Yeast Infections

Slide 1 · Yeast Infections

Candidiasis: pathogenic mechanisms, morphology, and clinical patterns

Candida albicans • Candida auris

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Distinguish yeast, pseudohyphae, and true hyphae in tissue.

Connect Candida virulence and host-defense defects to infection patterns.

Recognize mucocutaneous and disseminated candidiasis.

Differentiate the clinical significance of C. Albicans and C. Auris.

Slide 3 · Fungal growth forms frame diagnosis

Budding yeast

Pseudohyphae

Septate hyphae

Schematic fungal growth forms

Yeasts grow as individual round-to-oval cells, chiefly by budding.

Pseudohyphae are elongated buds remaining connected at constrictions.

Mold hyphae are filamentous structures; Fungi are eukaryotes with cell walls.

Slide 4 · Clinical categories of fungal infection

Category

Extent of involvement

Superficial / cutaneous

Superficial or keratinized skin, hair, and nails

Subcutaneous

Skin, subcutis, and lymphatics; rare systemic spread

Endemic

Dimorphic fungi capable of serious systemic illness

Opportunistic

May cause life-threatening illness with immunosuppression or devices

Slide 5 · Candida is not a single-species diagnosis

More than 200 Candida species.

Approximately 15–20 are frequently encountered in human infections.

Highlighted species include C. Albicans, C. Auris, C. Glabrata, C. Tropicalis, C. Parapsilosis, and C. Krusei.

C. Albicans and C. Auris are the focus of this lecture.

Slide 6 · Candida albicans normally lives with its host

Mouth

Gut

Vagina

Skin

Schematic site map

Typical colonization sites: Skin, mouth, gastrointestinal tract, and vagina.

Organisms are usually benign members of the commensal microbiota.

Infection commonly follows breach of epithelial or mucosal barriers.

Slide 7 · C. Albicans is adapted to human-host residence

No known environmental reservoir for C. Albicans.

The fungus has adaptations that permit completion of its life cycle within the human host.

This statement should not be extended to every Candida species.

Slide 8 · Colonization becomes disease when barriers fail

Commensal Candida

Barrier disruption

Local proliferation / invasion

Superficial disease

The same organism may be harmless on an intact surface yet pathogenic after breach.

Clinical pattern depends on the tissue involved and host defenses.

Slide 9 · Candidiasis spans localized and invasive disease

Localized disease

Systemic disease

Mucosal thrush, esophagitis, vaginitis

Bloodstream spread to distant tissues

Diaper rash and other cutaneous lesions

Abscesses, endocarditis, ocular or CNS disease

Often linked to surface or local defense changes

Strongly linked to profound neutropenia / devices

Slide 10 · Susceptibility differs by host context

Diabetes and burns predispose to superficial candidiasis.

Intravenous catheters and peritoneal dialysis facilitate bloodstream entry.

Neutropenia associated with leukemia, chemotherapy, or stem-cell transplantation predisposes to dissemination.

Slide 11 · Barrier-associated risk: Skin and mucosa

Candida near a weakened epithelial barrier

Schematic barrier crossing

Superficial infection appears where Candida encounters permissive mucosal or skin surfaces.

Wet and intertriginous sites can support cutaneous infection.

Antibiotic-associated loss of competing flora can precede oral thrush.

Slide 12 · Devices create a route to invasive candidiasis

Indwelling line / catheter

Organism gains access

Bloodstream infection

Distant organ seeding

An indwelling device provides a clinically important context for bloodstream dissemination.

Peritoneal dialysis is also identified as a risk setting.

Slide 13 · Profound neutropenia increases systemic risk

Leukemia / chemotherapy

Reduced neutrophil defense

Candida dissemination

Multiorgan lesions

Hematopoietic stem-cell transplantation is another source-listed setting.

Severe disease can cause shock and disseminated intravascular coagulation.

Slide 14 · Virulence reflects adaptation, not one toxin

C. Albicans adapts its cellular phenotype to host conditions.

Adhesion molecules bind host molecules and cellular surfaces.

Secreted enzymes, oxidative-stress resistance, and biofilms contribute to persistence and invasion.

Slide 15 · Phenotypic switching expands adaptive capacity

Yeast phenotype

Regulated switching

Alternate cell forms

Original schematic

That C. Albicans can adopt nine distinct cell shapes.

Coordinated transcription of phase-specific genes supports switching.

The forms can differ in colony appearance, antigenicity, and virulence.

Slide 16 · Environmental cues can drive switching

Temperature / nutrients

Antibiotic pressure

Host immune response

Phase-specific transcription

Source-listed cues can change the organism’s phenotypic state.

This is adaptive plasticity within the human host, not necessarily acquisition from the environment.

Slide 17 · Switching alters the host–pathogen interface

Yeast phenotype

Regulated switching

Altered properties

Original schematic

Phenotypic variants can differ in cell shape and colony morphology.

