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A.ANUSWEDHA
Associate Professor,
Department of Microbiology,
Justice Basheer Ahmed Sayeed College for
Women, Chennai
 Commonest infection – mucuous membrane, skin,
nail & internal organs
 In immunocompromised- disseminated- systemic
 C. AGENTS: C. albicans, C. krusei, C.guilliermondi,
C.parapsilosis, C. stellatoidea, C. tropicalis, C.
pseudotropicalis, C. lusitaniae, C. viswanthii
 Source: normal commensals –skin, GIT, Vagina
 PATHOGENESIS: entry- exogenous/ endogenous
 colonisation of local tissue
 invasion- facilitating by specific/non-specific
adherence factors
1. TOXINS-glycoprotein extracts of
candida cell wall- pyrogenic similar to
bacterial endotoxins.
2. ENZYMES-
proteases,lipases,esterases,phospholipa
ses,phosphatases-invasion of hyphae in
tissues
3. ADHESIN-adhesins on the surface of
candida that have receptors for
attachment to epithelial cells
4. COMPLEMENT RECEPTORs-mediates
engulfment of microorganisms that
have complement
5. PHENOTYPING SWITCHING-
6. PROTEINASES-
 A) MUCOCUTANEOUS INVOLVEMENT:
 1. oral candidiasis- oral thrush- diffused or
confined to gums, palate, tongue or buccal
mucosa- congestive reddening-dry, shiny,
varnish-like appearance
 2. oropharygneal candidiasis-
 Angular cheilitis- sore, erythematous fissured
lesions at the corners of the mouth.
 3. Alimentary candidiasis- esophagitis,
gastritis, peritonitis
 4. Vulvovaginitis, balanitis, balanoposthitis
 5. CMCC-
 6. ocular candidiasis-keratoconjuctivitis,
corneal ulcerations, conjuctival edema
INFECTION MODE OF
INFECTION
SYMPTOMS
1. INTERTRIGINOUS SKIN Inflammation of skin folds;
lymphangitis, lymphadenitis
2. PARONYCHIA &
ONYCHOMYCOSIS
Nails Nail folds, hand and
feet,nails-white, opaque,
thickened, brittle
3. DIAPER
DISEASE(infants)
Skin Maculopapules & vesicles,
coalescing to patches with
satellite pustules- gluteal
folds, perineum & inguinal
folds
4. CANDIDAL
GRANULOMA(Children)
skin Papules on face, scalp,
trunk, legs & pharynx
1. Urinary tract
candidiasis,
Candiduria
Vulva/vagina Infections of bladder
& kidneys
2. Pulmonary
candidiasis
Hematogenous spread Lung lesions
3. endocarditis “ Subacute endocarditis
in persons with
abnormal or prosthetic
valve
4. Meningitis Low birth wt infants,
neonates with
candidemia,
intracerebral
prosthetic devices,
neurosurgery
Hydrocephalus
5. Candidemia immunocompromised -
6. dissemination “ Systemic involvement
Arthritis Hematogenous spread/
joint surgery
Destruction of cartilage
osteomyelitis Hematogenous spread Osteolytic lesions with pus
endophthalmitis Disseminated candidiasis One or more focal, white
retinal lesions associated
with clouding vision
Candidemia, septicemia bloodstream
Nosocomial candidiasis invasive
1. Candidids
REASON: allergic manifestation of
metabolites- resolves after
treatment of primary
infection/desensitation
Vesicular lesions on the interdigital
spaces of fingers, side of wrists or
throughout the body
2Eczema(allergic), asthma(colonisation
of candida), gastritis(overgrowth of
candida)
Erythema-vesicles-rupture-ooze pus-
heals with scar
Irritable bowl syndrome
1. Asymptomatic oral carriage IN HIV PATIENTS
2. Oropharyngeal thrush
3. laryngitis, oesophagitis
4. vulvovaginitis, balanitis
5. Hematogenous dissemination
6. leukoplakia- white thickened patch occuring on the mucuous membrane of lips,
mouth or genitalia
7. perleche-(angular cheilitis)- inflammation of lips at the angles of the mouth with
fissures & crust formation
DIFFERENTIAL DIAGNOSIS – 1. leucoplakia 2. trichomonas
vaginitis 3. TB, 4. chronic bacterial infection
DIRECT MICROSCOPY-KOH , gram’s staining- budding yeast cells
with pseudohyphae
CULTURE- SDA, BA- colony morph- LPCB mount, CHROMagar
Candida-light green to bluish green
GERM TUBE TEST:Incubate 37C for 2-4 hrs in serum, wet
mount- germ tubes
CHLAMYDOSPORE FORMATION: CMA/rice starch agar- highly
