Whooping Cough: Not Just For Kids

Remember the last time you had a regular cold followed by weeks of annoying, dry coughing? Did it ever cross your mind that your problem might be whooping cough? Most likely, neither you nor your doctor gave the diagnosis a minute’s thought. Isn’t whooping cough is one of those childhood diseases, like measles and chicken pox, that immunizations have largely defeated? Yes and no. Yes, whooping cough is a serious illness in babies and toddlers, but it also afflicts adolescents and adults of all ages. And no, the disease has not gone the way of the dinosaurs, though immunization of babies and toddlers has dramatically cut morbidity and mortality rates from the infectious illness.

What is whooping cough?

Whooping cough is a highly infectious respiratory disease caused by the bacterium called Bordtella pertussis. The symptoms of whooping cough begin a week or so after exposure to someone who has the illness. At first, the stuffy, runny nose and mild cough, with little, if any, fever seem like ordinary cold symptoms. But within ten to fourteen days paroxysms of more severe, unproductive coughing begin. Coughing lasts, on average, six weeks. While coughing paroxysms are the signature feature of the illness in all age groups, older children and adults may lack the “whoop” on intake of breath that gives the illness its name.

Babies can die; adults break ribs 

In babies and children coughing bouts are frequently followed by vomiting. Infants can quickly develop respiratory distress and pneumonia, and most whooping cough fatalities occur in babies. Older children and adults suffer less severe disease, but the intensity of coughing can make life miserable for weeks, and can lead to hernias and broken ribs. Antibiotic treatment with erythromycin works, but only if the disease is suspected and confirmed early – before the worst of the coughing begins.

Many cases go undiagnosed

Many cases of whooping cough go undiagnosed because people do not seek medical help, or because the diagnosis is unsuspected. Even when whooping cough is suspected as the cause of a chronic cough, accurate laboratory diagnosis is difficult. By the time persistent cough finally brings people to the doctor, a throat or nasal swab may not pick up any bacteria. In addition, routine laboratory culture methods don’t work for pertussis bacteria like they do for streptococcal infections. Proof of infection can be inferred by the presence of blood antibodies against the bacteria, but blood tests to measure titers of are expensive and seldom done.

Vaccine development cut the death rate

Whooping cough occurs worldwide and causes an estimated 300,000 deaths per year across the globe. In the United States, death rates were in the 5,000-10,000/year range between the 1920s and 1940s, but the development of a pertussis vaccine reduced that toll enormously in the latter half of the 20th century. Recently, however, increasing numbers of whooping cough cases are being reported. In 2010 California declared a whooping cough epidemic based on 9,477 confirmed, probable and suspected cases. Washington State did the same in 2012. By that year, 48,000 confirmed cases were reported across the country. At the height of the California epidemic, there were 10 deaths – too many for a preventable disease, but a far cry from the tolls of the past.

Natural cycles, parental backlash and a  changed vaccine 

Bordtella pertussis has never disappeared from its niche in the human population, and several factors are at work in the recent, apparent increase in rates of infection. Foremost is a natural bacterial population cycle. Whooping cough bacteria seem to increase their numbers in 3-5 year cycles which probably correspond to naturally declining immunity in a population as children get older. This natural variation has coincided with some parental backlash against vaccinations because of fears that they do more harm than good, though childhood immunization rates as a whole are still very high. A third factor may be weaker population immunity because of alterations made to whooping cough vaccine in the 1990s.

Clearly, the original pertussis vaccine, derived from whole, dead pertussis bacteria and delivered as part of the first series of a baby’s shots, helped produce immunity sufficient to make death rates among babies drop dramatically. But in the early 1990s, the formulation of the vaccine was changed to decrease adverse responses to it – responses like fever, swelling at injection sites and rare cases of encephalitis. That change may be responsible for lessened immunity and more whooping cough cases among older schoolchildren. It also raised the number of shots that must be given over several months to achieve immunity in a baby.

Should drug companies fund vaccine research?

Some people who worry that too many vaccines are now being required and are less effective than advertised claim that the makers of the vaccines are anxious to find reasons to give booster shots to as many people as possible. Indeed, the largest and most influential of the scientific groups studying whooping cough – the Global Pertussis Initiative (GPI) – is funded by vaccine makers. But Dr. James D. Cherry has been studying whooping cough for several decades and maintains that the monetary sponsorship by pharmaceutical companies is necessary. Compiling data about infection rates and vaccine efficacy is expensive and surprisingly difficult. The prevention and treatment of infectious diseases depend on accurate assessment of disease rates and currently public health surveillance and reporting is hampered by lack of uniform standards for the diagnosis of whooping cough, especially in older children and adults. In addition, the development of vaccines is extraordinarily complicated and expensive, and will be of increasing importance as antibiotic resistant bacteria continue to evolve and thrive.

Who needs to be concerned about whooping cough?

