You may have heard about cases of bird flu lately in the news, but there’s no reason to panic. Here’s what you need to know about bird flu and how to keep your family safe.
What Is Bird Flu?
Bird flu is a form of the flu (influenza) virus that usually infects birds and other animals. It’s not the same as the flu that many people get during cold-weather months, but it can cause similar symptoms. There are different strains (kinds) of bird flu; a common strain is H5N1 or H5.
How Does Bird Flu Spread?
Wild birds — like ducks, geese, swans, and crows — can spread bird flu to birds on poultry farms and cows on dairy farms. Other animals have gotten infected, too. People who work with animals that have bird flu are more likely to get it.
Bird flu spreads through an animal’s saliva (spit), mucus, milk, pee, or poop. These can get on an animal’s feathers or skin, in their cages, or on nearby items like farm equipment. When people touch tiny droplets or specks that have the virus and then touch their eyes, nose, or mouth, they can get infected. They can also get infected by breathing in the droplets or dust that’s contaminated.
Sometimes bird flu can spread by eating undercooked eggs or poultry, like chicken or turkey, or by having raw milk from animals, like cows, infected with the virus.
What Are the Signs & Symptoms of Bird Flu?
Bird flu can appear like other flu viruses, and symptoms include:
Severe bird flu may cause a person to have trouble breathing or a high fever, feel confused, develop seizures, and even die.
How Is Bird Flu Diagnosed?
To check for bird flu, doctors will take a sample of mucus by wiping a cotton swab inside the nose or throat. If your child has pinkeye, they may swab the eye. The samples are sent to a lab for testing.
Be sure to tell your doctor if your child has been near any animals and has symptoms of bird flu.
How Is Bird Flu Treated?
Doctors may prescribe antiviral medicine for bird flu, and it works best if children start taking it when symptoms first start. Kids with more serious symptoms are treated in the hospital.
For children with mild symptoms, at-home care may help them feel better as they recover. Make sure your child drinks lots of liquids to prevent dehydration, gets plenty of sleep, and takes it easy. Kids might feel hot or cold, so have them wear layers that are easy to remove. For fever and aches, you can give acetaminophen or ibuprofen, but avoid aspirin because it’s linked to Reye syndrome.
To avoid spreading the virus to other people, your child should stay home from school or daycare — ask your doctor for how long.
Can Bird Flu Be Prevented?
There’s no vaccine for bird flu, but scientists are working on one to prevent people from getting the virus. Health officials in many countries are taking steps to help prevent bird flu from spreading.
To help keep your family healthy:
Avoid touching birds. Watch them from far away. If you plan to travel somewhere there’s been an outbreak of bird flu, stay away from live bird markets, poultry farms, or any other places where there might be infected poultry. Check with agencies like the CDC for travel updates.
Wash hands often when going to places like farms, petting zoos, or ponds that have birds. Also, take your shoes off before stepping inside your home to avoid bringing in germs.
Have your family wear gloves, masks, and goggles when working near wild animals, birds, cattle, and other livestock. Make sure everyone washes their hands and changes clothes afterward.
Report animals that may be sick with bird flu or died from it. Call your state health department and stay away from anything the animal touched.
Cook poultry, eggs, meat, and seafood to the right temperature to destroy any flu viruses in raw or undercooked food. Be sure to use different cutting boards and utensils (like forks, knives, spoons, and chopsticks) for uncooked meats and other foods. Wash hands before and after eating.
Avoid touching or having raw dairy products, like raw milk. Choose ones that have been pasteurized (heated to kill the bird flu virus and other germs) by checking the food label.
Get a flu shot. It won’t prevent bird flu, but it can help your child stay healthy by avoiding the seasonal flu. That way, there’s less chance of getting the two flus at the same time.
Can My Bird or Other Pets Get Bird Flu?
Birds and other pets may get bird flu if they go near another animal that has the virus. Making sure your pets are safe helps keep your family healthy, too. So follow these tips:
Keep your pet bird and its food and water inside, away from anyplace where it could be exposed to an infected animal. Avoid letting your pet drink or eat from ponds or other places where wild birds may have flown over and spread the virus.
