Let's talk infectious diseases, the reason for vaccines: ᴴᵃᵉᵐᵒᵖʰⁱˡᵘˢ ⁱⁿᶠˡᵘᵉⁿᶻᵃᵉ ᵗʸᵖᵉ ᵇ ⁽ᴴⁱᵇ⁾

Despite its name, Haemophilus influenzae type b – or Hib – doesn’t cause influenza. In the 1890s, doctors thought this bacteria might cause flu and – despite later research showing flu is caused by a virus – the name stuck. So what is it?

Haemophilus influenzae disease is a name for any infection caused by bacteria called H. influenzae. These bacteria live in people’s nose and throat, and usually cause no harm. However, the bacteria can sometimes move to other parts of the body and cause infection.

People spread H. influenzae, including Hib, to others through respiratory droplets. This happens when someone who has the bacteria in their nose or throat coughs or sneezes. People who are not sick but have the bacteria in their noses and throats can still spread the bacteria. Experts do not know how long it takes after H. influenzae enter a person’s body for someone to get sick. However, it could take as little as a few days before symptoms appear.

Hib bacteria can cause many types of invasive disease, including meningitis, pneumonia, cellulitis (skin infection), septic arthritis (joint infection), bloodstream infection, and epiglottitis (infection causing obstruction or closing of the windpipe). Prior to 1985 Hib disease was the leading cause of bacterial meningitis among U.S. children under 5 years old. Hib can also cause mild infections like bronchitis or ear infections.

Symptoms depend on the part of the body that is infected. Treatment depends on the kind of infection. Depending on how serious the infection is, people with H. influenzae disease may need care in a hospital. Even with appropriate treatment, some H. influenzae infections can result in long-term problems or death. For example, bloodstream infections can result in loss of limbs. Meningitis can cause brain damage or hearing loss.

In 1892, German physician Richard Pfeiffer isolated a bacterium from the lungs and sputum of influenza patients during a pandemic. Pfeiffer believed that he had found the cause of influenza. However, in the 1930s it was established that influenza is caused by a virus, not bacteria. But the bacteria Pfeiffer had isolated did prove to be useful in identifying several diseases.

In 1931, American researcher Margaret Pittman, PhD classified different types of Haemophilus influenzae bacteria and found that type b (called Hib) caused nearly all cases of Haemophilus influenzae meningitis. It would later be confirmed that Hib could also cause many other serious diseases, including infections of the blood, bone, and joints.

The first vaccine against Hib disease was licensed in the United States in 1985 and was used until 1988. It was replaced by the first conjugate vaccine against Hib. Today there are three conjugate Hib disease vaccines available in the United States, as well as two combination vaccines that provide protection against multiple diseases, including Hib disease.

With widespread use of the vaccine, the number of reported cases of invasive Hib disease in US children has been reduced by 99%.

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

Let's talk infectious diseases, the reason for vaccines: ᵀᵘᵇᵉʳᶜᵘˡᵒˢⁱˢ ⁽ᵀᴮ⁾

Tuberculosis (TB) is a contagious airborne disease caused by Mycobacterium tuberculosis, a bacterium that grows and divides inside of cells.

There are two kinds of TB, latent and active.

𝙻𝚊𝚝𝚎𝚗𝚝 𝚃𝙱

In most people, the immune system can contain the bacteria so that they do not replicate and cause disease. In this case, a person will have TB infection but not active disease.

Doctors refer to this as latent TB. A person may never experience symptoms and be unaware that they have the infection. There is also no risk of passing on a latent infection to another person. However, a person with latent TB still requires treatment. About 5% to 10% of infected people who do not receive treatment for latent TB infection will develop TB disease (active TB) at some time in their lives.

The CDC estimate that as many as 13 million people in the U.S. have latent TB.

𝙰𝚌𝚝𝚒𝚟𝚎 𝚃𝙱

The body may be unable to contain TB bacteria. This is more common when the immune system is weakened due to illness or the use of certain medications. When this happens, the bacteria can replicate and cause symptoms, resulting in active TB. People with active TB can spread the infection.

The infection, which starts in the lungs, causes nodules known as tubercles, or Ghon focii, which are spots left by dead infected tissue. With time, the disease can spread to other areas of the lung and larger areas of lung tissue may die off, causing cavities. Bacteria can also spread to other organs, including the kidney, brain, and spine.

The signature symptom of active TB is a bad cough that produces blood-tinged phlegm and can last three or more weeks. Other symptoms include chest pain, fatigue, loss of appetite, weight loss, fever, chills, and night sweats. Symptoms typically worsen over time, but they can also spontaneously go away and return.

