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Accession No.: 92055102.
Author: Saxena-S-B. Jenkins-R-R.
Title: Prevalence of Trichomonas vaginalis in men at high risk for
sexually transmitted diseases.
Source: Sex-Transm-Dis. 1991 Jul-Sep. 18(3). P 138-42.
Journal Title: SEXUALLY TRANSMITTED DISEASES.
Abstract:
This study determined the prevalence of Trichomonas vaginalis in young men
who were at high risk for sexually transmitted diseases; compared different
diagnostic tests for trichomonads; and compared sexual behavior of men with
positive and negative trichomonas test results. Men (85) aged 16-22 years
inclusive, were recruited from a job-training program to participate in this
study. Urethral specimens were obtained after prostatic massage for the
isolation of Neisseria gonorrhoeae, Chlamydia trachomatis, and trichomonads.
The diagnosis of trichomonas infection was made by urethral culture, urine
sediment culture, direct examination of urine sediment, direct specimen test
(DFA), and Papanicolaou (PAP) smear of urethral swab.
Trichomonas vaginalis was seen in 58% of the men, gonorrhoea in
23.5%, chlamydia in 29%, pediculosis in 6%, and condyloma acuminata in 7%,
respectively. There was no statistically significant difference in age of the
participants, frequency of intercourse, and number of sexual partners in the
last 3 months in men with positive and negative trichomonas test results. After
controlling for gonorrhoea, pyuria was significantly associated with
trichomonas-positive urine (P = .01).
No single test was ideal for the diagnosis of trichomonas infect
Using a combination of urethral culture and urine sediment culture as the "gold
standard," DFA was 60% sensitive and 73.0% specific. However, urine sediment
culture along with DFA identified 94% of all men with positive trichomonas test
results.
(Web Master's Note: STD clinic's still do not adequately test for this.
Even so, this article is in regard to ACUTE NGU. So I suspect it to
be EXTREMELY difficult to test for after being improperly treated.
So what Symptoms do all of these UNTREATED men have ? The other page
on NGU mentions 3-4 million men get NGU per year.
And this article say's that as many as 58% have trich. ???)
Holdings: Health Sciences K.K. Sherwood
SHELVED BY TITLE: Sexually transmitted diseases
CALL NUMBER: Per
LIB HAS: v.15(1988)--
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Source: Sexually Transmitted Diseases, March-April 1995 v22 n2 p83(14).
Title: Trichomoniasis in men: old issues and new data.(review article)
Author: John N. Krieger
Abstract: Trichomoniasis in men appears to be associated with urethral pain
but with little discharge. Trichomoniasis is the result of infection with the
protozoa Trichomonas vaginalis (T. vaginalis). It is thought to occur
predominantly in women. Traditionally, men were thought to be asymptomatic
carriers of the organism. However, a review of the medical literature suggests
that infection with T. vaginalis is associated with non-gonococcal urethritis
in some men. Some studies have attempted to link T. vaginalis infection in men
with prostatitis and other conditions, but results have been inconclusive.
Symptoms of infection in men are ill-defined as are the possible consequences
of infection. A recent study found that 45% of infected men had no discharge.
However, when discharge was present there was usually little of it and it was
clear. Testing for trichomoniasis may be warranted for sexually active men
with urethral symptoms and little or no discharge.
Author's Abstract: @ American Venereal Disease Association 1995
Background and Objectives: Trichomoniasis is common among sexualty active
women, but its importance as a cause of morbidity among sexually active men
remains uncertain. Study Design: The article outlines areas of controversy and
presents pertinent new data from case-control and natural history studies.
Results: Trichomonas vaginalis was documented in 11% of 447 men at risk for a
sexually transmitted disease. Although 54% of infected men complained of
urethral discharge, the discharge was only mild or moderately severe.
Elimination of Trichomonas vaginalis was associated with resolution of
urethritis. Conclusions: Trichomonas vaginalis is an important consideration
in sexually active men with urethral symptoms or inflammation but with little
or no evidence of discharge on physical examination.
