While most travelers will have onset and resolution of diarrhea during their trip, some will present with symptoms after return. Although most cases of travelers’ diarrhea (TD) are acute and self-limited, some people develop persistent (>14 days) gastrointestinal (GI) symptoms. Details on the management of TD during travel are available in the Travelers’ Diarrhea chapter.
Pathogenesis
While acute travelers’ diarrhea (i.e., diarrhea lasting less than 2 weeks) is usually self-limited and the etiologies are mostly infectious pathogens (see Travelers’ Diarrhea chapter), the pathogenesis of persistent diarrhea (i.e., diarrhea lasting 2 weeks or longer) in returned travelers generally falls into 1 of the following broad categories: ongoing infection or co-infection with a second organism not targeted by initial therapy; previously undiagnosed GI disease unmasked by the enteric infection; or a post-infectious phenomenon.
Ongoing infection
Most cases of TD are the result of bacterial or viral infection and are short-lived and self-limited. In addition to prolonged symptoms of typical pathogens among immunosuppressed persons and sequential infection with different pathogens, ongoing infection with parasites can cause prolonged diarrheal symptoms. Table 10.4.1 lists common bacterial, viral, and protozoal pathogens causing TD.
Table 10.4.1: Common bacterial, viral, and protozoal pathogens causing travelers’ diarrhea
Common Bacterial, Viral, and Protozoal Pathogens Causing Travelers’ Diarrhea – Table 10.4.1 – Bacteria
1Due to its narrower spectrum of activity, ciprofloxacin is slightly preferred over levofloxacin.
2Given the risk for hemolytic uremic syndrome, for patients with confirmed or suspected EHEC/STEC infection, hospitalization for aggressive fluid management and avoidance of antibiotics are recommended.
3Given risks of prolonged carriage associated with antibiotic use, antibiotics are recommended only for non-typhoidal Salmonella infection in infants, the elderly (>50 years), the immunocompromised, or those with severe disease.
4Given emergence of extensively drug-resistant strains, for patients with Shigella infection who have severe disease (e.g., bacteremia, hospitalized) or who are immunocompromised, empiric treatment with a carbapenem is recommended while awaiting results of drug susceptibility testing.
5Antibiotics are only indicated for moderate to severe illness.
6Tinidazole is preferred over metronidazole due to lower frequency of dosing and higher efficacy for some organisms.
7Intraluminal agents include paromomycin, iodoquinol, and diloxanide furoate.
Bacterial
While individual bacterial infections rarely cause persistent symptoms, travelers infected with bacteria known to cause mucosal inflammation, such as Campylobacter spp., Shigella spp., or Salmonella spp., as well as diarrheagenic Escherichia coli, can experience persistent diarrhea, including cases where the organism may be resistant against antibiotics commonly used for empiric treatment of TD (see Typhoid and Paratyphoid Fever chapter). A rare cause of post-travel persistent diarrhea is Yersinia spp., a foodborne bacterial infection which can present as a subacute febrile gastroenteritis.
Clostridioides difficile-associated diarrhea can occur after or during antibiotic use, including malaria chemoprophylaxis. The association between C. difficile and antimicrobial treatment is especially important to consider in patients with persistent TD that seems refractory to multiple courses of empiric antibiotic therapy. The initial workup of persistent TD should always include C. difficile testing. Healthcare professionals can prescribe oral vancomycin, fidaxomicin, or, less optimally, metronidazole, to treat C. difficile. Recurrent cases may be treated with fecal microbiota transplantation, now available by the oral route or as a retention enema. The monoclonal antibody bezlotoxumab is also an option.
Parasitic
As a group, parasites are the pathogens most likely to be isolated from patients with persistent diarrhea. Most parasitic infections have a less acute onset of symptoms than those caused by bacteria or viruses, and the probability of a traveler having a parasitic infection increases with increasing duration of symptoms. Parasites might also be the cause of persistent diarrhea in patients already treated for a bacterial pathogen.
Giardiasis
Giardia duodenalis is the most likely parasitic pathogen to cause persistent diarrhea. Suspect giardiasis particularly in patients with fatty stools, flatulence, or upper GI-predominant symptoms. When giardiasis is left untreated, symptoms can last for months, even in immunocompetent hosts. Diagnosis can be made by stool polymerase chain reaction (PCR), microscopy, enzyme immunoassay, or immunofluorescence (see Evaluation section below). In the absence of diagnostics (given the high prevalence of Giardia duodenalis as a cause for persistent TD), empiric therapy is a reasonable option in the appropriate clinical setting.
Amebiasis
Infection with Entamoeba histolytica, or amebiasis, can result in intestinal symptoms ranging from mild diarrhea to dysentery. Diagnosis can be made by stool PCR, microscopy, or enzyme immunoassay. Microscopy cannot distinguish between the pathogen E. histolytica and some non-pathogenic Entamoeba species such as Entamoeba dispar. Treatment is with metronidazole, followed by an intraluminal agent such as paromomycin or iodoquinol. Antibody testing for E. histolytica should be used for extra-intestinal infection only.
Cryptosporidiosis
Cryptosporidium spp. are emerging as common protozoans causing persistent diarrhea in both returning travelers and U.S. residents. Transmitted through contaminated food and water (including recreational water), most infections are asymptomatic or are self-limited. Symptoms may include watery diarrhea, nausea, or abdominal cramping. Disease may be more severe and prolonged in immunocompromised individuals. Diagnosis can be made by stool PCR, microscopy (modified acid-fast stain), immunofluorescence, or enzyme immunoassay. While most immunocompetent individuals recover with oral rehydration alone, in those with persistent symptoms, nitazoxanide may be used.
Cyclosporiasis
Cyclospora spp. may cause protozoal infection generally acquired by ingestion of contaminated food. It has been an increasingly recognized cause of persistent diarrhea in both U.S. residents and returning travelers. The oocyst of Cyclospora is resistant to chlorine disinfection. Diagnosis is through stool PCR or microscopy (modified acid-fast stain or wet mount confirmed by ultraviolet autofluorescence). Treatment is with trimethoprim-sulfamethoxazole.
Cystoisosporosis
Infection with Cystoisospora belli results in sudden onset of watery diarrhea that is self-resolving, although it may cause persistent diarrhea in immunocompromised individuals. Diagnosis can be made through detection of oocysts by stool microscopy (modified acid-fast stain). Most cases are self-resolving. Trimethoprim-sulfamethoxazole can be used if symptoms persist or if a patient is immunocompromised.
Dientamoeba fragilis infection
Dientamoeba fragilis is a protozoan that may be found in stools of both healthy individuals and in persons with abdominal symptoms. While it can be associated with diarrhea in returning travelers, its role as an intestinal pathogen is unclear. Diagnosis can be made by stool PCR or microscopy of permanently stained stool smears. Treatment options, none of which have been assessed in randomized controlled trials, include metronidazole and paromomycin.
Fungal
Microsporidiosis
Microsporidia are a group of fungi that can cause a self-limited watery diarrhea in travelers. In people living with HIV and rarely in immunocompetent persons, microsporidia can cause a chronic diarrhea. The route of transmission is not well known, and foodborne, waterborne, and animal-contact transmission have been reported. Diagnosis can be made by stool PCR or microscopy. Treatment depends on the species and includes albendazole.
Tropical sprue and brainerd diarrhea
Persistent TD also has been associated with tropical sprue and Brainerd diarrhea, both of which are believed to be caused by an infectious agent, although their culprit pathogens have yet to be identified. Tropical sprue is associated with deficiencies of vitamins absorbed in the proximal and distal small bowel and most commonly affects long-term travelers to tropical areas, as the name implies. The incidence of tropical sprue appears to have declined dramatically over the past 3 decades. Brainerd diarrhea is a syndrome of acute onset watery diarrhea lasting ≥4 weeks. Symptoms include 10–20 episodes of explosive, watery diarrhea per day, as well as fecal incontinence, abdominal cramping, gas, and fatigue. Nausea, vomiting, and fever are rare.
Underlying gastrointestinal disease
Celiac disease
In some cases, persistent symptoms relate to chronic underlying GI disease or to a susceptibility unmasked by the enteric infection. Most prominent among these is celiac disease, a systemic disease manifesting primarily with small bowel changes. In genetically susceptible people, exposure to antigens found in wheat causes villous atrophy, crypt hyperplasia, and malabsorption. Serologic tests, including tissue transglutaminase antibody testing, support the diagnosis; a small bowel biopsy showing villous atrophy confirms the diagnosis. Patients can be treated with a gluten-free diet.
Colorectal cancer
Depending on the clinical setting and age group, healthcare professionals might need to conduct a comprehensive search for other underlying causes of persistent diarrhea. Consider colorectal cancer in the differential diagnosis of patients passing occult or gross blood rectally or in patients with new-onset iron-deficiency anemia.
Inflammatory bowel disease
Idiopathic inflammatory bowel disease, including Crohn’s disease, microscopic colitis, and ulcerative colitis, can occur after acute bouts of TD. One prevailing hypothesis is that in genetically susceptible people, an initiating exogenous pathogen changes the microbiota of the gut, thereby triggering inflammatory bowel disease.
Lactose intolerance
Lactose intolerance is a syndrome caused by deficiency of lactase. Its prevalence varies across racial and ethnic groups, with the highest in Asian, African, and Native Americans, and increases with age. Symptoms include abdominal pain, flatulence, bloating, nausea, or diarrhea within hours after ingestion of lactose-containing foods.
Post-infectious phenomena
In some patients who present with persistent GI symptoms, healthcare professionals will not find a specific cause. After an acute diarrheal infection, patients might experience a temporary enteropathy characterized by villous atrophy, decreased absorptive surface area, and disaccharidase deficiencies, which can lead to osmotic diarrhea, particularly after consuming large amounts of fructose, lactose, sorbitol, or sucrose. Use of antimicrobial medications during the initial days of diarrhea might also lead to alterations in intestinal flora and diarrhea symptoms.
Occasionally, onset of irritable bowel syndrome (IBS) symptoms occurs after a bout of acute gastroenteritis, known as post-infectious IBS (PI-IBS). PI-IBS symptoms can occur after an episode of gastroenteritis or TD. The clinical workup for microbial pathogens and underlying GI disease in patients with PI-IBS will be negative. Whether using antibiotics to treat acute TD increases or decreases the likelihood of PI-IBS is unknown.
Small intestinal bacterial overgrowth is characterized by an excess of bacteria in the small intestine and is associated with intestinal motility disorders. Symptoms may include IBS-type symptoms such as abdominal discomfort, persistent diarrhea, or flatulence, and, in some cases, manifestations of nutrient malabsorption. Diagnosis is by carbohydrate breath testing, and treatment is with antibiotics.
Evaluation
Traditional methods of microbial diagnosis of diarrheal illness include stool culture, antigen detection using enzyme immunoassays, and microscopy. For detection of bacteria, routine stool culture will identify Campylobacter, Shigella, Salmonella, Aeromonas, and Plesiomonas. Special culture methods are required for Yersinia and Vibrio species. Diagnosis of C. difficile can be made by antigen detection and PCR. Identification of STEC/EHEC (E. coli O157:H7) is by culture and detection of Shiga-like toxin. Giardia and Cryptosporidium can be detected by antigen testing, and examination of serial stool specimens collected over 3 or more days for ova and parasites is appropriate for evaluation of persistent diarrhea when parasites are suspected, including the use of acid-fast staining for Cryptosporidium, Cyclospora, or Cystoisospora. In addition, a D-xylose absorption test can determine whether patients are properly absorbing nutrients. If underlying GI disease is suspected, include serologic testing for celiac disease and consider inflammatory bowel disease during initial evaluation. Subsequently, studies to visualize both the upper and lower GI tracts, with biopsies, might be indicated.
