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At least 19 recordsLinked to original sources
PubMed1976

Experimental alimentary infection of anole lizards (Anolis carolinensis) with Mycobacterium ulcerans.

Pathogenic Mycobacterium ulcerans were recovered from the stool of anole lizards up to 11 days after inoculation by stomach tube. M. ulcerans was isolated from the liver of 3 of 20 lizards and acid fast bacteria were seen in the mucosa of intrahepatic bile ducts in 2 of these 10 weeks post-inoculation. These results provide equivocal support for our hypothesis that herpetofauna are a reservoir of infection with M. ulcerans.

Administration, Oral↗
PubMed1978

Further characterization of Mycobacterium ulcerans toxin.

Mycobacterium ulcerans produces an exotoxin in culture which, when inoculated into guinea pig skin, causes inflammation, necrosis, edema, and other histopathological changes resembling those in infections of humans. The toxin was resistant to heat and to alkalies and was moderately acid labile. Toxic activity was destroyed by Pronase, phospholipase, lipase, amylase, and glucosidase but not by trypsin, collagenase, cellulase, lysozyme, hyaluronidase, or neuraminidase. Toxic activity was resistant to treatment with 2-mercaptoethanol, urea, guanidine hydrochloride, p-chloromercuribenzoate, ethylenediaminetetraacetate, and sodium deoxycholate but was destroyed by sodium m-periodate and sodium dodecyl sulfate. The toxin was precipitated by a wide range of ammonium sulfate concentrations. Extraction with chlorofrom-methanol or petroleum ether destroyed its activity. Isopycnic density gradient ultracentrifugation in KBr produced a high-density lipoprotein layer with a 24-fold increase in specific activity. The results indicate that this toxin is a high-molecular-weight phospholipoprotein-polysaccharide complex.

Centrifugation, Density Gradient↗
PubMedDate not supplied

Absence of an antibiotic effect of Mycobacterium ulcerans.

Fractions of Mycobacterium ulcerans were tested for the ability to inhibit growth of 39 bacterial strains. At protein concentrations of up to 280 mg/ml, there was no detectable effect on the growth of any of these bacterial strains.

Anti-Bacterial Agents↗
PubMed1975

Treatment of Mycobacterium ulcerans infection by hyperbaric oxygenation.

Mycobacterium ulcerans causes chronic nectotizing ulcers of the skin and subcutaneous tissue and is a serious health problem in some tropical countries. Chemotherapy has not been effective, and the treatment of choice is extensive debridement followed by skin grafting. In spite of this, many infections are complicated by disfiguring scars, contraction deformities, and--rarely--amputation. There are other procedures that may promote healing (e.g., heat treatment, rifampicin), but none has been completely evaluated. In our study, hyperbaric oxygenation (HBO), an effective treatment for many bacterial diseases, including some mycobacterial infections, was used to treat mice with M. ulcerans-infected footpads. Three groups (40 mice/group) were treated daily with 100% oxygen by three different protocols: 2.5 ATA for 2 h; 2.5 ATA for 1.25 h, twice a day; and 2 ATA for 3.5 h. The degree of infection in the treated mice was compared weekly with 40 positive controls (infected, not treated). The HBO therapy was more effective in the group treated at 2.5 ATA for 1.25 h, twice a day. After 25 weeks, there had been two feet autoamputated and only 12 deaths among the mice, as compared to 18 feet amputated and 24 deaths in the control group. Thus, hyperbaric oxygenation has a beneficial effect in mice and, if used in conjunction with other therapeutic procedures in man, may be an effective therapeutic adjunct in treating M. ulcerans infections.

Animals↗
PubMedDate not supplied

[Skin ulcer caused by Mycobacterium ulcerans in Cameroon. II. Bacteriological study].

