The Legacy of Smallpox: Immunization

Imagine a virus spreading disease in your city. Imagine sending your children and other loved ones to a rural area to be injected with infected material taken from people ill with the virus. Imagine the injections making them sick, but not as sick as they might be from contracting the disease naturally. They will require a month for recovery, but, from that time, they will no longer have to fear the virus. You have now imagined exactly what happened at the start of the age of immunization. The time was the mid to late 1700s, the place was the colonies that would become the United States, and the epidemic was smallpox, a dangerous disfiguring illness. One of the families involved, in 1776, belonged to John Quincy Adams.

At the time, there was no FDA to regulate the treatment, known as variolation (from the Latin word variola meaning spotted). People risked contracting severe cases of smallpox from the treatment, but they chose to go ahead because smallpox was a fearsome disease which, for centuries, swept through both the Old and New Worlds in epidemic waves, appearing and disappearing, killing millions, scarring survivors, and changing history as the scourge laid armies low on one side or the other.

An idea with a long history

The idea that suffering a mild case of smallpox prevented a severe case arose independently in several different parts of the world, with the first written reports dating back to the mid-16^thC in China. Cotton Mather, a Boston preacher, learned of the practice of deliberate infection from his African slave Onesimus in 1721 and introduced the practice to the Americas. Infected material or scabs from smallpox pustules were inhaled or scratched into the skin and while the practice killed 2-3% of the patients, that toll was considerably less than the 30% mortality rate of the epidemic disease.

How the variola virus causes smallpox

Pustules are the distinguishing marks of the disease called smallpox. The variola virus, whose only host is the human, enters the body via the mucous membranes of the mouth and nose. The virus multiplies quietly inside cells, producing no symptoms for 10-14 days. Then the body reacts with high fever, headache, and malaise. Patients take to their beds and develop a rash – at first, red spots, but then blisters which fill with pus. They spread from the mouth and nose, over the face, down the trunk and extremities. Coughing and sneezing spew infected material from pustules into the air, spreading the disease to caretakers. Deep skin lesions leave permanent pocked marks such as those scarring the faces of George Washington and Abraham Lincoln. Unlike many other viruses, variola is fairly hardy outside the body, which enabled its transmission from contaminated blankets given to native Americans by the British during the French and Indian war. The virus also traveled downwind from hospital ships on the Thames River in England in the 1890s.

The role of milkmaids in the history of immunization

The next chapter in the history of immunization occurred in Britain, where the fabled, beautiful skin of milkmaids was attributed to resistance to smallpox, conferred by prior infection with cowpox, a milder disease now known to be caused by the vaccinia (meaning cow) virus. In the late 1700s, Edward Jenner, a Gloucestershire physician, successfully prevented small pox by prior inoculations with the material from cowpox infections. The inoculations were called vaccinations, and Jenner became “the father of vaccination.”

Elimination of smallpox

The cowpox vaccine evolved over time into the standard vaccination procedure which eventually resulted in the elimination of the smallpox virus from the human population in the mid-1900s. The last natural case occurred in Somalia in 1977. Smallpox vaccinations, which had significant adverse effects in 1-2% of the population, were discontinued in the US in 1972 and the WHO declared smallpox eliminated from the world in 1980. Variola is the first and only virus to have been eliminated as a source of human illness, but other infectious diseases have been tamed in similar fashion and the hope is that new ways of creating vaccines will be even more effective.

How vaccines work

Smallpox vaccines were made from whole, live vaccinia viruses. Some vaccines for other diseases come from attenuated viruses (weakened viruses that transmit disease less effectively), or from killed viruses. Some vaccines are directed not at viruses, but at bacteria or at toxins like those produced by the diphtheria bacteria. All of them induce the immune system to create a memory of the specific organism or toxin, which will protect against future infection with the organism or the effects of a toxins like the ones produced by tetanus or diphtheria bacteria.

