what some term a “second skeleton,” which locks up joint movement and even making breathing difficult. However, new research shows that forming extra-skeletal bone might not be the only driver of the disease. Impaired muscle tissue regeneration allows unwanted bone to form instead of muscle regeneration after injury.

This study was published in NPJ Regenerative Medicine.

“While we have made great strides toward better understanding this disease, this work shows how basic biology can provide great insights into appropriate regenerative medicine therapies,” said the study’s lead author, Foteini Mourkioti, PhD. “From the lab, we’re now able to show that there is potential for a whole new realm of therapies for patients with this devastating condition.”

About 15 years ago, researchers discovered that a mutation in the ACVR1 gene was responsible for FOP. In that study, the team found that the mutation changed cells within muscles and connective tissues, causing them to behave like bone cells and create new, extraneus bone.

“However, while investigations of how the FOP mutation alters the regulation of cell fate decisions have been extensively pursued in recent years, little attention has been paid to the effects of the genetic mutation on muscle and its impact on the cells that repair muscle injuries,” Shore said. “We were convinced that pursuing research in this area could provide clues not only for preventing extra bone formation but also for improving muscle function and regeneration, bringing new clarity to FOP as a whole.”

The researchers studied muscle from mice with the same mutation in the ACVR1 gene that people with FOP have. They focused on two specific types of muscle tissue stem cells: fibro-adipogenetic progenitors (FAPs) and muscle stem cells (MuSCs). Typically, muscle injury repair requires a careful balance of these two cell types. Injured tissue responds by an expansion of FAP cells, which are assigned to recruit muscle stem cells that will regenerate the damaged muscle tissue. After about three days, FAPs die off, their job done. At the same time, MuSCs transition toward a more mature, differentiated state, called muscle fibre, essential to organised movement of our muscles.

In the mice with the ACVR1 mutation being studied, apoptosis – the process through which FAP cells die as a part of proper muscle regeneration – had slowed significantly, leading to a high presence of FAPs past their usual lifespan, altering their balance with the MuSCs. The injured tissue also showed a diminished capacity for muscle stem cell maturation and, as a result, muscle fibres were considerably smaller in mice carrying the ACVR1 mutation compared to muscle fibres in mice lacking the mutation.

“The prolonged persistence of diseased FAPs within the regenerating muscle contributes to the altered muscle environment in FOP, which reduces muscle regeneration and allows the over-abundant FAPs to contribute to the formation of extra-skeletal bone,” Mourkioti said. “This provides a completely new perspective on how excess extra-skeletal bone is formed – and how it could be prevented.”

The current targets for treating FOP focus on slowing extra-skeletal bone growth. This research may provide a pivotal new direction. “We propose that therapeutic interventions should consider promoting the regenerating potential of muscles together with the reduction of ectopic bone formation,” the authors wrote. “By addressing both stem cell populations and their roles in the origin of FOP, there is the possibility of greatly enhanced therapies.”

Source: University of Pennsylvania School of Medicine

Categories : Antibiotics Diseases, Syndromes and ConditionsTags :

Signs of Antibiotic ‘Pre-resistance’ Identified for the First Time

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Drug-resistant, Mycobacterium tuberculosis bacteria, the pathogen responsible for causing the disease tuberculosis (TB). A 3D computer-generated image. Credit: CDC

In a first of its kind study, researchers have spotted signs of antibiotic ‘pre-resistance’ in bacteria for the first time, indicating that they have the potential to develop drug resistance in the future.

The findings, published in Nature Communications, will allow doctors in the future to select the best treatments for bacterial infections.

Mycobacterium tuberculosis (TB) was the second leading infectious cause of death after COVID in 2020, killing 1.5m people. It can be cured if treated with the right antibiotics, but treatment is lengthy and many people most at risk lack access to adequate healthcare. Drug-resistant TB can develop when people do not finish their full course of treatment, or when drugs are not available or are of poor quality.

Multi-drug resistant TB represents a huge, unsustainable burden and totally drug resistant strains have been detected in a handful of countries. As health systems struggle to cope with the pandemic, progress on TB treatment globally has slowed.

To better understand TB for developing new drugs, this study has identified for the first time how to pre-empt drug resistance mutations before they have occurred. Dubbed ‘pre-resistance’ when a pathogen has a greater inherent risk of developing resistance to drugs in the future.

By analysing thousands of bacterial genomes, the study has potential application to other infectious diseases and paves the way towards personalised pathogen ‘genomic therapy’ – which chooses drugs according to the pathogen, preventing drug resistance.

The culmination of 17 years’ work, the study built up a TB bacterial ‘family tree’  from 3135 different tuberculosis samples. Computational analysis identified the ancestral genetic code of bacteria that then went on to develop drug resistance. The team identified the key changes associated with the development of resistance by looking through the ‘branches’ of the family tree to see which had the most potential for developing drug resistance.

Variations in the TB genome predicted that a particular branch would likely become drug resistant, and then validated their findings in an independent global TB data set.

