Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                
Jump to content

User:Naz7/sandbox

From Wikipedia, the free encyclopedia
< User:Naz7

This is an old revision of this page, as edited by Naz7 (talk | contribs) at 22:48, 15 November 2013 (→Management and Treatment). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

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 species of fungus responsible for paracoccidioidomycosis.[1][2][3] It is classified under Ascomycetous division and Onygenaceae family, even though for years its sexual phase or Teleomorph was not detected morphologically.[4] The ability of P.brasiliensis to grow as a soil-dwelling mold as well as a yeast at 25° and 37° respectively, makes it a Thermally dimorphic fungus.

Historical Aspects

P. brasiliensis was first discovered by Adolfo Lutz in 1908 in Brazil.[5] Although Lutz did not suggest a name for the disease caused by the fungus, he made note of the “pseudococcidica” and mycelical aspect of it in 25° C culture.[5] In 1911, Alfonse Splendore[6] suggested the denomination of Zymonema brasiliense and explained different features of the fungus in culture. [5] Finally in 1930, Floriano de Almeida offered the name of Paracoccidioides brasiliensis after distinguishing the fungus from a similar strain of C. immitis.[5]

Physiology

P. brasiliensis is a nonphotosyntehtic eukariotic organism with rigid cell wall and organelles very similar to those of higher organisms. [2] [7] Being a Thermally dimorphic fungus, it has the ability to grow an oval yeast-like form at 37° C and an elongated mycelial form at room temperature. [8] The two phases differ in their shape, biochemistry and ultra structural details. [7] The yeast-like form of P. brasiliensis has multiple nuclei, porous bi-layered nuclear membrane and a thick cell wall rich in fibers, whereas the mycelial phase has thinner cell wall, thin electron-dense outer layer, and separated hyphae. [7] In sexual reproduction of the yeast cell called Budding, layers of cell wall gain optical density, especially at the narrow neck between the mother and daughter cell. This is followed by a cleavage of the bud and formation followed by disappearance of a well-defined bud scar.[7] Typical budding must be apparent inside the Granulomatous foci, when examining the histopathologic material of the disease. [9] Hematoxylin and eosin (H&E) stainings are used for detection of fungal cells.[9] The cells without buds or with only one bud measure 5 to 15 µm in diameter, whereas those with multiple spherical buds are 10 to 20 µm in diameter.[9] Under the electron microscope the cells with multiple buds display peripherally located nuclei and cytoplasm in addition to a large central vacuole. [10] The tissue form of P. brasiliensis, yeast cells are usually larger and have thinner walls compared to those of Blastomycosis dermatitidis.[9] Hence, the tissue forms of two fungi are distinguished in that manner.

Dimorphism

  • Conversion from the mycelial to the yeast form of P. brasiliensis in vitro is achieved by transferring the mycelia onto Brain heart infusion broth or "blood-glucose-cysteine agar", and incubation for 10 to 20 days at 37° C.[9]
    • Hyphal cells either die or become transitional forms (6-30 µm in diameter) which would ultimately detach or remain on the hyphal cells to produce buds. [9] Final newly formed yeasts cells bud, become multinucleate, and embody mesosomes.[9]
  • The reverse conversion from yeast culture to a hyphal formed is attained by shifting the temperature of incubation from 37° to 25° C.[11]
  • Previously it was envisioned that nutritional requirements of both phases of P. brasiliensis are the same. [12]Later studies on the other hand, suggested an Auxotrophic condition for the yeast form. Thus, sulfur-containing amino acids such cysteine, or methionine are needed for growth. [13]

