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

Wound Care Advisor
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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NYU docs are using machine learning to stop a stealthy disease before it’s too late

Wound Care Advisor
lymphatic system disease

Researchers at NYU’s Tandon School of Engineering have teamed up with those from the university’s Rory Meyers College of Nursing to develop a machine-learning algorithm that could help detect a lymphatic system disease before doctors are able to.

There is no cure for lymphedema, only physical exercises that can keep the symptoms in check. (more…)

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Herpes zoster: Understanding the disease, its treatment, and prevention

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Herpes zoster: Understanding the disease, its treatment, and prevention

Herpes zoster (HZ, also called shingles) is a painful condition that produces a maculopapular and vesicular rash. Usually, the rash appears along a single dermatome (band) around one side of the body or face.

In most cases, pain, tingling, burning, or itching occurs a few days before the rash. Next, blisters form, scabbing over in 7 to 10 days. In rare cases, the rash is widespread, resembling varicella zoster (VZ, or chickenpox) rash. Pain can range from mild to severe and may be dull, burning, or gnawing. It may last weeks, months, or even years after the blisters heal. Shingles on the face may impair vision or hearing. (more…)

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Helping patients with lower-extremity disease benefit from exercise

Wound Care Advisor

By Jeri Lundgren, BSN, RN, PHN, CWS, CWCN

Research has shown that exercise can help ease symptoms in patients with arterial insufficiency, venous insufficiency, neuropathic disease, or a combination of these conditions. Here’s what you need to know to ensure your patients reap the most benefits from exercise. (more…)

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Hidden complications: A case study in peripheral arterial disease

Wound Care Advisor

By Pamela Anderson, MS, RN, APN-BC, CCRN, and Terri Townsend, MA, RN, CCRN-CMC, CVRN-BC

Jan Smith, age 59, is admitted to the coronary intensive care unit with an acute inferior myocardial infarction (MI). Recently diagnosed with hypertension and hyperlipidemia, she smokes a pack and a half of cigarettes daily. She reports she has always been healthy and can’t believe she has had a heart attack. (Note: Name is fictitious.)

On physical exam, the cardiologist finds decreased femoral pulses bilaterally and recommends immediate cardiac catheterization. Fortunately, primary percutaneous coronary intervention (PCI) is readily available at this hospital. PCI is the preferred reperfusion method when it can be provided by skilled cardiologists in a timely manner. (more…)

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Chronic venous insufficiency with lower extremity disease: Part 2

Wound Care Advisor

By Donald A. Wollheim, MD, WCC, DWC, FAPWCA

To begin appropriate treatment for chronic venous insufficiency (CVI), clinicians must be able to make the correct diagnosis. Part 1 (published in the March-April edition) described CVI and its presentation. This article provides details of the CVI diagnosis (including the differential diagnosis from other diseases), disease classification to help assess the extent of CVI, diagnostic studies used to diagnose CVI, and various treatment options to “rescue” the patient from CVI. (more…)

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Chronic venous insufficiency with lower extremity disease: Part 1

Wound Care Advisor

By Donald A. Wollheim, MD, WCC, DWC, FAPWCA

Chronic venous insufficiency (CVI) is the most common cause of lower extremity wounds. The venous tree is defective, incapable of moving all the blood from the lower extremity back to the heart. This causes pooling of blood and intravascular fluid at the lowest gravitational point of the body—the ankle.

This article has two parts. Part 1 enhances your understanding of the disease and its clinical presentation. Part 2, which will appear in a later issue, explores the differential diagnosis of similar common diseases, the role that coexisting peripheral artery disease (PAD) may play, disease classification of venous insufficiency, and a general approach to therapy.

The most common form of lower extremity vascular disease, CVI affects 6 to 7 million people in the United States. Incidence increases with age and other risk factors. One study of 600 patients with CVI ulcers revealed that 50% had these ulcers for 7 to 9 months, 8% to 34% had them for more than 5 years, and 75% had recurrent ulcers.

Thrombotic complications of CVI include thrombophlebitis, which may range from superficial to extensive. If the thrombophlebitis extends up toward the common femoral vein leaving the leg, proximal ligation may be needed to prevent clot extension or embolization.

