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Paracoccidioides brasiliensis
Scientific classification
Kingdom:
Fungi
Phylum:
Ascomycota
Subphylum:
Ascomycotina
Class:
Eurotiomycetes
Order:
Onygenales
Family:
Ajellomycetaceae
Genus:
Paracoccidioides
Species:
P. brasiliensis
Binomial name
Paracoccidioides brasiliensis
Synonyms

Zymonema brasiliensis Splend.,(1912)
Coccidioides brasiliensis Almeida, (1929)

Paracoccidioides brasiliensis is a dimorphic fungus and the causative agent of the disease, paracoccidioidomycosis.[1][2][3] The fungus has been affiliated with the Family Ajellomycetaceae (Phylum Ascomycota) although a sexual state or teleomorph has not yet been found.[4]

History[edit]

Paracoccidioides brasiliensis was first discovered by Adolfo Lutz in 1908 in Brazil.[5] Although Lutz did not suggest a name for the disease caused by this fungus, he made note of structures he called “pseudococcidica” together with mycelium in cultures grown at 25 °C.[5] In 1912, Alfonse Splendore[6] proposed the name Zymonema brasiliense and described the features of the fungus in culture. [5] Finally in 1930, Floriano de Almeida created the genus, Paracoccidioides to accommodate the species, noting its distinction from Coccidioides immitis.[5]

Physiology[edit]

Paracoccidioides brasiliensis is a nonphotosynthetic eukaryote with rigid cell wall and organelles very similar to those of higher eukaryotes.[2][7] 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.[8] The mycelial and yeast phases differ in their morphology, biochemistry and ultrastructure.[7] The yeast form contains large amounts of α 1–3 linked glucan. [9][10] The chitin content of the mycelial form is greater than that of the yeast form, but the lipid content of both phases is comparable.[9] 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 point that eventually give rise to the daughter cells.[2] Once the bud has expanded, a cleavage plane develops between the nascent cell and the mother cell. Following dehiscence, the bud scar disappears.[7] In tissue, budding occurs inside the granulomatous center of the disease lesion, as visualized by hematoxylin and eosin (H&E) staining of histologic sections.[9] Non-budding cells measure 5–15 µm in diameter whereas those with multiple spherical buds measure from 10–20 µm in diameter.[9] In electron microscopy, cells with multiple buds have been found to have peripherally located nuclei and cytoplasm surrounding a large central vacuole.[11] 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.[9] 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.[7]

Dimorphism[edit]

The yeast form of P. brasiliensis can be converted to the mycelial form in vitro by growth on Brain Heart Infusion agar or Blood-Glucose-Cysteine agar when incubated for 10–20 days at 37 °C.[9] Under these conditions, hyphal cells either die or convert to transitional forms measuring 6–30 µm in diameter which ultimately detach or remain on the hyphal cells, yielding buds. [9] New buds develop mesosomes and become multinucleate.[9]In contrast, yeast-like cultures can be converted to the mycelial form by reducing the incubation temperature from 37 to 25 °C.[12] Initally it was thought that nutritional requirements of both the yeast and mycelial phases of P. brasiliensis were identical; [13] however, later studies demonstrated the yeast form to be auxotrophic, requiring exogenous sulfur-containing amino acids including cysteine and methionine for growth.[14]

Ecology[edit]

Although the habitat of P. brasiliensis remains unknown, it is commonly associated with soils in which coffee is cultivated.[4][15][16] The disease caused by P. brasiliensis is mostly geographically restricted to Latin American countries such as Brazil, Colombia, and Venezuela, with greatest number of cases seen in Brazil.[9] The endemic areas are characterized by hot, humid summers, dry temperate winters, average annual temperatures between 17–23° C and annual rainfall between 500–800 mm.[17] However, the precise ecology regularities of the fungus remain elusive and P. brasiliensis has rarely been encountered in nature outside the human host.[2] One such rare example of environmental isolation was reported in 1971 by Maria B.de Albornoz and colleagues who isolated P. brasiliensis from samples of rural soil collected in Paracotos in the state of Miranda, Venezuela.[18] In in vitro studies, the fungus has been shown to grow when inoculated into soil and sterile horse or cow excrement.[19] The mycelial phase has also been shown to survive longer than the yeast phase in acidic soil.[20]

Epidemiology[edit]