Whooping cough is of most concern to people who work around and live with small babies who are too young to have completed their series of early DTaP immunization shots (against diphtheria, pertussis and tetanus). The booster vaccination has little risk and is probably advisable for all adults who are in regular close contact with susceptible infants. In the meantime, if you develop one of those miserable chronic coughs after a cold, stay away from vulnerable babies who have not yet had all their shots.

Chronic Fatigue Syndrome Gets Renamed

Imagine the way you felt the last time you had the flu. You were flattened, devoid of all energy. Staying upright to get dressed was more than you could handle. You slept – and slept – and slept – and still experienced none of the normal refreshment that a good night’s sleep provides. A fog descended on your mind and fuzzed up memory, destroyed drive and made your head ache. You could not concentrate on simple mental tasks like reading. Though you were doing nothing physical, your muscles ached. Then it all went away and you forgot about it.

But now imagine that it didn’t go away. The same misery persists and dramatically alters your life. You cannot work. You move from bed to couch and back to bed. You go to doctor after doctor and they find nothing wrong. Routine blood tests, X-ray and scan results are normal. Someone prescribes an antidepressant, confirming the suspicions of family, friends, and some doctors that your debilitating physical symptoms are “all in your head.” Eventually, you find your way to a doctor who makes a diagnosis. You have CFS which stands for chronic fatigue syndrome, and which, as of early 2015, has been renamed system exertion intolerance disease or, in our acronym-laden age, CFS/SEID.

A long history, with different names

CFS/SEID has probably been around for more than 200 years, making its appearance in the medical literature as “neurasthenia,” a term applied to patients who were lacking in physical, emotional and cognitive energy without any discernible disease to account for their malaise, without any improvement over time and without any progression that brought them to a worsened state. They were mostly ladies, whose frail constitutions prevented them from exerting themselves and who mysteriously took to their beds for weeks at a time.

The Yuppie flu

British doctors in the 1950s christened the symptom complex myalgic (painful muscles) encephalitis (inflammation of the brain), even though there was no evidence for inflammation to account for the headaches, difficulty concentrating and memory problems patients experienced. In the US in the 1980s, the syndrome was dubbed the Yuppie Flu because it seemed to follow viral infections like infectious mononucleosis and occurred in cities where young urban professionals (“yuppies”) congregated. When reported from other settings as well, the name was changed to chronic fatigue syndrome.

No apparent cause, but a real illness

Because no single infectious, hormonal or immunologic cause for CFS emerged from many attempts to identify its cause, because it was impossible to measure the subjective complaints constituting the syndrome, and because some improvements occurred when antidepressants were prescribed, CFS was, for decades, viewed as a psychological disorder. But this view became more and more untenable as it became clear that the illness hit people who had no history of depression or inability to cope with life. Many CFS patients continued to be very productive, learning how to manage their lives within the limitations of their fatigue and mental fog. Laura Hillenbrand, author of Seabiscuit and Unbroken is one outstanding example. Though no cause has yet been identified for the illness, the name change from chronic fatigue syndrome to systemic exertion intolerance disease signals that the illness is one rooted not in psychology but in an, as yet, unidentified physical cause.

Epidemiology and diagnostic criteria

It is estimated that there are about 1 million patients with CFS/ SEID in the US at any given time. There is no evidence that its incidence is increasing, but it is quite possible that some cases are hidden on among the legions of people who have been diagnosed only with depression. CFS/SEID is more common in women than in men. Sometimes it follows directly upon an acute flu-like illness, but at other times appears out of nowhere. The diagnostic criteria at this time include 6 months of unexplained, life-altering fatigue and orthostatic intolerance, which means the inability to stand for more than very short periods. Four of eight other symptoms are also required and these include disturbances in memory and concentration, persistent sore throat, tender lymph nodes, muscle pain, joint pain, headache, disturbed sleep patterns, and malaise following even minimal exertion. Additional symptoms may include increased sensitivity to tastes, odors, temperature and noise.

A relapsing illness

A small minority of CFS/SEID patients get completely better and never suffer a relapse. The majority suffer relapses for prolonged periods of time, perhaps the rest of their lives. Relapses are triggered by infections, surgery, temperature extremes and stressful events. Another minority are severely affected from the beginning of their illness and require support in the activities of daily living for the rest of their lives. Deterioration, though, is unusual and suggests the diagnosis of CFS is wrong and further attempts to find the correct diagnosis are indicated.

Problems in mitochondrial energy production?

While there is no identifiable single cause for CFS/SEID, poor energy production seems to be at the root of the many symptoms in this illness, which has focused some researchers’ attention on mitochondria – the powerhouses of all cells in the body. Mitochondria must continuously recycle the molecules they use to produce energy and there is some indication that this process is impaired in people with CFS/SEID. Perhaps this is why experience has taught many CFS/SEID patients to pace their lives, always allowing significant time for recovery from exertion.