Understanding normal anatomy and physiology

Lower extremity veins flow horizontally from the superficial veins to the perforating veins and then into the deep veins. Normally, overall venous blood flows vertically against gravity from the foot and ankle upward toward the inferior vena cava (IVC). This antigravity flow toward the IVC results from muscular contraction around nonobstructed veins and one-way valves that close as blood passes them. These valves prevent abnormal backward blood flow toward the foot and ankle region.

The lower extremities have four types of veins. Superficial veins are located within the subcutaneous tissue between the dermis and muscular fascia. Examples are the greater and lesser (smaller) saphenous veins. Perforating veins connect the superficial veins to the deep veins of the leg. The deep veins are located below the muscular fascia. The communicating veins con­nect veins within the same system.

The greater saphenous vein is on the leg’s medial (inner) side. It originates from the dorsal veins on top of the foot and eventually drains into the common femoral vein in the groin region. By way of perforating veins, the greater saphenous vein drains into the deep venous system of both the calf and thigh.

The lesser saphenous vein is situated on the lateral (outer) side of the leg and originates from the lateral foot veins. As it ascends, it drains into the deep system at the popliteal vein behind the knee. Communicating veins connect the greater saphenous vein medially and the lesser saphenous vein laterally.

Intramuscular veins are the deep veins within the muscle itself, while the intermuscular veins are located between the muscle groups. The intermuscular veins are more important than other veins in development of chronic venous disease. Below the knee, the intermuscular veins are paired and take on the name of the artery they accompany—for example, paired anterior tibial, paired posterior tibial, and paired peroneal veins. Eventually, these veins form the popliteal vein behind the knee, which ultimately drains into the femoral vein of the groin.

As the common femoral vein travels below the inguinal ligament of the groin, it’s called the external iliac vein. Eventually, it becomes the common iliac vein, which drains directly into the IVC.

Pathophysiology

Abnormally elevated venous pressure stems from the leg’s inability to adequately drain blood from the leg toward the heart. Blood drainage from the leg requires the muscular pumping action of the leg onto the veins, which pump blood from the leg toward the heart as well as from the superficial veins toward the deep veins. Functioning one-way valves within the veins close when blood passes them, preventing blood from flowing backward toward the ankle. This process resembles what happens when you climb a ladder with intact rungs: As you step up from one rung to the next, you’re able to ascend.

CVI and the “broken rung” analogy

If the one-way valves are damaged or incompetent, the “broken rung” situation occurs. Think how hard it would be to climb a ladder with broken rungs: You might be able to ascend the ladder, but probably you would fall downward off the ladder due to the defective, broken rungs.

Normally, one-way valves ensure that blood flows from the lower leg toward the IVC and that the superficial venous system flows toward the deep venous system. The venous system must be patent (open) so blood flowing from the leg can flow upward toward the IVC. Blockage of a vein may result from an acute thrombosis (clot) in the superficial or deep systems. With time, blood may be rerouted around an obstructed vein. If the acute thrombosis involves one or more of the one-way valves, as the obstructing thrombosis opens up within the vein’s lumen, permanent valvular damage may occur, leading to post-thrombotic syndrome—a form of CVI.

CVI may result from an abnormality of any or all of the processes needed to drain blood from the leg—poor pumping action of the leg muscles, damage to the one-way valves, and blockage in the venous system. CVI commonly causes venous hypertension due to reversal of blood flow in the leg. Such abnormal flow may cause one or more of the following local effects:

  • leg swelling
  • tissue anoxia, inflammation, or necrosis
  • subcutaneous fibrosis
  • Compromised flow of venous blood or lymphatic fluid from the extremity.

“Water balloon” analogy

The effect of elevated venous pressure or hypertension is worst at the lowest gravitational point (around the ankle). Pooling of blood and intravascular fluid around the ankle causes a “water balloon” effect. A balloon inflated with water has a thin, easily traumatized wall. When it bursts, a large volume of fluid drains out. Due to its thicker wall, a collapsed balloon that contains less fluid is more difficult to break than one distended with water.

In a leg with CVI, subcutaneous fluid that builds up requires a weaker force to break the skin and ulcerate than does a nondistended leg with less fluid. This principle is the basis for compression therapy in treating and preventing CVI ulcers.

