Let's talk infectious diseases, the reason for vaccines: ᴹᵉᵃˢˡᵉˢ

Measles is caused by an extremely contagious virus called paramyxovirus that replicates in your throat and nose. It's spread through respiratory droplets when an infected individual sneezes, coughs, or even talks. The virus can live in the air and on surfaces for up to two hours after a person with measles symptoms has left the area. It invades your respiratory system, causing fever and flu-like symptoms, and then spreads throughout your body. As your antibodies attack the virus, damage to the walls of tiny blood vessels occurs, leading to the measles rash.

An infected person is contagious for around eight days—four days before through four days after the measles rash appears. Measles is so contagious that one infected person who is exposed to 10 people who aren't immune to measles will infect 9 of the 10.

About 7 to 14 days after exposure to someone with measles, people without immunity to measles can develop measles symptoms, some of which are similar to the flu, including:

▪️Fever

▪️Dry cough

▪️Runny nose, sneezing, and congestion

▪️Red, watery eyes from conjunctivitis

▪️Sensitivity to light

▪️Poor appetite

▪️Swollen glands

▪️Koplik spots, small, bright red spots with a bluish-white central dot that are often found inside the mouth, on the inside of cheeks, and on the soft palate.

The classic measles rash is 3-5 days after the other symptoms appear. Unlike many other viral rashes, such as roseola and chickenpox, which typically start on the trunk, the measles rash starts on the face and head. Other things to watch for regarding the measles rash:

▪️This red, blotchy rash will spread down your or your child's body over the next three days, eventually reaching your hands and feet after starting around your hairline.

▪️It usually lasts about five to six days.

▪️After three to four days, the rash may no longer turn white when you push on it.

▪️Areas, where the measles rash was most severe, may start to peel.

▪️Once the rash begins to go away, it will fade in the same order that it started.

Measles is a serious, HIGHLY infectious disease that causes serious complications.

Although some people continue to claim that measles is a mild infection, it can have severe complications. In fact, one or more complications occur in around 30% of cases.

People who are at the highest risk for developing complications include: children under age 5, adults over age 20, pregnant women, and people with compromised immune systems.

Common complications include:

▪️Ear infections

▪️Diarrhea

More severe complications from measles include:

▪️Pneumonia: This lung infection is the main cause of measles death in children. Approximately 1 in 20 kids with measles develop pneumonia.

▪️Encephalitis: This is an inflammation of the brain that occurs in about 1 in 1,000 people. It involves more severe symptoms, such as fever, headache, vomiting, stiff neck, meningeal irritation, drowsiness, convulsions, and coma. This complication of measles usually begins about six days after the start of the measles rash and can lead to death, deafness, or permanent brain damage.

▪️Pregnancy issues: Measles can lead to preterm labor, low birth weight, and even pregnancy loss.

▪️Subacute sclerosing panencephalitis (SSPE): This is a deadly, but rare complication caused by defective measles virus. About seven to 10 years after having measles, children and young adults with SSPE develop progressive neurological symptoms, including memory loss, behavior changes, uncontrollable movements, and even seizures. As symptoms progress, they may become blind, develop stiff muscles, become unable to walk, and eventually deteriorate to a persistent vegetative state. Children who had measles before age 2 seem to be more at risk of developing this complication. People with SSPE usually die within one to three years of first developing symptoms. Fortunately, as the number of measles cases has been dropping in the post-vaccine era, so have the number of SSPE deaths.

▪️Seizures: In 0.6 percent to 0.7 percent of people, seizures with or without fever can occur as a complication of measles.

▪️Death: In the United States, measles is fatal in about 0.2 percent of cases.

Measles has a devastating impact on the body's immune system that could make it harder to fight infections for years.

The virus can cause "immune amnesia" - meaning the body forgets how to fight bugs it once knew how to beat.

Measles also resets the immune system to a "baby-like" state, compromising its ability to devise ways of tackling new infections.

"Measles is like the first 10 years of an untreated HIV infection compressed into a few weeks - that's the kind of immunological memory damage," said Dr. Michael Mina.

This is a serious problem because the measles are making a comeback due to a decrease in vaccinations.

Measles appeared in print as early as 0910 when a Persian physician published an account of measles and smallpox being two distinct and unique diseases.

In 1757, Scottish physician Francis Home transmitted measles from infected patients to healthy individuals via blood, demonstrating that the disease was caused by an infectious agent.

The Faroe Islands was experiencing a measles epidemic in 1846 so Danish physician Peter Panum traveled there and spent 5 months studying the disease. His observations were that measles was not just a childhood disease but affected people of all ages, the isolation of the Faroe Islands served to protect them from illness but also when illness hit the islands the mortality rate was high, the measles rash appeared 14 days after a person was exposed to the disease, and surviving the infection resulted in lifelong immunity against the disease.

Figuring out a cure for measles was proving to be difficult and very slow-going. Finally in 1916 French researchers Charles Nicolle, MD, and Ernest Conseil, MD showed that measles patients have specific protective antibodies in their blood. The researchers then demonstrated that serum from measles patients could be used to protect against the disease.

But it wasn't until 1954 that the measles virus was finally isolated and captured by Thomas Peebles, MD. The successful isolation of the virus was used to create a series of vaccines. In 1958 the first vaccine was tested on 11 children. All 11 vaccinated children developed measles antibodies, but nine also developed a mild rash—the vaccine didn’t cause full-blown measles, but it did cause symptoms. The researchers realized the virus used for the vaccine had to be weakened even more.

By 1960 there still wasn't a vaccine researchers felt good about mass producing. However, when an outbreak happened in February of 1960 and the 23 children who had been vaccinated with the most recent effort were exposed, they didn't fall ill. The vaccine still caused too many side effects but since it did its job and protected the children from the disease vaccine production went forward.

Successfully demonstrating its safety and efficacy, first in monkeys and then humans, John Enders and colleagues declared their measles vaccine capable of preventing infection in 1963.

Their Edmonston-B strain of measles virus was transformed into a vaccine licensed in the United States in 1963, and nearly 19 million doses would be administered over the next 12 years. In 1968 this vaccine was weakened (attenuated) enough to administer it without human blood proteins to lessen the side effects. Called the Moraten strain (More Attenuated Enders), it has been the only measles vaccine used in the United States since licensure.

In 1971 the MMR was licensed for use. It is a combination measles, mumps, and rubella vaccine. That combination will be discussed in a different post.

In 1978, the CDC declared a goal of eliminating measles from the United States by 1982. Although this goal would not be met, widespread vaccination drastically reduced the incidence of the disease, and it would be declared eliminated in the country by 2000. That was reversed in 2011 when the United States had 220 reported cases and since then the measles continue to have pockets of outbreaks every year. In 2020 the United States had 13 reported cases, in 2019 it was 31 cases which was the highest since 1992. That there continue to be outbreaks is concerning.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᶜᵒᵐᵇⁱⁿᵃᵗⁱᵒⁿ ⱽᵃᶜᶜⁱⁿᵉˢ: ᴰᵀᵃᴾ, ᵀᵈᵃᵖ, ᵃⁿᵈ ᵀᵈ

Because the bacterias that create the diseases pertussis, tetanus, and diphtheria all cause harmful proteins called toxins they are able to be combined into one vaccine and addressing three infectious diseases in one.

The vaccine components include diphtheria and tetanus toxoids and either killed whole cells of the bacterium that causes pertussis or pertussis antigens. DTaP and Tdap are both combination vaccines. The lower-case "d" and "p" indicate smaller concentrations of diphtheria toxoids and pertussis antigens, and "a" in "ap/aP" indicates that the pertussis toxoids are acellular.

