Tuesday, October 25, 2011

Germs : ( Part 3)

For most of you who still read this GERMS post, you may feel that this starts to get boring, but for some of you, I hope you still find it interesting, as I will continue to share as much knowledge as I can, without making you falling asleep. Let's talk more about germs, particularly about birth, infants as well as H. Pylori. 

Let's see. Like the colonization of the mouth and the skin, that of the human digestive tract, home to approximately 99% of the body's microflora, begins during birth, starting with the lactobacilli encountered in the birth canal. As the baby's head crowns, it compreses the mother's rectum, pushing out a small amount of stool. This head to anus position ensures that, of all billions of microbes, the baby will meet in its first day of life, the first will be those to which its mother immune system has already developed protective antibodies. Bear in mind, that a temporary supply of these antibodies have already passed to the fetus through the placenta. A chaser of breast milk delivers the second wave, millions of bifidobacteria. 

All incoming microbes, before they reach the intestines, must pass through the antechamber of the baby's stomach. In the stomachs of the older children and adults, high levels of hydrochloric acid present a microbe killing barrier. But, acid secretion doesn't begin until around 3 months of age, building gradually to adult levels over several years. This delay leaves open a welcoming door for the colonization of the stomach and intestinal tract during early life. Say, for example, a baby meets the stomach bug called H.Pylori during this period. For some people who known of this bug, he or she would know how destructive and 'durable' it is. 

Children typically do so on the hands or lips of someone already colonized. Once swallowed, this bacterium drills into the mucus layer that will protect the stomach from the hydrochloric acid bath to come. As the acid producing cells of the stomach mature, some strains of H.Pylori inject proteins that direct the cells to lower the  acidity to levels that are more tolerable to this bug, but still acidic enough to kill most of other kinds of microbes. In this way, H.Pylori has maintained a virtual monopoly over the human stomach for over decades. The strain H.Pylori carried by a particular family or population can even be trace ancestry as far back as the ancient migration patterns that began when Homo Sapiens first hiked out of Africa! 

H.Pylori, can triggers inflammation serious enough to produce gastric ulcers and stomach cancer in later life. In any case, H.Pylori is rapidly becoming extinct in the Western world, possibly leaving the stomach open for colonization by some other bugs. proceeding past the antechamber of the stomach, surviving microbes enter the switchback of the small intestine, where a forest of fingerlike extensions, called villi, maximize the surface area through which nutrients can enter thebloodstream. The low acidity or low pH, of the small intestine proves ideal doe bacterial growth. 

The small intestine is where incoming microbes most directly engage infant's dormant immune system. In places, the villi part to reveal barren hillsides, their surfaces a mosaic of oddly flattened and pitted cells. It's called the Peyer's patches, these domelike structures overlie the immune system's most important training academies. The pits on the surface of these flattened cells are pockets that continually snag passing bacteria, both live and dead. Like revolving doors, these pockets migrate to the cells inner surface, ushering their microbial passengers into the lymph tissues.

The internal structure of the Peyer's patch resembles that of the  lymph nodes that will mature in the infant's neck, groin and armpit. But, if lymph nodes resemble war rooms where immune system cells can learn what to attack, the lymph tissue of the Peyer's patch resembles a diplomatic center where incoming microbes get the benefit of the doubt, where they are presumed 'friendly' until proven other wise.

Well, if one say that the immune system learns to ignore the intestinal bacteria, however, would be wrong. Rather then inducing a microbe-killing inflammation, the interaction of the Peyer's patch triggers the production of an abundance of the antibody known as immunoglobulin A, or IgA. Like all antibodies, each IgA attaches to a specific target, in this case, a particular kind of intestinal bacteria. Whoever studied medical or health science, this would sound very familiar to you, unless, you did not pay attention during Immunology lectures. To meet and greet inside the neutral territory of the Peyer's patch, also leads to the proliferation of the T and B cells that will marshal an attack against these same bacteria should they turn up in forbidden territory, such as the blood.