Because the immune reaction to infection is complicated and involves many types of immune cells as well as production of antibodies to the infecting organism, immunity to future infection is best induced and longest lasting after actual infection. Immunity after smallpox infection is lifelong, but lasts only 5-7 years after smallpox immunization. Other vaccines, especially those made from live organisms, are very effective and, some provide lifelong protection, especially with periodic booster doses. They have made infections like polio, measles, diphtheria, whooping cough and tetanus so rare that many doctors have never seen such illnesses.

New technology

Like variolation, vaccines that rely on whole organisms can cause serious and unintended consequences. In the last two decades, genetic technology has enabled researchers to create vaccines from small parts of disease-causing organisms like COVID-19 or hepatitis viruses. Since sequencing genomes became automated and less expensive, the world of genetic virology and bacteriology has exploded. It is no longer necessary to rely on tedious and technically difficult culture methods to grow and identify microscopic and submicroscopic organisms. And it is possible to break down genetic information and use it to artificially produce components of these organisms or the proteins they produce, employing stock materials off laboratory shelves.

Using genetic material from viruses, researchers get living cells in laboratories to produce proteins specified by those genes and then create vaccines from the proteins. Or they inject the genetic material directly into people to get their cells to make the proteins. The immune system then recognizes these proteins as foreign and creates antibodies and memory cells against them. Theoretically, the induced immune memory prevents infection should the vaccinated person encounter the virus. But much work remains. Some of the vaccines tried do not produce robust or long lasting immunity. Some have had paradoxical effects, with the immunized individual responding to actual infection with worse disease, as if a small amount of immunity actually enhanced the ability of the live virus to cause illness. The widespread deployment of the new COVID-19 vaccines – apparently effective in test groups over a relatively short testing period (safety studies in the past have run for years) will provide an enormous amount of information as to long-term safety and efficacy over years to come. This will be the largest and most public trial so far for the vaccine industry’s newest technologies. If the results are as good as the researchers who have developed them expect them to be, you can expect more and more vaccines to appear on the market.

In the meantime, smallpox virus samples still exist in the US and in Russia. If these stocks had been eliminated, as once was planned, the smallpox virus would truly have disappeared from the world because, unlike most of the viruses that plague us, the small pox virus has no other animal hosts. And while there are long term plans to create new smallpox vaccines, it would be wise, in this uncertain world, to maintain the ability to rapidly understand the genetic makeup of the smallpox virus, as well as to rapidly implement old-fashioned smallpox immunization.

Posted by medical plaintalk

Physician turned medical writer.

The Headaches that Predict Catastrophe

One of the most treacherous problems a busy emergency room physician faces is headache. “Headache” is a very common symptom, different from focal head pains attributable to sinus, eye or ear problems. While very painful and sometimes associated with nausea and vomiting, the vast majority of headaches, even if frequent and debilitating, are benign. They do not signify underlying illnesses or impending danger. But the emergency physician cannot afford to be wrong about the rare headache that predicts oncoming catastrophe and provides a chance to intervene.

Two broad categories

Catastrophic headaches fall into two broad categories. The first category includes “space-occupying lesions” such as tumors, hemorrhages, abscesses, and hydrocephalus (known commonly as “water on the brain”). The second category involves infectious and autoimmune problems that produce inflammation, triggering pain receptors in the membranes surrounding the brain and its blood vessels. Catastrophes avoided by successful interventions in both categories include death, permanent brain damage and blindness.

Tumors and abscesses

The most common fear about a bad headache is that it is caused by a brain tumor, but tumors usually produce other symptoms, involving speech, thinking, coordination or vision before they produce headache. Since the brain tissue itself has no pain receptors, tumors cause headache when they distort surrounding membranes or blood vessels, which have pain receptors. Tumor-related headaches worsen with positions and activities that normally cause the pressure in the veins in the head to rise – coughing, sneezing, lying down, straining at a bowel movement or lifting something heavy. As tumor size and pressure increase, nausea and vomiting appear. Occasionally, brain abscesses – pockets of infection surrounded by capsules -may mimic tumors. They usually come from blood infections seeding bacterial or fungal organisms into the brain.