Ecology

The habitat of P. brasiliensis has been difficult to determine for mycologists, but it is presumed to be soils in which coffee can be grown. [4][14][15] There is an exclusive geographical distribution for the disease caused by P. brasiliensis. But the main territory has been identified to be Latin American countries such as Brazil, Colombia, and Venezuela with greatest number of cases diagnosed in Brazil (3000 cases). [9] These areas are endemic for paracoccidioidomycosis due to hot humid summers, dry temperate winters, average annual temperatures ranging from 17°-23° C and rainfalls of more than 500-800 mm.[16] However, because of rapid ability of P. brasiliensis to adapt itself to the environment, a distinctive ecology is difficult to pinpoint. No colonies of P. brasiliensis have been found alive in nature and outside human host.[2] But, the fungus is capable of cultivating in the soil and sterile horse or cow excrement based on in vitro studies. [17] In a study performed by Maria B.de Albornoz in 1971, P. brasiliensis was isolated from rural soil samples taken in areas of Paracactos in the state of Miranda, Venezuela. [18] According to another study performed in lab, when the fungus was subjected the fungus to different PH values and temperatures, it survived longer in acid soil due to higher resistance of mycelial phase compared to yeast phase in extreme conditions. [19]

Epidemiology

  • The disease caused by P. brasiliensis agent is more frequent in adult males than females, with a ratio of 38:1 and 12:1 according to Restrepo et al., as well as other reports. [9] [20]
  • The inhibitory effect of estrogen hormone on transformation of mycelial to yeast form of fungus is hypothesized to be a reason for females' resistance to paracoccidioidomycosis.[21]
  • The disease is not contagious.[9]
  • Due to high occurrence of oral lesions in patients, a former belief was the orpharyngeal mucosa role in entry of fungus. [2] However currently with strong support, the respiratory tract is considered to be the portal of entry for P. brasiliensis. [9] Londero et al. discovered the incidence of pulmonary lesions in at least 30% of progressive cases diagnosed with the disease. [22]

Immunology

  • The yeast form has large amounts of a glucan, which is extractable in 1 N sodium hydroxide (NaOH) with α 1-3 linkage. [9][23]
  • The mycelial form contains a β-glucan structure, which is both alkali-soluble and alkali-insoluble.[9]
  • There is more amount of chitin in mycelial form than yeast form.[9]
  • Lipid quantity is the same in both mycelial and yeast forms.[9]

Serology

A number of serologic tests have been used for diagnosis of the disease.[9] Double diffusion in agar gel and complement fixation test, are amongst 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 reported detection of 43-kD antigen in pooled sera of affected individuals, which might provide a possibility for planning a diagnostic test.[25]

Clinical Manifestations

  • The route of infection is assumed to be via inhalation [26] After the pathogen is inhaled, the conidia give rise to distinctive multipolar budding yeast forms in the lung. [8] Both immune-normal and immunocomromised persons could be infected by this fungus.[8] Notably, the organism produces multiple blastoconidia from a single cell, resulting in a "captain's wheel" appearance.
  • Features of pathology caused by the fungus in paracoccidioidomycosis examined at autopsy, are similar to those of Coccidioidomycosis and blastomycosis.[29] Lungs, lymph nodes, and mucous membrane of the mouth are the most frequently infected organs.[9] Extensive and occasional involvement of lymphoid and intestinal tract respectively, in paracoccidioidomycosis as well as lack of lesions in bone, and prostate make the pathogenicity of the fungus different from those of blastomycosis.[29][9]
  • Lesions caused by the fungi first appear in the lymphoid tissue and then extend to mucous membrane. [29] Focal or diffuse necrosis of the nodes is the ultimate result, if the nodes are involved completely.[29]
  • There are different formats and classes of infection caused by the fungus such as Subclinical, chronic unifocal, chronic multifocal, and sub-acute juvenile infections.[9]
    • Subclinical infection is diagnosed by a positive skin test only, since some of the patients may have been exposed to a cross reaction of fungus Histoplasma capsulatum and P. brasiliensis.[9]
    • Chronic unifocal infection occurs in only one organ, whereas chronic multifocal involves multiple organs. [9] Both occur mostly in adults and are rarely detected in children. [9]
    • Sub-acute juvenile infection could progress either acutely or subacutely regardless of the name, and it arises in juveniles of 30 years of age or younger. [9] However, the immune status could overshadow the age effect, as a fatal case of accute-disseminated paracoccidioidomycosis was reported in a 37-year-old man with AIDS. [30]

Management and Treatment

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.[31] 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 [32] Relapse occurs frequently with this drug, although only 2 out of 24 patients relapsed according to reports during their first year use of ketocnazole.[31] 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.[33] 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