Boosting energy production

In addition to pacing life to allow recovery time, lifestyle alterations that seem to help CFS/SEID patients minimize relapses also happen to be useful in maximizing mitochondrial function. These include avoidance of drugs and environmental toxins, avoidance of processed foods with high carbohydrate and sugar concentrations, addition of whole foods containing plenty of antioxidants and high quality protein, correction of hormonal problems, especially of the thyroid gland, and decreasing chronic inflammation associated with obesity and allergies. Gradual and graded programs of exercise, outdoors with some sun exposure help prevent the loss of muscle associated with inactivity and improve Vitamin D levels, with positive effects on immune function. Continued research will most likely show that CFS/SEID has many causes, all of which result in impaired mitochondrial function.

Lyme Disease: A Whodunit Tale

Some medical advances begin with old-fashioned detective work. Lyme disease, which was unknown in this country prior to 1975 is a good example.  That fall, two mothers from Old Lyme, Connecticut convinced the state Department of Public Health and Yale University to explore a mysterious outbreak of cases of inflammatory arthritis among the town’s children, because they were unsatisfied with the explanations they had been given for the cause. The investigation that winter centered on thirty-nine children and twelve adults from Old Lyme, all of whom had developed painful swelling of one or more joints between June and September.

Clues in clinical histories

Although blood tests and physical exams of the affected people had not previously revealed any known cause for the painful, swollen joints, investigators noted that there were striking similarities in the patients’ histories. Especially notable was a peculiar spreading rash that appeared about a month prior to the development of the arthritis and resembled an archer’s bull’s eye target. The affected people also lived close to one another, all in heavily wooded areas. The researchers concluded that the area where the cases clustered and the time of year in which they occurred were both crucial clues to the mystery. They believed that the illness could be an unknown type of infection but would have to await the next disease “season” for confirmation of this theory.

More clues in old European medical literature

In the meantime, investigators began combing through European medical literature, where they discovered similar descriptions of rashes going back to 1909. Over time, the Europeans had named the skin lesion erythema migrans and associated it with an illness that was similar to the one being reported in Connecticut, although without the arthritis. Some European reports mentioned tick bites in conjunction with the rashes, as well as successful treatment with antibiotics. Back in Connecticut, the next summer produced thirty more cases of what was by then being called “Lyme arthritis,” which investigators now believed was some kind of infection transmitted during outdoor activity.

Figuring out the tick relationship

The next pieces of evidence came from field studies of ticks. The distribution of a particular type of tick called Ixodes scapularis (variously known as the blacklegged tick, deer tick, or bear tick) near Old Lyme matched the distribution of local arthritis cases. Tick autopsies conducted in New York on Shelter Island, another hot spot for this mystery arthritis, showed that most of the ticks carried a spiral-shaped bacterium called Borrelia burgdorferi. Blood tests on affected individuals for antibodies to this organism tied it to the clinical cases of arthritis. Over the next two decades, the explosion of the deer population carrying the tick made the disease more common and widely known.As knowledge about and experience with the new disease accumulated, Lyme arthritis was renamed Lyme disease.

Early  Lyme disease symptoms

Lyme disease symptoms include an early stage of fatigue, muscle and joint pains, swollen glands, and headaches and fever that begin days to weeks after the infected tick bite. These symptoms represent the immune system’s response to the bacterial invasion. If a bull’s eye rash at the site of a former tick bite is present, diagnosis is easy. If not, diagnosis depends on a clear history of a tick bite and on the development of antibodies to the organism, which usually occurs later than the first few weeks of the illness.

Later symptoms

Left untreated, some, but not all infected patients develop symptoms within the next few weeks to months after the infected tick bite. Symptoms include arthritis, nerve pains, facial nerve paralysis, heart palpitations, shortness of breath, and chest pains. An even less common late phase that can occur up to two years after an infected tick bite might include migrating joint pains, muscle aches, abnormal muscle movements, weakness, heart arrhythmias, and cognitive complaints such as memory problems. These symptoms are not well understood and may represent a combination of the body’s ongoing fight against persistent bacteria and an autoimmune response that they trigger.

Treatment

Treatment of Lyme disease with oral antibiotics, either doxycycline or amoxicillin, is usually curative. If an infected tick is attached for more than thirty-six hours (the least amount of time it takes for transmission of the infection) and was encountered in an area where more than 20 percent of the deer tick population carries Borrelia burgdorferi, most patients are given a prophylactic one-time dose of doxycycline. Otherwise, treatment with antibiotics for two to four weeks begins as soon as the diagnosis of Lyme disease is made. The earlier the treatment, the faster the disease responds and symptoms subside. Late-phase treatment of neurological, cardiac, or arthritic symptoms may require intravenous delivery of antibiotics over longer periods. Although rare cases of persistent symptoms after treatment exist, no study has yet shown enough benefit from very long-term antibiotic use to justify the potential adverse effects of such a treatment.

