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Systemic MycosesSystemic Mycoses
Prepared By:
Saira RehmanSaira Rehman
Naila QamarNaila Qamar
Saba Aslam
Komal Javed
Hiza Hassan
Semester: 6th
,MLTMLT
Systemic Mycosis
These infections result from inhalation of the spores of dimorphic
fungi that have their mold forms in the soil.
Within the lungs, the spores differentiate into yeasts or other
specialized forms.
Most lung infections are asymptomatic and self-limited.
However, in some persons, disseminated disease develops in which
the organisms grow in other organs, cause destructive lesions, and
may result in death.
Infected persons do not communicate these diseases to others.
COCCIDIOIDECOCCIDIOIDEHISTOPLASMAHISTOPLASMABLASTOMYCESBLASTOMYCESPARACOCCIDIOIDESPARACOCCIDIOIDES
Systemic Mycoses
COCCIDIOIDECOCCIDIOIDE
General Characteristics
 Mode Of Transmission: Inhalation; Respiratory droplet
 Primary site of infection- LUNGS, 90% of infection is
asymptomatic or they resolved spontaneously
accompanied by high degree of specific resistance to
infections
 Causes dissemination to other sites
 Geographically restricted
 Dimorphic
 25 C- grows as filamentous mold
 37C- yeast cell
COCCIDIOIDE
 Disease
Coccidioides immitis causes coccidioidomycosis.
 Properties
C. immitis is a dimorphic fungus that exists as a
mold in soil and as a spherule in tissue
Transmission & Epidemiology Coccidioide
 The fungus is endemic in arid regions of the
southwestern United States and Latin America.
 People who live in Central and Southern California,
Arizona, New Mexico, Western Texas, and Northern
Mexico, a geographic region called the Lower
Sonoran Life Zone, are often infected.
 In soil, it forms hyphae with alternating
arthrospores
and empty cells.
 Arthrospores are very light
and are carried by the wind.
 They can be inhaled and
infect the lungs.
Pathogenesis of Coccidioide
 In the lungs, arthrospores form spherules that are large,
have a thick, doubly refractive wall, and are filled with
endospores.
 Upon rupture of the wall, endospores are released
and differentiate to form new spherules.
 The organism can spread within a person by direct
extension or via the bloodstream.
 Granulomatous lesions can occur in virtually any organ
but are found primarily in bones and the central
nervous system (meningitis)
 Dissemination from the lungs to other organs occurs in
people who have a defect in cell-mediated immunity.
Pathogenesis of Coccidioide
 Most people who are infected by C. immitis develop
a cell-mediated (delayed hypersensitivity) immune
response that restricts the growth of the organism.
 One way to determine whether a person has
produced adequate cell-mediated immunity to the
organism is to do a skin test (see below).
 In general, a person who has a positive skin test
reaction has developed sufficient immunity to
prevent disseminated disease from occurring.
 If, at a later time, a person's cellular immunity is
suppressed by drugs or disease, disseminated
disease can occur.
Clinical Findings of Coccidioide
 Infection of the lungs is often asymptomatic and is
evident only by a positive skin test and the presence of
antibodies.
 Some infected persons have an influenza like illness
with fever and cough.
 About. 50% have changes in the lungs (infiltrates,
adenopathy, or effusions) as seen on chest x-ray.
 10% develop erythema nodosum.
 This syndrome is called "valley fever" or "desert
rheumatism"; it tends to subside spontaneously.
 Disseminated disease can occur in almost any organ;
the meninges, bone, and skin are important sites.
Clinical Findings of Coccidioide
 The overall incidence of dissemination in
persons infected with C. imrnitis is 1%, although
the incidence in Filipinos and African Americans
is 10 times higher.
 Women in the third trimester of pregnancy also
have a markedly increased incidence of
dissemination.
 Erythema nodosum (EN) manifests as red, tender
nodules ("desert bumps") on extensor surfaces
such as the shins.