refractile thick walled terminal chlamydospores
BIOCHEMICAL TEST: CHO assimilation/ fermentation
DECTECTION OF METABOLITES: 1. D.mannose 2. D-
arabinitol- GLC
ANIMAL PATHOGENICITY: rabbit/mice
SEROLOGY
A) DECTECTION OF ANTIBODIES-slide
agglutination, ID, immunoprecipitation,
phytohaemagglutination, ELISA, RIA,
CIE
B) NON SPECIFIC CANDIDA AG- latex
agglutination, immunoblotting
C) CELL WALL COMPONENTS- cellwall
mannoprotein, beta(1,3 D glucan)
E) CANDIDA ENOLASE AG testing
SEROTYPING FOR EPIDEMIOLOGICAL
STUDIES- MR (morpho & resistotyping), PMS,
RFLP,Southern blotting
TREATMENT:
1.oral/ mucocutaneous- oral nystatin
2.Azole creams- clotrimazole
3.Systemic candidiasis- AmpB+ flucytosine
 Opportunistic systemic fungal infection
 SOURCE: excreta of pigeons; avian sps
 CLASSIFICATION: 5 serotypes based on the capsular
ag- A, B, C, D & AD
 3 varities based on ecological & epidemiological
differences
 1. Cr. neoformans var neoformans(world-wide)-
serotype D
 2. Cr. neoformans var gattii(tropical & subtropical)-
serotypes B & C
 3. Cr. neoformans var grubii( serotype A)
 4. Non-neoformans cryptococcus sp- non-
pathogenic/rarely pathogenic- Crypt.albidus,
 CLINICAL FEATURES: common in males than
females; gets disseminated in
immunocompromised.
 Incubation period: 2-4 weeks
!. PULMONARY CRYPTOCOCCOSIS Resp route: asymptomatic colonisation;
self-limited pneumonitis with dry cough,
dull chest pain, little or no fever
2. CNS CRYPTOCOCCOSIS A diffuse meningoencephalitis,
intracranial space occupying
lesions(ICSOL), well circumsribed
granuloma of brain or spinal
cord(cryptococcoma)-
Nausea, dizziness, irritability, vomiting,
impaired memory, fits, blurred vision,
nuchal rigidity- onset of coma- resp
arrest- death
3.CUTANEOUS CRYPTOCOCCOSIS-
hematogenous spread to skin
Painless papule, enlarges; centre
becomes shiny & flat, centre
depressed and ulcerates, draining a
thin fluid that contains cryptococci
4. OSSEOUS CRYPTOCOCCOSIS
Hematogenous spread-
Osteolytic lesions; no periosteal
proliferation, pain & swelling of the
local area for a long time
5. VISCERAL CRYPTOCOCCOSIS Lungs, meninges & any organ-
granulomatous lesion
6. CRYPTOCOCCAEMIA Disseminated in immunocompromised
PATHOGENESIS
Only capsulated yeast
infects man
Inhalation of spores or
dessicated yeast
Inflammatory resp to
inhaled yeast produces
lung lymph node complex
that restrains spread of
yeast
In lungs, cryptococcis
proliferated in the alveolar
space
In immunocompetent- gets
localised to lungs
In immunocompromised-
gets disseminated-CNS
VIRULENCE FACTORS
Capsule, melanin, high temp
growth,urease prod. of
extracellular phospholipase
DIFFERENTIA
L DIAGNOSIS
1. Malignant
neoplasia
2. TB
3. Bacterial
4. Fungal
Suspected
immunoco
mpromised
state of
patient
RADIOLOGY
1. CT
2. MRI
DIRECT MICROSCOPY
1. CSF- negative staining
2. Histopathogy- H & E, PAS,
GMS, Mayer’s mucicarmine
staining
Budding yeast cells in tissue
sections
CULTURE
1. SDA
mucoid,
buff-
coloured
colonies
2. Capsule
prod is
enhanced
–growth
on CA in
CO2
3. BSA/NSA-
brown
coloured
colonies
4. BA,
CHHA
BIOCHEMICAL
TEST
1. phenol-oxidase
2. Growth at 37C
3. Urease
4. Inositol& nitrate
assimilation
5. Morp of
blastospores
MICE
PATHOGENICITY
Infected material
Inoculated into
swiss albino mice-
IC, IV,IP
10-14 days
Autopsy exam of
body sites &
visceral organs for
cyptococci
SEROLOGY
1. Demo of
capsular ag in
serum/CSF-
Crypto LA test
Eiken LA test
2. Demo of AB
1. Agglutination
2. IFAbT
3. CFT
TYPING: serotyping,
RFLP, PMS
Causes, Symptoms and Diagnosis of Candidiasis Infection

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Causes, Symptoms and Diagnosis of Candidiasis Infection

  • 1. A.ANUSWEDHA Associate Professor, Department of Microbiology, Justice Basheer Ahmed Sayeed College for Women, Chennai
