1. SYSTEMIC MYCOSES Ma. Rosario L. Lacandula, MD, MPH
Department of Microbiology & Parasitology
College of Medicine
Our Lady of Fatima University

2. General Characteristics:
True Pathogenic fungi- causes infection in normal host
Highly virulent organism
MOT: 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

3. Small budding yeast 2-5 um in diameter and found inside macrophages
HISTOPLASMOSIS Darling’s disease, Reticuloendothelial cytomycosis, Cave disease & Spelunker’s disease
Thin branching hyphae that produce microconidia and tuberculate macroconidia
Small budding yeast 2-5 um in diameter and found inside macrophages

4. Histoplasmosis

5. Histoplasmosis

6. Histoplasmosis

7. Histoplasmosis
Etiologic agent: H. capsulatum var. capsulatum, H. capsulatum var duboisii
Natural reservoir: grows in soil with high nitrogen content especially areas contaminated by excreta of bats and birds( starlings & chicken)
High endemicity- Ohio & Mississippi Valley regions of the United States
Southern provinces of Ontario & Quebec in Canada
Scattered areas of Central & South America
Cases- Europe & Asia
Africa- H. capsulatum var. duboisii

8. HISTOPLASMOSIS CLINICAL SYNDROMES: Normal Host
Asymptomatic or mild flu like illness N exposure
Acute Pulmonary Histoplasmosis H exposure
Rare complications Pericarditis,mediastinal fibrosis
Opportunistic infection Disseminated histoplasmosis
Chronic Pulmonary histoplasmosis

9. Laboratory Diagnosis:
HISTOPLASMOSIS
Laboratory Diagnosis:
Serologic Test- complement fixation- standard test – (+) later in the disease 6 weeks or longer after symptoms, fourfold rise
Immunodiffusion- detects H & M antigens, more specific but less sensitive
Microscopic examination of infected tissue
Skin test- Histoplasmin test- ( +) after 2 weeks of exposure, no diagnostic value
Treatment:
Amphotericin B

10. Mold phase – typical pyriform microconidia 2-4 um in diameter
Blastomycosis Chicago Disease,Gilchrist’s disease, North American blastomycosis
Mold phase – typical pyriform microconidia 2-4 um in diameter
Tissue phase – 8-15 um in diameter; buds are produced singly & attached to parent cell by a broad base

11. Blastomycosis

12. Blastomycosis Etiologic Agent: Blastomyces dermatitidis
North America Continent & parts of Africa
Endemicity overlaps with histoplasmosis
Other endemic areas: Minnesota, Southern Manitoba, & Southwest Ontario
Epidemics- Wisconsin, Minnesota, Illinois, Eastern State of Virginia & North Carolina
Natural reservoir : not known, rarely cultured from soil of endemic areas
Infection can also occur among dogs and horses

13. Blastomycosis Clinical Syndromes:
Primary infection in the lungs- Inapparent
Ulcerative lesions of the skin & lytic bone lesion
Laboratory Diagnosis:
Serology
Microscopic findings
Treatment: Amphoterecin B

14. Blastomycosis

15. Blastomycosis

16. No typical pattern of sporulation
Paracoccidiodomycosis South American blastomycosis, Lutz Splendore-Almeida’s disease
Yeast with several budding cells attached to a parent cell; “pilot’s wheel”; 2-3 um in diameter
No typical pattern of sporulation

17. Paracoccidiodomycosis
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

18. Paracoccidiodomycosis
Clinical Syndromes:
Primary lung infection- asymptomatic
Ulcerative lesions of the buccal, nasal & occasionally GIT mucosa
Laboratory Diagnosis:
Serology
Microscopic findings
Treatment : Amphotericin B

19. Mycelia fragment to produce cylindrical arthroconidia
Coccidiodomycosis Posada’s Disease, San Joaquin Valley fever & Desert rheumatism
Spherule; multinucleated structure that undergoes internal cleavage to produce endospore
Mycelia fragment to produce cylindrical arthroconidia

20. Coccidioidomycosis

21. Coccidioidomycosis

22. Coccidioidomycosis Etiologic Agent: Coccidiodes immitis
“ New World”- North, Central & South American Continents
Highest endemicity- San Joaquin Valley in California, Maricopa & Pima Countries in Arizona, Texas
Endemic- Northern states of Mexico, parts of Venezuela, Paraquay & Argentina
Isolated in soil samples during summer
Inhibited by P. jantheniluem & B.subtilis during rainy season

