So you drive over to the lab to have your blood work? In the near future, that would totally be ‘old-school’. Even if you so much as consider making that journey, you have GOT to be tempted to please think again! Time has been proven, repeatedly, to be of the essence, both for the sake of the diagnosis & treatment and the patient’s quality of life. For instance, imagine the convenience it will provide for an HIV-infected patient, who is what a lab technician would probably call a regular customer, due to the regular follow-up tests needed to monitor the development and treatment. Through a $10 piece of hardware connected to your cell phone, you will have your medical test results ready on the go. All you’d have to do is insert a slide containing a drop or two of your blood and leave the rest of the work up to the chip, as demonstrated on a prototype. I will even bet that, those who choose not to use it, would be charged extra for lab work!!!

The Ozcan Research Group at UCLA will already begin their field tests in Africa concerning the new cell phone/microscope gadget. I had to see to believe. Aside from all the engineering & technological aspects, which I am sure are quite many, if this were to be actually implicated worldwide, the possibilities of its application are endless, including, but not necessarily limited to, pretty much all of the blood-borne diseases. For instance, malaria, which is fairly common in many African countries, can be instantly diagnosed. The hospital would get the patient’s blood picture, through the cellular networks for analysis by physicians and there you have it.

Tags: advances in medicine, blood borne, blood picture, blood test, blook work, cell phone, diagnosis, HIV, lab work, malaria, microscope

Did you see some one before who can fly without wings or move without legs? You will answer : definitely no, but I know someone, or better yet some living thing, who can do just both and it is called Borrelia burgdorferi; let’s share its story. It is a loosely coiled bacterium belonging to a class called spirochetes (moving bacteria).

Borrelia burgdorferi is motile through the undulation of its axial filaments. It is transmitted to humans by the bite of infected ticks (Ixodes scapularis and Ixodes pacificus) and cause a serious progressive disease called lyme disease.

The story of lyme disease began in 1975 when a mother, with her children in lyme city in the United States, was admitted to a hospital with signs of rheumatoid arthritis. It was a mysterious case until the discovery of Borrelia burgdorferi and that is how the disease got its name, when it was discovered in 1982. Symptoms and signs of lyme disease can be categorized into three phases:

Phase (1): An early localized skin rash, characterized by inflamed red edges with a clear white center at the site of insect bite, appears and is called “erythema migrans“.

Phase (2): The rash resolves as the bacteria begin to move into the blood stream towards their target organs like large joints, heart, and nervous system.

Phase (3): Inflammation of heart muscle leads to abnormal rhythm, meningitis, confusion and finally arthritis.

Treatment in the early phase is an easy mission by amoxicillin or doxycycline, orally for few weeks. However, the recommended regimen in late stages include parenteral ceftriaxone, analgesics to control the severe pain, and anti-inflammatory drugs, usually required for months .

Images credits:
Borrelia burgdorferi: http://www.wadsworth.org/databank/hirez/hechemy2.gif
Erythema migrans: http://phil.cdc.gov/PHIL_Images/9875/9875_lores.jpg

Tags: bacteria, Borrelia burgdorferi, erythema migrans, lyme disease, meningitis, outbreak, rheumatoid arthritis, ticks (Ixodes scapularis and Ixodes pacificus)

Hello, hello. You’re now tuned to your favorite blog: micro-writers.egybio.net. Tonight we have this very special guest, live, online. After two months of waiting, we finally got this exclusive interview with the emerged Streptococcus pyogenes strain, the most dangerous ever, M1T1. We have it here, with us, in the studio.

– Hello, M1T1. Welcome in our studio.
– Hey there.

– We knew from our resources, which are totally classified, that you got yourself in trouble recently.
– (Interrupting), I did NOT get myself in trouble. EID set me up.

– M1T1, Would you please calm down & tell us a little more about yourself?
– Well, I belong to Group A streptococci (GAS) aka Streptococcus pyogenes. M1T1 is my serotype; I’m just a clonal strain. As you know, S. pyogenes colonize human skin & throat causing either non-invasive (sore throat, tonsillitis & impetigo) or invasive (necrotizing fasciitis NF, scarlet fever & streptococcal toxic-shock syndrome STSS) infections. Actually, NF gave me my nick: Flesh-eating bacteria.

– So, you cause all people NF & STSS?
– No, kid. It depends on their genetic susceptibility, what you call “Host–pathogen interactions”. I was isolated from patients with invasive as well as non-invasive infections during 1992–2002. This is NOT entirely my fault; humans can make me extra virulent by selecting the most virulent members.

– Back to your history, when have you exactly been isolated?
– M1 & her sisters were the worst nightmare in US & UK in the 19^th century as they caused the famous pandemic of scarlet fever. “Nevertheless”, early 1980s was the golden age of my strain as well as my very close sisters M3T3 & M18. We caused STSS & NF in different parts of the world. Great times, great times!