The DTaP and Tdap vaccines both protect against three bacterial infections: diphtheria, tetanus and pertussis, whereas the Td vaccine only protects against diphtheria and tetanus. In addition, the vaccines vary in terms of who should receive them and the quantities of vaccine proteins they contain:

𝙳𝚃𝚊𝙿: The DTaP vaccine is given to infants and young children in a series of five shots ─ at 2 months, 4 months, 6 months, 15 to 18 months, and again at 4 to 6 years of age.

𝚃𝚍𝚊𝚙: The Tdap vaccine is different from the DTaP vaccine because it contains lesser quantities of diphtheria and pertussis proteins. For this reason, Tdap is much less likely than DTaP to cause side effects such as pain, redness and tenderness in adolescents and adults. The Tdap vaccine is recommended for most people 11 years and older who have not previously received it. People due for a tetanus booster and those with a wound that warrants tetanus vaccination can get Tdap or Td vaccine.

𝚃𝚍: The Td vaccine is the one people commonly think of when they think of getting their tetanus booster. Like Tdap, it contains lesser quantities of diphtheria protein to reduce the occurrence of side effects in adults. Adults should get a dose of Tdap or Td every 10 years as well as if they have a wound that warrants tetanus vaccination.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᴰⁱᵖʰᵗʰᵉʳⁱᵃ

Diphtheria can be caused by one of several strains of bacteria called Corynebacterium diphtheria (C. diphtheria). The bacteria that causes diphtheria is spread when someone inhales droplets from an infected person's cough or sneeze. It affects the mucous membranes of the throat and nose.

Once you’re infected, the bacteria release dangerous substances called toxins. The toxins spread through your bloodstream and often cause a thick, gray coating to form in these areas of the body: nose, throat, tongue, and airway. In some cases, these toxins can also damage other organs, including the heart, brain, and kidneys. This can lead to potentially life-threatening complications, such as: myocarditis (inflammation of the heart muscle), paralysis, and/or kidney failure.

After someone is exposed to diphtheria bacteria and becomes infected, the respiratory symptoms usually appear within two to five days, though the incubation period may be up to 10 days. Diphtheria infection can start out similarly to a normal respiratory infection. At first, symptoms may be mild. However, if the infection is not diagnosed and treated, severe complications can develop. The general symptoms of diphtheria include:

▪️Fever and chills

▪️Sore throat

▪️Runny nose

▪️Swollen glands in the neck ("bull's neck" appearance)

▪️Fatigue and feeling weak

▪️Wheezing and difficulty breathing

▪️Hoarseness and difficulty talking

▪️Racing heart (tachycardia)

▪️Nausea and vomiting (more common in children)

One of the hallmark features of diphtheria is the formation of a thick, hard, gray-colored coating (pseudomembrane) lining the throat. It may coat the tonsils, the nose, and other membranes in the respiratory tract. As the membrane builds up and thickens, it can make it difficult to breathe. When trying to remove or scrape off the membrane, bleeding of the tissue will occur. The membrane is highly infectious and filled with diphtheria toxin. Not only does this mean it can spread the infection, but it can also make the person with diphtheria very ill if the toxin spreads through the body.

Cutaneous diphtheria is another type of diphtheria infection, which is less common, that affects the skin. Cutaneous diphtheria is usually less severe than respiratory diphtheria. At first, the skin infections may appear very similar to other chronic conditions like eczema or psoriasis. Symptoms of cutaneous diphtheria include:

▪️Scaly rash

▪️Ulcers

▪️Secondary wound infections

Timely and accurate diagnosis is critical, as skin lesions caused by diphtheria bacterium are highly contagious, and the ease with which they shed makes the spread of the disease more likely.

Approximately 20% to 40% of people with diphtheria infection of the skin may develop the respiratory infection as well. Diphtheria infection is far more serious when it infects the mucous membranes of the respiratory tract, such as the nose, throat, and lungs.

Diphtheria is a serious condition, so your doctor will want to treat you quickly and aggressively.

The first step of treatment is an antitoxin injection. This is used to counteract the toxin produced by the bacteria. Your doctor will also prescribe antibiotics, such as erythromycin or penicillin, to help clear up the infection.

During treatment, your doctor may have you stay in the hospital so you can avoid passing your infection on to others. They may also prescribe antibiotics for those close to you.

Someone who has been severely ill from diphtheria may have a very long recovery and need to limit their activities to prevent complications. Once a person has recovered from diphtheria, they are required to get the vaccine, as getting sick with diphtheria does not make a person immune to the infection for the rest of her or his life.

1613 in Spain was known as “El Año de los Garotillos” (“strangulations”) for its epidemic of diphtheria. Since this disease wasn't named yet it was called by several names. In 1659 a Boston minister referred to it as Malady of Bladders in the Windpipe.

A terrifying diphtheria epidemic swept through New England in 1735. In some cases, entire families died of the disease. In one New Hampshire town, 32% of children under 10 died of diphtheria. The case-fatality ratio was almost 40%. There was no treatment proving successful in curing diphtheria.

The disease finally earned the name we now know it as in 1826 when French physician Pierre Bretonneau called it diphtérite. The origin was the Greek word for “leather” or “hide,” which describes the coating that appears in the throat. Bretonneau also distinguished diphtheria from scarlet fever, which until then there had been a lot of confusion about.

To relieve troubles breathing Dr. Bretonneau experimented with tracheotomy as a way to open the airway. This became another treatment method tried and at one point another physician, Armand Trousseau, reported about a 25% survival rate in the tracheotomies he performed on diphtheria sufferers.

Diphtheria was proving hard to understand and treat.

A small breakthrough happened in 1888 when scientists Émile Roux and Alexandre Yersin showed that a substance produced by C. diphtheriae caused symptoms of diphtheria in animals. Building on that find Shibasaburo Kitasato and Emil von Behring created a heat-treated diphtheria toxin in 1890 and studies showed it to be successful. They called the substance antitoxin and their treatment serum therapy.

Finally, there was some momentum building toward curing this awful disease.

In October 1894, two young Cincinnati physicians treated a two-year-old girl successfully with diphtheria antitoxin. This is one of the earliest documented uses of diphtheria antitoxin in the United States.

Until 1895 diphtheria antitoxin could only be procured outside of the United States. So in 1895, after some successful treatments were documented, Mulford Company of Philadelphia (later Merck Sharp & Dohme) began to produce and test diphtheria antitoxin in the United States.

The New York City Health Department began producing diphtheria antitoxin this year as well. Deaths from the disease began to drop as the treatment was increasingly used.

A first step in producing diphtheria antitoxin involved incubating the bacteria and then determining which samples were of adequate strength to produce antitoxin.

In 1907, Emil von Behring published a paper showing that a mixture of diphtheria toxin and antitoxin produced safe and lasting immunity to diphtheria in humans. The combination of toxin and antitoxin needed to be carefully balanced to provide enough toxin to elicit active immunity and the right amount of antitoxin to prevent the toxin from causing disease.

In 1914, William Park took Behring's work further by adjusting the amounts of the substances until he achieved a balance between lasting immunity and reactions to the mixture. This method was used for immunizing humans until toxoid immunization replaced it.

Working independently from one another, scientists Gaston Ramon and Alexander Thomas Glenny both developed diphtheria toxoid in 1923. It was able to induce antibodies that blocked natural toxin from attaching to cells. This breakthrough provided the simplest and most effective means to prevent diphtheria.

In 1926, Glenny increased the effectiveness of diphtheria toxoid by treating it with aluminum salts. Efforts to improve diphtheria toxoid were necessary because toxoid alone produced a lower level of antibody response than desired. Moreover, the immunity it produced was shorter than desired. Glenny began to add substances to the toxoid to trigger such a response. Today those substances are called adjuvants, and they are used in several types of vaccines.

Respiratory diphtheria has almost disappeared in the United States. Since 2004, the CDC has recorded no cases of respiratory diphtheria in the United States.

Diphtheria is now vaccinated against in a combination vaccine that addresses tetanus, pertussis, and diphtheria.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᵀᵉᵗᵃⁿᵘˢ

Tetanus is a disease that is spread by contact with an object or surface that has been contaminated with Clostridium tetani.