Clean the birdcage often. Wash your hands right away and after handling the bird or touching its poop.
Try to make sure any birds on your property (like those in a chicken coop) stay away from wild birds. To be extra safe, wear a mask when you’re near your birds.
Prevent other pets (like cats and dogs) from getting near wild birds, raw meat and poultry, and raw milk so they don’t get infected.
If you have a bird feeder, clean any surfaces that bird poop has touched and wash your hands.
The United States and other countries have stopped importing live birds and bird products (like meat and eggs) from countries where there have been outbreaks of bird flu. So if you buy a pet bird, it should not have been exposed to the virus.
Still, there is an illegal market for buying and selling exotic birds and other animals. Before you buy any animal as a pet, find out where it was born and raised. If you have more questions, talk with a veterinarian.
For some individuals in their late 60s, it may be worthwhile to get “catch-up” HPV testing, according to findings from a large study.
Credit: iStock
Testing for the presence of cancer-causing types of the human papillomavirus (HPV) is now a standard part of screening for cervical cancer, some times with simultaneous Pap tests (known as co-testing). But cervical cancer screening is recommended to stop at age 65 in many places and, for a variety of reasons, many older adults stop getting screened for cervical cancer well before that age.
In the new study, about 62% of women who were invited to undergo this “catch-up” testing for HPV (intervention group) had a test within the next year. In a comparison group of women not invited for catch-up testing, only about 2% had either a Pap test or an HPV test over the next year.
The rate of CIN2+ lesions diagnosed in the intervention group was significantly higher than in the comparison group (3.9 vs. 0.3 per 1,000 eligible women, respectively). CIN2+ lesions are often called precancers because these types of cell changes can go on to become cancer. Finding these lesions early allows doctors to remove them before they can progress.
Women who were furthest behind on regular screenings—that is, had one or no screenings since age 50—had nearly twice the rate of CIN2+ lesions as women who had been screened two or more times since age 50, the researchers found.
The study findings were published July 6 in PLOS Medicine.
“It may be time to reevaluate cervical cancer screening at older ages,” said lead investigator Mette Tranberg, Ph.D., of the University Research Clinic for Cancer Screening at Randers Regional Hospital in Denmark. “Our data show that it could really be beneficial to [offer catch-up HPV testing] for these older, insufficiently screened women.”
The findings support recommendations in some countries, such as the United States, where a history of negative screening results is recommended for stopping screening at age 65, after which the risk of a new HPV infection developing into cervical cancer is very low, said Nicolas Wentzensen, M.D., Ph.D., of NCI’s Division of Cancer Epidemiology and Genetics (DCEG), who was not involved in the study.
Dr. Tranberg cautioned, however, that catch-up HPV testing could have potential downsides.
As with any screening approach, she said, it’s important to weigh the potential benefits of catching precancers or early cancers with the potential harms. Those harms include being treated for lesions that would never have developed into cancer during a woman’s lifetime.
Overall, Dr. Wentzensen said, the study reinforces the importance of women continuing to stay up to date on cervical cancer screening as they get older.
“This study was able to evaluate the prevalence of precancer in this specific population. Understanding the prevalence of precancer is one part of the puzzle to inform screening recommendations in an any age group,” he said. “This study clearly shows that there [are potential precancers over age 65] and that offering an HPV test in this population to identify those who may need treatment could be helpful.”
The challenges of screening older individuals
Almost all cervical cancers are caused by infection with high-risk types of HPV, particularly HPV 16 and HPV 18. Most HPV infections go away on their own, but for some people an infection can persist for years and lead to abnormal cervical cells that form cervical lesions. If left untreated, these lesions may progress to cervical cancer.
Unlike Pap tests, which look for abnormal cells in a sample of cervical cells, an HPV test checks the cells for the presence of genetic material (DNA or RNA) from high-risk HPV types.
