How to choose a digital camera for wound documentation

By Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

Digital cameras have many helpful features, but the most important considerations for choosing a camera are hardware features. Focus on the following when choosing a camera:

Resolution. The resolution determines picture quality. The National Pressure Ulcer Advisory Panel recommends using a digital camera with a minimum of 3 megapixels
for wound photography. A megapixel is 1 million pixels. The more pixels used to produce a photo, the less grainy it will appear and the clearer any enlargements made from it will be. In essence, the more megapixels a camera produces, the clearer and more detailed the photograph will be. (more…)

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How to do a Semmes Weinstein monofilament exam

By Nancy Morgan, RN, BSN, MBA, WOC, WCC, DWC, OMS

Each month, Apple Bites brings you a tool you can apply in your daily practice.

Description

According to the American Diabetes Association, all patients with diabetes should be screened for loss of protective sensation in their feet (peripheral neuropathy) when they are diagnosed and at least annually thereafter, using simple clinical tests such as the Semmes-Weinstein monofilament exam.
The Semmes-Weinstein 5.07 monofilament nylon wire exerts 10 g of force when bowed into a C shape against the skin for 1 second. Patients who can’t reliably detect application of the 5.07, 10-g monofilament to designated sites on the plantar surface of their feet are considered to have lost protective sensation. (more…)

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How to write effective wound care orders

By Donna Sardina, RN, MHA, WCC, CWCMS, DWC, OMS

Writing effective orders for wound care is vital to ensure patients receive the right care at the right time, to protect yourself from possible litigation, and to facilitate appropriate reimbursement for clinicians and organizations.
Below are some overall strategies you can use:

  • Avoid “blanket” orders, for example, “continue previous treatment” or “resume treatment at home.” These types of general orders lack the specificity clinicians require to deliver care the patient needs and can be easily misinterpreted. For instance, treatments can change multiple times, and someone could pick a treatment from an incorrect date. (more…)
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How to manage incontinence-associated dermatitis

By Nancy Chatham, MSN, RN, ANP-BC, CWOCN, CWS, and Carrie Carls, BSN, RN, CWOCN, CHRN

Moisture-related skin breakdown has been called many things-perineal dermatitis, irritant dermatitis, contact dermatitis, heat rash, and anything else caregivers could think of to describe the damage occurring when moisture from urine or stool is left on the skin. At a 2005 consensus conference, attendees chose the term incontinence-associated dermatitis (IAD).

IAD can be painful, hard to properly identify, complicated to treat, and costly. It’s part of a larger group of moisture-associated skin damage that also includes intertrigo and periwound maceration. IAD prevalence and incidence vary widely with the care setting and study design. Appropriate diagnosis, prompt treatment, and management of the irritant source are crucial to long-term treatment.

Causes

IAD stems from the effects of urine, stool, and containment devices on the skin. The skin’s pH contributes to its barrier functions and defenses against bacteria and fungus; ideal pH is 5.0 to 5.9. Urine pH ranges from 4.5 to 8.0; the higher range is alkaline and contributes to skin damage.

Skin moisture isn’t necessarily damaging. But when moisture that contains irritating substances, such as alkaline urine, contacts the skin for a prolonged period, damage can occur. Urine on the skin alters the normal skin flora and increases permeability of the stratum corneum, weakening the skin and making it more susceptible to friction and erosion. Fecal incontinence leads to active fecal enzymes on the skin, which contribute to skin damage. Fecal bacteria can penetrate the skin, increasing the risk of secondary infection. Wet skin has a lower temperature than dry skin; wet skin under a pressure load has less blood flow than dry skin.

Containment devices, otherwise known as adult diapers or briefs, are multilayer disposable garments containing a superabsorbent polymer. The polymer is designed to wick and trap moisture in the containment device. This ultimately affects the skin by trapping heat and moisture, which may cause redness and inflammation that can progress to skin erosion. This trapping can lead to increased pressure against the skin, especially if the device has absorbed liquid and remains in contact with the skin.

Categorizing IAD

IAD is categorized as mild, moderate, or severe. (See Picturing IAD by clicking the PDF icon above.)

