Unpublished novel by Rakesh Biswas for all interested in the science and fantasy of medicine. Not about religion, but a postmodern multi genre combining elements of Science, Fantasy and Romance
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Settling down to a new dream

 

June’s diary Feb 4th 2003

 

The bus isn't crowded like a regular city bus. A few passengers get down at a nearby stop. A new passenger gets up and eyes me with a hint of recognition. One of my patient's relatives I presume.

The next bed in the special ward is a 90-year-young Second World War veteran. It has been years since he left the army and came down to his village, enjoying the gentle comforts of rural life. His abdomen was distended with fluid in the sac covering his intestines. This sac was made of a thin layer of cells and had been also covering his lungs since he was a fetus. At his age of 90 as the fluid in the sac covering his intestines increased water also seeped into his lung coverings. The cause of all this water accumulation was off course in his liver that over the years of dealing with a generous supply of Alcohol had fibrosed…or did it just age like all other cells of his body? No...Aging wouldn't cause fibrosis. Whatever it was, all this fibrosis was compressing the pipes supplying blood to his liver. The rivers inside those pipes were trying to find other avenues of drainage by trying to percolate into his visceral coverings. We thought it was alcoholic cirrhosis. We questioned him on his alcohol habits. He said he did take alcohol and with a wink added it was just to taste her daughter's home made local brew to make sure the taste was all right for their guests.

As the bus drove into the lakeside we made our way through a variety of stores selling items of tourist interest, trekking shoes, sleeping bags, instigating us to take off into the wild, away from this busy market place.

The lake was calm with a few boats gently drifting in its midst. There was an island which too seemed to be drifting. A few rain clouds had descended on the adjoining mountains full of lush green forests, a pagoda stared at us from its top. We watched our surroundings from a comfortable vantage point near the lake, inside an open air restaurant, a few buffaloes having a dip, children diving in to join them with a splash.

 

June felt relaxed swimming with her colleagues after having taken the plunge into her new job. She was a consultant trouble shooter now and a teacher-lecturer at that. Their hospital didn’t lack in system problems. Solving these were at the same time less taxing as the number of patients wasn’t very high like in city hospitals. She put all her heart and soul into dealing with them as best as she could and reveled in the questions asked by her students, an important way to keep learning.

 

 

 

 

 

 

 

The story of glomerular injury 1

 

It has been long since June met Professor Joatmon in his limestone cave of holistic medicine full of stalactites and stalagmites. At present if you move these curtains you can spot June looking smart in that suit, standing on the pulpit with a laser pointer in her hand. She’s become an Asstt professor herself now, teaching in the Macchapucchare College of medical sciences, Nepal. She’s at the moment presenting a paper on preventing and managing glomerular diseases in the community. You can stay on if you’d like to view her presentation.

June starts off with, “May we have the first slide please?”

 

 

The first slide is a picture of Macchapucchare teaching hospital, Pokhara, Nepal where I live and work.  To talk on renal diseases their impact and strategy for long-term solutions I am going to begin by relating a story, which has been synthesized from the stories of a number of our patients and doesn’t necessarily reflect any real life patient. Prem Bahadur Khadka (not his real name) is a 25 year old boy who hails from a remote village near Jumla, Nepal and had never seen a bus or car in his life before he left his village for higher studies.

This is his village where the only means of travel was an airstrip apart from the other option of a few days of walking

Prem was intelligent and soon after he finished his 10th grade exams he decided to leave his village for higher studies.

 

 

The story of glomerular injury 2

 

 

 

 

He came to Pokhara, enrolled in a good school and saw proper roads and vehicles for the first time.

As he was a good student he got into engineering and after finishing his degree, arrived in US as a software analyst. However he felt miserable there as he kept missing his relations and his mother’s cooking (among other things). He was actually relieved when he got the pink slip and lost his job after the economic slowdown.

 He came back to his village (and his mothers cooking) but found that by now he couldn’t adjust with his brothers who knew more than him about farming and all his knowledge of software was of no use in the village (which didn’t even have a single computer)

 

 

 

 

 

 

 

 

 

97

 

 

 

 

The story of glomerular injury 3

 

 

 

 

 

While all this was happening to Prem our protagonist in his macrocosm, quite unknown to him or anybody else a major war had already started inside his kidney where his glomeruli were being attacked by a lot of inflammatory cells.