Paracoccidioides brasiliensis causes a disease known as paracoccidioidomycosis characterized by slow, progressive granulomatous changes in the head mucosa, notably the nose and sinuses or the skin. Uncommonly the disease affects the lymphatic system, the central nervous system, the gastrointestinal tract or the skeletal system.[9] Due to the high proportion of cases affecting the oral mucosa, it was originally thought that these tissues were the primary route of entry of fungus.[2] However there is now strong evidence that the respiratory tract is the chief point of entry[9] and P. brasiliensis lung lesions occur in nearly a third of progressive cases.[21] The disease is not contagious.[9] Paracoccidioidomycosis is more frequently seen in adult males than females, favouring males by a factor of 12–38.[9][22] It is thought that the hormone estrogen inhibits the transformation of mycelial to yeast form, as shown by in vitro experiments, and that this factor may account for the relative resistance of women to infection.[23]

Detection[edit]

A number of serologic tests have been employed for the diagnosis of paracoccidioidomycosis.[9] Double diffusion in agar gel and complement fixation test, are amongst the mostly commonly used tests in serodiagnosis.[9] Culture extracts of the yeast or mycelia are exploited to produce effective, quick and reproducible antigens.[24][9] A study performed by Mendes-Giannini et al. reported detection of 43 kD antigen in pooled sera of affected individuals, which might provide a basis for the development of a diagnostic test.[25] It should be noted that tests targetting the presence of serum antibodies to P. brasiliensis simultaneously detect both active and historical infections and cannot descriminate active infection. The evaluation of populations in endemic zones has shown roughly equal rates of seroconversion between men and women, suggesting equal rates of exposure, despite the strong male predominance shown by the clinical disease.[9]

Clinical manifestation[edit]

Paracoccidioides brasiliensis causes mucous membrane ulceration of the mouth and nose with spreading through the lymphatic system. A hypothesis for entry of the fungus to the body is through periodontal membrane.[26][27] The route of infection is assumed to be inhalation following which the infective propagule gives rise to the distinctive multipolar budding yeast forms in the lung resembling a "ship's wheel" seen in histological sections.[28][8] Both immunologically normal and compromised people are at risk for infection.[8]

The lungs, lymph nodes, and mucous membrane of the mouth are the most frequently infected tissues.[9] The pathological features of paracoccidioidomycosis are similar to those seen in coccidioidomycosis and blastomycosis.[29] Hoewever in the former, the lesions first appear in the lymphoid tissue and then extend to mucous membranes,[29] producing localized to diffusive tissue necrosis of the lymph nodes.[29] The typically extensive involvement of lymphoid tissue and the limited occurrence of the gastrointestinal tract, bone and prostate set the clinical picture of paracoccidioidomycosis apart from that of blastomycosis.[29][9]

Management and Treatment[edit]

Successful Management and treatment of the disease caused by P. brasiliensis depends on physician's experience and knowledge of the fungi itself.[2] Since the portal of entry is the respiratory tract and due to asymptomatic primoinfection nature of the disease, diagnosis is only possible by skin testing.[2] However, even when the symptomatic forms of the disease are treated, the fungus can still become active when the immunologic state of host gets disturbed. [2] General circumstances of the host also make the treatment difficult. Undernutrition, alcoholism, socioeconomic and hygienic disadvantages, as well as taking late actions for treatment, are factors that favor the dissemination of the parasite.[2] The first step in treating the disease would be then a complete Anamnesis, checking for the climate where the patient lives and living conditions.[2] An anti fungal therapy is recommended for infected individuals with paracoccidioidomycosis.[9] Oral ketoconazole is now the drug mostly used for patients with no meningitis or any contradictions to use this drug.[30] Marques and colleagues reported successful results after 400mg daily treatment with ketoconazole in 22 people for 30-90 days and a following 200mg daily or every other day treatment for 18 months [31] Relapse occurs frequently with this drug, although only 2 out of 24 patients relapsed according to reports during their first year use of ketocnazole.[30] Intravenous amphotericin B is another well-established mode of therapy and has high levels of effectiveness.[9] Duration of therapy is less for Intravenous amphotericin B, compared to ketoconazole (usually 6-8 weeks) with only 16% of the patients not responding to this drug.[32] Regardless of the treatment used, late relapses are an issue with this pathogen.[9] Ideally, all clinical signs of infection should disappear after at least 6 months of therapy, although many patients are treated for duration of 1-2 years.[9]