Clostridium tetani is an anaerobic bacterium, meaning that it cannot live or grow where oxygen is present. When exposed to air, the bacterium will form a protective spore which allows it to remain in a dormant state, largely impervious to heat, dryness, ultraviolet radiation, or household disinfectants.

The spores can remain viable for years in soil and be reactivated when it is returned to a favorable moist environment. One such environment is a deep puncture wound in which the reactivated bacteria is able to establish an infection.

Once in the body, tetanus will release toxins—known as tetanospasmin toxins—that bind to nerve cells. The toxins will then spread through peripheral nerves until they finally reach the central nervous system (the brain and spinal cord). As the bacteria multiply and amplify this effect, the tetanospasmin toxins will begin to block the production of certain chemical messengers, known as neurotransmitters, that control voluntary muscle movement.

In terms of toxicity, tetanospasmin toxin is the second deadliest bacterial neurotoxin next to the botulinum toxin found in Botox.

In addition to generalized tetanus, there are other, less common forms of the disease.

▪️Local tetanus only affects the muscles around the immediate area of infection.

▪️Cephalic tetanus is limited only to the muscles of the head.

▪️Neonatal tetanus involves newborns of mothers who have not been vaccinated for tetanus. Because the baby has no inborn immunity to C. tetani, it is vulnerable to infection, most often as a result of an infected umbilical stump. While rare in the developed world, neonatal tetanus is the second leading cause of vaccine-preventable diseases among children worldwide.

Tetanus occurs almost exclusively in people who have not been vaccinated against C. tetani. If left untreated, a tetanus infection can progress from mild spasms to powerful whole-body contractions, suffocation, and heart attack. There is no cure for tetanus. The treatment of tetanus is based on vaccination status.

During the 1890s, the combined work of Shibasaburo Kitasato, Emil von Bering, and Edmond Nocard demonstrated that tetanus antitoxin had both protective and immunizing effects against tetanus toxins. In the early 1900s, medical organizations were reporting that untreated tetanus killed up to 85% of those infected.

World War I was instrumental in the effort to find a way to treat tetanus. Much of the fighting occurred in fields, where wounds were constantly exposed to tetanus spores. Further, the explosive power of modern weapons drove dirt and shrapnel deep into wounded tissue, where conditions are conducive to the bacterium’s growth.

Desperate to avoid tetanus’s enormous fatality rate, military doctors invested heavily in the new serum therapy. They used antitoxin for both prevention and treatment, experimenting with the size and number of doses which led to serum sickness in hundreds of soldiers. However, tetanus antitoxin is credited with saving hundreds of thousands of lives during the war.

A vaccine to prevent tetanus – tetanus toxoid – was introduced in 1924. Tetanus toxoid is an inactivated form of the toxin; it teaches the body to recognize and produce antibodies against the toxin, but is not able to damage the body itself. Yet, the vaccine was not frequently used until World War II, when it became one of the routine vaccinations given to all American soldiers.

On the heels of the war, vaccination with tetanus toxoid became common for all Americans. Routine vaccination has ensured that death from tetanus is rare in the United States. However, a vaccination booster must be repeated every ten years to keep that immunity. People who do contract tetanus may be treated with a modern form of antitoxin, tetanus immune globulin.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᵂʰᵒᵒᵖⁱⁿᵍ ᶜᵒᵘᵍʰ ⁽ᴾᵉʳᵗᵘˢˢⁱˢ⁾

Whooping cough is caused by a type of bacteria called Bordetella pertussis. It is a HIGHLY contagious respiratory tract infection. When an infected person coughs or sneezes, tiny germ-laden droplets are sprayed into the air and breathed into the lungs of anyone who happens to be nearby. In many people, it's marked by a severe hacking cough followed by a high-pitched intake of breath that sounds like "whoop."

The disease usually starts with cold-like symptoms and maybe a mild cough or fever. In babies, the cough can be minimal or not even there. Babies may have a symptom known as “apnea.” Apnea is a pause in breathing pattern. Pertussis is most dangerous for babies. About half of babies younger than 1 year who get the disease need care in the hospital.

Early symptoms can last for 1-2 weeks and usually include:

▪️Runny nose

▪️Low-grade fever

▪️Mild, occasional cough

▪️Apnea (in babies)

Pertussis in its early stages appears to be nothing more than the common cold. Therefore, healthcare professionals often do not suspect or diagnose it until the more severe symptoms appear.

After 1-2 weeks and as the disease progresses, the traditional symptoms of pertussis may appear and include:

▪️Paroxysms (fits) of many, rapid coughs followed by a high-pitched “whoop” sound

▪️Vomiting during or after coughing fits

▪️Exhaustion after coughing fits

Healthcare providers generally treat pertussis with antibiotics and early treatment is very important. Treatment may make your infection less serious if you start it early, before coughing fits begin.

Who is at risk for whooping cough? It turns out EVERYONE is! The whooping cough vaccine you receive as a child eventually wears off. This leaves most teenagers and adults susceptible to the infection during an outbreak — and there continue to be regular outbreaks. Infants who are younger than age 12 months who are unvaccinated or haven't received the full set of recommended vaccines have the highest risk for severe complications and death.

In 1578 there was an epidemic of pertussis in Paris. Guillaume De Baillou referred to it as “quinte,” which was a common name for the disease that was circulating. De Baillou suggested the name might have to do with the sound of the characteristic “whoop” cough.

Pertussis remained unnamed and unexplored until 1900. Scientists Jules Bordet and Octave Gengou observed the causative agent of pertussis, Bordetella pertussis. In 1906 they succeeded in isolating the bacteria for further study. In 1912 the same scientists attempted a vaccine from killed whole-cell B. pertussis preparations but it was not effective.

In 1925 Thorvald Madsen, a Danish physician, tested his pertussis vaccine in children in the Faroe Islands. The vaccine seemed to provide protection against disease. But in 1933 Madsen released a report that he believed two of the children had died as a result of potential reactions to the vaccine.

Finally, in 1939 it was girl power for the win! American bacteriologist Pearl Kendrick, PhD, and her colleague Grace Elderding, PhD demonstrated the effectiveness of a vaccine when compared with a control group that did not receive the vaccine: the annual attack rates per 100 children were 2.3 in the vaccinated group and 15.1 in the control group, respectively, with no deaths in either group. In addition, the disease was milder in the group that had been vaccinated.

In 1948 a combined vaccine for diphtheria, tetanus, and pertussis became available in the United States. This type of combined shot used a whole-cell pertussis vaccine; decades later, in the mid-1990s, the whole-cell vaccine would be replaced with an acellular version that resulted in fewer adverse reactions.

Immunity from the vaccine tends to wane by age 11 so a booster shot is needed as is for pregnant women between 27 and 36 weeks for every single pregnancy. Some varieties of the every-10-year tetanus and diphtheria vaccine also include protection against whooping cough. This vaccine will also reduce the risk of you transmitting whooping cough to infants.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᵀʸᵖʰᵒⁱᵈ ᶠᵉᵛᵉʳ

Typhoid fever is caused by Salmonella typhi bacteria. Salmonella typhi is related to the bacteria that cause salmonellosis, another serious intestinal infection, but they aren't the same.

Typhoid fever is a serious worldwide threat and affects about 27 million or more people each year. It is rare in developed countries and still a serious health threat in the developing world, especially for children.

Contaminated food and water or close contact with an infected person cause typhoid fever. Salmonella typhi is passed in the feces and sometimes in the urine of infected people. If you eat food that has been handled by someone who has typhoid fever and who hasn't washed carefully after using the toilet, you can become infected. In developing countries, where typhoid fever is established, most people become infected by drinking contaminated water. The bacteria may also spread through contaminated food and through direct contact with someone who is infected.