 This is a cartoon borrowed from Harrison’s principles of Internal Medicine, which shows in molecular detail the happenings inside a cell in Prem Bahadur’s glomerulus. You can see how the antigens are processed and finally parceled into an endosomal compartment containing the MHC class II molecule .The antigen settles down into the groove of the MHC and sets off a chain reaction stimulating a clonal proliferation of hordes of inflammatory T cells.  

 

 

 

 

 

The story of glomerular injury 4

 

 

 

 

This is the strong inflammatory response inside Prem Bahadur’s glomerulus as a result of which we expect to see a lot of protein and RBCs in his urine (if only we could have examined it earlier). However Prem Bahadur didn’t notice anything wrong with his urine. His neighbors noticed him growing plump day by day and complimented him on this sign of prosperity. At first Prem Bahadur was also happy that he was getting fat but later noticed that he was unable to enjoy his mother’s cooking due to a feeling of extreme nausea. This too was ignored by him until one day he developed extreme breathlessness and had to be rushed to our hospital in Pokhara. 

 

 

 This is a picture of our hospital on a stormy night. When I saw him in our casualty (for the first time) I found him gasping for breath, his lungs were full of crepitations which we quickly treated with Lasix and referred him to Katmandu for dialysis. At Katmandu they dialyzed him for fluid overload and a urine analysis subsequently showed 3+ proteins and plenty of RBCs suggesting acute glomerular injury. He was immediately treated with high dose steroids and a renal biopsy was done.

 

The biopsy showed focal areas of glomeruli that were sclerosed in segments.

 

 

 

 

 

The story of glomerular injury 5

 

The fire was too severe to be quenched with steroids and it was already too late to prevent Prem Bahadur’s kidney from blowing up in smoke.

 

 

 

He received a few more dialysis from Katmandu and spent whatever money he had earned over the past few months. His brothers came forward to donate their kidneys for transplantation but that would mean selling off their land and cattle to go to one of the hospitals in India and Prem Bahadur wasn’t keen on that. The next slide is a Haiku sequence, which was mailed to me by a friend right after 9/11.

 

 

The story of glomerular injury 6

 

The last I heard of him was through one of our medical students also from the same village. Prem was spending his last days in deathbed with his family praying for him daily and it would be a matter of days or months before death would take him.

 

 

 

 

This is a summary of the story of glomerular injury which describes how it’s initiated by breakdown of tolerance leading to reactivity of antibodies with planted glomerular antigens which in turn generates a chemical cytokine mediated response leading to proliferation of inflammatory cells and subsequent irreversible renal damage (in a substantial number of people).

 

 

 

 

 

 

 

 

 

 

 

The story of glomerular injury 7

 

 

The key word here is tolerance and (next slide)

 

 

 

 

 Tolerance is fast becoming popular in transplantation research but we need tolerance urgently before the need for transplantation arises to save our native kidneys (before the inflammatory cells attack them). As much as we need tolerance to save this Earth before a full-fledged war breaks out. That is the problem of glomerular injury for we don’t really know why this breakdown of tolerance occurs. We don’t even know why hypertension or diabetes occurs (for that matter). Our present strategy is only to control them in the hope of slowing the progression of renal disease.    

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Going up and down tops and bottoms

 

June had begun the most crucial learning phase of her life that God was looking for. There were two traditional approaches to learning, the top down and the bottoms up. Like her friend Paul from the complexity list elaborated in an email, “Top down is a pre-formed idea and we can choose to say yes or no. Bottom up is an exploratory idea where new direction can be woven from multiple diverse strands (many of which can be "top down"). Top down is essential; bottom up is existential. Top down relates to realist ontology - it is really objectively there; bottom up relates to relativist ontology - it is there if it is meaningful to you. Today's bottom up can be tomorrow's top down and vice versa. Top down in one place is bottom up in another.  The two are constantly (and rightly) interwoven at all levels.

June's undergrad years had been more top down assimilating her tools, a knowledge base accumulated over decades of bottoms up research by physicians of yore. Now was the time to use the tools she had acquired to fix human systems independently in a judicious mixture of the two approaches”.