Screening for IAD

Screen the patient’s skin for persistent redness, inflammation, rash, pain, and itching at least daily. To differentiate IAD from pressure ulcers, keep in mind that:

  • IAD can occur wherever urine or stool contacts the skin. In contrast, pressure ulcers arise over bony prominences in the absence of moisture.
  • With IAD, affected skin is red or bright red. With a pressure ulcer, skin may take on a bluish purple, red, yellow, or black discoloration.
  • The skin-damage pattern in IAD usually is diffuse. With a pressure ulcer, edges are well defined.
  • The depth of IAD-related skin damage usually is partial-thickness without necrotic tissue. With a pressure ulcer, skin damage depth may vary.

Preventing IAD

The three essentials of IAD prevention are to cleanse, moisturize, and protect.

  • Cleanse the skin with a mild soap that’s balanced to skin pH and contains surfactants that lift stool and urine from the skin. Clean the skin routinely and at the time of soiling. Use warm (not hot) water, and avoid excess force and friction to avoid further skin damage.
  • Moisturize the skin daily and as needed. Moisturizers may be applied alone or
    incorporated into a cleanser. Typically, they contain an emollient such as lanolin to replace lost lipids in the stratum corneum.
  • To protect the skin, apply a moisture-barrier cream or spray if the patent has significant urinary or fecal incontinence (or both). The barrier may be zinc-based, petrolatum-based, dimethicone-based, an acrylic polymer, or another type. Consider using an algorithm developed by wound and skin care specialists that’s customized for skin care products your facility uses. (See Skin care algorithm by clicking the PDF icon above.)

If the treatment protocol fails, the patient should be referred to an appropriate skin care specialist promptly.

To help prevent urine or stool from contacting the patient’s skin, consider using a male external catheter, a female urinary pouch, a fecal pouch, or a bowel management system. Avoid containment devices. If the patient has a containment pad, make sure it’s highly absorbent and not layered, to decrease pressure under the patient.

Managing IAD

A comprehensive multidisciplinary approach to IAD is essential to the success of any skin care protocol. Identify skin care champions within your facility and educate them on IAD. Incorporating administrators, physicians, nursing staff, therapists, and care assistants makes implementation of protocols and algorithms within an institution seamless.

Administrators support the skin care program in the facility, including authorizing a budget so product purchases can be made. The certified wound clinician is the team expert regarding skin care, incontinence, prevention, and product recommendation. The physician oversees protocol development and evaluates and prescribes additional treatment when a patients fails to respond to treatment algorithms. Nursing staff identify patients at risk, incorporate the algorithm into the patient’s plan of care, and direct care
assistants
. Therapists address function, strength, and endurance issues to improve the patient’s self-care abilities in activities of daily living to manage or prevent episodes of incontinence.

In severe inflammation, topical dressings, such as alginates and foam dressings, may be used along with topical corticosteroids. In complex IAD, antifungals or antibiotics may be required if a secondary fungal or bacterial infection is suspected.

Additional diagnostic tests may be done to identify and treat secondary infections. These tests may include skin scraping, potassium hydroxide test or Gram’s stain for fungal components, or a swab culture and sensitivity for bacterial infections. If your patient has a suspected secondary fungal or bacterial infection, use appropriate treatments for the full course of recommended therapy. In severe secondary fungal infection, an oral agent may be added to topical therapy. If cost is a concern, consider using a pharmacy knowledgeable about compounding for topical combination therapies.

Referrals and education

For assessment and treatment of under-lying incontinence, refer the patient to a continence specialist if appropriate. Teach the patient strategies for managing incontinence through dietary measures, toileting programs, pelvic-floor muscle training, clothing modification, and mobility aids.

Selected references

Beguin A, Malaquin-Pavan E, Guihaire C, et al., Improving diaper design to address incontinence associated dermatitis. BMC Geriatrics. 2010;10:86. http://www.biomedcentral.com/1471-2318/10/86. Accessed March 15, 2012.

Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis. J Wound Ostomy Continence Nurs. 2011; 38(4):359-370.

Bliss DZ, Zehrer C, Savik K, et al. An economic evaluation of four skin damage prevention regimens in nursing home residents with incontinence: economics of skin damage prevention. J Wound Ostomy Continence Nurs. 2007;34(2):143-152.

Denat Y, Khorshid L. The effect of 2 different care products on incontinence-associated dermatitis in patients with fecal incontinence. J Wound Ostomy Continence Nurs. 2011;38(2):171-176.

