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Four Dangers Lurking In Your Garden—and How To Protect Yourself

Many people see gardening as a relaxing pastime—an easygoing way to spend hours outdoors when the weather's nice. But as a consultant in emergency medicine, I deal with all manner of medical emergencies and injuries arising from what may appear to be a harmless hobby.

Over the years, I have seen hand wounds from cutting implements and foot wounds from lawn mowers and garden forks. In recent weeks, I have seen falls from ladders, head wounds from falls on concrete—and, sadly, confirmed the death of a person in their later years whose enthusiastic shoveling proved too much.

Even in times past, the garden could be quite the health hazard. One of the first patients to be treated with penicillin was a police officer who had apparently contracted sepsis after a scratch from a rose thorn. In those days, the most minor of wounds could have the deadliest of consequences—and it turns out this can still happen, with a UK woman recently dying from sepsis after scratching her hand while gardening.

But these aren't the only dangers lurking in your garden. Here are just a few things to look out for before you next head out to tend your plants:

1. Tetanus

Tetanus is a particularly nasty disease. The muscles go into spasm due to the effects of the toxin from the bacteria, Clostridium tetani. The suffering is almost indescribable, causing painful muscle spasms and a locked jaw.

Many associate tetanus with objects such as rusty nails. But this surprisingly common organism is also found in the soil, particularly if manured, because clostidia are found in the gut. Roses like soil with manure, so this could turn these beloved flowers deadly if you get cut by contaminated thorns or if the soil gets into a cut.

Luckily, I have yet to see any cases in the emergency room because the UK immunizes against tetanus. And I never want to see a case, because of how nasty it is. The case fatality rate can exceed 50% in people who aren't immunized. This is why it's important to check that your tetanus jab is up to date.

2. Bacteria and fungi

Lurking in a humble bag of compost is an ingredient many of us wouldn't expect: Legionella.

This bacteria can cause an infection called Legionnaires' disease which is particularly harmful for the elderly and people with a compromised immune system. It can lead to a nasty and often fatal pneumonia when inhaled. Warm, stagnant water involved in the composting process may account for its presence.

It isn't only pre-packaged compost that's hazardous. Your own compost heap is also be filled with various bacteria and fungi, which, if properly maintained, should cause you no trouble. But often the mold Aspergillus can grow when it's hot outside. This can give rise to some nasty lung lesions and may even become more widespread in the body—especially in the elderly and immunosuppressed and can be fatal.

Mold spores can also trigger allergies in some people, a condition known as extrinsic allergic alveolitis or "farmer's lung". This condition was classically due to exposure to moldy hay, but compost heaps can also do the same because of the presence of organisms such as Aspergillus and the bacteria Actinomycetes.

3. Leptospirosis

Leptospira is a bacterium that may be found in water contaminated with rat urine. With rats often building habitats near humans, it might be best to take care near the pond or rainwater barrels when gardening.

Leptospira can cause leptospirosis, a rather unpleasant infection that causes headaches, fevers, chills, vomiting, jaundice and then later, liver failure, kidney failure and meninigitis.

4. Power tools

While power tools can make our work easier in the garden, they can also make it much easier to injure ourselves, too. Hedge trimmers may be a great way to tame trees and bushes, but they can also amputate digits and inflict wounds very efficiently. Be sure to wait until the hedge trimmer is fully turned off before clearing any branches you've removed.

Hedge trimmers and lawn mowers can also easily cut through electric cables, which can lead to electrocution. Power tools can also be disastrous if you fall while up a ladder and if you have power lines crossing your garden, then please avoid them.

Stay safe

While these hidden dangers are certainly a risk, luckily there are many simple things you can do to avoid harm from them, including:

Cleaning and covering wounds while gardening.

Make sure your immunisations are up to date (especially for tetanus).

Keeping compost bags away from your face when you open them.

Deter rats by not putting cooked food on compost heaps, covering water butts and setting up traps if you have an infestation.

Set up ladders firmly on even ground away from power lines.

Enjoy having wildlife but leave it alone (snakes can be just as much a danger as rats).

And one last piece of advice from me. Every year the burns unit at my hospital sees a number of people who have tried to speed up the process of lighting their barbecue or bonfire by using petrol. Not all survive. So if you are planning to cook the fruits of your labors on a barbecue in your garden, make sure you don't use inflammable liquids to get the flame started, and have a fire extinguisher on hand just in case.

Gardening is a rewarding hobby that has many health benefits. Just be sure to take sensible precautions.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Citation: Four dangers lurking in your garden—and how to protect yourself (2023, May 31) retrieved 31 May 2023 from https://medicalxpress.Com/news/2023-05-dangers-lurking-gardenand.Html

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The Sepsis Seesaw: Tilting Toward Immunosuppression

The immune response goes haywire during sepsis, a deadly condition triggered by infection. Richard S. Hotchkiss and his colleagues take the focus off of the prevailing view that the key aspect of this response is an exuberant inflammatory reaction. They assess recent human studies bolstering the notion that immunosuppression is also a major contributor to the disease. Many people with sepsis succumb to cardiac dysfunction, a process examined by Peter Ward. He showcases the factors that cause cardiomyocyte contractility to wane during the disease.