Diagnostic tests to determine specific microbial etiologies in cases of post-travel diarrhea have advanced in the past number of years. While culture, microscopy, and antigen detection have been the mainstay of diagnostics, PCR-based diagnostics (including as part of multiplex panels, which uses a single stool specimen to detect multiple enteropathogens simultaneously) are becoming increasingly available for detection of bacterial, viral, fungal, and protozoal pathogens. While these assays have high sensitivity and specificity, the clinical utility and economic impact of these diagnostic molecular panels have not been determined fully. In some cases, molecular testing detects colonization rather than infection, potentially making it difficult for healthcare professionals to interpret and apply the results properly. For persistent diarrhea, the use of a protozoa-dedicated multiplex panel would be most appropriate because bacteria and viruses are unlikely causes.
If you are someone taking a cinnamon supplement for its health perks, you might want to think twice. New research suggests it might be time to go back to getting nutrients from your plate, not a pill. Researchers now found that a compound in cinnamon supplements could interfere with how your body processes medications, something plain old cinnamon in food does not seem to do.
Cinnamon is an age-old spice that has long been used as a flavoring agent in foods like breakfast cereals, snacks, bagels, teas, and hot chocolate. In recent years, cinnamon supplements have gained popularity among health enthusiasts, praised for their potential anti-inflammatory benefits and blood sugar-lowering effects.
The latest study, published in the journal Food Chemistry: Molecular Sciences, uncovers a surprising twist for supplement users. Researchers found that cinnamaldehyde, the compound responsible for cinnamon’s distinctive flavor and many of its medicinal properties, can interfere with how the body processes certain medications when taken in concentrated supplement form. This interference could either reduce the effectiveness of common drugs or amplify their side effects, posing unexpected risks for people who rely on regular medications.
However, adding a dash of cinnamon to your coffee or oatmeal is harmless and might even offer small health perks. But when cinnamon is taken in concentrated supplement form, the story changes.
The new findings are a reminder that more is not always better, especially for those who turn to supplements as a shortcut for nutrition. “Health concerns could arise if excessive amounts of supplements are consumed without the knowledge of health care provider or prescriber of the medications. Overconsumption of supplements could lead to a rapid clearance of the prescription medicine from the body, and that could result in making the medicine less effective,” Shabana Khan, a principal scientist at the National Center for Natural Products Research in a news release.
“People who suffer from chronic diseases – like hypertension, diabetes, cancer, arthritis, asthma, obesity, HIV, AIDS or depression – should be cautious when using cinnamon or any other supplements. Our best advice is to talk to a healthcare provider before using any supplements along with the prescription medicine. By definition, supplements are not meant to treat, cure or mitigate any disease,” Khan added.
All orders are protected by SSL encryption – the highest industry standard for online security from trusted vendors.
Natural Neuropathy Relief is backed with a 60 Day No Questions Asked Money Back Guarantee. If within the first 60 days of receipt you are not satisfied with Wake Up Lean™, you can request a refund by sending an email to the address given inside the product and we will immediately refund your entire purchase price, with no questions asked.
What do hospitals have to say for themselves about serving meals that appear to be designed to inspire repeat business?
“Hospital food needs a revolution.” I was surprised to learn that most inpatient meals served in hospitals are “not required to meet national nutrition standards for a healthy diet.” An analysis of the nutritional value of food served to patients in teaching hospitals found that many did not meet dietary recommendations. “Warning: Hospital food bad for health,” read the headline.
A registered dietitian wrote to defend hospitals and point out how stringent the guidelines are, saying that “over half the hospitals met or exceeded more than half the guidelines….It would not take more than choosing eggs for breakfast and 2 percent milk with meals to exceed the recommended intake of cholesterol and fat…The provocative conclusions of Singer et al. only lead the media and the public to conclude that we are a bunch of dunces who have no understanding of the relation between nutrition and disease prevention.”
Well, if the white coat fits…
“We spend a fortune on training doctors, but then don’t follow through on the simplest things, like food.” “Good diet is as necessary to recovery of health as good nursing, surgery, or medicine, and it is folly to pretend that it is beyond the power of our profession to change this reproach.” That was written 75 years ago, yet still there is pushback: “Perhaps we should question whether a ‘healthy diet’ given to a helpless patient during a 2- to 10-day hospital stay benefits anyone or anything other than the dietitian’s sense of ‘doing good,’” responded one doctor. He added, “I am always bothered when a healthy 75-year-old…is deprived of a desired morning egg because a ‘healthy’ low-cholesterol diet has been ordered.” I mean, what is a few days of a little heart-unfriendly diet in the scheme of things…
But it’s the message that’s being sent. “The presence of foods on the [hospital] tray sends a message to patients as to what is healthy and acceptable for them to eat,” responded the researchers who did the hospital foods analysis. “We still can think of no better place or opportunity to set an example of good nutrition than when patients are in hospitals.”
After all, public schools in California, for instance, have banned the sale of sodas for more than a decade. Why not children’s hospitals? In a study of California healthcare facilities serving children, 75 percent of beverages and 81 percent of foods sold in vending machines wouldn’t have been allowed to be sold in schools. We’re talking soda and candy. “Having unhealthy items in health care facilities and seeing staff consume these products…contradicts the nutrition and health messages children often receive from health care providers.”
On adult menus, nearly all meals contained excess salt, with 100 percent of daily menus exceeding the American Heart Association’s recommendation for staying under 1,500 mg of sodium a day. This means meals offered to patients may actually “contribute to the exacerbation or slow resolution of the very conditions that may have led to the hospitalization,” as I discuss in my video Just How Bad Is Hospital Food?.
But if hospitals adhered to the recommended limits of salt, the food wouldn’t taste as good, responded an executive from the Salt Institute, to which the researchers replied: Taste as good? “Hospital food is often criticized as having poor palatability, despite the fact that it likely already contains high levels of sodium.” It doesn’t taste good, no matter how much salt it has.
At the very least, we should “prepare all meals with low sodium content and make optional table salt available for those patients who do not have additional restrictions.” Then, if individuals want to add salt, it’s their choice. If they want to get someone to wheel them out into the parking lot and smoke, that’s their business, but we shouldn’t be blowing cigarette smoke into patients’ rooms three times a day, whether they want it or not. Interestingly, studies suggest that when people are allowed to salt food to taste, they rarely add as much sodium as may come in prepackaged foods.
As you can see below and at 3:55 in my video, when researchers switched study participants to a low-sodium diet, they used their saltshakers more, but, overall, their salt intake dipped way down. And they said their food tasted just as salty, because salt added to the surface of foods makes it taste saltier. But when a hospital meal is served pre-salted, “most inpatients may not actually have the option to consume healthy levels of sodium while they are hospitalized.”
In defense of their unhealthy food, one hospital food service provider explained that they’re just giving people what they want: “People are in the hospital and they are stressed and they need something that they consider comfort food, so I don’t want to deny that to people if that’s what makes them feel better.” That’s a reason one clinical director sends ice cream and candy bars to cancer patients: “We focus on familiar comfort foods, an approach that has enhanced patient satisfaction and improved intake.” You know what else might help? A nice, long drag on a cigarette. Hospitals used to sell cigarettes, “primarily…for ‘patient convenience.’” “‘I don’t think I can deny a paying patient the right to smoke a cigarette,’” said a medical center administrator. “‘As a service to the patient, I will have to insist we have cigarette machines in the hospital.” But others suggested that tobacco products shouldn’t be sold in hospitals at all. This wasn’t from the 1950s, but from the 1980s. Yet, at the time, the “irony of hospitals allowing the sale of cigarettes, which are the major cause of preventable illness and death in this country, has rarely been discussed in the literature…It is especially ironic that smoking is permitted in 89% of doctors’ lounges.”
To their credit, though, U.S. hospitals underwent “the first industry-wide ban on smoking in the workplace” by the mid-1990s. Now, “hospitals again have the opportunity to take the lead and to create food environments that are consistent with their mission to cure the sick and to promote health. Through the simple act of serving food that meets national nutritional standards, our hospitals will act in the best health interests of their patients, and their staff, and will undoubtedly again be leaders in our ongoing dialogue on how to improve our food supply, which in turn will improve the health of us all.”
“Strict antismoking regulations have frequently been criticized as too harsh or difficult to enforce, as if disease and premature death brought on by smoking were any easier to accept and control.” Think my smoking-diet parallel is hyperbole? Well, guess what? Today, the major cause of preventable illness and death in this country is no longer tobacco. The leading cause of death in America is now the American diet, as shown below and at 6:29 in my video. Hospitals in the United States serve “millions of patient meals each day and are optimally positioned to model a healthy diet through patient food.”
It is time to pay attention to your teen’s health. Even adolescents who look healthy and fall within a normal weight range could be on the path to heart damage if they have one hidden health condition, warns a recent study.
Teens with prediabetes, a condition marked by elevated blood sugar levels and insulin resistance, may face a much higher risk of heart trouble than previously thought. According to the latest study published in the journal Diabetes Care, adolescents with prediabetes are nearly three times more likely to have worsening of both structural and functional heart damage during growth to young adulthood.
Even more striking was the discovery that heart damage progresses five times faster in females than in males, highlighting the urgent need for parents and health professionals to pay closer attention to adolescent girls when it comes to early detection and prevention of prediabetes.
In the study, researchers followed 1,595 adolescents from age 17 to 24, using data from the University of Bristol’s Children of the 90s cohort. The prevalence of high blood sugar, insulin resistance, and heart enlargement of the participants was evaluated during the period.
Teens with fasting blood sugar levels of ≥5.6 mmol/L during the follow-up period faced a 46% higher risk of developing left ventricular hypertrophy, a thickening of the heart muscle that can lead to serious heart issues. For those with even higher blood sugar (≥6.1 mmol/L), the risk tripled. Researchers also noted that insulin resistance also played a role, raising the risk of premature heart damage by 10%.
“Earlier results from the same cohort indicate that late adolescence is a critical period in the evolution of cardiometabolic diseases. The current findings further confirm that even healthy-looking adolescents and young adults who are mostly normal weight may be on a path towards cardiovascular diseases, if they have high blood glucose and insulin resistance,” said researcher Andrew Agbaje, in a news release.
“Worsening insulin resistance and increased fat mass have a bidirectional reinforcing vicious cycle. In the new study, we observed that two-thirds of the effect of insulin resistance on excessive heart enlargement was explained by increased total body fat. The five-fold increase in the prevalence of prediabetes within seven years of growth from adolescence to young adulthood underscores the critical importance of lifestyle behavior and dietary habits, especially after adolescents have become independent from their families,” Agbaje added.
Skin and soft tissue problems, including rashes, are among the most frequent medical concerns of returned travelers. Several large reviews of dermatologic conditions in returned travelers have shown that insect bite reactions, superficial bacterial infections (often superimposed on insect bites), and non-specific “itchy rashes” are consistently among the most common skin problems identified at post-travel medical visits (Table 10.5.1).