  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 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.. PMID 8472249. {{cite journal}}: Check |doi= value (help)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. {{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. 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 x y z aa ab ac Kwon-Chung, K.J (1992). Medical Mycology. Philadelphia: Philadelphia: Lea & Febiger. ISBN 0812114639. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  10. ^ Furtado, J.S (1967). "The structure and reproduction of Paracoccidioides brasiliensis in human tissue". Sabouraudia. 5: 226–229. PMID 6036228. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  11. ^ Ramirez-Martinez, J.R (1971). "Paracoccidioides brasiliensis: Conversion of yeast-like forms into mycelia in submerged culture". J. Bacteriol. 105: 523–526. PMID 5541529.
  12. ^ Gilardi, G.L (1965). "Nutrition of systematic and subcutaneous pathogenic fungi". Bact. Rev. 29: 406–424.
  13. ^ Paris, S (1985). "Nutritional studies on Paracoccidioides brasiliensis": the role of organic sulfur in dimorphism". Sabouraudia. 23: 85–92. PMID 4012515. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  14. ^ Flannigan, Brian (2001). Microorganisms in Home and Indoor Work Environments: Diversity, Health Impacts, Investigation and Control. New York: Taylor & Francis. p. 479. ISBN 9780203302934.
  15. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  16. ^ Borelli, D (1969). "Reservareas de algunos agentes de micosis". Med Cut(Barcelona). 3: 367–370.
  17. ^ Borelli, D (1961). "Hipotesis sobre ecologia de Paracoccidioides". Derm Venez. 3: 130–132.
  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. ^ Restrepo, M (1969). "Effect of hydrogen ion concentration and of temperature on the growth of "Paracoccidioides brasiliensis in soil extract". Sabouraudia. 7: 207–215. PMID 5385156. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  20. ^ Restrepo, M (1970). "Paracoccidiomycosis (South American blastomycosis): a study of 39 cases observed in Medellin, Colombia". Am. J. Trop. Med. Hyg. 19: 68–76. PMID 4984585. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  21. ^ Restrepo, M (1984). "Estrogens inhibit mycelial to yeast transformation in the fungus Paracoccidioides brasiliensis: implications for resisance of females to paracoccidioidomycosis". Infect. Immun. 46: 346–353. PMID 6500694. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  22. ^ Londero, A.T (1972). "Paracoccidioidomycosis: a clinical and mycologic study in forty one cases observed in Santa Maria, RS, Brazil". Am. J. Med. 52: 771–775. PMID 5030174. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  23. ^ Kanetsuna, F (1969). "Cell wall composition of the yeast and mycelial forms of Paracoccidioides brasiliensis". J. Bacteriol. 97: 1036–1041. PMID 5776517. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  24. ^ Blumer, S.O (1984). "Rapid and reliable method for production of a specific Paracoccidioides brasiliensis immunodiffucsion test antigen". J. Clin. Microbiol. 19: 404–407. PMID 6425358. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  25. ^ Mendes-Giannini, M.J.S (1989). "Detection of the 43,000-molecular-weight glycoprotein in sera of patients with paracoccidioidomycosis". J. Clin. Microbiol. 27: 2842–2845. PMID 2592544. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  26. ^ 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)
  27. ^ 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.
  28. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)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. ^ Pedro, R.J (1989). "Paracoccidioidomicose e infeccao pelo virus da imunodeficiencia humana". Rev. Inst. Med. Trop. Sao Paulo. 31: 119–125. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  31. ^ a b Restrepo, A (1993). "Post-therapy status of paracoccidioidomycosistreated with ketoconazole". Am. J. Med. 74: 53–57. PMID 6295152. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  32. ^ 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). PMID 3982489. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  33. ^ Negro, G. del (1982). Negro, G. del (ed.). "In Paracoccidioidomicose: Blastomicose sul-americana": 271–283. {{cite journal}}: Cite journal requires |journal= (help)


Stub icon

This Eurotiomycetes-related article is a stub. You can help Wikipedia by expanding it.

Retrieved from "https://en.wikipedia.org/w/index.php?title=User:Naz7/sandbox&oldid=581834561"