Systemic Endemic Mycoses

1. Endemic systemic Mycoses
Dr Sumitha J
Associate Professor
JBAS College for Women
Chennai-18

2. Endemic Systemic Mycoses
Histoplasma
Blastomyces
Coccidiodes
Paracoccidiodes

3. Morphology
Dimorphic
Exists in mould forms in the
Environment and in yeast
form at 37degree Celsius

4. Tissue Morphology

5. Geographical distribution
Fungi Geographical area
Histoplasma Tropical
American continent and some
tropical regions of the world
Blastomyces Temperature
North America and Central
and East Africa
Coccidiodes Semi-desert Areas Central and South America
Paracoccidiodes Tropical
American continent and some
tropical regions of the world

6. Pathogenesis
The inoculum enters the host through the respiratory
tract
lymphatic and hematogenous dissemination
Most cases are observed in returning
travellers from endemic areas, aid
workers, archaeologists, speleologist
and immigrants
Cutaneous manifestations are secondary

7. Histoplasma capsulatum
Histoplasmosis is an intracellular mycotic infection of the
reticuloendothelial system caused by the inhalation of conidia from
the fungus Histoplasma capsulatum.
Three varieties of Histoplasma capsulatum are recognised, depending
on the clinical disease: var.capsulatum is the common cause of
histoplasmosis; var. duboisii is the African type and
var. farciminosum causes lymphangitis in horses.

8. Clinical manifestations
Approximately 95% of cases of histoplasmosis are inapparent,
subclinical or benign.
Five percent of the cases have chronic progressive lung disease,
chronic cutaneous or systemic disease or an acute fulminating
fatal systemic disease.
All stages of this disease may mimic tuberculosis

9. Blastomyces dermatitis
Blastomycosis is a chronic granulomatous and suppurative disease
having a primary pulmonary stage that is frequently followed by
dissemination to other body sites, chiefly the skin and bone.
Mostly soil borne

10. Clinical manifestations-Pulmonary
blastomycosis
Pulmonary lesions are asymptomatic
Some develop symptoms after an incubation period of 3-15 weeks.
Blastomycosis is indolent in onset and patients present with chronic symptoms
such as cough, fever, malaise and weight loss
The lesions become more extensive, with continued suppuration and eventual
necrosis and cavitation
Occasional patients present with an acute onset of infection, with development
of high fever, chills, productive cough, myalgia, arthralgia and pleuritic chest
pain. Often these patient appear to recover after 2-12 weeks of symptoms

11. Clinical manifestations-
Cutaneous blastomycosis
Haematogenous spread gives rise to cutaneous lesions in over
70% of patients.
These tend to be painless and present either as raised verrucous
lesions with irregular borders, or as ulcers.
The face, upper limbs, neck and scalp are the most frequent sites
involved.

12. Clinical manifestations-
Osteoarticular blastomycosis
Occurs in about 30% of patients with the spine, pelvis, cranial
bones, ribs and long bones most commonly involved.
Patients often remain asymptomatic until the infection spreads
into contiguous joints, or into adjacent soft tissue causing
subcutaneous abscesses.
Radiological findings are often non-specific and arthritis occurs
in up to 10% of patients.

13. Clinical manifestations-
Osteoarticular blastomycosis
genitourinary blastomycosis involving the prostrate, epididymis
or testis
haematogenous spread to the brain causing meningitis, and
spinal or brain abscess.
Radiological findings are often non-specific and arthritis occurs
in up to 10% of patients.

14. Paracoccidioides brasiliensis
Paracoccidioidomycosis is a chronic granulomatous disease that
characteristically produces a primary pulmonary infection, often
inapparent, and then disseminates to form ulcerative granulomata of the
buccal, nasal and occasionally the gastrointestinal mucosa.
The disease in its inception and development is similar to blastomycosis
and coccidioidomycosis.
The only etiological agent, Paracoccidioides brasiliensis is geographically
restricted to areas of South and Central America.