Hemorrhages in the brain

Brain hemorrhages occupy space and increase pressure in the head. Deep small blood vessels, damaged by high blood pressure or arteriosclerosis, are usually the culprits. While these intracerebral hemorrhages can cause sudden headache, stroke-like symptoms such as paralysis, confusion, trouble speaking and loss of consciousness occur first or soon after the onset of headache.

Hemorrhages outside the brain, but inside the head

Headaches are also a symptom of epidural and subdural hematomas – collections of blood that accumulate over the surface of the brain hours to weeks after some closed head injuries (meaning no skull fracture). The history of injury, even seemingly trivial injury in an elderly patient, is crucial to correct evaluation of these headaches and there may be no other accompanying neurological symptoms. A head blow in the temple, where the skull is the thinnest is a common history. Young children and older adults are more susceptible to epidural hematomas (located between the inner skull and the the dural membrane over the brain) than those in between those age groups. Both epidural and subdural (between the dural membrane and the surface of the brain) collections of blood usually require surgical removal, sometimes as an emergency if symptoms such as change in level consciousness appear. Actor Liam Neeson’s wife Natasha Richardson did not survive an epidural hematoma incurred in a skiing related fall in 2009.

The “sentinel headache” of the aneurysm

Bleeding from brain aneurysms – weak spots at branch points of arteries – can be immediately catastrophic, even causing sudden death. But a tiny, warning leak before an aneurysm actually ruptures may cause a “sentinel headache” which allows time for life-saving surgical repair to prevent the oncoming, big rupture which typically occurs sometime in the next 10 days. A sentinel headache is sudden and severe pain involving all or part of the head, It is sometimes described like a “thunderclap.” As the little warning squirt of blood dissipates in the spinal fluid around the base of the brain, the headache dulls but a peculiar, longer-lasting pain may appear in the middle of the upper back, usually worsened with movement and probably indicating irritation from blood in the spinal fluid around the spinal cord. Diagnosis involves brain imaging with dye to study the arteries, and possibly a spinal tap to make certain bleeding has occurred. Unruptured cerebral artery aneurysms are found incidentally in 2% of autopsies so the problem is not rare.

Hydrocephalus

Hydrocephalus is a rare cause of headache, but one that should never be overlooked. The rise in pressure in the head comes from spinal fluid being trapped in the ventricles, hollow structures in the center of the brain where spinal fluid is made. Normally the spinal fluid circulates out of the ventricles via a very small channel, and bathes the surface of the brain and spinal cord before being absorbed into special veins at the top of the head. If flow is blocked, the ventricles begin to enlarge putting pressure on the surrounding brain. Most times, the onset of hydrocephalus is gradual, with headache, nausea, vomiting and balance problems gradually increasing. Unrecognized and untreated, obstructed spinal fluid flow leads to lethargy, coma and death, within 24 hours if the obstruction is sudden. Causes of obstruction include congenital anatomical abnormalities, tumors blocking the ventricular outflow tracts, scarring of these passages by inflammation from past meningitis or bleeding. Hydrocephalus most often requires surgical intervention to either remove the obstruction or to place a shunt around it, allowing cerebrospinal fluid to escape from the ventricles.

Headache from infection

Headache producing infections mainly involve the meninges, the membranes covering the brain and the spinal cord and are caused by viruses, bacteria or fungi. Viral and bacterial meningitis both cause severe headache, neck pain and rigidity and photophobia – inability to tolerate bright light. Movements of head and trunk and even eye movements are painful. Someone suffering from bacterial meningitis has a high fever, looks extremely ill and deteriorates rapidly. Identification of the infection type requires spinal fluid, obtained via spinal tap – insertion of a large needle into the spinal canal in the low back. Antibiotics are lifesaving. Viral meningitis, though painful, is less dramatic, and gets better on its own. Fungal meningitis is rare and much slower and less dramatic in its presentation than bacterial meningitis. It most often occurs in people who have impaired immune systems and requires prolonged treatment with antifungal drugs.