Many countries, including the United States, have begun transitioning to HPV testing as the primary approach to cervical cancer screening. Women who test positive for HPV are referred for follow-up testing, which may include a Pap test or colposcopy (visual inspection of the cervix under magnification) and a biopsy to see how abnormal the cells are and how much of the cervical tissue is affected.
HPV tests are very good at detecting infection with the virus, but because these tests have only been available for the past 10 or so years, most women over age 65 have never had one. Instead, most older women have had Pap tests for routine cervical cancer screening.
However, Pap tests are less effective in older women compared to younger women because physiological changes after menopause make it more difficult for doctors to collect samples from the part of the cervix where cell changes typically start.
Even though cervical cancer tends to be diagnosed at younger ages than many cancers—in the United States the median age at diagnosis is 50 years—it does affect older women.
Experts say new approaches to prevent cervical cancer in women over the age of 65 are needed because women over this age continue to be diagnosed with and die from the disease. In the United States, for example, women 65 and older account for more than 20% of new cases of cervical cancer and around 37% of deaths from the disease.
Dr. Tranberg and her colleagues wondered whether giving women over age 65, particularly those who have fallen behind on screening, a catch-up HPV test could help bridge this gap in cervical cancer prevention.
Catching up with an HPV test
In the study, more than 11,000 Danish women aged 65 to 69 from one region of Denmark were invited to get an HPV test. They were able to choose between having a cervical sample collected by their doctor or using a vaginal self-collection kit to be mailed back for testing, known as self-sampling.
Women were included if they had no record of screening in the past 5.5 years. A comparison group of about 33,400 Danish women from Denmark’s remaining four regions were offered usual care, which included getting a Pap test or HPV test as needed—for example, if they had vaginal bleeding.
About 62% of women in the catch-up testing group had an HPV test within 12 months, while only 2% of women in the comparison group got either a Pap test or HPV test within the same time frame.
Using patient records from a centralized data network in Denmark, the researchers compared the rates CIN2+ lesions diagnosed in the two groups. In the catch-up group, 3.9 out of every 1,000 eligible women were found to have a CIN2+ lesion, compared with 0.3 out of every 1,000 eligible women in the comparison group.
Those who had rarely or never been screened in their 50s and early 60s (“insufficiently screened”) were more than twice as likely to have CIN2+ lesions as those who had been screened at least twice during that same time (“routinely screened”).
Overall, more women in the catch-up testing group chose to get a cervical sample collected by a clinician than to do self-sampling. But those who were insufficiently screened were much more likely to choose self-collection than those who were routinely screened.
Among the 2,000 women who conducted the testing via self-collection at home, 161 were found to be HPV-positive. Of this group, all except one completed follow-up testing with their doctor within the next 6 months.
This finding, Dr. Tranberg said, suggests that offering the opportunity for self-collection may be appealing to women who prefer not to get screening from a provider.
Balancing risk versus benefit
The study’s findings, Dr. Wentzensen said, highlight the importance of the recommendation in US cervical cancer screening guidelines that calls for women over 65 to continue screening until they have a series of normal results.
“We know there is risk [in this age group],” he said. “So clinicians need to work with patients to make sure they have had several consecutive normal HPV test results. For their patients who haven’t, he added, “you can’t just release them from screening.”
However, he cautioned that CIN2+ is not the best indicator of cervical cancer risk, because many of these lesions will never progress to cancer. A better measure, he said, would be CIN3+ lesions, which are much more likely to develop into cancer.
Dr. Tranberg acknowledged that CIN3+ would have been a better primary measure but, from a statistical standpoint, would have required an even larger study. However, the researchers did find that rates of CIN3+ were higher in the catch-up testing group than the comparison group.
Ultimately, Dr. Tranberg said, better tests and biomarkers are needed to differentiate between abnormalities that are harmless and abnormalities that will progress to cancer.
She also pointed out that given the potential harms of screening, such as overdiagnosis and overtreatment, it’s important to determine who would benefit most from receiving a catch-up HPV test.
