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by Murder

  The initial symptoms are like a flu: fever, chills, malaise, headache, muscular soreness and stiffness, poor appetite, nausea, and vomiting. Soon the classic cycle of fever, chills, and rigors (uncontrollable shaking) occurs about every forty-eight hours along with the rupturing of the RBCs and the release of large numbers of the organisms into the bloodstream. Obviously, the continued destruction of RBCs in this fashion leads to anemia. The victim may also appear jaundiced (a yellow hue to the skin). Over time, the liver and/or the kidneys can fail, and death may follow.

  Quinine comes from the bark of the cinchona tree, originally found in Peru. The bark was ground and used to treat "intermittent fevers" as early as 1712. In 1820 two French chemists, Pierre Pelletier and Joseph Caventou, extracted quinine from the bark and made a powder of sulfate of quinine that proved to be more effective in treating the fevers than the bark itself.

  During the nineteenth century, quinine was the major treatment for malaria. Not a pleasant medicine, it tastes bitter and causes nausea, vomiting, diarrhea, skin rashes, ringing in the ears, and even hearing loss for high-pitched frequencies. Used in smaller doses, as you suggested, it would have fewer of these side effects and would only blunt the symptoms of the disease, as you guessed. Without full and aggressive treatment the malaria would never resolve, and the person would be infected for life. Africa and South America have millions of people who live just this way. Many eventually die of the anemia, liver or kidney failure, or another infection such as pneumonia—victims of malaria are more prone to other infections than the norm.

  Boneset (Eupatorium perfoliatum), also known as feverwort, ague-weed, or sweatplant, is a flowering plant that was dried and used to make a bitter tea. It causes flushing and sweating, and was used to treat fevers and also as a laxative. Several North American Indian

  tribes found it useful, and it was adopted from them by European settlers. I know of no evidence that it was effective against malaria. Its use as a folk remedy, both then and now, is due to its ability to cause sweating, which was seen as beneficial. It is not.

  What Exotic Diseases Are Prevalent in the Caribbean?

  Q: My heroine's daughter returns from a trip to the Caribbean very ill, requiring that she be hospitalized. I thought of severe "turista" and hepatitis as possible illnesses but would prefer something a little more exotic. Any thoughts?

  A: Schistosomiasis. Exotic enough?

  A mouthful for sure, it is pronounced: shish-toe-so-my-a-sis. It is an infection caused by a trematode (a worm in the fluke family) and there are several species worldwide. In the Caribbean the most likely type would be Schistosoma mansoni (S. mansoni). It is endemic to many parts of the Caribbean, and victims contract it if they swim or bathe in water infected with the parasite. Any freshwater pond or stream can contain S. mansoni.

  The life cycle of this parasite is complex and interesting (Figure 9). It requires the cooperation of two hosts (human and snail) and the metamorphosis of the organism into several distinct forms. The infective form is called a cercaria. It is a microscopic wormlike organism with a forked tail. It enters the body through unbroken skin that comes in contact with infected water. After entry it transforms into a form called a schistomule and migrates via the bloodstream to the lungs and then to the portal vein of the liver, where it matures into an adult schistosome. Males and females then pair up and migrate to the intestinal lining, where they set up housekeeping, mate, and begin to produce eggs. The eggs either remain in the intestinal tissues or are swept back to the liver. Either way,

  they are ultimately excreted, and when they contact water again, they hatch into a miracidium, a free-swimming form that moves by way of cilia (external hairlike structures that function as paddles). These forms seek out and invade a specific species of snail. Within the snail they develop into cercariae, and are released into the water, and the cycle repeats itself

  Within the human body the invasion, migration, and maturation period lasts about four to five weeks. During this time the victim typically has no symptoms, with the possible exception of mild itching for a day or so after initial exposure. Symptoms begin with the egg-laying stage. The most common symptoms are fever, chills, headache, hives or angioedema (puffy swelling of the hands, feet, and face, especially the lips and eyes), cough, weight loss, fatigue, abdominal pain, and diarrhea. Occasionally the diarrhea may be bloody.

