philamom

(Table 1) didn't open with post - so here it is. Several factors are associated with the risk of infection as well as the different manifestations of Lyme borreliosis: PREDISPOSING FACTORS HLA DR2, HLA DR4 genotype Compromised immune system Coinfections that cause immunosuppression Ecosystem that fosters tick-borne disease (infection) Outdoor activities (infection) PRECIPITATING FACTORS Tick bite (initial infection) Episode of acute stress (relapse) Immunosuppression (relapse) Vaccination (relapse) Childbirth (relapse) Auto accident (relapse) Coinfection (relapse) PERPETUATING FACTORS High bacterial load Reinfections Coinfections Chronic unremitting stress Sleep deprivation Corticosteroid exposure Misdiagnosis Undertreatment

I have to really consider mold being another issue for us. When I was 7-8 months pregnant and on bedrest our finished basement flooded. The days following we had a company come out that used industrial machines to suck up the water & place fans around. My husband was out of town so I took care of supervising the ordeal (big no-no). We didn't replace the carpet or padding. A couple weeks later I was diagnosed with H.E.L.P (liver toxicity) and needed to deliver asap. Three years later had another flood. We replaced the carpet this time with no padding underneath. The company said there were no signs of mold, but I always wonder about behind the drywall. We still occasionally get flooding in one area when there's a lot of rain. And, in our bathroom, there is green stuff in the handle to turn the shower on-off. Yikes.

Good timing. Filter change is on my list this week. I will hold off and check online. Thanks for sharing Michael!