Signs and symptoms are likely to develop gradually — often appearing one to three weeks after exposure to the disease. Early illness signs and symptoms include:

▪️Fever that starts low and increases daily, possibly reaching as high as 104.9 F

▪️Headache

▪️Weakness and fatigue

▪️Muscle aches

▪️Sweating

▪️Dry cough

▪️Loss of appetite and weight loss

▪️Stomach pain

▪️Diarrhea or constipation

▪️Rash

▪️Extremely swollen stomach

Without treatment, you may:

▪️Become delirious

▪️Lie motionless and exhausted with your eyes half-closed in what's known as the typhoid state

▪️Life-threatening complications often develop at this time.

Most people who have typhoid fever feel better a few days after they start antibiotic treatment, but a small number of them may die of complications. Vaccines against typhoid fever are only partially effective. Vaccines usually are reserved for those who may be exposed to the disease or who are traveling to areas where typhoid fever is common.

Henry Prince of Wales, the oldest son of King James I, died at age 18 in 1612 after a “short illness” which was not identified or described other than as a fever. In 1882, Norman Moore, MD, based on his studies of the autopsy on the prince as well as detailed descriptions of the illness, alleged that the prince had died of typhoid fever. If he was correct (today it is generally assumed that he was) this would have been the earliest English case of typhoid fever on record.

Fast forward to 1896 when finally there was momentum on typhoid treatment. Richard Pfeiffer and Wilhelm Kolle demonstrated that inoculation with killed typhoid bacteria resulted in human immunity against typhoid fever. Almroth E. Wright published a paper a few months later in 1897, in which he described a similar finding.

U.S. Army physician Frederick F. Russell developed the first U.S. typhoid fever vaccine in 1909. In 1914 Almroth E. Wright developed an effective typhoid vaccine as well.

Early forms of the typhoid vaccine were used by the British Army in 1899 during the Second Boer War in southern Africa. Nearly 15,000 soldiers were immunized; among these men, there were approximately 11 cases of typhoid fever per 1,000 soldiers. In contrast, unimmunized soldiers saw approximately 31 cases of typhoid fever per 1,000 men.

Typhoid vaccination would become an important part of military life. Mandatory typhoid vaccination for a division of 15,000 men in the United States Army began in 1911, with the mandate expanded to include all soldiers only a few months later.

By 1914, typhoid vaccination had moved beyond military forces in the United States and into use for the general public, specifically for those traveling.

Two typhoid vaccines are licensed for use in the United States. The Ty21a is a live, attenuated vaccine given in oral capsule form. Vi capsular polysaccharide (ViCPS) is an injected subunit vaccine. These are typically reserved for people traveling to areas where typhoid fever is common or for people who may come into direct contact with the disease.

We can't talk about Typhoid without talking about Mary Mallon, or Typhoid Mary as she is better known. Mary Mallon was an asymptomatic carrier of Typhoid.

Mallon, an Irish immigrant who worked as a cook for wealthy New York families, first gained the attention of public health officials in 1906. A Long Island family for whom Mallon had worked as a cook had fallen ill with typhoid fever. Though Mallon was no longer with the family, officials trying to locate her discovered that other families she’d worked for had also developed typhoid fever. In one outbreak at a household of nine in Dark Harbor, Maine, in 1902, Mallon and Mr. Coleman Drayton, head of the household, were the only two not to fall ill (Drayton had contracted typhoid fever years before).

In 1907, Mallon was detained by the New York City Department of Health for three years, first at a hospital for contagious diseases in Manhattan, and then at Riverside Hospital on North Brother’s Island in the East River to be kept in isolation. She was released in 1910 under the conditions that she would no longer work as a cook and would take steps to prevent spreading typhoid.

In 1915, however, Mallon was caught once again working as a cook (this time under the assumed name Mary Brown) after infecting 25 people with typhoid, one of whom died. Mallon was eventually sent back to North Brother Island and remained there for the next 23 years until her death in 1938.

At the time of her death in 1938, she was officially blamed for 10 outbreaks totaling 51 cases of typhoid fever, and three deaths from the disease.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ʸᵉˡˡᵒʷ ᶠᵉᵛᵉʳ

Yellow fever virus is an RNA virus that belongs to the genus Flavivirus. Yellow fever virus is transmitted to people primarily through the bite of infected Aedes or Haemagogus species mosquitoes. Mosquitoes acquire the virus by feeding on infected primates (human or non-human) and then can transmit the virus to other primates (human or non-human).

It is found in tropical and subtropical areas of Africa and South America. Yellow fever is a very rare cause of illness in U.S. travelers. It is diagnosed based on laboratory testing, a person’s symptoms, and travel history. There is no medicine to treat or cure infection.

The majority of people infected with yellow fever virus will either not have symptoms, or have mild symptoms and completely recover.

For people who develop symptoms, the time from infection until illness is typically 3 to 6 days. Initial symptoms include:

▪️Sudden onset of fever

▪️Chills

▪️Severe headache

▪️Back pain

▪️General body aches

▪️Nausea

▪️Vomiting

▪️Fatigue

▪️Weakness

▪️Most people with the initial symptoms improve within one week.

For some people who recover, weakness and fatigue (feeling tired) might last several months.

Severe symptoms include:

▪️High fever

▪️Jaundice

▪️Bleeding

▪️Shock

▪️Organ failure

Severe yellow fever disease can be deadly. Among those who develop severe disease, 30-60% die.

The most effective way to prevent infection from Yellow Fever virus is to prevent mosquito bites. Mosquitoes bite during the day and night. Use insect repellent, wear long-sleeved shirts and pants, treat clothing and gear, and get vaccinated before traveling, if vaccination is recommended for you.

Prior to 1741 doctors referred to the disease, and others that were similar to it, by a variety of names, such as pestilential fever, malignant fever, putrid bilious fever, and the like. Then the term yellow fever began to be used. The name comes from the yellowed appearance of the skin and eyes that results from damage to the liver: toxic materials build up in the blood and cause the tell-tale color to appear.

During the 1793 Yellow fever epidemic in Philadelphia Dr. Benjamin Rush observed the symptoms and spread of the disease closely, hoping to uncover some definite cause and means of prevention. Rush, however, did not seem to draw any conclusions about the presence of the mosquitoes in relation to yellow fever. He favored the “miasma” theory of the disease—literally “pollution”—which was widely accepted in Philadelphia at the time.

Yellow fever killed more than 13,000 people in the lower Mississippi Valley in 1878. At the time, it was one of the worst medical disasters in U.S. history. Marine Hospital Service Surgeon General John Woodworth reported to Congress that “Yellow fever should be dealt with as an enemy which imperils life and cripples commerce and industry.”

Spurred by the massive yellow fever-related casualties in the Spanish-American War, members of the U.S. Army Yellow Fever Commission, headed by Walter Reed, traveled to Cuba to study the disease in 1900. The Commission was successful with Jesse Lazear even giving his life toward the pursuit of an answer. It was determined that it was, in fact, caused through the transmission of mosquito bites.

Following this finding, efforts began to reduce and remove the mosquito population in areas where the disease was most evident. Workers drained or covered open water containers and fumigated areas to kill adult mosquitoes. Yellow fever cases began to drop, and reports of malaria dropped as well.

Due to the discovery that infected mosquitos were the culprits and there were preventative measures that could be taken, the last yellow fever epidemic on the North American continent occurred in 1905. But the need for a vaccine existed in other continents.

It wasn't until 1931 that a Yellow fever vaccine started to gain some traction. Max Theiler demonstrated that mice injected with serum from previously infected monkeys or humans were protected from yellow fever infection.

And finally, in 1936 Theiler and his colleagues successfully developed a live attenuated vaccine for yellow fever using tissue cultures prepared from embryonated chicken eggs. Among the many subcultures of the yellow fever virus in the laboratory, the one designated “17D” was used, giving the vaccine its name. He published results of U.S. vaccine trials in humans in 1937. The vaccine was easily adapted for mass production and became the universal standard.

