My PWP was admitted to the hospital with a hematoma of the leg that had become infected. He was placed on an intravenous antibiotic, 400mg moxifloxacin HCL (Avelox) every 24 hours. No other meds were given. After 4 days he was released and is now on 500mg of cefuroxime (generic for ceftin) 2x's daily. Since coming home, he has no endurance, feels tired and weak, and wants to sleep if he doesn't keep on his feet doing something.

Do antibiotics have a negative effect on PD medications? He is taking the "usual" meds (stalevo, requip, azilect and carbadopa/levodopa). I know stress plays a role in PD, but what about antibiotics?

He has an appointment tomorrow with the doctor who saw him in the hospital, but I'm not sure how knowledgeable he is when dealing with Parkinsons. Just wondered if anyone here has had a similar experience. (We will see his neurologist if this condition does not change.)

now he needs to be given a probiotic - kefir usually sold as kefir

found in organic yogurts - puts the flora back into the gi tract to help his immmune system stay strong...
Lactobacillus kefiranofaciens -go to www.answers.com

and he may need essential minerals,
found in fiji water but not gator aid - sugar is horrid on PD patients,
all things in balance are great - yet it is hard to find the body's pH balance...
so research - or google
intestinal flora -Intestinal Flora
"The entire world is covered with a layer of feces. Granted it is thicker in some places than in others, but a solid layer, nevertheless. . . ." This is how a wizened professor used to begin his clinical parasitology course for microbiology graduate students. Naturally all the students laughed, only to learn during the ensuing months that the statement is profoundly true. The lesson also bears truth in that fecal microorganisms arise from within the bowels of the digestive tract. The human intestine is home to an invisible and remarkable biosphere of living organisms dedicated to preserving its own existence. Humans serve as host to these billions and trillions of organisms that function in effect as a single living entity.

In fair exchange, during our lifespan, our gut flora provides us with health, protects us from disease, and serves as the major labor force to digest almost everything we eat—from artichokes to zebu.

The population of microbes that inhabit our intestines is made up of hundreds of different species of bacteria and other organisms. By far the vast majority of these are anaerobic, which means they do not multiply in the presence of oxygen. Since few if any anaerobes are defined as classic pathogens, by and large these anaerobes are only of interest to culinarians because they function to metabolize and break down what we eat and make it available to be absorbed and used as fuel and energy for our own body. Other species that require air (oxygen) to live are more commonly known by the general public, and a few have even achieved stardom, mainly because of their predilection to cause disease. Thus, certain bacteria such as staphylococcus, E. coli, salmonella, shigella, enterobacter, and others have become well recognized, if not feared—almost to the point of being a phobia—by some people, especially in the United States. Most people seem to be confused by too many overstated, highly publicized warnings, along with too many recommendations from too many different sources.

A list of the scientific names of all the different microorganisms that inhabit the human gut, sometimes described as autochthonous flora, would be very lengthy. Some understanding of science is required, however, in order to appreciate the very complex relationship we have with the microbial world living inside and on our bodies, which in turn help maintain the delicate balance between health and disease. Most important is the fact that each living human being has a rather steadfast and distinct microbial profile. This profile is almost as identifiable as a fingerprint.

When foreign bacteria are introduced to our profile, the ecosystem reacts rather quickly to disallow these species to proliferate. Accordingly, disease is not a normal finding; rather, we, for most of our existence, maintain ourselves in a general state of good health.

Some remarkable studies have demonstrated that even when our intestinal microbiologic profile is disrupted to the point of causing disease, for instance, in the case of traveler's diarrhea, the body mounts a tremendous effort to return itself to its normal healthful state, and in doing so somehow the original microbial profile returns. What we eat and how old we are does play a major role in the overall state of our live-in microbial population, and on occasion shifts of our profile do occur. For example, this happens when the microbes adjust to accommodate the various types of food we ingest. So, if we eat a diet of all starches, those species of organisms which thrive on starches will increase their relative numbers in relation to the frequency and amount of starch which we consume. When one considers diseases that are due to intestinal microbiota, it is also important to know what "pathologic bolus" means. Simply put, this phrase refers to the minimal number of pathogenic organisms needed to be ingested in order to cause a specific disease. It is usually expressed as numbers in powers of ten per gram or milliliter of menstruum. This number ranges from very large to very small, depending on the specific organism and disease. So, while certain diseases require huge numbers of bacteria in order to initiate illness, others require very few bacteria.