 It is a delayed (cell-mediated) hypersensitivity
response to fungal antigens and thus is an
indicator of a good prognosis.
Clinical Findings of Coccidioide
 There are no organisms in these lesions; they are not
a sign of disseminated disease. EN is not specific for
coccidioidomycosis; it occurs in other granulomatous
diseases, e.g, histoplasmosis, tuberculosis, and
leprosy.
 In infected persons, skin tests with fungal extracts
cause at least a 5mm induration 48 hours after
injection (delayed hypersensitivity reaction).
 Skin tests become positive within 2-4 weeks of
infection and remain so for years but are often
negative in patients with disseminated disease.
Laboratory Diagnosis of Coccidioide
 In tissue specimens,
spherules are seen
microscopically.
 Cultures on
Sabouraud's agar
incubated at 25 °C show
hyphae with arthrospores.
 (Caution: Cultures are highly
infectious; precautions against
inhaling arthrospores must be
taken.)
Laboratory Diagnosis of Coccidioide
 In serologic tests, IgM and IgG precipitins appear
within 2-4 weeks of infection and then decline
in subsequent months.
 Complement-fixing antibodies occur at low titer
initially, but the titer rises greatly if
dissemination occurs
Treatment & Prevention of Coccidioide
 No treatment is needed in asymptomatic or mild
primary infection.
 Amphotericin B (Fungizone) or itraconazole is used
for persisting lung lesions or disseminated disease.
 Ketoconazole is also effective in lung disease.
 Fluconazole is the drug of choice for meningitis.
 Intrathecal amphotericin B may be required and
may induce remission, but long-term results are
often poor.
 There are no means of prevention
except avoiding travel to endemic areas.
PARACOCCIDIOIDESPARACOCCIDIOIDES
General characteristics
 Etiologic Agent: P. brazieliensis
 Central & South America & has high incidence in Brazil,
Venezuela & Colombia
 Natural reservoir: isolated in soil that have high
humidity & average temperature of 23 C
 Equal distribution among males & females, but clinical
disease is about 9X higher in males
 Transition of fungi from mold to yeast can be induced in
vitro by raising the temperature of 25 C to 37 C
 M-17-beta- estradiol inhibits transformation of the fungi
 Testosterone,corticosterone & 17 alpha estradiol had
NO inhibitory on the transformation
Disease of Paracoccidioides
 Paracoccidioides brasiliensis causes
paracoccidioidomycosis,
also known as South American blastomycosis.
Paracoccidioidomycosis
 Etiologic Agent: P. brazieliensis
 Central & South America & has high incidence in Brazil,
Venezuela & Colombia
 Natural reservoir: isolated in soil that have high humidity &
average temperature of 23 C
 Equal distribution among males & females, but clinical
disease is about 9X higher in males
 Transition of fungi from mold to yeast can be induced in
vitro by raising the temperature of 25 C to 37 C
Properties of Paracoccidioides
 P. brasiliensis is a dimorphic fungus that exists
as a mold in soil and as a yeast in tissue.
 The yeast is thick walled with multiple buds, in
contrast to B. derrnatitidis, which has a single
bud .
Transmission & Epidemiology of Paracoccidioides
 The spores are inhaled, and early lesions occur
in the lungs.
 Asymptomatic infection is common.
 This fungus grows in the soil and is endemic in
rural Latin America. Disease occurs only in that
region.
Pathogenesis & Clinical Findings of Paracoccidioides
 The spores are inhaled, and early lesions occur in the lungs.
 Asymptomatic infection is common.
 Alternatively oral mucous membrane lesions, lymph node
enlargement, and sometimes dissemination to many organs
develop.
 Ulceration, granulomatous infection of oral and nasal mucosa
Laboratory Diagnosis of Paracoccidioides
 In pus or tissues, yeast cells with multiple buds
are seen microscopically.
 A specimen cultured for 2-4 weeks may grow
typical organisms.
 Skin tests are rarely helpful.