Jung Bahadur Gurung was a retired Indian army soldier who came into her outpatient chamber with a complaint of fever for a month. For a number of years he had had severe pain abdomen coming on intermittently for a number of years. He had yellow eyes that looked quite unwell and he kept scratching his body. June did a quick system river check and his blood tests indicated an inflamed liver evidenced by the enzymes. It also suggested the inflammation was obstructing the outflow of bile from his liver and this was producing all the scratching. June's gut feeling told her it was a granulomatous inflammation of the liver possibly due to tuberculosis.

Jung Bahadur was admitted for a liver biopsy after June asked her radiologist friend to look for and rule out any dilated bile pipes inside the liver that might suggest a block to the pipes carrying bile into the liver. He took a quick look with an ultrasound beam and reassured her that the liver pipes were all right. June went ahead with the liver biopsy and got her liver tissue but was shocked to find that she was hitting pus. That night the pressures inside Jung Bahadur’s system rivers hit an all time low at 60 mm of mercury even as his temperatures swung up to a high of 40 degrees cent and June thought she would lose him. The commonest complication of a liver biopsy is bleeding from the liver bed but June was puzzled as his hemoglobin was not dropping. A repeat ultrasound examination revealed a large sub diaphragmatic abscess that had been overlooked in the previous ultrasound. June realized she was partly responsible for this as she had hurried the radiologist into simply ruling out a specific top down problem and not having allowed him a complete bottoms up look. Jung Bahadur was operated for the abscess below the diaphragm and the surgeons also discovered a perforated gall bladder. The pus had obviously come from an infected gall bladder and the organism was found to be Salmonella paratyphi. Salmonella getting into the blood stream was a common cause of fever in this part of the world but this one had got into the gall bladder, perforated it and caused an abscess manifesting as prolonged fever. Jung Bahadur followed up with June for years to come after his complete recovery.

 

 

Fever bugs in system-rivers

 

Apart from the unusual presentations of fever the usual fevers were no less interesting. Typhoid was endemic in the area, possibly as compensation to malaria that was less common. Typhoid meant, ‘like Typhus’, which was less common but present nevertheless. Systems afflicted had this splitting headache, apathy and loss of appetite. Most systems malfunctions could be classified into that affecting the system from outside (bugs getting in through online attachments) or from inside due to the systems anti-bug defense software gone awry. June got to see more of system problems due to outside bugs. Fever was indicative of the anti-bug software working overtime, producing chemicals like lymphokines that when dumped into system rivers would naturally heat up the system. The commonest bug to cause seasonal fevers was off course the common cold virus where systems would start blowing their nose along with sneezing and dripping secretions everywhere. Most of these malfunctions would be temporary and would subside on their own hardly requiring any anti-bug software. The Typhoid bug on the other hand would also produce high grade fever that would characteristically refuse to touch normal baseline in the first few days. June found monitoring system temperatures by plotting a 4 hourly graph quite useful in differentiating between viral and typhoid fevers at least in the initial two or three days. It was all the more necessary to prevent misuse of anti-bug software in the community. In fact anti-bug misuse was assuming epidemic proportions in the community far greater than the bug epidemic. Once anti-bug software was used frequently the bugs would get to recognize their weak spots and modify their codes accordingly so they could escape their next onslaught. Most community practitioners, health assistants and physicians alike resorted to prescribing antibiotics under the mistaken assumption that they would bring prompt relief. June found it was paracetamol that would be able to give them better relief. Anti-bugs more often would just add to the misery by producing diarrhea. She began to design a prospective trial in the community to see if distributing fever charts to patients could really help to bring down this present epidemic of anti-bug misuse. Apart from the common typhoid, June noticed another particularly different pattern of fevers, as high grade as typhoid. It was however intermittent in pattern even in the very first days of its appearance and was remarkably resistant to anti-typhoid software. It would come in epidemics every monsoon and most people affected were farmers. They had biochemical abnormalities in the form of raised enzymes in their liver function tests and mild degree of proteinuria and WBC casts suggesting a liver and renal involvement. This was Typhus which responded remarkably to another software, doxycycline. The name Typhoid was actually derived from Typhus meaning typhoid like and yet Typhoid ruled the roost as an endemic disease while Typhus was just an epidemic visitor. There were systems met infrequently that would present with continuous fever where no amount of investigations would reveal any clue. Very often they would demonstrate multi-component involvement, be it in the joints, or skin, or kidney filters, or heart, lung coverings or even the bone marrow affecting their cell producing assembly lines. Here it was the systems own anti-bug defense gone awry attacking and corrupting own files. Most of them responded to software termed immunosuppressive. Sometimes they would respond to nothing.          