Sepsis, the systemic inflammatory response syndrome that occurs during severe infection, kills more than 210,000 people in the US annually1. Developing new therapies for sepsis has been particularly frustrating, and over 25 trials of new agents have failed1. This failure has been partly due to a lack of understanding of the pathogenic mechanisms driving sepsis.

Two recent studies in human subjects shed light on one of the most important and relatively underrecognized mechanisms of sepsis immunopathology. Limaye et al.2 and Luyt et al.3 provide evidence that the otherwise dormant viruses cytomegalovirus (CMV) and herpes simplex virus (HSV) are reactivated in critically ill individuals—adding strength to the concept that a key aspect of critical illness is immunosuppression2,3. Most experimental therapies for sepsis have focused on attenuating the initial inflammatory response, ignoring—and possibly exacerbating—the progressive development of immunosuppression4,5,6,7. Although these approaches have demonstrated modest benefits in select groups of patients, the majority of deaths occur in patients with sepsis who are immune suppressed5,6,7. These two new studies should direct researchers toward fresh diagnostic and therapeutic approaches to sepsis.

Limaye et al.2 examined the incidence of reactivation of CMV in 120 CMV-seropositive critically ill individuals, many of whom apparently had sepsis2. Before their illness, these people had normal immunity. CMV viremia, as assessed by real-time PCR, occurred in 40 subjects (33%), indicating that CMV reactivation occurs frequently in the critically ill. CMV reactivation was associated with prolonged stay and death. These findings dovetail with an earlier study by Luyt et al.3 who reported a 21% incidence of HSV bronchopneumonitis that was attributed to viral reactivation in critically ill, immunocompetent individuals requiring prolonged mechanical ventilation3.

It is likely that only a modest number of the subjects in these two studies had clinically important viral infections. Rather, these studies show that critically ill individuals who had normal immunity before hospitalization become profoundly immunocompromised during a protracted illness, thereby enabling reactivation of latent viruses that may become clinically relevant.

Although the investigators didn't specifically state the incidence of sepsis in their study populations, many of the subjects in these two studies had bacterial or fungal sepsis during their intensive care unit (ICU) stay2,3. For example, a number of patients in the CMV trial were hospitalized in the burn ICU, in which a substantial fraction of individuals invariably develop sepsis because of loss of barrier function. The HSV study population included subjects requiring prolonged mechanical ventilation, and ventilator-associated pneumonia occurs in up to 85% of this population. Clearly, CMV or HSV reactivation occurred in the setting of sepsis in many of the subjects.

Sepsis initiates a complex immunologic response that varies over time (Fig. 1)4,5. Although recent studies show that both inflammatory and anti-inflammatory responses occur simultaneously in sepsis, the early net result is characterized by a hyperinflammatory response. The magnitude of this response varies depending on many factors, including the number and virulence of pathogens, and other disease conditions afflicting the patient4. With contemporary standard-of-care measures, the majority of patients survive the hyperinflammatory phase and enter a stage of protracted immunosuppression that has been termed 'immunoparalysis'6,7. This immunosuppression in sepsis is manifested by loss of delayed type hypersensitivity response to positive control antigens, failure to clear the primary infection and development of new secondary infections6,7. Secondary, hospital-acquired infections include both virulent organisms such as Staphylococcus aureus and Clostridium difficile as well as organisms that are not particularly dangerous to nonimmunosuppressed individuals, such as Stenotrophomonas maltophila, Acinetobacter calcoaceticus-baumannii and Candida albicans. Infection with these latter organisms, as with CMV and HSV reactivation, highlights the marked immunosuppression in critically ill patients.

Figure 1: Immunologic response in sepsis over time.

Although both pro- and anti-inflammatory responses are activated early in sepsis, the proinflammatory response predominates. As sepsis progresses, the anti-inflammatory response becomes predominant, and it is during this later phase that secondary infections and viral reactivation occur. Early deaths during the early proinflammatory response phase are due to cytokine storm–mediated events, whereas later deaths during the anti-inflammatory phase are due to failure to control pathogens.

Multiple cellular mechanisms underlie immunosuppression in patients with sepsis, including activation of T regulatory cells and myeloid-derived suppressor cells8,9. Additionally, an early and ongoing immunopathology in sepsis is the apoptotic depletion of cells of both the innate and adaptive immune system10. Uptake of apoptotic cells further impairs host immunity by inducing an anti-inflammatory phenotype in phagocytic cells that consume the cellular corpses11. Prevention of this sepsis-induced apoptosis apparently attenuates the immunosuppressive cascade and leads to sustained immunity10. From this perspective, sepsis may be simply a race to the death between the host immune system and the pathogens, and pathogens gain an early advantage by inducing the death of billions of immune effector cells.