  Diagnosis is difficult, mostly because schistosomiasis isn't considered. It is often confused with typhoid fever, amoebic dysentery, and other diarrheal or prolonged febrile diseases. Lab tests would show an increase in the white blood cell (WBC) count, particularly an elevation of eosinophils (a type of white blood cell) to greater than 50 percent of all WBCs (a normal level would be 3 to 5 percent). Diagnosis is established by finding the eggs in a stool specimen, from a biopsy of rectal tissues, or by a positive immunofluorescent antibody test.

  Once diagnosed, treatment is fairly straightforward: a single dose of Oxamniquine (15 milligrams [mg] per kilogram [kg] of body weight [1 kg equals 2.2 pounds]) and three doses of Praziquantel, (20 mg per kg) given six hours apart. Let's say your character weighs about 120 pounds, or 55 kilograms. She would be given 825 mg of Oxamniquine at one time and three 1200-mg doses of Praziquantel six hours apart.

  In your story the young victim could have gone swimming in a pool, perhaps near a romantic waterfall or in a tree-shaded stream. She would return home full of stories and feel completely normal. Six weeks later she could develop the "flu." Fever, chills, cough, and mild diarrhea would suggest such a diagnosis. Her M.D. would treat her with aspirin, fluids, and chicken soup, but she would become worse. More fever and chills, weight loss, and bloody diarrhea could develop. She would be hospitalized and evaluated for hepatitis, amoebic dysentery, and perhaps typhoid. Blood tests, bar

  ium enemas, and cultures of her blood would reveal nothing except an elevation of the WBC and eosinophil counts. Liver and kidney studies would be normal. Finally, a stool specimen, sent to the lab to look for amoeba organisms, would show the schistosome eggs, and an immunofluorescent antibody test would be performed on a blood sample. The cute young doctor on whom she has developed a crush would make the diagnosis, treatment would be given, and she would go on with her life, none the worse for wear.

  What Are the Symptoms and Signs of Spinal Muscular Atrophy?

  Q: I've afflicted a major character in my book with chronic spinal muscular atrophy. The book is set in fifteenth-century Brittany and France. I chose this disease because I wanted one that would waste the character away, not be contagious, and be quite rare, so that no one would know what to do about it.

  At the time my heroine meets him, he is in his twenties and his legs have already atrophied. He knows he is going to die as his brother did, but because the progress of the disease has temporarily slowed, he has hope that he has more years to live.

  My critique group keeps asking for more symptoms of his suffering, though I do say his strength is going as the wasting and paralysis moves up his body, and he is in pain as it happens.

  Does this scenario ring true? What else can you tell me about this rare disease?

  A: Yes, your scenario works well, and you have obviously done your research.

  Spinal muscular atrophy (SMA) comes in at least three varieties:

  1. SMA I, Infantile SMA or Werdnig-Hoffmann disease, is apparent at birth and has a rapidly fatal course. The infant has weak, floppy limbs and poor reflexes, and usually dies in the first year. Not suitable for your story.

  2. SMA II, Chronic Childhood SMA, begins in later childhood and has a slowly progressive course.

  3. SMA III, Juvenile SMA or Wohlfart-Kugelberg-Welander disease, begins during late childhood and has a slowly progressive course. This is probably best for your scenario.

  These are all what we call "lower motor neuron diseases." They affect the neurons (nerve cells) of the lower spinal cord rather than those of the brain. Motor neurons are those involved in movement as opposed to sensati
on (sensory neurons). Other diseases in this family include amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease). Stephen Hawking, the brilliant theoretical physicist, is afflicted with ALS.

  SMA is an inherited disease, so the fact that your character's brother died from the same disease fits perfectly and adds a note of fear since the character knows what to expect. Of course, in the 1400s absolutely nothing was known about this disease, and it obviously wouldn't have a name. It is very likely that he would be considered a sinner or possessed or otherwise dangerous. At that time religion had a much stronger hold on people's beliefs than did science.

