Tetracycline Wolbachia treatment of heartworms

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Tetracycline Wolbachia treatment of heartworms

Postby malernee » Fri Nov 19, 2004 2:45 pm

Vet Parasitol. 2003 Nov 3;117(1-2):73-83.

Immunological role of the endosymbionts of Dirofilaria immitis: the Wolbachia surface protein activates canine neutrophils with production of IL-8.

Bazzocchi C, Genchi C, Paltrinieri S, Lecchi C, Mortarino M, Bandi C.

Dipartimento di Patologia Animale Igiene e Sanita Pubblica Veterinaria, Sezione di Patologia Generale e Parassitologia, Universita di Milano, Via Celoria 10, 20133 Milan, Italy.

Filarial nematodes, including Dirofilaria immitis and D. repens, harbour intracellular bacteria belonging to the genus Wolbachia. These bacteria have been implicated in the pathogenesis of filarial diseases, possibly through their endotoxins. Recent studies have shown that a major surface protein of Wolbachia (WSP) induces a specific IgG response in hosts infected by D. immitis. WSP from the Wolbachia of D. immitis was produced in recombinant form. The purified protein was used in stimulation assays on canine neutrophils. The assays performed using a modified Boyden chamber showed that WSP stimulates neutrophil chemokinesis. In addition, RT-PCR revealed increased production of chemokine IL-8 by cells incubated with this protein. Neutrophils have been shown to play a major role in the pathogenesis of river blindness, and to accumulate in the nodules of onchocerciasis patients. In dogs infected by D. immitis, neutrophils accumulate in kidneys and in the wall of pulmonary arteries. As shown by our studies, Wolbachia could contribute to these inflammatory phenomena through its surface protein WSP, independently from its endotoxin component.

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Exp Parasitol. 2000 Aug;95(4):265-70.

Tetracycline inhibits development of the infective-stage larvae of filarial nematodes in vitro.

Smith HL, Rajan TV.

Department of Pathology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut, 06030-3105, USA.

In recent years, studies have linked tetracycline treatment of filaria-infected animals with reduced adult worm burdens and decreased levels of microfilaremia. These observations are believed to be attributable to clearance of Wolbachia, intracellular rickettsial-like organisms found within filarial tissues. Although maximal worm reductions were observed when treatment was initiated early in infection, it is not known whether tetracycline inhibits development of infective-stage larvae. To address this issue, we studied the effect of tetracycline on three different species of filarial nematodes, Brugia malayi, Brugia pahangi, and Dirofilaria immitis, in a serumfree in vitro system supporting molting to the fourth larval stage. Tetracycline was capable of inhibiting L3 to L4 molting within a dosage range similar to that reported for susceptible rickettsial organisms. However, Wolbachia DNA could still be detected in nematodes from tetracycline-treated cultures. In addition, three other antibiotics with anti-rickettsial and anti-chlamydial activity (chloramphenicol, erythromycin, and ciprofloxacin) failed to inhibit L3 to L4 molting. Although tetracycline is capable of completely blocking molting of infective-stage larvae, it remains possible that this effect is due to pharmacological activities unrelated to its anti-rickettsial functions.
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Wolbachia heartworms tetracycline human and animals study

Postby malernee » Mon Nov 22, 2004 8:50 pm

http://cdli.asm.org/cgi/content/full/10/1/180






Immunoglobulin G Antibodies against the Endosymbionts of Filarial Nematodes (Wolbachia) in Patients with Pulmonary Dirofilariasis
F. Simón,1 G. Prieto,1 R. Morchón,1 C. Bazzocchi,2 C. Bandi,2 and C. Genchi2*
Laboratorio di Parassitologia, Facultad de Farmacia, Universidad de Salamanca, 37007 Salamanca, Spain,1 Dipartimento di Patologia Animale, Igiene e Sanità Pubblica Veterinaria, Sezione di Patologia Generale e Parassitologia, 20133 Milan, Italy2

Received 28 May 2002/ Returned for modification 7 August 2002/ Accepted 19 September 2002


ABSTRACT


The dog parasite Dirofilaria immitis can infect humans. Patients with pulmonary dirofilariasis were tested for immunoglobulin G (IgG) antibodies against the surface protein of Wolbachia, the bacterial endosymbiont of D. immitis. These patients showed significantly higher IgG titers than healthy individuals from areas in which D. immitis was endemic as well as areas in which it was not endemic. Titration of anti-Wolbachia surface protein IgG could become useful for diagnostic applications.