So, an infant's immature immune system learns to tolerate swallowed bacteria while warily keeping them at a distance. over the course of childhood, the numbers of Peyer's patches lining the small intestine dwindles from several hundred to around thirty? Not entirely sure, but I think that's the approximated figure I could still remember.  This remnant group of Peyer's patches clusters along the final segment of the small intestine just before it opens into the expansive bacterial holding chamber of the colon. Within this remnant, a much reduced diplomatic corps  of immune cells continues to monitor the daily passage of millions of microbes, recognizing the vast majority as normal and worthy of tolerance.

Once they have passed through the forceful contractions and microbe snagging cells of the small intestine, bacteria enter the settling tank of the large intestine. Though it is sterile at birth, it will become the microbial rain forest of the human body. At the end of the vaginally delivered baby's first day of life, the scattering of bacteria in his poop reflects that of his mother vaginal and intestinal tract.

By contrast, that of the cesarean-born baby contains a more random assortment of microbes from the hands of the birth attendants and the general hospital environment. Whatever the method of delivery, by the third day , a breast fed infant es excreting a near monoculture of bifidobacteria, which continues to predominate until the introduction of solid food. Bear in mind that the intestinal flora of a 'formula-fed' infant also contains bifidobacteria, but the source is unknown, and far much smaller numbers and as a small part of an unstable mixture of other mibrobes. So parents, this is a very important point to take note.

In the intestine, as on the baby's skin and in its mouth, the bifidobacteria discourage the growth of potential troublemakers such as staph and help to select the first permanent resident. Studies also show that an abundance of intestinal bifidobacteria boosts the level of protective antibodies in a baby's blood, antibodies that target not only problematic bacteria but many kinds of diarheaa inducing gastrointestinal viruses. This phenomenon may also explain why in Third World countries with poor water sanitation, the mortality rates of breast fed infants are as much as six times lower then formula fed babies during the first six months of life, regardless the family income or education level.

The first wave of intestinal microbes also triggers the maturation of the colon's lining. Underlying blood vessels extend to the lining's surface and there form the dense network of tiny capillaries needed both to keep it healthy and to carry away the nutrients liberated by resident bacteria. At the same time, the first touch of bacteria awakens millions of intestinal stem cells. Once activated, these cells begin endlessly dividing, and their proliferation continually refreshes the intestinal lining's delicate layer of surface cells.

The surface cells, in turn begin shedding at a rate of several billion cells per day! This replacement renders the intestinal tract resilient to the kind of injuries that inevitably occur when a child starts eating solid food, with its abundance of natural toxins as well as the occasional sharp object or disease causing microbe.

Folks, I know this is one pretty darn boring read. A lot of science and too much of germs stuff. Well, if you are into microorganisms' world, you might like what you read here. Till then, stay tuned.


Thursday, October 20, 2011

Germs : ( Part 2)

In this post, I will write a bit bout how germs evolve around our body as ecosystem, our mouths, its life on the surface and inside as well. I have discovered that writing this topic is quite a challenge for me, compared to the rest of the other health discussions I've written earlier. Though I will try to elaborate and explain as laymen as possible, this topic about germs will always be one of my favorite learning till today.

Preparations for the human-microbe alliance begin before birth. Midway through pregnancy, a hormonal shift directs the cells lining a woman's vagina to begin stockpilling sugary glycogen, the favorite food of the bacteria called lactobacilli. By fermenting the sugar into lactic acid, these bacteria lower the pH of the vagina to levels that discourage the growth of potentially dangerous invaders. These threats include the occasional intestinal bacterium that might stray from anus to vagina, then overgrow and spread into the uterus to cause a pregnancy-threatening infection. The acid secreting lactobacilli also provide partial protection against the sexually transmitted bacteria Neisseria gonorrhoeae and Chlamydia trachomatis, which can cause blindness in newborns infected during passage through the birth canal.