Doughty DB. Urinary and Fecal Incontinence: Current Management Concepts. 3rd ed. St. Louis, MO: Mosby Elsevier; 2006.

Gray, M. Optimal management of incontinence-associated dermatitis in the elderly. Am J Clin Dermatol. 2010;11(3):201-210.

Gray M, Beeckman D, Bliss DZ, et al. Incontinence-associated dermatitis: a comprehensive review and update. J Wound Ostomy Continence Nurs. 2012;39(1):61-74

Gray M, Bliss DZ, Doughty DB, et al. Incontinence-associated dermatitis: a consensus. J Wound Ostomy Continence Nurs. 2007;34(1):45-54.

Gray M, Bohacek L, Weir D, et al. Moisture vs pressure: making sense out of perineal wounds. J Wound Ostomy Continence Nurs. 2007;34(2):134-42.

Institute for Clinical Systems Improvement. Health care protocol: Pressure ulcer prevention and treatment. Bloomington, MN: Institute for Clinical Systems Improvement. January 2012. http://www.icsi.org/pressure_ulcer_treatment_protocol__review_and_comment_/pressure_ulcer_treatment__protocol__.html. Accessed March 15, 2012.

Junkin J, Lerner-Selekof JL. Prevalence of incontinence and associated skin injury in the acute care inpatient. J Wound Ostomy Continence Nurs. 2007;34(3):260-269.

Landefeld CS, Bowers BJ, Feld AD, et al. National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. Ann Intern Med. 2008;148(6):449-458.

Langemo D, Hanson D, Hunter S, et al. Incontinence and incontinence-associated dermatitis. Adv Skin Wound Care. 2011;24(3):126-142.

Scheinfeld NS. Cutaneous candidiasis workup. 2011 update. http://emedicine.medscape.com/article/1090632-workup. Accessed March 15, 2012.

U.S. Census Bureau. The older population 2010. November 2011. www.census.gov/prod/cen2010/briefs/c2010br-09.pdf. Accessed March 15, 2012.

Nancy Chatham is an advanced practice nurse at Passavant Physician Associates in Jacksonville, Illinois. Carrie Carls is the nursing director of advanced wound healing and hyperbaric medicine at Passavant Area Hospital in Jacksonville, Illinois.

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A young Black scientist discovered a pivotal leprosy treatment in the 1920s − but an older colleague took the credit

Dr. Isabel Kerr, a European missionary, administering to a patient a chaulmoogra oil treatment in 1915, prior to the invention of the Ball Method. George McGlashan Kerr, CC BY

By Mark M. Lambert, Des Moines University

Hansen’s disease, also called leprosy, is treatable today – and that’s partly thanks to a curious tree and the work of a pioneering young scientist in the 1920s. Centuries prior to her discovery, sufferers had no remedy for leprosy’s debilitating symptoms or its social stigma.

This young scientist, Alice Ball, laid fundamental groundwork for the first effective leprosy treatment globally. But her legacy still prompts conversations about the marginalization of women and people of color in science today.

As a bioethicist and historian of medicine, I’ve studied Ball’s contributions to medicine, and I’m pleased to see her receive increasing recognition for her work, especially on a disease that remains stigmatized.

Who was Alice Ball?

Alice Augusta Ball, born in Seattle, Washington, in 1892, became the first woman and first African American to earn a master’s degree in science from the College of Hawaii in 1915, after completing her studies in pharmaceutical chemistry the year prior.

After she finished her master’s degree, the college hired her as a research chemist and instructor, and she became the first African American with that title in the chemistry department.

Impressed by her master’s thesis on the chemistry of the kava plant, Dr. Harry Hollmann with the Leprosy Investigation Station of the U.S. Public Health Service in Hawaii recruited Ball. At the time, leprosy was a major public health issue in Hawaii.

Doctors now understand that leprosy, also called Hansen’s disease, is minimally contagious. But in 1865, the fear and stigma associated with leprosy led authorities in Hawaii to implement a mandatory segregation policy, which ultimately isolated those with the disease on a remote peninsula on the island of Molokai. In 1910, over 600 leprosy sufferers were living in Molokai.

This policy overwhelmingly affected Native Hawaiians, who accounted for over 90% of all those exiled to Molokai.

The significance of chaulmoogra oil

Doctors had attempted to use nearly every remedy imaginable to treat leprosy, even experimenting with dangerous substances such as arsenic and strychnine. But the lone consistently effective treatment was chaulmoogra oil.