Table 10.5.1: Most common causes of skin lesions in returned travelers
Most common causes of skin lesions in returned travelers – Table 10.5.1
Diagnosis
Percentage of All Dermatologic Diagnoses (n = 4,742)
Cutaneous larva migrans
9.8%
Insect bite
8.2%
Skin abscess
7.7%
Superinfected insect bite
6.8%
Allergic rash
5.5%
Rash, unknown origin
5.5%
Dog bite
4.3%
Superficial fungal infection
4.0%
Dengue
3.4%
Leishmaniasis
3.3%
Myiasis
2.7%
Spotted fever group rickettsiosis
1.5%
Scabies
1.5%
Cellulitis
1.5%
Other
32.5%
Notes
Source: Modified from Lederman, E. R., Weld, L. H., Elyazar, I. R., von Sonnenburg, F., Loutan, L., Schwartz, E., Keystone, J. S., & GeoSentinel Surveillance Network (2008). Dermatologic conditions of the ill returned traveler: an analysis from the GeoSentinel Surveillance Network. International Journal of Infectious Diseases, 12(6), 593–602. The data in the table represent returning travelers who presented to travel clinics that were part of the GeoSentinel network. Many travelers returned from the Caribbean, so cutaneous larva migrans was likely more prevalent than what may have been seen after travel to other destinations.
Healthcare professionals generally use several approaches concurrently when examining a returned traveler with a new onset skin condition (Box 10.5.1). Few travelers’ dermatoses constitute a medical emergency. Any skin condition accompanied by fever, obtunded mental status, petechiae/purpura, or other signs of systemic illness needs a prompt, if not urgent, and thorough diagnostic evaluation. Travel destinations, types (and duration) of exposure, and safety precautions (e.g., vaccinations, use of bed nets, sanitary conditions, etc.) are the next echelon of inquiry. Next, the healthcare professional should consider the morphology of skin lesions noted on physical examination. Primary lesions (i.e., those that are unaltered by time, scratching, crusting, or medical treatment) are most useful. The clinical diagnosis may be straightforward or may require laboratory confirmation using cultures, serologies, skin biopsy, or microscopy.
Box 10.5.1
Assessing returned travelers presenting with skin problems: essential elements
Pertinent Past Medical History
Systemic diseases and chronic conditions, including preexisting skin conditions
Current medications (and any change in medications or adherence while traveling)
Evolution of skin lesions (what did they look like when they first appeared, and does the patient have photographs of early lesions?)
Travel History
Location and duration of travel
Exposure history: freshwater, seawater, insects, animals, plants, occupational and recreational exposures, sexual and other human-contact exposures
Companion travelers with similar findings
Vaccination status
Adherence to standard travel precautions (e.g., safe food and water precautions, insect bite precautions)
Medications taken during travel (could provide adequate prophylaxis for specific conditions or might have cutaneous side effects)
Ingestion of aquatic plants, undercooked fish, crustaceans, reptiles, or amphibians
Physical Examination
Shape of skin lesions (e.g., macules, nodules, papules, plaques, ulcers)
Number, pattern, and distribution of lesions
Location of lesions: exposed versus unexposed skin surfaces
Many dermatologic problems in returned travelers represent a flare of an existing condition, sometimes because the usual treatment regimen was interrupted while away from home. Other skin disorders might coincide with travel or appear shortly thereafter but are unrelated to travel itself, such as the appearance of actinic keratoses (sun-induced cutaneous precancers) in older travelers with extensive sun exposure history.
Fever and rash
Many illnesses fall into the category of fever with a rash. In returned travelers, fever and rash are most often, but not always, due to viral infections. Nevertheless, bacterial infections, parasitic infections, systemic fungal infections, and some noninfectious conditions can also cause fever and rash. If the rash is characterized by petechiae/purpura or by abundant vesicles, pustules, or widespread blisters, the evaluation should be prompt and thorough.
Systemic viral infections and illnesses
The first 3 conditions discussed—dengue, chikungunya, and Zika—are viral diseases transmitted by Aedes spp. mosquitoes and often present as undifferentiated fevers. Rashes, particularly widespread petechial eruptions, provide important diagnostic information. Viral illnesses often occur in small outbreaks, so epidemiologic clues are significant.
Dengue
Dengue is characterized by an abrupt onset of high fever, frontal headache (often accompanied by retro-orbital pain), and myalgia (see Dengue chapter). A widespread but faint macular rash, interrupted by islands of uninvolved pallid skin, may appear 2–4 days after illness onset. A petechial rash may occur in classic and severe dengue (Figure 10.5.1).
Figure 10.5.1
Figure 10.5.1: Dengue
Chikungunya
The rash associated with chikungunya resembles that of dengue, but hemorrhage, shock, and death are rare (see Chikungunya chapter). A major distinguishing feature of chikungunya is its associated arthritis, arthralgia, or tenosynovitis that can persist for months, particularly in older adults.
Zika
The course of Zika is generally subclinical or mild, characterized by arthralgia, conjunctivitis, fever, lymphadenopathy, and a morbilliform (“maculopapular”) rash (see Zika chapter).
Other hemorrhagic fever viruses
Many viruses that are naturally present in rodents, bats, or non-human primates have the potential to spill over into human populations. Ebola and Marburg viruses are examples. Such viruses might cause serious, hemorrhagic, or otherwise deadly diseases. Subsequently, if the virus is easily transmitted from person to person, then clusters, outbreaks, or even an epidemic might ensue.
Healthcare professionals concerned that a returned traveler may have a possible viral hemorrhagic fever should notify public health authorities and initiate precautions to protect the patient and others. Features of a viral hemorrhagic fever include morbilliform eruptions, bleeding in the skin such as petechiae (pinpoint bleeding) and ecchymoses (bruises), gingival bleeding, epistaxis, and other features such as jaundice.
Morbilliform eruptions
Measles
Measles typically presents with a prodrome that includes fever, cough, runny nose (coryza), and red watery eyes (bilateral conjunctivitis). Koplik spots (small red spots with bluish/white center on the buccal mucosa) begin 2–3 days after symptoms first appear. Within another few days, the typical rash begins, usually first on the head and neck, then spreading downward to the trunk and extremities. The measles rash consists of innumerable small pink-to-red macules and slightly elevated papules, referred to as a morbilliform or maculopapular eruption. Measles can be spread easily (see Measles [Rubeola] chapter).
COVID-19
During the course of acute COVID-19 infection, many people develop cutaneous findings (see COVID-19 chapter). The data are imperfect but seem to show that rashes fall into 2 large groups:
Morbilliform and urticarial eruptions that resemble common non-specific viral exanthems
Eruptions associated with hypercoagulability; these are areas of net-like erythema (livedo reticularis, presumably due to altered vascular perfusion) or pathologic hypercoagulability (retiform purpura)
Non-specific acute morbilliform eruptions are widely reported as the most common skin finding in COVID-19. Many other types of eruptions have been attributed to COVID-19. Understanding of the clinical significance, pathophysiology, and epidemiology continues to evolve.
Children and young adults may develop a condition known as “COVID toes,” characterized by sudden onset of painful, dusky red macules and patches, typically on the plantar aspect of the distal phalanges of one or more toes. The clinical and histological appearance of COVID toes resembles a condition known as chilblains (a type of cold exposure injury).
Acute HIV infection
Acute retroviral syndrome is the initial presentation of newly acquired HIV infection (see Sex and Travel chapter). It presents as an influenza-like syndrome that includes fever, generalized lymphadenopathy, and malaise, often accompanied by a generalized skin eruption. In acute HIV infection, associated skin lesions present as pink to deeply red macules or papules, or as a morbilliform eruption. Urticarial and pustular lesions also have been described. Oral ulcers might be present. The clinical appearance is not diagnostic and resembles rashes seen in many acute viral syndromes.
Acute, febrile, vesiculopustular eruptions
This section includes diseases caused by true poxviruses (family: Orthopoxviridae) and a much more common condition, chickenpox or varicella, caused by the varicella-zoster virus (family: Herpesviridae). These viral infections can cause an acute illness with fever and vesiculopustules that can spread easily from person to person.
Early presentations of a poxvirus infection and a case of chickenpox may resemble each other, even though they are virologically, clinically, and epidemiologically dissimilar. The clinical appearance of each type of infection resembles the other, superficially.
Poxvirus diseases
Orthopoxvirus infections present similarly with fever, headache, malaise, and characteristic deep-seated, firm, well-circumscribed lesions that evolve through various stages (including papules, vesicles, and pustules). After 2–4 weeks (longer in immunocompromised people), lesions mature into crusts that resolve in most individuals.
The most significant orthopoxvirus disease is smallpox, caused by variola virus. The virus and the disease have been eradicated in nature, largely due to the global campaign using smallpox vaccine, made from a related orthopoxvirus, vaccinia virus. In 2022, another orthopoxvirus disease, mpox, which was once considered a geographically focal zoonosis, emerged worldwide. During the global outbreak, mpox virus infected mostly men who have sex with men. Most cases were transmitted through skin-to-skin contact. Consequently, the lesions on many patients with mpox appeared mainly or exclusively on anogenital surfaces. In patients with advanced HIV disease or other immunocompromised states, the disease can be particularly virulent and can cause death.
Several other poxviruses cause mild disease with relatively few lesions, often 1–5. In northern Europe, cowpox is present and tends to cause disease when people have direct contact with an infected domestic cat that acquired the disease from a recently caught, infected rodent.
Orf and milker’s nodule are caused by closely related parapoxviruses. Most people acquire these zoonoses occupationally, usually by handling or feeding infected sheep, cattle, or goats. Although less common, there have been parapoxvirus infections in individuals with recent exposure to white-tail deer through handling of carcasses in the United States. A localized lesion at the site of inoculation (often through a skin break) presents after 3–7 days of exposure and can evolve through multiple clinical stages; resolution usually happens after approximately 4–6 weeks. Fever, malaise, or lymphadenopathy may occur but are uncommon.
Varicella (chickenpox)
Varicella (chickenpox) can be mild in children and more severe in adults or immunocompromised patients. It presents with 1–2 days of fever, followed by a generalized pruritic rash consisting of macules that evolve through the papular stage (red bumps) to form vesicles (small, clear, fluid-filled blisters) and pustules (pus-filled blisters) on an erythematous base, which resolve by crusting. Lesions often occur in crops, and various stages of evolution are often present simultaneously, so papules, vesicles, pustules, and crusts may all occur at the same time.
Systemic bacterial infections and illnesses
Meningococcemia
Invasive Neisseria meningitidis disease occurs worldwide and is often associated with outbreaks, especially in the meningitis belt of Sub-Saharan Africa (see Meningococcal Disease chapter). Meningococcemia is often characterized by acute onset of fever and a petechial or purpuric rash, commonly accompanied by hypotension, mental status changes, or multiorgan failure. Rapid diagnosis and immediate treatment (often started empirically before laboratory confirmation is obtained) can be lifesaving.
Rickettsioses
Most rickettsial infections have distinctive geographic and epidemiologic features based on the ecological preferences and behavioral habits of reservoir animals, arthropod vectors, and pathogens. Many of these “geographic rickettsioses” induce a spotted fever that characteristically starts with the bite of an infected tick or mite. After a several-day incubation period, the first cutaneous finding is often an eschar at the bite site. Often called a tache noire (black stain), these are mildly painful, dark brown or black, necrotic lesions with a red rim. The systemic illness begins over the next few days, usually accompanied by a maculopapular, petechial, or vesicular rash.
African tick-bite fever
Rickettsia africae, the bacteria responsible for African tick-bite fever (South African tick typhus), is transmitted by the bite of a hard tick (Hyalomma spp.; Figure 10.5.2). Travelers who hike or camp outdoors or are on safari are particularly at risk for this disease, a frequent cause of fever and rash in southern Africa (see Rickettsial Diseases chapter).
Figure 10.5.2
Figure 10.5.2: African tick-bite fever
The disease is characterized by fever and an eschar at the site of the tick bite. The eschar, or tache noire, is a mildly painful, dark brown or black, necrotic lesion with a red rim. Several lesions might be present because exposed individuals often suffer multiple tick bites. Within a few days, patients develop a fine petechial or papular rash, associated with regional lymphadenopathy near the bite.