Subjects: Trichomoniasis - Care and treatment
Trichomonas vaginalis - Infective ability
Men - Health aspects
Urethritis, Nongonococcal - Causes of
RN: A16795288
( Please see additional information (Bib.) after this Abstract.
Also- Mycoplasma Infection's Co-Infecting ??? )
MEDLINE: Biomedicine, 1990- Fri Jul 17 18:43:26 1998Document 1
Accession No.: 95369889.Author: Provenzano-D. Alderete-J-F.
Title: Analysis of human immunoglobulin-degrading cysteine
proteinases of Trichomonas vaginalis.
Source: Infect-Immun. 1995 Sep. 63(9). P 3388-95.
Journal Title: INFECTION AND IMMUNITY.
Antibody Test's For STD's Blocked ???
Scan of Text pert. info.
( Second Col. First Paragraph )
Abstract:
Trichomonas vaginalis is a protozoan parasite that causes a
widely distributed sexually transmitted disease (STD).Since
immunoglobulin G (IgG) antibodies to specific trichomonad
immunogens are found in serum and vaginal washes (VWs) from
patients with trichomoniasis, a potential mechanism of
immune evasion by this parasite might be the ability of
T. vaginalis proteinases to degrade human immunoglobulins (Igs).
Incubation of human IgG with lysates of T. vaginalis
organisms resulted in time- and concentration-dependent
degradation of the heavy chain. Secretory IgA was degraded
similarly. Inhibitors of cysteine proteinases, when added
to trichomonal lysates, abolished IgG and IgA degradation,
while EDTA, a metalloproteinase inhibitor, did not.
Substrate-gel electrophoresis with human IgG, IgM, or IgA
copolymerized with acrylamide revealed several distinct
cysteine proteinases in both lysates and culture supernatants
from logarithmically growing parasites that degraded all
classes of human antibodies. Trichomonal lysates and
supernatants of numerous isolates tested all had Ig-degrading
activity. Finally, proteolytic activity against IgG was
detected in most (26 of 33; 78%) VWs from patients with
trichomoniasis. In contrast, 18 of 28 (65%) VWs from women
without trichomoniasis or from patients infected with other
STDs had no detectable proteinases when tested in an identical
manner. The other 10 of these 28 VWs (35%) had smaller amounts
of detectable Ig-degrading proteinases. These differences in
Ig-degrading proteinase activity between patients with and
without trichomoniasis, regardless of coinfecting STDs, were
statistically significant (P = 0.001). These results illustrate
that T. vaginalis is capable of degrading human Igs.
Holdings: Health Sciences Serials
SHELVED BY TITLE: Infection and immunity
CALL NUMBER: W 1 IN405 LIB HAS: v.1(1970)--
===============================================
Plus
MYCOPLASMA-ASSOCIATED IMMUNOSUPPRESSION,
Infect Immun, 1974, v9, p410-415.
THE IMMUNOSUPPRESSIVE EFFECT OF MYCOPLASMA INFECTION,
Immunol, 1972, v22, p695-702.
MYCOPLASMA IMMUNOLOGICAL PROBLEMS,
Ann NY Acad Sci, 143(1),
704-706, 1967.
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Since it has been shown that people can and do cross contaminate themselves
with vernal warts, just how catchy is this Trichomonas vaginalis ???
Crohn's Disease, Ulcerative Colitis ??? Read On.
Accession No.: 97392567.
Author: Addis-M-F. Rappelli-P. Cappuccinelli-P. Fiori-P-L.
Title: Extracellular release by Trichomonas vaginalis of a
NADP+ dependent malic enzyme involved in pathogenicity.
Source: Microb-Pathog. 1997 Jul. 23(1). P 55-61.
Journal Title: MICROBIAL PATHOGENESIS.