 

 

The cranky irritable bowel

 

June’s diary (draft of a mail to Jo- on her experiences with the irritable bowel)5

 

My first acquaintance with the disease was possibly at a time when I didn't have any connection with medicine. It began with my father. He was a very meticulous man and was by profession an anthropologist-teacher. His abdomen at that point of time while I was in school oblivious of my future medical career was gradually putting on a paunch. It was not however his paunch that bothered him, it was gas. Gas always used to have ticklish connotations for us young ones probably as it came out from banal orifices producing an offensive sound and odor. However it was not the coming out of gas that seemed to bother him. It was the not coming out part that was most worrisome. He used to feel miserable about his intermittent abdominal bloating, producing a diffuse pain. Very often he would express his anguish by percussing various parts of his abdomen, even while moving around with his daily activities until it became a habit. He even developed a philosophy of happiness which stated that all cause of human misery lay in the abdomen. If only abdominal organs functioned well, everything would be perfectly alright in this world. Surprisingly he grew out of it although it took him years and I no longer find him percussing his own abdomen. I went on to meet similar people in my human trouble shooting career. At first I used to attribute them to protozoan infestations like Giardia or Entamoeba so very endemic in our part of the world but gradually realized that most often no cause could be detected. There were so many criteria to identify the irritable bowel and most of these problem patients would satisfy quite a few. The treatment was however dismal as the cause wasn’t clear. It was a disturbance of bowel movement alright but then why should the bowel move so mischievously at times? A typical scenario was the bowel moving in alternate contraction and relaxations and suddenly at one point of time stopping randomly followed by distension of that halted segment until the human carrying the bowel winced in pain. Mercifully it would pass off after some time, the distended colonic gas coming out silently or otherwise and you’d find a relieved expression on his face. Another way it would present was an urge to defecate at times especially when the subject was engaged in some kind of work, tedious and boring but important nevertheless. However what would come out could hardly be called fecal matter rather than that which was normally present on the surface of the colonic mucus membrane, ‘mucus.’ Each time one passed stools one felt there was more to pass, a sensation termed tenesmus that was possibly due to colonic spasm. Eighty of hundred patients in my outpatient clinic with abdominal pain going on for a very long time could be classified into this pattern.     

 

 

 

 

 

 

A dysfunctional dyspeptic stomach

 

Vatta- an Ayurvedic concept: People with predominance of disorders of movement or motion in the body

 

It was not just the lower bowel whose movement was at fault but even the upper bowel along with the stomach would refuse to budge at times. This produced an upper abdominal epigastric discomfort frequently labeled dyspepsia. June would put in flexible telescopes with lighted lens into these mischievous bowels either from above or below to look for anything that could be treated but no it was something to do with the electrical wiring of their slow moving pipes that wouldn’t move because of frequent current failures. There was no way she could have their wiring replaced. What could have led to their movements getting awry? She decided to drop a mail to her old professor Joatmon.

Dear June, Sitting in a busy OPD (with both patients and students) and evaluating dyspepsia (which happens to be one of the commonest patient complaints in the OPD closely rivaling headaches and chest pain) one needs to develop a quick but full proof strategy to evaluate these patients. We had been taught a lot of clinical features to distinguish between duodenal and gastric ulcers in our undergraduate days but what we possibly needed more was to distinguish between ulcer and non- ulcer dyspepsia.