Rocky mountain spotted fever
Rocky Mountain spotted fever (RMSF) is a tick-borne rickettsial disease that is more severe than other spotted fevers. RMSF occurs in North America (U.S. and Mexico) and parts of Central and South America. Because of its potential severity and lethality and the need for early treatment, consider RMSF when evaluating patients with fever and rash.
Most patients with RMSF develop a rash 3–5 days after illness onset. The typical rash of RMSF starts as a blanching maculopapular eruption. Cutaneous blood vessels become inflamed and leaky, sometimes resulting in necrosis. Red blood cells leak from inflamed blood vessels, leading to non-blanching petechiae that are especially prominent on the ankles and wrists. It usually spreads to palms and soles, then becomes generalized. Patients with RMSF are usually very ill with high fever and severe headaches.
Bacterial infections localized to skin and soft tissues
Bacterial skin infections occur most frequently when skin surface has been interrupted, often by abrasions, bites, or minor scratches, particularly under circumstances when it is difficult to maintain good hygiene. Common organisms responsible are Staphylococcus aureus and Streptococcus pyogenes. Resulting infections are collectively called pyodermas (Greek for “pus skin”) and can present as impetigo, folliculitis, ecthyma (ulcers or open sores), furuncles (also called abscesses or boils), cellulitis and erysipelas, or lymphangitis.
Impetigo
Impetigo is a common, highly contagious, superficial bacterial skin infection. S. aureus and S. pyogenes are the most common pathogens. Streptococcal impetigo classically presents in children with golden or “honey-colored” crusts formed from dried serum. Staphylococcal impetigo often appears in body folds, especially the axillae, and might present as fragile pustules.
In temperate climates, most impetigo is caused by S. aureus, either alone or mixed with S. pyogenes. In many tropical areas, however, streptococcal impetigo remains especially common in children. It often arises as a secondary skin infection after the epidermal barrier is disrupted by insect bites, scabies, or scratches. Treatment for impetigo varies based on the severity or extent of the infection and by the suspected pathogen. Mupirocin, a topical antibiotic, is an excellent treatment for mild, localized impetigo caused by either pathogen. More extensive infections may require oral antibiotics, but the regimen differs by pathogen.
Folliculitis (hair follicle infections) and furunculosis (boils or abscesses)
People whose skin or nasal mucosa is colonized with S. aureus are at risk for recurrent folliculitis or furunculosis. By its very nature, folliculitis occurs only on hair-bearing surfaces. People can easily but unintentionally spread the infection (autoinoculation) when they shave the hair from various body surfaces.
Furuncles may continue occurring weeks or months after a traveler’s return. If staphylococcal boils recur frequently, treatment may require a decolonization regimen with nasal mupirocin and a skin wash with an antimicrobial skin cleanser. Some decolonization protocols advise similar treatment for household members and close contacts.
Many travelers who develop boils when abroad mistakenly attribute the tender lesions to spider bites. However, outside a few endemic areas (mainly the south-central U.S.), necrotizing spider bites are extremely rare. The lesions in these cases are far more likely to be abscesses caused by methicillin-resistant S. aureus and should be treated accordingly.
Cellulitis and erysipelas
Cellulitis and erysipelas manifest as red, warm, edematous areas that might start at the site of a minor injury, at an opening in the skin, or without an obvious underlying suppurative focus. Erysipelas tends to have a clearly raised line of demarcation at the edge of the lesion. This is due to involvement of superficial lymphatics and is more likely to be associated with fever. Cellulitis, erysipelas, and lymphangitis are usually caused by S. pyogenes and other β-hemolytic streptococci or S. aureus (including methicillin-resistant strains), but gram-negative aerobic bacteria also can cause cellulitis.
Treatment
Use soap and water for local cleansing of bacterial skin infections. A topical antibiotic, preferably mupirocin, can also be used; bacitracin zinc and polymyxin sulfate (often in combination) are alternatives. Topical antibiotic ointments are widely available in other countries and may contain neomycin (a well-recognized cause of acute allergic contact dermatitis), fusidic acid, or gentamicin.
In low- and middle-income countries, “triple cream” products may be available over the counter. These often contain ultrapotent corticosteroids that can interfere with the healing of common infections and have their own side effects. In many low- and middle-income countries, an application of gentian violet or potassium permanganate is the treatment of choice for impetigo.
Minor skin abscesses often respond to incision and drainage without needing antibiotics. Oral or parenteral antibiotics might be required if the skin infection is deep, expanding, extensive, painful, or associated with systemic symptoms (e.g., fever). Consider antibiotic resistance if the condition does not respond to empiric therapy. Bites and scratches from animals (both domestic and wild) can lead to infections with anaerobic bacteria or unusual gram-negative organisms. Appropriate treatment might require care from specialists who can obtain bacterial cultures, prescribe focused antibiotic therapy, and perform surgical debridement, as needed (see Zoonotic Exposures: Bites, Scratches, and Other Hazards chapter).
Skin lesion morphology
Linear lesions
Cutaneous larva migrans
Cutaneous larva migrans, a condition in which the skin is infested with zoonotic hookworms (often Ancyclostoma spp.), presents as an extremely itchy, linear, or serpiginous lesion (Figure 10.5.3). The migrating larvae advance slowly in the skin’s uppermost layers. Cutaneous larva migrans is usually self-limiting after 4–6 weeks. Albendazole and ivermectin are both effective therapies, and topical corticosteroids can be used to relieve severe pruritus, which is often present. Infrequently, more serious disease can result from invasion of deeper organs.
Figure 10.5.3
Figure 10.5.3: Cutaneous larva migrans
A deeper lesion that resembles urticarial patches and that progresses rapidly might be due to larva currens (“running larvae”), caused by cutaneous migration of filariform larva of Strongyloides stercoralis. Call or email the CDC for recommendations on diagnosis and treatment of cutaneous larva migrans or larva currens (404-718-4745; parasites@cdc.gov).
Lymphocutaneous or sporotrichoid spread of infection
Lymphocutaneous or sporotrichoid spread of infection occurs when organisms ascend proximally along superficial cutaneous lymphatics, producing raised, cord-like, linear lesions. Alternatively, this condition can present as an ascending chain of discontinuous, sometimes ulcerated nodules (termed nodular lymphangitis) that arise after primary percutaneous inoculation of specific pathogens. Causative pathogens can be bacterial (e.g., Francisella tularensis; Nocardia spp.; atypical Mycobacterium spp. [such as Mycobacterium marinum after exposure to brackish water or rapidly growing Mycobacteria after pedicure footbaths]); parasitic (e.g., Leishmania spp., particularly those responsible for causing Western Hemisphere leishmaniasis); or fungal (e.g., Coccidioides spp., Sporothrix spp.).
Phytophotodermatitis and other noninfectious exposures
Phytophotodermatitis is a noninfectious condition resulting from the interaction of natural psoralens, most common in the juice of limes, and solar ultraviolet A radiation. This often occurs on tropical vacations after travelers are outside, preparing food or drinks with locally purchased limes. Several days later, the involved surfaces may develop painful streaks of blisters, essentially the equivalent of an exaggerated sunburn. The area heals slowly, evolving into asymptomatic hyperpigmented lines that may take weeks or months to resolve. Because of the several-day delay between the exposure to lime juice and sunlight, people rarely self-identify the cause of this painful rash.
Long linear lesions caused by cnidarian envenomation (e.g., stings from the tentacles of jellyfish or Portuguese man o’ war [Physalia physalis]), often resemble phytophotodermatitis (see Poisonings, Envenomations, and Toxic Exposures During Travel chapter). Another common but self-evident cause of an itchy, often blistering eruption is acute contact dermatitis due to black henna. In places where henna is commonly used, the compound paraphenylenediamine is often added to red or brown henna to make a longer-lasting pigment, black henna. Travelers who receive temporary tattoos using black henna (rather than the more traditional red or brown henna) are at risk for severe, often blistering, acute allergic contact dermatitis due to paraphenylenediamine.
Macular lesions
Macules and patches (flat lesions) are common, often non-specific, and frequently due to medication reactions or viral exanthems. Purpura are typically macular, and any purpura associated with fever could indicate a life-threatening emergency (e.g., meningococcemia).
Leprosy/Hansen’s disease
Leprosy frequently presents with hypopigmented or erythematous patches that are hypoesthetic to pinprick and associated with peripheral nerve enlargement. Newly diagnosed leprosy cases occur almost exclusively in immigrants arriving from low- or middle-income countries where the disease is endemic. Diagnosis is made by skin lesion biopsies. The National Hansen’s Disease Clinical Center in Baton Rouge, Louisiana, provides consultations (nhdped@hrsa.gov; 800-642-2477).
Lyme disease
Lyme disease is caused by the spirochete Borrelia burgdorferi sensu lato. Endemic to temperate latitudes in North America, Asia, and Europe, the bacterium that causes Lyme disease is transmitted through the bite of infected hard ticks, genus Ixodes.
Infected travelers present with ≥1 large erythematous patches (erythema migrans). If ≥1 lesions are present, the first lesion appears where the tick bite occurred; subsequent lesions are due to secondary, probably hematogenous, spread of Borrelia, not multiple tick bites. Erythema migrans often is described as targetoid, but many cases lack central clearing or red-and-white bands. Lesions generally are asymptomatic. Pruritus, if present, is usually intermittent and very mild. Lesions that are severely or persistently pruritic are unlikely to be erythema migrans.
Tinea (dermatophyte infections)
Tinea (ringworm) is caused by a several closely related superficial fungi (Microsporum, Trichophyton, and Epidermophyton). Typical lesions appear as expanding, red, raised rings, with an area of central clearing. Diagnostic methods include fungal culture, microscopy (prepare skin scraping samples with a 10% solution of potassium hydroxide [KOH]), and polymerase chain reaction. Treatment usually involves application of a topical antifungal (e.g., clotrimazole, ketoconazole, miconazole, terbinafine) for several weeks or a course of an oral antifungal (e.g., terbinafine, fluconazole, itraconazole). Nystatin-based topical agents are ineffective.
When a returned traveler has a recalcitrant fungal infection, consider obtaining culture for species identification. A longer course of high-dose oral antifungals might be needed to treat severe or recurrent infections caused by emerging drug-resistant Trichophyton species, such as Trichophyton indotineae, that have been detected in travelers returning from South and Southeast Asia.
Topical medications that combine an antifungal agent with a potent corticosteroid (e.g., betamethasone, clobetasol) are available in many countries; caution travelers against their use. Adverse events associated with steroid-containing antifungal preparations include longer-lasting infections; more extensive spread of the infection over large areas of the body; invasion of the fungal pathogen into the deeper skin layers; unusual presentation of infection (making diagnosis more challenging); and severe redness and burning (Figure 10.5.4).
Figure 10.5.4
Figure 10.5.4: Ringworm after use of a steroid cream
Tinea versicolor (also called pityriasis versicolor)
Caused by several species of the fungus Malassezia (e.g., Malassezia furfur [previously Pityrosporum ovale], Malassezia globosa), tinea versicolor is characterized by abundant, asymptomatic, round to oval skin patches. Lesions are often 1–3 cm in diameter, but dozens of lesions can coalesce to form a “map-like” appearance on the upper chest and back. Affected skin typically has a dry or dusty surface. Lesions can be skin-colored, slightly hypopigmented, or slightly hyperpigmented (versicolor means “changed color”), but all the lesions on any one individual have a uniform color (Figure 10.5.5).
