3. FUNGI
• EUKARYOTES WITH CELL WALL.
• EXIST AS INDIVIDUAL CELLS/ IN CHAINS (YEAST)/ IN MULTICELLULAR FILAMENTS
(MOLD)
• MANY MEDICALLY IMPORTANT FUNGI ARE DIMORPHIC
-EXIST AS YEAST FORM IN HUMAN BODY TEMPERATURE AND MOLD FORM
AT ROOM TEMPERATURE.
• FUNGAL INFECTIONS CAN BE DIAGNOSED BY HISTOLOGIC EXAMINATION,
ALTHOUGH DEFINITIVE IDENTIFICATION OF SOME SPECIES REQUIRES CULTURE.
4. FUNGAL INFECTIONS/ MYCOSES
• FOUR MAJOR TYPES
SUPERFICIAL/ CUTANEOUS MYCOSES : COMMON AND LIMITED TO VERY
SUPERFICIAL OR KERATINIZED LAYERS OF SKIN, HAIR, AND NAILS.
SUBCUTANEOUS MYCOSES : INVOLVE THE SKIN, SUBCUTANEOUS TISSUE,
LYMPHATICS AND RARELY DISSEMINATE SYSTEMATICALLY.
5. ENDEMIC MYCOSES : ARE CAUSED BY DIMORPHIC FUNGI THAT CAN PRODUCE
SERIOUS SYSTEMIC ILLNESS IN HEALTHY INDIVIDUALS.
OPPORTUNISTIC MYCOSES : CAN CAUSE LIFE THREATENING SYSTEMIC DISEASE IN
INDIVIDUALS WHO ARE IMMUNOSUPPRESSED OR WHO CARRY IMPLANTED
PROSTHETIC DEVICES OR VASCULAR CATHETERS
6. CANDIDIASIS
ETIOLOGY :
• ORIGINATES WHEN NORMAL COMMENSAL FLORA BREACH THE SKIN OR MUCOSAL
BARRIERS.
• USUALLY LIVES AS BENIGN COMMENSALS AND SELDOM PRODUCE DISEASE IN
HEALTHY PEOPLE.
• INDIVIDUALS WITH DIABETES AND BURN PATIENTS ARE PARTICULARLY SUSCEPTIBLE
TO SUPERFICIAL CANDIDIASIS.
• SEVERE DISSEMINATED CANDIDIASIS MOST COMMONLY OCCUR IN PATIENTS WHO
ARE NEUTROPENIC.
7. PATHOGENESIS :
• PRODUCTION OF ADHESINS
• PRODUCTION OF ENZYMES THAT CONTRIBUTE INVASIVENESS.
• C . ALBICANS CAN FORM BIOFILMS ON IMPLANTED MEDICAL DEVICES THAT REDUCED
THE ORGANISM’S SUSCEPTIBILITY TO IMMUNE RESPONSES AND ANTIFUNGAL DRUG
THERAPY.
• NEUTROPHILS, MACROPHAGES AND TH17 CELLS ARE IMPORTANT FOR PROTECTION
AGAINST CANDIDA INFECTIONS.
8. MORPHOLOGY :
• C . ALBICANS EXIST AS YEAST – PSEUDOHYPHAE
• ORGANISMS MAY SEEN IN ROUTINE
HEMATOXYLIN AND EOSIN STAINS, BUT A
VARIETY OF SPECIAL FUNGAL STAINS (GOMORI
METHANAMINE-SILVER, PERIODIC ACID-SCHIFF)
ARE COMMONLY USED TO VISUALIZE THEM.
10. CRYPTOCOCCOSIS
MAJOR SPECIES THAT CAUSE INFECTION ARE :
C . NEOFORMANS
• MAY CAUSE MENINGOENCEPHALITIS IN HEALTHY INDIVIDUALS
• FREQUENTLY OCCURS AS AN OPPORTUNISTIC INFECTION.
• HIGH DOSE OF CORTICOSTEROIDS –A MAJOR RISK
• PRESENT IN SOIL AND BIRD DROPPINGS AND INFECTS WHEN IT IS INHALED.
11. C . GATTI
• MORE LIKELY THAN C.NEOFORMANS TO CAUSE INFECTION IN IMMUNOLOGICALLY
HEALTHY INDIVIDUALS.