For example, not all salmonella species are pathogenic, and those that are generally require that a large pathologic bolus be ingested to produce illness. On the other hand, most species of shigella are intrinsically "pathogenic," and it takes only a small number to cause symptoms. It has been found, in this example, that salmonellae generally are susceptible to destruction by acidity of the stomach, and few survive to enter the intestines where the actual infection takes place. Shigellae, on the other hand, are able to withstand the acidity of our gastric juices and arrive in the intestine viable and ready to set up (unwanted) residence and cause disease.

Other major factors also play heavily in defining health and disease. Paramount to this struggle are the status of our overall nutritional habits and secondly the maintenance of the immune system and understanding how it functions to protect us from invading organisms.

In general, well-fed people are less likely to catch infectious diseases of any sort, and with some exceptions, the incidence and severity of dysenterylike diseases are also lessened if we follow a well-balanced diet. The amazing increase in the average height of individuals after the introduction of better food and balanced diets in certain Third World populations, which occurred in one single generation, is testimony to the tremendous impact diet plays in this regard. Individuals who suffer from underlying diseases and conditions that compromise the normal function of our immune system are much more vulnerable to life-threatening diseases caused by bacteria, viruses, and other organisms than are average citizens. Likewise, those who have lost protection due to impairment or destruction of the skin are much more likely to become ill. The causative agents in these cases are produced not only by recognized pathogens, but also come from normally benign species of so-called normal (or commensal) flora. Almost 90 percent of mortalities in burn patients are due to infection and sepsis. Furthermore, most of these deadly infections are produced by the patient's own intrinsic internal microorganisms. Notable for this discussion is that most foodborne diseases are indeed usually attributed to microbial species of the enteric type—"enteric" meaning those normally found in the digestive tract. When they are allowed to proliferate in nutrient-rich unrefrigerated foods such as potato salad, bacterial and viral "food poisoning" is likely, and outbreaks continue to afflict even the most civilized nations.

The most common cause of both direct and crosscontamination of foods, which ultimately can lead to such outbreaks, is unofficially labeled in medical vernacular the "fecal/hand/mouth" route—not a polite description, but accurate. Furthermore, although refrigeration and proper storage—and to a lesser degree chemical disinfection—are important, human hands remain the most villainous of vectors of food-borne disease. More important, frequent handwashing with regular soap and hot water remains the absolute best means of prevention.

Bibliography

Blank, Fritz. "Food on the Move: Travelers' Diarrhea: The Science of 'Montezuma's Revenge.' " Proceedings of the Oxford Symposium on Food and Cookery. Oxford, U.K., 1996.

Schaedler, Russell W., and René Dubos. "The Ecology of the Digestive Tract." Proceedings of the Cholera Research Symposium. Washington, D.C.: U.S. Department of Health, Education and Welfare, 1965.

Dubos, René, and Russell W. Schaedler. "Some Biological Effects of the Digestive Flora." American Journal of the Medical Sciences 244, no. 3 (September 1962).

—Fritz Blank



look up - electrolyte minerals -

and read about the bloods ph balance and health...
and ~~~~~~~~`
and everyone should know who Otto Warburg is:
Biochemist Otto Warburg (1883-1970) discovered cell oxidation and identified the iron-enzyme complex, which catalyzes cell oxidation. For this work, he was awarded the Nobel Prize in physiology or medicine in 1931.

Otto Warburg is considered one of the world's foremost biochemists. His achievements include discovering the mechanism of cell oxidation and identifying the iron-enzyme complex, which catalyzes this process. He also made great strides in developing new experimental techniques, such as a method for studying the respiration of intact cells using a device he invented. His work was recognized with a Nobel Prize for medicine and physiology in 1931.

Otto Heinrich Warburg was born on October 8, 1883, in Freiburg, Germany, to Emil Gabriel Warburg and Elizabeth Gaertner. Warburg was one of four children and the only boy. His father was a physicist of note and held the prestigious Chair in Physics at University of Berlin. The Warburg household often hosted prominent guests from the German scientific community, such as physicists Albert Einstein, Max Planck, Emil Fischer - the leading organic chemist of the late-nineteenth century, and Walther Nernst - the period's leading physical chemist.

you are a good person - thank you for caring for your husband w/ PD,
sincerely -

I will add some links at the bottom of this for you to print out and take to your doctor.

A large percentage of people, including PWP, have a colony of bacteria in their stomach called Helicobacter pylori (HP). Among other things, it causes ulcers. The two Australians who discovered it won a Nobel Prize two years ago. It is that important.