Although the 17D yellow fever vaccine is highly effective, vaccination rates in at-risk regions remain lower than is necessary to prevent outbreaks. The World Health Organization warns that epidemics in unvaccinated populations can result in case-fatality ratios of more than 50%. WHO encourages both mass immunization efforts and routine infant immunization, as well as vaccination for travelers to countries where the disease is endemic. American travelers are required by WHO International Health Regulations to receive a yellow fever vaccination before visiting some countries in tropical South America and sub-Saharan Africa.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᶜʰᵒˡᵉʳᵃ

A bacterium called Vibrio cholerae causes cholera infection. The deadly effects of the disease are the result of a toxin the bacteria produces in the small intestine. The toxin causes the body to secrete enormous amounts of water, leading to diarrhea and a rapid loss of fluids and salts (electrolytes).

Cholera bacteria might not cause illness in all people who are exposed to them, but they still pass the bacteria in their stool, which can contaminate food and water supplies.

Contaminated water supplies are the main source of cholera infection. The bacterium can be found in:

▪️Surface or well water.

▪️Seafood.

▪️Raw fruits and vegetables. Raw, unpeeled fruits and vegetables are a frequent source of cholera infection in areas where uncomposted manure fertilizers or irrigation water containing raw sewage can contaminate produce in the field.

▪️Grains. In regions where cholera is widespread, grains that are contaminated after cooking and kept at room temperature for several hours can grow cholera bacteria.

Everyone is susceptible to cholera, with the exception of infants who get immunity from nursing mothers who have previously had cholera. Still, certain factors can make you more vulnerable to the disease or more likely to have severe signs and symptoms.

Risk factors for cholera include:

▪️Poor sanitary conditions.

▪️Reduced or nonexistent stomach acid.

▪️Household exposure. You're at increased risk of cholera if you live with someone who has the disease.

▪️Type O blood. For reasons that aren't entirely clear, people with type O blood are twice as likely to develop cholera compared with people with other blood types.

▪️Raw or undercooked shellfish.

Although shock and severe dehydration are the worst complications of cholera, other problems can occur, such as:

▪️Low blood sugar

▪️Low potassium levels

▪️Kidney failure

Cholera can quickly become fatal. In the most severe cases, the rapid loss of large amounts of fluids and electrolytes can lead to death within hours. In less extreme situations, people who don't receive treatment can die of dehydration and shock hours to days after cholera symptoms first appear.

In 1849, English doctor John Snow proposed that cholera was spread by contaminated water. He rejected the commonly held idea that “bad air,” or miasma, was responsible for cholera. Rather, based on his careful examination of a London outbreak, he suggested that the disease occurred when people ingested certain tiny particles in water.

In 1854, Italian physician Filippo Pacini linked the cholera bacterium to the disease itself. Pacini microscopically observed samples from the intestines of cholera victims and noted the presence of tiny, comma-shaped particles that he suggested were the cause of the disease. He suggested that the cholera vibrio acted on the lining of the intestine to cause massive fluid and electrolyte loss, and he suggested that cholera patients be treated with intravenous injections of water to which salt had been added. Though most of his ideas have been shown to be correct, the scientific world largely ignored his work during his lifetime.

In 1885, Spanish physician Jaime Ferrán developed a live, attenuated cholera vaccine. His vaccine was the first to immunize humans against a bacterial disease. He created the vaccine by cultivating bacteria taken from the waste of a person ill with cholera and growing the bacteria on nutrient culture at room temperature. The material was then administered to subjects via one to three injections in the arm. During the rest of his career, Ferrán would develop vaccines for plague, tetanus, typhus, tuberculosis, and rabies.

In 1896, Wilhelm Kolle developed a heat-inactivated cholera vaccine that came to serve as a model for cholera vaccines for the next century.

In 1927, Alexandre Besredka developed a vaccine for cholera known as a bilivaccine, which used bile salts. It was the first oral vaccine developed. Besredka’s bilivaccine was given in doses on three successive days and consisted of a bile tablet followed by a tablet containing cholera vibrios.

In the United States, an oral cholera vaccine (Vaxchora®) is approved for adults age 18-64 traveling to cholera-afflicted areas. Other cholera vaccines are currently in the development pipeline.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᴿᵃᵇⁱᵉˢ

Rabies is a deadly virus spread to people from the saliva of infected animals. The rabies virus is usually transmitted through a bite. In rare cases, rabies can be spread when infected saliva gets into an open wound or the mucous membranes, such as the mouth or eyes. This could occur if an infected animal were to lick an open cut on your skin.

Any mammal can transmit the rabies virus. The animals most likely to transmit the rabies virus to people include: Cats, Cows, Dogs, Ferrets, Goats, Horses, Bats, Beavers, Coyotes, Foxes, Monkeys, Raccoons, Skunks, Woodchucks.

To reduce your risk of coming in contact with rabid animals:

▪️Vaccinate your pets.

▪️Keep your pets confined.

▪️Protect small pets from predators.

▪️Report stray animals to local authorities.

▪️Don't approach wild animals.

▪️Keep bats out of your home.

▪️Consider the rabies vaccine if you're traveling. If you're traveling to a country where rabies is common and you'll be there for an extended period of time, ask your doctor whether you should receive the rabies vaccine. This includes traveling to remote areas where medical care is difficult to find.

Despite being rare in the United States, rabies remains a frightening prospect due to the speed neurological symptoms can develop and progress.

This type of virus, known the lyssavirus, moves through the network of nerve cells, causing progressive symptoms as it gradually infiltrates the brain and central nervous system. That's why, unlike some infectious diseases, you cannot wait for signs of the illness to appear. You must seek treatment the moment you come you are bitten or scratched by an animal that has or is suspected to have rabies.

The symptoms of rabies can be characterized by the stages of infection, broadly described as the incubation period, the prodromal period, the acute neurologic period, and coma preceding death.

The incubation period is the time between exposure to the virus and the first appearance of symptoms. Symptoms of rabies during the incubation period may include:

▪️Fever

▪️Headache

▪️Tingling or burning sensation at the site of the exposure (known as paresthesia)

The prodromal period is described by the first appearance of symptoms. This is when the virus first enters the central nervous system and begins to cause damage.

The prodromal phase tends to run from two to 10 days on average and may cause such symptoms as:

▪️Fatigue

▪️A general feeling of unwellness

▪️Loss of appetite

▪️A sore, swollen throat

▪️Nausea

▪️Vomiting

▪️Diarrhea

▪️Agitation

▪️Insomnia

▪️Anxiety and depression

The acute neurologic period lasts anywhere from two to ten days and will almost invariably end in death. The types and characteristics of symptoms can vary, depending largely on how severe or mild the initial exposure was.

Symptoms of rabies occurring during the acute neurologic period may include:

▪️Hyperactivity

▪️Excessive salivation

▪️Hydrophobia

▪️Priapism

▪️Extreme sensitivity to light

▪️Paranoia

▪️Confusion and incoherence

▪️Aggression

▪️Hallucinations

▪️Seizures

▪️Partial paralysis

▪️Delirium

These symptoms will soon lead to a coma as the rabies infection causes massive brain inflammation. Without intensive supportive care, death will usually occur within hours or days.

There are three types of rabies that can be contracted.

(1) 𝙁𝙪𝙧𝙞𝙤𝙪𝙨 𝙧𝙖𝙗𝙞𝙚𝙨 is the type most people with experience. As its name suggests, this form of rabies is characterized by violent physical and neurologic symptoms. Symptoms may come and go, and will often be interspersed with moments of calm and lucidity. Death will most often be caused by cardio-respiratory arrest.