• PRESENT WITH LARGE LESIONS THAT PRODUCE MASS EFFECTS OR THAT MIMIC THE
RADIOLOGIC APPEARANCE OF NEOPLASM
• ASSOCIATED WITH CERTAIN TREE SPECIES , IS FOUND IN SOIL.
• ACQUIRED BY INHALATION
12. PATHOGENESIS :
• POLYSACCHARIDE CAPSULE : INHIBIT PHAGOCYTOSIS BY ALVEOLAR MACROPHAGES,
LEUKOCYTE MIGRATION AND RECRUITMENT OF INFLAMMATORY CELLS.
• MELANIN PRODUCTION : HAS ANTIOXIDANT PROPERTIES,DECREASE ANTIBODY
MEDIATED PHAGOCYTOSIS, COUNTERACTS EFFECTS OF ANTIFUNGAL AGENTS, BINDS
IRON,PROVIDE CELL WALL INTEGRITY.
• ENZYMES : AID TISSUE INVASION
13. MORPHOLOGY :
• THICK GELATINOUS CAPSULE CONTAINING A
POLYSACCHARIDE THAT STAINS INTENSE RED WITH
PERIODIC ACID-SCHIFF AND MUCICARMINE IN TISSUES.
CLINICAL FEATURES :
• MAJOR LESIONS ARE IN THE CNS , INVOLVING THE MENINGES, CORTICAL GREY
MATTER AND BASAL NUCLEI.
14. ASPERGILLOSIS
ETIOLOGY :
• CAUSE ALLERGIES IN HEALTHY PEOPLE AND SERIOUS SINUSITIS, PNEUMONIA AND
INVASIVE DISEASE IN IMMUNOCOMPROMISED INDIVIDUALS.
• NEUTROPENIA AND USE OF CORTICOSTEROIDS PREDISPOSE ASPERGILLUS
INFECTION.(MOST COMMON A.FUMIGATUS)
PATHOGENESIS :
• LUNG IS THE MAJOR PORTAL OD ENTRY.
• PRODUCE SEVERAL VIRULENT FACTORS INCLUDING ADHESINS, ANTIOXIDANTS,
ENZYMES AND TOXINS.
15. MORPHOLOGY :
• SEPTATE HYPHAE
• BRANCHING AT ACUTE ANGLES (40 DEGREES)
CLINICAL FEATURES :
• ASPERGILLOMA (FUNGUS BALL) SEEN IN; PARANASAL SINUS, LUNG AND SOMETIME
INTRACRANIAL INVOLVING BRAIN.
16. INVASIVE ASPERGILLOSIS :
• OPPORTUNISTIC INFECTION
• PRIMARY LESION USUALLY IN THE LUNG
• WIDESPREAD HEMATOGENOUS DISSEMINATION
WITH THE INVOLVEMENT OF HEART VALVES AND
BRAIN IS COMMON
17. MUCORMYCOSIS
ETIOLOGY :
• OPPORTUNISTIC INFECTION CAUSES BY MUCORMYCETES
• ALSO CALLED ZYGOMYCOSIS
• MAJOR PREDISPOSING FACTORS :NEUTROPENIA, CORTICOSTEROID USE, DM, IRON
OVERLOAD, BREAKDOWN OF CUTANEOUS BARRIER.
PATHOGENESIS :
• INHALED SPORES COMMONLY PRODUCE INFECTIONS IN THE SINUSES AND THE LUNGS
• ANGIOINVASIVE : HYPHAE GROWING IN AND ROUND BLOOD VESSELS CAUSE
ISCHEMIA
18. MORPHOLOGY :
• NON- SEPTATE HYPHAE WITH RIGHT ANGLED
BRANCHING.
CLINICAL FEATURES :
• SPREAD FROM NASAL SINUS TO ORBIT AND BRAIN
GIVES RISE TO RHINOCEREBRAL MUCORMYCOSIS.
• INVADE ARTERIES AND INDUCE THROMBOSIS.
• LUNG IVOLVEMENT- SECONDARY TO RHINOCEREBRAL DISEASE/PRIMARY IN PEOPLE
WITH SEVERE IMMUNODEFICIENCY.