Figure 10.5.5
Figure 10.5.5: Tinea (Pityriasis) versicolor
Tinea versicolor can be diagnosed in various ways. A clinical diagnosis often is based on the appearance of the lesions. Under the light of a Wood ultraviolet lamp, the lesion produces a subtle yellowish-green hue, corroborating the diagnosis. Microscopic examination using a KOH preparation can be confirmatory. The fungi that cause tinea versicolor are difficult to grow in standard culture media.
Topical azole products (e.g., clotrimazole cream, ketoconazole shampoo used as a body wash), selenium sulfide shampoo, or topical zinc pyrithione are recommended treatments. Systemic azoles (e.g., fluconazole) can be used to treat severe, relapsing infections, or those recalcitrant to first-line therapies. In many countries, the most common treatment is Whitfield ointment (salicylic acid 3% and benzoic acid 6%, mixed in a vehicle such as petrolatum). Oral griseofulvin, topical nystatin, and both oral and topical terbinafine are ineffective against Malassezia.
Nodular and subcutaneous lesions
Gnathostomiasis
Gnathostomiasis is a nematode infection that occurs mainly in Southeast Asia, along the Pacific coast of Ecuador and Peru, in parts of Mexico, and Sub-Saharan Africa. People acquire gnathostomiasis by eating raw or undercooked, infected freshwater fish, amphibians, or reptiles. Infected individuals experience transient, migratory, subcutaneous nodules often described as both itchy and painful. Several reports suggest that initial symptoms can occur weeks or even years after exposure. Symptoms are due to nematode larvae migrating through cutaneous and subcutaneous soft tissues. Humans are accidental, dead-end hosts for gnathostomes. Tissue (skin) and peripheral eosinophilia is common. Reliable serologic tests are not widely available but could be used for diagnosis. Call or email CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).
Loiasis
Loiasis is caused by Loa loa, a filarial nematode transmitted by day-biting African deer flies (Chrysops spp.). Among travelers, the disease is seen mostly in people who have lived or worked in endemic areas for several months or longer. Clinical manifestations vary among patients; many people develop edematous subcutaneous nodules, often painful or pruritic and located around large joints. These nodules are known as Calabar swellings, named for the Nigeria-Cameroon coastal area where the disease is prevalent. Some people with loiasis have generalized itchy skin with no other cutaneous findings. Adult worms are occasionally observed crossing the bulbar conjunctivae or the soft eyelid tissues, leading to another name for loiasis, African eyeworm disease. Peripheral eosinophilia is common in travelers.
Loiasis is diagnosed using conventional light microscopy to find microfilariae (larvae of the worm) on a blood smear. The blood should be collected during midday hours (i.e., between 10 a.m. and 2 p.m.). In travelers who have crossed time zones, blood should be collected during midday hours of the location where the infection was acquired. Nevertheless, microfilaremia might be undetectable; such cases require serologic testing, although infection with other nematodes may produce a false positive test result.
The drug of choice for the treatment of loiasis is diethylcarbamazine (DEC). Most patients will achieve cure, defined as resolution of symptoms, resolution of eosinophilia, and decreasing antifilarial antibody titers, with 1 or 2 courses of DEC. Some will require additional courses of DEC or a trial of albendazole. DEC is the treatment of choice because there is solid evidence that it kills both the microfilariae and the adult worms, resulting in quicker resolution of the infection. The risk of fatal encephalopathy or other severe adverse neurologic events is related to the microfilarial load. Quantitative blood smears are required before initiating treatment. Prophylactic DEC (300 mg once a week) can be used to prevent infection in long-term travelers to endemic areas. DEC, which is not Food and Drug Administration (FDA)-approved in the United States, can be obtained through consultation with the Parasitic Diseases Branch at CDC (parasites@cdc.gov; 404-718-4745). Albendazole may play a role in the treatment of loiasis in cases of failed DEC treatment or in order to try to lower microfilarial loads so that DEC may be used safely. Ivermectin may play a role in lowering microfilarial loads so that DEC may be safely used in certain circumstances.
Furuncular myiasis
In Sub-Saharan Africa, furuncular myiasis is caused by a skin infestation with larvae of the tumbu fly, also known as the mango or mputsi fly (Cordylobia anthropophaga and related species; Figure 10.5.6). In the Western Hemisphere, larvae of the botfly (Dermatobia hominis) cause similar-appearing furuncular myiasis. The botfly’s range extends from central Mexico to the northern half of South America. Typical lesions are solitary; there can also be multiple painful nodules that resemble furuncles (boils). Each nodule holds only a single larva. The center of a lesion has a small punctum through which the larva both breathes and expels waste.
Figure 10.5.6
Figure 10.5.6: Myiasis Cordylobia anthropophaga
More mature larvae sometimes exit on their own, or they can be gently compressed out of nodules. Extracting larvae can be difficult and may take several methods. Start with obstructing the breathing punctum by applying an occlusive substance or dressing (such as petroleum jelly) for several hours. Larvae may emerge from their dermal domicile in search of air to breathe. Removal may require a small, superficial incision that permits gentle extraction of the larvae. The process should be performed carefully to avoid puncturing the larval body, which could result in residual parts retained in the skin. Once a larva has been extracted, the newly vacant cavity should be flushed with sterile water. Additional lesions are often hidden in the scalp, particularly in the case of infestation with Dermatobia. The patient may require treatment for secondary bacterial infection and appropriate prophylaxis for tetanus. Call or email CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).
Tungiasis
Tungiasis is a skin infestation caused by adult female sand fleas (Tunga penetrans) and is endemic to parts of the Caribbean, South America, and Sub-Saharan Africa. Typically, 1 or more gravid female fleas burrow into the thick skin on a person’s sole or around the toes. Most people with tungiasis have multiple lesions. Individual lesions have a strikingly uniform appearance with a round, 5 mm diameter, white, slightly elevated surface. In the center of the lesion, a minute, frequently black, opening is present, through which the embedded flea breathes, eliminates waste, and eventually extrudes her eggs. Clustered lesions can appear as crusty, dirty, or draining plaques. The lesions, which are itchy and painful, continue to expand as the uterus of the sand flea fills with eggs.
Treatment includes extracting the burrowed fleas, consideration of antibiotics for secondary bacterial infection, and prophylaxis for tetanus, if required. Extraction performed in endemic areas using non-sterile procedures has been associated with significant complications. Promising emerging topical therapies include dimeticones (silicone oils) and a neem/coconut oil mixture. Call or email CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).
Papular lesions
Bites by insects and other arthropods
Insect bites are probably the most common cause of papular lesions. Biting insects include bed bugs, fleas, head lice, midges, mosquitoes, and sand flies. Most bites are itchy because of hypersensitivity reactions to proteins and other components in the insect’s saliva.
Individual bites usually appear as small (4–10 mm diameter), edematous, pink to red papules with a gentle “watch-glass” profile. The center of many bites will have a small, subtle break in the epidermis where the arthropod’s mouth parts entered the surface of the skin. The pink to red color is generally limited to the elevated part of the lesion and is surrounded by a subtly pale hypovascular rim.
Lesions are often pruritic, thereby inducing patients to scratch their bites. Scratching often excoriates or erodes the skin’s surface, putting the site at risk for secondary bacterial infections, usually with Staphylococcus spp. or Streptococcus spp. Many arthropods produce bite reactions that have characteristic shapes, patterns, and distributions. For example, bites from bed bugs and fleas often appear as clusters of discrete red papules on unclothed surfaces of the body (Figure 10.5.7).
Figure 10.5.7a
Figure 10.5.7a: Bedbug bites
Figure 10.5.7b
Figure 10.5.7b: Bedbug bites
Scabies
Scabies infestation usually manifests as a generalized or regional pruritic papular rash with erythema, abundant excoriations, and secondarily infected pustules. Scabies generally presents in a regionally symmetric manner (Figure 10.5.8). For example, 2 of the most commonly involved sites are the volar wrists and finger web spaces; the left and right sides are usually involved in a nearly identical fashion. Also, boys and men with scabies often develop nodular lesions on the scrotum and penis. When considering scabies in any male older than 2 years, a genital examination can be extremely helpful. Scabies burrows are short, delicate, linear lesions that involve the most superficial part of the epidermis; burrows are pathognomonic but are challenging to detect. See treatment information.
Figure 10.5.8a
Figure 10.5.8a: Scabies
Figure 10.5.8b
Figure 10.5.8b: Scabies
Other papular lesions
Many other conditions present as widespread, extremely pruritic eruptions, often with numerous fine, slightly elevated, somewhat indistinct papules. Examples include acute allergic contact dermatitis (perhaps due to plants) and photosensitive dermatitis (often associated with photosensitizing medications, e.g., doxycycline, sulfonamides). Onchocerciasis (specifically onchocercal dermatitis due to the inflammatory reaction to dying microfilaria in the skin) can occur in expatriates living in endemic areas in Sub-Saharan Africa. Onchocercal dermatitis manifests as a generalized pruritic, finely papular dermatitis, a rare finding in travelers that occurs years after exposure. Swimmer’s itch (cercarial dermatitis) and hookworm folliculitis are extremely itchy eruptions composed of papules on skin surfaces exposed to freshwater and fecally-contaminated soils, respectively.
Skin ulcers
Skin ulcers form when a destructive process damages or erodes the epidermis, the skin’s superficial layer, and then enters the dermis, the skin’s deeper, more leathery layer. The most frequent causes of acute (duration Staphylococcus and Streptococcus. Infection with these organisms creates well-demarcated, shallow ulcers with sharp “punched out” borders known as bacterial or common ecthyma. Treatment for ecthyma is described earlier in this chapter.
Ulcers seen in some conditions, such as the chancre of primary syphilis, are ulcerated when they first appear. However, most skin ulcers start as an elevated lesion, typically a papule or vesicle (or perhaps a larger plaque, nodule, or bulla), with an intact surface. As the epidermal surface breaks down, the lesion evolves into an erosion or an ulcer. This is the case with the next conditions to be discussed, anthrax and cutaneous leishmaniasis, along with many other diseases.
Anthrax
Cutaneous anthrax starts as a large, edematous swelling. Within a few days, the skin surface develops a shallow ulcer that progresses into a necrotic black eschar. In all stages, anthrax lesions are surprisingly painless. Most cases of travel-associated anthrax are cutaneous (rather than inhalational or gastrointestinal) and are acquired via exposure to live ruminants (hoofed mammals that chew their cud, such as cattle, goats, and sheep) or from handling unprocessed products made from animal hides or wool.
Any case of human anthrax should be reported immediately to public health authorities. Anthrax spores can be used as a bioweapon (in warfare or in bioterrorism). Therefore, cases of anthrax, which are extremely rare in the developed world, will raise concern for a bioterror or biowarfare attack.
Anthrax treatment requires antibiotics to kill the pathogen, Bacillus anthracis, and antitoxins to neutralize the toxins that the pathogen produces. An FDA-approved vaccine is available to people in certain occupations (veterinarians and other animal handlers; ground soldiers).
Buruli ulcer (Mycobacterium ulcerans infection)
Buruli ulcer is rare in travelers. It is caused by a toxin produced by Mycobacterium ulcerans, a freshwater bacterium found most commonly in equatorial Africa (mainly Ghana and Nigeria) and in the Australian state of Victoria. Buruli ulcers typically start as edematous nodules that arise at sites of minor skin injury. The nodules ultimately break down and form expanding invasive wounds. Despite extensive wounds, Buruli ulcers often lack signs of inflammation; in other words, they are surprisingly painless and do not generate a pustular response.
A condition known as tropical ulcer has a similar appearance, but it is exceptionally painful. Like Buruli ulcer, it commonly appears on the shins. Unlike Buruli ulcer, tropical ulcer is felt to be caused by a polymicrobial bacterial infection, possibly including some mycobacteria.