  • 2.  Commonest infection – mucuous membrane, skin, nail & internal organs  In immunocompromised- disseminated- systemic  C. AGENTS: C. albicans, C. krusei, C.guilliermondi, C.parapsilosis, C. stellatoidea, C. tropicalis, C. pseudotropicalis, C. lusitaniae, C. viswanthii  Source: normal commensals –skin, GIT, Vagina  PATHOGENESIS: entry- exogenous/ endogenous  colonisation of local tissue  invasion- facilitating by specific/non-specific adherence factors
  • 3. 1. TOXINS-glycoprotein extracts of candida cell wall- pyrogenic similar to bacterial endotoxins. 2. ENZYMES- proteases,lipases,esterases,phospholipa ses,phosphatases-invasion of hyphae in tissues 3. ADHESIN-adhesins on the surface of candida that have receptors for attachment to epithelial cells 4. COMPLEMENT RECEPTORs-mediates engulfment of microorganisms that have complement 5. PHENOTYPING SWITCHING- 6. PROTEINASES-
  • 4.  A) MUCOCUTANEOUS INVOLVEMENT:  1. oral candidiasis- oral thrush- diffused or confined to gums, palate, tongue or buccal mucosa- congestive reddening-dry, shiny, varnish-like appearance  2. oropharygneal candidiasis-  Angular cheilitis- sore, erythematous fissured lesions at the corners of the mouth.  3. Alimentary candidiasis- esophagitis, gastritis, peritonitis  4. Vulvovaginitis, balanitis, balanoposthitis  5. CMCC-  6. ocular candidiasis-keratoconjuctivitis, corneal ulcerations, conjuctival edema
  • 5.
  • 6. INFECTION MODE OF INFECTION SYMPTOMS 1. INTERTRIGINOUS SKIN Inflammation of skin folds; lymphangitis, lymphadenitis 2. PARONYCHIA & ONYCHOMYCOSIS Nails Nail folds, hand and feet,nails-white, opaque, thickened, brittle 3. DIAPER DISEASE(infants) Skin Maculopapules & vesicles, coalescing to patches with satellite pustules- gluteal folds, perineum & inguinal folds 4. CANDIDAL GRANULOMA(Children) skin Papules on face, scalp, trunk, legs & pharynx
  • 7.
  • 8. 1. Urinary tract candidiasis, Candiduria Vulva/vagina Infections of bladder & kidneys 2. Pulmonary candidiasis Hematogenous spread Lung lesions 3. endocarditis “ Subacute endocarditis in persons with abnormal or prosthetic valve 4. Meningitis Low birth wt infants, neonates with candidemia, intracerebral prosthetic devices, neurosurgery Hydrocephalus 5. Candidemia immunocompromised - 6. dissemination “ Systemic involvement
  • 9. Arthritis Hematogenous spread/ joint surgery Destruction of cartilage osteomyelitis Hematogenous spread Osteolytic lesions with pus endophthalmitis Disseminated candidiasis One or more focal, white retinal lesions associated with clouding vision Candidemia, septicemia bloodstream Nosocomial candidiasis invasive
  • 10. 1. Candidids REASON: allergic manifestation of metabolites- resolves after treatment of primary infection/desensitation Vesicular lesions on the interdigital spaces of fingers, side of wrists or throughout the body 2Eczema(allergic), asthma(colonisation of candida), gastritis(overgrowth of candida) Erythema-vesicles-rupture-ooze pus- heals with scar Irritable bowl syndrome 1. Asymptomatic oral carriage IN HIV PATIENTS 2. Oropharyngeal thrush 3. laryngitis, oesophagitis 4. vulvovaginitis, balanitis 5. Hematogenous dissemination 6. leukoplakia- white thickened patch occuring on the mucuous membrane of lips, mouth or genitalia 7. perleche-(angular cheilitis)- inflammation of lips at the angles of the mouth with fissures & crust formation
  • 11. DIFFERENTIAL DIAGNOSIS – 1. leucoplakia 2. trichomonas vaginitis 3. TB, 4. chronic bacterial infection DIRECT MICROSCOPY-KOH , gram’s staining- budding yeast cells with pseudohyphae CULTURE- SDA, BA- colony morph- LPCB mount, CHROMagar Candida-light green to bluish green GERM TUBE TEST:Incubate 37C for 2-4 hrs in serum, wet mount- germ tubes CHLAMYDOSPORE FORMATION: CMA/rice starch agar- highly refractile thick walled terminal chlamydospores BIOCHEMICAL TEST: CHO assimilation/ fermentation DECTECTION OF METABOLITES: 1. D.mannose 2. D- arabinitol- GLC ANIMAL PATHOGENICITY: rabbit/mice
  • 12.
