Community immunity won’t help you with tetanus (AKA “lockjaw”). The bacteria that cause tetanus are common in the environment. Any contaminated wound can have a nice case of tetanus associated.
Tetanus causes prolonged contractions of the skeletal muscles. That’s what locks the ol’ jaw. That’s also what can bend you over backwards like a bow until you’re supported by just your heels and your head. (Photo) (Another photo) (Painting) (Child with tetanus, Photo) (Infant with tetanus, Photo)
I’ll fix your feet til you can’t walk
I’ll lock your jaw til you can’t talk
I’ll close your eyes so you can’t see
This very hour, come and go with me
I’m death I come to take the soul
Leave the body and leave it cold
To draw up the flesh off of the frame
Dirt and worm both have a claim
Signs and symptoms may include:
Spasms in the facial muscles
Muscle spasms (may be strong enough to break bones or dislocate joints)
Tetanus is life-threatening. Once the patient is symptomatic, in the US, the mortality rate is 25%. Worldwide it’s 50%.
We routinely inquire about a patient’s tetanus immunization status any time a tetanus-prone wound shows up, and routinely give the immunization any time the patient isn’t 100% sure he/she has had the shot within the past five years.
One of the early signs of tetanus is the rictus sardonicus, a smile like the Joker in the comic books. A highly accurate (and highly specific) test for tetanus is this: tickle the back of the patient’s throat with a tongue depressor. If the patient coughs, gags, or chokes, that’s negative. If, on the other hand, the patient bites down on the tongue depressor, that’s a positive: he’s got lockjaw.
If you have a deep or dirty wound, particularly a puncture wound, get it seen in an Emergency Room. If you have a wound and subsequently start feeling muscle cramps in the area … get to an Emergency Room now. We have people standing by. “L. B.” IN MEMORY OF LYMAN SON OF MR. JACOB AND MRS. ABIGAIL BLACK WHO DIED SEPT 10TH 1801 AGED 6 YRS 10 MONTHS 23 DA
Haemophilus influenzae type B
This is the disease that inspired this post. The news story read, Rare sickness kills child; officials urge vaccination
A childhood illness that has mostly been curbed through vaccinations has killed one child and sickened four others in Minnesota, health officials said Friday.
The five children were infected with a bacterial infection known as Hib: Haemophilus influenzae type b.
Three of the affected children had not received any vaccinations, including the 7-month-old who died, according to the Centers for Disease Control and Prevention.
“The situation is of concern,” said Dr. Anne Schuchat, director of the National Center for Immunization and Respiratory Disease at the CDC. “It could be happening elsewhere, and of course it’s tragic that one of the children actually died from a preventable disease.”
One of the infected children, a 5-month old, had not completed the three-dose series of the vaccination, and a 15-month old child had received all doses but had an immune deficiency.
Before the immunization was developed, 43 per 100,000 children got meningitis associated with Hib.
Of those 43, 20% would die. 8.6 out of those 43. One in five.
So, you see, five sick and one dead falls right into the expected mortality rate. It’s a mortality rate that’s worse than you’d get playing Russian Roulette (where the odds are one in six that you’ll die).
How about the ones who get Hib meningitis and don’t die?
15%-30% of survivors suffer some permanent neurologic damage, including blindness, deafness, and mental retardation.
Another 17% of invasive Hib cases include epiglottitis, an infection and swelling in the throat that can cause life-threatening airway blockage. Other forms of invasive Hib disease include: joint infection (8%), skin infection (6%), pneumonia (15%), and bone infection (2%).
With Hib vaccine, the rate of Hib meningitis is 0.11 per 100,000. JOHN N. SON OF JOHN AND MARY HUBBARD DIED MARCH 21, 1836 AGED 1 YR (8 MO 1 DA)
Complications of measles are comparatively rare. But given that measles’ infection rate is around 90%, a small percent of a large number is still a large number. And in third-world countries, the fatality rate for measles runs around 28%. Among immuno-compromised folks right here, measles is around 30% fatal. (That’s where community immunity comes in handy—if the immuno-compromised folks never run into measles because everyone else is immune, they skate.) Photo. Photo. Photo.
Measles is comparatively mild in children; it can be devastating in adults. The 1911 measles epidemic killed 5% of the US Army.
And even “comparatively mild” is still nothing to laugh at. Those complications can include blindness and deafness from scarring. In The Five Little Peppers and How They Grew the children all get the measles, and there’s quite a bit of concern that Polly will go blind.