Cutaneous leishmaniasis
The main areas of risk for cutaneous leishmaniasis (CL) are Africa’s northeastern quadrant, Latin America, South Asia, Central Asia, Mediterranean coastal areas, and the Middle East (see Leishmaniasis chapter). The bite of an infected sand fly transmits the Leishmania parasite, and CL lesions start as localized, typical insect bite reactions that are papules or nodules. Over several weeks, the lesions evolve slowly into shallow ulcers with raised margins. This resembles a broad, shallow, volcanic caldera. The ulcer’s surface is often covered by a dried crust or a raw, fibrinous coat. In the absence of secondary bacterial infection, leishmanial ulcers are generally painless. Lesions may remain as nodules or papules without ulceration, which is more commonly seen in Old World Disease (Figure 10.5.9; Figure 10.5.10).
Figure 10.5.9
Classic chiclero ulcer Leishmania mexicana
Figure 10.5.10
Figure 10.5.10: Cutaneous leishmaniasis
Special techniques are necessary to confirm a diagnosis of CL. The simplest (and office-based) technique is a modified skin scraping with material placed on a glass slide and examined by a dermatopathologist. In travelers, pathogen speciation is often necessary to determine whether the lesion will remain strictly cutaneous and self-healing or if it will require treatment with medication (i.e., oral, topical, or intravenous) or possibly cryotherapy or heat therapy. Refer to the CDC webpage or contact CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).
Spider bites
An important consideration when evaluating a patient who reports a spider bite is that most alleged spider bites are simply not spider bites (see Poisonings, Envenomations, and Toxic Exposures During Travel chapter). The sudden appearance of a warm, tender lesion with a necrotic center is often diagnosed (by patients, family members, and emergency medical staff) as a spider bite. However, few purported spider bites involve a spider observed to either bite the patient or to merely be present. Indeed, a painful necrotic lesion in this context is more likely to be a bacterial skin infection that likely requires antibiotics.
Nevertheless, necrotizing spider bites can occur and are most often caused by recluse spiders (Loxosceles spp.). In the United States, the most common culprit is the brown recluse (or fiddleback) spider (Loxosceles reclusa), found in the south-central United States. The Mediterranean recluse spider (Loxosceles rufescens) resembles the brown recluse. It is native to the Mediterranean basin and the Near East. This species has become widespread, leading to a large, nearly worldwide distribution. It rarely bites people, and its venom has low toxicity, but it has been implicated in true spider bites. In contrast, many studies show that outside a few endemic areas, most alleged spider bites are, in fact, methicillin-resistant S. aureus infections and should be treated accordingly.
Uncommon causes
A less common cause of skin ulcers is cutaneous diphtheria (Corynebacterium diphtheriae), which creates a shallow ulcer on the skin. Just as in oropharyngeal diphtheria, the involved surface typically has a gray membranous surface.
Haemophilus ducreyi causes chancroid, a sexually transmitted infection, but on several island groups in the southwestern Pacific, H. ducreyi causes nonvenereal cutaneous ulcers. Another sexually transmitted infection, syphilis (Treponema pallidum), can also ulcerate the skin.
Trypanosoma brucei rhodesiense, the protozoal pathogen that causes African trypanosomiasis, can produce a chancre at the bite site of the transmitting tsetse fly (Glossina spp.).
Miscellaneous skin infections
Bite-associated infections
Wound infections after cat and dog bites are caused by a variety of microorganisms (see Zoonotic Exposures: Bites, Scratches, and Other Hazards chapter). This includes S. aureus, alpha, beta, and gamma hemolytic streptococci, several genera of gram-negative organisms, and several anaerobes. Pasteurella multocida infection classically occurs after cat bites but can also occur after dog bites; lesions caused by this organism develop quickly and are often painful. Patients lacking spleens are at particular risk for severe cellulitis and sepsis due to Capnocytophaga canimorsus infection after dog bites. Management of cat and dog bites includes consideration of rabies post-exposure prophylaxis (see Rabies chapter), as well as tetanus immunization and antibiotic treatment. Avoid primary closure of dog bites to the hand or puncture wounds anywhere on the body.
Monkey bite management includes wound care, tetanus immunization, rabies post-exposure prophylaxis, and consideration of antimicrobial prophylaxis. Bites and scratches from Old World macaque monkeys, even those that appear healthy, have been associated with fatal encephalomyelitis due to B virus infection in humans; valacyclovir is the recommended post-exposure prophylaxis after high-risk macaque exposure.
Water-associated infections
Skin and soft tissue infections (SSTI) can occur after exposure to fresh, brackish, or salt water, particularly if the skin’s surface is compromised. Infections with water-associated organisms can follow from a variety of types of skin trauma, including: abrasions or lacerations sustained during swimming or wading; bites or stings from marine or aquatic creatures (see Poisonings, Envenomations, and Toxic Exposures During Travel chapter); and punctures from fishhooks.
The most virulent SSTI associated with marine and estuarine exposures are due to Vibrio vulnificus and related non-cholera Vibrio spp. For freshwater exposures, Aeromonas hydrophila is the most dangerous pathogen. Various skin and soft tissue manifestations can occur in association with either infection, including abscess formation, cellulitis, ecthyma gangrenosum, and necrotizing fasciitis.
Pending identification of a specific organism, treat acute infections related to aquatic injury with an antibiotic that provides both gram-positive and gram-negative coverage (e.g., fluoroquinolone or third-generation cephalosporin).
Mycobacterium marinum infection
Mycobacterium marinum is a free-living environmental bacterium found worldwide in warm, preferably brackish, water. The usual onset of infection is when the bacteria enter the skin after a minor abrasion or shallow puncture injury occurs in or around open water. Typical locations for M. marinum infection include knees, shins, and the dorsal surfaces of hands and feet, where water-associated minor trauma occurs most commonly.is rarely painful, warm, or purulent.
Patients describe a variety of healing patterns after minor water-associated injury—areas that were injured but not infected heal quickly. In contrast, injured areas that were infected with M. marinum will develop the irregularly bordered, expanding, multinodular violaceous plaques characteristic of this infection. Treatment with antimycobacterial agents for weeks to months is required because lesions do not resolve spontaneously. Occasionally, the infection extends proximally along superficial lymphatics, a process known as lymphocutaneous or sporotrichoid spread.
Pseudomonas aeruginosa infection
So-called hot tub folliculitis can occur after using inadequately disinfected swimming pools or hot tubs. Folliculitis (tender or pruritic folliculocentric red papules, papulopustules, or nodules) typically develops 8–48 hours after exposure to water contaminated with Pseudomonas aeruginosa. Usually, several dozen discrete lesions occur on skin surfaces submerged in the infectious water. Most patients have malaise; some have a low-grade fever. The condition is self-limited to 2–12 days; antibiotic therapy is rarely required.
Vibrio vulnificus infection
Necrotizing Vibrio vulnificus infections can be acquired in 2 ways: (1) when open skin surfaces are exposed to contaminated brackish or saltwater; and (2) when people eat Vibrio-contaminated raw or undercooked shellfish, resulting in severe systemic infection. The illness is especially severe in people with underlying liver disease, often from alcoholism or conditions such as hemochromatosis. V. vulnificus skin infections usually start as dramatic cellulitis with hemorrhagic bullae, leading to necrotizing fasciitis and fulminant sepsis. In general, infections caused by these organisms can be more severe in immunocompromised people (see Immunocompromised Travelers chapter).
Shewanella infection
Shewanella, a genus of motile gram-negative bacilli found in warm marine waters worldwide, causes SSTIs that clinically and epidemiologically resemble V. vulnificus infections. Patients, often those with chronic liver disease, can develop sepsis and multiple organ failure. Small outbreaks of Shewanella infections have been reported among people who cross the Mediterranean Sea in crowded, unsound boats. Under such conditions, travelers who have had prolonged exposure of their feet and legs to contaminated seawater are at high risk for Shewanella infection.
In the United States in January 2025 alone, approximately 20 million commercially-raised birds, mostly egg-laying hens, were affected by the highly pathogenic avian influenza (H5N1). These numbers are staggering yet barely scratch the surface of a potentially larger threat looming over the country. If action is not taken now, the next pandemic could be far deadlier than the 1918 influenza and COVID-19.
What Was the 1918 Influenza?
According to the World Health Organization (WHO), “The 1918 influenza pandemic killed more people in less time than any other disease before or since”; it was the “most deadly disease event in the history of humanity.” Indeed, it killed more people in a single year than the bubonic plague—the “black death”—in the Middle Ages killed in a century. The 1918 virus also killed more people in twenty-five weeks than AIDS killed in twenty-five years. According to one academic reviewer, this “single, brief epidemic generated more fatalities, more suffering, and more demographic change in the United States than all the wars of the Twentieth Century.”
What Caused the 1918 Flu Pandemic?
Although the human influenza virus wasn’t even discovered until 1933, an inspector with the U.S. Bureau of Animal Industry had been publishing research as early as 1919 that suggested a role for farm animals in the pandemic. Inspector J.S. Koen of Fort Dodge, Iowa, wrote: “The similarity of the epidemic among people and the epidemic among pigs was so close, the reports so frequent, that an outbreak in the family would be followed immediately by an outbreak among the hogs, and vice versa, as to present a most striking coincidence if not suggesting a close relation between the two conditions. It looked like ‘flu,’ and until proven it was not ‘flu,’ I shall stand by that diagnosis.”
The answer to where the 1918 virus came from was published in October 2005. Humanity’s greatest killer appeared to originally come from avian influenza—bird flu.
What Is Bird Flu?
Evidence now suggests that all pandemic influenza viruses—in fact all human and mammalian flu viruses in general—owe their origins to avian influenza. Back in 1918, schoolchildren jumped rope to a morbid little rhyme:
I had a little bird, Its name was Enza. I opened the window, And in-flu-enza.
Leading public health authorities, from the U.S. Centers for Disease Control and Prevention (CDC) to the World Health Organization, feared that this bird flu virus was but mutations away from spreading efficiently though the human population, triggering the next pandemic. “The lethal capacity of this virus is very, very high; so it’s a deadly virus that humans have not been exposed to before. That’s a very bad combination,” said Irwin Redlener, former director of the National Center for Disaster Preparedness at Columbia University. Scientists speculate worst-case scenarios in which H5N1 could end up killing a billionor more people around the world. “The only thing I can think of that could take a larger human death toll would be thermonuclear war,” said Council on Foreign Relations senior fellow Laurie Garrett. H5N1 has the potential to become a virus as ferocious as Ebola and as contagious as the common cold.
H1N1 vs. H5N1
The 1918 pandemic virus was H1N1. The annual flu strain remained H1N1, infecting relatively few people every year for decades until 1957, when an H2N2 virus suddenly appeared as the “Asian flu” pandemic. Because the world’s population had essentially only acquired immunity to H1 spikes, the virus raced around the globe, infecting a significant portion of the world’s population. For example, half of U.S. schoolchildren fell ill. H2N2 held seasonal sway for 11 years. In 1968, the H3N2 “Hong Kong Flu” virus triggered another pandemic and has been with us every year since.
So there were three influenza pandemics in the twentieth century—in 1918, 1957, and 1968—but, as the director of the National Institute for Allergy and Infectious Diseases has said, “There are pandemics and then there are pandemics.” The half-and-half bird/human hybrid viruses of 1957 and 1968 evidently contained enough previously recognizable human structure that the human population’s prior partial exposure dampened the pandemic’s potential to do harm. In contrast, the pandemic strain of 1918 was wholly avian-like. Instead of diluting its alien avian nature, the 1918 bird flu virus “likely jumped straight to humans and began killing them,” noted Taubenberger, the man who helped resurrect it. The same could be happening with the new spate of avian influenza viruses sporadically infecting people in more recent years, like H5N1. The human immune system had never been known to be exposed to an H5 virus before. As the WHO points out, “Population vulnerability to an H5N1-like pandemic virus would be universal.”