Chaulmoogra oil is derived from the seeds of the chaulmoogra tree. Health practitioners in India and Burma had been using this oil for centuries as a treatment for various skin diseases. But there were limitations with the treatment, and it had only marginal effects on leprosy.

The oil is very thick and sticky, which makes it hard to rub into the skin. The drug is also notoriously bitter, and patients who ingested it would often start vomiting. Some physicians experimented with injections of the oil, but this produced painful pustules.

Dr. Isabel Kerr, a European missionary, administering to a patient a chaulmoogra oil treatment in 1915, prior to the invention of the Ball Method. George McGlashan Kerr, CC BY
Dr. Isabel Kerr, a European missionary, administering to a patient a chaulmoogra oil treatment in 1915, prior to the invention of the Ball Method. George McGlashan Kerr, CC BY

The Ball Method

If researchers could harness chaulmoogra’s curative potential without the nasty side effects, the tree’s seeds could revolutionize leprosy treatment. So, Hollmann turned to Ball. In a 1922 article, Hollmann documents how the 23-year-old Ball discovered how to chemically adapt chaulmoogra into an injection that had none of the side effects.

The Ball Method, as Hollmann called her discovery, transformed chaulmoogra oil into the most effective treatment for leprosy until the introduction of sulfones in the late 1940s.

In 1920, the Ball Method successfully treated 78 patients in Honolulu. A year later, it treated 94 more, with the Public Health Service noting that the morale of all the patients drastically improved. For the first time, there was hope for a cure.

Tragically, Ball did not have the opportunity to revel in this achievement, as she passed away within a year at only 24, likely from exposure to chlorine gas in the lab.

Ball’s legacy, lost and found

Ball’s death meant she didn’t have the opportunity to publish her research. Arthur Dean, chair of the College of Hawaii’s chemistry department, took over the project.

Dean mass-produced the treatment and published a series of articles on chaulmoogra oil. He renamed Ball’s method the “Dean Method,” and he never credited Ball for her work.

Ball’s other colleagues did attempt to protect Ball’s legacy. A 1920 article in the Journal of the American Medical Association praises the Ball Method, while Hollmann clearly credits Ball in his own 1922 article.

Ball is described at length in a 1922 article in volume 15, issue 5, of Current History, an academic publication on international affairs. That feature is excerpted in a June 1941 issue of Carter G. Woodson’s “Negro History Bulletin,” referring to Ball’s achievement and untimely death.

Joseph Dutton, a well-regarded religious volunteer at the leprosy settlements on Molokai, further referenced Ball’s work in a 1932 memoir broadly published for a popular audience.

Historians such as Paul Wermager later prompted a modern reckoning with Ball’s poor treatment by Dean and others, ensuring that Ball received proper credit for her work. Following Wermager’s and others’ work, the University of Hawaii honored Ball in 2000 with a bronze plaque, affixed to the last remaining chaulmoogra tree on campus.

In 2019, the London School of Hygiene and Tropical Medicine added Ball’s name to the outside of its building. Ball’s story was even featured in a 2020 short film, “The Ball Method.”

The Ball Method represents both a scientific achievement and a history of marginalization. A young woman of color pioneered a medical treatment for a highly stigmatizing disease that disproportionately affected an already disenfranchised Indigenous population.

In 2022, then-Gov. David Ige declared Feb. 28 Alice Augusta Ball Day in Hawaii. It was only fitting that the ceremony took place on the Mānoa campus in the shade of the chaulmoogra tree.The Conversation


Mark M. Lambert, Assistant Professor of Behavioral Medicine, Medical Humanities, and Bioethics, Des Moines University

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

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Leprosy cases are rising in the US – what is the ancient disease and why is it spreading now?

leprosy

By Robert A. Schwartz, Rutgers University

The word “leprosy” conjures images of biblical plagues, but the disease is still with us today. Caused by infectious bacteria, some 200,000 new cases are reported each year, according to the World Health Organization. In the United States, leprosy has been entrenched for more than a century in parts of the South where people came into contact with armadillos, the principle proven linkage from animal to humans. However, the more recent outbreaks in the Southeast, especially Florida, have not been associated with animal exposure.