15. Clinical manifestations-
Mucocutaneous paracoccidioidomycosis
The mouth and nose are the most usual mucosal sites of infection.
Painful ulcerated lesions develop on the gums, tongue, lips or
palate and can progress over weeks or months.
Perforation of the palate or nasal septum may occur.
Cutaneous lesions often appear on the face around the mouth and
nose, although patient with severe infection can have widespread
lesions.

16. Clinical manifestations-Pulmonary
paracoccidioidomycosis
Most cases have an indolent onset and patients present with
chronic symptoms such as cough, fever, night sweats, malaise and
weight loss. Chest x-rays are characteristic but not diagnostic.
The infection must be distinguished from histoplasmosis and
tuberculosis

17. Clinical manifestations-Lymphonodular
paracoccidioidomycosis
Lymphadenitis is common in younger patients. Cervical and
submandibular chains are the most obvious manifestation and
lymph nodes may progress to form abscesses with draining sinuses.

18. Clinical manifestations-Disseminated
paracoccidioidomycosis
Haematogenous spread of P. brasiliensis can result in widespread
disseminated disease; including lesions of the small or large
intestine, hepatic lesions, adrenal gland destruction, osteomyelitis,
arthritis, endophthalmitis and meningoencephalitis or focal cerebral
lesions.

19. Coccidioides immitis
Coccidioidomycosis is initially, a respiratory infection, resulting from the
inhalation of conidia, that typically resolves rapidly leaving the patient with a
strong specific immunity to re-infection.
However, in some individuals the disease may progress to a chronic
pulmonary condition or to a systemic disease involving the meninges, bones,
joints and subcutaneous and cutaneous tissues.
Coccidioides immitis is a soil inhabiting fungus endemic in south-western
U.S.A., northern Mexico and various centres in South America. Several cases
have now been diagnosed in Australia, all in patients with a history of travel
to endemic areas.

20. Clinical manifestations
However, 5-10% of patients that do develop symptoms are left
with pulmonary residual nodule or cavity that is usually detected
several months or years later.
Another 5% of patients may develop metapulmonary
dissemination to the meninges, bones, joints and subcutaneous
and cutaneous tissues, within the first few weeks to months after
the onset of primary infection .

21. Clinical manifestations
60% of individuals suffer a benign and transient chest infection
that does not require medical attention.
Of the 40% who develop symptoms, most will have an acute
febrile "flu-like" illness starting 7-28 days (average 10-16 days)
after exposure and most patients will recover completely.
The main symptoms are fever, pleuritic chest pain, cough,
malaise, headache, myalgia, night sweats and loss of appetite.
Many patients also develop a mild, diffuse erythematous or
maculopapular rash on the trunk and limbs.

22. LABORATORY DIAGNOSIS-Histoplasmosis
Clinical Material :Skin scrapings, sputum and bronchial washings, cerebrospinal
fluid, pleural fluid and blood, bone marrow, urine and tissue biopsies from various
visceral organs.
Direct microscopy:
(a) Skin scrapings should be examined using 10% KOH and Parker ink or
calcofluor white mounts
(b) Exudates and body fluids should be centrifuged and the sediment examined
using either 10% KOH and Parker ink or calcofluor white mounts,
(c) Tissue sections should be stained using PAS digest, Grocott's methenamine
silver (GMS) or Gram stain.

23. LABORATORY DIAGNOSIS-Histoplasmosis
Histopathology is especially useful and is one of the most important ways of
alerting the laboratory that they may be dealing with a potential pathogen.
Culture: Clinical specimens should be inoculated onto primary isolation
media, like Sabouraud's dextrose agar and Brain heart infusion agar
supplemented with 5% sheep blood.
Serology: Immunodiffusion and/or complement fixation tests for the
detection of antibody have proven to be useful in the diagnosis of
Histoplasmosis, especially in immunocompetent patients. However,
detection of antibodies in immunosuppressed patients is often difficult,
with between 20-50% of patients testing negative.

24. Histoplasmosis
T i s s u e m o r p h o l o g y o f H .
capsulatum var. capsulatum (left)
showing numerous small narrow base
budding yeast cells (1-5um diam)
i n s i d e m a c r o p h a g e s a n d H .
capsulatum var. duboisii (right)
showing larger sized budding yeast
cells (5-12 um in diam).