Dirofilaria immitis is the causative agent of heartworm disease in dogs and cats. The disease is found worldwide in subtropical and temperate areas (8). In dogs and cats, the parasite develops to the adult stage in the pulmonary arteries and in the right cardiac chambers (6, 10). The infection is transmitted by several species of mosquitoes that are frequently able to bite both humans and animals. People living in areas of endemicity are thus at risk of infection. Humans are, however, "dead-end hosts," since larvae do not normally develop into the adult stage in humans. Human pulmonary dirofilariasis develops when the nematode dies, embolizes and travels to the lung, and lodges in a small branch of the pulmonary artery. In these cases, chest radiography shows well-circumscribed, noncalcified or calcified nodules (5, 9, 12).

In areas in which heartworm infection in dogs is endemic, clinically healthy people are frequently found positive for antibodies against D. immitis antigens. For example, Prieto et al. (14) recently recorded seroprevalence values ranging from 26 to 37% in three areas of southern Europe. The high percentage of seroprevalence in healthy people in areas of endemicity hampers the serological diagnosis of pulmonary dirofilariasis. Two methods have been proposed for the experimental diagnosis of this disease; they are based on the use of recombinant or native D. immitis proteins (13, 18). However, neither method allows clear-cut distinction between healthy humans from areas of endemicity and patients with pulmonary nodules. Serological studies have also shown different antibody profiles in humans: immunoglobulin G (IgG), IgM, and predominantly IgE antibodies against D. immitis antigens were detectable in healthy individuals, while in patients with pulmonary lesions, the IgE response was not observed (7, 17). Evaluation of immunoglobulin profiles could aid in diagnosis. However, the IgG, IgM, and IgE responses in healthy individuals vary throughout the year (7, 11).

Filarial nematodes, including D. immitis, harbor obligate, intracellular, gram-negative bacteria belonging to the genus Wolbachia (Rickettsiales). Wolbachia is a stable and abundant component of the body of filarial nematodes (1, 2). It was recently shown that Wolbachia surface protein (WSP) induces a specific IgG response in cats infected with D. immitis (3) and in monkeys infected with lymphatic filariae (15). In addition, Wolbachia appears to play a role in the immunopathogenesis of filarial diseases (4, 16).

So far, all studies which have shown a specific antibody response against Wolbachia proteins have been performed with natural hosts of filarial nematodes, with hosts in which the parasite can develop to the adult stage, or after inoculation of hundreds of infective larvae (e.g., see reference 3). Whether an antibody response against Wolbachia develops in dead-end hosts under natural conditions (such as for D. immitis in humans) is not known. The aim of this study was to investigate the IgG response against a Wolbachia protein in humans living in areas in which dog heartworm disease is endemic.

Forty-two serum samples from humans were assigned to the following groups. Group 1 (G1) contains 10 serum samples from patients with pulmonary nodules due to D. immitis infection (these samples were kindly supplied by Patrick Lammie, Centers for Disease Control and Prevention, Atlanta Ga.; diagnosis was made by bioptisy sampling). Group 2 (G2) contains 18 serum samples from clinically healthy humans living in areas in which heartworm infection is endemic (Po River Valley, northern Italy: 10 samples; Colombian Amazonia, South America: 8 samples) and previously found by an enzyme-linked immunosorbent assay (ELISA) to be IgG positive for D. immitis by use of both somatic and excretory or secretory antigens from adult nematodes (14, 19). Group 3 (G3) contains 14 serum samples from healthy humans living in a mountainous area of the province of Salamanca, Spain, where D. immitis infection in dogs and mosquitoes has not been recorded; these donors were found by the ELISA to be seronegative for D. immitis infection.

The WSP of D. immitis, produced in recombinant form and purified as described by Bazzocchi et al. (3), was used as an antigen in an ELISA for the detection of IgG in the 42 serum samples. The ELISA was performed as described by Perera et al. (13), with minor modifications. Briefly, microplate wells were coated with 0.8 µg of recombinant WSP; serum samples were analyzed at a 1:30 dilution, and anti-human peroxidase-conjugated IgG was diluted 1:4,000. The optical density (OD) was measured at 492 nm. The cutoff (0.5) was the OD arithmetical average plus three standard deviations for the 14 serum samples from the clinically healthy blood donors living in the D. immitis-free area.