  As you noted, the loss of motor nerve stimulation in your character leads to progressive atrophy of the muscles. This is usually more prominent in the larger proximal muscles of the shoulder and hip girdles. The thighs, upper arms, and shoulders become progressively weak and wasted, month by month and year by year.

  Pain is not typical with these syndromes since they involve the motor neurons rather than the sensory ones.

  The symptoms are simply a progressive loss of strength and muscle size, beginning in the larger muscles and progressing to the smaller ones. As the weakness advances, loss of coordination and the finer movements of the hands, for example, deteriorate. Handwriting, drawing, and playing with small objects would suffer. Handling eating utensils or other tools would become awkward and clumsy. Walking would become wider of gait (for better balance) and more shuffling in quality. Trips and falls would be common. The ability to stand, walk, and rise from a chair would become increasingly difficult. Eventually the victim would become chair- or bed-bound and more and more dependent on the help of others for feeding, bathing, dressing, and so forth. Through all this his mind would be completely intact, since this disease does not affect the brain. Of course, depression, sullenness, anger, and thoughts of suicide could appear.

  What Type of Bacterial Meningitis Is Most Likely to Infect Adolescents?

  Q: I have an unusual question. I am writing a fictional story that is loosely autobiographical. At age twelve, while attending a summer camp, I became very ill, was hospitalized for a couple of weeks, and nearly died. I remember little of the experience but later was told I had had bacterial meningitis and that many of the other kids at camp had the same thing. I want to use this event in my story and would appreciate your thoughts on what this might have been.

  A: Meningitis is an inflammation of the meninges, which are the membranes that cover the brain and spinal cord. The most common at age eleven would be viral meningitis (caused by several different types of viruses) or bacterial meningitis (caused by either Haemophilus influenzae or Neisseria meningitidis, both of which are bacteria). The most likely culprit in the scenario you describe would be meningococcal meningitis, which is caused by N. meningitidis.

  Meningococcal meningitis most commonly occurs in children under three years of age or in adolescents between fourteen and twenty. It can become epidemic in closed communities such as camps, military bases, and schools, particularly where people come from varied parts of the country. Let me explain why this is so.

  Many different strains or types of N. meningitidis exist. We all carry these and other bacteria in our nasopharynx (nose and throat). We are immune to them, as are most people in our immediate geographic area. After all, we live with them on a daily basis. When we go to another area of the country, we are exposed to people who carry different strains of the same bacteria. We may have no immunity against these strains because we have not been exposed to them on a regular basis and thus have not developed antibodies against them. Alternatively, someone may come into our area from another part of the country and expose us to their particular strain. Either way, we are at risk of developing an infection from this foreign bacterium.

  This is particularly true for viruses. How many times have you or someone you know developed a flu or cold after a vacation or trip? When you travel in an airplane and visit other areas of the country or world, you are exposed to viruses that are not part of your normal environment. Since your immunity to these viruses is minimal or absent, you become ill.

  N. meningitidis is a common bacterium in our nasopharynx. When people from diverse areas gather, as in a camp or military base, someone may bring in a particularly virulent strain to which many of the group, if not most, do not possess immunity; that is, the carrier is immune, but the other members of the group are not. The bacteria can spread from person to person by direct contact (sharing food or drink or by kissing) or through the air by coughing or sneezing. This sets the stage for those without immunity to

  develop a throat infection. From the nasopharynx these bacteria can enter the bloodstream, spread to the brain, and become meningitis. As it spreads from person to person, an epidemic of meningococcal meningitis occurs. This is probably what happened to you and your friends.

  The incubation period is as short as twenty-four hours, so the epidemic spreads rapidly. By the time the first person becomes ill, many others are already exposed and will themselves become symptomatic in short order.

  The major symptoms are fever, chills, sore throat, severe headache, stiff neck, photophobia (irritation of the eyes with exposure to light), generalized aches and pains, and nausea. Since it is an infection of the brain, lethargy, disorientation, confusion, and even coma can occur. This may explain why you remember little of the event.