Effects of elevated venous pressure or hypertension

Increased pressure in the venous system causes:

  • abnormally high pressure in the superficial veins—60 to 90 mm Hg, compared to the normal pressure of 20 to 30 mm Hg
  • dilation and distortion of leg veins, because blood refluxes abnormally away from the heart and toward the lower leg and may move from the deep venous system into the superficial veins.

Abnormal vein swelling from elevated pressure in itself may impair an already abnormally functioning one-way valve. For instance, the valve may become more displaced due to the increase in intraluminal fluid, which may in turn worsen hypertension and cause an increase in leg swelling. Increased pressure from swollen veins also may dilate the capillary beds that drain into the veins; this may cause leakage of fluid and red blood cells from capillaries into the interstitial space, exacerbating leg swelling. Also, increased venous pressure may cause fibrinogen to leak from the intravascular plasma into the interstitial space. This leakage may create a fibrin cuff around the capillary bed, which may decrease the amount of oxygen entering the epidermis, increase tissue hypoxia, trigger leukocyte activation, increase capillary permeability, and cause local inflammation. These changes may lead to ulceration, lipodermatosclerosis, or both.

Visible changes may include dilated superficial veins, hemosiderin staining due to blood leakage from the venous tree, atrophie blanche, and lipodermatosclerosis. (See CVI glossary by clicking the PDF icon above.) Both atrophie blanche and lipodermatosclerosis result from local tissue scarring secondary to an inflammatory reaction of the leg distended with fluid.

Lipodermatosclerosis refers to scarring of subcutaneous tissue in severe venous insufficiency. Induration is associated with inflammation, which can cause the skin to bind to the subcutaneous tissue, causing narrowing of leg circumference. Lymphatic flow from the leg also may become compromised and inhibited in severe venous hypertension, causing additional leg swelling.

Patient history

In a patient with known or suspected CVI, a thorough history may lead to a working diagnosis. Be sure to ask the patient these questions:

  • Do you have pain?
  • Is your pain worse toward the end of the day?
  • Is the pain relieved with leg elevation at night?
  • Is it relieved with leg elevation during the day?
  • Do you have leg pain that awakens you at night?
  • How would you describe the pain?
  • Does the skin on your leg feel tight or irritated?
  • Have you noticed visible changes of your leg?
  • Do you have a leg ulcer?

Also determine if the patient has comorbidities that may exacerbate CVI, including PAD, renal failure, venous thrombosis, lymphedema, diabetes mellitus, heart failure, or malnutrition. (See CVI risk factors by clicking the PDF icon above .)

Common CVI symptoms

Approximately 20% of CVI patients have symptoms of the disease without physical findings. These symptoms may include:

  • tired, “heavy” legs that feel worse toward the end of the day
  • discomfort that worsens on standing
  • legs that feel best in the morning after sleeping or after the legs have been
  • elevated during the day.

Although patients may report leg discomfort, the history indicates that it doesn’t awaken them at night. Be aware that discomfort from CVI differs from that caused by PAD. With PAD, patients may report pain on exercise (claudication), pain with elevation (nocturnal pain), or constant pain (resting pain).

Signs of CVI (with or without ulcers) include:

  • leg swelling (seen in 25% to 75% of patients)
  • skin changes (such as hemosiderin staining or dermatitis)
  • telangiectasia, reticular veins, or both; while these are the most common signs, they represent an overall less severe finding
  • varicose veins with or without bleeding, occurring in one-third of patients with CVI.

Venous ulcers

Venous ulcers are the most common type of lower extremity ulcer. They’re commonly found on the medial aspect of the lower extremity, from the ankle to the more proximal calf area. Usually, they arise along the course of the greater saphenous vein, but also may be lateral and may occur at multiple locations. They aren’t found above the knee or on the forefoot. Venous ulcers are shallower than arterial ulcers and have considerable exudate consistent with drainage from a ruptured water balloon. They may extend completely around the leg.

CVI: From a heavy sensation to visible changes

In patients with CVI, blood flows within a lower extremity in an abnormal, reverse direction, causing build-up of blood and intravascular fluid around the ankle. Initially, this may cause only a sensation of heavy legs toward the end of the day, with no visible changes. Eventually, it may lead to venous ulcers or other visible changes. This abnormal blood flow results from dysfunction of the normal mechanisms that drain blood from the leg against gravity into the IVC.