Nine stains of Mycobacterium ulcerans isolated in Kamerun, in Congo and in France, were compared with six reference strains found in Zaïre, Australia and Mexico and M. intracellulare, M. simiae, M. paratuberculosis. These fiveteen strains constitutets an species whose typical features were: the difficult and slow growth at the optimum temperature of 30 degrees C, the biochemical tests and the sensitivity to rifampin, streptomycin, kanamycin, viomycin, cycloserin and probably capreomycin. In mice inoculated by the intravenous route, M. ulcerans gives ulcerations of external teguments and sometimes, internal lesions.

Anti-Bacterial Agents↗
PubMed1979

Tumoricidal effects of Mycobacterium ulcerans toxin on murine adenocarcinoma (C3HBA).

Fresh homogenized mammary gland adenocarcinoma (C3HBA) material was subcutaneously inoculated in the anterior right thigh of transplant host mice (C3H/HeJ). When tumors were palpable, the mice were separated into three groups. The test group received biweekly intratumoral injections of Mycobacterium ulcerans filtrate containing 40 mg of protein per ml. One control group received intratumoral injections of normal physiological saline, and the remaining group received no treatment at all. The survival rate of toxin-treated animals was 13.5% at 15 weeks when compared with the control groups. Additionally, tumor metastasis was apparently abrogated in test animals when compared to the control animals. Marked necrosis of the tumors in the test animals was noted by histological examination. Controls showed slight to moderate degrees of tumor necrosis. In this model Mycobacterium ulcerans toxin appears to have therapeutic value as an antitumor agent.

Adenocarcinoma↗
PubMed1975

The production and preliminary investigation of Burulin, a new skin test reagent for Mycobacterium ulcerans infection.

The preparation of a skin test antigen from Mycobacterium ulcerans by ultrasonic disintegration and filtration is described. The reagent, called Burulin, was tested in Africa in normal school children, and in patients with leprosy, tuberculosis or M. ulcerans disease. Those with tuberculosis or M. ulcerans disease were simultaneously tested with Tuberculin PPD. Burulin was found to be highly specific for patients in the reactive stage of M. ulcerans disease, and there was no cross-reaction in patients with other mycobacterioses. On the other hand, the majority of patients with M. ulcerans disease reacting to Burulin also produce positive reactions to Tuberculin PPD.

Antigens, Bacterial↗
PubMed1992

Mycobacterium ulcerans infection; is the "Bairnsdale ulcer" also a Ceylonese disease?

Mycobacterium ulcerans infection produces progressive skin ulceration in man and other mammalia. The disease was first described in 1984 in patients from the Bairnsdale district in Australia, but was known in Africa well before this time. It has since been reported from many, mostly tropical countries in Africa, central and south America, and south-east Asia. The infection characteristically occurs in closely defined areas which are related to river or lacustrian systems draining tropical or warm temperate rain forest. Like the flora to which it relates, the mycobacterium shows a Gondwanian distribution which is evidence of its great antiquity. There is evidence that cases of the infection have occurred on the Indian subcontinent. Infection if it does occur would support the theory that the mycobacterial infection is related to tropical or warm temperate rain forest plant species with a Gondwanian distribution.

Humans↗
PubMed1975

Mycobacterium ulcerans in Australia.

The epidemiology of 39 case reports of infection with Mycobacterium ulcerans published during the past 25 years in Australia is presented. A review is made of the laboratory findings of the strains found in Australia and of the contribution of Australian workers to the description, treatment and prevention of this disfiguring disease.

Adolescent↗
PubMed1976

Mycobacterium ulcerans (Buruli) skin ulceration in Nigeria.

Twenty-two of 24 cases of Mycobacterium ulcerans infection in Ibadan are reviewed. The patients included Africans, Caucasians, and Indians. There were no differences between races in the manifestations of the disease. The average age of the patients was higher than that in other reports in the literature. The fact that most cases were originally wrongly diagnosed reemphasizes the need to search for M. ulcerans in cases of "tropical" ulcer that fail to respond to adequate therapy. Early recognition and surgery are the mainstay of treatment. Comexazole seems more effective than clofazimine in the treatment of these ulcers.

