No abstract

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 chloroform-methanol or petroleum ether destroyed its activity. Isopycnic density gradient ultracentrifugation in KBr produced a highdensity lipoprotein layer with a 24-fold increase in specific activity. The results indicate that this toxin is a high-molecular-weight phospholipoprotein-polysaccharide complex.

Abstract. Animal models for Mycobacterium ulcerans infections (Buruli ulcer) include guinea pigs, rats, and mice, but each has limitations in replicating the spectrum of human disease. Here, 19 adult nine-banded armadillos were inoculated intradermally with M. ulcerans. Injection sites were examined and skin samples obtained for histologic and microbiology studies. Necropsies were conducted to assess systemic involvement. In group 1 (n ϭ 4), 2 animals developed progressive skin ulcers with undermined borders at the injection sites within 6-10 weeks. Biopsies showed features similar to human disease including extensive necrosis in the deep dermis and subcutaneous fat, mixed cellular infiltrates, and acid-fast bacilli (AFB). In group 2 (n ϭ 15), 5 animals developed progressive skin ulcers, 3 had evanescent papulo-nodules, 3 died shortly after inoculation of unknown causes, and 4 showed no signs of infection. Lesion samples from 3 animals with progressive ulcers were culture positive for AFB. Our findings indicate that nine-banded armadillos are susceptible to M. ulcerans and may develop cutaneous lesions that closely mimic Buruli ulcer.In tropical countries, skin ulcers caused by infectious agents are common. Mycobacterium ulcerans, the causative organism of Buruli ulcer first isolated in Australia, is considered a public health threat, especially in Africa. [1][2][3][4][5][6][7][8][9][10] Recent observations suggest that environmental sources of M. ulcerans include swamps, with subsequent transmission by insects. 11 The clinical features of Buruli ulcer are variable. In uncomplicated disease, painless skin ulcers, typically on the extremities, develop without fever or malaise. 12,13 However, progressive lesions may result in large areas of ulceration, necrosis, and osteomyelitis. Many lesions tend to heal, but this may take years without medical intervention. Advanced disease requires surgical excision and skin grafts or amputation. Crippling contractures and lymphedema may accompany healing. Medical therapies include clofazimine, dapsone, rifampicin, phenytoin, cotrimoxazole, macrolide compounds, and heat. However, cure rates are generally low. [14][15][16][17][18][19] Understanding the pathogenesis of human M. ulcerans infections has been slowed by the lack of an animal model that develops features resembling human disease. Rats, mice, and guinea pigs are used as animal models for M. ulcerans infections, but each is limited in replicating the spectrum of features found in human disease. Rats and mice develop lesions after cutaneous inoculation with M. ulcerans, but lack the extensive ulceration characteristic of human disease. In the mouse footpad, the organisms multiply but necrosis without ulceration destroys the limb and causes death. 20,21 Guinea pigs develop inflammatory lesions at the inoculation sites that usually resolve without ulcer formation. 21,22 The nine-banded armadillo is highly susceptible to M. leprae and has been a useful animal model for leprosy. 23 Here, we report that armadillos are also s...

No abstract

A numerical study was made of 53 organisms, representing 12 genera of the family Enterobacteriaceae and 4 members of the genus Aeromonas. A total of 105 features was determined for each culture. Matching coefficients were computed, and the organisms were sorted into phenetic groups by use of the "highest-link" criterion. The genera Enterobacter (Aerobacter), Escherichia, Citrobacter, Arizona, Shigella, and Salmonella formed a single, large cluster with little or no evidence of subdivisions into tribes or genera. Paracolobactrum and Klebsiella were joined to the large group as subclusters. Members of the genera Erwinia and Serratia formed separate, distinct clusters related to the large group at a lower level of similarity. At a still lower level were appended Aeromonas, Proteus, Providencia, and some individual species from other genera. These organisms were no more closely related to one another than to the larger group.

No abstract

In spring 1991, Belizian health officials expressed concern about a possible hepatitis outbreak in a banana farming district. A study was designed to identify cases and to address the serological prevalence of hepatitis virus markers. Three populations were studied: (i) persons meeting a clinical case definition for hepatitis; (ii) designated banana workers; and (iii) people in a random sample of households in the community. Information was collected using questionnaires and sera were collected for laboratory testing. This report presents the preliminary results of a study conducted in June 1991. Among people who met the clinical case definition, 24% of 42 tested had immunoglobulin M antibody to hepatitis B virus (HBV) core antigen (anti-HBc IgM). In the worker and household survey populations, 284 and 280 people, respectively, were tested for anti-HBc IgM. In each group, 4% were positive. HBV surface antigen was found in 37% of 43 clinical cases, 18% of workers, and 13% of people in the household survey. Among the 3 study populations, the prevalence of HBV core antibody (anti-HBc) ranged from 73% to 81%. Almost all tested persons had evidence of prior hepatitis A virus infection. Evidence of prior infection with hepatitis viruses A and B was widespread, but an aetiology could not be established for most of the clinical cases. However, the prevalence of hepatitis B markers in this population was very high compared to other reports from the Caribbean.

No abstract