TB usually affects the lungs, though symptoms can develop in other parts of the body. This is more common in people with weakened immune systems. TB can also cause:

▪️persistently swollen lymph nodes, or “swollen glands”

▪️abdominal pain

▪️joint or bone pain

▪️confusion

▪️a persistent headache

▪️seizures

People should ask for a TB test if they:

▪️have spent time with a person who has or is at risk of TB

▪️have spent time in a country with high rates of TB

▪️work in an environment where TB may be present

Two tests can show whether TB bacteria are present:

▪️the TB skin test

▪️the TB blood test

However, these cannot indicate whether TB is active or latent. To test for active TB disease, the doctor may recommend a sputum test and a chest X-ray.

Everyone with TB needs treatment, regardless of whether the infection is active or latent.

The right type of antibiotic and length of treatment will depend on:

▪️the person’s age and overall health

▪️whether they have latent or active TB

▪️the location of the infection

▪️whether the strain of TB is drug-resistant

Treatment for latent TB can vary. It may involve taking an antibiotic once a week for 12 weeks or every day for 9 months.

Treatment for active TB may involve taking several drugs for 6–9 months. When a person has a drug-resistant strain of TB, the treatment will be more complex.

TB is not something that is typically vaccinated against in the United States and it can be fatal if left untreated.

TB has been around for tens of thousands of years. It was often called "consumption" because of the dramatic weight loss it can cause. Before the 1940s, when the antibiotic streptomycin became available, there wasn't much that could be done for the illness. Fresh air, good nutrition, and sunlight were thought to be helpful but didn't always work. In some cases, doctors attempted to remove a diseased lung. From the 17th through the 19th centuries, it is believed that one in five people died from tuberculosis.

It wasn't until 1882 that TB was identified. Robert Koch isolated and cultured Mycobacterium tuberculosis. He immediately began to work on a vaccine for treatment and prevention of tuberculosis.

Between 1904 and 1921 Albert Calmette and Camille Guérin worked on attenuated tuberculosis bacilli to test on humans. They used TB from cows to weaken the bacteria enough to place in humans in hopes of providing some immunity. Their preparation is called Bacillus Calmette-Guérin, or BCG in shorthand.

In 1928, the Health Committee of the League of Nations adopted BCG as a recommended tuberculosis vaccine. Between 1947 and 1951 a total of 8 million babies and nearly 14 million people were given the BCG vaccine in the International Tuberculosis Campaign. The project initially began in Europe in the aftermath of World War II. However, the program extended beyond Europe when UNICEF contributed $2 million to expand the program to other continents.

In 1974 WHO included BCG in the list of recommended vaccines for developing countries. In 1974 fewer than 5% of children worldwide were immunized by age 1 against diphtheria, polio, tuberculosis, pertussis, measles, and tetanus. The Expanded Programme on Immunization would help bring vaccination against these six diseases to many underserved areas.

Still a leading killer worldwide, tuberculosis is less prevalent in the United States than it used to be. According to the CDC, 9,029 new cases of TB were reported in the United States in 2018.

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

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

Pneumococcal disease is caused by common bacteria (Streptococcus pneumoniae) that can attack different parts of the body.

When these bacteria invade the lungs, they can cause pneumonia; when they invade the bloodstream, they can cause sepsis; and when they invade the covering of the brain, they can cause meningitis. These invasive infections are serious, often require treatment in the hospital, and can lead to death. The bacteria can also cause milder common conditions like middle-ear infection (otitis media) and sinusitis.

Pneumococcal disease is a leading cause of serious illness throughout the world. About 1.3 million persons visit emergency departments in the US each year with pneumonia, which is often caused by pneumococcal infections, and nearly 50,000 people will die from pneumonia. Fewer people will get pneumococcal meningitis or bloodstream infection, but the mortality rate for these infections is higher, even with proper treatment.

There are two main types of pneumococcal disease: non-invasive and invasive. The non-invasive form of the disease is less serious, whereas invasive is fatal in 10% of cases.

Non-invasive pneumococcal disease causes a mild infection where the s. pneumoniae bacteria can spread through the nose, throat, and upper and lower respiratory tracts. The bacteria is associated with a number of conditions: acute bronchitis, sinusitis, and otitis media (inflammation in the middle ear).

Invasive PD is more serious than the non-invasive type and occurs inside the blood or in a major organ. There are several types of invasive pneumococcal disease including pneumonia, meningitis, sepsis, bacteremia, osteomyelitis, and septic arthritis.

