INFECTIOUS DISEASE OF
Dr. Naila Awal
• Fungi are the eukaryotic, saprophytic,
parasitic micro organism, unicellular or
multicellular having chitin in their cell wall
& ergosterol & zymosterol in their cell
Morphological classification1) Mold- fungi which are
multicellular & form a
round/oval like fungi
reproduction by budding.
3) Yeast like fungusFungus that reproduction
by budding, but bud fails
to separate from parent
cell & ultimately form a
structure that looks like a
chain of elongated cell.
• Ex- Cryptococcus
• 4) Dimorphic fungus
• Fungi that can remain
either mold/ yeast form
depending upon the
temperature of the
• Ex- Histoplasma
• 37C-->change to yeast
• 25C --> mold form
Depending upon the site of infection
1) Superficial mycosesThose fungal infection
,caused by the fungus that
lies on the surface of the
2) Cutaneous mycosescaused by the fungus that
liberate keratinase enzyme &
therefore can invade deep
into keratin layer of skin &
also nail &hair.
• ExMalassezia furfur -->
• Pityriasis versicolor
dermatophytoses (Ring worm)
3) Sub cutaneous
mycoses- caused by
the fungus that lies on
the surface of the
4)Deep mycoses- caused
by the fungus that infect
• Ex• Rhinosporidium seeberi–
• Ex• Candida–Candidiasis.
• Histoplasma capsulatumHistoplasmosis.
• Disease- Malassezia furfur
• Clinical manifestationLesions are macular, non-inflammatory, well
demarcated & hypopigmented.
• Sample- Skin scrapping
• Lab procedure• The scrapping material is placed on glass slide few
drops of KOH is added cover slip wait for 20 mins.
• Observation-Cluster of rounded yeast cell & short ,stout,
curve, septate hyphae.
• Genus1)Trichophyton- Nail & Hair
C/FSkin-->Ring like lesion.
Ring- Scaly, hypopigmented & inflammatory.
Nail yellow, brittle & thick.
• SampleSkin- Skin scrapping
Hair- Hair clipping. If infection present in scalp, then skin
adjoining scalp is taken.
Nail Nail shaving at the margin between healthy &
unhealthy area & from the deeper portion of nail.
1)The material is placed on glass slide few drops of KOH
is added cover slip wait for 30 mins (skin)/10mins
• Observation- long thin, branched & septate hyphae.
2) Culture- Sabouraud's dextrose agar media25-28 C for 3-4 weeks.
• Colony morphology- colony is picked up place on
glass slide Lacto phenol cotton blue dye is added
cover slip examine under microscope.
Sub cutaneous mycoses
• Definition- It is a granulomatous disease of
subcutaneous tissue caused by various fungi & bacteria
where there is gradual destruction of tissue leading to
loss of function of the affected area.
Disease- Maduromycosis /Madura foot
Actinomycetoma when madura foot is caused by
Eumycetoma when madura foot is caused by
Site- 1)Foot most common site
• Local trauma of skin
Micro organism enters to the body
• Sample- muco pus
• Lab procedure• Muco pus is taken in 3 separate glass slides.
• 1st slide- 1 drop of normal saline is added cover slip
viewed by hand glass
• Observation• If granules are black- Madurella grisea
yellow white-Pseudallescheria boydii
2nd glass slide
• Add few drops of 20% KOH in muco pus wait for 10
• Observation• If fine fillamentous branch with no chlamydospore
• If thick septate branched hyphae with chlamydospore
3rd glass slide• Granules are crushed on a slide Z-N stain
decolorized with 1% H2SO4 Red branching filament
• Definition- It is a chronic granulomatous disease
characterized by production of large polyp / wart like
• Causative organism- Rhinosporidium seeberi
• Site- Common site –Nose-78%
Fungus is inoculated into the mucosal epithelium of nasal
Replication of fungus
Hyperplasic growth of host tissue & immune response
• The lesions are polypoid, reddish & granular.
• May be multiple & pedunculated.
• Highly vascular & bleed on touch.
M/E• Papillomatous hyperplesia of nasal mucosa.
• Multiple mature & immature cyst (sporangia) are packed
• Infiltration of chronic inflammatory cells into normal
• ClassificationDeep mycoses
Primary deep mycoses
(Fungal infection that
infect healthy Individual)
(Fungal infection that
infect immunosuppressive individual)
• Causative organism- Histoplasma capsulatum.