References[edit]

  1. ^ Ryan, KJ (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. p. 683. ISBN 0-8385-8529-9.
  2. ^ a b c d e f g h i j Pan American Health Organization. Scientific Publication No. 254 (1971). Paracoccidioidomycosis (1st ed.). Washington Pan American Health Organization. p. 325.{{cite book}}: CS1 maint: numeric names: authors list (link)
  3. ^ Brummer E, Castaneda E, Restrepo A (1993). "Paracoccidioidomycosis: an update". Clin. Microbiol. Rev. 6 (2): 89–117. doi:10.1128/CMR.6.2.89. PMC 358272. PMID 8472249.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ a b Bagagli E, Theodoro RC,Bosco SMG; et al. (2008). "Paracoccidioides brasiliensis: phylogenetic and ecological aspects". Mycopathologia. 165 (4–5): 197–207. doi:10.1007/s11046-007-9050-7. PMID 18777629. S2CID 4877112. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  5. ^ a b c d Lacaz, CS (1994). "Historical evolution of the knowledge on paracoccidioidomycosis and its etiologic agent, Paracoccidioides brasiliensis". Boca Raton:CRC Press: 1–11. {{cite journal}}: Cite journal requires |journal= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ http://www.whonamedit.com/doctor.cfm/1534.html
  7. ^ a b c d Carbonell, Luis M (1963). "Ultrastructure of Paracoccidiodes brasiliensis". Mycopathologia et Mycologia Applicata. 19: 184–204. doi:10.1007/BF02051247. ISSN 0027-5530. PMID 14045074.
  8. ^ a b c Reiss, E (2011). Fundamental Medical Mycology. New Jersey:Wiley-Blackwell: Hoboken. p. 624. ISBN 9780470177914.
  9. ^ a b c d e f g h i j k l m n o p q r s t u v w Kwon-Chung, K.J (1992). Medical Mycology. Philadelphia: Philadelphia: Lea & Febiger. ISBN 0812114639. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  10. ^ Kanetsuna, F.; Carbonell, L. M.; Moreno, R. E.; Rodriguez, J. (1969). "Cell wall composition of the yeast and mycelial forms of Paracoccidioides brasiliensis". J. Bacteriol. 97 (3): 1036–1041. doi:10.1128/jb.97.3.1036-1041.1969. PMC 249811. PMID 5776517.{{cite journal}}: CS1 maint: date and year (link)
  11. ^ Furtado, J. S.; De Brito, T.; Freymuller, E. (1967). "The structure and reproduction of Paracoccidioides brasiliensis in human tissue". Sabouraudia. 5 (3): 226–229. doi:10.1080/00362176785190431. PMID 6036228.{{cite journal}}: CS1 maint: date and year (link)
  12. ^ Ramirez-Martinez, J.R (1971). "Paracoccidioides brasiliensis: Conversion of yeast-like forms into mycelia in submerged culture". J. Bacteriol. 105 (2): 523–526. doi:10.1128/jb.105.2.523-526.1971. PMC 248414. PMID 5541529.
  13. ^ Gilardi, G.L (1965). "Nutrition of systematic and subcutaneous pathogenic fungi". Bact. Rev. 29 (3): 406–424. doi:10.1128/br.29.3.406-424.1965. PMC 441289. PMID 5318450.
  14. ^ Paris, S (1985). "Nutritional studies on Paracoccidioides brasiliensis": the role of organic sulfur in dimorphism". Sabouraudia. 23 (2): 85–92. doi:10.1080/00362178585380151. PMID 4012515. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  15. ^ Flannigan, Brian (2001). Microorganisms in Home and Indoor Work Environments: Diversity, Health Impacts, Investigation and Control. New York: Taylor & Francis. p. 479. ISBN 9780203302934.
  16. ^ Terçarioli GR, Bagagli E, Reis GC; et al. (2007). "Ecological study of Paracoccidioides brasiliensis in soil: growth ability, conidia production and molecular detection". BMC Microbiol. 7: 92–99. doi:10.1186/1471-2180-7-92. PMC 2180180. PMID 17953742. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  17. ^ Borelli, D (1969). "Reservareas de algunos agentes de micosis". Med Cut(Barcelona). 3: 367–370.
  18. ^ Albornoz, M (1971). "Estudio de la sensibilidad especifica en residents de un area endemica a la paracoccidiodomycosis en Venezuela". Mycopathologia. 45: 65–75. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  19. ^ Borelli, D (1961). "Hipotesis sobre ecologia de Paracoccidioides". Derm Venez. 3: 130–132.
