Clindamycin, “clindy” for short, is a bacteriostatic antibiotic used by patients on the Marshall Protocol (MP). Clindamycin comes in 75, 150 and 300mg capsules. There are no reported problems with the generic equivalent.
Prior to the MP, clindamycin has been used to treat acne, bacterial infections with anaerobic bacteria, protozoal diseases such as malaria, and can be useful against some methicillin-resistant Staphylococcus aureus (MRSA) infections.1 Clindamycin binds to the 50S subunit of the bacterial ribosome.
Clindamycin is particularly effective at eliminating infected nerve tissue. Consequently, immunopathological reactions often involve exacerbation of Th1-related psychological symptoms. Therefore, patients with anxiety, depression, obsessive compulsive disorder, etc. should use clindamycin cautiously, as symptoms allow, and be monitored closely.
Clindamycin is typically used in three-antibiotic combinations. When used in combination with just minocycline, it is called a “Modified Phase Two.”
Clindamycin typically comes in pills, but the liquid preparation of clindamycin is acceptable. The pediatric form is called Cleocin and comes in flavored granules for oral solution at 75mg per 5 ml. Patients' pharmacists can instruct them on how to mix it and how long the solution would be good after it has been mixed.
Some patients have complained about the taste of liquid clindamycin.
The maximum recommended dose of clindamycin is 150mg. The maximum recommended frequency is every other day. As with other MP antibiotics, patients are advised to increase their dose of clindamycin incrementally, which insures safety and that a range of pathogens are being targeted.
The standard amount to increase clindamycin is 37.5mg, which is 1/4 of a 150mg pill or 1/8 of a 300mg pill.
Patients concerned about intolerable immunopathology can increment their dose by 25mg, which is 1/6 of a 150mg pill or 1/12 of a 300mg pill.
Clindamycin should be taken at the same time as any other every-other-day antibiotics.
A compounding pharmacy will make up capsules in whatever size clindamycin a patient needs, including 37.5mg, which equals 1/4 a clindamycin pill, the typical starting dose for Phase 3.
There are patients that find smaller doses are sufficient for stimulating adequate immune response. Some have had clindamycin compounded at 5, 10, or 20 mg dose levels.
Patients who wish to maximize their insurance benefit should ask their doctors to prescribe the highest number of clindamycin capsules they feel comfortable with. Because clindamycin is often used in much higher amounts for acute infections, this dosing schedule is typically not questioned by insurance companies. However, there are usually no refills ordered with this type of prescription.
Two examples of these prescriptions are “ninety 150mg capsules” and “sixty 300mg capsules.”
Azithromycin is no longer recommended for use while on the MP. As specified in greater detail in the Protocol Guidelines, patients on the Marshall Protocol begin by taking regular doses of olmesartan (Benicar) and then, later on, increasing doses of minocycline. When ready to experience additional immunopathology, patients begin to take a second antibiotic.
That second antibiotic has historically been azithromycin (Zithromax) or clindamycin. Under certain circumstances, patients and their physicians may wish to use Sulfamethoxazole/Trimethoprim (Bactrim/Septra).
Patients who are still experiencing significant immunopathology from the Olmesartan / 100mg minocycline combination are not yet ready to add a second antibiotic because the two antibiotic combination, especially when Zithromax is used, is very much stronger than minocycline alone.
A special consideration for patients with high levels of 25-D – Patients should not begin azithromycin until their serum level of 25-D drops below 12ng/ml, at which point, they may carefully introduce it. The reason for this caution is because a high level of 25-D suggests a relatively inactive immune response. By taking shorter-acting antibiotics such as clindamycin (as opposed to azithromycin), patients may minimize the length of time they experience a profound response to their antibiotics. An exception may be made for patients who are healthy enough to handle a substantial increase in immunopathology. In this case, physicians may want to wait until a patient's 25-D drops below 20ng/ml.