Some vaginal lactobacilli also produce hydrogen peroxide, and these extra aggressive lactobacilli are particularly effective at beating back the growth of Streptococcus agalactiae, or group B strep. Commonly found in vaginas of women who lack hydrogen peroxide producing lactobacilli, group B strep remains a leading cause of infant mortality.

Each year, we noticed hundreds and even thousands of life threatening cases of pneumonia, meningitis, and blood infections primarily in babies under one month of age. Because the natural protection of lactobacillus is far from foolproof, Western obstetricians routinely put women who tested positive for group B strep on antibiotics during labor. Ironically, previous courses of antibiotics are often to be blamed or allowing group B strep to move into the birth canal in the first place, as these drugs tend to disrupt the woman's protective lactobacilli.

Now, let's talk about germs and our mouths. How about infant's mouth? Typically, the infant mouth's first innoculation of bacteria includes a generous sampling of the lactobacilli present in the mother's canal. With the first gulp of breast milk, these lactobacilli are joined by millions of bifidobacteria, a related group of acid-producing microbes. 

These microbes mysteriously appear in and around the nipples of a woman's swelling breasts during the eight month of pregnancy. There, the bifidobacteria secrete a potent combination of acids and antibiotic chemicals to repel potentially dangerous microbes. Though, the bifidobacteria themselves perish in the open air, they leave behind acids that linger for hours on the breast and in a baby's mouth.

If the newborn is fortunate, her neisseria population will include globes of Neisseria lactamica, which thrives on lactose, or milk sugar. Early colonization by this species builds strong immunity against Neisseria meningitidis, the most common cause of meningitis, a potentially deadly inflammation of the membrane covering the brain and spinal cord.

Where do all these early colonizers come from? By identifying the specific subtypes of bacteria in children's mouths, researchers have found that the vast majority trace directly to the mouths of their mothers. The maternal antibodies still circulating in a newborn's blood, which was passed during pregnancy, may further encourage the growth of microbes that they recognize as their own.

The mouth's salivary glands secrete a more constant but less intense source of bacterial food, a watery mix of protein, sugars and minerals. The mouth's first wave of aerobic bacteria consumes enough oxygen to create an underlying zone where anaerobic bacteria can thrive. These anaerobic bacteria bacteria feed on the biochemical waste products of their microbial neighbors and so help stabilize their ecosystem as it grows crowded.

Next, let's move on the discussion about germs' life on the surface. As with the mouth and nose, the colonization of the human skin begins during birth, with the lactobacilli in the mother's birth canal. These protective bacteria contribute their lactic acid and hydrogen peroxide to the bacteria-killing enzymes in the creamy vernix that covers the emerging baby. 

Like the bifidobacteria of breast milk, lactobacilli don't survive long in open air. The hands and exhalations of parents and birth attendants likewise transfer bacteria to the baby's skin. Twenty four hours after birth, the suburbanization of the baby's skin has gone far, with more than a thousand bacteria per square. This rapid pace of growth continues through the second day, surpassing ten thousand per square centimeter at forty eight hours, and hitting the one hundred thousand mark by six weeks. At such densities, the skin's largely aerobic pioneers begin to deplete the limited oxygen inside hair follicles and glands, preparing them for second wave of settlers.

For most part, the skin's microflora stabilize by middle childhood. Though family and friends continuously trade microbes, fewer and fewer of these later visitors remain for long. Then, when we reach adolescence, the pimple inducing Propionibacterium acnes lives up to it name. It becomes trapped and overgrows inside overeactive oil glands. Next, the high estrogen levels of female adolescence also foster the growth of vaginal lactobacilli. A girl does not have to be sexually active to accidentally introduce a small number of these troublesome microbes into her vagina. She may do so when she wipes after a bowel movement.

Because antibiotics, especially broad spectrum antibiotics, tend to disrupt this ecological balance, they frequently trigger either yeast infections or bacteria vaginosis, which is caused by intestinal bacteria.

