Emphysema: Symptoms, stages, causes, treatments, and outlook

Antibiotic Resistance, Mutation Rates And MRSA

As worrisome as MRSA is, it is just the tip of the iceberg, so to speak. In fact, there are a number of far more threatening drug-resistant bacteria in existence, such as Pseudomonas aeruginosa. P. Aeruginosa poses a greater threat because it has certain biological features that make it more readily resistant to antibiotics than MRSA. For example, P. Aeruginosa has a highly impermeable outer membrane, whereas MRSA does not. This outer membrane makes it more difficult for antibiotic chemical compounds to actually get inside the bacterial cell so that they can inflict damage. Moreover, once the antibiotic compounds are inside it, P. Aeruginosa has what are known as efflux pumps, which can very quickly pump foreign compounds like antibiotics back out of the cell before they have a chance to do damage. MRSA does not have efflux pumps. Because of these biological features, P. Aeruginosa infections either quickly evolve multidrug resistance or are drug-resistant from the start. Unlike with MRSA, however, the likelihood of picking up a P. Aeruginosa infection from a doorknob in a school building is practically nil. P. Aeruginosa infections occur mostly among hospital patients—at least for now.

In both the hospital and the community, antibiotic resistance has emerged as a major public health problem. In fact, some scientists consider it the most important public health problem of the twenty-first century. The problem exists not just because bacterial mutation rates lead to a rapid accumulation of mutations (including drug-resistant mutations), but also because of the selective pressures that antibiotics impose. If a drug-resistant phenotype were to evolve and there were no antibiotic present, then that phenotype would fare no better than any other bacterial phenotype. In other words, it wouldn't flourish, and it might even die out. It is only when antibiotics are used that drug-resistant phenotypes have a selective advantage and survive.

Of course, not all mutations confer resistance, and most probably have nothing at all to do with resistance. That said, bacterial populations with especially high mutation rates (so-called "hypermutable" strains) often have higher antibiotic resistance rates. For example, in a study of cystic fibrosis (CF) patients infected with P. Aeruginosa (which is a major cause of sickness and death among CF patients), where more than a third of all CF patients had hypermutable P. Aeruginosa infections, the hypermutable populations had higher resistance rates than isolates with "normal" mutation rates (Oliver et al., 2000). Plus, there are other ways that bacteria evolve resistance, in addition to spontaneous nucleotide base mutations. For instance, bacteria can acquire resistance genes through conjugation (i.E., from plasmid DNA) and from recombination with other bacterial DNA following transformation.

The emergence and spread of antibiotic resistance has become such an important public health problem that many federal and state public health agencies now distribute educational posters to encourage "good hygiene" practices—practices that prevent the spread of antibiotic-resistant bacteria from one person to another and help keep those mutant S. Aureus bacteria off doorknobs. Maybe you have seen one of these posters in a school hallway, in a locker room, or in a public bathroom, imploring you to wash your hands with soap and water to help prevent disease.

To make MRSA matters even worse, in 2002, health care workers reported the first cases of vancomycin-resistant MRSA. In other words, even "last-resort" vancomycin doesn't always work. Therein lies the crisis: People are dying from "simple" bacterial infections, all because of a very low mutation rate.

How Antibiotics And Vaccines Work

Some vaccines are effective against bacterial infections such as typhoid but most work against viruses.

Unlike antibiotics treating bacterial infections, vaccines do not actually kill the viral infection. Vaccines are given before infection to protect the person.

Vaccines are often 'dead' or weakened versions of the virus. Some more recent vaccines are small sections of the virus's genetic information (RNAcloseRNAA form of genetic information made of four bases (A, U, G and C). Or DNAcloseDNAGenetic information made from four bases (A, T, G and C) arranged in a double helix.). Vaccines do not infect the person receiving them with the illness, but do cause an immune responsecloseimmune responseThe effect that an infection or vaccine has upon a person which protects them from further infection. When given. This can make some people a little ill shortly after vaccination, but these symptoms are almost always much less severe than the infection itself.