One approach might be to offer catch-up testing to only those older women who have been insufficiently screened, and to make self-collection kits more widely available. HPV self-collection kits are already being used in several countries, including Denmark, and are under FDA review in the United States.
Meanwhile, Dr. Wentzensen and other DCEG colleagues are engaged in several collaborative efforts related to cervical cancer screening. They include initiatives to improve screening in communities where screening rates continue to lag (see below).
Screening centered around HPV testing “is now the preferred approach in most places in the world, and now it’s really a question of implementation and making sure that new developments reach the populations that need them the most,” he said.
A bimanual pelvic examination (BPE) is used to check a woman’s internal pelvic organs. The health care provider inserts two fingers into the vagina and then places pressure with the other hand to the lower part of the belly.
The American College of Obstetricians and Gynecologists recommends BPEs only if young women have a medical history or certain symptoms like pelvic pain and unusual bleeding. The American College of Physicians and the American Academy of Family Physicians do not recommend performing BPEs on women who are not pregnant and are not having health problems.
BPEs are not recommended before prescribing most hormonal contraceptives (including birth control pills), or during screening for sexually transmitted infections.
A Pap test is used to check for cervical cancer by placing a speculum (medical tool) inside the vagina to collect cells from the cervix.
Cervical cancer screening is not recommended for women younger than 21 years, according to leading professional organizations.
The harms of unnecessary tests
Unnecessary BPE and Pap tests could cause several harms, such as:
Fear.
Anxiety.
A false positive test result (a test result that tells you a disease or condition is present, when in reality, there is no disease).
Unnecessary treatments.
Unnecessary costs.
Given these possible harms, it’s important for young women to receive BPEs and Pap tests only when necessary. BPEs and Pap tests should be a shared decision between the patient and the health care provider.
About the study
CDC researchers used data from the National Survey of Family Growth to estimate the number of potentially unnecessary tests in young women aged 15 to 20 in the United States. The data were combined from the years 2011 to 2017.
Survey participants were asked if they had received a Pap test or a BPE in the past 12 months.
The BPEs were classified as either medically needed (the test was necessary) or potentially unnecessary.
The exam was considered medically needed if the young woman:
Was pregnant.
Used an intrauterine contraceptive device (IUD).
Received the test because of a medical problem.
Received treatment for a sexually transmitted infection such as chlamydia, gonorrhea, syphilis, or genital herpes.
Key findings
The study estimated that 1.4 million BPEs and 1.6 million Pap tests performed on females in the United States aged 15 to 20 in a single year may have been medically unnecessary.
The study also found:
Young women who had a Pap test were 7 times more likely to report also receiving a BPE, compared with young women who did not have a Pap test.
Young women who had been screened for a sexually transmitted infection were 4 times more likely to receive a Pap test and 60% more likely to receive a BPE, compared with young women who had not been screened.
Young women who used a hormonal contraception method other than an IUD were 75% more likely to receive a Pap test and 31% more likely to receive a BPE, compared with young women who did not use non-IUD hormonal contraception methods.
How to avoid unnecessary BPEs and Pap tests
The study concluded that efforts to avoid unnecessary BPEs and Pap tests among young women could include:
Educating health care providers and women about when exams and tests are necessary.
Encouraging parents and patients to ask health care providers about when exams are appropriate.
Making a shared decision between the patient and the health care provider about whether exams and tests are necessary.
When a parent is sent away for military service (deployment), family life changes. You may wonder how your child will handle it all, but parents and caregivers can help kids cope.
Telling your child about deployment is the first step. Being honest, talking to kids in terms they can understand, and making plans to stay in touch are key.
To help your child adjust to this new transition, try the tips below.
How Can I Help My Child During Deployment?
While your family member is gone, there are lots of things you can do to keep home life normal and stay strong as a family:
Stick to a routine. When there are big changes in life, keeping some things the same at home can be a comfort. Try to stick to your child’s regular routines, like getting ready for bed or doing a fun Saturday morning activity.