The ELISA results are reported in Table 1. All of the serum samples from patients with pulmonary nodules due to D. immitis (G1) showed high ODs that were consistently above the cutoff. Serum samples from healthy donors found serologically positive for D. immitis (G2) and from donors living in areas of nonendemicity (G3) had significantly lower ODs (one-way analysis of variance; F, 49.04; P, <0.0001; degrees of freedom, 39).








Our results show that the IgG response against the WSP of D. immitis is consistently detectable only in patients with pulmonary nodules due to the parasite. In healthy blood donors from areas in which D. immitis is endemic and who have IgG against somatic and excretory or secretory antigens of adult parasites, the IgG levels against WSP are lower. Only in 3 cases out of 14 were the IgG titers in this group above the cutoff of our ELISA. This result suggests that the surface protein of Wolbachia endosymbionts stimulates the host immune system only after the death of preadult worms in the small branches of pulmonary arteries, or at least when the development of D. immitis has progressed to a stage at which nematode death can lead to the release of a sufficient amount of bacteria. In any case, our results provide further evidence for the immunological role of Wolbachia in filarial infection, with special reference to humans, and also show that IgG titers are related in some way to the clinical status of the patient.
Our results may suggest an interesting method for the serodiagnosis of pulmonary dirofilariasis. Differential diagnosis (e.g., to exclude pulmonary cancer) requires surgical biopsy, and even a reliable serological assay would not necessarily exclude the need for histological analysis. However, a reliable serologial test for pulmonary dirofilariasis would aid in the final diagnosis, allowing better treatment of patients and better planning of invasive diagnostic procedures, such as thoracoscopy. Based on our results, titration of anti-WSP IgG appears to be a very promising tool for the diagnosis of pulmonary dirofilariasis, possibly in combination with titration of IgE against D. immitis antigens. Of course, examination of additional serum samples from healthy individuals, from patients with pulmonary nodules, and from patients with different parasitoses is needed before an anti-WSP assay can be proposed as a test for the diagnosis of human dirofilariasis.



ACKNOWLEDGMENTS

We thank Patrick Lammie for providing serum samples from humans with pulmonary nodules, Laura Kramer for critical reading of the manuscript, and Stefano Novati for suggestions.

This work was supported by Consejería de Educación y Cultura Junta de Castilla y Léon (grant SA01/00F given to F. Simón) and by MIUR-COFIN 2001 (support given to C. Genchi).


FOOTNOTES

* Corresponding author. Mailing address: Dipartimento di Patologia Animale, Igiene e Sanità Pubblica Veterinaria, Sezione di Patologia Generale e Parassitologia, Via Celoria 10, 20133 Milan, Italy. Phone: 39 02 50318101. Fax: 39 02 50318095. E-mail: claudio.genchi@unimi.it.







