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1.
Article in English | MEDLINE | ID: mdl-38747851

ABSTRACT

Microsporum canis, one of the most widespread dermatophytes worldwide, is a zoonotic microorganism that transmits infection from reservoirs such as cats and dogs to humans. This microorganism is associated with Tinea corporis and other clinical manifestations; however, few studies have used genetic surveillance to determine and characterize the process of zoonotic transmission. In this study, we show a clear example of zoonotic transmission from a cat to an intrafamilial environment, where it caused Tinea corporis by infection with M. canis. Molecular characterization using the b-tubulin gene and Random Amplified Polymorphic DNA analysis made it possible to determine that the six isolates of M. canis obtained in this study belonged to the same genetic variant or clone responsible for reservoir-reservoir or reservoir-human transmission.


Subject(s)
Cat Diseases , Microsporum , Tinea , Zoonoses , Microsporum/isolation & purification , Microsporum/genetics , Microsporum/classification , Cats/microbiology , Animals , Tinea/microbiology , Tinea/transmission , Tinea/veterinary , Cat Diseases/microbiology , Cat Diseases/transmission , Zoonoses/microbiology , Zoonoses/transmission , Pets/microbiology , Humans , Dogs , Random Amplified Polymorphic DNA Technique , Male , Female , Dog Diseases/microbiology , Dog Diseases/transmission , DNA, Fungal/genetics
2.
Vet Res Commun ; 48(1): 49-60, 2024 Feb.
Article in English | MEDLINE | ID: mdl-37490241

ABSTRACT

Salmonella's virulence genes are located in two regions known as Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2). SPI-1 allows the bacteria to invade the intestine, while SPI-2 is important for intracellular survival and replication, although it is also necessary for intestinal disease. The aim of this study was to evaluate the effect of the deletion of SPI-1 or SPI-2 genes on the intestinal and systemic salmonellosis using the avian model. Groups of chickens were orally infected with 1010 Colony-Forming Units (CFU) of S. Typhimurium SL1344 WT strain, as well as mutants ∆SPI-1 or ∆SPI-2. At different times post-infection, 5 chickens from each group were euthanized and examined postmortem. Cecum and liver were taken from each chicken for determination of CFU's, histopathological analysis and immunochemistry. Bacterial colonies were recovered from the liver and cecum samples infected with WT strain, while in the cultures from the organs infected with the mutant strains no colonies were recovered or were drastically affected in the ability to survive. In histopathological analysis, the WT strain produced lesions in liver and ceca, and it was detected by immunohistochemistry throughout the course of the infection. On the other hand, organs of chickens infected with ∆SPI-1 or ∆SPI-2 showed attenuated lesions and the immunohistochemistry revealed less bacteria compared to the WT strain. Taken together, our results show the importance of SPI-1 and SPI-2 genes for the complete intestinal and systemic disease in an in vivo avian model.


Subject(s)
Chickens , Intercellular Signaling Peptides and Proteins , Salmonella Infections, Animal , Animals , Chickens/genetics , Genomic Islands/genetics , Intestines , Salmonella/genetics , Bacterial Proteins/genetics
3.
Antibiotics (Basel) ; 12(12)2023 Dec 09.
Article in English | MEDLINE | ID: mdl-38136747

ABSTRACT

Chromoblastomycosis is a chronic granulomatous mycosis of the skin and subcutaneous tissue caused by traumatic inoculation with dematiaceous fungi. This disease primarily affects agricultural workers, who are mostly men. We present a case of chromoblastomycosis in a 63-year-old male farmer patient with dermatosis over 50 years of evolution, with warty, erythematous, and scaly plaques that predominate on the left hemithorax. Direct examination with potassium hydroxide (KOH) revealed numerous fumagoid cells. Amplification and sequencing of the internal transcribed spacer (ITS) and translation elongation factor 1-alpha (TEF-1a) gene revealed that chromoblastomycosis was caused by Cladosporium cladosporioides. The chromoblastomycosis was treated with itraconazole and fluconazole without any improvement, and amphotericin B was administered with partial improvement.

4.
Jpn J Infect Dis ; 75(4): 427-430, 2022 Jul 22.
Article in English | MEDLINE | ID: mdl-35354704

ABSTRACT

The causative agents of leprosy are Mycobacterium leprae and M. lepromatosis. Mycobacterium lepromatosis was found in 2008 to cause diffuse lepromatous leprosy in Mexican patients. This study aimed to identify M. leprae and M. lepromatosis in paraffin-embedded skin samples from Caribbean patients with leprosy. A total of six skin samples were obtained from the Dominican Republic. All cases presented the multibacillary form; five were nodular lepromatous leprosy, and one was borderline lepromatous leprosy. All patients received multidrug therapy. Molecular identification was achieved using the M. leprae-specific repetitive element for M. leprae and the hemN gene for M. lepromatosis. Mycobacterium leprae was identified in two lepromatous leprosy cases, and one borderline lepromatous leprosy case; M. lepromatosis was found in one nodular lepromatous leprosy case. Both Mycobacterium species were present in two nodular lepromatous leprosy cases. This is the first report of M. lepromatosis in the Dominican Republic.


Subject(s)
Leprosy, Lepromatous , Leprosy , Dominican Republic , Drug Therapy, Combination , Humans , Leprostatic Agents/therapeutic use , Mycobacterium , Mycobacterium leprae/genetics
5.
Braz J Microbiol ; 51(4): 2009-2014, 2020 Dec.
Article in English | MEDLINE | ID: mdl-32897511

ABSTRACT

Using molecular and whole-genome sequencing tools, we investigated colistin-resistant Escherichia coli isolates from wild sea lions. Two unrelated E. coli colistin-resistant isolates, ST8259 and ST4218, were identified, both belonging to the B2 phylogroup and different serotypes. Polymorphisms in PmrA, PmrB, and PhoQ proteins were identified, and the role of PmrB and PhoQ in contributing to colistin resistance was determined by complementation assays. However, the mutations characterized in the present study are not involved in colistin resistance, which have been described in E. coli isolates from clinical settings. Therefore, the acquired mutations in pmrB and phoQ genes in resistance to colistin in bacteria related to marine environment animals are different. This work contributes to the surveillance and characterization of colistin resistance in Escherichia coli obtained from animals from aquatic environments.


Subject(s)
Anti-Bacterial Agents/pharmacology , Colistin/pharmacology , Escherichia coli/classification , Escherichia coli/drug effects , Genome, Bacterial , Sea Lions/microbiology , Animals , Animals, Wild/microbiology , Drug Resistance, Multiple, Bacterial/genetics , Escherichia coli Proteins/genetics , Microbial Sensitivity Tests , Serogroup , Whole Genome Sequencing
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