  20. ^ Restrepo, A.; Moncada, L. H.; Quintero, M. (1969). "Effect of hydrogen ion concentration and of temperature on the growth of "Paracoccidioides brasiliensis in soil extract". Sabouraudia. 7 (3): 207–215. doi:10.1080/00362177085190371. PMID 5385156.{{cite journal}}: CS1 maint: date and year (link)
  21. ^ Londero, A. T.; Ramos, C. D. (1972). "Paracoccidioidomycosis: a clinical and mycologic study in forty one cases observed in Santa Maria, RS, Brazil". Am. J. Med. 52 (6): 771–775. doi:10.1016/0002-9343(72)90083-6. PMID 5030174.{{cite journal}}: CS1 maint: date and year (link)
  22. ^ Restrepo, M (1970). "Paracoccidiomycosis (South American blastomycosis): a study of 39 cases observed in Medellin, Colombia". Am. J. Trop. Med. Hyg. 19 (1): 68–76. doi:10.4269/ajtmh.1970.19.68. PMID 4984585. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  23. ^ Restrepo, M (1984). "Estrogens inhibit mycelial to yeast transformation in the fungus Paracoccidioides brasiliensis: implications for resisance of females to paracoccidioidomycosis". Infect. Immun. 46 (2): 346–353. doi:10.1128/iai.46.2.346-353.1984. PMC 261537. PMID 6500694. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  24. ^ Blumer, S. O.; Jalbert, M.; Kaufman, L. (1984). "Rapid and reliable method for production of a specific Paracoccidioides brasiliensis immunodiffucsion test antigen". J. Clin. Microbiol. 19 (3): 404–407. doi:10.1128/jcm.19.3.404-407.1984. PMC 271074. PMID 6425358.{{cite journal}}: CS1 maint: date and year (link)
  25. ^ Mendes-Giannini, M. J.; Bueno, J. P.; Shikanai-Yasuda, M. A.; Ferreira, A. W.; Masuda, A. (1989). "Detection of the 43,000-molecular-weight glycoprotein in sera of patients with paracoccidioidomycosis". J. Clin. Microbiol. 27 (12): 2842–2845. doi:10.1128/jcm.27.12.2842-2845.1989. PMC 267138. PMID 2592544.{{cite journal}}: CS1 maint: date and year (link)
  26. ^ Smith J M (1969). "Mycoses of the alimentary tract". Gut. 10 (12): 1035–1040. doi:10.1136/gut.10.12.1035. PMC 1553013. PMID 4904223.
  27. ^ García AM, Hernández O, Aristizabal BH; et al. (2010). "Gene expression analysis of Paracoccidioides brasiliensis transition from conidium to yeast cell". Med. Mycol. 48 (1): 147–154. doi:10.3109/13693780903055673. PMID 19568977. S2CID 22151171. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  28. ^ Restrepo A, McEwen JG, Castañeda E (2001). "The habitat of Paracoccidioides brasiliensis: how far from solving the riddle?". Med. Mycol. 39 (3): 233–41. doi:10.1080/714031028. PMID 11446526.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. ^ a b c d Rippon, John (1982). Medical mycology : the pathogenic fungi and the pathogenic actinomycetes (2nd ed.). Philadelphia: Saunders. ISBN 0721675867.
  30. ^ a b Restrepo, A (1993). "Post-therapy status of paracoccidioidomycosistreated with ketoconazole". Am. J. Med. 74 (1B): 53–57. doi:10.1016/0002-9343(83)90514-4. PMID 6295152. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  31. ^ Marques, S.A (1985). "Paracoccidioidomycosis: a comparative study of the evolutionary serologic, clincal and radiologic results for patients treated with ketoconzazole or amphotericin B plus sulfon-amides". Mycopathologia. 89 (19–23): 19–23. doi:10.1007/BF00437128. PMID 3982489. S2CID 2126796. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  32. ^ Negro, G. del (1982). Negro, G. del (ed.). "In Paracoccidioidomicose: Blastomicose sul-americana": 271–283. {{cite journal}}: Cite journal requires |journal= (help)

External links[edit]

Category:Eurotiomycetes


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