  • 13. SEROLOGY A) DECTECTION OF ANTIBODIES-slide agglutination, ID, immunoprecipitation, phytohaemagglutination, ELISA, RIA, CIE B) NON SPECIFIC CANDIDA AG- latex agglutination, immunoblotting C) CELL WALL COMPONENTS- cellwall mannoprotein, beta(1,3 D glucan) E) CANDIDA ENOLASE AG testing SEROTYPING FOR EPIDEMIOLOGICAL STUDIES- MR (morpho & resistotyping), PMS, RFLP,Southern blotting TREATMENT: 1.oral/ mucocutaneous- oral nystatin 2.Azole creams- clotrimazole 3.Systemic candidiasis- AmpB+ flucytosine
  • 14.  Opportunistic systemic fungal infection  SOURCE: excreta of pigeons; avian sps  CLASSIFICATION: 5 serotypes based on the capsular ag- A, B, C, D & AD  3 varities based on ecological & epidemiological differences  1. Cr. neoformans var neoformans(world-wide)- serotype D  2. Cr. neoformans var gattii(tropical & subtropical)- serotypes B & C  3. Cr. neoformans var grubii( serotype A)  4. Non-neoformans cryptococcus sp- non- pathogenic/rarely pathogenic- Crypt.albidus,
  • 15.  CLINICAL FEATURES: common in males than females; gets disseminated in immunocompromised.  Incubation period: 2-4 weeks !. PULMONARY CRYPTOCOCCOSIS Resp route: asymptomatic colonisation; self-limited pneumonitis with dry cough, dull chest pain, little or no fever 2. CNS CRYPTOCOCCOSIS A diffuse meningoencephalitis, intracranial space occupying lesions(ICSOL), well circumsribed granuloma of brain or spinal cord(cryptococcoma)- Nausea, dizziness, irritability, vomiting, impaired memory, fits, blurred vision, nuchal rigidity- onset of coma- resp arrest- death
  • 16. 3.CUTANEOUS CRYPTOCOCCOSIS- hematogenous spread to skin Painless papule, enlarges; centre becomes shiny & flat, centre depressed and ulcerates, draining a thin fluid that contains cryptococci 4. OSSEOUS CRYPTOCOCCOSIS Hematogenous spread- Osteolytic lesions; no periosteal proliferation, pain & swelling of the local area for a long time 5. VISCERAL CRYPTOCOCCOSIS Lungs, meninges & any organ- granulomatous lesion 6. CRYPTOCOCCAEMIA Disseminated in immunocompromised
  • 17. PATHOGENESIS Only capsulated yeast infects man Inhalation of spores or dessicated yeast Inflammatory resp to inhaled yeast produces lung lymph node complex that restrains spread of yeast In lungs, cryptococcis proliferated in the alveolar space In immunocompetent- gets localised to lungs In immunocompromised- gets disseminated-CNS VIRULENCE FACTORS Capsule, melanin, high temp growth,urease prod. of extracellular phospholipase
  • 18.
  • 19. DIFFERENTIA L DIAGNOSIS 1. Malignant neoplasia 2. TB 3. Bacterial 4. Fungal Suspected immunoco mpromised state of patient RADIOLOGY 1. CT 2. MRI DIRECT MICROSCOPY 1. CSF- negative staining 2. Histopathogy- H & E, PAS, GMS, Mayer’s mucicarmine staining Budding yeast cells in tissue sections
  • 20.
  • 21. CULTURE 1. SDA mucoid, buff- coloured colonies 2. Capsule prod is enhanced –growth on CA in CO2 3. BSA/NSA- brown coloured colonies 4. BA, CHHA BIOCHEMICAL TEST 1. phenol-oxidase 2. Growth at 37C 3. Urease 4. Inositol& nitrate assimilation 5. Morp of blastospores MICE PATHOGENICITY Infected material Inoculated into swiss albino mice- IC, IV,IP 10-14 days Autopsy exam of body sites & visceral organs for cyptococci SEROLOGY 1. Demo of capsular ag in serum/CSF- Crypto LA test Eiken LA test 2. Demo of AB 1. Agglutination 2. IFAbT 3. CFT TYPING: serotyping, RFLP, PMS