posted
Has anyone tried Ketoconazole (Nizoral) or Clotrimazole (Lotrimin or Mycelex) for Babesia?
Hubby has a candida rash on his groin area. Plan to call his primary care provider on Tuesday and request oral Nizoral -- he will probably start with 1/2 of a 200 mg tablet. Will report back in a couple of weeks. Usual dose for candida is 200 -400 mg for 1 -2 weeks and up to 6 months for other systemic infections.
Note that Nizoral has lots of drug interactions -- especially with antibiotics -- Rifampin, Biaxin, Ketek. Also with valium and quinine.
Not sure about interactions with Clotrimazole.
Hubby is off all antibiotics again. Elevated bilirubin from 75 mg Rifampin and 100 mg Doxy so will give the Nizoral a try.
1: Parasitology. 2003 Oct;127(Pt 4):311-5. Related Articles, Links
Clotrimazole, ketoconazole, and clodinafop-propargyl inhibit the in vitro growth of Babesia bigemina and Babesia bovis (Phylum Apicomplexa).
Bork S, Yokoyama N, Matsuo T, Claveria FG, Fujisaki K, Igarashi I.
National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
We evaluated the growth inhibitory efficacy of the imidazole derivatives, clotrimazole (CLT) and ketoconazole (KC), and the herbicide clodinafop-propargyl (CP), in in vitro cultures of Babesia bovis and B. bigemina. Clotrimazole was effective in a dose range of 15 to 60 microM (IC50: 11 and 23.5 microM), followed by KC (50 to 100 microM; IC50: 50 and 32 microM) and CP (500 microM; IC50: 265 and 390 microM). In transmission electron microscopy, extensive damage was observed in the cytoplasm of drug-treated parasites. Combinations of CLT/KC, CLT/CP and CLT/KC/CP acted synergistically in both parasites. In contrast, the combination of KC/CP was exclusively effective in B. bovis, but not in B. bigemina.
PMID: 14636017 [PubMed - indexed for MEDLINE]
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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posted
Haven't heard of this. Surprised that azoles would be used for babesia. Wonder why they tried these?
Posts: 8430 | From Not available | Registered: Oct 2000
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I have been on both nizoral and mycelex for yeast while undergoing treatment for babesia (mepron, ketek and plaquenil), and I didn't observe any benefit from either drug.
Posts: 187 | From Washington, DC | Registered: Dec 2004
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bpeck
Frequent Contributor (1K+ posts)
Member # 3235
posted
Ketonazole cream (or miconazole- aka Monistat 7) will clear the skin candida.. but he'd better be taking something orally too... in case he'sot it systemically or in the gut (and not all the gut meds are systemic.. i.e. Nystatin, Candex)
Does anyone think Nizoral (ketoconazole) or Lotrimin or Mycelex (clotrimazole) has any effect on Lyme cysts?
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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troutscout
Frequent Contributor (5K+ posts)
Member # 3121
posted
hmmmmmmmmmmmmmmmmmm
I am taking nasal spray of 2% Keto... for 2 months now...haven't noticed anything... alos on ketek/mepron and bicillin w/pulsed flagyl
Didn't notice anything
Trout
-------------------- Now is the time in your life to find the "tiger" within. Let the claws be bared, and Lyme BEWARE!!! www.iowalymedisease.com [/URL] Posts: 5262 | From North East Iowa | Registered: Sep 2002
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posted
There may be an assumption that Babesia is vulnerable to the azoles because p. falcicarum, the blood parasite that causes malaria, has been found to have this vulnerability.
Here are some abstracts.
Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):331-6.
Potent antimalarial activity of clotrimazole in in vitro cultures of Plasmodium falciparum.
Tiffert T, Ginsburg H, Krugliak M, Elford BC, Lew VL.
Physiological Laboratory, University of Cambridge, Downing Street, Cambridge CB2 3EG, United Kingdom.
The increasing resistance of the malaria parasite Plasmodium falciparum to currently available drugs demands a continuous effort to develop new antimalarial agents.
In this quest, the identification of antimalarial effects of drugs already in use for other therapies represents an attractive approach with potentially rapid clinical application.
We have found that the extensively used antimycotic drug clotrimazole (CLT) effectively and rapidly inhibited parasite growth in five different strains of P. falciparum, in vitro, irrespective of their chloroquine sensitivity. The concentrations for 50% inhibition (IC(50)), assessed by parasite incorporation of [(3)H]hypoxanthine, were between 0.2 and 1.1 microM. CLT concentrations of 2 microM and above caused a sharp decline in parasitemia, complete inhibition of parasite replication, and destruction of parasites and host cells within a single intraerythrocytic asexual cycle (approximately 48 hr).
These concentrations are within the plasma levels known to be attained in humans after oral administration of the drug. The effects were associated with distinct morphological changes. Transient exposure of ring-stage parasites to 2.5 microM CLT for a period of 12 hr caused a delay in development in a fraction of parasites that reverted to normal after drug removal; 24-hr exposure to the same concentration caused total destruction of parasites and parasitized cells. Chloroquine antagonized the effects of CLT whereas mefloquine was synergistic. The present study suggests that CLT holds much promise as an antimalarial agent and that it is suitable for a clinical study in P. falciparum malaria.