Bandi, C., T. J. C. Anderson, C. Genchi, and M. L. Blaxter. 1998. Phylogeny of Wolbachia in filarial nematodes. Proc. R. Soc. Lond. B 265:2407-2413.[CrossRef][Medline]
Bandi, C., A. J. Trees, and N. W. Brattig. 2001. Wolbachia in filarial nematodes: evolutionary aspects and implications for the pathogenesis and treatment of filarial diseases. Vet. Parasitol. 98:215-238.[CrossRef][Medline]
Bazzocchi, C., F. Ceciliani, J. W. McCall, I. Ricci, C. Genchi, and C. Bandi. 2000. Antigenic role of the endosymbionts of filarial nematodes: IgG response against the Wolbachia surface protein in cats infected with Dirofilaria immitis. Proc. R. Soc. Lond. B 267:2511-2516.[CrossRef][Medline]
Brattig, N. W., U. Rathjens, M. Ernst, F. Geisinger, A. Renz, and F. W. Tischendorf. 2000. Lipopolysaccharide-like molecules derived from Wolbachia endobacteria of the filaria Onchocerca volvulus are candidate mediators in the sequence of inflammatory and anti-inflammatory responses of human monocytes. Microbes Infect. 2:1147-1157.[CrossRef][Medline]
Cordero, M., M. R. Muñoz, A. Muro, F. Simón, and L. Perera. 1992. Small calcified nodule: an undescribed radiologic manifestation of human pulmonary dirofilariasis. J. Infect. Dis. 165:398-399.[Medline]
Dillon, R. 1984. Feline dirofilariasis. Vet. Clin. N. Am. Small Anim. Pract. 14:1185-1199.
Espinoza, E., M. Cordero, A. Muro, F. Lorente, and F. Simon. 1993. Anti-Dirofilaria immitis IgE: seroepidemiology and seasonal variation in an exposed human population. Trop. Med. Parasitol. 44:172-176.[Medline]
Genchi, C., L. H. Kramer, and G. Prieto. 2001. Epidemiology of canine and feline dirofilariasis: a global view, p. 121-133. In F. Simon and C. Genchi (ed.), Heartworm infection in humans and animals. Ediciones Universidad Salamanca, Salamanca, Spain.
Harrison, E. G., and J. H. Thompson. 1971. Dirofilariasis, p. 903-916. In R. A. Marcial-Rojas (ed.), Pathology of protozoal and helminthic diseases. The Williams & Wilkins Co., Baltimore, Md.
Kume, S., and S. Itagaki. 1955. On the life-cycle of Dirofilaria immitis in the dog final host. Br. Vet. J. 111:16-24.
Muro, A., M. Cordero, A. Ramos, and F. Simón. 1991. Seasonal changes in the levels of anti-Dirofilaria immitis antibodies in an exposed human population. Trop. Med. Parasitol. 42:371-374.[Medline]
Orihel, T. C., and M. L. Eberhard. 1998. Zoonotic filariasis. Clin. Microbiol. Rev. 11:366-381.[Abstract/Free Full Text]
Perera, L., A. Muro, M. Cordero, E. Villar, and F. Simón. 1994. Evaluation of a 22 kDa Dirofilaria immitis antigen for the immunodiagnosis of human pulmonary dirofilariosis. Trop. Med. Parasitol. 45:249-252.[Medline]
Prieto, G., G. Cancrini, A. Muro, C. Genchi, and F. Simon. 2000. Seroepidemiology of Dirofilaria immitis and Dirofilaria repens in humans from three areas of southern Europe. Res. Rev. Parasitol. 60:95-98.
Punkosdy, G. A., V. A. Dennis, B. L. Lasater, G. Tzertzinis, J. M. Foster, and P. J. Lammie. 2001. Detection of serum IgG antibodies specific for Wolbachia surface protein in rhesus monkeys infected with Brugia malayi. J. Infect. Dis. 184:385-389.[CrossRef][Medline]
Saint André, A., N. M. Blackwell, L. R. Hall, A. Hoerauf, N. W. Brattig, L. Volkmann, M. J. Taylor, L. Ford, A. G. Hise, J. H. Lass, E. Diaconu, and E. Pearlman. 2002. The role of endosymbiotic Wolbachia bacteria in the pathogenesis of river blindness. Science 295:1892-1895.[Abstract/Free Full Text]
Simon, F., A. Muro, M. Cordero, and J. Martin. 1991. A seroepidemiologic survey of human dirofilariosis in western Spain. Trop. Med. Parasitol. 42:106-108.[Medline]
Sun, S., and K. Sugane. 1992. Immunodiagnosis of human dirofilariosis by enzime linked immunosorbent assay using recombinant DNA-derived fusion protein. J. Helminthol. 66:220-226.[Medline]
Viera, C., I. D. Vélez, M. N. Montoya, S. Agudelo, C. Genchi, and F. Simón. 1998. Dirofilaria immitis in Tikuna Indians and their dogs in the Colombian Amazon. Ann. Trop. Med. Parasitol. 92:123-125.[CrossRef][Medline]


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Clinical and Diagnostic Laboratory Immunology, January 2003, p. 180-181, Vol. 10, No. 1
1071-412X/03/$08.00+0 DOI: 10.1128/CDLI.10.1.180-181.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:


Punkosdy, G. A., Addiss, D. G., Lammie, P. J. (2003). Characterization of Antibody Responses to Wolbachia Surface Protein in Humans with Lymphatic Filariasis. Infect. Immun. 71: 5104-5114 [Abstract] [Full Text]
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heartworm Wolbachia associated molecules