The Conversation talked with Robert A. Schwartz, professor and head of dermatology at Rutgers New Jersey Medical School, to explain what researchers know about the disease.

What is leprosy and why is it resurfacing in the US?

Leprosy is caused by two different but similar bacteria — Mycobacterium leprae and Mycobacterium lepromatosis — the latter having just been identified in 2008. Leprosy, also known as Hansen’s disease, is avoidable. Transmission among the most vulnerable in society, including migrant and impoverished populations, remains a pressing issue.

This age-old neglected tropical disease, which is still present in more than 120 countries, is now a growing challenge in parts of North America.

Leprosy is beginning to occur regularly within parts of the southeastern United States. Most recently, Florida has seen a heightened incidence of leprosy, accounting for many of the newly diagnosed cases in the U.S.

The surge in new cases in central Florida highlights the urgent need for health care providers to report them immediately. Contact tracing is critical to identifying sources and reducing transmission.

Traditional risk factors include zoonotic exposure and having recently lived in leprosy-endemic countries. Brazil, India and Indonesia have each noted more than 10,000 new cases since 2019, according to the World Health Organization data, and more than a dozen countries have reported between 1,000 to 10,000 new cases over the same time period.

Why was leprosy stigmatized in biblical times?

Evidence suggests that leprosy has plagued civilization since at least the second millennium B.C.

From that time until the mid-20th century, limited treatments were available, so the bacteria could infiltrate the body and cause prominent physical deformities such as disfigured hands and feet. Advanced cases of leprosy cause facial features resembling that of a lion in humans.

Many mutilating and distressing skin disorders such as skin cancers and deep fungal infections were also confused with leprosy by the general public.

Fear of contagion has led to tremendous stigmatization and social exclusion. It was such a serious concern that the Kingdom of Jerusalem had a specialized hospital to care for those suffering from leprosy.

How infectious is leprosy?

Research shows that prolonged in-person contact via respiratory droplets is the primary mode of transmission, rather than through normal, everyday contact such as embracing, shaking hands or sitting near a person with leprosy. People with leprosy generally do not transmit the disease once they begin treatment.

Armadillos represent the only known zoonotic reservoir of leprosy-causing bacteria that threaten humans. These small mammals are common in Central and South America and in parts of Texas, Louisiana, Missouri and other states, where they are sometimes kept as pets or farmed as meat. Eating armadillo meat is not a clear cause of leprosy, but capturing and raising armadillos, along with preparing its meat, are risk factors.

The transmission mechanism between zoonotic reservoirs and susceptible individuals is unknown, but it is strongly suspected that direct contact with an infected armadillo poses a significant risk of developing leprosy. However, many cases reported in the U.S. have demonstrated an absence of either zoonotic exposure or person-to-person transmission outside of North America, suggesting that transmission may be happening where the infected person lives. But in many cases, the source remains an enigma.

Some people’s genetics might make them more susceptible to leprosy infections, or their immune systems are less capable of resisting the disease.

Stigma and discrimination have prevented people from seeking treatment, and as a result, “concealed” cases contribute to transmission.

How do you recognize it?

Leprosy primarily affects the skin and peripheral nervous system, causing physical deformity and desensitizing one’s ability to feel pain on affected skin.

It may begin with loss of sensation on whitish patches of skin or reddened skin. As the bacteria spread in the skin, they can cause the skin to thicken with or without nodules. If this occurs on a person’s face, it may rarely produce a smooth, attractive-appearing facial contour known as lepra bonita, or “pretty leprosy.” The disease can progress to causing eyebrow loss, enlarged nerves in the neck, nasal deformities and nerve damage.

The onset of symptoms can sometimes take as long as 20 years because the infectious bacteria have a lengthy incubation period and proliferate slowly in the human body. So presumably many people are infected long before they know that they are.

Fortunately, worldwide efforts to screen for leprosy are being enhanced thanks to organizations like the Order of Saint Lazarus, which was originally founded in the 11th century to combat leprosy, and the Armauer Hansen Research Institute, which conducts immunologic, epidemiological and translational research in Ethiopia. The nongovernmental organization Bombay Leprosy Project in India does the same.

How treatable is it?

Leprosy is not only preventable but treatable. Defying stigma and advancing early diagnosis via proactive measures are critical to the mission of controlling and eradicating it worldwide.

Notably, the World Health Organization and other agencies provide multi-drug therapy at no cost to patients.