(2) 𝙋𝙖𝙧𝙖𝙡𝙮𝙩𝙞𝙘 𝙧𝙖𝙗𝙞𝙚𝙨 affects up to 20% of people and will cause muscles to gradually weaken, starting from the site of the exposure and expanding outward. Paralysis and death will eventually ensue (usually by respiratory failure). Most paralytic cases are believed to be caused by a minor injury, such as a nip, that has gone unnoticed.

(3) 𝘼𝙩𝙮𝙥𝙞𝙘𝙖𝙡 𝙧𝙖𝙗𝙞𝙚𝙨 is a type most often associated with bat bites. It may involve symptoms from both furious and paralytic forms of the disease. The variations in symptoms and severity can often make it hard to recognize a case as rabies.

In 1831 a schoolboy in Arbois, France, observed first hand a rabies outbreak spread by the bites of rabid animals. He never forgot that. His name? Louis Pasteur.

Fast forward to 1880. Pasteur had successfully created the first laboratory-created vaccine and he started studying rabies in earnest. One of the difficulties with studying rabies is that the time between introduction of the infectious agent and signs of the disease varies greatly. Pasteur was able to advance his studies by shortening this period: first, he selected for the most lethal, fast-acting strains of the virus, and, second, he injected infectious material directly into rabbit brains (in the wild, the virus is introduced via a bite and travels slowly up a nerve to the brain).

In 1884 Pasteur was able to successfully use a series of less-attenuated vaccines over several days to prevent rabies in dogs that had been infected. The work was dangerous: he and his assistants often had to handle the rabid animals and take samples from them.

In July 1885, he successfully prevented rabies in 9 year old Joseph Meister by post-exposure vaccination. And in October of that same year Pasteur successfully repeated his rabies vaccinations on a shepherd who had been severely bitten by a rabid dog. After Pasteur published word of the success, people fearing rabies from animal bites began to seek him out for the series of vaccinations.

It wasn't until 1946 that Pasteur's rabies vaccine was looked at again. Physician Hilary Koprowski adapted a rabies virus strain in chick embryos. He hoped to avoid using nervous system tissue as a medium for cultivating rabies virus because vaccine containing such tissue could cause serious side effects, such as encephalitis.

Additionally, Koprowski wanted to improve upon the immunogenicity of the older vaccines and to create a vaccine that would not result in as many vaccine failures as the older vaccines.

His new strain was successful and he called it HEP (for high-egg passage), as he continued to work on a new rabies vaccine.

In 1961, scientists tested different live virus preparations of Koprowski’s HEP rabies vaccine virus in animal and human trials. Most studies showed adequate antibody response and minimal side effects.

Jump forward to 1971. Koprowski’s team of scientists wanted to improve on the antibody response created by the experimental HEP live-virus vaccines. They looked to a cell line created from human embryonic cells as a medium for cultivating the rabies virus. Their initial tests successfully used live vaccine virus, as had the previous HEP tests. But medical resistance was strong to using a live virus rabies vaccine. The risk for inadvertent infection with a fatal illness was seen to be too high. Accordingly, Koprowski’s team used a chemical disinfectant to inactivate their rabies vaccine virus.

The rabies vaccine produced by Koprowski’s team at the Wistar Institute, called HDCV (human diploid cell vaccine), was licensed in Europe in 1976 and in the United States in 1980. One of its principal advantages was that the vaccine was given in five injections rather than the course of 14-21 injections used in the older vaccines.

HDCV is still widely used, but it is expensive to produce. Other rabies vaccines containing viruses grown in other types of cell culture have been licensed in different parts of the world. A few vaccines created with nervous system tissue continue to be used in Asia, Africa, and South America.

{You can find all the sources I used by clicking here.}

Let's talk infectious diseases, the reason for vaccines: ᴬⁿᵗʰʳᵃˣ

Anthrax is a serious infectious disease caused by bacteria known as Bacillus anthracis.

Anthrax can be found naturally in soil and commonly affects domestic and wild animals around the world. Although it is rare in the United States, people can get sick with anthrax if they come in contact with infected animals or contaminated animal products. Anthrax can cause severe illness in both humans and animals.

People get infected when anthrax spores get inside the body and they “activate.” When they become active, the bacteria can multiply, spread out in the body, produce toxins, and cause severe illness. This can happen when people breathe in spores, eat food or drink water that is contaminated with spores, or get spores in a cut or scrape in the skin.

There are four types of anthrax and the type of illness a person develops depends on how anthrax enters the body. Typically, anthrax gets into the body through the skin, lungs, or gastrointestinal system. All types of anthrax can eventually spread throughout the body and cause death if they are not treated with antibiotics.

Cutaneous anthrax is the most common form of anthrax infection, and it is also considered to be the least dangerous. Without treatment, up to 20% of people with cutaneous anthrax die. However, with proper treatment, almost all patients with cutaneous anthrax survive.

Inhalation anthrax is considered to be the most deadly form of anthrax. Infection usually develops within a week after exposure, but it can take up to 2 months. Without treatment, inhalation anthrax is almost always fatal. However, with aggressive treatment, about 55% of patients survive.

When a person eats raw or undercooked meat from an animal infected with anthrax, they can develop gastrointestinal anthrax. Gastrointestinal anthrax has rarely been reported in the United States. Without treatment, more than half of patients with gastrointestinal anthrax die. However, with proper treatment, 60% of patients survive.

Recently, another type of anthrax infection has been identified in heroin-injecting drug users in northern Europe. This type of infection has never been reported in the United States.

During the 1800s, doctors saw cases of anthrax but did not yet have a diagnosis for the disease. During this time, the organism that causes anthrax had not yet been discovered, but doctors had noticed a link between the disease and the animal hair industry. Because of this, the disease became known as “wool sorters disease.”

In 1877 Robert Koch studied Bacillus anthracis, from these studies, he was able to determine the life cycle of the anthrax bacteria, and was able to demonstrate what became known as Koch’s postulates, which demonstrate a causal relationship between a specific microorganism and a disease.

Louis Pasteur took Koch’s work a step further, trying to fully prove how anthrax was spread and how it made people or animals sick. Pasteur also worked to create a vaccine for anthrax. In his experiment, Pasteur gave 25 animals two shots of an anthrax vaccine he had created with weakened anthrax bacteria. After he gave both rounds of the vaccine to these animals, he injected them with live anthrax bacteria. He also injected live bacteria into 25 other animals that had not been vaccinated. Each of the vaccinated animals survived, while the 25 that were not vaccinated died.

In the 1950s the first anthrax vaccine for humans was created. This anthrax vaccine was tested in a group of goat hair mill workers. This study determined that the vaccine was 92.5% effective in preventing cutaneous anthrax. After the study, the vaccine was made available to people working in goat hair processing mills in the United States. In 1970 an updated human anthrax vaccine was released, replacing the 1950s vaccine. This is essentially the same vaccine used today.

Anthrax Vaccine Adsorbed (AVA) protects against anthrax. It does not contain any anthrax bacteria and cannot give people anthrax. It is not typically available to the general public. It is approved for use in three groups of adults 18 to 65 years of age who may be at risk of coming in contact with anthrax because of their job. To build up protection against anthrax, these groups should get 5 shots of anthrax vaccine over 18 months. To stay protected, they should get annual boosters.

{You can find all the sources I used by clicking here.} 

Let's talk vaccines: ᴴᵉʳᵈ ᴵᵐᵐᵘⁿⁱᵗʸ

Herd immunity occurs when a large portion of a community becomes immune to a disease, making the spread of disease from person to person unlikely. As a result, the whole community becomes protected — not just those who are immune.

Often, a percentage of the population must be capable of getting a disease in order for it to spread. This is called a threshold proportion. If the proportion of the population that is immune to the disease is greater than this threshold, the spread of the disease will decline. This is known as the herd immunity threshold.

What percentage of a community needs to be immune in order to achieve herd immunity? It varies from disease to disease. The more contagious a disease is, the greater the proportion of the population that needs to be immune to the disease to stop its spread. For example, the measles is a highly contagious illness. It's estimated that 94% of the population must be immune to interrupt the chain of transmission.