• Pathogenesis• Source of infection- Soil
• Mode of transmission- Inhalation.
macro & microconidia enters into lung
engulf by alveolar macrophage
through macrophage they spread to the various tissue.
(Liver, spleen, lymph node)
2)Pulmonary histoplasmosis- fever, dry cough.
More severe case- granulomatous lesion in lung.
3)Localized lesion in extrapulmonary sitemediastinum, adrenal,liver, meninges.
4) Disseminated histoplasmosis- Immunosuppressed
• Specimen1)Pulmonary histoplasmosis- Sputum.
2)Buffy coat of blood.
3)Bone marrow aspirate.
4)Biopsy specimen from different internal organ.
• Lab procedure• 1) Direct microscopy- Specimen is taken on the glass
slide Giemsa staining Microscopic examination.
• Findings- Yeast like fungus within the cytoplasm of
2)CultureSabouraud’s dextrose agar media- incubate at 37 C for 4
Observation of colony morphologyhyphae with macro & micro conidia.
3) SerologyPatient’s serum-Anti histoplasma
4)SkinHistoplasmin skin test.
5) HistopathologyPulmonary histoplasmosisEpithelioid granuloma with
central caseous necrosis,
areas of consolidation.
Disseminated histoplasmosis-->Mononuclear phagocytes filled with fungal yeast.
-->Epithelioid granuloma are not formed.
• Definition- It is a true yeast surrounded by thick
• Causative organism- Cryptococcus neoformans.
• Nice to knowCapsulated bacteriaStreptococcus pneumoniae
Mode of transmission- Inhalation of yeast
• Pathogenesis• It is asymptomatic / produce influenza like
symptoms which resolves automatically in
But in immunocompromised person Through inhalation enters into lung via
blood meninges cryptococcal meningitis.
Lab procedure1)Wet film microscopy- circular/oval yeast cell.
2)India ink preparation- CSF is centrifuged deposit is
taken on glass slide1 drop of india ink is added
cover slip examine under microscope.
Observation- against dark background darkly illuminated
single circular/oval yeast with budding.
Blood agar media- 37 C for 24 hours
Saborauds dextrose agar media-37 C for 2 days.
• 2 days after, colonies are picked up on glass slide
examine under the microscope
• ObservationSpherical yeast cell
4)Serological test- Anti cryptococcal Ab +
• CNS• In immunosuppressed personSoap bubble lesion- gelatinous masses of fungi in
meninges or may expand the perivascular VirchowRobin space within the grey matter.
• In non immunosuppressed personChronic granulomatous lesion composed of macrophage,
lymphocyte & foreign body giant cell. Suppuration may
• Lung- Solitary pulmonary granuloma.
• Causative agent- Aspergillus fumigatus.
• Mode of transmission- By the inhalation of
• Spectrum of disease1) No infection- b/c alveolar macrophage engulf & destroy
2)Person who have allergic to Aspergillus antigen, manifest
as Allergic bronchopulmonary Aspergillosis (ABPA).
3)Person who have cavity to lung (due to TB, sarcoidosis),
conidia after reaching the cavity they germinate &
produce abundant hyphae in lung cavity. This clinical
condition is known as Aspergilloma.
• They manifest asHaemoptysis
4)Person who are in steroid therapy (leukemia, bone
marrow transplantation) inhale conidia produce
severe manifestation of disease Invasive
Aspergillosis which is clinically manifest as pneumonia.
• After lung infection hyphae invade blood vessels
haematogenous spread to different internal organ
Abscess (brain, liver, kidney).
• Lab procedure• 1) Gram staining- Septate hyphae
with dichotomous branching.
• 2)CultureBlood agar
Sabouraud's dextrose agar media
• Observation of colony- Aspergillus colonies are usually
fast growing, white, yellow, yellow-brown, brown to black
or shades of green.
• 3) Serological test- Immunodiffusion tests for the
detection of antibodies to Aspergillus species .
• 4) Histopathology• AspergillomaProliferative mass of hyphae form fungal ball which lies
freely within the cavities.
Surrounding inflammatory reaction may be
sparse/chronic inflammation/ fibrosis.