Dyspepsia subgroups

 

 Reflux-like dyspepsia

  • Heartburn plus dyspepsia
  • Acid regurgitation plus dyspepsia

Ulcer-like dyspepsia

  • Localised epigastric pain
  • Pain when hungry
  • Pain relieved by food
  • Pain relieved by antacids or acid reducing drugs
  • Pain that wakens the patient from sleep
  • Pain with remission and relapses

Dysmotility-like dyspepsia

  • Upper abdominal discomfort (pain is not a dominant symptom)
  • Early satiety
  • Postprandial fullness
  • Nausea
  • Retching or vomiting
  • Bloating in the upper abdomen (without visible distension)
  • Upper abdominal discomfort often aggravated by food                                                  pg 106

 

 

 

Setting gas purely unconditionally free

There are a lot of clinical subgroups initially devised in the hope of achieving therapy tailored to specific symptoms but they don’t help in distinguishing clinically between ulcer and non ulcer dyspepsia. In fact the only thing, which might give us a clue to an ulcer or an endoscopically verifiable structural lesion, is the presence of recent onset dyspepsia. Patients having symptoms of long-term dyspepsia do generally turn out to have no ulcer disease on Endoscopy. In a Western series, only four out of 165 dyspeptic patients who did not have a peptic ulcer at initial Endoscopy developed an ulcer over 10 years of follow up, although 62 (58%) of the 106 who still had dyspepsia 10 years later had ulcer- like symptoms. What then is the cause of this dyspepsia, which is so very distressing to our patients? If most of them are supposed to have ulcers only when the dyspepsia is recent could it be that the ulcers heal and leave no trace of organic lesion but do cause some neural damage on the long run affecting gastric/bowel function.

In many patients, failure of the peristaltic wave to propagate results in upper abdominal discomfort, early satiety or post-prandial fullness (doomma houni) or a sense of gano-gola formation. There are no medicines yet in the market to really improve bowel motility ( Cisapride, metoclopramide and domperidone aren’t practically that effective) , however there may be some benefit in walking after meals, at least this has been demonstrated to improve gastric motility in diabetics. It’s rather surprising that it hasn’t yet been tried or verified in non ulcer dyspepsia.

There are many questions, which remain unanswered even in ulcer dyspepsia. Like why does H. Pylori eradication only improve ulcer healing and doesn’t have much benefit in non-ulcer dyspeptics who harbor H. Pylori? Is it because H. Pylori is not really the causative agent of ulcers but only responsible for delayed ulcer healing?

I would suggest that you counsel your patients to optimize their bowel movements such that their bowel doesn’t get confused. All they need to do is move it everyday at particular fixed times. In other words eat and pass stools at the same time every day. As these bowels are autonomic and do not directly take orders from the brain they can only be regulated by timely stimuli or signals to their electrical apparatus. Walking regularly in addition would also offer a timely stimulus to their regular movement. Same could be inferred about sleep I guess but all these definitely need to be validated by controlled trials and why don’t you take up the challenge? Jo.

 

 

 

  A blackening lady

One day, June noticed in her outpatient department a middle aged lady who appeared strikingly black, a complexion never noticed in her part of the world. She quickly asked her in and admitted her after a brief history.

She was a 40 year old lady from Mustang valley, Nepal and her main complaint was progressive blackening of her whole body since one year. She also had associated weakness along with loss of weight (>50%) and appetite. Since one month she had also developed progressive contractures of her knees and hips and was virtually bed ridden. She had taken some indigenous medicines for her troubles that continued however. The exact nature of the medicines could not be ascertained. She was also amenorrhoeic since a year. Fifteen years ago, she reported having fallen very ill once with cough and fever and was treated again by indigenous medicines. The illness had lasted for 1-2 months after which she recovered almost as if from death-bed.