Abstract:
This report presents evidence showing that Trichomonas vaginalis
releases in the extracellular environment a functional form of
NADP(+)-dependent malic enzyme. The protein which is likely responsible
for the oxidative decarboxilase activity had already been identified in
previous studies as P65, one of the five adhesive proteins of the
protozoan. The same protein had also been described as AP65 by other
authors, which identified it as one of the four surface proteins
specifically responsible for binding of the parasite to the
target cell in a ligand-receptor fashion. Gene characterization
studies performed on P65 by different authors revealed that the
nucleotide sequences of the genes coding for P65 display a striking
homology with the ones coding for the trichomonad malic enzyme. The
experiments performed in this work demonstrate that P65 is secreted and
retains its adhesive properties in the extracellular environment, being
able to bind both erythrocytes and HeLa cells. Therefore, an oxidative
decarboxylase activity assay was performed on T. vaginalis
cell-free filtrates, in order to assess if the released P65
displays cathalitic properties. The assay revealed that parasite-free
supernatants exhibit an oxidative decarboxylase activity which is
NADP(+)-dependent. On the basis of the most recent findings on T.
vaginalis pathogenetic mechanism, which involves pH-dependent perforins,
a role for the secreted enzyme as part of the system is proposed.
Holdings: Available on the Internet
LIB HAS: For issues available online, check:
http://www.idealibrary.com/cgi-bin/links/toc/mi
Health Sciences Serials
SHELVED BY TITLE: Microbial pathogenesis
CALL NUMBER: W1 MI265
LIB HAS: v.1(1986)--
Source: The Lancet, Oct 17, 1998 p1286(1).
Title: Mycoplasma hominis parasitism of Trichomonas vaginalis.(Research
Letters)
Author: Paola Rappelli, Maria Filippa Addis, Franco Carta and Pier Luigi
Fiori
Subjects: Trichomonas vaginalis - Physiological aspects
Mycoplasma infections - Physiological aspects
Comorbidity - Immunological aspects
Trichomoniasis - Physiological aspects
Locations: Italy; Mozambique; Angola
SIC code: 8730
Electronic Collection: A53108655
RN: A53108655
Full Text COPYRIGHT 1998 Lancet Ltd.
Vaginal infections during pregnancy are a risk factor for intrauterine growth
retardation, preterm birth, and perinatal mortality or morbidity.1 Studies of
pregnant1 and non-pregnant2 women have shown an association between
Trichomonas vaginalis and Mycoplasma hominis infections. In an African area
with a high prevalence of trichomoniasis, we noticed anti-Mycoplasma
antibodies in an unexpectedly high number of women with anti-Trichomonas
antibodies. Because an electron-microscopy study showed Mycoplasma organisms
in food vacuoles of protozoa,3 we investigated the cohabitation of the two
micro-organisms in the vagina.
35 T vaginalis isolates were obtained from Italian, Mozambican, and Angolan
women. Parasites were cultured for 7 days in an incubator and culture medium,
which were monitored weekly to ensure they were Mycoplasma-free, then stored
in liquid nitrogen. A sample of each isolate was cultured for 3 months, in the
same Mycoplasma-free conditions. DNA samples, obtained from both the 7 day and
the 3 month cultures of each isolate, were then tested with a Mycoplasma
group-specific PCR. Only two isolates were PCR-negative in both short-term and
long-term cultures. To verify that the presence of Mycoplasma in T vaginalis
cultures was not due to in-vitro contamination, we tested all isolates by PCR
for the detection of Mycoplasma species commonly found as cell-culture
contaminants (M arginini, M hyorhinis, M orale, M fermentans, and Acholeplasma
laidlawii). In all tests there was no specific amplification. The use of
specific primers for the detection of Mycoplasma species frequently associated
with genitourinary tract infections (Ureaplasma urealyticum, M genitalium, and
M hominis), showed that the mycoplasmas associated with all 33 PCR-positive T
vaginalis isolates belonged to the species M hominis. We were able to isolate
Mycoplasma colonies from all infected T vaginalis cultures, and to confirm the
molecular identification by standard biochemical techniques and growth
characteristics in selective media.