HP belongs to a family called "gram negative" bacteia, named for the way they stain in the lab. These bacteria produce a neurotoxin called lipopolysaccharide (LPS) and use it as a part of their cell wall. It is harmless there. But when the bacterium dies, it sends out a tiny cloud of a major toxin. And sometimes when it detects particular antibiotics and knows that it is under attack, some strains ramp up their toxin production. Two hundred fold.

One of the leading factors that set the stage for later PD is exposure of the fetus to LPS. This sets up a chain of events that sensitizes the adult to further exposure and leads to the brain's immune cells (microglia) over reacting and damaging neurons. Plus, LPS is, itself, a potent neurotoxin.

So, with all that preamble, your husband may be drowning in poison from the dead bacteria. I don't want to be overly dramatic, but if this scenario is true then certain steps must be taken as quickly as possible to get the toxin out of the bowel and to dampen the immune response. If your husband is constipated that makes it easy. Your doctor can just flush him out good. If he is not then it gets tougher and changing antibiotics might be in order.

Two things that have research behind them to calm the microglia and that you can start right now are green tea extract and silymarin.

I learned this the hard way and have two wonky fingers on my right hand to remind me. This is something each and every one of us could run into tomorrow. Wlk into the hospital with a bad bug and come out in a wheel chair.So everyone print this out and keep a copy in your wallet and give each of your doctors one. This is not something they are going to know. If they do then you have an unusually good doctor.


Here is an abstract for your doctor. I did not notice if you were in USA or UK, but Dr. Sylvia Dobbs at King's College in London might be worth your doc's call if it gets complicated. Good luck and let us know how it goes.


: Helicobacter. 2005 Aug;10(4):276-87.

Erratum in:
Helicobacter. 2005 Oct;10(5):557. Bjarnason, Inguar T [corrected to Bjarnason,
Ingvar T].

Role of chronic infection and inflammation in the gastrointestinal tract in the
etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets
of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A
randomized, double-blind, placebo-controlled efficacy study.

Bjarnason IT, Charlett A, Dobbs RJ, Dobbs SM, Ibrahim MA, Kerwin RW, Mahler RF,
Oxlade NL, Peterson DW, Plant JM, Price AB, Weller C.

Section of Neuropharmacology, Institute of Psychiatry, London, UK.

BACKGROUND: Links between etiology/pathogenesis of neuropsychiatric disease and
infection are increasingly recognized. AIM: Proof-of-principle that infection
contributes to idiopathic parkinsonism. METHODS: Randomized, double-blind,
placebo-controlled efficacy study of proven Helicobacter pylori eradication on
the time course of facets of parkinsonism. Intervention was 1 week's triple
eradication therapy/placebos. Routine deblinding at 1 year (those still infected
received open-active), with follow-up to 5 years post-eradication. Primary
outcome was mean stride length at free-walking speed, sample size 56 for a
difference, active vs. placebo, of 3/4 (between-subject standard deviation).
Recruitment of subjects with idiopathic parkinsonism and H. pylori infection was
stopped at 31, because of marked deterioration with eradication failure. Interim
analysis was made in the 20 who had reached deblinding, seven of whom were
receiving antiparkinsonian medication (long-t(1/2), evenly spaced) which remained
unchanged. RESULTS: Improvement in stride-length, on active (n = 9) vs. placebo
(11), exceeded size of effect on which the sample size was calculated when
analyzed on intention-to-treat basis (p = .02), and on protocol analysis of six
weekly assessments, including (p = .02) and excluding (p = .05) those on
antiparkinsonian medication. Active eradication (blind or open) failed in 4/20,
in whom B-lymphocyte count was lower. Their mean time course was: for
stride-length, -243 (95% CI -427, -60) vs. 45 (-10, 100) mm/year in the remainder
(p = .001); for the ratio, torque to extend to flex relaxed arm, 349 (146, 718)
vs. 58 (27, 96)%/ year (p < .001); and for independently rated, visual-analog
scale of stance-walk videos (worst-best per individual identical with 0-100 mm),
-64 vs. -3 mm from anterior and -50 vs. 11 lateral (p = .004 and .02).
CONCLUSIONS: Interim analysis points to a direct or surrogate (not necessarily
unique) role of a particular infection in the pathogenesis of parkinsonism. With
eradication failure, bolus release of antigen from killed bacteria could
aggravate an effect of ongoing infection.



PMID: 16104943 [PubMed - indexed for MEDLINE]




By the way, that first bold part is "Scientese" for "We scared ourselves silly and backed off real quick because we were afraid someone was going to get hurt."