Additional mechanistic insights from these two studies can be obtained by comparison to studies of individuals with congenital immune deficiencies that confer susceptibility to particular classes of pathogens. HSV and CMV reactivation in critically ill patients suggests a T cell defect, and studies in ICU patients, especially those with sepsis, report extensive loss of CD4+ and CD8+ T cells. Natural killer cell counts are almost certainly reduced in sepsis, as well, and may also have a role in viral reactivation. Individuals with sepsis probably have multiple, interrelated immunologic defects owing to the extensive cross-talk between the specialized cells of the immune system that coordinate function to eradicate specific pathogens. For example, T cells make interferon-γ, a powerful macrophage activator, and, therefore, T cell dysfunction may result in macrophage defects.

Perhaps the most important implication of these two studies is that newer antibiotics alone are unlikely to substantially affect sepsis mortality. The fundamental problem in critically ill individuals is loss of immune competence; eradicating a particular class of pathogens will probably result in superinfection with other microorganisms. In addition to developing clinical practices to avoid infections, attention should be directed toward methods to enhance or restore immune function in critically ill individuals. Although there is risk of exacerbating the early hyperinflammatory phase of sepsis, methods to quantify the immune competence of each patient and appropriately time immunotherapy should minimize this danger.

Immunotherapy is being aggressively pursued in cancer research12. Similar to patients with sepsis, many people with cancer are immunosuppressed as a result of their underlying disease, and similar mechanisms, such as activation of myeloid-derived suppressor cells and T regulatory cells, may be involved in both disorders13. In this regard, a number of the immune-enhancing agents being investigated in cancer, such as antibody to programmed death-1 (ref. 14), agonistic antibody to CD40 (ref. 15) and interleukin-7 (R.S.H., J. Unsinger, D. Hildeman and C. Caldwell, unpublished data) are reported to improve survival in animal models of sepsis.

Research over the last few years has provided insight into the mediators of immune suppression during sepsis; the findings of Limaye et al.2 and Luyt et al.3 highlight the profound impact of prolonged critical illness on immune function and should stimulate basic research and development of methods to enhance immunity. In our opinion, reengaging or preserving host immune function will be the next major advance in the management of patients with sepsis.

Preterm Birth Complications: Jaundice, Distressed Breathing Among Others

While some babies might go on to lead healthy lives, some might encounter serious medical complications and long-term health problems. According to WHO, preterm birth complications are the leading cause of death among children under 5 years of age.

As per a recent UN report, India ranks among the top 5 countries having the highest rates of preterm births. The report shows that an estimated 13.4 million babies were born pre-term in 2020, with nearly 1 million dying from preterm complications. A typical pregnancy lasts about 40 weeks. Premature birth happens when an infant is born before 37 weeks of gestation.

As per studies, children who are born prematurely are at a high risk of stillbirth, neonatal death, and later childhood mortality. According to WHO, preterm birth complications are the leading cause of death among children under 5 years of age.

While some babies might go on to lead healthy lives, some might encounter serious medical complications and long-term health problems. As per reports, the advancement in the development of the Neonatal Intensive Care Unit (NICU) has improved the clinical outcomes of these babies and created hope for their survival and healthy lives.

Medical complications of premature births

Premature babies have a high risk of encountering medical complications after birth, the reason being their arrival much before the developmental cycle completed a circle. The following are some medical conditions that might affect the newborn.

Respiratory Distress Syndrome- Breathing problems in premature babies are due to an immature respiratory system. In this condition, there is harsh, irregular breathing due to the lack of a certain surfactant in the lungs that prevents them from collapsing. Some babies also go on to develop apnea where they can pause their breathing for at least 20 seconds. Many babies that develop respiratory complications are put on ventilators in the NICUs. If they are on the breathing assisting device for long, there are chances that they might develop lung infections. Sometimes, the lungs are too immature to withstand the pressure from the respirator.

Pneumonia- Complications with respiratory problems in premature babies can lead to pneumonia in some cases. It is an infection of the lungs and causes inflammation and breathing difficulties. Treatments usually include antibiotics and oxygen support. If left untreated, it can turn into deadly infections or sepsis or meningitis.

Neonatal Jaundice- Jaundice in newborns is common and usually harmless. The condition is caused by the build-up of bilirubin in the blood, a chemical associated with the break-down of blood cells. Babies have high levels of red blood cells which are broken down and replaced frequently. As per an estimate, 8 among 10 premature babies might develop the condition.

Infections- A premature baby can develop infections in any part of the body. The reason is a less developed immune system. Also, premature babies often require several medical procedures, including the insertion of intravenous (IV) lines, catheters, and breathing-assisting ventilators. Each time these devices are used, there is a chance of introducing bacteria, fungi, viruses and other pathogens into the baby's body.

Heart and brain problems- A premature baby can be affected by certain heart conditions like the failure to the closing of a duct that connects two major blood vessels of the heart. This can further cause more blood to be passed through the lungs and this can result in complications both in the heart and lungs. Premature babies can also have an intraventricular haemorrhage in the brain that can lead to bleeding (mild to severe).

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