Stay connected. Keep the deployed parent part of your child’s life. Besides having phone and video calls, kids might:
Make an online photo album to share or send handwritten letters or care packages.
Start a scrapbook with things like artwork, pictures, and report cards for when the parent returns home.
Think good wishes about the parent at the same time each day, like at bedtime.
Talk often and listen. Chat with your kids about the things that upset them. Let them know it’s OK to be worried sometimes and that you feel that way too. Simply listening and letting children know that you understand can comfort them.
Make sure kids are active, eat right, and sleep well. Stress can lead to eating foods that aren’t healthy or spending too much time online, watching TV, or playing video games. Exercising, choosing healthy foods, and getting enough sleep can help kids stay at their best.
Try not to overload kids. It’s not your child’s job to take on the household duties of the deployed parent. Kids should focus on school and their after-school activities. If they’d like to help, letting them do a few extra things can make them feel like they’re pitching in. Small helpful tasks can include watching younger siblings once in a while or making dinner one day a week.
Limit the news. Your child may be tempted to keep checking the news to learn about where the deployed parent is. Set limits on what kids read and watch, and talk with them about what they see. Set aside time to chat about what your child has heard on the news or from other people.
Help kids feel calm. Encourage children to do what soothes them. They may want to draw, write, read, listen to music, go for a walk, or play with a pet.
Volunteer. Your deployed family member is helping other people. Doing the same can make your family feel connected. Look for ways you and your kids can volunteer in the community.
Get support. When a parent is deployed, it can put a lot of pressure on the other family members to take on extra tasks. Ask for support from relatives, friends, community members, and other military families. You can also see what programs the military offers to help you get through tough times. Check with your installation’s Military & Family Support Center or visit Military OneSource (800- 342-9647).
How Can I Help My Family Adjust When a Parent Returns?
When a deployed parent comes home, most families need time to find their balance. Here are some ideas to make the shift easier:
Talk with each other. A lot can change when a parent has been away. The kids are older and may have new interests and ways of doing things. Everyone may be more self-reliant. Talking with your newly returned family member and being honest can help everyone figure out where they fit into the new routine.
Give it time. The first few days and weeks of being together as a family might be rocky. Putting pressure on yourself or your loved ones to act or feel a certain way makes things harder. Be patient as you get to know each other again. Give the whole family plenty of chances to connect.
How Do I Know if My Family Needs Help?
Family members may react to a parent’s absence for military service in different ways. For example, if your child has anxiety, the signs might be subtle. Babies and toddlers may be withdrawn or clingy. Preschoolers may act as they did when they were younger (like regressing in potty training) or have new fears (like monsters under the bed).
Older kids and teens who feel anxious may:
eat less than usual or have stomachaches
have sleep problems and nightmares
be restless
seem aggressive, angry, or sad
withdraw from activities
have trouble at school
If your child has any of these problems, try to be calm and understanding. Talk with kids often and let them know things will be OK. It’s also important to be clear about what behaviors aren’t acceptable. Everyone still needs to follow the household rules.
Help children express their strongest feelings in words. Keeping a journal is a good way for older kids to do this. Tell them when you’re feeling proud of their good behavior, kindness, and helpfulness.
It’s also common for parents to be stressed during and after a military deployment. Finding ways to ease stress may help.
What if We Need Extra Support?
Sometimes you or your family may need more help. This is often the case if a deployed parent has been injured or has a mental health condition like posttraumatic stress disorder (PTSD). The military can offer counseling for the parent who has returned. Therapy may help you and your kids too, giving everyone a safe way to share feelings and get support. You can ask your doctor to suggest someone local.
Military OneSource has both child and adult counseling services available. You also can call (800) 342-9647.
Your provider will take samples from your blood and may also take a sample from your CSF to do a spinal tap (lumbar puncture) to check for the Neisseria meningitidis bacteria in your body. These samples will then be sent to a laboratory to test for meningococcal disease and figure out which antibiotic will work best for treatment.