Lyme Disease, Comorbid Tick-Borne Diseases, and Neuropsychiatric Disorders By Robert C. Bransfield, MD | December 1, 2007 Dr Bransfield is associate director of psychiatry at Riverview Medical Center in Red Bank, NJ. Psychiatrists interested in joining the Microbes and Mental Illness Discussion Group may e-mail the author at bransfield@comcast.net. He is President Elect of the International Lyme and Associated Diseases Society. The author reports that he is on the Speakers' Bureau of Abbott, AstraZeneca, Cephalon, Forest, GlaxoSmithKline, Jazz, Lilly, Pfizer, Sanofi Aventis, Takeda, UCB, and Wyeth; and he is on the advisory board for the Lyme Disease Association, Turn the Corner Foundation, Morgellons Research Foundation, and Lyme Induced Foundation. -------------------------------------------------------------------------------- Many recall the phrase "To know syphilis is to know medicine." Now Lyme disease (Lyme borreliosis), the new "great imitator,"1 is the ultimate challenge to the breadth and depth of our knowledge. In psychiatry, we generally treat mental symptoms or syndromes rather than the underlying cause of a disorder. A greater awareness of immune reactions to infections and other contributors to mental illness enhances our psychiatric capabilities. Lyme disease, like syphilis, is caused by a spirochete with a multitude of pos-sible manifestations and 3 stages: early with dermatological symptoms, disseminated, and late stage. Unlike Treponema pallidum, the cause of syphilis, the causative agent of Lyme disease, Borrelia burgdorferi, can be much more difficult to eliminate, diagnostic testing is less reliable, and interactive copathogens are major contributors in the pathophysiology.2,3 B burgdorferi is highly adaptable with 6 times as many genes as T pallidum and 3 times as many plasmids as any other bacteria that allow rapid genetic adaptations.4,5 It is a stealth pathogen that can evade the immune system and pathophysiological mechanisms.6,7 Knowingly or not, most psychiatrists have at some point been perplexed by patients with late-stage psychiatric manifestations of Lyme borreliosis. Several factors are associated with the risk of infection as well as the different manifestations of Lyme borreliosis (Table 1). A problematic case The following composite case illustrates a number of problems that may make diagnosis and treatment of Lyme borreliosis anything but straightforward. The patient is in good health and enjoys outdoor activities. Often this person has the HLA DR4 genotype. He or she may acquire a small tick bite that goes unnoticed because the subsequent rash may not be of the classic bull's-eye type, may be easily overlooked in dark-skinned individuals, may be misdiagnosed, or may occur only with a second or subsequent infection. There may be flu-like symptoms with migratory musculoskeletal aches and pains. If a diagnosis of Lyme disease is made, the initial course of antibiotic treatment may not have been sufficient to eliminate the infection. (Although standardized by 1 set of guidelines, psychiatrists often see the failures of some of the "standard" treatments.) Low-grade symptoms may remit and periodically relapse over time. An accident, emotional stress, vaccination, or childbirth can trigger an exacerbation of symptoms. The patient, who did not have psychosomatic symptoms and was not hypochondriacal in the past, now complains of an increasing number of somatic, cognitive, neurological, and psychiatric symptoms. Although Lyme disease may be suspected, the laboratory tests available to most clinicians often lack sensitivity and thus are read as negative for Lyme disease. Fibromyalgia, chronic fatigue syndrome, or multiple sclerosis (MS) may be erroneously diagnosed. Treatment of some symptoms with corticosteroids may initially provide relief, but a more rapid decline often follows. The patient sees multiple specialists, each of whom restricts the examination to his area of expertise. Nothing is resolved, and the patient is frustrated that his symptoms cannot be explained. In view of the growing list of unexplained symptoms, including psychiatric symptoms, the patient is treated with tranquilizers and antidepressants with some benefit, but gradual decline persists. The major complaints include fatigue, multiple cognitive impairments, depression, anxiety, irritability, head-aches, and a multitude of other symptoms. When general medical treatment fails, the patient may be referred to a psychiatrist for 3 reasons: the unexplained medical symptoms give the appearance of a psychosomatic or somatoform condition; complex mental symptoms are thought to require psychiatric assessment; and a psychiatrist is thought to be needed to more effectively manage psychiatric treatments. The Figure presents single photon emission CT (SPECT) images of the brain of a depressed 51-year-old woman with Lyme disease, before and after treatment with ceftriaxone(Drug information on ceftriaxone). She walked on nature trails at home and on vacations, recalled frequent tick bites and an expanding bull's-eye rash on her abdomen with no other symptoms, but considered it of no special significance at the time. Over 8 years, there was a progressive development of unexplained symptoms that began with GI complaints, followed by cognitive impairment, fatigue, depression, arthritis, and shortness of breath. The primary diagnosis was atypical depression. Although the patient failed to respond to 51 different drug trials, the treating psychopharmacologist assured her the mental symptoms could not possibly be caused by an underlying physical condition. The initial SPECT scan demonstrated "extensive hypoperfusion... predominantly in the frontal and temporal lobes and to a less degree in the parietal and occipital lobes," which is consistent with Lyme disease and neurodysfunction. Neurocognitive testing demonstrated significant abnormalities. An MRI scan ruled out frontal temporal dementia. The patient tested negative for Lyme disease by CDC epidemiological criteria, but the Lyme IgG Western blot test result was positive at one laboratory and equivocal at another. The CD57 lymphocyte count was low at 17/µL (60 to 360) and the patient tested positive for 4 other tick-borne infections (Mycoplasma fermentans, Babesia microti, Babesia WA-1, and Bartonella henselae). The patient was intolerant to oral antibiotics and was treated with 8 months