Postby guest » Fri Dec 03, 2004 11:16 am

The host-parasite relationship is a complex phenomenon with the immunomodulating effects of the parasite, the host reponse and now throw in Wolbachia associated molecules (WAMs) like Wolbachia Surface Protein (WSP). Below is an excerpt from an article by Kramer et al, "Wolbachia endosymbionts and the immunopathogenesis of filarial disease"
D. immitis and WAMs
"Bazzocchi et al. (2003) have recently studied the effect of Wolbachia Surface Protein from D. immitis on canine neutrophils. The authors showed that WSP stimulates neutrophil chemokinesis and IL-8 production. Neutrophils have been shown to play a major role in the pathogenesis of river blindness, and to accumulate in the nodules of onchocerciasis patients. In dogs infected by D. immitis, neutrophils accumulate in kidneys and in the wall of pulmonary arteries. Wolbachia could contribute to these inflammatory phenomena through its surface protein WSP. Several studies have also been carried out on the humoral response to D. immitis WSP. Infected cats have circulating anti-WSP antibodies, as shown by Western Blot analysis (Bazzocchi et al., 2000). Humans living in D. immitis-endemic areas have circulating anti-WSP antibodies and, more interestingly, patients diagnosed with pulmonary nodules caused by D. immitis have much higher titres (Simòn et al., 2003). Human infection with D. immitis is often aborted; however, in certain cases, the worm may develop and migrate, often reaching the lungs, where it is subsequently sequestered in an inflammatory nodule. The high level of circulating antibodies against a Wolbachia protein in these patients confirms the hypothesis that contact between Wolbachia and the host immune system is more likely following worm death and degeneration."

I know I keep going back to the Wolbachia issue, but the point I am trying to make i
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Wolbachia heartworm infection appears to be 100%

Postby guest » Sun Dec 05, 2004 12:02 pm

Wolbachia organisms can be found in both male and female worms and in all stages of development from embryos, L1-adults. Below is another excerpt from the aforementioned article.
"Wolbachia is present in many of the filarial nematodes that cause disease in humans and animals, including Onchocerca volvulus, Wuchereria bancrofti, Brugia malayi and Dirofilaria immitis. In species harbouring Wolbachia, the prevalence of infection appears to be 100%. Moreover, the infection appears stable along evolutionary times: main branches of filarial evolution are composed of species harbouring Wolbachia (Casiraghi et al., 2001). In adult nematodes, Wolbachia is present in the hypodermal cells of the lateral chords; the cytoplasm of some of these cells is filled with Wolbachia and resemble insect bacteriocytes. In females, Wolbachia is also present in the ovaries and in developing embryos, but has not been demonstrated in the male reproductive apparatus (Sacchi et al., 2002). The bacterium is vertically transmitted through the cytoplasm of the egg, and there is no evidence for horizontal transmission or for paternal transmission. Indeed, the phylogeny of Wolbachia matches that of the host filariae (Casiraghi et al., 2001)."
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adult heartworms are weakened by doxy wolbachia treatment

Postby guest » Sun Dec 05, 2004 3:19 pm

Wolbachia is a Rickettsialis organism that has a symbiotic relationship with Dirofilaria immitis. It produces metabolites that MAY contribute to the pathogenesis of HWD. Doxy will eliminate the organsism for a few months at which time microfilaria are no longer produced and the adult worms are weakened.
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webpage about Wolbachia

Postby malernee » Mon Jul 17, 2006 12:40 pm

Heartworm Prevention and Treatment
Important New Information Regarding Treatment of Heartworm!
Recent research has led to the discovery of a parasite called Wolbachia that lives symbiotically inside heartworms. Studies indicate that this parasite contributes to the adverse effects of both heartworm infection and heartworm treatment, including inflammation, embolism and allergic reaction. Treatment with doxycycline for 30 days to kill the Wolbachia parasite weakens the heartworms and makes them unable to reproduce, lessens their adverse effects on the body and greatly reduces the chance of adverse reaction during heartworm treatment.
Any dog that is currently infected with heartworms should be treated with doxycycline for 30 days. If the infected dog will be treated with Immiticide (fast-kill method), it is best to give the doxycycline prior to beginning Immiticide treatment, as this should make the treatment much safer, by greatly reducing the potential for embolism and allergic reaction to the death of the worms. There may also be benefit in continuing to give doxycycline during treatment. If anyone has dogs currently undergoing treatment with Immiticide, I would start doxycycline immediately, as it may be beneficial even if prior treatment was not done.

Doxycycline should also be given to dogs that are being treated with monthly Heartgard (slow kill method) or any type of alternative heartworm treatment method, as it will weaken the heartworms, prevent them from reproducing, and reduce the chance of adverse effects caused by the heartworm infection itself, and by the worms dying.

It appears unlikely that the Wolbachia parasite persists in the body after the heartworms have been cleared, though we do not know for certain at this time. To be safe, it may be best to give doxycycline for 30 days to any dogs that have completed heartworm treatment in the past, to clear any possible remaining Wolbachia.