If the meningococcal bacteria are in the samples, the laboratory will be able to culture (grow) them using the meningococcal culture test. If it’s not clear from this test whether your samples have the meningococcal bacteria in them, your provider may order additional tests such as the meningococcal antigen test or PCR test.
During a blood test:
If your provider thinks you might have a meningococcal infection, they may collect a blood sample for a meningococcal culture test, PCR test, or antigen test.
A health care professional will take a blood sample from a vein in your arm, using a small needle. After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes.
During a spinal tap:
If your provider thinks you might have a meningococcal infection, they may collect a CSF sample for a meningococcal culture test, PCR test, or antigen test.
To get a sample of CSF, a provider will do a procedure called a spinal tap, also known as a lumbar puncture. A spinal tap is usually done in a hospital. During the procedure:
You will lie on your side or sit on an exam table.
Your provider will clean your back and inject an anesthetic into your skin, so you won’t feel pain during the procedure. They may put a numbing cream on your back before this injection.
When the area on your back is completely numb, your provider will insert a thin, hollow needle between two vertebrae in your lower spine. Vertebrae are the small backbones that make up your spine.
Your provider will withdraw a small amount of cerebrospinal fluid for testing. This will take about five minutes.
You’ll need to stay very still while the fluid is being withdrawn.
Your provider may ask you to lie on your back for an hour or two after the procedure. This may prevent you from getting a headache afterward.
Different oral diabetes medicines work in different ways to help control diabetes:
Help the body produce insulin
Increase the sensitivity of body tissues to insulin
Help with carbohydrate digestion and absorption in the body
There are eight major classes of oral medicines for diabetes:
Biguanides
SGLT2 inhibitors
Sulfonylureas
DPP-4 Inhibitors
Thiazolidinediones
Alpha-glucosidase inhibitors
Meglitinides
Bile acid sequestrants
These medicines may be used alone or in combination.
BIGUANIDES
Metformin (Glucophage, Glumetza, Riomet, and Fortamet) is a biguanide. This is often the first oral medicine health care providers prescribe for type 2 diabetes.
Metformin is a medicine that stops the liver from making glucose. It also makes body tissues more sensitive to insulin.
Sustained-release: Taken as a single dose every day, most often with an evening meal
The most common side effect of metformin is diarrhea. Sometimes people taking metformin will become deficient in vitamin B12. If you have liver or kidney disease, tell your provider. People with liver or kidney disease or who are heavy drinkers should not take metformin.
SGLT2 INHIBITORS
SGLT2 inhibitors increase the amount of glucose that goes out in the urine. They may also lead to some weight loss and lower blood pressure in people with diabetes.
SGLT2 inhibitors include:
Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)
If you have kidney disease, tell your provider before taking these medicines. Side effects include urinary tract infections and yeast infections due to the presence of more sugar in the urine.
SULFONYLUREAS
These medicines help the pancreas produce insulin and help the body use glucose (blood sugar) for energy. Sulfonylureas include:
Glipizide (Glucotrol)
Glyburide (Diabeta, Glynase)
Glimepiride (Amaryl)
Glipizide is taken 30 minutes before a meal. Glyburide and glimepiride are taken with meals.
In the beginning, your provider will:
Start you on a low dose, taken once a day.
Increase the dose every 1 to 2 weeks until your blood sugar level comes in range.
When you take sulfonylureas:
Do not skip meals.
Limit alcohol (ask your provider how much is safe for you).
Always carry candy, juice, or sugar in case your blood sugar gets too low.
The most common side effect of sulfonylureas is hypoglycemia. Other side effects include weight gain, irritability, stomach upset, and skin rashes.
Tell your provider if your weight changes or if your blood sugar level is regularly low. Your provider will adjust the dosage of the medicine.
DPP-4 INHIBITORS
These medicines help the body release more insulin. They also lower the amount of glucose made by your body. DPP-4 inhibitors help lower blood sugar without causing hypoglycemia.