The ability of protozoa specifically to allow the replication of M hominis was
then studied. In-vitro infection experiments showed that only M hominis (but
neither U urealyticum nor M genitalium) was able to infect a Mycoplasma-free T
vaginalis isolate. Upon laboratory infection of T vaginalis, M hominis DNA was
detectable after several weeks of daily 1:16 dilutions in fresh T vaginalis
culture medium. We were also able to reisolate M hominis from
laboratory-infected T vaginalis after prolonged cultivation, showing that the
bacterium is able not only to infect T vaginalis cells, but also to replicate
in association with them. We also showed, in vitro, that T vaginalis infected
with M hominis are able to transmit the infection to human epithelial cells,
and that infected epithelial cells are able to transmit M hominis to T
vaginalis.
The clinical association between the two pathogens2 cannot be explained by the
fact that both infections share the same route of transmission. The ability of
the M hominis to parasitise and to replicate in association with T vaginalis
could play a key role in this association. The association between T vaginalis
and M hominis is not unique among human pathogens; the mutual replication of
protozoa and bacteria has been shown for Acanthamoeba and Legionella
pneumophila,4 and for Acanthamoeba and Mycobacterium avium.5
1. Germain M, Krohn MA, Hillier SL, Eschenbach DA. Genital flora in pregnancy
and its association with intrauterine growth retardation. J Clin Microbiol
1994; 32: 2162-68.
2. Koch A, Bilina A, Teodorowicz L, Stary A. Mycoplasma hominis and Ureaplasma
urealyticum in patients with sexually transmitted diseases. Wien Klin
Wochenschr 1997; 109: 584-89.
3. Nielsen MH. The ultrastructure of Trichomonas vaginalis Donne before and
after transfer from vaginal secretion to diamonds medium. Acta Pathol
Microbiol Scand 1975; 83: 381-89.
4. Rowbotham TJ. Preliminary report on the pathogenicity of Legionella
pneumophila for freshwater and soil amoebae. J Clin Pathol 1980; 33: 1179-83.
5. Cirillo JD, Falkow S, Tompkins LS, Bermudez LE. Interaction of
Mycobacterium avium with environmental amoebae enhances virulence. Infect
Immun 1997; 65: 3759-67.
Department of Biomedical Sciences, Division of Experimental and Clinical
Microbiology, University of Sassari, 07100 Sassari, Italy (P L Fiori;
e-mail:
fioripl@assmain.uniss.it)
Prof. Stevens,
STEVENS@ADRENALINE.Berkeley.EDU
Subject:Trichomonas vaginalis and it's pathogenic enzyme
CC:
Alderete@UThscsa.edu, cdherter@u.washington.edu, Duesberg@uclink4.berkeley.edu,
J1mS1@aol.com, jkrieger@u.washington.edu, larson1@u.washington.edu,
gnicimm@ix.netcom.com, soross@u.washington.edu
It was with great interest that I came across your test
for E.Coli .
http://www.rimag.com/07/rep_coli.htm
It is my hope that you can develop a similar test for
Trichomonas vaginalis. It goes undetected in a large number
of patients. Please see this link for posted articles,
suitable for writing a research grant.
https://www.angelfire.com/wa/thestrangest/tricho.html
Fresh Trichomonas vaginalis isolates can be obtained from
STD-Collaborative Research Center (STD-CRC)
Department of Microbiology
University of Texas Health Science Center
San Antonio, Texas.
The authors of this attached report at the above link,
specifically the article on the immunoglobulin-degrading
effects of Trichomonas vaginalis and it's ability to thwart
antibody tests (scanned and posted page from article)
https://www.angelfire.com/wa/thestrangest/images/TVD2.jpg
are ;
Alderete-J-F. Alderete@UThscsa.edu
and
Provenzano-D.
The corresponding author is listed as;
Mailing address
DEPT OF MICROBIOLOGY
UTHSCSA
7703 FLOYD CURL DR.
SAN ANTONIO, TEXAS 78284-7758
PHONE- 210-567-3940
FAX- 210-567-6612
Frankly sir, I have a hypothesis that say's this is
much more common that currently suspected. That it can
work with mycoplasma infections as well as other infectious
agents. While rendering them undetectable to most diagnostic
tests. Some of this is outlined by clicking on the links
at again
https://www.angelfire.com/wa/thestrangest/images/TVD2.jpg
One such plausible explanation is that of patients cross
infecting themselves from their genitals to their rectums.