Prevention of tick bites

Prevention of Lyme disease is the best way to deal with the illness, and there are things you can do to protect yourself. In the states where most cases occur (the New England states and New York, New Jersey, Maryland, Virginia, Wisconsin, and Minnesota), be aware that ticks tend to cling to high grasses and shrubbery in areas where deer roam. By hiking in the center of paths, away from tall grasses and shrubs, and wearing protective clothing, such as long sleeves and pants, you can reduce the chances of a tick bite. Shirt tails should be kept tucked in at the waist, sleeves should be kept closed at the wrists, and pants cuffs should be kept tucked into socks at the ankles. Additionally, spraying with insect repellent containing 20 to 30 percent DEET can help.

Self-examination is very important after potential tick exposure

The type of tick that transmits Lyme disease is Ixodes scapularis. It may be either a six-legged, immature tick nymph the size of a poppy seed or the slightly larger, eight-legged mature tick. Both forms excrete an anesthetic in their saliva that prevents you from feeling their bite, so close examination of your body is necessary after potential exposure. Bathe within two hours of coming inside and do a full body exam, with the aid of a mirror, paying close attention to areas covered with hair. Inspect all gear, clothing, and pets for ticks, and tumble clothing in a dryer at high heat to kill any hidden ticks.

Tick removal

Should you find an attached tick on your body, to remove it place the tip of a clean, fine-tipped tweezer as close to the skin as possible and pull gently, in a straight line. Dispose of all ticks in a toilet or drown them in alcohol and then seal them in a plastic bag for disposal. Clean bites with alcohol or iodine. Because the transmission of an infection from a tick to a human requires thirty-six to forty-eight hours of attachment, ridding yourself of ticks in the first twenty-four hours is effective prevention. Longer attachments that occur in high-risk parts of the country merit a single dose of doxycycline within seventy-two hours of a bite. Otherwise, be alert for symptoms or a rash, and seek treatment as soon as possible if they occur.  (See blow for a link to an interesting tick removal tool.*)

Research continues

The detective work surrounding the unraveling of the Lyme disease mystery continues today in the laboratory. Now researchers tend to focus on the rare people who, despite receiving adequate antibiotic treatment after contracting Lyme disease, experience persistent, unexplained, or recurring symptoms. These people remain almost as much of a mystery to researchers today as the initial thirty-nine children and twelve adult with arthritis were to researchers in the mid-1970s.

 

*Tick removal tool

https://www.thegrommet.com/tickease?utm_campaign=20180626&utm_content=49931&utm_medium=email&utm_source=CC&trk_msg=77TUPK4NDPL4R992MUGHP52NOS&trk_contact=4ACPOO38FT83AKKO084SUBGRPC&trk_sid=ICRD996NV2C3PQ9D216CFKVDLG

 

Fever: Resetting the Thermostat

 

Humanity has but three great enemies: fever, famine, and war; of these by far the greatest, by far the most terrible, is fever.
―William Osler, MD

    In Dr. William Osler’s world of the late 1800s, doctors had not yet seen antibiotics rescue people from death caused by infectious diseases. Osler, one of the founders of Johns Hopkins Hospital routinely saw children die from meningitis, scarlet fever and diphtheria. He watched adults die from wound infections and cholera and the threat of mortal infection loomed over every surgical procedure. Fever was an unwelcome herald of trouble that often ended in death.

However, since antiquity fever was also thought to be therapeutic for some ailments of the brain, including melancholy and seizures. In the 1920s, a German psychiatrist, Julius Wagner-Jauregg, attempted to use the recurring high fevers of malarial infection to treat syphilis, then an incurable disease that eventually robbed patients of their minds and motor coordination.  Wagner-Jauregg was a eugenicist and later a Nazi sympathizer, and gave his patients malaria without their consent, but the fact that six of his nine patients recovered earned him the Nobel prize in medicine in 1927. He remains the only psychiatrist ever to be so honored in that discipline. Fever asylums popped up in many locations on both sides of the Atlantic in the 1930s, but were relegated to history by the discovery of antibiotics in the next decade.

How does the body temperature rise?

Fever begins when a “pyrogen” – some kind of viral or bacterial protein, or a protein made by the body as part of an inflammatory response — stimulates a tiny, deep part of the brain called the hypothalamus.  There, “warm sensitive neurons,” normally responsible for keeping the body temperature stable, act as if the temperature has fallen and slow their firing rates, triggering physiologic responses throughout the body that produce more heat. The incipient fever sufferer feels cold and sometimes begins to shiver. Blood vessels in the skin clamp down, sacrificing their flow to the core of the body in an effort raise the temperature. Heart and breathing rates go up, core temperature rises and the forehead begins to feel warm to the touch, even though the patient still feels chilled.