How Dangerous Is H5N1 Bird Flu?
H5N1 developed a level of human lethality not thought possible for influenza. So far, about half of those known to have come down with this flu have died. H5N1 is good at killing, but not at spreading. To trigger a pandemic, the virus has to learn how to spread efficiently from person to person. Now that the genome of the 1918 virus has been completely sequenced, we understand that it may have taken only a few dozen mutations to turn a bird flu virus into humanity’s greatest killer, and we have seen some of those changes taking form in H5N1. The further H5N1 spreads and the more people it infects, the greater the likelihood that it might lock in mutations that could allow for efficient human-to-human transmission. “And that’s what keeps us up at night,” said the chair of the Infectious Diseases Society of America’s task force on pandemic influenza.
How Did Bird Flu Emerge?
More than a century ago, researchers confirmed the first outbreak of a particularly lethal form of avian influenza that they called “fowl plague.” Plague comes from the Greek word meaning “blow” or “strike.” Later, the name “fowl plague” was abandoned and replaced by “highly pathogenic avian influenza” or HPAI.
Domesticated poultry can also become infected with a low-grade influenza, so-called low pathogenic avian influenza, or LPAI, which may cause a few ruffled feathers and a drop in egg production. Influenza viruses with H5 or H7 spikes, however, are able to mutate into the high-grade variety that can cause devastating illness among the birds. Webster’s term for H5 and H7 strains of flu says it all: “the nasty bastards.” And you don’t get nastier than H5.
Avian Influenza, Poultry, and Eggs
To avoid contracting bird flu, an influenza expert at the UK Health Protection Agency warned, “[a]void being in touching distance [of birds who could be affected]. Don’t kiss chickens.” Kissing aside, what is the risk of putting our lips on them in other ways?
In 2001, the virus was found and confirmed in frozen duck meat. The investigators concluded, “The isolation of an H5N1 influenza virus from duck meat and the presence of infectious virus in muscle tissue of experimentally infected ducks raises concern that meat produced by this species may serve as a vehicle for the transmission of H5N1 virus to humans.”
The finding of H5N1-contaminated poultry meat triggered a more extensive survey. Top flu researchers at the U.S. Department of Agriculture (USDA) looked into chicken meat. Chickens who inhaled H5N1 became infected even more systemically than did ducks. The virus spread through the internal organs, into the muscle tissue, and even out into the skin. Virus was found in both white and dark meat.
There is a precedent for bird-borne virus-infected meat. Unlike bacteria, viruses can remain infective for prolonged periods even in processed foods. Some methods of preservation, like refrigeration, freezing, or salting, may even extend the persistence of viruses in food.On the other hand, since viruses cannot replicate without living tissue, improper storage of food is less problematic.
What about eggs? “Be careful with eggs,” the World Health Organization has warned. “Eggs from infected poultry could also be contaminated with the [H5N1] virus…”
Mutating and Getting More Virulent
Within a single individual, a virus evolves, adapts, learns. It hits dead ends and tries something new, slowly notching up mutations that may lock into place the ability to effectively survive in, and transmit between, people. Every single person who gets infected presents a risk of spawning the pandemic virus. Describes one virologist, “You’re playing Russian roulette every time you have a human infection.” Experts fear that as more and more people become infected, a virus will finally figure out the combination—the right combination of mutations to spread not just in one elevator or building, but in every building, everywhere, around the globe. Then it won’t just be peasant farmers in Vietnam dying after handling dead birds or raw poultry—it will be New Yorkers, Parisians, Londoners, and people in every city, township, and village in the world dying after shaking someone’s hand, touching a doorknob, or simply inhaling in the wrong place at the wrong time. It’s happened before, and it may soon happen again.
Said a WHO spokesperson about a virus like H5N1, “All the indications are that we are living on borrowed time.” A senior associate at the Center for Biosecurity listed the indications: “The lethality of the virus is unprecedented for influenza, the scope of the bird outbreak is completely unprecedented and the change that needs to happen to create a pandemic is such a small change—it could literally happen any day.”
Never before H5N1 had bird flu spread so far, so fast, and the longer the virus circulates in poultry production systems the higher the likelihood of additional human exposure.
Can H5N1 Be Eradicated?
H5N1 may be here to stay. “This virus cannot now be eradicated from the planet,” said Center for Biosecurity director O’Toole. “It is in too many birds in too many places.” The virus seemed to be getting more entrenched. “If you described it as a war, we’ve been losing more battles than we’ve won,” a WHO spokesperson told TheFinancial Times. “From a public health point of view, and an animal health point of view, this virus is just getting a stronger and stronger grip on the region.”
In a tone uncharacteristic of international policy institutions, the FAO wrote: “Over this bleak landscape sits a black cloud of fear that the virus might become adapted to enable human-to-human transmission and then spread around the globe.” The urgency and alarm among those tracking H5N1’s building momentum was palpable. “It’s like watching a volcano getting ready to erupt,” described a spokesperson of the World Organization for Animal Health (known as OIE, for Office Internationale des Epizooties). “We’re all holding our breath,” said Julie Gerberding, former head of the CDC.
Breeding Grounds for Disease
The world’s three leading authorities—the Food and Agriculture Organization of the United Nations, the World Health Organization, and the World Organization for Animal Health—held a joint consultation in 2004 to determine the key underlying causes. Four main risk factors for the emergence and spread of these diseases were identified. Bulleted first: “Increasing demand for animal protein.” This has led to what the CDC refers to as “the intensification of food-animal production,” the factor blamed in part for the increasing threat.
The way we kept animals when we first domesticated them ten thousand years ago is a far cry from how they are reared today. Chickens used to run around the barnyard on small farms. Now, “broiler” chickens—those raised for meat—are typically warehoused in long sheds confining an average of 20,000 to 25,000 birds. A single corporation, Tyson, can churn out more than 20 million pounds of chicken meat a day. Worldwide, an estimated 70 to 80 percent of egg-laying chickens are intensively confined in battery cages, small barren wire enclosures stacked several tiers high and extending down long rows in windowless sheds. The cages are stocked at such densities that each hen is typically allotted less floor space than a standard letter-sized piece of paper. It is not uncommon for egg producers to keep hundreds of thousands—or even a million—hens confined on a single farm. Half the world’s pig population—now approaching one billion—is also crowded into industrial confinement operations. This represents the most profound alteration of the animal-human relationship in ten thousand years.
What Can We Do?
To reduce the emergence of viruses like H5N1, humanity must shift toward raising birds in smaller flocks, under less stressful, less crowded, and more hygienic conditions, with outdoor access, no use of human antivirals, and with an end to the practice of breeding for rapid growth or unnatural egg production at the expense of immunity. This would also be expected to reduce rates of increasingly antibiotic-resistant pathogens such as Salmonella, the number one foodborne killer in the United States. We need to move away from the industry’s fire-fighting approach to infectious disease to a more proactive preventive health approach that makes birds less susceptible—even resilient—to disease in the first place.
In the United States, the American Public Health Association (APHA) is among those advocating for “radical” (from the Latin radix, for “root”) change. In 2003, the APHA passed a “Precautionary Moratorium on New Concentrated Animal Feed Operations,” in which it urged all federal, state, and local authorities to impose an immediate moratorium on the building of new factory farms—including industrial turkey, laying hen, broiler chicken, and duck facilities. In November 2019, it reiterated its stance, publishing a new policy statement calling once again for a moratorium on new factory farms, as well as a moratorium on the expansion of existing ones.
Eating to Beat Bird Flu
The journal of the APHA published an editorial entitled “The Chickens Come Home to Roost” that went beyond just calling for a deintensification of the pork and poultry industries. The editorial questioned the prudence of raising so many animals for food in the first place, given the pandemic threat they may pose: “It is curious, therefore, that changing the way humans treat animals, most basically ceasing to eat them, or at the very least, radically limiting the quantity of them that are eaten—is largely off the radar as a significant preventive measure. Such a change, if sufficiently adopted or imposed, could still reduce the chances of the much-feared influenza epidemic. It would be even more likely to prevent unknown future diseases that, in the absence of this change, may result from farming animals intensively and killing them for food. Yet humanity doesn’t even consider this option.”
However, thanks to food innovations, this may be changing, with plant-based meats, milks, and eggs growing in popularity with expanded options in supermarkets. And, making healthier choices could also help mediate the next coronavirus epidemic by also decreasing the rates of comorbidities found to increase the risk in SARS, MERS, and COVID-19. For example, consider the underlying risk factors for COVID-19 severity and death—obesity, heart disease, hypertension, and type 2 diabetes—all of which can be controlled or even reversed with a healthy enough plant-based diet and lifestyle.
Egg-Free Eggs
There are so many delicious egg-free egg recipes, like this Garden Veggie Tempeh Scramble created by NutritionFacts.org’s own executive director.
Conclusion
H5N1 was discovered in chickens decades ago, a flu virus that would forever change our understanding of how bad pandemics could get—a flu virus that appears capable of killing half the people it infects. Imagine if a virus like that started explosively spreading from human to human. Consider a pandemic a hundred times worse than COVID-19, one with a fatality rate not of one in two hundred but rather a coin flip of one in two. Thankfully, H5N1 has so far remained a virus mainly of poultry, not people, but H5N1 and other new and deadly animal viruses like it are still out there, still mutating, with an eye on the eight-billion-strong buffet of human hosts. With pandemics, it’s never a matter of if, but when. A universal outbreak with more than a few percent mortality wouldn’t just threaten financial markets but civilization itself as we know it.
A pandemic triggered by a bird flu virus could leave hundreds of millions dead. “An influenza pandemic of even moderate impact,” Michael Osterholm, the director of the Center for Infectious Disease Research and Policy at the University of Minnesota, wrote, “will result in the biggest single human disaster ever—far greater than AIDS, 9/11, all wars in the 20th century and the recent tsunami combined. It has the potential to redirect world history as the Black Death redirected European history in the 14th century.”1 Hopefully, for humanity’s sake, the direction world history will take is away from raising birds by the billions under intensive confinement so as to potentially lower the risk of us ever being in this same precarious place in the future. The silver lining of COVID-19 is that the world will be better prepared for the next global health crisis. Tragically, it may take a pandemic with a virus like H5N1 before the world realizes the true cost of cheap chicken.
1 Kennedy M. 2005. Bird flu could kill millions: global pandemic warning from WHO. “We’re not crying wolf. There is a wolf. We just don’t know when it’s coming.” Gazette (Montreal), March 9, p. A1.
You do not smoke, and you do not have a persistent cough: so you might think lung cancer is not your concern. But think again. While smoking remains the leading cause of lung cancer deaths, about 20% of people diagnosed have never touched a cigarette. Spotting early signs is crucial, yet many symptoms are so subtle they are easy to miss.
People with lung cancer may experience a persistent cough, repeated chest infections, coughing up blood, breathlessness, chest pain, constant fatigue, and unexplained weight loss. While these are the common signs people typically associate with lung cancer, we are going to explore the silent warnings the body may send that are often easy to overlook.
Face and Neck Swelling: Lung cancer patients can develop tumors near the superior vena cava, a large vein that carries deoxygenated blood from the head, neck, upper limbs, and torso back to the heart. This complication, known as superior vena cava syndrome, occurs when the tumor presses against the vein and nearby lymph nodes, causing blood to back up and resulting in swelling in the face and neck.
