View Full Version : Ack

29-08-2006, 20:30:41
I just discovered my Brita Water filter had green stuff growing in it

I am generally only home at night, and we don't have lots of lights in our apartment...

I drank out of it this morning. (I know it didn't haev green stuff in it when I changed the water a week ago or so)

I felt bad yesterday, and today, so that might explain why.

Am I going to die?

Jon Miller

29-08-2006, 20:32:23
Now I feel sick to my stomach..


C.G.B. Spender
29-08-2006, 21:58:21
You will die. Don't know when though

29-08-2006, 22:07:14
Yes, you will indeed be dead as a doornail.

I can predict the time better then Vincent, it will be during this century, count on it!

29-08-2006, 22:07:43
Was the green stuff algae or pseudomonas?

29-08-2006, 22:08:58
not sure?


29-08-2006, 22:09:34
Uhhh ohh....

--Pseudomonas aeruginosa has very simple nutritional requirements. It is often observed "growing in distilled water" which is evidence of its minimal nutritional needs. In the laboratory, the simplest medium for growth of Pseudomonas aeruginosa consists of acetate for carbon and ammonium sulfate for nitrogen.

--P. aeruginosa possesses the metabolic versatility for which pseudomonads are so renowned. Organic growth factors are not required, and it can use more than seventy-five organic compounds for growth.

--Its optimum temperature for growth is 37 degrees, and it is able to grow at temperatures as high as 42 degrees.

--It is tolerant to a wide variety of physical conditions, including temperature. It is resistant to high concentrations of salts and dyes, weak antiseptics, and many commonly used antibiotics.

--Pseudomonas aeruginosa has a predilection for growth in moist environments, which is probably a reflection of its natural existence in soil and water.

29-08-2006, 22:09:37
it was from the bottom, not surface sitting..


29-08-2006, 22:11:11

Most Pseudomonas infections are both invasive and toxinogenic. The ultimate Pseudomonas infection may be seen as composed of three distinct stages: (1) bacterial attachment and colonization; (2) local invasion; (3) disseminated systemic disease. However, the disease process may stop at any stage. Particular bacterial determinants of virulence mediate each of these stages and are ultimately responsible for the characteristic syndromes that accompany the disease.


Although colonization usually precedes infections by Pseudomonas aeruginosa, the exact source and mode of transmission of the pathogen are often unclear because of its ubiquitous presence in the environment. It is sometimes present as part of the normal flora of humans, although the prevalence of colonization of healthy individuals outside the hospital is relatively low (estimates range from 0 to 24 percent depending on the anatomical locale).

The fimbriae of Pseudomonas will adhere to the epithelial cells of the upper respiratory tract and, by inference, to other epithelial cells as well. These adhesins appear to bind to specific galactose or mannose or sialic acid receptors on epithelial cells. Colonization of the respiratory tract by Pseudomonas requires fimbrial adherence and may be aided by production of a protease enzyme that degrades fibronectin in order to expose the underlying fimbrial receptors on the epithelial cell surface. Tissue injury may also play a role in colonization of the respiratory tract since P. aeruginosa will adhere to tracheal epithelial cells of mice infected with Influenza virus but not to normal tracheal epithelium. This has been called opportunistic adherence, and it may be an important step in Pseudomonas keratitis and urinary tract infections, as well as infections of the respiratory tract.

The receptor on tracheal epithelial cells for Pseudomonas pili is probably sialic acid (N-acetylneuraminic acid). Mucoid strains, which produce an exopolysaccharide (alginate) have an additional or alternative adhesin which attaches to the tracheobronchial mucin (N-acetylglucosamine). Besides pili and the mucoid polysaccharide, there are possibly two other cell surface adhesins utilized by Pseudomonas to colonize the respiratory epithelium or mucin. Also, it is likely that surface-bound exoenzyme S could serve as an adhesin for glycolipids on respiratory cells.