of intravenous ceftriaxone. The second SPECT scan demonstrated "marked improvement of the hypoperfusion pattern in the temporal, frontal, and parietal lobes and small areas of hypoperfusion pattern remain." The depression never returned, but some mild residual symptoms persist, including fatigue, neuropathy, and arthritis; however, she has mostly returned to her active lifestyle. The failure to diagnose and treat these infections for several years resulted in an escalation of symptoms and a loss 8 years of her life that could have been prevented by earlier diagnosis and treatment. General theoretical issues The causes of most psychiatric illnesses are unknown. The catecholamine hypothesis does not adequately explain the cause of abnormal neurotransmitter functioning. Mendel stated that human traits are determined by individual genes that function independently of other genes and environmental influences. Koch believed that many human diseases are caused by microbes that exert their effect independently of other microbes, environmental factors, and genes. The cause of most mental illnesses cannot be explained by neurotransmitters, genes, or infections alone. Instead, as stated by Yolken,8 most common human diseases are caused by the interaction of environmental insults and susceptibility genes.Many of the susceptibility genes are diverse determinants of human response to environmental factors, including infections, and prevention or treatment of the infections may result in the effective treatment of complex disorders. Neuropsychiatric disease is often associated with an interaction of environmental insults and susceptibility factors that frequently results in a pathological interaction including inflammation, oxidative stress, mitochondrial dysfunction, and excitotoxicity, which leads to neuronal dysfunction.3 Numerous studies document that infections, such as pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, syphilis, hepatitis C, and zoonotic (animal) diseases, can cause mental illness.9-13 The same syndrome may be caused by different infections in different individuals, and the same infection can cause different syndromes in different individuals. For example, obsessive-compulsive disorder has been caused by infection with Streptococcus, B burgdorferi, Japanese B encephalitis virus, herpes simplex virus 1, Borna disease virus, Epstein-Barr virus, and Mycoplasma, as well as by thepandemic influenza of 191814-16; I have also observed cases caused by Hong Kong influenza and coxsackievirus infection. Of course, many of these infections have also been shown to cause other psychiatric and somatic symptoms. Some infections result in residual injury even after the infection itself no longer persists, while other infections may persist in a chronic relapsing and remitting state. Chronic infections are most commonly viral, venereal, and vector-borne zoonotic.8 Tick-borne diseases and chronic infectious diseases B burgdorferi, the principal organism associated with Lyme borreliosis, is one of the most complex bacteria known to man. In addition, a tick bite can presumably transmit more than 1 disease-causing organism. Thus, 2 major clinical hurdles in diagnosis and management are the absence of a clear therapeutic end point in treating Lyme borreliosis and the potential presence of tick-borne coinfections that may complicate the course of the illness.3 The more common interactive coinfections may be caused by M fermentans, Mycoplasma pneumoniae, B microti, Ba- besia WA-1, Chlamydia pneumoniae, Ehrlichia, Anaplasma, and B henselae, and multiple viruses and fungi.2,3,17 When multiple microbes grow together, they can promote immunosuppressive effects and cause marked symbiotic changes that alter their functioning.18 Neuroborreliosis is an infection within the brain; however, infections in the body that do not pass through the blood-brain barrier may also impact the brain indirectly via immune effects. All the clinical manifestations, acute or chronic, of infection with B burgdorferi are characterized by strong inflammation with the production of several proinflammatory and anti-inflammatory cytokineswith an aberrant innate proinflammatory response19 and inflammatory brain changes.20 Most of the dysfunction caused by these infections is associated with immune reactions. Lyme borreliosis and other tick-borne infections are associated with a combination of inflammatory reactions and autoimmune symptoms. The proinflammatory cytokines associated with these infections increase indoleamine 2,3-dioxygenase, which decreases serotonin and kynurenic acid, a neuroprotective glutamate antagonist. In addition, the cytokines increase the level ofquinolinic acid, an N-methyl d-aspartic acid (NMDA) agonist and neurotoxin, which contributes to the neurological and cognitive deficits seen in patients with tick-borne infections.21-23 This change may produce over-stimulation of hippocampal (NMDA) receptors leading to apoptosis and hippocampal atrophy. Hippocampal atrophy in the temporal lobes caused by NMDA overstimulation has been associated with depression and dementia.24 Lyme borreliosis and other tick-borne infections can exist as an asymptomatic chronic carrier state, they can present with occasional or chronic fluctuating low-level symptoms, or they can lead to severe multisystem dysfunction and a multitude of psychiatric presentations.2 Assessment Some helpful screening questions for a person with suspected late or complicated B burgdorferi infection are listed in Table 2. Positive responses require a thorough history, review of systems, and assessment of cognitive, emotional, vegetative, behavioral, psychiatric, neurological, and somatic symptoms. TABLE 2 Screening for suspected late or complicated Lyme disease 1. Do you live or have you vacationed in areas that may expose you to ticks? 2. Have you engaged in activities that may have exposed you to ticks? expectations 3. Have family members, neighbors, or the family dog been infected? 4. Is there a history of a tick bite, possibly with a flu-like illness and/or a bull's-eye or other rash? 5. Is there a point at which the patient’s health declined, followed by a relapsing progression and development of multisystemic symptoms, including cognitive, psychiatric, neurological, and physical symptoms? 6. Have antibiotics ever caused a sudden worsening followed by an improvement of symptoms?