Definition of normal and abnormal body temperatures

Normal body temperatures vary over the course of the day and from individual to individual, within a degree above or below 98.6°F (37°C). Oral temperatures are about a degree lower than ear and rectal temperatures.  Fever is defined in adults as 100.4° orally or 101°F (38.3°C) rectally, and 101° orally in children. These elevated temperatures seem to work, along with the body’s immune system, to undermine the success of an invaders like viruses and bacteria……up to a point. Temperatures rising to 103-104° begin to have deleterious effects on cells, making their membranes unstable and triggering faults in the workings of cellular machinery. Organ failure can result, complicating already serious illness with kidney and liver problems.

Why do babies and little children get fevers so often?

Babies and small children, who are at the beginning of their life experience with infections, develop fevers more often than adults do. Their fevers may be the first or only symptoms of illness, and the illness may be brief and self-limited. Fevers which indicate worrisome problems in children are accompanied by other symptoms like rash, stiff neck, lethargy, breathing difficulties or abdominal pain.

Adult fevers 

In adults, other symptoms of trouble often come before a fever and point to a body part in some kind of trouble.  When fever occurs along with GI symptoms like abdominal pain, nausea, vomiting and diarrhea, a significant abdominal problem requiring medical or surgical attention may be present. Fever along with cough and sputum production may mean a bacterial pneumonia. Fever that develops as a part of the flu is usually accompanied by profound fatigue, muscle aches and pains and headache.

What causes fever?

About 75% of elevated temperatures come from infections. What causes account for the other 25%?  This “non-pyrogenic category” includes fevers from some cancers, from inflammation of all kinds, from brain injuries like hemorrhages and strokes, and from major bodily injuries with crushed or otherwise damaged tissues. In addition, overactive thyroid glands elevate body temperatures. Some drugs, particularly the neuroleptics used for depression and other psychiatric disorders can cause fever, as can some genetic problems.  Familial Mediterranean Fever comes from mutations in genes that control inflammation responses. Malignant hyperthermia, a potentially fatal rise in temperature in response to anesthetics, comes from a muscle gene mutation.

To treat or not to treat fever?

Treatment of fever is straightforward – body temperature drops in response to an antipyretic drug such as acetaminophen (Tylenol) or aspirin. But fever appears to be an evolutionary response in almost the entire animal kingdom, aimed at protecting the body from invasion by other living forms. In other words, fever induced by infection may be helpful.  Why try to normalize the temperature during the illness?

Most of the time, with temperatures in the 101-102 range, treatment beyond making the patient comfortable is not necessary. But the deleterious effects of raising body temperature begin to show up in the 104 range, and perhaps sooner in people who have underlying medical problems that affect their ability to tolerate higher heart and breathing rates or to maintain adequate hydration. Fever makes demands upon the body that young and otherwise healthy people can tolerate, but older, sicker people may not. Elevated temperatures in heat stroke from a hostile environment or from excessive exertion without adequate hydration serve no useful purpose and should always be treated promptly, with external cooling and hydration.

In the modern age of medicine, antibiotics have reduced Osler’s greatest enemy to a symptom of illness. But it is a symptom that deserves respect. When fever is present, something is wrong and the wrong thing usually involves and invasion of the body by another living form, or a significant area of tissue inflammation or decay. Careful evaluation of other symptoms is the first priority in discovering the cause of fever, for that is what needs treatment more than the fever itself. Should we overuse antibiotics and render them ineffective against our most common infections though, Osler’s great enemy will regain its fearsomeness.

More On Shingles

Readers wanting to know more about some topics  pose very good questions. My original magazine column about immunization to prevent shingles (September 2011) generated enough reader mail to warrant another column sharing some of the answers.

Recognizing recurrent shingles episodes:

One reader had suffered through an eruption of ophthalmic shingles, which involves the nerve that carries sensation from the eye, including the cornea, from the skin around the eye, and also from the forehead. The reader wanted to know “What are the signs and symptoms for a re-occurrence of the zoster virus in the eye so I would know what to look for if I am getting an attack?”  As in other areas of the body, symptoms that come before the rash erupts  in the eye and the face are sensory  – tingling, burning, itching and pain. Warning sensations in ophthalmic shingles might also include irritating dryness and a sense something lodged in the eye. Our reader understood that taking an antiviral drug early in the course of an eruption might lessen the likelihood of scarring of the cornea, so paying attention to early symptoms has therapeutic consequences.   If an abnormal sensation persists for several hours without explanation or response to simple measures like rinsing the eye out, then the symptom is worth bringing to the attention of the doctor. That said, the use of antiviral drugs early in the course of a shingles outbreak does not prevent the eruption from progressing, but it may shorten the duration and lessen its intensity.  When the surface of the eye is involved, anything that can be done to prevent corneal scarring is of some value.