 Serologic testing shows that when significant
antibody titers (by immunodiffusion or complement
fixation) are found, active disease is present
Treatment & Prevention of Paracoccidioides
 The drug of choice is itraconazole taken orally
for several months.
 There are no means of prevention.
Systemic_MycosesM

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Systemic_MycosesM

  • 1. Systemic MycosesSystemic Mycoses Prepared By: Saira RehmanSaira Rehman Naila QamarNaila Qamar Saba Aslam Komal Javed Hiza Hassan Semester: 6th ,MLTMLT
  • 2. Systemic Mycosis These infections result from inhalation of the spores of dimorphic fungi that have their mold forms in the soil. Within the lungs, the spores differentiate into yeasts or other specialized forms. Most lung infections are asymptomatic and self-limited. However, in some persons, disseminated disease develops in which the organisms grow in other organs, cause destructive lesions, and may result in death. Infected persons do not communicate these diseases to others.
  • 5. General Characteristics  Mode Of Transmission: Inhalation; Respiratory droplet  Primary site of infection- LUNGS, 90% of infection is asymptomatic or they resolved spontaneously accompanied by high degree of specific resistance to infections  Causes dissemination to other sites  Geographically restricted  Dimorphic  25 C- grows as filamentous mold  37C- yeast cell
  • 6. COCCIDIOIDE  Disease Coccidioides immitis causes coccidioidomycosis.  Properties C. immitis is a dimorphic fungus that exists as a mold in soil and as a spherule in tissue
  • 7. Transmission & Epidemiology Coccidioide  The fungus is endemic in arid regions of the southwestern United States and Latin America.  People who live in Central and Southern California, Arizona, New Mexico, Western Texas, and Northern Mexico, a geographic region called the Lower Sonoran Life Zone, are often infected.  In soil, it forms hyphae with alternating arthrospores and empty cells.  Arthrospores are very light and are carried by the wind.  They can be inhaled and infect the lungs.
  • 8. Pathogenesis of Coccidioide  In the lungs, arthrospores form spherules that are large, have a thick, doubly refractive wall, and are filled with endospores.  Upon rupture of the wall, endospores are released and differentiate to form new spherules.  The organism can spread within a person by direct extension or via the bloodstream.  Granulomatous lesions can occur in virtually any organ but are found primarily in bones and the central nervous system (meningitis)  Dissemination from the lungs to other organs occurs in people who have a defect in cell-mediated immunity.
  • 9. Pathogenesis of Coccidioide  Most people who are infected by C. immitis develop a cell-mediated (delayed hypersensitivity) immune response that restricts the growth of the organism.  One way to determine whether a person has produced adequate cell-mediated immunity to the organism is to do a skin test (see below).  In general, a person who has a positive skin test reaction has developed sufficient immunity to prevent disseminated disease from occurring.  If, at a later time, a person's cellular immunity is suppressed by drugs or disease, disseminated disease can occur.
  • 10.
  • 11. Clinical Findings of Coccidioide  Infection of the lungs is often asymptomatic and is evident only by a positive skin test and the presence of antibodies.  Some infected persons have an influenza like illness with fever and cough.  About. 50% have changes in the lungs (infiltrates, adenopathy, or effusions) as seen on chest x-ray.  10% develop erythema nodosum.  This syndrome is called "valley fever" or "desert rheumatism"; it tends to subside spontaneously.  Disseminated disease can occur in almost any organ; the meninges, bone, and skin are important sites.
  • 12. Clinical Findings of Coccidioide  The overall incidence of dissemination in persons infected with C. imrnitis is 1%, although the incidence in Filipinos and African Americans is 10 times higher.  Women in the third trimester of pregnancy also have a markedly increased incidence of dissemination.  Erythema nodosum (EN) manifests as red, tender nodules ("desert bumps") on extensor surfaces such as the shins.  It is a delayed (cell-mediated) hypersensitivity response to fungal antigens and thus is an indicator of a good prognosis.