There are two main paths to herd immunity — infection and vaccines.

𝙽𝚊𝚝𝚞𝚛𝚊𝚕 𝚒𝚗𝚏𝚎𝚌𝚝𝚒𝚘𝚗

Herd immunity can be reached when enough people in the population have recovered from a disease and have developed protective antibodies against future infection.

However, there are some major problems with relying on community infection to create herd immunity: reinfection and health impact.

𝚅𝚊𝚌𝚌𝚒𝚗𝚎𝚜

Herd immunity also can be reached when enough people have been vaccinated against a disease and have developed protective antibodies against future infection. Unlike the natural infection method, vaccines create immunity without causing illness or resulting complications.

Herd immunity makes it possible to protect the population from a disease, including those who can't be vaccinated, such as newborns or those who have compromised immune systems.

Herd immunity, or community immunity, as it’s sometimes called, is a powerful public health tool. By ensuring those who can be vaccinated do get vaccinated we can achieve herd immunity and prevent the illness and suffering that comes from the spread of infectious diseases.

{You can find all the sources I used by clicking here.}

Let's talk vaccines: ⱽᵃᶜᶜⁱⁿᵉ ᵀʸᵖᵉˢ

There are several different types of vaccines. Each type is designed to teach your immune system how to fight off certain kinds of germs—and the serious diseases they cause.

When scientists create vaccines, they consider:

▪️How your immune system responds to the germ

▪️Who needs to be vaccinated against the germ

▪️The best technology or approach to create the vaccine

Vaccines are generally classified as live or non-live (sometimes loosely referred to as ‘inactivated’) to distinguish those vaccines that contain attenuated replicating strains of the relevant pathogenic organism from those that contain only components of a pathogen or killed whole organisms. In addition to the ‘traditional’ live and non-live vaccines, several other platforms have been developed over the past few decades.

There are several types of vaccines, including:

▪️Inactivated vaccines

▪️Live-attenuated vaccines

▪️Messenger RNA (mRNA) vaccines

▪️Subunit, recombinant, polysaccharide, and conjugate vaccines

▪️Toxoid vaccines

▪️Viral vector vaccines

𝙸𝚗𝚊𝚌𝚝𝚒𝚟𝚊𝚝𝚎𝚍 𝚟𝚊𝚌𝚌𝚒𝚗𝚎𝚜 (𝙺𝚒𝚕𝚕𝚎𝚍 𝙰𝚗𝚝𝚒𝚐𝚎𝚗)

Inactivated vaccines use the killed version of the germ that causes a disease. They are made by making a pathogen safe for use in a vaccine by treatment with heat or chemicals. This kills the pathogen, making it incapable of replication, but still allows it to induce an immune response to at least some of the antigens contained within the organism.

Inactivated vaccines usually don’t provide immunity that’s as strong as live vaccines. So you may need several doses over time (booster shots) in order to get ongoing immunity against diseases.

Inactivated vaccines are used to protect against:

▪️Hepatitis A

▪️Flu (shot only)

▪️Polio (shot only)

▪️Rabies

𝙻𝚒𝚟𝚎-𝚊𝚝𝚝𝚎𝚗𝚞𝚊𝚝𝚎𝚍 𝚟𝚊𝚌𝚌𝚒𝚗𝚎𝚜

Live vaccines use an attenuated form of the germ that causes a disease. (Attenuated means having been reduced in force, effect, or value.) In some cases, microorganisms can be attenuated or disabled so that they lose their ability to cause significant disease (pathogenicity) but retain their capacity for transient growth within an inoculated host. Attenuation can often be achieved by growing a pathogenic bacterium or virus for prolonged periods under abnormal culture conditions.

Because these vaccines are so similar to the natural infection that they help prevent, they create a strong and long-lasting immune response. Just 1 or 2 doses of most live vaccines can give you a lifetime of protection against a germ and the disease it causes.

Live vaccines are used to protect against:

▪️Measles, mumps, rubella (MMR combined vaccine)

▪️Rotavirus

▪️Smallpox

▪️Chickenpox

▪️Yellow fever

▪️Influenza (nasal spray)

▪️Shingles

𝚂𝚞𝚋𝚞𝚗𝚒𝚝, 𝚛𝚎𝚌𝚘𝚖𝚋𝚒𝚗𝚊𝚗𝚝, 𝚙𝚘𝚕𝚢𝚜𝚊𝚌𝚌𝚑𝚊𝚛𝚒𝚍𝚎, 𝚊𝚗𝚍 𝚌𝚘𝚗𝚓𝚞𝚐𝚊𝚝𝚎 𝚟𝚊𝚌𝚌𝚒𝚗𝚎𝚜

Subunit, recombinant, polysaccharide, and conjugate vaccines use specific pieces of the germ—like its protein, sugar, or capsid (a casing around the germ).

Because these vaccines use only specific pieces of the germ, they give a very strong immune response that’s targeted to key parts of the germ. They can also be used on almost everyone who needs them, including people with weakened immune systems and long-term health problems.

One limitation of these vaccines is that you may need booster shots to get ongoing protection against diseases.

These vaccines are used to protect against:

▪️Hib (Haemophilus influenzae type b) disease

▪️Hepatitis B

▪️HPV (Human papillomavirus)

▪️Whooping cough (part of the DTaP combined vaccine)

▪️Pneumococcal disease

▪️Meningococcal disease

▪️Shingles

▪️Influenza (injection)

𝚃𝚘𝚡𝚘𝚒𝚍 𝚟𝚊𝚌𝚌𝚒𝚗𝚎𝚜

Toxoid vaccines use a toxin (harmful product) made by the germ that causes a disease. They create immunity to the parts of the germ that cause a disease instead of the germ itself. That means the immune response is targeted to the toxin instead of the whole germ.

Like some other types of vaccines, you may need booster shots to get ongoing protection against diseases.

Toxoid vaccines are used to protect against:

▪️Diphtheria

▪️Tetanus

𝚅𝚒𝚛𝚊𝚕 𝚟𝚎𝚌𝚝𝚘𝚛 𝚟𝚊𝚌𝚌𝚒𝚗𝚎𝚜

For decades, scientists studied viral vector vaccines. Some vaccines recently used for Ebola outbreaks have used viral vector technology, and a number of studies have focused on viral vector vaccines against other infectious diseases such as Zika, flu, and HIV. Scientists used this technology to make COVID-19 vaccines as well.

Viral vector vaccines use a modified version of a different virus as a vector to deliver protection. Several different viruses have been used as vectors, including influenza, vesicular stomatitis virus (VSV), measles virus, and adenovirus, which causes the common cold. Adenovirus is one of the viral vectors used in some COVID-19 vaccines being studied in clinical trials.

Viral vector vaccines are used to protect against:

▪️COVID-19

𝙼𝚎𝚜𝚜𝚎𝚗𝚐𝚎𝚛 𝚁𝙽𝙰 (𝚖𝚁𝙽𝙰) 𝚟𝚊𝚌𝚌𝚒𝚗𝚎𝚜

mRNA vaccines are a new type of vaccine to protect against infectious diseases. To trigger an immune response, many vaccines put a weakened or inactivated germ into our bodies. Not mRNA vaccines. Instead, they teach our cells how to make a protein—or even just a piece of a protein—that triggers an immune response inside our bodies. That immune response, which produces antibodies, is what protects us from getting infected if the real virus enters our bodies.

COVID-19 mRNA vaccines give instructions for our cells to make a harmless piece of what is called the “spike protein.” The spike protein is found on the surface of the virus that causes COVID-19.

Once the instructions (mRNA) are inside the muscle cells, the cells use them to make the protein piece. After the protein piece is made, the cell breaks down the instructions and gets rid of them.

Next, the cell displays the protein piece on its surface. Our immune systems recognize that the protein doesn’t belong there and begin building an immune response and making antibodies, like what happens in natural infection against COVID-19.