The problem here is that it generally goes undetected, even when
in it's acute stage. This may also explain why arthritis
patients generally have negative antibody test's for everything.
Thank you, and God's speed,
Tom Krohmer
-----------------------------------------------------------------
Document 4
Accession No.: 97392567.
Author: Addis-M-F. Rappelli-P. Cappuccinelli-P. Fiori-P-L.
Title: Extracellular release by Trichomonas vaginalis of a
NADP+ dependent malic enzyme involved in pathogenicity.
Source: Microb-Pathog. 1997 Jul. 23(1). P 55-61.
Journal Title: MICROBIAL PATHOGENESIS.
Abstract:
This report presents evidence showing that Trichomonas vaginalis
releases in the extracellular environment a functional form of
NADP(+)-dependent malic enzyme. The protein which is likely responsible
for the oxidative decarboxilase activity had already been identified in
previous studies as P65, one of the five adhesive proteins of the
protozoan. The same protein had also been described as AP65 by other
authors, which identified it as one of the four surface proteins
specifically responsible for binding of the parasite to the
target cell in a ligand-receptor fashion. Gene characterization
studies performed on P65 by different authors revealed that the
nucleotide sequences of the genes coding for P65 display a striking
homology with the ones coding for the trichomonad malic enzyme. The
experiments performed in this work demonstrate that P65 is secreted and
retains its adhesive properties in the extracellular environment, being
able to bind both erythrocytes and HeLa cells. Therefore, an oxidative
decarboxylase activity assay was performed on T. vaginalis
cell-free filtrates, in order to assess if the released P65
displays cathalitic properties. The assay revealed that parasite-free
supernatants exhibit an oxidative decarboxylase activity which is
NADP(+)-dependent. On the basis of the most recent findings on T.
vaginalis pathogenetic mechanism, which involves pH-dependent perforins,
a role for the secreted enzyme as part of the system is proposed.
Holdings: Available on the Internet
LIB HAS: For issues available online, check:
http://www.idealibrary.com/cgi-bin/links/toc/mi
Health Sciences Serials
SHELVED BY TITLE: Microbial pathogenesis
CALL NUMBER: W1 MI265
LIB HAS: v.1(1986)--
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April 1, 1997
R&I Report
Red Alert!
E. coli!
A cheap, instantaneous sensor that can detect toxins of
the
deadly E. coli
0157:H7 strain is being shopped around for commercial
development by
Lawrence Berkeley Laboratory at the University of
California, Berkeley.
In the presence of E. coli toxins, the sensor changes
from
blue to red. The
redder the sensor, the higher the concentration of
toxins.
The color change is
instantaneous—a big improvement over current detection
methods that
require samples be cultured for 24 hours.
Chemist Raymond Stevens, whose team at Berkeley Lab
invented the
sensor, says it could be incorporated into plastic,
paper
or glass. Since it's
relatively inexpensive, it could easily become part of
a
bottle cap or container
lid, warning of E. coli before the food within is
consumed.
The ingenious device is based on multiple copies of a
single molecule,
fabricated into a thin film. While the molecule's
surface
locks onto the telltale
bacteria, another layer of the same molecule changes
color
to signal their
presence.
--RITA ROUSSEAU
===============================================
Plus
MYCOPLASMA-ASSOCIATED IMMUNOSUPPRESSION,
Infect Immun, 1974, v9, p410-415.
THE IMMUNOSUPPRESSIVE EFFECT OF MYCOPLASMA INFECTION,
Immunol, 1972, v22, p695-702.
MYCOPLASMA IMMUNOLOGICAL PROBLEMS,
Ann NY Acad Sci, 143(1),
704-706, 1967.
Web Master "Tom"
a.k.a.
krohmer@hotmail.com
thechiron@hotmail.com