  • 13. Clinical Findings of Coccidioide  There are no organisms in these lesions; they are not a sign of disseminated disease. EN is not specific for coccidioidomycosis; it occurs in other granulomatous diseases, e.g, histoplasmosis, tuberculosis, and leprosy.  In infected persons, skin tests with fungal extracts cause at least a 5mm induration 48 hours after injection (delayed hypersensitivity reaction).  Skin tests become positive within 2-4 weeks of infection and remain so for years but are often negative in patients with disseminated disease.
  • 14. Laboratory Diagnosis of Coccidioide  In tissue specimens, spherules are seen microscopically.  Cultures on Sabouraud's agar incubated at 25 °C show hyphae with arthrospores.  (Caution: Cultures are highly infectious; precautions against inhaling arthrospores must be taken.)
  • 15. Laboratory Diagnosis of Coccidioide  In serologic tests, IgM and IgG precipitins appear within 2-4 weeks of infection and then decline in subsequent months.  Complement-fixing antibodies occur at low titer initially, but the titer rises greatly if dissemination occurs
  • 16. Treatment & Prevention of Coccidioide  No treatment is needed in asymptomatic or mild primary infection.  Amphotericin B (Fungizone) or itraconazole is used for persisting lung lesions or disseminated disease.  Ketoconazole is also effective in lung disease.  Fluconazole is the drug of choice for meningitis.  Intrathecal amphotericin B may be required and may induce remission, but long-term results are often poor.  There are no means of prevention except avoiding travel to endemic areas.
  • 18. General characteristics  Etiologic Agent: P. brazieliensis  Central & South America & has high incidence in Brazil, Venezuela & Colombia  Natural reservoir: isolated in soil that have high humidity & average temperature of 23 C  Equal distribution among males & females, but clinical disease is about 9X higher in males  Transition of fungi from mold to yeast can be induced in vitro by raising the temperature of 25 C to 37 C  M-17-beta- estradiol inhibits transformation of the fungi  Testosterone,corticosterone & 17 alpha estradiol had NO inhibitory on the transformation
  • 19. Disease of Paracoccidioides  Paracoccidioides brasiliensis causes paracoccidioidomycosis, also known as South American blastomycosis.
  • 20. Paracoccidioidomycosis  Etiologic Agent: P. brazieliensis  Central & South America & has high incidence in Brazil, Venezuela & Colombia  Natural reservoir: isolated in soil that have high humidity & average temperature of 23 C  Equal distribution among males & females, but clinical disease is about 9X higher in males  Transition of fungi from mold to yeast can be induced in vitro by raising the temperature of 25 C to 37 C
  • 21. Properties of Paracoccidioides  P. brasiliensis is a dimorphic fungus that exists as a mold in soil and as a yeast in tissue.  The yeast is thick walled with multiple buds, in contrast to B. derrnatitidis, which has a single bud .
  • 22. Transmission & Epidemiology of Paracoccidioides  The spores are inhaled, and early lesions occur in the lungs.  Asymptomatic infection is common.  This fungus grows in the soil and is endemic in rural Latin America. Disease occurs only in that region.
  • 23. Pathogenesis & Clinical Findings of Paracoccidioides  The spores are inhaled, and early lesions occur in the lungs.  Asymptomatic infection is common.  Alternatively oral mucous membrane lesions, lymph node enlargement, and sometimes dissemination to many organs develop.  Ulceration, granulomatous infection of oral and nasal mucosa
  • 24.
  • 25. Laboratory Diagnosis of Paracoccidioides  In pus or tissues, yeast cells with multiple buds are seen microscopically.
  • 26.  A specimen cultured for 2-4 weeks may grow typical organisms.  Skin tests are rarely helpful.  Serologic testing shows that when significant antibody titers (by immunodiffusion or complement fixation) are found, active disease is present
  • 27. Treatment & Prevention of Paracoccidioides  The drug of choice is itraconazole taken orally for several months.  There are no means of prevention.