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Colonies of Strepto-bacillus moniliformis
In the late 1930's Emmy Klieneberger-Noble found that colonies of Strepto-bacillus moniliformis were often accompanied by smaller colonies which in structure and component units exactly duplicated a mycoplasma.1,2
Years later, Dr. T. McP. Brown also became aware of a relationship between mycoplasma and strep. "It has been well established that toxins from streptococci, as well as those from mycoplasma, have an affinity for joints.Strep is an organism that is very susceptible to penicillin . . but even after it has been knocked out as a source of infection, streptococcus hangs on for years, in tonsils, around teeth and in other hidden places - not causing infection, but serving as another source of antigen, or toxin with that demon-strated specificity for joints. . . The streptococcus often alters its form (becomes an L-form) which further compounds the problem (in RA). Treatment of the strep takes one kind of medication; treatment of the altered form requires yet another."3
In a study of 12 patients with associated Mycoplasma pneumoniae infection, A. Ponka noted two patients had an elevated ASO titre and deduced the arthritis was caused by a streptococcal infection.4
It was also noted that "the non-respiratory manifestations of M. pneumoniae infections, e.g. arthritis, carditis and central nervous system infections, might also be due to an im-munological process. . . the arthritis may be reactive in quality, as in rheumatic fever. In this context it should be recalled that M. pneumoniae and Streptococcus group A have antigenic properties in common. Brunner et al5 have demonstrated radioimmuno-precipitating antibodies to M. pneumoniae were blocked by lipids from selected strains of Streptococcus group A and Staphlococcus aureus. . . It has also been suggested that the rise in M. pneumoniae CF titres in arthritis might be unspecific, and caused by cross-reacting antibodies. . . It is possible that the arthritis is caused by direct invasion of mycoplasma into the joints."4
Arnold and Tyndall found DNAase B and ASO to be effective in identifying a reactive arthritis which is migratory and transient and directly linked to recent strep infections. In several cases, the ASO was normal as was ANA, RF and SED rate, but the DNAase was elevated to a significant degree.7
If the patient has an elevated ASO, DNAase B and/or a history of strepto-coccal infection, 250 mg. of ampicillin is prescribed to be taken once daily (preferably in the evenings and not at the same time as the tetracycline). This is continued until the ASO titre is negative after which the medicine is discontinued and the patient is monitored for recurrence.6
A reading other than negative is normal for these tests (varying with age). It has been the experience of several of our patients that any titre cannot be tolerated, and can result in an exacerbation of rheumatic disease symptoms, so it is recommended that the penicillin derivative be continued until a negative titre is achieved. At such time it can usually be discontinued with no exacerbation of rheumatic disease symptoms.
References:
1 E Klieneberger, The natural occurrence of pleomorphic-like organisms known as L, associated with Streptobacillus moniliformis, J Hyg 42, 1935, pg 485-496.
2 E Klieneberger-Noble, Origin, development and significance of L-forms in bacterial cultures, J Gen Microbiol, 3, 1949, pgs 434-442.
3 Synopsis of "Antimycoplasma approach to the mechanism and the control of rheumatic disease, The Scanner, The Arthritis Institute of the National Hospital for Orthopedics, 1:6; 1982.
4 A Ponka, Arthritis associated with Mycoplasma pneumoniae infection, Scand J Rhu, 8:27; 1979, pgs 27-32.
5 H Brunner, B Prescott, H Greenberg, WD James, R Horswood, RM Chanock, Unexpectedly high frequency of antibody to Mycoplasma pneumoniae in human sera as measured by sensitive technique, J Infect Dis, 135; 1977, pg. 524.
6 Protocol for using antibiotics in the treatment of inflammatory rheumatic diseases, The Road Back Foundation, 1995, pgs 1-4.
7 MH Arnold, A Tyndall, Poststreptococcal reactive arthritis, Ann Rhu Dis, 1989; 48:pgs 686-688.
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