Drugs that make the virus awaken

The same reader also wanted to know what drugs might predispose her to another eruption, and how to avoid them. The drugs that put people at most risk for a herpes zoster outbreak are the ones that suppress the function of immune cells in the body. The most common offenders belong to the steroid class on anti-inflammatory drugs, and have names like prednisone, dexamethasone, decadron, and prednisolone.  They are used to treat conditions like multiple sclerosis and lupus and rheumatoid arthritis and when used for periods longer than a week, they begin to impair immune response.  Sometimes they are part of a chemotherapy regimen for cancer. Other chemotherapy drugs and radiation also impair immune cell function, so shingles eruptions are not surprising in patients undergoing cancer treatment.  Paradoxically, steroids are part of the treatment for shingles – but they are used for only a short time, to decrease inflammation.

Vaccine questions

Another reader wrote:” My husband never had Chicken Pox and yet he did have a severe case of shingles and he was in his 40’s when they occurred. At that time we were told the opposite of the article…we were told he got shingles because he had never had Chicken Pox.  This was over 20 years ago so perhaps research has changed that.  Does the fact he had shingles mean he cannot get the vaccine?” There are many people whose childhood chicken pox was so mild that they have no memory of the disease. Blood testing will show whether or not there is any trace of immunity to the virus in people who think they did not have the disease. An adult who contracts chicken pox for the first time has a rash that involves much more of his body than the shingles rash does.  He is also extremely sick, much more so than a child with the disease. So if an adult develops what is a typical shingles rash, it is considered proof that he has had chicken pox in the past.

You probably did have chicken pox

Age 40 is on the young side for shingles, but there are many idiosyncrasies in the immune system, with some people have worse immune “memory” for specific viruses than others do. Having had a shingles eruption does not prevent this reader’s husband from getting the vaccine, and given that it is now over 20 years since the last time the virus stimulated his immune system, immunization might be a very good idea.  Guidelines for vaccine administration also do not exclude people who think they did not have chicken pox as a child, even though, in theory, a vaccine made from a live, weakened virus could cause a full blown case of chicken pox in a chicken pox virgin (more on different vaccine constructions below).  It is estimated that 99% of people in the US have had chickenpox, whether or not they are aware of it.

Being refused the vaccine

Getting an immunization proved difficult for another reader. He went to his county health department seeking a shingles immunization, but he was turned down because he has non-Hodgkin’s lymphoma, a form of lymphatic system cancer. While his disease is in remission and his blood work indicates good immune cell function, there is a theoretical risk that the vaccine, which contains a live, weakened version of the virus, will reactivate the line of white cells that caused his lymphoma. Many people face this type of risk-balancing problem in choosing whether or not to get a vaccine, and each individual case requires weighing risks versus benefits. In some cases, for example someone with AIDS who has good white blood cell tests and is not sick, the patient’s doctor may advise getting the vaccine because the risk of the effect of a shingles outbreak is greater than the risk that the virus in the vaccine will cause trouble. In the case of people with history of cancers that arise directly from immune system cells, however, no one wants to take a chance of triggering cells to become cancerous by the introduction of a live virus in the form of a vaccine.  In addition, no one wants to  introduce an infection that the immune system cannot control.  These problems are the reason that researchers have pushed to develop a new vaccine, just becoming widely available in in 2017-18, which does not contain any live virus.

The old and the new vaccines

Lastly, several readers inquired about the frequency of the zoster vaccination.  Immunizing for shingles is relatively new, and recommendations may change, but right now, Zostavax, the old vaccine, is recommended for all people over age 60,  as a one time shot. Zostavax cuts the rate of shingles by 51% and the development of post-herpetic shingles pain by 65%.  The new vaccine, Shingrix, is recommended beginning at age fifty and in tests improves these prevention rates to 98% and 85% respectively. Shingrix requires two separate doses. The effectiveness of the vaccines does wane over time, and there is more experience with the old one. Currently there are not any guidelines about repeat administration, but there are no contraindications to getting the new vaccine for people who have already had the old one.

Where to get immunized

Immunizations are available at pharmacies, grocery stores, county health offices, and walk in clinics and all of these facilities have guidelines which will exclude some people.  Anyone excluded by general criteria should review the reason with a doctor who cares for the problem that caused the exclusion.

Shingles:Chicken Pox Re-Awakened

Chicken pox is a common and usually mild childhood disease caused by the varicella virus. The  same virus is also the cause of a very painful skin rash known as shingles in adults.  These two very different illnesses demonstrate the two missions of all viruses – to reproduce themselves and to stay alive.   Reproduction keeps the varicella virus spreading from child to child. Hibernation keeps it alive in adults, giving it another chance to reproduce. While chicken pox is usually a mild disease, shingles is painful and at times disabling.