Bactrim was prescribed for suspected bartonella. Not sure if it crosses the BBB but the zith she is on does for sure. Not sure if she is worse in symptoms since probiotics and detox...I have been increasing those all along from info on this forum since January. Do you think that could make things worse? What exactly would consitute drainage? She won't take baths or put on deoderant or patches or anything like that. I think a phone call to his office would be a good idea to check about the bactrim. I don't have any experience with the supps that support drainage...hopefully Jodie will chime in. I just mentioned it because in our situation when I add in a large quantity of supplements, it often leads to increased behaviors. Just my experience...don't know enough about it. I would call Dr. J and update him with your situation.

laure-have you spoken with Dr J's office recently. I'm just wondering if the Bactrim was prescribed for the lyme and Bartonella? Does the Bactrim cross the BBB? My dd is on Minocin for the co-infection and was recently increased to help with ocd. Also, is she worse in symptoms since the bent pills and large probiotic dose? Is it too much in detox, but not enough drainage. This is not coming from my experience - just remember reading how important it is to rid of the critters after detox. I would call and see if you can get in earlier for your follow-up. Thinking of you!!

Justine- can you elaborate on the test for chronic lyme...what test was it? Also, what HLA's were positive? Thanks! Thank you Justine. Anyone else have + HLA's?

Familyof5- How did you figure out it was mold in your attic, if disguised as dust? thx

Justine- can you elaborate on the test for chronic lyme...what test was it? Also, what HLA's were positive? Thanks!

I plan to begin focusing on detox/drainage at the end of this month. I just wanted my daughter to finish the school year (she missed half of last year). She seems to react to anything ingested, viruses, blood draws, dental, you name it, so we've been keeping it minimal. Now it's time to make some changes. Can you please let us know what you learn about the positive HLA's at your appointments? thx

Thank you. I did some googling last night (sigh). I saw it was linked to chronic lyme and resistant to treatment. I guess I can expect a longer time.

In decoding his notes, it say's she is positive for HLA-DR4. She is negative for HLA-B27. Do you know anything about the DR4? Same? Sorry to hear about your son's joint pain.

3 days? how long did you do 2 days? Still do it 2 days (4 doses of 250mg). Friday pm, Saturday am & pm, Sunday am. Has that helped with the herxing? Or so that he is in better shape for school on Monday? Just curious, I'll probably be asking questions till the end of time. Exactly...better shape for school in the morning (though I still have to drag her out of the bed ). My dd's llmd said to first start on Sat/Sun morning to watch for any reaction.

During my daughter's recent llmd appointment I mentioned some of my ailments (mild rheum arthritis, raynauds, IBS, exc) and the doctor said "now I know where your daughter got the positive HLA gene from". At the time I didn't know what he was talking about. When I got home and looked at her previous labs, it is written down that she is positive for HLA- B for one number and negative for three others. Can't understand his penmanship. I assume it can't be too significant since he never brought it to my attention before. I thought I would ask you really smart folks. Anyone know?

3 days? how long did you do 2 days? Still do it 2 days (4 doses of 250mg). Friday pm, Saturday am & pm, Sunday am.

Ok...that's good. I don't recall too many children being on it daily. We started with Sat/Sun, but now do it Friday evening - Sun morning.

If the doctor wrote the script then I would call and request to have a new one faxed over to the pharmacy. If the pharmacy made the change, then I would tell them you will have your child take it until they get the correct size pills in. They should switch it without any additional cost. I don't like to mess around because my dd had difficulty swallowing last year which led to a refusal of taking meds. She can now swallow pills again but I still ask for the small size. Good luck...I hope she takes it. btw- is it daily?

My soon to be 10 year old (60lbs?) takes 500mg daily on weekends. 250mg am/pm for 2 days.

Good idea!

LLM- Thanks for posting your update. I need some strength right now. Since mid-end of January, we have spiraled back to my daughter's baseline before lyme treatment. She is not at her worst, but back to where she was in September. I hold onto the hope that even though she has regressed, we did see her at the best she's been in two years, prior to this happening. Just need to get her back there again! Her doctor increased her Minocin, but haven't started it yet, because she has a cold and is SO emotional. Tonight begins the weekend Tindamax so we'll probably wait till next week. When you start the Tindamax back up, it might be wise to take it slow. Maybe begin with 1/2 tablet...see what your llmd thinks. We recently took a break from it and my daughter had a really, really difficult time when she resumed it. She started with one tablet. I can't wait until this is your NORM all the time!! Yay!

Thank you.

Very nicely done. Great Job!!

How about for a 10 yr old? Jr. or adult capsules?

My daughter's LFT has been elevated for at least a year and a half. We now run it every 3 months.

Vickie- do you give your son the D-Hist Jr. daily? thx