In addition, vaccine technology to combat leprosy is in the clinical trials stage and could become available in coming years. In studies involving nine-banded armadillos, this protein-based vaccine delayed or diminished leprous nerve damage and kept bacteria at bay. Researchers believe that the vaccine can be produced in a low-cost, highly efficient manner, with the long-term prospect of eradicating leprosy.

If health care professionals, biomedical researchers and lawmakers do not markedly enhance their efforts to eliminate leprosy worldwide, the disease will continue to spread and could become a far more serious problem in areas that have been largely free of leprosy for decades.

The World Health Organization launched a plan in 2021 for achieving zero leprosy.The Conversation

Robert A. Schwartz, Professor and Head of Dermatology, Rutgers New Jersey Medical School, Rutgers University

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

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Flesh-eating bacteria infections are on the rise in the US

Vibrio vulnificus

By Bill Sullivan, Indiana University

Flesh-eating bacteria sounds like the premise of a bad horror movie, but it’s a growing – and potentially fatal – threat to people.

In September 2023, the Centers for Disease Control and Prevention issued a health advisory alerting doctors and public health officials of an increase in flesh-eating bacteria cases that can cause serious wound infections.

I’m a professor at the Indiana University School of Medicine, where my laboratory studies microbiology and infectious disease. Here’s why the CDC is so concerned about this deadly infection – and ways to avoid contracting it.

What does ‘flesh-eating’ mean?

There are several types of bacteria that can infect open wounds and cause a rare condition called necrotizing fasciitis. These bacteria do not merely damage the surface of the skin – they release toxins that destroy the underlying tissue, including muscles, nerves and blood vessels. Once the bacteria reach the bloodstream, they gain ready access to additional tissues and organ systems. If left untreated, necrotizing fasciitis can be fatal, sometimes within 48 hours.

The bacterial species group A Streptococcus, or group A strep, is the most common culprit behind necrotizing fasciitis. But the CDC’s latest warning points to an additional suspect, a type of bacteria called Vibrio vulnificus. There are only 150 to 200 cases of Vibrio vulnificus in the U.S. each year, but the mortality rate is high, with 1 in 5 people succumbing to the infection.

How do you catch flesh-eating bacteria?

Vibrio vulnificus primarily lives in warm seawater but can also be found in brackish water – areas where the ocean mixes with freshwater. Most infections in the U.S. occur in the warmer months, between May and October. People who swim, fish or wade in these bodies of water can contract the bacteria through an open wound or sore.

Vibrio vulnificus can also get into seafood harvested from these waters, especially shellfish like oysters. Eating such foods raw or undercooked can lead to food poisoning, and handling them while having an open wound can provide an entry point for the bacteria to cause necrotizing fasciitis. In the U.S., Vibrio vulnificus is a leading cause of seafood-associated fatality.

Why are flesh-eating bacteria infections rising?

Vibrio vulnificus is found in warm coastal waters around the world. In the U.S., this includes southern Gulf Coast states. But rising ocean temperatures due to global warming are creating new habitats for this type of bacteria, which can now be found along the East Coast as far north as New York and Connecticut. A recent study noted that Vibrio vulnificus wound infections increased eightfold between 1988 and 2018 in the eastern U.S.

Climate change is also fueling stronger hurricanes and storm surges, which have been associated with spikes in flesh-eating bacteria infection cases.

Aside from increasing water temperatures, the number of people who are most vulnerable to severe infection, including those with diabetes and those taking medications that suppress immunity, is on the rise.

What are symptoms of necrotizing fasciitis? How is it treated?

Early symptoms of an infected wound include fever, redness, intense pain or swelling at the site of injury. If you have these symptoms, seek medical attention without delay. Necrotizing fasciitis can progress quickly, producing ulcers, blisters, skin discoloration and pus.

Treating flesh-eating bacteria is a race against time. Clinicians administer antibiotics directly into the bloodstream to kill the bacteria. In many cases, damaged tissue needs to be surgically removed to stop the rapid spread of the infection. This sometimes results in amputation of affected limbs.

Researchers are concerned that an increasing number of cases are becoming impossible to treat because Vibrio vulnificus has evolved resistance to certain antibiotics.

How do I protect myself?

The CDC offers several recommendations to help prevent infection.