On physical examination she was cachectic (weighing 30 kgs) and pale along with diffuse hyper-pigmentation of skin and dorsum of the tongue. The blood pressure was 84/60 mmHg in the right upper limb and pulse rate was normal. The abdomen revealed a mild diffuse tenderness and the knee and hip joints showed bilaterally symmetrical contractures. There were no other remarkable findings on systemic examination. Her Hemoglobin was 11g/dl and total leukocyte count was 6,200 with a normal differential count. The serum sodium was the lower limit of normal at134 mmol/L and the serum potassium was 3.3mmol/L. The liver function tests showed a mild rise of enzymes. The chest X-ray showed a small calcified focus in the left upper lobe of lung. An ultrasound revealed a right suprarenal hypo echoic mass posterior to the Inferior vena-cava, measuring 2.5 X 1.8 X 1.6 cm. Displaced retroperitoneal fat planes seen between the mass and adjacent liver parenchyma suggested it was an adrenal mass. There was no similar obvious mass in the left adrenal area. An ultrasound guided fine needle aspiration was performed which showed frank pus. This on further microscopic examination showed gram negative bacilli that on culture grew mucoid colonies indicating Klebsiella pneumonia sensitive to ciprofloxacin, Gentamicin, Cephazolin, ceftazidime and resistant to Ampicillin. The patient was already put on Anti- tubercular therapy after a clinical diagnosis of Addisons disease along with steroids. After the report of the pus culture sensitivity oral Ciprofloxacin was also added for 2 weeks. On follow up after 6 months, the patient reported an increase in appetite and strength, the blood pressure was 100/70mmHg on the average along with a 4 kg weight gain and the contractures improved with physiotherapy as the patient gradually became ambulant. A repeat liver function test showed normalization of the enzymes level.

 

 

 

 

A web based doctor patient relationship

The patient gave June and her colleagues a lot of surprises. Although C.T scans are known to reveal enlarged adrenals at advanced stages of tubercular Addison's disease, it is not very common to visualize them on ultrasound, let alone do an ultrasound guided fine needle aspiration. To her further wonder it turned out to be pus, which revealed the bug Klebsiella pneumonia as a possible source, hitherto unheard of as producing Addison's disease. There were two possibilities, either it was secondary bacterial infection on top of primary involvement of the adrenals with tuberculosis or it was a primary infection of the Klebsiella Pneumonia involving the adrenal gland. Odd for the bug Klebsiella was the remarkable lack of fever, or any other symptoms to suggest the portal of entry (unless it was the febrile pneumonia like illness she had had 15 years back). However a source could also have been from the urinary tract as Klebsiella is known to cause asymptomatic bacteruria. June posted her experience on a medical web site and one fine day was surprised to receive a mail from another patient long after she had put the whole thing at the back of her mind.

Dear June, I read your case report "A blackening Lady".  I found it interesting. 

 

I am currently treating Klebsiella pneumonia bacterial infection. 

 

Would you please respond with your thoughts on the following question...

 

I'd struggled with recurring symptoms related to klebsiella infection for the past 15 years.  In the beginning of those years, I was suffering with recurring flu-like symptoms.  Bronchial infections began then as well and continued to return (with the "current jelly sputum").  Urinary tract infections recurred often, a back problem began 7 years ago and progressively grew worse...I was told it was termed ankylosing spondylitis.

 

Here's my question...How long can an overgrowth of klebsiella pneumonia bacteria be present?  Is it reasonable to assume that this has been the underlying problem for these past 15 years?  According to the research I'm finding it would seem logical, yet I cannot locate any information regarding how long this overgrowth can remain in the body. 

 

The one mention of that issue was stated "death occurs within 48 hours", I believe that is inaccurate information.  Can you assist me with this question? 

 

I'd greatly appreciate you're response. Chris Jestus, Minnesota

 

 A web based relationship 2

 

Thanks for your mail. Could I ask how you chanced upon my article? Before I attempt to answer your questions I need to clarify your symptoms in the history. Where was the klebsiella in your case isolated from? Was it the sputum or the urine? How many times has it been detected in your sputum/urine? Klebsiella can present in a variety of ways and our "blackening lady" was one of them. It can present as severe sepsis where the bacteria continue to divide relentlessly and can definitely kill a patient in days. However in your case its presentation seems to be what I understand from your history as a recurrent respiratory tract infection in which case it’s unlikely that it will do much damage. Please let me know the details, particularly if there is any finding in your Chest X-ray. Thanks for writing and do reply for I want to help you solve your problem, yours sincerely

Juneli Sen. MD, Asstt Prof,

Dept of Internal Medicine,

Macchapucchare College of medicine, Pokhara,

Nepal. PIN -33701

Phone: 00977-61-26416-extn-189,

Fax-00977-61-27862

 

Dear Juneli, Thank you for responding.   