But Polly’s eyes didn’t get any better, with all the care; and the lines of worry on Mrs. Pepper’s face grew deeper and deeper. At last, she just confronted Dr. Fisher in the kitchen, one day after his visit to Polly, and boldly asked him if they ever could be cured. “I know she’s—and there isn’t any use keeping it from me,” said the poor woman—“she’s going to be stone-blind!”
“My good woman,” Dr. Fisher’s voice was very gentle; and he took the hard, brown hand in his own—“your little girl will not be blind; I tell you the truth; but it will take some time to make her eyes quite strong—time, and rest. She has strained them in some way, but she will come out of it.”
To poor Polly, lying in the darkened room, or sitting up in the big rocking-chair—for Polly wasn’t really very sick in other respects, the disease having all gone into the merry brown eyes—the time seemed interminable. Not to do anything! The very idea at any time would have filled her active, wide-awake little body with horror; and now, here she was!
Signs and symptoms of measles include:
Inflamed eyes (conjunctivitis)
Sensitivity to light
Tiny white spots with bluish-white centers found inside the mouth on the inner lining of the cheek, called Koplik’s spots
A skin rash made up of large, flat blotches that often flow into one another
Ear infection. Measles causes an ear infection in nearly one out of every 10 children.
Encephalitis. About one in 1,000 people with measles develops encephalitis, an inflammation of the brain caused by a viral infection, which may cause vomiting, convulsions and, rarely, coma. Encephalitis can closely follow measles, or it can occur years later during adolescence as a result of a slow virus infection. The late form, called Dawson’s encephalitis, is rare.
Pneumonia. As many as one in 15 with measles gets pneumonia, which can be life-threatening.
Diarrhea or vomiting. These complications are more common in infants and small children.
Bronchitis, laryngitis or croup. Measles may lead to inflammation of your voice box (larynx) or inflammation of the inner walls that line the main air passageways of your lungs (bronchial tubes).
Pregnancy problems. Pregnant women need to take special care to avoid measles, because the disease can cause miscarriage, premature labor or babies with low birth weights.
Low platelet count (thrombocytopenia). Measles may lead to a decrease in platelets — the type of blood cells that are essential for blood clotting.
In 2007, there were 197,000 measles deaths globally - nearly 540 deaths every day or 22 deaths every hour, mostly children under the age of five.
It remains a leading cause of death among young children globally, despite the availability of a safe and effective vaccine.BETSEY HUBBARD DIED JULY 17, 1799 AGED 9 MO 5 DS
EBER DIED OCT 27, 1802 AGED 7 MO 16 DS
LUCINDA DIED AUG 29, 1810 AGED 1 YR 2 MO 20 DS
HARRIET DIED JAN 22, 1820 AGED 6 YR 4 MO 6 DS
PETER B. DIED MAR 10, 1820 AGED 9 MO 8 DS
CHILDREN OF PETER & POLLY HUBBARD
Mumps is caused by a virus. The usual route of transmission is through droplets (coughing and sneezing). Photo. Photo. The most common presentation is a parotitis (inflammation of the major salivary glands located on either side of the face), which occurs in 30-40% of patients. Other reported sites of infection are the testes, pancreas, eyes, ovaries, central nervous system, joints, and kidneys.
Central Nervous System involvement is common, but symptomatic meningitis only occurs in about 15% of patients. It usually resolves without complications, but adults are at a higher risk for sequelae. Encephalitis is rare and is seen in fewer than 2 per 100,000 cases. It has a mortality rate of 1.4%.
Orchitis (inflammation of the testicles) can occur in 50% of postpubertal males. It causes testicular atrophy in as many as 50% of persons affected but rarely causes sterility.
Pancreatitis occurs in 5% of persons infected with mumps. The hyperglycemia that results is usually transient, but a few cases of diabetes mellitus have been reported. It is not conclusive that the mumps virus has been the definitive cause.
Deafness has been reported in 1 per 20,000 cases of mumps. In 80% of cases, the hearing loss is reported to be unilateral.
Some deaths due to myocarditis (inflammation of the heart muscle) have been reported. The incidence of this complication is reported to be up to 15%, but it is usually asymptomatic.
The risk of spontaneous abortion is increased in a woman who contracts mumps in the first trimester.
Other complications reported are chronic arthritis, arthralgias (joint pain), and nephritis (inflammation of the kidneys).
Serious complications are more common in adults.