  There are several significant and even lethal complications of this disease. Brain or spinal cord abscesses, pneumonia, meningococcal arthritis, endocarditis (infection of the heart valves), and meningococcemia (a severe infection of the bloodstream that can kill quickly) are not uncommon.

  Treatment is with high doses of intravenous penicillin to which the bacterium is very sensitive. Most victims of this illness recover completely with proper treatment.

  Is Shock Therapy Effective Treatment for Severe Depression?

  Q: I need to know about shock therapy for depression. One of my characters is severely depressed and has tried all the medications. Is shock therapy still done? How is it done? Does it work? What are the complications?

  A: Major clinical depression is a common and significant medical problem. It robs the sufferer of all that is good about life. The person is sad and lonely, sees no future, enjoys no one's company, avoids

  social activities, cries, and often fails to care for himself. In its severest form the person's clothes are dirty: he doesn't bathe and eats poorly, if at all; and his health declines from this personal neglect. The mortality rate in severe depression approaches 15 percent, mostly due to suicide.

  Electroconvulsive therapy (ECT) was discovered in the 1930s. Over the years many methods have been used to invoke the convulsions necessary for this type of treatment. Initially, drugs were used and then insulin, which drops the blood sugar to such low levels that a seizure occurs. Finally, electric shock delivered to the brain was employed.

  The mechanism of its action and benefit are poorly understood. It seems as though the chaotic electrical activity that rages through the brain during the generalized (grand mal) seizure that the ECT produces somehow alters the mood center of the brain. No one knows for sure, but the results can be dramatic.

  In the early years ECT was done without anesthesia so that when the seizures occurred, the recipients would sometimes severely bite their tongues, vomit and aspirate, or even break bones in their extremities from the violent nature of the provoked convulsions.

  In 1975 the movie One Flew over the Cuckoo's Nest hit the screen and painted a negative picture of ECT. Here it was used as a punitive device, as opposed to a therapeutic endeavor. Currently, it is making a comeback, simply because it works. It is safe and effective as the first line of treatment for severe depression, with response rates of 80 to 90 percent. In people who have failed medical therapy, as in your character, it is effective in 50 to 60 percent of cases. As with any therapy, relapses after ECT may occur.

  The procedure is much less barbaric than it once was. The patie
nt is placed on a stretcher, an IV is started, cardiac monitoring electrodes are placed on the chest, and the ECT electrode patches are applied to each side of the head. Either an Ambu bag with face mask is placed over the mouth and nose or an endotracheal tube is introduced into the trachea (windpipe) in order to ventilate the patient during the procedure and until the anesthetic and muscular paralytic agents wear off.

  The patient is then given a short-acting general anesthetic and a muscle relaxant, which prevent the outward manifestations of the seizure and thus prevent the tongue biting and bone breaking of the past. Short-acting anesthetic agents used in this circumstance might include 25 to 50 milligrams of Diprivan (propofol) given by IV and repeated as necessary or 2 to 5 milligrams of Versed (midazolam HCL) given by IV and repeated as necessary. Their effects are seen immediately and wear off quickly. Muscle paralytics used might include .10 milligrams per kilogram (1 kilogram equals 2.2 pounds) of Norcuron (vecuronium bromide) given by IV or 1 to 4 miligrams of Pavulon (pancuronium bromide) given by IV. Each of these takes effect immediately. Dosing can be repeated as necessary and wears off over twenty to thirty minutes.

  The physician performing the ECT pays close attention to the patient's heart rhythm and airway to prevent complications from aspiration or cardiac arrhythmias. The electrical current is applied to the brain, and the seizure activity is induced. Since the patient is anesthetized and paralyzed, no tonic-clonic jerking, which happens in generalized seizures, occurs.

  For severe depression six to twelve treatments are given at the rate of three times a week or longer, until the desired response occurs. Long-term side effects appear to be minimal, if any. In the short term there may be a dulling of cognitive function (thinking and problem solving) for a few days or weeks. There may also be amnesia, which can be retrograde (events that occurred prior to the ECT) or anterograde (events that occur in the period just after the ECT). In either case, these tend to resolve over a few days or weeks.