Treatment depends on the type of pneumococcal disease. Noninvasive pneumococcal infections may not need treatment. Invasive pneumococcal infections will require antibiotics.

The best prevention of pneumococcal disease is vaccination. While there are numerous strains of s. pneumoniae and vaccination cannot prevent all of them, pneumococcal vaccines can protect you from the most common strains.

In 1881, Louis Pasteur and U.S. Army physician George Miller Sternberg both independently discovered the Streptococcus pneumoniae bacterium that is responsible for cases of pneumonia and meningitis, as well as other illnesses.

The first whole-cell vaccine was tested on 50,000 miners in Africa in 1911. However, the date was inconclusive so the vaccine was abandoned. Another vaccine was introduced in 1945 but coincided with the advent of widespread penicillin use. With penicillin being viewed as an effective treatment for pneumococcal infections, the vaccine did not gain much traction.

One challenge in producing a pneumococcal vaccine involved determining which of the more than 90 types of pneumococcal bacteria produced the most disease. Finally, in 1977 a vaccine was licensed that protected against 14 types of pneumococcal bacteria. In 1983, Merck expanded on this work by producing a vaccine against 23 types of pneumococcal bacteria. This vaccine is still used today in adults 65 and older, as well as for individuals aged two or older who are at high risk for disease.

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

Let's talk infectious diseases, the reason for vaccines: ᶜᵒᵐᵇⁱⁿᵃᵗⁱᵒⁿ ⱽᵃᶜᶜⁱⁿᵉ: ᴹᴹᴿ

In 1971 the measles, mumps, and rubella (MMR) combination vaccine was licensed for use. Combination vaccines have several advantages over single vaccines. They reduce the need for several separate injections, and they reduce the costs of stocking and shipping multiple containers. Combination vaccines can help improve overall vaccination rates by simplifying the vaccination process.

One dose of MMR vaccine is 93% effective against measles, 78% effective against mumps, and 97% effective against rubella.

Two doses of MMR vaccine are 97% effective against measles and 88% effective against mumps.

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

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

The disease rubella is caused by the rubella virus from the family matonaviridae. Rubella spreads when an infected person coughs or sneezes. Also, if a woman is infected with rubella while she is pregnant, she can pass it to her developing baby and cause serious harm.

The signs and symptoms of rubella are often difficult to notice, especially in children. Signs and symptoms generally appear between two and three weeks after exposure to the virus. They usually last about one to five days and may include:

▪️Mild fever of 102 F or lower

▪️Headache

▪️Stuffy or runny nose

▪️Inflamed, red eyes

▪️Enlarged, tender lymph nodes at the base of the skull, the back of the neck and behind the ears

▪️A fine, pink rash that begins on the face and quickly spreads to the trunk and then the arms and legs, before disappearing in the same sequence

▪️Aching joints, especially in young women

▪️Some adults may also have a headache, pink eye, and general discomfort before the rash appears.

No treatment will shorten the course of rubella infection, and symptoms don't usually need to be treated because they're often mild. However, doctors often recommend isolation from others — especially pregnant women — during the infectious period.

Mild symptoms can be managed with bed rest and medicines for fever, such as acetaminophen.

Rubella is the most dangerous for pregnant women. Infection with rubella virus causes the most severe damage when the mother is infected early in pregnancy, especially in the first 12 weeks.

A mother who has been infected with rubella and is pregnant develops congenital rubella syndrome (CRS). If she doesn't miscarry or experience a stillbirth, her developing baby is at risk for severe birth defects with devastating, lifelong consequences. CRS can affect almost everything in the developing baby’s body.

The most common birth defects from CRS can include:

▪️Deafness

▪️Cataracts

▪️Heart defects

▪️Intellectual disabilities

▪️Liver and spleen damage

▪️Low birth weight

▪️Skin rash at birth

Less common complications from CRS can include:

▪️Glaucoma

▪️Brain damage

▪️Thyroid and other hormone problems

▪️Inflammation of the lungs

Although specific symptoms can be treated, there is no cure for CRS.

German physician Friedrich Hoffmann was the first to give a clinical description of the disease that would later come to be known as rubella. It was first called German measles and was known that way for the next one hundred years. In 1841, after an outbreak in an India boys' school, rubella appeared as the suggested name. Rubella means "little red".

The rubella virus was eventually isolated in 1960 by Thomas Weller, MD. His 10 year old son contracted a severe case of rubella so he inoculated cultures of human cells with his son’s urine, and was eventually able to isolate the causative agent. However, Weller came to this discovery about the same time as several other researchers. Rubella's time had come.