Non-infectious inflammatory headache: temporal arteritis

Headache from a non-infectious inflammatory condition called temporal arteritis usually presents itself in the seventh or eighth decade of life as a constant, often one-sided pain. Other symptoms that provide clues to this diagnosis are pain in the jaw muscle, especially with chewing, and tenderness of the artery just under the skin of the temple – the origin of the name for auto-immune inflammation that affects the arteries that supply the skull and brain with blood and can cause blindness and strokes. Diagnosis is confirmed when a blood test called ESR (erythrocyte sedimentation rate) is elevated and a temporal artery biopsy shows characteristic inflammatory cells in the artery wall. Treatment with steroids like prednisone, undertaken soon enough, prevents blindness and takes the headache away, but must be continued for many months.

A very useful question

One of the most useful questions an emergency room physician, or any other professional evaluating a headache complaint can ask the patient is “How worried are you about this headache?” People know themselves and have an innate sense about the nature of their symptoms. They will very often know the difference between a catastrophic headache and all the others.

Posted by medical plaintalk

Physician turned medical writer.

Epidemic Fear

“How many valiant men, how many fair ladies, breakfast with their kinfolk and the same night supped with their ancestors in the next world! The condition of the people was pitiable to behold. They sickened by the thousands daily, and died unattended and without help. Many died in the open street, others dying in their houses, made it known by the stench of their rotting bodies. Consecrated churchyards did not suffice for the burial of the vast multitude of bodies, which were heaped by the hundreds in vast trenches, like goods in a ships hold and covered with a little earth.” -Giovanni Boccaccio, 1313-1375

Conjuring up fear about epidemic infectious illnesses is easy. First bring up the black death that swept the European continent in the middle ages. A little bug wiped out half the population. Fast forward to the Spanish Flu of the early twentieth century. That one was a bird flu that made the jump to humans. Then dip into the African continent where the fiendish Ebola virus rises up periodically and passes easily among villagers, killing virtually everyone infected. And finally move onto SARS, other corona viruses, mad cow disease, AIDS, and flesh-eating bacterial infections. The complacency of the last seven decades of antibiotic and immunization successes succumbs easily to visions of new horrors, which happen to sell well in the crisis-oriented media.

The trick to dealing with the fear of epidemic illnesses is to separate substantiated facts from breathless commentary, identify things within the sphere of your influence, learn what you can and cannot do about them, do those things and quit worrying about the rest. Worry, after all, undermines the immune system, which is the first line of defense against infections of all kinds.

Many of the infectious horrors trumpeted in the press are, for the time being, hypothetical worries that depend on things that might happen, but have not yet and may not ever. That is not to say that our leaders shouldn’t have plans for an epidemic requiring difficult decisions about allocation of resources or for immunizing large numbers of people as fast as possible. But for the average individual trying to lead as healthy and happy a life possible, attention has to go to the “worth-worrying-about category,” – bacteria and viruses likely to be encountered and about which there are things to do to diminish the risk of allowing them to set up shop in the body.

Examples of the “worth-worrying about” category

Three examples of organisms in this category are two different bacteria, MERSA (methicillin resistant Staphylococcus aureus) and clostridium difficile, and the “flu” viruses – influenza type, other upper respiratory viruses that travel in the same circles (corona viruses included here). Ironically, the two bacterial enemies have set up shop in our health care facilities, making trips to the hospital risky ventures for reasons more than whatever brings you there in the first place. The SARS virus did most of its interpersonal traveling in health care facilities, and currently the new coronavirus is most lethal in chronic health care facilities. So, barring bad luck, it is also worthwhile keeping yourself healthy enough to stay out of these places.

MERSA in hospitals – invader of wounds

MERSA first appeared in 1961, two years after the introduction of methicillin, an antibiotic designed to counter bacteria which had become resistant to penicillin. Because bacteria reproduce by the billions, the lucky few that are naturally resistant to antibiotics like penicillin generate millions of equally resistant offspring like themselves in short order. Nevertheless, it took many more years of widespread antibiotic use to spread the methicillin resistant strains around the world. Now they are well entrenched, and account for 40% pf the hospital acquired infections. They travel around the hospitals and nursing homes on the hands and in the noses of health care workers, 40% of whom are “carriers,” and they live on the surfaces of blood pressure cuffs and computer keyboards, waiting to hitch a ride on a hand. Good hand-washing practices are very effective in reducing infection rates, but compliance is surprisingly difficult to achieve. Hospitals in England are contemplating re-instituting the practice of having a matron on each ward to oversee the hygiene practices of doctors, nurses, technicians and patients.