Selected references

Alguire PC, Mathes BM. Clinical evaluation of lower extremity chronic venous disease. UpToDate. Last updated April 18, 2012. http://www.uptodate.com/contents/clinical-evaluation-of-lower-extremity-chronic-venous-disease?source=search_result&
search=Clinical+evaluation+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150.  Accessed March 3, 2013.

Alguire PC, Mathes BM. Diagnostic evaluation of chronic venous insufficiency. UpToDate. Last updated May 7, 2012. www.uptodate.com/contents/diagnostic-evaluation-of-chronic-venous-insufficiency?source=search_result&search=Diagnostic+evaluation
+of+chronic+venous+insufficiency&selectedTitle=1%7E127. Accessed March 3, 2013.

Alguire PC, Mathes BM. Pathophysiology of chronic venous disease. UpToDate. Last updated April 12, 2012. www.uptodate.com/contents/pathophysiology-of-chronic-venous-disease?source=search_result&search=Pathophysiology+of+chronic+venous+disease
&selectedTitle=1%7E127. Accessed March 3, 2013.

Alguire PC, Scovell S. Overview and management of lower extremity chronic venous disease. UpToDate. Last updated June 27, 2012. www.uptodate.com/contents/overview-and-management-of-lower-extremity-chronic-venous-disease?source=search_
result&search=Overview+and+management+of+lower+extremity+chronic+venous+disease&selectedTitle=1%7E150. Accessed March 3, 2013.

Moneta G. Classification of lower extremity chronic venous disorders. UpToDate. Last updated October 22, 2011. www.uptodate.com/contents/classification-of-lower-extremity-chronic-venous-disorders. Accessed March 3, 2013.

Sardina D. Skin and Wound Management Course; Seminar Workbook. Wound Care Education Institute; 2011:92-112.

Donald A. Wollheim is a practicing wound care physician in southeastern Wisconsin. He also is an instructor for Wound Care Education Institute and Madison College. He serves on the Editorial Board for Wound Care Advisor.

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Necrotizing fasciitis: Frightening disease, potentially grim prognosis

Wound Care Advisor

By Lydia Meyers, BSN, RN, CWCN

Necrotizing fasciitis (NF) results from an infection that attacks the fascia and subcutaneous tissues. The primary bacterial etiology is group A streptococcus, a facultative anaerobic bacterium. However, other bacteria may contribute. Sometimes called the “flesh-eating” disease because of the potentially devastating effect on the afflicted patient, NF can be monomicrobial or polymicrobial.

The four typical settings for NF are:

  • surgical bowel or abdominal trauma surgery
  • pressure ulcer and perianal abscess
  • injection sites (especially in drug users)
  • Bartholin abscess or minor vulvovaginal infection.

Because of the rapid course and ravaging nature of acute NF, clinicians must maintain a high index of suspicion if the patient has suggestive signs and symptoms. In 1990, puppeteer Jim Henson (best known for creating the Muppets) died from NF. At that time, little was known about the progression of group A streptococcal infection.
The disease can quickly cause death, so starting immediate treatment is even more crucial than confirming the diagnosis. Once the disease is suspected, antibiotics must be given immediately and the patient must be prepared for surgery at once. NF spreads rapidly, capable of progressing from a small lesion to death in days to weeks. Thus, delayed diagnosis increases the risk of death. Lack of knowledge about the disease and inability to recognize it promptly are the main reasons many victims die. This article can improve your knowledge base.

Overview

NF was discovered in 1871 by Joseph Jones, a Confederate Army surgeon. At that time, it was called hemolytic streptococcal gangrene, nonclostridial gas gangrene, nonclostridial crepitant cellulitis, necrotizing or gangrenous erysipelas, necrotizing cellulitis, bacterial synergistic gangrene, or synergistic necrotizing cellulitis.
NF involves the fascia, muscle compartments, or both. It can affect not only the muscle fascia but the superficial fascia. NF and cellulitis differ in the amount of tissue involved and extent of tissue involvement.
The most common areas of infection are the abdominal wall, perineum, and extremities. When NF affects the perineum and scrotum, it’s called Fournier gangrene, after the French dermatologist and virologist Alfred Jean Fournier.
The most common causes are trauma, surgery, and insect bites. The disease can affect persons of any age. Such comorbidities as diabetes, chronic renal failure, immunosuppressive therapy, hypertension, obesity, and malnutrition increase susceptibility.

