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Another Look at Mycoplasma.

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Another Look at Mycoplasma
To the Editor:
The recent article by the mycoplasmatologists
and rheumatologists Cole, Taylor, and Ward (ARTHRITIS
RHEUM 18:435-441, 1975) could be misleading to less
experienced investigators. In ruling out likely etiologic
strains, the authors apparently did not evaluate the three
more prevalent human strains of mycoplasma antigens-M salivarium, M orale. and Ureoplasma (T mycoplasma)-in their search for humoral and cell-bound
mycoplasma antibodies in RA. Since our first report in
1964 on the incidence of mycoplasma C F antibodies in
arthritis patients (l), we have followed mycoplasma antibody levels in several thousand patients and still find
M salivarium and M orale (pharyngis) to be the more
prevalent antibody strains. The highest incidence
(60-80%) of humoral mycoplasma antibodies has been
found in female patients attending pulmonary, OBGYN, or VD clinics.
We and other investigators have reported that
rheumatoid factor positive RA patients have a significantly lower incidence of circulating antibodies, including mycoplasma, than do seronegative and nonrheumatoid patients (2,3). It should also be noted that
mycoplasma have been isolated, although infrequently,
from the tissues and even the pleural fluid of RA
patients in the absence of humoral antibodies, while the
cell-mediated responses (skin test and leukocyte migration inhibition tests) were positive (4). Humoral mycoplasma antibodies (single type) have also been observed
persisting for several years in osteoarthritic and asymptomatic controls with negative cell-mediated responses.
The reporting of mycoplasma antibody levels in a single
serum sample may not be representative because concurrent infections can apparently reduce mycoplasma
antibody titers to zero for several weeks. In addition,
mycoplasma antibodies have been found to be low or
absent in the sera of patients ( 5 ) and swine (6), although significant antibody levels were found in the
synovial fluid.
We have found cell-mediated responses to different human mycoplasma strains in both RA and non-RA
patients (including several MS patients) using primarily
the delayed type cutaneous skin reaction. However
neither this test nor the peripheral leukocyte transformation technique directly measures cell-bound antibodies in other tissue cells. The higher blastogenic
transformation by phytohemagglutinin found in the RA
Arthritis and Rheumatism, Vol. 19, No. 3 (May-June 1976)
patients by Cole and coworkers does not seem to agree
with the depressed response reported by other investigators (7,8). Actually the role of mycoplasma in
suppressing this and other immunologic responses
should be given careful consideration and extensive investigation.
In another rheumatology journal, noted mycoplasmatologists and rheumatologists in Finland concurrently reported finding a high (50%) incidence of
mycoplasma antibodies in RA sera (9). Although two
comparable strains-M fermentans and M arthritidiswere cultured and used by both groups of investigators,
the indirect hemagglutination (IHA) test apparently
may be more sensitive and nonspecific than the growth
inhibition tests (metabolic or mycoplasmacidal). It is
particularly significant that these investigators found
both increased and decreased IHA antibody levels in
RA and non-RA sera after it was adsorbed on aggregated IgG t o remove the rheumatoid factor activity. The
adsorption is important because mycoplasma, especially
M fermentans. binds globulin proteins from the horse
serum enriched culture media. A 20% incidence of
mycoplasma antibodies in the serum of healthy blood
donors to only these two human strains may be a somewhat high finding, especially when the more prevalent
strains-M salivarium, M orale, M hominis, and M
pneumoniae-were excluded. Although we have used
both growth inhibition and agglutination tests, the complement fixation (CF) test has proved to be the most
satisfactory for screening patients’ sera for mycoplasma
antibodies. The CF test is also particularly applicable
for patients on drugs known to inhibit mycoplasma
growth in vitro, such as gold salts, chloroquine, and
tetracyclines, which might interfere with growth inhibition tests.
Finding antibodies t o the human mycoplasma
strains in both rheumatoid and nonrheumatoid captive
great apes does not prove that the mycoplasma were
acquired from their human caretakers (10). Conversely
the M salivarium strain isolated from an early rheumatoid patient with autologous humoral antibodies who
had been bitten by a pet monkey does not prove its
primate origin, even though the human oral strains have
been found primarily in monkeys (1 1). However there is
growing concern that humans might further contaminate the great apes now being investigated in the
wild. The isolation and detection of the arthritogenic
swine strain M hyorhinis in humans may prove to have
some significance, but presently it appears to be more of
a laboratory characteristic than a species characteristic.