MERSA in the community – boils and other skin infections

MERSA has appeared in the community as well, and it is becoming difficult to tell which bacterial strains originated in hospitals. Typically, the infections caused by MERSA in the community are skin abscesses and inflammation around hair follicles. They afflict people who live in close quarters or share dressing. Prisons, barracks, locker rooms, and communal bathing facilities have all been implicated. While the scary stories told about MERSA have involved rapid deterioration from a quick spread of bacteria along the lines of the connective tissue in an extremity (necrotizing fasciitis), or in the lungs, these cases are rare. The development of a pus-containing, red lump on the skin, around a hair follicle or not, is the most likely presentation, and often can be cleared by a surgical drainage of the abscess.

What can you do to avoid this bug? Take care of any skin breaks promptly, by cleaning them with soap and water and peroxide, and covering them until they are sealed over. Regular baths or showers with good attention to the hair covered areas not only keeps the bacteria count down, but makes you aware of any areas of inflammation, especially if you have been in locker rooms. Keeping sports equipment and clothing clean and dry, especially pieces that come into contact with skin. Alcohol based cleaners are the most effective.

Clostridium Difficile – invader of the colon

Another bacteria making the rounds of health care facilities affects the colon and produces a very nasty smelling diarrheal illness that prolongs hospitalizations, or triggers re-hospitalizations when it appears after a patient has been sent home, in addition to spreading outside the health care setting. Clostridium difficile is aptly named because ridding hospitals of it has been difficult. This bacterium is not a stranger to the colon – over 50% of infants carry it without any symptoms. But when a patient has been taking antibiotics for other reasons, the normal bacterial population of the colon suffers and allows Clostridum D. to move in and irritate its lining, producing diarrhea that in turn requires more antibiotics, which will gradually produce more antibiotic resistance. For the time being C.difficile is still responsive to a variety of antibiotics, and to fecal transplants, but before a patient is adequately treated, his illness spreads the organism further and other sick patients are most at risk. As in MERSA infections, excellent hygiene practices are key to not transmitting clostridial infection.

Flu viruses and other colonizers of the airways

Viral “flus” and upper respiratory infections come around each year in different forms, which may or may not be susceptible to the current vaccines. Vaccines are best guesses as to the from the flu virus will take for the year. Immunization helps protect some people, and is generally recommended for the elderly, the very young and the chronically ill. Because the flu is spread through respiratory droplets, the actions required to minimize the spread of any particularly virulent strain of viruses – the kind that caused the Spanish flu, for instance – depend on an educated and responsible public. Staying out of crowded places, keeping hands away from mouths and noses, adhering to rigorous hand-washing with soap and water before meals and after contact with others, covering mouths with the crook of the elbow when coughing and sneezing, careful washing of food, utensils, countertops, and door handles and use of face masks in public by sick people are all effective ways of curtailing the spread of all respiratory illnesses including the common cold.

Public Defense

The more the public becomes practiced in good hygiene and avoids unnecessary antibiotic use (viruses do not respond to or require antibiotic treatment), the more robust a community’s response to the inevitable breakout of a viral infection will be and the better chance we have of not increasing the numbers of our antibiotic resistant bacterial enemies. Good hygiene also includes maintenance of good general health habits – diet, sleep, and exercise – to keep the immune system primed to ward off invaders and keep individuals out of the chronically ill groups that are susceptible to epidemics when they hit.

You cannot cram for good health but you can keep chronic health problems at bay with slow, steady discipline, a worthwhile endeavor since infections are always worse when other health problems such as diabetes complicate them. Your immune system functions best when you are rested, unstressed, well- nourished, and well-exercised, and exposed regularly to the natural world and sunshine (better than Vitamin D supplements). All of these things are within your sphere of influence and good antidotes to epidemic fear.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

No more posts.