One of the objections to the germ theory of disease was that not everyone who’s exposed to the germs gets sick. (Some debunkers deliberately ingested pure cultures of disease germs with no ill effects and used this as proof that germs don’t cause illness.) But it isn’t necessary for everyone to become ill for a contagious disease to be a serious public health problem. In order to have a pandemic as few as 15-40% of the population need to be affected. VIANA DAUGHTER OF ASA & MARGARET ANDREWS DIED SEPT 2, 1823 AGED 2 YEARS
Mild in children (a rash, low-grade fever, and aching joints), rubella (AKA German measles, three-day measles) is devastating in pregnant women.
In the first trimester, there’s a 90% chance that rubella would pass from the pregnant woman to her fetus, causing congenital rubella syndrome (CRS). In 20% of cases this results in spontaneous abortion.
Among those born alive:
Signs and symptoms in the infant may include:
Cloudy corneas or white appearance to pupil (43%)
Low birth weight
Small head size
Skin rash at birth
Heart defects (50%)
It is important for women to become immune to rubella before they reach child-bearing age. Herd immunity is also important to protect those who are either not immune or whose immunity is not complete. Photo. Photo.
Rubella is a virus; it is transmitted by contact or airborne droplets.
If you are pregnant and suspect you have rubella, do not visit your OB/GYN directly. Call ahead, to avoid contact with other pregnant women. HIRAM BORN JAN 14, 1827 DIED FEB 14, 1827
CHESTER G. BORN MAY 5, 1832 DIED FEB 19, 1833
EMELINE BORN MARCH 24, 1825 DIED FEB 21, 1833
SUSAN BORN APRIL 14, 1836 DIED DEC 10, 1836
CHILDREN OF HIRAM & EMILY TAYLOR
Chicken pox (AKA varicella). A red itchy rash marked with blisters, low-grade fever, and aching joints that lasts for a few days. The rash appears primarily on the torso. Caused by a virus and spread by droplets or direct contact. Photo. Photo. Photo.
When a woman who is not immune catches chicken pox any time during pregnancy, but particularly in the first 28 weeks of pregnancy, the virus can infect her fetus, resulting in fetal varicella syndrome:
Under-developed fingers and toes
Anal and urinary bladder sphincter abnormalities
Spinal cord malformation
Damage to the eyes
Absent deep tendon reflexes
Maternal infection at any time in pregnancy exposes the fetus to a high risk of transplacental contamination and is indicative of fetal follow-up. The risk of fetal anomalies, however, is higher during the first and second trimesters. Sonographic signs of fetal disease include fetal demise, growth restriction, musculoskeletal abnormalities such as clubfeet and abnormal position of the hands (caused by both necrosis and denervation of the affected tissue), limitation of limb extension due to cicatrices formation, cutaneous scars, limb hypoplasia, chorioretinitis, congenital cataracts, microphthalmia, hydrops, polyhydramnios, hyperechogenic hepatic foci, cerebral anomalies such as ventriculomegaly or atrophy, and microcephaly, disseminated foci of necrosis and microcalcifications, encephalitis, echogenic bowel in the second trimester. The placenta can show a multifocal chronic villitis with multinucleated giant cells. Fetal infection can be demonstrated by detection of varicella-zoster virus DNA by polymerase chain reaction (PCR) in fetal blood and amniotic fluid or by detection of the specific IgM antibody, in the same fluids.
You don’t want that, now do you?
Immunization prevents it.
Chicken pox is the gift that keeps on giving. It never goes away—it just becomes inactive living along the nerve pathways in the body. It can return in the form of shingles later on, when the patient is under stress, immunocompromised, or otherwise has reduced resistance.
People who have had chickenpox (varicella zoster) in their youth can develop shingles (herpes zoster) in later years. During an acute attack of the chickenpox virus, most of the viral organisms are destroyed, but some survive, travel up nerve fibers along the spine, and lodge in nerve cells where they may lie dormant for many years. A decrease in the body’s resistance can cause the virus to reawaken decades later. It then travels back down the nerve fibers to the skin’s surface. Photo. Photo. Photo.
The reawakened virus generally causes a vague burning sensation or tingling over an area of skin. A painful rash usually occurs two to five days after the first symptoms appear. A cluster of small bumps (1) turns into blisters (2) that resemble chickenpox lesions. The blisters fill with pus, break open (3), crust over (4), and finally disappear. This process takes four to five weeks.
A painful condition called post-herpetic neuralgia can sometimes occur. This condition is thought to be caused by damage to the nerves (5), and can last from weeks to years after the rash disappears. HERE LIE TWO SONS OF ELIJAH & MABEL ANDREWS.
ELISHA DIED OCT 21, 1802 AGED 1 YR & 5 MONTHS
RICHARD DIED OCT 25, 1797 AGED 2 YRS & 1 MONTH
Why do we immunize? Because if we don’t…these diseases come back.