The arthritogenic rat strains M arthritidis (reference
6 50
strain PG-6) have been found to cross-react with those
strains that were isolated from humans a n d were formerly called M horninis, Type 11. Our laboratory recently reported the isolation of such a strain from the
pleural fluid of a patient with severe rheumatoid arthritis who had a negative humoral antibody titer with a
positive rheumatoid factor but gave a positive, delayed
type skin test and leukocyte migration inhibition tests to
the isolated strain (4). Several other strains of the M
horninis, Type 11, or M arthritidis have been isolated in
our laboratory. This finding supports those of Jansson
a n d coworkers, who found that many of their mycoplasma isolates from R A and SLE patients cross-reacted
primarily with M arthritidis (12).
Until more is known a b o u t mycoplasma and
their host relationships, we would like to suggest the
importance of not ruling o u t any possible etiologic
strains until a more likely candidate is found. T h e caution is especially advised for the M arthritidis strains
that produce large amounts of DNase, for the etiologic
source(s) of DNase inhibition, a n d for the still unknown
anti-DNA antibodies in SLE patients (13).
1. Clark HW, Bailey JS, Brown TMcP: Determination of
mycoplasma antibodies in humans. Bacteriol Proc 6459,
2. Brown TMcP, Clark HW, Bailey JS: Relationship be-
tween mycoplasma antibodies and rheumatoid factors
(RF). Arthritis Rheum 13:309-310, 1970
Stanford F: Comparison of complement-fixing antibody
titers i n patients with rheumatoid arthritis and matched
controls. Ann Rheum Dis 31:330-333, 1972
Brown TMcP, Bailey JS, Clark HW: Mycoplasma in
pleural effusion of rheumatoid arthritis, XI11 International Congress on Rheumatology. Excerpta Medica
International Congress Series No. 299. Amsterdam, Elsevier/Excerpta Medica, 1973, p 172
Brown TMcP, Bailey JS, Felts WR, et al: Mycoplasma
antibodies in synovia. Arthritis Rheum 9:495, 1966
Barden JA, Decker JL: M. hyorhinis swine arthritis. I.
Clinical and microbiotogical features. Arthritis Rheum
14:193-201, 1971
7. Rosenthal CJ, Franklin EC: Depression of cellular-me-
diated immunity in systemic lupus erythematosus: relation
to disease activity. Arthritis Rheum 18:207-217, 1975
8. Lockshin MD, Eisenhauer AC, Kohn R, et al: Cell-mediated immunity in rheumatic diseases. 11. Mitogen responses in RA, SLE, and other illnesses: correlation with
T- and B-lymphocyte populations. Arthritis Rheum
18~245-250, 1975
9. Jansson E, Makisara P, Tuuri S: Mycoplasma antibodies
Arthritis and Rheumatism, Vol. 19, No. 3 (May-June 1976)
in rheumatoid arthritis. Scand J Rheumatol 4: 165-168,
10. Brown TMcP, Clark HW, Bailey JS: Natural occurrence
of rheumatoid arthritis in great apes-a new animal
model. (Experience with captive gorillas in the US. including the Philadelphia Zoo.) Proceedings of the Zoological Society of Philadelphia Centennial Symposium on
Science and Research, 1974
1 I . B a d e MF: Mycoplasmal flora of simians. J Infect Dis
127: 17-20, 1973 (suppl)
12. Jansson E, Makisara P, Vainio K, et al: An 8-year study
on mycoplasma in rheumatoid arthritis. Ann Rheum Dis
30506-508, 1971
13. Bailey JS, Clark HW, Brown TMcP, et al: Radial diffu-
sion analysis of mycoplasma desoxyribonuclease. American Society of Microbiology Abstracts, 1975, p 59
M c P . BROWN,M.D.
Arthritis Institute
National Orthopaedic and
Rehabilitation Hospital
Arlington, Virginia 22206
To the Editor:
I would like to add two other mnemonics to the
o n e suggested by Dr. Schumacher (ARTHRITIS RHEUM
18:626, 1975) to help remember the color of the crystal
a s related to its orientation to the axis of the slow vibration of light when viewed under compensated polarized
light microscopy.
BRAG: Blue a t Right Angle-Gout
IPPPB: Positive Parallel Pyrophosphate Blue, a
take off on IPPB: intermittent positive pressure breathing.
Emory University School of Medicine
Atlanta, Georgia 30303
...and More Mnemonics
To the Editor:
I liked Dr. Schumacher’s little verse that helps
him remember the polarizing characteristics of the monosodium urate crystal (ARTHRITIS
RHEUM 18:626, 1975).
O n this side of the Atlantic, I have been helped by the
letters BAPM, which is actually the abbreviation for the
British Association of Physical Medicine but which reminds m e of Blue Across Purine Metabolite, a mne-
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another, look, mycoplasma
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