Now, let's talk a bit about the bacteria called E.coli. I'm not sure how many of you readers heard and know of this bacteria, but allow me to share some of my knowledge with you on this one. This bacteria, remains the best known of all the intestinal bacteria. It was the one bacterium that consistently showed up in stoll cultures and sewage-contaminated water supplies. In truth, E.coli was simply the easiest of the intestinal bacteria to grow outside the body. Anyone of you heard about the contamination of beef burgers years back in countries such as USA would surely learn one of two things about this bacteria. In this case, we are talking about commercial processed meat.

Stay tuned...


Friday, October 14, 2011

Germs : ( Part 1)

Today, I would like to write about something slightly different. Germs! Microbes! Well, I know it is not most people's favorite subject, but from my point of view, it is very important, and it plays key role to our health since millions of years ago. I will discuss about our primal ancestors, how they were associated with these organisms since long time ago. 

Over the millions of years that human and their ancestors lived as hunter-gatherers, they populations remain too small to allow a deadly infection to last long, or to travel far before killing everyone off. Microbes, use humans as secondary homes, while residing primarily in  animals such as insects. Of these, the mosquito-borne malaria parasite, maybe the oldest and the deadliest.

When tribes of Homo sapiens first hiked north of Africa some thirty thousand years ago,  they largely escaped their tropical parasites and enjoyed a prolong era of robust health. This is not to say that hunter gatherers enjoyed an idyllic existence. Starvation and injury made for a short and brutal lifespan, but it was nonetheless a life span largely free of infectious disease.

With civilization, well behaved microbes abruptly lost their near-monopoly over the human body and a new microbial lifestyle arose. Thee real carriers of the infectious organism, rats and their attendant fleas, had massively multiplied. thriving in the household waste that the working poor tossed from their windows for lack of a better option.

Now, let's talk about the reborn of germ theory. Does anyone know when does the first maternity wards open in Europe? Well, the answer is late 1700's. That time proven to be especially deadly as well, with childbed and fever racing through the newly popular maternity wards and killing thousands of people. And no wonder, for the doctors and midwives were constantly moving between the sick and the merely birthing, thrusting contaminated hands and instruments high into raw and torn birth canals and wombs. But the idea that medical workers might be spreading infection was shared by few and shunned by many.

In fact, the controversial concept would destroy many careers. The first was that of the Scottish surgeon Alexander Gordon. He noted the resemblance between the milky substance seen in the wombs of women dead of puerperal fever and the wound infections. Gordon's proposed cure for puerperal fever was all but medieval, but his recipe for preventing its spread was spot on. He noted that the patient's apparel and bedcloths ought be burnt or thoroughly purified, and the nurses and physicians who have attended the patients affected with the puerperal fever ought carefully to wash themselves and get their apparel properly fumigated before it be put on again.

Then, a half century later, Oliver Wendell Holmes tried unsuccessfully to hector doctors of the Atlantic into recognizing the infectious nature of puerperal fever. He was then dismissed as another crazy 'contagionist' physician, and he left medical practice few years later. The same year Holmes abandon medical practice, the Hungarian physician Ignaz Summelweis supplied clear proof of both Gordon's and Holmes's contagionist theories. But, after Ignaz Summelweis died, European and American doctors had largely split into two camps, the contagionist and the sanitarians. The contagionists are the ones who advocated germ theories, and sanitarians, are the ones who clung to the idea of miasmas. Fyi, the miasma theory, refers to the believe of diseases such as cholera and chlamydia were caused by 'poisonous aires' arose from filth and decay.

On the contagionist side, a number of researchers had glimpsed the presence of microscopic organisms in diseased tissues. But, many countered that if, in fact, bacteria existed in the blood and tissues of the sick, they did not cause the disease, rather they sprang spontaneously from the dead and dying tissue.

The early microbe hunters could not discern the profound differences between the ultrasimple 'prokaryotic' cell of a bacterium, and the larger, more sophisticated 'eukaryotic' cells of microscopic parasites such as protozoa and fungi. They also mistakenly assumed that viruses were infectious microorganisms that were too tiny for them to see with their most powerful microscopes. We now know them to be nonliving particles of protein wrapped nucleic acids (which is our DNA and RNA), that enter our cells and there get mistakenly copied, to fuel a new round of infection.

