Paracoccidioidomycosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac
Overview
Spores of Paracoccidioides spp. are transmitted via the respiratory route to the human host. Following transmission, Paracoccidiodes spp. conidia and mycelial particles invade the terminal brochioles and alveoli and convert into yeast cells. [1] On microscopic histopathological analysis, a pilot's wheel-like appearance is a characteristic finding of PMC. [2]
Pathogenesis
- Spores of Paracoccidioides spp. are transmitted via the respiratory route to the human host.
- Following transmission, Paracoccidiodes spp. conidia and mycelial particles invade the terminal brochioles and alveoli and convert into yeast cells. [1]
- "The infection can spread to other tissues via lymphatic and hematic" routes. [1]
- "The fungi developed mechanisms (such as adhesion to host cells), to avoid entrapment within mucus and their elimination by mucigen cilliary cells" [3]
- "Their effective adherence contributes to higher speed invasion of host cells, allowing for evasion of the immune system" [3]
Associated Conditions
Paracoccidioidomycosis is a opportunistic disease in Latin America. Associated conditions are:
- HIV/AIDS: Endemic areas of Paracoccidioides spp. in Brazil have the majority of HIV/AIDS patients.[4] Nevertheless, the incidence of HIV/AIDS and paracoccidioidomycosis is minimum, this may be because the prophylaxis (trimetropin-sulfamethoxazole) used for Pneumocystis jiroveci is the one of the possible treatments for PCM. [4]
- Carcinoma: The majority of patients with carcinoma and PCM, have the same organ or adjacent tissues involved. A risk factor for carcinoma is chronic inflammation with squamous metaplasia, which has been described in 33% cases of PCM in a study. [4]
- Transplants: The small amount of cases may be because of the use of trimetropin-sulfamethoxazole as prophylaxis for Pneumocystis jiroveci, which is one of the possible treatments for PCM. [4]
- Carpal Tunnel Syndrome: Only seen in Immunosupressed patients. [5]
Microscopic Pathology
s a nonphotosynthetic eukaryote with a rigid cell wall and organelles very similar to those of higher eukaryotes. Being a dimorphic fungus, it has the ability to grow an oval yeast-like form at 37°C and an elongated mycelial form produced at room temperature. The mycelial and yeast phases differ in their morphology, biochemistry, and ultrastructure. The yeast form contains large amounts of α-(1,3)-linked glucan. The chitin content of the mycelial form is greater than that of the yeast form, but the lipid content of both phases is comparable. The yeast reproduces by asexual budding, where daughter cells are borne asynchronously at multiple, random positions across the cell surface. Buds begin by layers of cell wall increasing in optical density at a point that eventually gives rise to the daughter cell. Once the bud has expanded, a cleavage plane develops between the nascent cell and the mother cell. Following dehiscence, the bud scar disappears. In tissue, budding occurs inside the granulomatous center of the disease lesion, as visualized by hematoxylin and eosin (H&E) staining of histologic sections. Nonbudding cells measure 5–15 µm in diameter, whereas those with multiple spherical buds measure from 10–20 µm in diameter. In electron microscopy, cells with multiple buds have been found to have peripherally located nuclei and cytoplasm surrounding a large central vacuole. In the tissue form of P. brasiliensis, yeast cells are larger with thinner walls and a narrower bud base than those of the related dimorphic fungus, Blastomycosis dermatitidis. The yeast-like form of P. brasiliensis contains multiple nuclei, a porous two-layered nuclear membrane, and a thick cell wall rich in fibers, whereas the mycelial phase has thinner cell walls with a thin, electron-dense outer layer. [6] In biopsies, the fungus appears as a polygemulating yeast with a pilot's wheel-like appearance. [7]
References
- ↑ 1.0 1.1 1.2 Fortes MR, Miot HA, Kurokawa CS, Marques ME, Marques SA (2011). "Immunology of paracoccidioidomycosis". An Bras Dermatol. 86 (3): 516–24. PMID 21738969.
- ↑ Paracoccidioidomycosis. Wikipedia.https://en.wikipedia.org/wiki/Paracoccidioidomycosis. Accessed on January 12, 2015
- ↑ 3.0 3.1 de Oliveira HC, Assato PA, Marcos CM, Scorzoni L, de Paula E Silva AC, Da Silva Jde F; et al. (2015). "Paracoccidioides-host Interaction: An Overview on Recent Advances in the Paracoccidioidomycosis". Front Microbiol. 6: 1319. doi:10.3389/fmicb.2015.01319. PMC 4658449. PMID 26635779.
- ↑ 4.0 4.1 4.2 4.3 Brummer E, Castaneda E, Restrepo A. Paracoccidioidomycosis: An Update. 'Clin. Microbiol. Rev.1993;Vol 6(2):89-117
- ↑ Lytkin MI, Petlenko VP (1988). "[A methodological analysis of the theory of traumatic disease]". Voen Med Zh (4): 11–4. PMID 3414040.
- ↑ Paracoccidioides brasiliensis. Wikipedia.https://en.wikipedia.org/wiki/Paracoccidioidesbrasiliensis. Accessed on January 12, 2015
- ↑ Paracoccidioidomycosis. Wikipedia.https://en.wikipedia.org/wiki/Paracoccidioidomycosis. Accessed on January 12, 2015