Dr Grandjean, senior author of the study, said: “We’re running out of options in antibiotics and the options we have are often toxic – we have to get smarter at using what we have to prevent drug resistance.

“This is the first example of showing that we can get ahead of drug resistance. That will allow us in the future to use the pathogen genome to select the best treatments.”

Source: EurekAlert!

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Apaxiban is an Option in Severe Renal Dysfunction

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The anticoagulation options for patients with concomitant renal impairment are limited and until recently, warfarin was the only recommended option due to insufficient data supporting alternative drugs in such patients. A new study published in Blood Advances suggests that apixaban is a viable option in patients with severe renal dysfunction.

Apixaban in patients with impaired renal function is supported by limited data. Landmark clinical trials evaluating apixaban in patients with atrial fibrillation and/or acute venous thromboembolism excluded patients with creatinine clearance (CrCl) <25 mL/min. 

A multicentre, retrospective chart review was conducted to evaluate the safety and effectiveness of apixaban compared with warfarin in patients with CrCl <25 mL/min. Included patients were newly initiated on apixaban or warfarin for at least 45 days with a CrCl <25 mL/min.


Patients were evaluated for thrombosis and bleeding outcomes six  months following initiation of anticoagulation. The primary outcome was the time to first bleeding or thrombosis event. A total of 128 patients met inclusion criteria in the apixaban group and 733 patients in the warfarin group. 

Time to first bleeding or thrombosis event was significantly different between the apixaban and warfarin groups. After controlling for atrial fibrillation and coronary artery bypass grafting, risk of thrombotic and bleeding events was lower in the apixaban group (hazard ratio 0.47). There was no statistical difference between time to thrombosis (83 days vs 54 days, P = .648), rate of thrombosis (5.5% vs 10.3%, P = .08), time to bleeding (46 days vs 54 days, P = .886), or rate of bleeding (5.5% vs 10.9%, P = .06). The severity of bleeding and thrombotic events was not different between groups. 

The results suggest apixaban may be a reasonable option for patients with severe renal dysfunction despite the known increase in apixaban exposure, the researchers concluded. They add that, “These results add to the growing body of evidence of real-world data that apixaban is a reasonable option for patients with severe renal dysfunction.”

The researchers recommend investigating the use of apixaban in patients with a severe renal dysfunction, especially those on haemodialysis, in order to definitively determine the role of apixaban in this patient population.

Source: Blood Advances

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A Surprising Use for Ivermectin in Fighting West Nile Virus

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Mosquito
Photo by Егор Камелев on Unsplash

Putting ivermectin in bird-feeders in places where Culex mosquitoes congregate showed promise in reducing the number of infectious mosquitoes that could transmit West Nile virus to humans, according to a researcher presenting at the American Society of Tropical Medicine & Hygiene (ASTMH) virtual meeting.

A pilot trial found that when ivermectin-treated bird-feeders were placed in contiguous lots, there was up to a 16% additional reduction in infectious mosquito days compared to when the bird-feeders were randomly placed, where there was only a 5% additional decline, reported Karen Holcomb, PhD, of the University of California Davis.

Furthermore, with just 33% coverage of ivermectin-treated bird-feeders in a neighbourhood, infectious mosquito days fell by 15% to 45%, she stated.
Since no human vaccine exists for West Nile Virus, the primary strategy has been vector control, she added. However, insecticide has a low specificity in targeting mosquitoes involved in West Nile transmission, and Holcomb also discussed some “non-targeted effects” of spraying in the human population.

Her group hypothesised that because ivermectin could kill mosquitoes while being minimally toxic in mammals and birds, it might be possible to treat bird-feeders with ivermectin, where the mosquitoes would bite the birds, ingest the ivermectin, and die before they could pass the virus on to humans.

Two earlier studies laid the groundwork: one that treated chickens with ivermectin and found a decrease in seroconversion and fewer older mosquitoes near the treated flocks, and an increase in mortality of mosquitoes following a blood meal on treated chickens.

Nevertheless, “the link between ivermectin and West Nile virus transmission was not fully elucidated,” Dr Holcomb said, adding there was no significant difference in mosquito abundance or infection prevalence, as well as variable serum concentrations in chickens.

Next steps of the study included determining what type of set-up worked best for ivermectin-treated bird-feeders in neighborhoods: either contiguous (with all treated bird-feeders in a row) or random. Dr Holcomb’s group found similar reductions in infections in mosquitoes and birds, but the greatest reductions in treated lots were from contiguous, not random placement, she said.

Uncertainty about ivermectin-induced mortality in wild mosquitoes remains, as well as the proper dose of ivermectin to induce mortality.

As a result of ivermectin’s controversial demand during the COVID pandemic, Dr Holcomb said she encountered logistical hurdles.

“During the past year, our collaborators noted it’s become harder to obtain ivermectin, and the ivermectin they were getting was lower quality than prior to COVID,” she told MedPage Today.

In any case, this strategy won’t be used in field control trials for at least a couple more years, Dr Holcomb noted, and “during that time, there should be a reduction in demand for ivermectin.”.

Source: MedPage Today