The first rubella vaccine was licensed in 1969. 10 years later this first vaccine was replaced in the United States by American physician Stanley A. Plotkin’s newly licensed RA27/3 vaccine, which had been used in Europe for years and provided superior protection to that of the earlier vaccines. This new updated vaccine also replaced the original rubella vaccine in the combined MMR shot, and is still used today.

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

Let's talk infectious diseases, the reason for vaccines: ᴬʳᵉ ᵐᵉᵃˢˡᵉˢ ᵃⁿᵈ ʳᵘᵇᵉˡˡᵃ ᵗʰᵉ ˢᵃᵐᵉ?

𝘼𝙧𝙚 𝙢𝙚𝙖𝙨𝙡𝙚𝙨 𝙖𝙣𝙙 𝙧𝙪𝙗𝙚𝙡𝙡𝙖 𝙩𝙝𝙚 𝙨𝙖𝙢𝙚?

Short answer: No.

Longer answer: It would be easy to think that measles and rubella, also called German Measles, are the same disease. It would be easy to think that because of the name German Measles assigned to the disease rubella. And because measles is also known as rubeola. Really, how much more confusing can it get? 🤷‍♀️

While they do have some similarities, they have some pretty big differences.

Let's outline the similarities first:

▪️ Both diseases are caused by an RNA virus.

▪️ They have similar symptoms and are spread by respiratory droplets.

▪️ Rashes are a distinct marker of each disease.

And now the differences:

▪️ Even though both are caused by RNA viruses, it is two different families. Measles belongs to the Paramyxoviridae family and Rubella belongs to the Matonaviridae family.

▪️ German measles are mild while measles cannot, and should not, be considered mild. German measles are not life-threatening while measles are.

▪️ Both the appearance and the length of the rashes differ.

▪️ Symptoms for measles lasts twice as long as rubella.

▪️ The virus that causes measles specifically invades the respiratory system while the virus that causes rubella invades lymph nodes, eyes, and skin.

▪️ Symptoms for measles are more severe and numerous.

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

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

Mumps is caused by a virus that enters the body through the mucous membranes, which are the areas that line the inside of your mouth, nose, and throat. The virus that causes mumps is a paramyxovirus.

Mumps is easily transmitted through casual contact and therefore HIGHLY contagious. The virus can survive in respiratory fluids, and this is how it is transmitted from person to person. You can also catch the virus if you touch objects that have the virus on them. Sharing cups, utensils, and other objects, or being in close contact with someone who has mumps can also increase your chances of getting the infection. Lack of good hygiene, such as hand washing, can increase the spread of the virus. The incubation period for mumps is about two to three weeks. Infection with mumps is not common because many people are vaccinated. However, you can get the infection if you have not been vaccinated, or, in rare instances are immunosuppressed.

The paramyxovirus causes an immune reaction as the body tries to fight it, which exacerbates the symptoms, causing the flu-like symptoms and the characteristic swelling of the face and neck. It is also described as a neurotrophic virus, which means that it has a tendency to travel to the nervous system. The virus can also affect other parts of the body, including the pancreas and testes, often causing painful enlargement and swelling of these areas.

Symptoms usually appear about two days after infection and can last as long as two weeks. Typically, the initial symptoms include:

▪️Fever

▪️A headache

▪️Swollen, painful salivary glands under the ears or jaw (in about 30% to 40% of cases)

▪️Ear pain

▪️Facial pain

There is no specific antiviral treatment and antibiotics will have no effect on the disease. The only course of treatment is reactive - acetaminophen or ibuprofen can be used to reduce the fever and relieve pain, cold and warm compresses can be used for the swollen glands - or proactive, i.e. vaccinate.

The first written description of mumps as a disease can be found as far back as the 5th century BC. The father of medicine Hippocrates described an outbreak of mumps on the Greek island of Thasos in approximately 410BC, which modern physicians today still refer back to as a masterful documentation of the disease.

“Swellings appeared about the ears, in many on either side, and in the greatest number on both sides,” the passage reads. “They were of a lax, large, diffused character, without inflammation or pain, and they went away without any critical sign.”

But then not another word about mumps appears in medical history accounts until 1934! The cause of mumps was finally discovered and documented by Claud D. Johnson and Ernest W. Goodpasture. But it took another 11 years to isolate the virus and by 1948 an inactivated vaccine had been developed. However, it had a short immunity life and was soon replaced with other more effective versions.

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.

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

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.}