– Only for you, I suppose! So, what made you hypervirulent? What caused you this “epidemiologic shift”?
– Two reasons Dr Ramy K. Aziz identified that improved my fitness to humans: the new genes I got from phages & “host-imposed pressure”. Both resulted in the selection & survival of me M1T1 the hypervirulent strain. Dr Aziz’s work at Dr Kotb’s lab resulted in identification of a group of genes I got from phages that changed my entire life.

– Interesting! Tell us more about that. How did phages “change your life”?
– Dr Aziz proved that I differ from my ancestral M1 when he found that I have 2 extra prophages (lysogenized phages didn’t get the chance to lyse me, so they became integrated in my genome):
1. SPhinX which carries a gene encodes the potent superantigen SpeA or pyrogenic exotoxin A (scarlet fever toxin).
2. PhiRamid which carries another gene encodes the most potent streptococcal nuclease ever, Sda1.
3. He also found that phages conversion from the lytic state to the lysogenic state resulted in exchange of toxins between our different strains (aka Horizontal Gene Transfer). Phages are very good genetic material transporters, what makes “strains belonging to the same serotype may have different virulence components carried by the same or highly similar phages & those belonging to different serotypes may have identical phage-encoded toxins.” What a quote from Rise and Persistence of Global M1T1 Clone of Streptococcus pyogenes.

– Well, It was not that interesting. So, what? What’s the significance? How that made you hypervirulent?
– You can’t get it? You’re not that smart, are you? Tell me, what made M1 hypervirulent causing scarlet fever in the 1920s and me hypervirulent causing STSS in the 1980s with a 50-years decline period?

– Superantigen?
– Exactly. You do have your moments! Superantigen encoding-gene was present in us and absent in strains isolated in the period between them. The interesting part, for me of course, that humans after 50 years of absence of hypervirulent strains had absolutely no superantigen-neutralizing antibodies. That was the real invasive party. Superantigen causes high inflammatory response because of its non-specific binding to immune system components (antibodies & complements) causing an extremely high inflammatory response. In fact, SuperAg inflammatory response is “host-controlled”.

– So, what about Sda1?
– Streptodornase (streptococcal extracellular nuclease) helps me to degrade neutrophils that entrap me in the neutrophil extracellular traps (NETs). So, I can invade humans freely & efficiently and be able to live in their neutrophils. Dr Aziz proved in his paper “Post-proteomic identification of a novel phage-encoded streptodornase, Sda1, in invasive M1T1 Streptococcus pyogenes” that it’s all about C-terminus in my Sda1; the frame-shift mutation increased my virulence while deletion decreased it.

– Now we know about your SuperAg & nuclease (DNase), what’s the “host-imposed pressure”?
– I have my own SpeB (Protease), I use it to degrade my other proteins (virulence factors), which provides me with a good camouflage & gives me access to blood. When the host immune system recognizes me, it traps me in NETs. At this time, I secret Sda1 to degrade neutrophils. Actually, SpeB protects you, humans, from my Sda1& my other toxins. When SpeB was compared in patients with severe & non-severe strep infections, it was found that SpeB wasn’t expressed in case of severe infection. Expression of SpeB may be host-controlled, as host selects the mutants with a mutation in covS, a part of my regulatory system which regulates my gene expression including SpeB gene.

– Finally, M1T1. How do you see your future?
– More new phage-encoded genes, more selection of the hypervirulent strains by the host & more regulation of expression of my virulence factors. Pretty good future! I also count on humans to not develop immunity against me like what happened in 1980, when I got new virulence factors or allelic variations in my old ones.

Thank you, M1T1. Pleasure talking to you…….M1T1? M1T1, where are you? Why do I feel this strange pain in my throat?

Image credits:
Streptococcus pyogenes: http://adoptamicrobe.blogspot.com/

Tags: covS, epidemiologic shift, flesh-eating bacteria, global M1T1 clone, group A streptococci (GAS), horizontal gene transfer, host-imposed pressure, host–pathogen interactions, impetigo, M1T1, Malak Kotb, necrotizing fasciitis, neutrophil extracellular traps (NETs), phage-encoded toxins, pyrogenic exotoxin A, Ramy K. Aziz, S. pyogenes, scarlet fever, sore throat, streptococcal nuclease Sda1, streptodornase, STSS, superantigen SpeA, tonsillitis

It’s hard to talk about someone you know who passed away, but, believe me; it’s harder when you talk about someone you know nothing about. To know someone better, you have to read his writings or, simply, read what his friends wrote about him. Reading what a disciple of his, David M. Morens the director of the National Institute of Allergy and Infectious Diseases, wrote about him made me believe that Dr. Gregg is the luckiest person on the planet by gaining this undeniable love & appreciation from his students. Dr. Gregg died on July 9, 2008 at the age 78.