    

I chanced upon your article by researching Klebsiella Pneumonia bacteria; I've been looking into many sights to confirm my belief that the Klebsiella has been the underlying issue in my situation.  I believe, based on the research I'm finding, that it is possible.

 

The Klebsiella bacterium was detected through Comprehensive Stool Analysis, through Great Shakes Diagnostic Lab.

 

Regarding the sputum and urine... the sputum was never tested, yet in the past have had sputum that was very concentrated (almost a rubbery consistency, with a darker color)...recognizably different from the normal phlegm consistency.  I've noticed this when the bronchial infections are most severe.

 

 In past urine tests, E. coli showed up a couple of times.  I'm seeing pictures that show a resemblance to klebsiella.  A webpage that shows the similarities is http://www.mfi.ku.dk/ppaulev/chapter33/images/33-4.jpg  I question if it's possible that klebsiella may have been present.  Urinary tract infections had been recurring at least a few times a month throughout the years since then.  I kept a good supply of cranberry capsules on hand, as they were often needed. I also consumed a lot of garlic throughout the years to fight off frequent illnesses.

 

My ongoing struggle with recurring symptoms began 25 years back.  At that time my medical report noted " diarrhea, cramps, acute viral gastrointestinitis, Leg aches, fibromyalgia symptoms, blood tests showed neutrophils low (46.7) lymphocytes high (44.2), IgG antibodies".  From then on ....I never felt completely healthy.  

 A web based relationship 3

 

I had been prescribed many antibiotics from that time through 1994...at which time I started researching natural approaches to help control the many recurring yeast infections, thrush, allergies etc. (which I understand leads back to overuse of antibiotics).

 

The following notes are taken from my medical reports.... 

 

Over the past 15 years I was to doctors many times with complaints of overwhelming fatigue, depression, and bronchial infections that would last for weeks, subside, and then return within a few weeks again. 

 

 My blood pressure would usually be on the low side (98/36, 96/40, 84/60, 80/50 ),  

 I frequently felt ill with flu-like symptoms, often had low temps as well (97*, 96.4*, 95.7*, 94*);

 I was having fibromyalgia symptoms (often aching in various parts of my body, which came and went, recurring in different areas with each onset, more noticed in the morning). 

 I had chronic constipation that began in 1993... For the past 10 years I could not pass fecal matter without an enema and when I did, I often suffered from hemorrhoids and bleeding from straining.  I became too thin and was often told by my husband and friends that I needed to gain weight. I often felt weak and periodically got dizzy.

 

 Over the past couple of years, I was becoming more forgetful and struggled with confusion and unclear thinking.  I struggled with manic-depression as well for the past few years.  I also struggled with Pre menstrual syndrome, a lot prior to my monthly cycle along with recurring headaches often.

 

I would get sore lumps under my armpit (assuming swollen lymph node).  My breast had become continuously tender and painful for the past year or so.

 

  I'd began seeing chiropractors in 1996 with lower back pain which progressively grew worse, and eventually affected my entire back and neck, was particularly painful on left side between shoulder blade and spine.  I wasn't able to sleep well, my eyes were often red and I was told I had Ankylosing Spondylitis.  There's a good study mentioned by the university of Florida relating Ankylosing Spondylitis to Klebsiella bacteria overgrowth http://www.chem.fsu.edu/learn/kleb.htm  and http://www.chem.fsu.edu/learn/radio.htm   

 

X-ray (1996) L5 sacralized as per chiropractor.  In 2002 another chiropractors notes read "Chris has bone spurs @ the 4, 5, 6th lumbar vertebra, the 5th lumbar is fused with the sacrum".  Range of motion has fluctuated throughout the years from 30% to 90%...stiffness came and went but continued to grow worse in general.

 

Bone scan (3-16-01) showed right increase activity in upper left costal vertebra junction at T3 level, noted possible degenerative activity, no significant abnormalities within the verterbal bodies along with mild scoliosis of thoracic spine.

A web based relationship 4 

 

Chris’s medical history contd

 

A CT scan (5-01-01) noted cyst within the left kidney.