Vaccinations

Since 1995, vaccination against the varicella virus has been very successful in reducing the number of childhood chicken pox cases.  In 2005, a vaccine designed to boost adult immunity cut the number of cases of shingles in adults in half and a vaccine about to be introduced now, in 2017, promises much better protection against shingles for older adults, especially for older adults.  Both chicken pox and shingles vaccines mark significant progress against the varicella virus, which infects 95% of unvaccinated people.

Who gets shingles

Shingles typically afflicts older people or in people with weakened immune systems. In them, the long-sleeping varicella virus has suddenly awakened, erupting in an intensely itchy, blistered rash known confined to one patch of skin, usually on the trunk, but sometimes on the head or extremities. Doctors call shingles herpes zoster, which sometimes causes confusion with the common cold sore, caused by the herpes simplex virus. Both herpes simplex and varicella viruses are members of a larger family of “alphaherpes” viruses, with similar abilities to live in peace inside the body and revive periodically.

Why name it shingles?

Shingles is a more descriptive name than herpes zoster. When fully developed and severe, the shingles rash has a rough, red, pebbled surface formed by multiple blisters packed in tight formation, often rectangular in shape. Like a roof shingle, the patch of virus- laden blisters can look like it has been laid on top of the skin. The distribution of this adult eruption of the varicella virus is very different from the random and widespread distribution of blisters in chicken pox.  The difference between rashes caused by exactly the same virus is a visual lesson in the way the varicella virus infects, reproduces, goes into hiding and reemerges.

The initial infection: chicken pox

The varicella virus enters the body through the nose or mouth. It is picked up by immune cells in the lymphatic fluid and then makes its way through the rest of the body in a trip that takes 7-10 days. Since the immune system doesn’t see the virus as much of a threat, there are often no symptoms of any illness in this period. But once the virus reaches the skin, real battle begins.  Troops of immune cells produce small red dots on the skin, then red bumps and finally blisters which rupture and release new viral particles to the air.  Mission number one, reproduction is accomplished.

The virus goes into hiding

Mission number two, staying alive, is more complicated.  While varicella viruses spread easily from ruptured blisters or via coughing and sneezing, once the viruses dry out, they die.  Dried, crusted rashes are no longer contagious. But underneath the skin, some viruses begin another journey. They travel up long thin nerve fibers that carry sensory information from the skin to the spinal cord. Their first stop is the nerve cell bodies that sit in little clumps of tissue called ganglia, just outside the spinal cord. Here, for reasons that are unknown, the viruses are allowed to integrate their genetic material into the nucleus of the cells, alongside the DNA and RNA responsible for normal protein production.

Re-awakening

For years, varicella viruses demand nothing of their host nerve cells. Then in later life, or sooner in people who have suppressed immune systems from diseases like AIDS  or treatment of diseases like cancer, the varicella virus may suddenly commandeer the protein-making machinery in the  ganglionic nerve cell. It makes multiple copies of itself, sending them back out to the skin along the same nerves by which they entered the ganglia.  The rash that appears affects only the part of the skin innervated by those nerves. The sensory nerves are arranged in “stripes” around the trunk and down the limbs, and the rash looks like a portion of that stripe.

Why the re-awakened virus causes so much pain

Pain is a central feature of shingles because the immune system attacks the virus for a second time. This time, the attack starts in the ganglia where the virus has emerged from hiding. When the immune battle against the virus begins, the nerve cells report the action to the brain, even before a skin rash appears. The unwitting patient begins to feel sharp and shooting pains, as well as numbness, tingling and itching sensations in the skin as long as two or three days before a rash appears. Occasionally fever, headache and back pain appear.  Sometimes pain remains even after the rash resolves, a distressing condition called post-herpetic neuralgia, which is often difficult to manage.

Other complications

Pain is not the only complication of shingles. Permanent damage may result from re-emergence of the virus in a sensory distribution that involves organs other than skin. Rashes that involve the eye can cause scarring the cornea, and those that involve the ear sometimes cause permanent deafness.  Shingles cannot be transmitted, but if someone who has never had chicken pox or been vaccinated against it comes in contact with blister fluid from the shingles rash, they will get chicken pox. Adult chicken pox is a far worse illness than the pediatric version.

Immunity

Immunity to the chicken pox virus diminishes with age, and shingles rarely appears before the late 50s.  About one in every three people who’ve had chicken pox will get shingles;  the risk of a second episode is also about one in three and higher if pain persists more than 30-60 days. Recurrences rarely happen more than twice, indicating that the reawakened virus stimulates renewed immunity.

Avoiding the often disabling pain of an acute shingles episode and diminishing the risk of post-herpetic neuralgia are both good reasons to consider adult immunization against the chicken pox virus. Not only does the adult vaccine cut the risk of getting shingles in half, it makes cases that do occur significantly less severe. The large study that yielded these results also turned up no vaccine safety issues.   When you next think about getting a flu shot, give some consideration to prevention of shingles too.