Michael B. Gregg, M.D. was born in 1930 in Paris, France. He was educated at Stanford University and Western Reserve University School of Medicine. He entered the Public Health Service in 1959 right after he completed his residency in internal medicine at Columbia Presbyterian Hospital in NY. He first served at the National Institutes of Health Rocky Mountain Laboratory. He then trained in infectious diseases in Lahore, Pakistan before he joined CDC (it was known as the Communicable Disease Center) in 1966 as Chief Epidemic Intelligence Service Officer (EISO). From 1967-1988, Dr. Gregg (or Mike like everyone in the CDC used to call him) was the editor of the MMWR. His writing style “just the facts” made thousands of epidemiologists believe that good medical writing indicates clear thinking, which is the only thing needed in Epidemiology. In 1975, Mike was the MMWR editor, Viral Diseases Division director and deputy director of the Bureau of Epidemiology.

Mike was not only a MMWR editor, but he taught hundreds of students in NIH & CDC to become leaders in epidemiology & public health. Mike’s textbook “Field Epidemiology” (Don’t get extremely excited, It’s a link to the review not the book itself. My apologies.) is the “go to” book in breakout investigation & to solve public health issues. As David M. Morens says, it reflects his very wide experience in national as well as international epidemiology including:

1. Pontiac fever/Legionnaires’ disease (1968/1976) [Ligeonella pneumophila – Philadelphia] First, it was thought to be a 1918-like influenza pandemic, but Mike kept running through the history of Influenza & other respiratory diseases, the epidemic ones. After a couple of days of collecting info, Mike was the first to say: “This is beginning to look like Pontiac fever.”
2. Swine flu (1975–1976) [Hsw1N1 – New Jersey]
3. Guillain-Barré syndrome (1977)
4. Ebola hemorrhagic fever (1976) [(-)ssRNA virus – Zaire & Sudan]
5. In the June 5, 1981 issue, he published a report about 5 Pneumocystis carinii pneumonia cases. Such disease was rare, so he wrote a note saying: “the case histories suggested a cellular-immune dysfunction related to a common exposure, a disease acquired through sexual contact”, which we know now as HIV/ AIDS. It was the first report about it.
6. He helped in putting on the epidemiology map of Reye syndrome (1973–1977) [A fatal disease associated with Aspirin consumption when having a viral-disease e.g. Varicella – Ohio] , Kawasaki disease (1977), and toxic-shock syndrome (1980) [S. aureus]. He was consulted in the SARS outbreak in 2003 [Severe acute respiratory syndrome (+)ssRNA coronavirus] even after his full retirement.

Mike used to give the epidemiology course each July. The first subject was: “How to investigate an epidemic”. His first words were: “First, you need to find a good map…” He was teaching his students to keep an open and interested mind, to remain flexible and creative, to rethink and to assemble the puzzle pieces quickly to get the big picture.

“It’s better to be approximately right today than exactly right tomorrow,” a phrase said by Michael O’Leary, a former epidemiology student of Mike rephrasing his description of epidemiologists’ work: “Quick and dirty”.

Image credits:
Michael B. Gregg: http://www.cdc.gov/

Tags: ebola hemorrhagic fever, field epidemiology, Guillain-Barré syndrome, Michael B. Gregg, MMWR, Pneumocystis carinii, pontiac fever, reye syndrome, SARS outbreak, swine flu, toxic-shock syndrome

Researchers at Yale & the University of Chicago were faced with a surprising conclusion based on their scientific experimentation on mice. Unlike the common belief that microbes are in fact “bad” & possess a harmful threat to our health, some of these bacteria prove their innocence. Mice, that were exposed to common bacteria in the normal gut flora, were protected against the development of Type I diabetes. Previous research had shown that mice, exposed to killed Mycobacterium tuberculosis, were also protected. So, this means that mice that grow in their natural habitat are better off than the ones raised in the much improved sanitary conditions of the lab.

This comes to support the hypothesis many scientists have lately adopted. They tend to believe in a directly proportional realtionship between a person’s exposure to parasites, bacteria, worms, etc.. within the surrounding evironment and his immunity. The more, the better..that is within limits of course.

This actually makes perfect sense to me. It is really obvious when you see, for example, people living in third world countries with mosquitoes hovering around and considered normal. But when they travel abroad for a while and come back, they get different sorts of allergies & rashes from those previously “harmless” mosquitoes. What parasites and microbes do for you is not all bad. Unfortunately, I had to experience this dilemma.

Source: ScienceDaily

Tags: bacteria, diabetes, flora, immunity, mice, tuberculosis, Yale