25. Histoplasmosis
C u l t u r e o f H i s t o p l a s m a
capsulatum showing growth as a
mould at 25C and as a yeast at
37C.

26. LABORATORY DIAGNOSIS-Blastomycosis
Clinical material: Skin scrapings, sputum and bronchial washings, cerebrospinal
fluid, pleural fluid and blood, bone marrow, urine and tissue biopsies from various
visceral organs.
Direct microscopy:
(a) Skin scrapings should be examined using 10% KOH and Parker ink or
calcofluor white mounts
(b) Exudates and body fluids should be centrifuged and the sediment examined
using either 10% KOH and Parker ink or calcofluor white mounts,
(c) Tissue sections should be stained using PAS digest, Grocott's methenamine
silver (GMS) or Gram stain.

27. LABORATORY DIAGNOSIS-Blastomycosis
Histopathology is especially useful and is one of the most important ways of
alerting the laboratory that they may be dealing with a potential pathogen.
Culture:Clinical specimens should be inoculated onto primary isolation
media, like Sabouraud's dextrose agar and Brain heart infusion agar
supplemented with 5% sheep blood.
Serology: Serological tests are of limited value in the diagnosis of
Blastomycosis.

28. Blastomycosis

29. LABORATORY DIAGNOSIS-
Coccidioidomycosis
Clinical material: Skin scrapings, sputum and bronchial washings, cerebrospinal
fluid, pleural fluid and blood, bone marrow, urine and tissue biopsies from various
visceral organs.
Direct microscopy:
(a) Skin scrapings should be examined using 10% KOH and Parker ink or
calcofluor white mounts
(b) Exudates and body fluids should be centrifuged and the sediment examined
using either 10% KOH and Parker ink or calcofluor white mounts,
(c) Tissue sections should be stained using PAS digest, Grocott's methenamine
silver (GMS) or Gram stain.

30. LABORATORY DIAGNOSIS-
Coccidioidomycosis
Histopathology is especially useful and is one of the most important ways of
alerting the laboratory that they may be dealing with a potential pathogen.
Culture:Clinical specimens should be inoculated onto primary isolation
media, like Sabouraud's dextrose agar and Brain heart infusion agar
supplemented with 5% sheep blood.
Serology: Immunodiffusion and/or complement fixation tests for the
detection of antibody have proven to be useful in the diagnosis of
Coccidioidomycosis especially in immunocompetent patients. However,
detection of antibodies in immunosuppressed patients is often difficult,
with between 20-50% of patients testing negative.

31. Coccidioidomycosis

32. LABORATORY DIAGNOSIS-
ParaCoccidioidomycosis
Clinical material: Skin scrapings, sputum and bronchial washings, cerebrospinal
fluid, pleural fluid and blood, bone marrow, urine and tissue biopsies from various
visceral organs.
Direct microscopy:
(a) Skin scrapings should be examined using 10% KOH and Parker ink or
calcofluor white mounts
(b) Exudates and body fluids should be centrifuged and the sediment examined
using either 10% KOH and Parker ink or calcofluor white mounts,
(c) Tissue sections should be stained using PAS digest, Grocott's methenamine
silver (GMS) or Gram stain.

33. LABORATORY DIAGNOSIS-
ParaCoccidioidomycosis
Histopathology is especially useful and is one of the most important ways of
alerting the laboratory that they may be dealing with a potential pathogen.
Culture:Clinical specimens should be inoculated onto primary isolation
media, like Sabouraud's dextrose agar and Brain heart infusion agar
supplemented with 5% sheep blood.
Serology: Immunodiffusion and/or complement fixation tests for the
detection of antibody have proven to be useful in the diagnosis of
Coccidioidomycosis especially in immunocompetent patients. However,
detection of antibodies in immunosuppressed patients is often difficult,
with between 20-50% of patients testing negative.

34. ParaCoccidioidomycosis
Multiple, narrow base,
budding yeast cells (steering
wheels) of P. brasiliensis.
GMS stained lung section
(left) and phase contrast of
cells from a culture (right).