I was unable to find information on the recommended dosage of doxycycline for dogs with heartworm infection. Because Wolbachia is a rickettsial organism, similar to those that cause tick disease, it may be advisable to use the higher dose of doxycycline that is recommended for treatment of tick disease, which is 10 mg/kg, twice a day.

Veterinarians may contact Merial, the manufacturer of Immiticide, for more information on this topic, if needed.

Here is some additional info on the topic that I was able to find, though most of it is highly technical and still in preliminary stages of research:

http://www.veterinarypartner.com/Content.plx?P=A&A=610
"Wolbachia is a genus of rickettsial organisms (sort of like bacteria, but not exactly). They live inside the adult heartworm. These organisms seem to be protective or beneficial to heartworms and treating the dog with the antibiotic doxycycline seems to sterilize female heartworms (meaning they cannot reproduce). Wolbachia is also thought to be involved in the embolism and shock that result when heartworms die. The role of this organism is still being investigated. If your veterinarian wants to pre-treat your heartworm positive dog with doxycycline, it may be because of concerns regarding this organism. As new information emerges, we will post here."

http://www.vetmed.auburn.edu/~blagbbl/B ... posium.pdf
"Wolbachia are intracellular bacteria that infect numerous species of filarial worms including heartworms. Many contend that these friendly inhabitants (endosymbionts) play a role in the pathogenesis of diseases caused by heartworms and other filarids. Contention is that host immune responses directed at Wolbachia can actually go awry and enhance the disease process in heartworm infections. Some also contend that elimination of Wolbachia spp. from heartworms may affect the survival of adult heartworms and may decrease the host’s errant immunologic responses when adult worms are killed or die."

http://www.vin.com/proceedings/Proceedi ... &O=Generic
"Dirofilaria immitis [heartworms] the cause of heartworm disease in dogs and cats harbours an endosymbiont intracellular bacteria of the genus Wolbachia (a Rickettsia). Studies performed recently indicate that these bacteria may play an important role in the pathogenesis and immune response to filarial infection (Bandi et al, 2001)." This article goes on to say that Wolbachia may contribute to many of the side effects of heartworm disease, including inflammation, kidney disease, lung problems and allergic reactions.

http://www.vin.com/proceedings/Proceedi ... &O=Generic
"Furthermore, preliminary data from our laboratory indicates that antibiotic treatment before adulticide therapy in dogs with heartworm disease leads to a decrease in pro-inflammatory cytokines, particularly IL-8."

http://lib.bioinfo.pl/meid:13044
This site has numerous other studies on human treatment, indicating that doxycycline, oxytetracycline (of which doxycycline is a derivative) and rifampicin (sometimes use in conjunction with doxycycline) are all effective against Wolbachia.

http://www.pnas.org/cgi/content/full/94/21/11154
"Bacterial relatives of Wolbachia include a number of agents that have arthropods as vectors and cause serious human diseases such as typhus, scrub typhus, erhlichiosis, and Rocky Mountain spotted fever. Studies of these bacteria require special containment facilities. In contrast, Wolbachia have so far been found only in invertebrates and are not known to cause mammalian disease."


Where to find Diethylcarbamazine Citrate, the generic form of Filaribits (daily heartworm preventative):
Doctors Foster & Smith
There is also a product called Dimmitrol that is sold in Australia and can be shipped to the US:
Interpet
CanadaVet (ships from Australia)
Pets Megastore
Vet-Pet-Supplies-Online


Links
http://www.heartwormsociety.org Overview on heartworm disease and map of incidence. See Veterinary Information for treatment guidelines.
Heartworm The information here is slightly outdated, but it gives a very good overview of heartworm infection, prevention and testing, with some info on treatment.

Information on timing heartworm preventatives:
http://www.citadeltm.com/Heartworm.html (US)
http://www.heartworm-hotline.org/ (California only)
http://www.veterinarypartner.com/Content.plx?A=595 see When to Start Prevention Each Year

Emerging Issues in Heartworm Disease Detailed info on diagnosis

Canine Heartworm Disease: Prevention and Treatment

http://www.vetmed.wsu.edu/depts-VCPL/ Information on Ivermectin sensitivity and testing

Heartworm Treatment:
Heartworm-positive dog requires tailored treatment
Heartworm Treatment Aftecare

Articles I wrote for the Whole Dog Journal on heartworm prevention and treatment will be added to this site in September/October, 2006.








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