• 1) lungAspergillus form fruiting bodies (usually in lung cavities) &
Septate filaments, branching at right angles (40 degrees)
Definition- It is an opportunistic infection caused by ‘bread
mould fungi’ including- Mucor, Rhizopus, Abscidia &
Breakdown of cutaneous barrier as a result of burning,
surgical wound/ trauma.
Major route of infection- 1) Inhalation
3) Traumatic inoculation.
Clinical presentation• 5 clinical form of Mucormycosis- Rhino cerebral,
pulmonary, gastrointestinal, primary cutaneous &
• Rhino cerebral MucormycosisInitial symptoms- acute sinusitis, congestion, purulent nasal
discharge, fever, unilateral headache, peri orbital edema,
proptosis, facial numbness, cranial nerve palsy.
• Pulmonary MucormycosisFever, haemoptysis
• Gastrointestinal Mucormycosis• Bowel perforation, peritonitis, GIT hemorrhage.
• Severe immunocompromised person manifest as
primary cutaneous lesion.
• They do not harm in immunocompetent
individual but infect immunosuppressed person.
• It is transmitted by air borne asexual spore.
• After inhalation of spore
Colonize into nasal sinus
Engulf by alveolar macrophage
& oxidative killing
• Specimen- Biopsy from suspicious areas.
• Lab procedure1) Staining• H&E stain- often hard to see
– GMS, PAS stains better
irregularly wide fungal
hyphae with frequent
right angle branching.
2) Histopathology- Common site• nasal sinus, lung &GIT
Rhino cerebral Mucormycosis• Local tissue necrosis
• Invade arterial wall
• Penetrate peri orbital tissue.
• Pulmonary Mucormycosis• Areas of hemorrhagic pneumonia with
• Vascular thrombi &
• Distal infraction.
• Species1)Candida albicans.
• Features1) Dimorphic fungus•
25 C-True hyphae.
37C-Pseudohyphae with yeast.
produce chlamydospore- Sexual spore.
3) Causes opportunistic infection.
• Predisposing factor of candidiasis1) Immunosuppression due to prolong use of – Anti cancer
3)Prolong use of antibiotic
6)Bone marrow transplant recipient
8)Very young & very old age.
Clinical spectrum of candidiasis• 1) Mucosal candidiasis•
Vulvo vaginal candidiasis
2) Cutaneous CandidiasisNail proper- Onychomycosis
Nail fold- Paronychia
Armpit/ web of the fingers & toes- Intertrigo
Hair follicle- Folliculitis
Penile skin- Balanitis
Perineum of infant- Diaper rash
• Definition- It is the superficial fungal infection on the
mucous membrane of oral cavity.
• Seen inNewborn
Children receiving oral steroid
HIV positive patient
for asthma & following a course of
broad spectrum antibiotics that destroy normal bacterial flora.
• Morphology- They form grey-white dirty looking pseudo
membrane, composed of matted organism &
• Deep to the surface there is mucosal hyperemia &
• Common in• Women withDM
• Clinical manifestationIntense itching
Thick curd like discharge
• Definition- It is a candidiasis which is caused
by blood borne dissemination of organisms into
various tissue / organs.
• Persons risk for developing candidiasis1) ICU patient
2) Surgical patient
3)Patient with central venous catheter
4) Immunocompromised person.
5) Very LBW infant
Lab diagnosis of candidiasis
-->Scrapping from superficial lesion
-->Blood, CSF, Urine
-->Material from I/V catheter
1) Wet film preparation- From
Swab, exudates, CSF (centrifuge), urine (centrifuge)
• FindingsSpherical/ oval yeast cell with budding.
2)StainingA) Gram staining- Gram + round/oval yeast cell with
B) Immuno fluorescence staining- calcoflor white stain.
3) CultureA) Sabouraud's dextrose agar media
B) Blood agar media
• 37 C for 48 hours in aerobic condition.
Colony morphology• 2-4 mm in diameter, circular, white/creamy, soft with
4)Confirmation – Gram staining from the culture plate.
• Gram + yeast with budding.
5)Germ tube test (Confirmatory test for Candida albicans)
• 0.5ml human serum is taken in a test tube
• Test fungal colony is added
• Incubate at 37C for 4 hours
• Then 1 drop of serum is collected & place on glass slide
• Cover slip
• Microscopic examination
• Observation- Yeast like cell with finger like projection.
• Comment+ for Candida albicans
7) Sugar fermentation test• It differs for different species.