At the end of the process, our bodies have learned how to protect against future infection. The benefit of mRNA vaccines, like all vaccines, is those vaccinated gain this protection without ever having to risk the serious consequences of getting sick with COVID-19.

mRNA vaccines do not use the live virus that causes COVID-19.

They do not affect or interact with our DNA in any way. mRNA never enters the nucleus of the cell, which is where our DNA is kept.

The cell breaks down and gets rid of the mRNA soon after it is finished using the instructions.

Future mRNA vaccine technology may allow for one vaccine to provide protection for multiple diseases, thus decreasing the number of shots needed for protection against common vaccine-preventable diseases.

Beyond vaccines, cancer research has used mRNA to trigger the immune system to target specific cancer cells.

Scientists predict that mRNA is going to transform vaccines in the future and it already has with COVID. It's one of the reasons the vaccine was created so fast.

{You can find all the sources I used by clicking here.}

Let's talk vaccines: ᵂʰʸ ᵃʳᵉⁿ'ᵗ ᵛᵃᶜᶜⁱⁿᵉˢ ¹⁰⁰% ᵉᶠᶠᵉᶜᵗⁱᵛᵉ?

Why aren't vaccines 100% effective?

The short answer: Because nothing is.

The longer answer:

Individual immune systems are different enough that in some cases, a person’s immune system will not generate an adequate response. As a result, he or she will not be effectively protected after immunization.

That said, the effectiveness of most vaccines is high. After receiving the second dose of the MMR vaccine (measles, mumps, and rubella) or the standalone measles vaccine, 99.7% of vaccinated individuals are immune to measles. The inactivated polio vaccine offers 99% effectiveness after three doses. The varicella (chickenpox) vaccine is between 85% and 90% effective in preventing all varicella infections, but 100% effective in preventing moderate and severe chicken pox.

In every single article, every single piece of literature I read - and it has been A LOT - there hasn't yet been a claim that any vaccine is 100% effective. The claim that has been made is that vaccines are our best chance against either never contracting an infectious disease at all or contracting only a mild case.

It's worth noting that natural infection also does not provide 100% protection.

{You can find all the sources I used by clicking here.} 

Let's talk vaccines: ᴬⁿᵗⁱᵇᵒᵈⁱᵉˢ ᶠʳᵒᵐ ⁱⁿᶠᵉᶜᵗⁱᵒⁿ ᵃⁿᵈ ᶠʳᵒᵐ ᵛᵃᶜᶜⁱⁿᵃᵗⁱᵒⁿ

Is there a difference between the antibodies created through natural infection and the antibodies created in response to a vaccine? 

Even though antibodies are important for eliminating and preventing many kinds of infections, not all antibodies the body produces against a virus are effective.

Different B cells in the body will produce multiple different antibodies that bind to different sites on the body. But only binding to some of these sites will actually inactivate the virus. For a vaccine to work, it must produce a neutralizing antibody.

When you develop antibodies through natural infection, your immune system goes through this process of identifying the virus and eventually making effective antibodies. Your B cells make antibodies to different parts of the virus, some of which are effective and some of which are not. These help you eliminate the virus and recover. Hopefully, some of these antibodies also help protect you from future infection.

The process of vaccination allows the formation of the memory B cells, just like they do in natural infection. If you are ever exposed to the virus, these B cells go into action right away and release antibodies that can target the virus. They inactivate the virus before you get sick. Or, in some cases, you might get sick but with a much milder case.

For the most part, the antibodies that you form from getting vaccinated are the same kind of antibodies you would get from a natural infection. One difference is that certain types of vaccines only show the immune system part of the relevant virus. Because of that, the immune system doesn’t form as many different types of antibodies as it would in the course of a natural infection.

However, this doesn’t mean that the antibodies formed are any less effective than those formed in a natural infection. And getting vaccinated gives your immune system a head start over potential infection down the road.

{You can find all the sources I used by clicking here.} 

Let's talk vaccines: ᴼⁿᵉ ˢʰᵒᵗ, ᵐᵘˡᵗⁱᵖˡᵉ ᵈᵒˢᵉˢ, ᵃⁿᵈ ᵇᵒᵒˢᵗᵉʳˢ

So, what's up with the multiple doses and/or booster shots needed? It depends on the disease, the kind of vaccine, and the kind of antibodies created.

Let's first look at the reasons why we might need to receive multiple doses of a vaccine.

▪️For some vaccines (primarily inactivated vaccines), the first dose does not provide as much immunity as possible. So, more than one dose is needed to build more complete immunity. The vaccine that protects against the bacteria Hib, which causes meningitis, is a good example.

▪️For some vaccines (primarily live vaccines), studies have shown that more than one dose is needed for everyone to develop the best immune response. For example, after one dose of the MMR vaccine, some people may not develop enough antibodies to fight off infection. The second dose helps make sure that almost everyone is protected.

▪️In the case of flu vaccines, adults and children (6 months and older) need to get a dose every year because the flu viruses causing disease may be different from season to season. Every year, flu vaccines are made to protect against the viruses that research suggests will be most common. This is the only vaccine, to date, that needs to be received every year to be effective. In fact, to date, this is the only disease that mutates as often as it does. (To date is used because it is still undetermined whether or not the COVID-19 disease will behave in the same way or not.)

Now what about those booster shots?

For some vaccines, after a while, immunity begins to wear off. At that point, a “booster” dose is needed to bring immunity levels back up. For example, in the case of the DTaP vaccine, which protects against diphtheria, tetanus and pertussis, the initial series of four shots that children receive as part of their infant immunizations helps build immunity. But a booster dose is needed at 4-6 years old. Another booster against these diseases is needed at 11-12 years of age. This booster for older children—and teens and adults, too—is called Tdap.

A booster dose serves as a reminder to the immune system. It says, "Hey, remember me? I'm still a potential threat so keep making those antibodies against me!"

{You can find all the sources I used by clicking here.} 

Let's talk vaccines: ᴵᵐᵐᵘⁿⁱᵗʸ

The immune system could be its own series, there's so much to talk about in regards to it. But we aren't going to go *there* so here's some basic info about the immune system as it pertains to our look at vaccines.

There are three types of immunity: innate, adaptive (also called active or acquired), and passive.

Innate immunity is what we are all born with. We are all born with some level of immunity to invaders. Human immune systems, similarly to those of many animals, will attack foreign invaders from day one. This innate immunity includes the external barriers of our body — the first line of defense against pathogens — such as the skin and mucous membranes of the throat and gut.

Active immunity results when exposure to an antigen triggers the immune system to produce antibodies to that disease. Exposure to the disease can occur through infection with the actual disease (resulting in natural immunity), or introduction of a killed or weakened form of the disease through vaccination. Active immunity is long-lasting, and sometimes life-long.

Passive immunity is provided when a person is given antibodies to a disease rather than producing them through his or her own immune system. A newborn baby acquires passive immunity from its mother through the placenta. A person can also get passive immunity through antibody-containing blood products such as immune globulin. Passive immunity lasts only for a few weeks or months.

Vaccines are also called immunizations because it introduces antigens or weakened pathogens to a person in such a way that the individual does not become sick but still produces antibodies. Because the body saves copies of the antibodies, it is protected if the threat should reappear later in life, therefore putting the person in a state of active immunity.

Some people believe that naturally acquired immunity—immunity from having the disease itself—is better than the immunity provided by vaccines. However, natural infections can cause severe complications and be deadly. This is true even for diseases that many people consider mild, like chickenpox. It is impossible to predict who will get serious infections that may lead to hospitalization.

A white blood cell (yellow) is shown here eating an anthrax bacteria (orange).
The white line in the bottom left-hand corner of the slide denotes a 5 micrometer
(one MILLIONTH of a meter) measurement.

{You can find all the sources I used by clicking here.}