The mucoid exopolysaccharide produced by P. aeruginosa is a repeating polymer of mannuronic and glucuronic acid referred to as alginate. Alginate slime forms the matrix of the Pseudomonas biofilm which anchors the cells to their environment and, in medical situations, it protects the bacteria from the host defenses such as lymphocytes, phagocytes, the ciliary action of the respiratory tract, antibodies and complement. Biofilm mucoid strains of P. aeruginosa are also less susceptible to antibiotics than their planktonic counterparts. Mucoid strains of P. aeruginosa are most often isolated from patients with cystic fibrosis and they are usually found in post mortem lung tissues from such individuals.


The ability of Pseudomonas aeruginosa to invade tissues depends upon production of extracellular enzymes and toxins that break down physical barriers and damage host cells, as well as resistance to phagocytosis and the host immune defenses. As mentioned above, the bacterial capsule or slime layer effectively protects cells from opsonization by antibodies, complement deposition, and phagocyte engulfment.

Two extracellular proteases have been associated with virulence that exert their activity at the invasive stage: elastase and alkaline protease. Elastase has several activities that relate to virulence. The enzyme cleaves collagen, IgG, IgA, and complement. It also lyses fibronectin to expose receptors for bacterial attachment on the mucosa of the lung. Elastase disrupts the respiratory epithelium and interferes with ciliary function. Alkaline protease interferes with fibrin formation and will lyse fibrin. Together, elastase and alkaline protease destroy the ground substance of the cornea and other supporting structures composed of fibrin and elastin. Elastase and alkaline protease together are also reported to cause the inactivation of gamma Interferon (IFN) and Tumor Necrosis Factor (TNF).

P. aeruginosa produces three other soluble proteins involved in invasion: a cytotoxin (mw 25 kDa) and two hemolysins. The cytotoxin is a pore-forming protein. It was originally named leukocidin because of its effect on neutrophils, but it appears to be cytotoxic for most eukaryotic cells. Of the two hemolysins, one is a phospholipase and the other is a lecithinase. They appear to act synergistically to break down lipids and lecithin. The cytotoxin and hemolysins contribute to invasion through their cytotoxic effects on eukaryotic cells.

One Pseudomonas pigment is probably a determinant of virulence for the pathogen. The blue pigment, pyocyanin, impairs the normal function of human nasal cilia, disrupts the respiratory epithelium, and exerts a proinflammatory effect on phagocytes. A derivative of pyocyanin, pyochelin, is a siderophore that is produced under low-iron conditions to sequester iron from the environment for growth of the pathogen. No role in virulence is known for the fluorescent pigments.


Blood stream invasion and dissemination of Pseudomonas from local sites of infection is probably mediated by the same cell-associated and extracellular products responsible for the localized disease, although it is not entirely clear how the bacterium produces systemic illness. P. aeruginosa is resistant to phagocytosis and the serum bactericidal response due to its mucoid capsule and possibly LPS. The proteases inactivate complement, cleave IgG antibodies, and inactivate IFN, TNF and probably other cytokines . The Lipid A moiety of Pseudomonas LPS (endotoxin) mediates the usual pathologic aspects of Gram-negative septicemia, e.g. fever, hypotension, intravascular coagulation, etc. It is also assumed that PseudomonasExotoxin A exerts some pathologic activity during the dissemination stage (see below).


P. aeruginosa produces two extracellular protein toxins, Exoenzyme S and Exotoxin A. Exoenzyme S is probably an exotoxin. It has the characteristic subunit structure of the A-component of a bacterial toxin, and it has ADP-ribosylating activity (for a variety of eukaryotic proteins) characteristic of exotoxins. Exoenzyme S is produced by bacteria growing in burned tissue and may be detected in the blood before the bacteria are. It has been suggested that exoenzyme S may act to impair the function of phagocytic cells in the bloodstream and internal organs to prepare for invasion by P. aeruginosa.

Exotoxin A has exactly the same mechanism of action as the diphtheria toxin, it causes the ADP ribosylation of eukaryotic elongation factor 2. It is partially-identical to diphtheria toxin, but it is antigenically-distinct. It utilizes a different receptor on host cells, but otherwise it enters cells in the same manner as the diphtheria toxin and it has the exact enzymatic mechanism. The production of Exotoxin A in is regulated by exogenous iron, but the details of the regulatory process are distinctly different in C. diphtheriae and P. aeruginosa.