The immune response causes the vaccinated person's white blood cellsclosewhite blood cells Cells made in bone marrow which fight infection. To produce specific antibodiescloseantibodiesProteins made by white blood cells that are specific to an infection. They help fight off the illness. Which fight the infection. If the person then catches the virus, their white blood cells can make these antibodies faster and often stop them becoming severely ill. At this point, a vaccinated person now has increased immunitycloseimmuneWhen a person has either been infected or has received a vaccine against a viral infection. To infection.

Natural immunity is when a person gets the infection and manages to fight it without a vaccine. The symptoms for chickenpox are generally mild and so the vaccine is only given in the UK to those people with less effective immune systems. Most people have natural immunity from chickenpox as they had the illness as a child.

Scientists, doctors and nurses overwhelmingly agree that vaccination is a vital way of protecting from infection.

Dear Doctor: Are Wound Infections After Open-heart Surgery Common? How Are They Treated?

DEAR DR. ROACH: In December 2023, I had an open-heart aortic valve replacement. All went well, but then I contracted a staph infection. I had to have a second procedure to remove the top four sternal wires, leaving me with a baseball-sized wound that required a vacuum drain and antibiotics.

During my treatment course, my infectious disease doctor informed me that there was another bacterium found that was unidentifiable and sent out of province to find out what it was. It turned out to be Mycobacterium cosmeticus, for which there are no known antibiotics to fight it, as it is very rare.

With this new information, I had all the sternum wires removed, which required a third procedure. My vacuum drain was removed, and I am now being treated with wound dressings. I was again noted to have a staph infection, and I am now starting my second round of cefazolin today. But still, there were no antibiotics found to kill the mycobacterium.

My question is: Why am I not dead? If it won't kill me, there surely must be some kind of symptoms to expect. No one can answer these questions. -- K.D.

ANSWER: Infectious complications, such as a wound infection, after an open-heart surgery are not rare. Staphylococcus aureus is a frequent culprit, and cefazolin is an excellent treatment. Proper wound care and antibiotics are the mainstays of treatment.

Mycobacteria are a unique class of bacteria. Tuberculosis is the most important disease caused by mycobacteria, but there are many others in this family. M. Cosmeticus is a newly described bacteria, which was first reported in 2004 from a nail salon (hence the name).

First, it is not true that there aren't any antibiotics to treat this. A rare case of a lung infection from M. Cosmeticus was successfully treated with a combination of four medicines that are commonly used to treat tuberculosis.

Second, not all infections, especially not all skin infections, need to be treated with antibiotics. Abscesses are commonly treated by draining them. Although we often also use antibiotics, drainage is the key part of treatment, and these usually heal without antibiotics.

It's useful to remember that before antibiotics were discovered in the early 20th century, most people were successfully cured of infections with wound care and supportive measures. Now that some bacteria have become resistant to all antibiotics, we occasionally need to rely once again on the surgical techniques that have been used to treat serious infections for centuries.

DEAR DR. ROACH: I have a venous lake on my lip. My dermatologist referred me to a plastic surgeon, but after consulting with him, I am hesitant to have a procedure that drastic. I am considering asking the dermatologist for a different type of referral, but what? -- S.L.

ANSWER: A venous lake is a benign condition of the skin, and although they can show up on the face or ears, I most commonly see these on the lips, where it looks like a bluish blister. They seem to disappear when compressed with a glass slide.

You don't need to do anything about it at all if you don't want to, but if its appearance bothers you, or it frequently bleeds, it can be treated with surgery. An alternative is laser treatment. Most plastic surgeons have experience with this, too.

Dr. Roach regrets that he is unable to answer individual letters, but will incorporate them in the column whenever possible. Readers may email questions to ToYourGoodHealth@med.Cornell.Edu or send mail to 628 Virginia Dr., Orlando, FL 32803.

(c) 2022 North America Syndicate Inc.

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