 

Echocardiogram (5-4-01) no significant findings noted.  Estimated ejection fraction is approximately 65-70%.  I had been experiencing bouts of intense chest pain that made it hard to breathe, and would let up a little when I bent over. Recently I found mention of tachycardia at some sights for Klebsiella...tachycardia seems to describe my chest pain. This previous note of tachycardia symptoms was more severe than the often recurring general tightness/hard to breathe feeling that I experienced often as well.

 

In regards to helping me solve my problem...thank you for your interest...I sincerely appreciate that.

 

  The above issues have all significantly improved. (I would say at least 80%).  I now am sleeping well at night; the back pain is very minimal compared to before.  The last bout of severe chest pain was over 3 months ago; I feel all the psychological issues have been gone since January, I am able to stay focused and my memory is better; I no longer get urinary tract infections like I used to, no headaches or P.M.S. symptoms in the past few months; I'm not aching in various places any more...I wake in the morning without pain.  My eyes are not red all the time; I have no swollen lumps under my arm, my breasts are not hurting all the time etc. etc.  In general...I've come a long way and I am so very thankful for that.

 

The improvements began to happen when I began passing long strands of mucous in my stools in November of 2002.   I believed they were worms, but two different lab tests reported no worms.  They were defined as "mucoid matter".  (One test was done at a local lab, the other at Great Shakes Diagnostic Lab…the tests were done about 2 months after I began passing a lot of these strands)  These mucous strands have ranged up to 26" long.  I've preserved some in jars in hopes that someone working in the research of Klebsiella bacteria would be interested in studying this.  I'm reading that Klebsiella is a highly mucoid bacteria and my doctor had told me that it is possible that the klebsiella are responsible for these mucous strands...any thoughts on that? 

 

I still continue to pass some of these mucous strands, much less than at first, but still some.  

 

I feel that the Klebsiella is the underlying issue, but I'd like your opinion...does that seem logical?  I think it does, but I'm not a doctor or specialist. 

 

I am so thankful to be regaining my health in significant ways...I hope that by sharing my experience, it may help others in some way. Yours Chris Jestus

 

 

All humans are born physicians

June was perplexed initially as to how she should respond to Chris’s letter as her letter could be obviously labeled as that of a hypochondriac by contemporary medical school teaching but then she had also studied in a different school part time. Joatmon’s teachings in post modern holistic medicine always emphasized that all humans were born physicians by virtue of their ownership right on their systems. The role of a formally trained trouble shooter was simply to act as a facilitator in a global understanding of the nature of the human system and its afflictions. She wrote back…

Thanks Chris, for giving me the opportunity to go through your case sheet. I believe I have been able to solve your problem. I enclose a paragraph from Harrison's Principles of internal medicine below:

Klebsiella species are broadly prevalent in the environment and colonize mucosal surfaces of mammals. In healthy humans, K. pneumonia colonization rates range from 5 to 35% in the colon and from 1 to 5% in the oropharynx; the skin is usually colonized only transiently. In long-term-care facilities and hospitals, colonization occurs with K. oxytoxa as well, and carriage rates are significant among both workers and patients. Person-to-person spread is thought to be the predominant mode of acquisition.

Most of us carry a world of bacteria inside our systems where they live and die continuing their cycles of existence. Your klebsiella was one such isolated from your stool where it was living a normal life with minimum damage to your system. However the troubles which started in your system since 1988 definitely signifies the entry of a virus (something which may be likened to software programs which affect our computer systems) and it really troubled you all these days starting from an acute diarrhea, cramps, moving on to Leg aches and fibromyalgia symptoms followed by constipation which made you suffer so much. There is nothing in your medical investigations to suggest Ankylosing spondylitis as the X-ray changes described in ankylosing spondylitis are very much different from the ones described in your imaging findings. They are non specific changes possibly normal for your age...by the way I don't know your age accurately. Although klebsiella antigens are related to ank-spond they are hypothesized to cause so by acting as a trigger for an autoimmune reaction to the antigen by the body's cellular defense system. MUCUS is a normal constituent which layers the bowels of all normal human beings and is passed out when stools are scanty inside the bowels. The klebsiella is unlikely to remain alive for this long inside the jars where you have stored them. Yours June

 

 

 

 

 

 


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Unpublished novel for all interested in the science and fantasy of medicine. Not about religion, but a postmodern multi genre combining elements of Science, Fantasy and Romance