More from the CDC
Copyright © 2009 by James D. Macdonald
I am not a physician. I can neither diagnose nor prescribe. This post is presented for entertainment purposes only. Nothing here is meant to be advice for your particular condition or situation.
Index to Medical Posts
From Elizabeth Moon:
My mother had polio as a small child, and late in life developed post-polio syndrome. During WWII, she was working as liaison engineer for the Army Air Corps at a Douglas Aircraft factory outside Chicago when there was an outbreak of polio and a shortage of nurses because of the war…and power outages that meant more people were needed to hand pump the iron lungs that kept the most severely disabled alive. There was an emergency call for anyone with nurse’s training (which she also had.) She left the factory, and her boss threatened her—she was, after all, on a defense contract. “If it were your wife or child in that ward?” She worked long shifts at the hospital until the worst was over.
Polio was the terror of my early childhood…in bad years, we had “block quarantines” when children were not supposed to leave the block on which they lived. (And we sometimes did and we got in big trouble for it, if caught, which we always were.) One of my good friends in first and second grade had had polio and had the heavy leg braces and crutches; she was in my Brownie troop. When a second-grade teacher came down with polio, when I was in first grade, many of the children in that school (including me) were given gamma globulin shots, then the only “maybe” preventive. It hurt like anything—huge shot, bigger than a penicillin shot. Didn’t matter.
We had outbreaks yearly, where I grew up, and big ones on occasion. When I was five, and again when I was seven, I was sent to Colorado to escape the local outbreak, on the grounds that a cabin 12 miles from the nearest town might be safer, the air and water purer. But the second year, a Scout camp had been built upstream of the cabin on the same river, and the water was definitely not purer. Every child knew about polio. Every child (let alone the parents) had seen the pictures of polio wards, the rows of children in wheel chairs and braces, the rows of iron lungs with just heads sticking out. Every child knew someone who had died, or been crippled, by polio. Every family collected dimes for the March of Dimes; in school we were given worksheets to stick them on, and the Mothers of the Mother’s March handed out similar cards with little pockets. (Yes, mothers did actually march through the streets, and go door to door to collect donations.)
The year before the vaccine came out two children in one family came down with polio the day after a swimming party I’d been to. I will never forget my mother’s face as she turned to look at me—still holding the receiver—and said harshly “Put your chin on your chest!” (A test of nuchal rigidity, this was a command every child in that era knew.) She was terrified. Though the children had only shown clear symptoms that day, they would’ve been contagious the day before. One boy died; the other had permanent disabilities. Back in the day, no accommodations were made for disabled children in school—many kids with polio sequelae were sent to residential facilities where they did get schooling, because local schools routinely excluded kids with disabilities.
Every febrile illness in summer was suspect. Every febrile illness after children had played in water (in the street, for instance, if it rained, or in a swimming pool) was suspect. I had a different serious illness, an encephalitis, and at first it was thought it might be polio (and I’m sure other mothers, hearing that I was sick, told their children to “put your chin on your chest.”)
Then came the vaccines—first the Salk, then then Sabin. Three shots for the Salk, one or two weeks apart: they lined us up in the halls of a school, and bang-bang-bang it was done. Then a year or two later, we had another series of three shots. By then, the outbreaks were noticeably smaller. In five years, hardly a new case—a new case was news.
That didn’t cure those who’d already had it. When I went off to college, I did some volunteer work in a children’s hospital. There was only one polio patient: one of the last cases, then a teenager, in an iron lung. By then there were no more specialty polio centers, no more polio wards, in which at least the inhabitants could talk to someone who understood. In a ward for children, where the other patients were kids who’d had some other treatable illness or injuries, there was his iron lung. He wanted no part of the cheerfulness we tried to bring to the ward.
And no wonder. Unless he could adapt to one of the smaller respiratory assists that came later, he was stuck for life in a huge, unwieldy, scary case…immobile, having to be tended by people who reached in through portholes on the side to clean him up, change his diaper…and who, increasingly, would not have a clue what his life was like because people like him were so few now. He could not see his body, engulfed in the machine that kept him alive. He could see only what was directly above him or reflected in the mirror over his head. None of the electronic aids for the disabled existed then…or for another decade or two.
There were, and are, more lethal diseases than polio: those with a higher mortality, and greater infectivity as well. But polio had a special horror to it.
Children’s gravestones from the Black Cemetery, Berlin, VT. I learned about the Black Cemetery from this song, and I recommend it to everyone.
Why We Immunize by James D. Macdonald is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 License.
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