Pathophysiology

NF falls into four classifications based on wound microbiology. Type 1, the most common, involves polymicrobial bacteria. Type 2 results from trauma and is associated with comorbidities. Type 3, rare in this country, stems from gram-negative marine bacteria. Type 4 is a fungal infection occurring mostly in immunocompromised persons. (See Comparing types of necrotizing fasciitis by clicking the PDF icon above.)

Disease progression

The four types of NF progress in a similar way. Bacteria secrete pyrogenic exotoxin A, which stimulates cytokines. These cyto­kines damage the endothelial lining; fluid then leaks into the extravascular space.
M proteins in streptococci and β-hemolytic streptococci exacerbate the immune reaction by inhibiting phagocytosis of polymorphonuclear leukocytes and normal neutrophil chemotaxis. As the immune reaction increases, blood vessels dilate, allowing toxins to leak through vessel walls, which in turn decreases blood flow. As the cascade continues, hypoxic conditions cause facultative aerobic organisms to grow and become anaerobic. These bacteria exacerbate destruction of surrounding cells and lead to release of carbon dioxide, water, hydrogen, nitrogen, hydrogen sulfide, and methane. As the infection continues to progress, toxins spread throughout the bloodstream and the patient becomes septic.

Assessment

Obtain the patient’s medical history and description of the wound. Determine when the changes first appeared and whether the affected area seemed to get worse recently.
In all NF types, patients commonly present with a small, painful area (possibly with entry marks) but no other signs or symptoms. The wound may appear as a bulla, cellulitis, or dermatitis, representing an infection developing in underlying tissues. The skin may have a wooden-hard feel as the infection progresses to the subcutaneous space and causes necrosis. The wound becomes discolored and necrotic; drainage is rare until surgical debridement begins. The patient quickly develops fever, chills, nausea, and vomiting. As NF progresses, bullae become dark purple with darkened edges; the patient grows disoriented and lethargic, and organ failure and respiratory failure
ensue. Without treatment, the patient dies.

Diagnosis

Diagnostic tests usually include magnetic resonance imaging, complete blood count with differential, comprehensive metabolic panel, and cultures. (See Diagnostic findings in necrotizing fasciitis by clicking the PDF icon above.)

Treatment

Immediate surgical debridement and broad-spectrum antibiotics are needed to stop the immune response to infection. Clindamycin, gentamicin, penicillin, or metronidazole may be given alone or in combination until culture results are available. Supportive care includes total parenteral nutrition for nutritional support, I.V. fluids, and oxygen. Limb amputation should be done only as a last resort.
Surgical debridement involves penetrating deep into the fascia and removing all necrotic tissue. After the first debridement, release of “dishwater fluid” may occur.
Administering hyperbaric oxygen therapy (HBOT) after the first debridement increases tissue oxygenation, thus reducing tissue destruction by anaerobic bacteria. During HBOT (usually given as a 90-minute treatment), the patient breathes 100% oxygen in an environment of increasing atmospheric pressure.
HBOT should be given in conjunction with surgical debridement (usually after each debridement) and should continue until necrotic tissue ceases and cell destruction stops. HBOT also promotes collagen synthesis and neoangiogenesis (new blood vessel growth), which boosts blood supply and oxygen to tissues.
Adverse effects of HBOT include ear pain, oxygen toxicity, and seizures. Ear pain can be minimized by swallowing or yawning. If the patient continues to have ear pain, ear tubes may be inserted by an otolaryngologist. During HBOT, air breaks (intervals of breathing room air) are important in controlling oxygen toxicity (the main cause of seizures).
Throughout the HBOT treatment period, wound dressings must be simple. Well-moistened gauze dressings and an abdominal pad provide good support. Once necrotic destruction occurs, dressings depend on wound size and the need to fill cavities. The patient may require a diverting colostomy, depending on wound
location and the amount of uncontrolled diarrhea. Blood glucose levels must be monitored before and after HBOT, as this treatment affects blood glucose.