In later stages of the treatments, demeclocycline may be combined with other MP antibiotics in the following fashion:
Perhaps add these studies:
Infect Immun. 2011 Oct 17. [Epub ahead of print] Profound alterations of intestinal microbiota following a single dose of Clindamycin results in sustained susceptibility to C. difficile-induced colitis. Buffie CG, Jarchum I, Equinda M, Lipuma L, Gobourne A, Viale A, Ubeda-Morant C, Xavier J, Pamer EG. SourceInfectious Diseases Service, Department of Medicine, Lucille Castori Center for Microbes, Inflammation and Cancer, Immunology and Computational Biology Programs and Genomics and Molecular Microbiology Core Laboratories, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center.
Abstract Antibiotic-induced changes in the intestinal microbiota predispose mammalian hosts to infection with antibiotic-resistant pathogens. Clostridium difficile is a Gram-positive intestinal pathogen that causes colitis and diarrhea in patients following antibiotic treatment. Clindamycin predisposes patients to C. difficile colitis. Herein, we have used Roche-454 16s rDNA pyrosequencing to longitudinally characterize the intestinal microbiota of mice following clindamycin treatment in the presence or absence of C. difficile infection. We show that a single dose of clindamycin markedly reduces the diversity of the intestinal microbiota for at least 28 days, with an enduring loss of approximately 90% of normal microbial taxa from the cecum. Loss of microbial complexity results in dramatic sequential expansion and contraction of a subset of bacterial taxa that are minor contributors to the microbial consortium prior to antibiotic treatment. Inoculation of clindamycin-treated mice with C. difficile (VPI 10463) spores results in rapid development of diarrhea and colitis, with a 4 to 5 day period of profound weight loss and an associated 40 to 50 % mortality rate. Recovering mice resolve diarrhea and regain weight but remain highly infected with toxin-producing vegetative C. difficile bacteria and, in comparison to the acute stage of infection, have persistent, albeit ameliorated cecal and colonic inflammation. The microbiota of “recovered” mice remains highly restricted and mice remain susceptible to C. difficile infection at least 10 days following clindamycin, suggesting that resolution of diarrhea and weight gain may result from the activation of mucosal immune defenses.
J Med Microbiol. 2008 Aug;57(Pt 8):1007-14. Impact of antibiotics on the gut microbiota of critically ill patients. Iapichino G, Callegari ML, Marzorati S, Cigada M, Corbella D, Ferrari S, Morelli L. SourceIstituto di Anestesiologia e Rianimazione, Università degli Studi, Polo San Paolo, via Di Rudinì 8, I-20142 Milano, Italy.
Abstract We evaluated the relationship between the intestinal microbiota composition and clinical outcome in a group of 15 high-risk patients admitted for acute infection and/or surgical/accidental trauma who were treated with systemic antibiotics according to standard intensive care unit (ICU) protocols. There was a high mortality rate amongst these patients, each of whom had a considerable organ failure score at admission, respiratory assistance during the most of their ICU stay and a long length of stay. All of these individuals received sedation and enteral nutrition, and the majority also received insulin, vasoactive drugs and some stress-ulcer prophylaxis agents. The intestinal microbiota composition was assessed using denaturing gradient gel electrophoresis (DGGE), a molecular biology tool used to characterize bacterial ecosystems. As all of the patient subjects were in good health prior to their acute illness and admission to the ICU, the first faecal samples obtained from this group showed a DGGE banding pattern that was similar to that of healthy subjects. After 1 week of critical illness, coupled with intensive care treatment, including antibiotics, a very definite alteration in the overall microbiota composition was evident, as revealed by a reduction in the number of DGGE bands. Further pronounced changes to the DGGE banding profiles could be observed in patients remaining in the ICU for 2 weeks. Moreover, a dominant band, identified by sequencing as highly related to Enterococcus, was detected in the DGGE profile of some of our patient subjects. We also performed real-time PCR and obtained results that were in agreement with our qualitative evaluations using DGGE. The degree of organ failure and ICU mortality was significantly higher in patients for whom a high reduction in microbiota biodiversity was coupled with a massive presence of enterococci. A statistically significant link between these two ecological traits and the use of clindamycin was also found.