23. Coccidioidomycosis Clinical Syndromes 60 % asymptomatic
40 % develop symptomatic pulmonary infection.Most common symptoms of primary disease are cough, fever, and chest pain. Night sweats and joint pains are not unusual
Primary infections usually self limited
Dissemination mainly in the meninges and/or skin
HLA A9, Type B blood, do not develop toxic erythemas
Blacks/ Asian are susceptible

24. Coccidioidomycosis Laboratory Diagnosis
Complement fixation and tube precepitin
Latex agglutination and agar immunodiffusion- two lines of precipitation appear to be significant
2 sources of antigen, both cell-free culture filtrates
Coccidiodin
Spherulin
Treatment: Amphotericin B, ketoconazole

25. Coccidioidomycosis

26. OPPORTUNISTIC MYCOSES
Ma. Rosario L. Lacandula, MD, MPH
Department of Microbiology & Parasitology
College of Medicine
Our Lady of Fatima University

27. Opportunistic mycoses
General Characteristic:
Low virulent fungi
Monomorphic
Causes infection in immunocompromised host
Healthy individual develop high degree of innate resistance to fungal colonization

28. Crytococcosis Busse-Buschke’s disease, torulosis, and European Blastomycosis
Etiologic agent: Crytococcus neoformans
Monomorphic
Encapsulated- inhibits phagocytosis
Phenoloxidase- converts phenolic compounds to melanin
Lungs- Primary site of infection
High predilection for systemic spread to the brain- leading cause of fungal meningitis

29. Cryptococcosis

30. Cryptococcosis
Survive well in dessicated, alkaline, nitrogen rich, and hypertonic environment- recovered from excreta and debris of pigeons
Organism that not cause infection of pigeons
Worldwide distribution
Clinical Syndromes:
Primary pulmonary infection-asymptomatic detected as an incidental finding on routine chest X ray- solitary nodule
Symptomatic pneumonia-diffuse pulmonary infiltrates
Skin cryptococcosis, Cryptococcal meningitis, osteolytic bone lesions

31. Cryptococcosis

32. Cryptococcosis

33. Cryptococcosis Laboratory Diagnosis
Detection based on the presence of antigen
Latex agglutination test for detection of the capsule
Rapid test- use of India Ink preparation of CSF- seen as clear halo
Treatment: Amphotericin B

34. Candidiasis Etiologic agent: Specie of Candida Endogenous normal flora
Major disease problem of immunocompromised host
Clinical disease ranges from superficial skin infection to systemic life threatening disease
Rarely isolated from the surface of human skin except from certain intertrigenous areas
Organs involved- lungs, spleen,kidney,liver,heart and brain
Pseudohyphae & septate hyphae

35. Candidiasis Clinical Syndromes
CMC Chronic mucocutaneous candidiasis- heterogenous group of clinical syndromes characterized by chronic, treatment resistant superficial Candida infections of the skin, nails and oropharynx
No dissemination seen in visceral organs
Defect in CMI
Laboratory Diagnosis
Rapid diagnosis- germ tube test
Budding yeast cells, pseudohyphae and septate hyphae
Treatment: Amphotericin B , 5-fluorocytosine, ketoconazole and fluconazole

36. Development of germ tubes by Candida albicans yeast cells after incubation in serum x 2 hours @ 37oC

37. Candidiasis (Moniliasis)

38. Candidiasis (Moniliasis)

39. Aspergillosis Etiologic agent: A. fumigatus; A. niger; A. flavus
Common in the environment
Exogenous source
Normal individual not susceptible to systemic aspergillosis

40. Aspergillosis Clinical syndromes
Mycotoxicosis- ingestion of contaminated peanuts
Allergic aspergillosis- allergic bronchopulmonary disease
Secondary Colonization- fungal colonization of pre existing cavity ( e.g. pulmonary abscess) w/o invasion.
Fungus ball- spherical mass of intertwined septate branching hyphal elements
Systemic disease- Invasive disease involving multiple organs
Laboratory Diagnosis: septate hyphae that branch at regular intervals seen in clinical specimens

41. Mucormycosis
Susceptibility to the fungi- metabolic acidosis, DM, leukopenis and hyperglycemia
Grows rapidly on all laboratory media
Form coenocytic hyphae
Ubiquitous in the environment and encountered as contaminants
Clinical Syndromes
Rhinocerebral zygomycosis-most common-originate in the paranasal sinuses can involve the ocular orbit and palate with extension to the brain
Lungs, GIT, subcutaneous tissue

42. Mucormycosis
In severely burned patients- colonize the damaged tissues and tend to become invasive.
In disseminated disease- predilection for invading major bood vessel. Clot that result can cause ischemia and necrosis of adjacent tissues.
Laboratory Diagnosis:
Microscopic findings

43. Mucormycosis

44. Mucormycosis