People who have a fresh cut, including a new piercing or tattoo, are advised to stay out of water that could be home to Vibrio vulnificus. Otherwise, the wound should be completely covered with a waterproof bandage.

People with an open wound should also avoid handling raw seafood or fish. Wounds that occur while fishing, preparing seafood or swimming should be washed immediately and thoroughly with soap and water.

Anyone can contract necrotizing fasciitis, but people with weakened immune systems are most susceptible to severe disease. This includes people taking immunosuppressive medications or those who have pre-existing conditions such as liver disease, cancer, HIV or diabetes.

It is important to bear in mind that necrotizing fasciitis presently remains very rare. But given its severity, it is beneficial to stay informed.The Conversation


Bill Sullivan, Professor of Pharmacology & Toxicology, Indiana University

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

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Rare ‘Flesh-Eating’ Bacterium Spreads North as Oceans Warm

Map of cases of the flesh eating bacteria Vibrio vulnificus

Debbie King barely gave it a second thought when she scraped her right shin climbing onto her friend’s pontoon for a day of boating in the Gulf of Mexico on Aug. 13.

Even though her friend immediately dressed the slight cut, her shin was red and sore when King awoke the next day. It must be a sunburn, she thought.

But three days later, the red and blistered area had grown. Her doctor took one look and sent King, 72, to the emergency room.

Doctors at HCA Florida Citrus Hospital in Inverness, Florida, rushed King into surgery after recognizing the infection as Vibrio vulnificus, a potentially fatal bacterium that kills healthy tissue around a wound. While King lay on the operating table, the surgeon told her husband she would likely die if they didn’t amputate.

Just four days after the scrape, King lost her leg then spent four days in intensive care.

“The flesh was gone; it was just bone,” she said of her leg.

Cases of V. vulnificus are rare. Between 150 and 200 are reported to the Centers for Disease Control and Prevention every year, with about 20% resulting in death. Most are in states along the Gulf of Mexico, but, in 2019, 7% were on the Pacific Coast. Florida averages about 37 cases and 10 deaths a year.

But a rise in cases nationally and the spread of the disease to states farther north — into coastal communities in states such as Connecticut, New York, and North Carolina — have heightened concerns about the bacterium, which can result in amputations or extensive removal of tissue even in those who survive its infections. And warmer coastal waters caused by climate change, combined with a growing population of older adults, may result in infections doubling by 2060, a study in Scientific Reports warned earlier this year.

“Vibrio distributions are driven in large part by temperature,” said Tracy Mincer, an assistant professor at Florida Atlantic University. “The warmer waters are, the more favorable it is for them.”

 

The eastern United States has seen an eightfold increase in infections over a 30-year period through 2018 as the geographic range of infections shifted north by about 30 miles a year, according to the study, which was cited in a CDC health advisory last month.

The advisory was intended to make doctors more aware of the bacterium when treating infected wounds exposed to coastal waters. Infections can also arise from eating raw or undercooked seafood, particularly oysters, it warned. That can cause symptoms as common as diarrhea and as serious as bloodstream infections and severe blistered skin lesions.

New York and Connecticut this summer issued health warnings about the risk of infection as well. It’s not the first year either state has recorded cases.

“There’s very few cases but when they happen, they’re devastating,” said Paul A. Gulig, a professor in the Department of Molecular Genetics and Microbiology at the University of Florida College of Medicine.

‘An Accident of Nature’

Vibrio has more than 100 strains, including the bacterium that causes cholera, a disease that causes tens of thousands of deaths worldwide each year.

The V. vulnificus strain likes warm brackish waters close to shorelines where the salinity is not as high as in the open sea. Unlike some other Vibrio strains, it has no mechanism to spread between humans.

It’s found in oysters because the mollusks feed by filtering water, meaning the bacterium can become concentrated in oyster flesh. It can enter humans who swim in salty or brackish waters through the slightest cut in the skin. Infections are treated with antibiotics and, if needed, surgery.

“It’s almost an accident of nature,” Gulig said. “They have all these virulence factors that make them really destructive, but we’re not a part of this bug’s life cycle.”

Once inside the human body, the bacteria thrive.

Scientists don’t believe the bacteria eat flesh, despite how they’re often described. Rather, enzymes and toxins secreted by the bacterium as it multiplies break down the human tissue in the area below the skin, causing necrosis, or death of tissue cells.

