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» LymeNet Flash » Questions and Discussion » Medical Questions » One infection after another: (re)activating sub-clinical infections

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Author Topic: One infection after another: (re)activating sub-clinical infections
Brussels
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Subclinical infection

Clinicians have long reported a phenomenon known as ‘minocycline-induced lupus’ in which certain patients administered with minocycline appear to develop the autoimmune condition.

In fact, there is no plausible mechanism that explains how minocycline can cause lupus—or any other disease.

A more logical explanation may be that certain patients harbor persistent bacterial species that predispose for subclinical lupus.

When minocycline is administered, some of these bacteria are killed, resulting in immunopathological reactions that are mistakenly interpreted as clinical manifestation of the disease.

As Krawitt has argued, the same is likely true for ‘minocycline-induced hepatitis’.

Many of the patients on our immunostimulative therapy have also reported the temporary development of new symptoms, suggesting that the UNMASKED SUB CLINICAL INFECTIONS MAY BE MORE COMMON THAN CURRENTLY SUPPOSED.
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JM is a 54-year-old female diagnosed with endometriosis (diagnosed in 1986), chronic fatigue syndrome (2000) and a number of comorbidities.

In January 2006, JM was administered with 40 mg of olmesartan four times daily.

(Brussel's: Olmesartan stimulates the immune system, as being an antagonist to VDR, vit D receptor)

In April, she was also administered with 25 mg of minocycline every other day.

JM reported increases in symptoms including but not limited to the following: body pain, fatigue, lightheadedness, insomnia, photosensitivity, anxiety and depression.

In August 2009, she developed acute shingles with distribution of the left greater occipital nerve branch.

Shingles were managed with oral and topical Valtrex.

By November 2009, JM's symptoms were stable and tolerable, although she reported an increase in fatigue after beginning 125 mg of Bactrim DS every other day.

In March 2010, JM discontinued taking all antibiotics but remained on 40 mg of olmesartan four times daily.

By April 2010, JM reported global improvement.


Most of the symptoms that JM found exacerbated upon olmesartan and subinhibitory antibiotic administration were symptoms that she had previously experienced before starting therapy.

However, JM had NEVER REPORTED ANY HISTORY OF SHINGLES infections.

It is likely that her activated immune response unmasked a previously subclinical infection.

This same phenomenon, including treatment-induced appearance of shingles, has also been reported in IRIS.

Posts: 6199 | From Brussels | Registered: Oct 2007  |  IP: Logged | Report this post to a Moderator
Brussels
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Immune reconstitution inflammatory syndrome (IRIS)

http://www.uptodate.com/contents/immune-reconstitution-inflammatory-syndrome

The term "immune reconstitution inflammatory syndrome" (IRIS) describes a collection of inflammatory disorders associated with paradoxical worsening of preexisting infectious processes following the initiation of highly active antiretroviral therapy (HAART) in HIV-infected individuals.


Preexisting infections in individuals with IRIS may have been previously diagnosed and treated or they may be subclinical and later unmasked by the host's regained capacity to mount an inflammatory response.


If immune function improves rapidly following the commencement of HAART, systemic or local inflammatory reactions may occur at the site or sites of the preexisting infection.
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http://www.nature.com/cmi/journal/v8/n3/full/cmi201077a.html

More recently, a type of immunopathology has been observed in HIV/AIDS patients (called IRIS).

During IRIS, HIV/AIDS patients experience the worsening or onset of systemic inflammatory clinical signs and symptoms following treatment with highly active antiretroviral therapy (HAART).

(Br: this looks like herxheimer?).


This syndrome results when HAART allows for partial recovery of the immune response.

This causes renewed and exuberant host immunological responses towards opportunistic infectious agents, agents that the host accumulated during prior periods of immunosuppression.

A number of well-known readily cultured pathogens have been conclusively linked to IRIS:

- the herpes viruses,
- cytomegalovirus,
- hepatitis B and C,
- M. tuberculosis,
- Mycobacterium avium complex
- Cryptococcus neoformans.


Interestingly, patients experiencing IRIS often ‘develop’ AUTOIMMUNE conditions as a manifestation of immune restoration.

These include sarcoidosis and other granulomatous reactions, diabetes mellitus, rheumatoid arthritis,....

.... systemic lupus erythematosus, Guillain–Barre syndrome, Graves disease and autoimmune thyroid disease.


This suggests that these patients accumulated microbes that are directly involved in the pathogenesis of these disease states.

Posts: 6199 | From Brussels | Registered: Oct 2007  |  IP: Logged | Report this post to a Moderator
Brussels
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Kill one infection, you may get another showing up (an old infection, known to you), or a new one, totally unknown.

These microbes were not outside, but just living dormant. Peeling the onion concept.

They call here subclinical infection!

-------------------

Second post about IRIS: it is described as a pathology for AIDS patients, after their immune system gets reactivated.

Well, the second article does expand it's view to other types of patients (not only AIDS).

I do feel chronic lyme sufferers who start different therapies fall very much in a similar picture:

- developing autoimmune conditions,

- developing a series of subclinical infections that are part of healing (unfortunately), like herpes / shingles, Mycobact. tuberculosis, cryptococcus neoformans, and I am pretty sure Candida albicans and other candidas are inside that picture!

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Brussels
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the good part of it, is that if other infections are getting activated, reactivated, but dealt with

.... (with abx, killers, your immune system, or therapies like that one proposed in the article (Olmesartan),

.... it means you're getting better, not worse (even though it may feel you are getting worse).

During lyme, I suffered terribly from Mycobacterium tuberculosis, that almost cost my life.

I never had that before, it was just there dormant, I suppose.

Cryptococcus neoformans, I just had it a few weeks ago. A bad infection too, but not as crippling as TB.

And it was not the first time for me (I remember clearly that pathogen name, when lyme was active).

I'm just posting that, because the article proposes another treatment for auto immune diseases, and chronic infections...

Their suggestion is to add a VDR agonist together with antimicrobials.

and I'm also posting that, because I find it so interesting to read in a scientific paper what we all live

...(one infection showing up, one after another, specially when we think we are getting better).

It is normal that such things happen, it seems!

[ 07-29-2015, 02:58 PM: Message edited by: Brussels ]

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Judie
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Wow! Good stuff!
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