Right now, I conclude the first post of this 'Germs' series. Stay tuned as I will make time to write the second post hopefully in few days time. Take care.


Thursday, October 6, 2011

Chlamydophila Pneumoniae : Infectious bacterium

I've been spending some time researching about germs, bacteria and viruses as well as parasites and yeast. One pretty rare bacterium which came across my attention, Chlamydophila Pneumoniae. It is also known as Chlamydia Pneumoniae, but it is NOT the same Chlamydia sexually transmitted disease. Why is it so interesting and dangerous? 

Now, a lot of doctors have yet to know about this bacteria, and if being told, they often mixed up with the STD Chlamydia. The popular Chlamydia, is actually a STD based bacterium, which can destroy a woman's reproductive system, causing infertility and so on. For men, it can cause fluid discharge and burning sensation on the penis and other complications as well. It is one of the most common sexually infected diseases in developed countries, but I will not discuss on this type of bacteria for today. Let's focus on the much more destructive bacterium, Chlamydia Pneumoniae.

Although I'm not an expert or have sufficient knowledge about this germ, but I hope to share some information regarding this bacterium, to whoever is reading this post right now. The most common question asked is "How can I be infected with this bacteria?" Well, it mainly started off with respiratory infection, then could well spread to other parts of the organs in the body and infect other tissues such as nerve tissues, brain, muscles, blood vessels and even immune cells. It can be spread by droplet infection, coughing, sneezing, and if you accidentally touched a surface or objects which has the infected droplets, there is a high chance you may be infected too.

First of all, this bacteria contains endotoxins, which are toxic chemicals that can damage tissues and cause inflammation. It can also increase the load of toxic in the body and trigger chronic immune activation. It infects inside the cells and steals the energy from your body, making you feel as if you have low energy levels and sluggish most of the time. 

One of the interesting is, this bacterium, it loves cortisol! It actually triggers production of cortisol and feeds on these stress hormones! It makes your immune system susceptible to other infections as it causes the immune system white blood cells to dysfunction. Thus, one after another infections are stacking up on top of each other and making the body more vulnerable and weak.

Approximately 100 diseases or health conditions are associated with Chlamydia Pneumoniae. A long list of health conditions from  diarrhea, chronic fatigue, chronic sinusitis, shortness of breath, muscle pain, depression, prostate inflammation, asthma, joint problems, to a more severe conditions such as stroke, heart disease, multiple sclerosis, atherosclerosis, diabetes mellitus, chronic fatigue syndrome, Alzheimer's, rheumatoid arthritis

In most infections with Chlamydia pneumoniae, it run silently, or with common cold symptoms. Only in immune system suppressed individuals such as patients with cancer, HIV infection and in elderly people so acquired pneumonia to serious complications, sometimes leading to fatal outcome. Approximately 80% of those over 60 years of age have blood antibodies against Chlamydia Pneumoniae, are affected, whereas only about 20-30% of the 10-year schoolchildren are hit by this bacteria.

Question is, how can one know if he or she is infected with this bacterium? Well, there are few ways to perform diagnosis and get tested out to confirm if your body has Chlamydia Pneumoniae. However, detection of Chlamydia pneumoniae is very complicated because they are not like other bacteria can be grown. They trive in a host cell and behave like parasites. Below are the few diagnostic methods which certain respective hospitals could perform, but most conventional doctors never even heard of this bacterium before.


- IgG, IgM and IgA antibody detection
- Nucleic acid detection
- Real Time PCR

Finally, what types of treatment can be used to combat or cure this infection? Below are some of the tested and proven effective treatment for Chlamydia Pneumoniae infection.


- NAC (amino acid )
- Glutathione (anti-oxidant )
- Amoxicillin (antibiotic)
- Azithromycin (antibiotic)
- Minocycline (antibiotic)