DPP-4 inhibitors include:
Alogliptin (Nesina)
Linagliptin (Tradjenta)
Saxagliptin (Onglyza)
Sitagliptin (Januvia)
These medicines are taken once a day. Common side effects are:
Muscle pain
Stuffy nose
Sore throat
Respiratory infection
Headache
Stomach ache
These medicines can also cause severe joint pain. If you notice joint pain, contact your provider right away.
THIAZOLIDINEDIONES (GLITAZONES)
Pioglitazone (Actos) and rosiglitazone (Avandia) are in this group of medicines. They lower insulin resistance by making body tissues more sensitive to insulin. These medicines are taken 1 to 2 times a day with or without meals.
Side effects include:
Weight gain
Water retention (edema)
Decreased bone density
Increased risk of heart failure
Increased risk for bladder cancer
If you have heart disease or liver disease, and are prescribed a thiazolidinedione medicine, ask your provider if it is safe to take it. If you have side effects, stop taking the medicine right away and tell your provider.
ALPHA-GLUCOSIDASE INHIBITORS
These medicines delay the digestion of carbohydrates (starches and sugars) in the body. This helps lower blood sugar after a meal. Acarbose (Precose) and miglitol (Glyset) are alpha-glucosidase inhibitors.
These medicines are taken with the first bite of each meal. Side effects include bloating, flatulence, and diarrhea.
MEGLITINIDES
Meglitinides such as repaglinide (Prandin) and nateglinide (Starlix) increase insulin production in the pancreas. Avoid alcohol when you are on these medicines.
These medicines:
Are useful if you don’t eat meals at regular times
Can be taken anytime between 30 minutes before a meal up to mealtime
Side effects can include low blood sugar and stomach upset.
BILE ACID SEQUESTRANTS
These medicines lower blood sugar and cholesterol in people with diabetes. Bile acid sequestrants were originally used to treat high LDL (bad) cholesterol. These medicines also help lower blood sugar.
These medicines are often prescribed for people with type 2 diabetes who also have high cholesterol. They also may be used for people who have liver problems and can’t take other medicines.
Cholestyramine (Prevalite, Questran) and colesevelam (Welchol) are bile acid sequestrants. Side effects include flatulence and constipation.
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.
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.
Find information for patients and families to understand and navigate organ donation and transplantation below:
Questions and answers for transplant candidates about:
The heart
Functions of the heart
The heart is a strong, muscular, cone-shaped organ. It is located behind the breastbone between the lungs. It pumps blood throughout the body.
Blood that no longer carries oxygen flows from the heart to the lungs, where it gives up wastes and gets new oxygen. From there, the blood returns to the heart and is pumped to the rest of the body.
Heart failure happens when the heart cannot pump enough blood to meet the body’s needs. Birth defects, or any condition that damages or overloads the heart muscle, can cause it. Treatment depends on the cause of heart failure and the age and condition of the patient.
Heart transplant procedures
Most heart transplants involve replacing the patient’s heart with the heart from a deceased donor. In rare cases, the patient’s native heart is not removed; this is known as a heterotopic transplant.
There also have been a few transplants involving a living heart donor. This may occur if one patient receives a heart-lung combination transplant but their heart is in good condition. This patient’s heart may then be transplanted into another recipient. This is known as a “domino” heart transplant.
Reasons for heart transplant
Heart diagnosis categories
Heart diagnoses
Cardiomyopathy
Dilated Myopathy: Idiopathic
Dilated Myopathy: Myocarditis
Dilated Myopathy: Other Specify
Dilated Myopathy: Post Partum
Dilated Myopathy: Familial
Dilated Myopathy: Adriamycin
Dilated Myopathy: Viral
Dilated Myopathy: Alcoholic
Hypertrophic Cardiomyopathy
Restrictive Myopathy: Idiopathic
Restrictive Myopathy: Amyloidosis
Restrictive Myopathy: Sarcoidosis
Restrictive Myopathy: Endocardial Fibrosis
Restrictive Myopathy: Other Specify
Restrictive Myopathy: Secondary to Radiation/Chemotherapy