Tetanus: Poster Child for Preventive Medicine

 

True preventive medicine is an intervention that stops a disease from developing, not one which simply slows disease progress. The body’s immune system is the master of disease prevention and it is no accident that one of the first medical efforts at preventing disease stemmed from the observation in the late 1700s that suffering a mild infection like cowpox prevented a similar but more severe infection – smallpox. Immunization was born, and to this date is the single most effective form of prevention of lethal disease. In the current age of rejection of routine immunization by a significant number of people, the disease called tetanus and its prevention by immunization is a story worth reviewing.

What causes tetanus?

Tetanus a disease is caused by a type of bacteria called Clostridia tetani, a fragile little organism that can’t tolerate oxygen or high temperatures but which changes itself into a tough intermediate form called a spore to lie in wait for potential victims. C. tetani spores survive indefinitely, are common in soil, particularly manure rich soil, and are found in intestinal tracts of farm animal, cats, guinea pigs, rats and people. They can survive oxygen rich environments, the usual antiseptics and even the temperatures used to sterilize medical instruments. Once the spores gain entry into body tissues, they revert to fragile bacterial form, reproduce and begin to manufacture tetanospasmin, one of the most lethal toxins known to man and the substance responsible for the symptoms of the disease. Though farm animals and people are susceptible to tetanus infection, dogs and cats are not.

Development of symptoms

Tetanus infections are usually acquired when C. tetani spores enter the body through a deep wound in the skin that air does not reach. Contaminated batches of heroin are also sources of infection when the drug is injected under the skin or intravenously. In the first few days after C. tetani spores come to life inside the body, no symptoms or tests indicate anything amiss. As the toxin producing bacteria increase in number, and the toxin produced finds its way to the spaces between nerves and muscle and between motor nerve cells in the brain and spinal cord, profound muscle spasms begin. Tetanospasmin works by the blocking normal neurochemical signals that inhibit muscle tone and motor nerve excitability.
The time from infection to development of symptoms in any infection is known as the incubation period. In human tetanus, the closer the entrance point of the bacteria to the brain or spinal cord the shorter the incubation period. On average symptoms begin about a week after injury. Though localized forms of tetanus can occur, with muscle spasm limited to the area around the wound, most cases are general and symptoms begin in the muscles of the head and neck. Spasm of the powerful masseter muscles of the jaw is the origin of the term “lockjaw,” a commonly used name for tetanus infection. Vocal cord and respiratory muscle involvement can interfere with breathing. Abdominal, trunk and skeletal muscle involvement are extremely painful and spasms can be strong enough to fracture long bones and spinal vertebrae. Other complications arise from involvement of the central nervous system: fever, high blood pressure, heart rhythm abnormalities and seizures. Secondary complications like bladder infections, pneumonia and blood clots in the legs and lungs also contribute to the lethality of the disease. In the pre-immunization era, treatment was confined to supporting the patient through the four weeks it takes for the toxin’s effects to wane.

Making the immune system remember the disease

Unlike cow pox, in which the natural immune response directed against the cowpox virus prevents more cowpox episodes but also smallpox, a full-blown case of tetanus does not confer any immunity because the minute amounts of toxin that produce the symptoms are not sufficient to stimulate the immune system to make antibodies against it. Immunization to tetanus is accomplished by presenting the immune system with a much larger amount of a formaldehyde weakened version of the toxin, to which it will produce antibodies which will neutralize the real toxin should it ever appear. This process takes a few weeks and several doses are required over time to reach full potency of an antibody response.

Immunization programs have made tetanus rare enough for people to forget how terrible an illness it is. In the US, since routine, active immunization began in the 1940s, tetanus rates declined steadily and were at an all-time low of .01 cases per 100,000 people in 2009. In addition, with better supportive care, mortality rates declined from 30% in the mid-1900s to 10% in the first decade of the 21st C.

Borrowing someone else’s immunity

Nevertheless, tetanus infections still occur and may increase in frequency if immunization rates drop. Fortunately, another type of immunization helps when tetanus develops in people who have not been immunized – a passive immunization process that allows patients to borrow antibodies produced in the blood of other people who have been immunized against C.tetani. This “antitoxin” is a mixture of human gamma globulin from screened donors and antibodies in it that “recognize” tetanus toxin react with the toxin circulating in the tetanus victim’s body, neutralizing a lot of its potency.

Boosting weakened immunity

The antibody response to tetanus toxoid wanes over time, but a repeat injection brings it up to full speed quickly. Booster doses are recommended for all adults every 10 years and in the event of penetrating wounds, especially if immunization status is unknown. Awareness of the symptoms of tetanus and the status of immunization of anyone someone suffering from heroin addiction, a sad and growing problem, is crucial for anyone who cares for them. Tetanus is the poster child for preventive medicine and no one should have to suffer this disease. The earlier it is recognized, the better the outcome is likely to be.

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