Adolescent↗
PubMed1975

Experimental infection of anole lizards (Anolis carolinensis) with Mycobacterium ulcerans by the subcutaneous route.

To test whether herpetofauna could be a laboratory model for Mycobacterium ulcerans, 21 anole lizards were inoculated subcutaneously with viable M. ulcerans, 21 with autoclaved organisms, and 14 with an aqueous solution of 0.01% Tween 80. M. ulcerans was recovered in culture from the slowly progressive lesions which developed at the inoculation site in lizards receiving the viable bacteria. Progressive lesions did not occur in the two control groups. Three patterns of inflammatory response to viable M. ulcerans were observed: 14 lizards developed a diffuse, granulomatous reaction in which acid fast bacilli (AFB) were predominantly intracellular; 1 developed focal, encapsulated granulomas; 5 developed a diffuse, necrotizing granulomatous response in which most AFB were extracellular--similar to the characteristic lesion found in human infections.

Animals↗
PubMed1976

The protective effect of BCG against Mycobacterium ulcerans disease: a controlled trial in an endemic area of Uganda.

In a BCG vaccination trial in an area of Uganda endemic for Mycobacterium ulcerans disease ("Buruli Ulcer"), 8,856 persons were examined for the disease in mid-1970 and tuberculin tested; BCG was given by intradermal injection to a random 50% of all those with negative, low or middle grade tuberculin reactions; Twelve months later the study group was re-examined for M. ulcerans lesions and, subsequently, new cases of the disease were detected, using a hospital registration system, to December 1974. One hundred and forty-nine patients with onset since July 1970 were thus ascertained and BCG was found to offer an overall protection of 47% against the disease, similar to that observed in a previous smaller trial by the Uganda Buruli Group (UBG, 1969). However, the protective effect was confined to those with tuberculin reactions of less than 4 mm before vaccination and was apparent only in the first year of the study. BCG offered no additional protection to those with previous M. ulcerans disease or an existing BCG scar at entry into the trial, although both these groups appeared to be protected against the disease, the protective effects being 88% and 82% respectively. An initial tuberculin reaction of 4 mm (or greater) offered some protection against the disease (37%). Lesions developing in the vaccinated group, or in those with initial tuberculin reactions of 4 mm or more, were smaller than those in unvaccinated persons. No relationship was found between the protective effect of BCG and either the prevalence of persons with evidence of previous M. ulcerans disease in different geographical areas, or the incidence of new cases in different areas during the first year of the study. A decline in the incidence was observed over the study period. The findings are consistent with BCG producing only short-lasting protection against M. ulcerans disease. However, long-lasting protection and a delay in onset of the disease in vaccinated persons, as suggested by the UBG in 1969, cannot be excluded on the basis of the data currently available from this trial.

Adolescent↗
PubMed1979

Mycobacterium ulcerans infection: treatment with rifampin, hyperbaric oxygenation, and heat.

The effectiveness of hyperbaric oxygenation (HBO), heat, and rifampin for treating mice infected with Mycobacterium ulcerans was analyzed. Four hundred mice were innouclated in the hind footpads with 10(8) organisms. The seven treatment groups (50 mice each) were HBO (2.5 ATA for 1.5 h, twice a day), rifampin (RIF) (20 mg/kg body weight/d), heat (mice maintained at 37 degrees C), and all combinations of the three treatments. The severity of infection in the treated mice was compared weekly for 20 weeks with that of infected controls. The most effective treatments were RIF/HEAT and RIF/HBO/HEAT, RIF/HBO/HEAT treatment was further evaluated to determine the effectiveness of treating mice at various stages of infection. Three hundred mice were inoculated in the hind footpads, and, as the infection progressed, they were separated into groups (50 mice/group) according to the severity of infection. The treatment groups were compared to positive controls. The effectiveness of therapy was indirectly proportional to the severity of infection.

Animals↗