Exotoxin A appears to mediate both local and systemic disease processes caused by Pseudomonas aeruginosa. It has necrotizing activity at the site of bacterial colonization and is thereby thought to contribute to the colonization process. Toxinogenic strains cause a more virulent form of pneumonia than nontoxinogenic strains. In terms of its systemic role in virulence, purified Exotoxin A is highly lethal for animals including primates. Indirect evidence involving the role of exotoxin A in disease is seen in the increased chance of survival in patients with Pseudomonas septicemia that is correlated with the titer of anti-exotoxin A antibodies in the serum. Also, tox- mutants show a reduced virulence in some models.

You are soooo dead.

29-08-2006, 22:13:19
I am going to see the doctor on Monday, should I go to the imergency room?


29-08-2006, 22:14:44
Either that or the undertaker.

29-08-2006, 22:14:51
Do you have AIDS, SCID, take chronic glucocorticoids, have leukemia, are on blood thinners, etc?

29-08-2006, 22:15:26
I am on Beta Blockers..


29-08-2006, 22:16:42
Here is what it looks like under the nail!!!


Here is what it looks like in an HIV patient after treatment

http://www.hivdent.org/slides/images/major_aph_ulcer_supra_inf_with_pseudo_post_treat.j pg

29-08-2006, 22:17:39
My blood pressure is elevated, and I am perhaps hotter then usual and thirstier than usual.


29-08-2006, 22:17:46
Originally posted by JM^3
I am on Beta Blockers..


This is a picture of someone who has it and was on beta blockers


29-08-2006, 22:18:53
Hmmm, I'm hungry.

29-08-2006, 22:28:58
Now you have me worried.


29-08-2006, 22:31:31
Check your PMs. I sent you pictures of what happens to other parts that shouldn't be posted.

C.G.B. Spender
30-08-2006, 05:33:15
too late, he can't read them anymore

30-08-2006, 06:48:53
bye Jon

this would be his final episode......I miss him already

Lazarus and the Gimp
30-08-2006, 07:32:15
Why don't people just drink water from the tap any more? Filters are wrong.

Jon- it's probably just algae. The worst case scenario is that you may start photosynthesising a bit.

30-08-2006, 07:36:34
Originally posted by JM^3
I am on Beta Blockers..


what did I do to get put on ignore?

Lazarus and the Gimp
30-08-2006, 08:11:11
Place your bets now-

5/4 on- he turns out fine.
2/1- bar a spot of arsehole-ripping squits, he's fine.
5/1- death.
10/1- he gets a lycra costume, and fights crime.

30-08-2006, 08:14:00
:lol: Jon and fine...............:lol:

30-08-2006, 08:24:52
Originally posted by Lazarus and the Gimp

10/1- he gets a lycra costume, and fights crime.


hell of a mental image

30-08-2006, 08:44:56
:lol: Jonman nanna nanna nanna nannaa JONMAN!!!!

30-08-2006, 10:54:09

30-08-2006, 11:22:28
I survived.. and am feeling better


30-08-2006, 11:59:42
Get the lycra suit anyway.

30-08-2006, 12:00:30
a hell of an avatar Jon.
Now it's the time

30-08-2006, 12:25:32
If someone resized it..

(although my flashing florescent one is still my favorite)

30-08-2006, 12:29:05

30-08-2006, 12:51:39
This incident is now episode 12 in "The Jon Miller Experience"

30-08-2006, 16:24:36
Damn it, he survived.

C.G.B. Spender
30-08-2006, 16:50:41
It's all your fault

30-08-2006, 18:25:31
pseudomonas is an oppurtunistic pathogen- If you catch it, its probably because your immune system is messed up

common with AIDS and burn victims

30-08-2006, 18:27:30
OTOH, if its algae, there could be all sorts of other nasty things in there feeding on that. Yum, its like you just drank a whole terrarium.

30-08-2006, 18:45:05
Originally posted by C.G.B. Spender
It's all your fault Next time I'll make sure the poison is more potent.