Mental Health Symptoms: Studies have shown that people who were later diagnosed with lung cancer often developed mental health issues such as confusion, anxiety, and depression. These symptoms could be caused by tumors affecting the brain, the impact of cancer on the immune system or hormones, or high calcium levels related to cancer.
Finger clubbing: Finger clubbing is a notable yet often overlooked symptom associated with lung cancer. It occurs when certain lung tumors produce hormone-like substances that increase blood flow and fluid accumulation in the fingertips, leading to their enlargement. This condition is characterized by rounded, bulging fingertips and nails that may appear shiny or curve more than usual.
Stomach Problems: It is estimated that around 40% of lung cancer patients develop tumors that release substances that could disrupt normal calcium levels. Excessive calcium in the blood affects digestion and causes stomach cramps, nausea, and constipation.
Shoulder and back pain: Not all lung cancers affect the respiratory system. For example, a Pancoast tumor is a type of lung cancer that grows in the upper part of the lung and can spread to the ribs, vertebrae, nerves, and blood vessels. This type of lung cancer can cause pain in the shoulder blade, upper back, and arm.
Early detection of lung cancer:
The survival rate for lung cancer largely depends on how far the cancer has spread at the time of diagnosis. If detected early, when the cancer is still localized, and treated promptly, some lung cancers can go into remission. Therefore, if you experience any symptoms, it’s important to consult with a doctor. However, keep in mind that these symptoms may not necessarily indicate lung cancer, as they could be linked to other conditions.
All orders are protected by SSL encryption – the highest industry standard for online security from trusted vendors.
Sonu’s Diabetes Secret is backed with a 60 Day No Questions Asked Money Back Guarantee. If within the first 60 days of receipt you are not satisfied with Wake Up Lean™, you can request a refund by sending an email to the address given inside the product and we will immediately refund your entire purchase price, with no questions asked.
While this article has been reviewed for accuracy and fairness by Mindful editors, some material in this article was generated by AI. To learn more about our AI practices and why we sometimes use AI to generate content, please see our statement here.
We often imagine a standard meditation practice taking place in a seated position, but sitting is certainly not the only way to get a great meditation session. In fact, one of the most accessible places to meditate is a space where we already spend a third of our lives: in bed. If you’re wondering how to meditate in bed, you’ll find what you need to get started in this simple guide, complete with techniques, benefits, and tips to make the most of this restful practice.
Whether you’re looking to begin your day with clarity, or you’re seeking a soothing practice to quiet your body and mind before sleep, meditating in bed offers a gentle and practical way to weave mindfulness into your routine.
Why Learn How to Meditate in Bed?
Meditating in bed isn’t just convenient—it can also be beneficial. Here’s why this practice is worth exploring:
Accessibility: First of all, at the beginning or end of each day, you’re already there! No need for a special cushion or designated space. Plus, this position can be easier and more comfortable for people with chronic pain or mobility challenges that make traditional seated postures painful or impossible.
A Versatile Option to Add to Your Mindfulness Toolkit: You can meditate in bed while sitting, lying on your back, or resting on your side. And while you might not feel like meditating in bed every day, it can be a great option for times when you aren’t feeling well, or you’re recovering from an injury or medical procedure that makes sitting uncomfortable.
A Gentle Start or End to the Day: Morning meditations set the tone for mindfulness and focus, while evening meditations help transition from the day’s busyness to restful sleep.
Stress and Sleep Support: Mindfulness meditation has been shown to reduce stress and improve sleep quality, making it an ideal practice for those struggling with insomnia or racing thoughts at night.
Body Awareness and Relaxation: In bed, you’re naturally lying down or reclining, a posture that can encourage deep relaxation and help you connect with your body in a soothing way.
How to Prepare for Meditating in Bed
Creating the right environment can significantly enhance your meditation experience. Here are a few steps we recommend to set the stage:
Reduce Distraction: This can include anything from taking a few minutes to declutter the space, making sure your phone is silenced or off, or taking care of a small to-do that might be nagging your mind.
Dim the Lights: Soft lighting or total darkness can help signal your brain that it’s time to wind down. If it’s safe to do so, a lit candle can also be soothing. (For example, if you know you’re prone to falling asleep during this type of meditation, candles might not be the best option.)
Limit Noise: Use earplugs, a white noise machine, or calming background sounds like ocean waves or rain if you’re in a noisy environment.
Dress Comfortably: Wear loose, comfortable clothing or pajamas that don’t restrict your movement or breath.
Avoid Screens: If you’re using this time to wind down at night, minimize screen time for at least 30 minutes before bed to reduce blue light exposure and prepare your mind for stillness.
Techniques for Meditating in Bed
While most meditations can be done sitting, standing, or reclining, there are several meditation methods tailored for bed, each addressing different goals like relaxation, mindfulness, or stress relief. Here are some of our favorites:
1. Body Scan Meditation
The body scan is a soothing technique that helps you become aware of physical sensations, tension, and areas of relaxation.
How to Meditate In Bed with a Body Scan:
Lie flat on your back with your arms resting at your sides. Close your eyes.
Begin by focusing on your breath. Take slow, deep breaths in through your nose and out through your mouth.
Starting at the top of your head, bring your awareness to each part of your body. Notice sensations—warmth, tension, or lightness.
Slowly work your way down your body: forehead, jaw, neck, shoulders, arms, chest, stomach, hips, legs, and feet.
If you notice tension, imagine sending your breath there to gently release it.
Once you’ve scanned your whole body, rest in the stillness you’ve created.
2. Breath Awareness Meditation
Focusing on the breath is a foundational meditation practice that calms the mind and anchors you in the present moment.
How to Meditate In Bed with Breath Awareness:
Lie comfortably on your back or side, closing your eyes.
Inhale deeply through your nose for a count of four, hold for a count of two, and exhale slowly through your mouth for a count of six.
Pay attention to the sensation of air moving in and out—cool air entering, warm air leaving.
If your mind wanders, gently guide it back to the rhythm of your breath.
Continue for 5–15 minutes or until you feel a sense of calm.
3. Guided Visualization
This technique uses imagery to create a sense of peace and relaxation, perfect for setting a vision for your upcoming day, or winding down before sleep.
How to Meditate In Bed with a Guided Visualization:
Find a guided meditation app or audio recording, or create your own imagery.
As you lie in bed, close your eyes and picture a serene setting, like a tranquil beach, a quiet forest, or a warm, glowing light surrounding you.
Use all your senses: imagine the sounds, scents, and textures of your visualization.
Let the imagery carry you into a deep state of relaxation.
4. Loving-Kindness Meditation (Metta)
Loving-kindness meditation is a practice of directing goodwill and compassion toward yourself and others. This can be particularly powerful before you head into work (focusing your attention on compassion for those you’ll encounter during the day) or as a way to re-center after a stressful day.
How to Meditate In Bed with Metta Meditation:
Begin in a comfortable lying position, eyes closed.
Take a few deep breaths and focus on feelings of warmth and love.
Silently repeat phrases like:
“May I be happy.”
“May I be healthy.”
“May I be safe.”
Gradually expand your focus to others: first someone you love, then a neutral person, and finally someone you’ve struggled with.
End by sending loving-kindness to all beings everywhere.
5. Counting or Word Meditation
For those who struggle with a racing mind, creating a single, simple point of focus can help to slow thoughts and bring calm to the body and mind. Counting works, or choosing a short word or phrase can also be useful.
How to Meditate In Bed with Counting or a Simple Word:
Lie on your back and close your eyes.
Begin counting your breaths: inhale as “one,” exhale as “two,” and so on up to ten.
If you’re using a word or phrase, you can repeat it on each inhale and exhale, or you can use the inhale for the first part of the phrase and the exhale for the second. For example, you could say something like, (inhale) I greet this day, (exhale) with gratitude and openness.
If your mind wanders, which it will, just start again without judgment.
Repeat this process until you feel centered and calm.
While it has many overlaps with traditional meditations practices, Yoga Nidra is a restorative and intention-setting practice that’s been around for centuries. It is a form of non-sleep deep rest (NSDR) that activates the brain’s delta waves, which allows the body to enter the “rest and digest” state. It has been shown to bring deep relaxation, mental clarity, and a calm, revitalized energy. Notably, it’s an effective practice for reducing anxiety.
How to Meditate in Bed with Yoga Nidra:
Get comfortable on your back with your feet about shoulder width apart and your arms by your sides.
Set an intention (called a Sankalpa) for your practice. This could be something like, I am courageous, My true nature is love, or, I am a conduit for peace in the world.
Remind yourself that you will remain awake throughout the practice.
Focus on different parts of your body, feeling their weight and then their lightness.
Witness all thoughts and feelings that arise, welcoming them with compassion, not trying to “fix” them, and just allowing them to pass.
Reflect on your intention for the practice and affirm it with your mind and body.
You can learn more about the practice of Yoga Nidra and experience seven full guided sessions with teacher Kelly Boys in our Yoga Nidra course.
Tips for Meditating In Bed as an Ongoing Practice
As with any meditation practice, it might take some time to find what works best for you. As you explore adding this approach to your mindfulness toolkit, here are a few tips to keep in mind:
Be Patient with Yourself: Your mind will wander—this is normal. Gently bring your focus back to the practice without self-criticism.
Experiment with Positions: While lying on your back is common, this might be uncomfortable for people with low back issues. It’s okay to lie on your side, prop your knees up, or lie at a 45º angle with pillows under your shoulders, neck, and head if that’s more comfortable.
Use Props for Comfort: Pillows under your knees or a weighted blanket can enhance relaxation.
Set a Time Limit (or Don’t): Meditate for a specific duration, or simply let the practice carry you into sleep.
Be Consistent: Make meditation a nightly or morning ritual. The more you practice, the easier it becomes to slip into a meditative state.
How to Meditate In Bed: Benefits You Can Experience
As you experiment with different techniques and times of day, see what you notice about how you’re feeling. Here are some benefits you might experience as you develop your practice:
Improved Sleep Quality: Meditating before bed can help quiet the mind, release tension, and prepare your body for restful sleep.
Reduced Anxiety and Stress: Mindfulness lowers cortisol levels, promoting a sense of calm and balance.
Enhanced Emotional Regulation: Regular meditation can help you approach challenges with greater resilience and clarity.
Improved mindset or outlook: Morning meditation sets a positive tone, fostering mindfulness, curiosity, and focus throughout the day.
Deepened Self-Awareness: Spending time with your thoughts and body creates a stronger connection with yourself.
A Cozy, Comfy Way to Grow Your Mindfulness Practice
Meditating in bed is a versatile, gentle way to bring mindfulness into your life. Whether you’re looking to start your day with clarity or unwind into restful sleep, the techniques shared here can help you create a sense of peace and connection.
The beauty of bed meditation lies in its simplicity—you don’t need fancy tools or hours of practice. All you need is your breath, your body, and a willingness to be present. Over time, this practice can transform not just your sleep but also your overall well-being.
FAQs
What if I fall asleep during meditation?
It’s common to fall asleep while meditating in bed, especially at night. This isn’t necessarily a bad thing! If your goal is to wind down and sleep better, drifting off during meditation means your practice is working. However, if you’re aiming for focused mindfulness, consider meditating sitting upright earlier in the day.
Can I combine meditating in bed with other types of meditation?
Of course! Meditation can be done anytime, anywhere, and any way you like. Just find what works for you. You can even combine practices if you like—for example, using yoga stretches to help you relax before bed.
When I learn how to meditate in bed, do I get the same benefits as other types of meditation?
Yep! Meditating in bed still increases relaxation, lessens stress, balances the nervous system, enable better sleep, improves mood, and offers a host of other physical, emotional, and mental benefits.