PMID: 10618418 [PubMed - indexed for MEDLINE]
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J Biol Chem. 2002 Feb 8;277(6):4152-8. Epub 2001 Nov 13.
Clotrimazole binds to heme and enhances heme-dependent hemolysis: proposed antimalarial mechanism of clotrimazole.
Huy NT, Kamei K, Yamamoto T, Kondo Y, Kanaori K, Takano R, Tajima K, Hara S.
Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan.
Two recent studies have demonstrated that clotrimazole, a potent antifungal agent, inhibits the growth of chloroquine-resistant strains of the malaria parasite, Plasmodium falciparum, in vitro.
We explored the mechanism of antimalarial activity of clotrimazole in relation to hemoglobin catabolism in the malaria parasite. Because free heme produced from hemoglobin catabolism is highly toxic to the malaria parasite, the parasite protects itself by polymerizing heme into insoluble nontoxic hemozoin or by decomposing heme coupled to reduced glutathione.
We have shown that clotrimazole has a high binding affinity for heme in aqueous 40% dimethyl sulfoxide solution (association equilibrium constant: K(a) = 6.54 x 10(8) m(-2)). Even in water, clotrimazole formed a stable and soluble complex with heme and suppressed its aggregation. The results of optical absorption spectroscopy and electron spin resonance spectroscopy revealed that the heme-clotrimazole complex assumes a ferric low spin state (S = 1/2), having two nitrogenous ligands derived from the imidazole moieties of two clotrimazole molecules.
Furthermore, we found that the formation of heme-clotrimazole complexes protects heme from degradation by reduced glutathione, and the complex damages the cell membrane more than free heme. The results described herein indicate that the antimalarial activity of clotrimazole might be due to a disturbance of hemoglobin catabolism in the malaria parasite.
PMID: 11707446 [PubMed - indexed for MEDLINE]
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J Biochem (Tokyo). 2002 Mar;131(3):437-44.
Effect of antifungal azoles on the heme detoxification system of malarial parasite.
Huy NT, Kamei K, Kondo Y, Serada S, Kanaori K, Takano R, Tajima K, Hara S.
Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan.
The antimalarial activities of some antifungal azole agents (ketoconazole, miconazole, and clotrimazole) have been known for several years, however, their antimalarial mechanism remains equivocal.
Our recent study showed that clotrimazole has a relative high affinity for heme, inhibits reduced glutathione-dependent heme catabolism, and enhances heme-induced hemolysis. In the present study, we have found that clotrimazole can remove heme from histidine rich peptide-heme complex, which initiates heme-polymerization in malaria.
In addition, we show that two other azoles (ketoconazole and miconazole) behave similarly to clotrimazole in binding to heme: they bind to heme with similar affinities, remove heme from the histidine rich peptide-heme complex and from the reduced glutathione-heme complex to form stable heme-azole complexes with two nitrogenous ligands derived from the imidazole moieties of two azole molecules. We have also revealed that clotrimazole and miconazole have stronger promoting activities for heme-induced hemolysis than ketoconazole, implying that the stronger antimalarial activities of clotrimazole and miconazole might arise from their stronger ability to promote heme-induced hemolysis of clotrimazole and clotrimazole than that of ketoconazole.
These results also suggest that ketoconazole and miconazole, like clotrimazole, might possess an antimalarial mechanism relating to their inhibition of heme polymerization and the degradation of reduced glutathione-dependent heme.
PMID: 11872173 [PubMed - indexed for MEDLINE]
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Biol Pharm Bull. 2004 Mar;27(3):361-5.
Enhancement of heme-induced membrane damage by the anti-malarial clotrimazole: the role of colloid-osmotic forces.
Huy NT, Takano R, Hara S, Kamei K.
Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Kyoto, Japan.
Two recent studies have demonstrated that clotrimazole, a well-known potential antifungal agent, inhibits the in vitro growth of chloroquine-resistant strains of the malaria parasite, Plasmodium falciparum.
In a previous study, we suggested that clotrimazole acts as an anti-malarial agent by inhibiting heme catabolism in the malaria parasite and by enhancing heme-induced membrane damage. In this paper, we examined the mechanism of action by measuring hemolysis as an indicator of membrane damage.
Our results showed that clotrimazole does not promote the binding of heme to membranes, and that the enhancement of heme-induced hemolysis by clotrimazole is not caused by lipid peroxidation or by oxidation of thiol groups in membrane proteins.
Instead, clotrimazole inhibits glutathione-dependent heme degradation, resulting in an enhancement of heme-induced hemolysis. We also found that clotrimazole increases the susceptibility of erythrocytes to hypotonic lysis in the presence of heme and that sucrose could inhibit hemolysis induced by heme-clotrimazole complexes.
Thus, it appears that the enhancement of heme-induced hemolysis by clotrimazole in our experiments is due to a colloid osmotic hemolysis mechanism. The hydrophobicity and the large molecular size of the heme-clotrimazole complex might be key factors for induction of hemolysis.
PMID: 14993803 [PubMed - indexed for MEDLINE]
paulscha
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