Supportive care and follow-up treatment

During initial treatment, patients need supportive care and monitoring. Once they’re out of danger, begin teaching them how to prevent NF recurrences. Advise them to control blood glucose levels, keeping the glycated hemoglobin (HbA1c) level to 7% or less. Caution patients to keep needles capped until use and not to reuse needles. Instruct them to clean the skin thoroughly before blood glucose testing or insulin injection, and to use alcohol pads to clean the area afterward.
Before discharge, help arrange the patient’s aftercare, including home health care for wound management and teaching, social services to promote adjustment to lifestyle changes and financial concerns, and physical therapy to help rebuild strength and promote the return to optimal physical health. One helpful patient resource is the National Necrotizing Fasciitis Foundation. The Centers for Disease Control and Prevention section on necrotizing fasciitis includes “Common sense and great wound care are the best ways to prevent a bacterial skin infection.”
The life-threatening nature of NF, scarring caused by the disease, and in some cases the need for limb amputation can alter the patient’s attitude and viewpoint, so be sure to take a holistic approach when dealing with the patient and family. Today, NF has a much better survival rate than 2 decades ago when Jim Henson died. In my practice, I’ve seen four NF cases. Thanks to early identification, good wound care, and HBOT, these patients suffered only minimal damage.

Selected references

Boyer A, Vargas F, Coste F, et al. Influence of surgical treatment timing on mortality from necrotizing soft tissue infections requiring intensive care management. Intensive Care Med. 2009;35(5):847-853. doi:10.1007/s00134-008-1373-4.

Cain S. Necrotizing fasciitis: recognition and care. Practice Nurs. 2010;21(6):297-302.

Centers for Disease Control and Prevention. Notes from the field: fatal fungal soft-tissue infections after a tornado—Joplin, Missouri, 2011. MMWR. 2011;60(29):992.

Chamber AC, Leaper DJ. Role of oxygen in wound healing: a review of evidence. J Wound Care. 2011; 20(4):160-164.

Christophoros K, Achilleas K, Vasilia D, et al. Postraumatic zygomycotic necrotizing abdominal wall fasciitis with intraabdominal invasion in a non immunosuppressed patient. Internet J Surg. 2007;11(1). doi:10.5580/17a8.

Ecker K-W, Baars A, Topfer J, Frank J. Necrotizing fasciitis of the perineum and the abdominal wall-surgical approach. Europ J Trauma Emerg Surg. 2008;
34(3):219-228. doi:10.1007/s00068-008-8072-2.

Hunter J, Quarterman C, Waseem M, Wills A. Diagnosis and management of necrotizing fasciitis. Br J Hosp Med. 2011;72(7):391-395.

Magel DC. The nurse’s role in managing necrotizing fasciitis. AORN J. 2008;88(6):977-982.

Phanzu MD, Bafende AE, Imposo BB, Meyers WM, Portaels F. Under treated necrotizing fasciitis masquerading as ulcerated edematous Mycobacterium ulcerans infection (Buruli ulcer). Am J Trop Med Hyg. 2012;82(3):478-481.

Ruth-Sahd LA, Gonzales M. Multiple dimensions of caring for a patient with acute necrotizing fasciitis. Dimens Crit Care Nurs. 2006;25(1):15-21.

Stevens DL, Bisno AL, Chambers HF, et al; Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-1406.

Su YC, Chen HW, Hong YC, Chen CT, et al. Laboratory risk indicator for necrotizing fasciitis score and the outcomes. ANZ J Surg. 2008;78(11):968-972.

Taviloglu K, Yanar H. Necrotizing fasciitis: strategies for diagnosis and management. World J Emerg Surg. 2007;2:19.

Lydia Meyers is a medical reviewer for National Government Services in Castleton, Indiana, and a clinical liaison at CTI Nutrition in Indianapolis. She has 11 years of wound care experience in nursing homes, wound clinics, and home health.

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

Wound Care Advisor
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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Flesh-eating bacteria infections are on the rise in the US

Wound Care Advisor
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

Wound Care Advisor
Map of cases of the flesh eating bacteria Vibrio vulnificus

By Christopher O’Donnell, Tampa Bay Times

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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