The infection spreads like wildfire, Gulig said, making early detection critical.

“If you take a pen and mark where the edge of the redness is and then look at that two or four hours later, the redness would have moved,” Gulig said. “You can almost sit there and watch this spread.”

Researchers have conducted studies on the bacteria, but the small number of cases and deaths make it tough to secure funding, said Gulig. He said he switched his research focus to other areas because of the lack of money.

But growing interest in the bacteria has prompted talk about new research at his university’s Emerging Pathogens Institute.

Examining the bacteria’s genome sequence and comparing it with those of Vibrio strains that don’t attack human flesh could yield insights into potential drugs to interfere with that process, Gulig said.

Shock and Loss

Inside the operating room at HCA Florida Citrus, the only signs of King’s infection were on her shin. The surgeon opened that area and began cutting away a bright red mush of dead flesh.

Hoping to save as much of the leg as possible, the doctor first amputated below her knee.

But the bacteria had spread farther than doctors had hoped. A second amputation, this time 5 inches above the knee, had to be performed.

After surgery, King remained in critical care for four days with sepsis, a reaction to infection that can cause organs to fail.

Her son was there when she awakened. He was the one who told her she had lost her leg, but she was too woozy from medication to take it in.

It wasn’t until she was transferred to a rehab hospital in nearby Brooksville run by Encompass Health that the loss sank in.

A former radiation protection technician, King had always been self-reliant. The idea of needing a wheelchair, of being dependent on others — it felt like she had lost part of her identity.

One morning, she could just not stop crying. “It hit me like a ton of bricks,” she said.

Six different rehab staffers told her she needed to meet with the hospital’s consulting psychologist. She thought she didn’t need help, but she eventually gave in and met with Gerald Todoroff.

In four sessions with King, he said, he worked to redirect her perception of what happened. Amputation is not who you are but what you will learn to deal with, he told her. Your life can be as full as you wish.

“They were magic words that made me feel like a new person,” King said. “They went through me like music.”

Physical therapy moved her forward, too. She learned how to stand longer on her remaining leg, to use her wheelchair, and to maneuver in and out of a car.

Now, back in her Gulf Coast community of Homosassa, those skills have become routine. Her husband, Jim, a former oil company worker and carpenter, built an access ramp out of concrete and pressure-treated wood for their single-story home.

But she is determined to walk with the aid of a prosthetic leg. It’s the motivation for a one-hour regimen of physical therapy she does on her own every day in addition to twice-weekly sessions with a physical therapist.

Recovery still feels like a journey but one marked by progress. She has nicknamed her “stump” Peg. She’s now comfortable sharing before and after pictures of her leg.

And she’s made it her mission to talk about what happened so more people will learn about the danger.

“This is the most horrific thing that can happen to anybody,” she said. “But I’d sit back and think, ‘God put you here for a reason — you’ve got more things to do.’”

What to Know About ‘Flesh-Eating’ Bacterium Vibrio vulnificus

Infection Symptoms:

  • Diarrhea, often accompanied by stomach cramping, nausea, vomiting, and fever.
  • Wound infections cause redness, pain, swelling, warmth, discoloration, and discharge. They may spread to the rest of the body and cause fever.
  • Bloodstream infections cause fever, chills, dangerously low blood pressure, and blistering skin lesions.

To Protect Against Vibrio Infections:

  • Stay out of saltwater or brackish water if you have a wound or a recent surgery, piercing, or tattoo.
  • Cover wounds with a waterproof bandage if they could come into contact with seawater or raw or undercooked seafood and its juices.
  • Wash wounds and cuts thoroughly with soap and water after contact with saltwater, brackish water, raw seafood, or its juices.

Who Is Most at Risk:

  • Anyone can get a wound infection. People with liver disease, cancer, or diabetes, and those over 40 or with weakened immune systems, are more likely to get an infection and have severe complications.

Sources:

This article was produced in partnership with the Tampa Bay Times.

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

 

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Topics Covered:

  • The Indications and Contraindications for Collagen
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As a visionary and entrepreneur in the field of mobile medicine, she has operated mobile wound care practices nationwide for many years. She enjoys educating on the art and science of wound healing and how practical solutions apply to healthcare professionals today. Martha enjoys being a positive change in healthcare impacting clients suf­fering from wounds and skin issues of all etiologies.


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