Antigenicity can vary across phenotypic forms.

The resulting states may exhibit different virulence properties.

Slide 18 · Adhesins tether Candida to host surfaces

Candida cell

Adhesion molecules

Host surface

ECM ligands and epithelial/endothelial cells

Original schematic

C. Albicans expresses many functionally distinct adhesion molecules.

Binding substrates include fibrinogen, fibronectin, and laminin.

Adhesion also occurs to epithelial and endothelial cells.

Slide 19 · Adherence is the gateway to persistence

Candida contacts surface

Adhesion molecules bind

Stable association

Opportunity for invasion / biofilm

The first adhesive interaction contributes to host-surface colonization and device-associated communities.

A schematic causal summary of source-described mechanisms.

Slide 20 · Secreted proteinases facilitate tissue invasion

Secreted enzymes may degrade ECM

Original schematic

At least nine secreted aspartyl proteinases are described.

Degradation of extracellular matrix proteins may promote invasion.

The source qualifies this role as a proposed contribution rather than a universal prerequisite.

Slide 21 · Catalase counteracts a host killing pathway

Phagocyte oxidative attack

Candida catalase activity

Reduced oxidative damage

Potential survival advantage

Candida catalases may permit resistance to oxidative killing.

Do not interpret this as complete protection from phagocytes.

Slide 22 · Candida biofilms are mixed communities

Yeast + filamentous forms + fungal matrix

Implanted substrate

Original schematic

Biofilms contain yeast and filamentous fungal forms.

A fungal-derived extracellular matrix surrounds the community.

At least 30 factors participating in biofilm formation.

Slide 23 · Biofilm formation includes a dispersal phase

Initial adhesion

Maturation

Structured community

Dispersion

Adhesion, maturation, and dispersion as regulated contributors.

This diagram is a conceptual sequence rather than a precise time course.

Slide 24 · Implanted devices can support biofilms

Yeast + filamentous forms + fungal matrix

Implanted substrate

Original schematic

C. Albicans can form biofilms on implanted medical devices.

Biofilms reduce susceptibility to immune responses.

The same architecture reduces susceptibility to antifungal drug therapy.

Slide 25 · Biofilm biology explains clinical persistence

Biofilm-associated cells occupy a shared extracellular matrix.

The microbial community can include cells in several morphologic states.

The combination of adhesion and reduced clearance matters in catheter-associated disease.

Slide 26 · Three host-defense arms are emphasized

Candida

Neutrophils

Macrophages

Th17 response

Original schematic

Neutrophils provide rapid cellular defense.

Macrophages phagocytose Candida and participate in oxidative killing.

Th17 responses recruit additional inflammatory cells, supporting mucosal protection.

Slide 27 · Phagocytes are an immediate barrier

Candida encountered

Neutrophil / macrophage uptake

Oxidative killing

Reduced organism survival

Neutrophils and macrophages are both important first-line defenses.

The pathway is compromised in specific phagocytic deficiencies.

Slide 28 · Phagocytic defects have predictable consequences

Impairment

Source-described implication

Neutropenia

Increased risk of C. albicans infection

Defective phagocyte oxidase

Reduced oxidative antimicrobial activity

Myeloperoxidase defects

Increased vulnerability to Candida infection

Slide 29 · Filamentous forms can evade phagosomes

Filamentous forms may escape phagosome

Original schematic

Candida morphotypes after phagocytosis.

Filamentous forms can escape from the phagosome into the cytoplasm.

Yeast forms do not show this escape behavior.

Slide 30 · Dendritic sensing starts a protective cascade

Candida yeast

Dendritic-cell recognition

IL-6 / IL-23

Th17 responses

Yeast forms can activate dendritic cells by several pathways.

This example highlights one source-described β-glucan pathway.

Slide 31 · β-1,3-glucan engages dectin

β-1,3-glucan

Dectin

Original schematic

Candida yeast expresses β-1,3-glucan.

The fungal ligand interacts with dectin on dendritic cells.

Downstream cytokine production promotes Th17 responses.

Slide 32 · IL-6 and IL-23 support Th17 responses

β-glucan–dectin engagement

Dendritic-cell signaling

IL-6 + IL-23

Th17 response

The source links the lectin recognition event to cytokines and adaptive immune support.

Cytokine labels are mechanistic; No unreported concentrations are inferred.

Slide 33 · Th17 responses reinforce cellular recruitment

Candida recognition

Th17-cell response

Neutrophil recruitment

Monocyte recruitment

Th17-mediated recruitment is important in protection from mucocutaneous Candida infection.

The source does not equate Th17 activity with a single antimicrobial effector.

Slide 34 · Defective T-cell/Th17 immunity causes recurrence

Low T-cell counts due to HIV are associated with recurrent mucocutaneous candidiasis.

Inherited defects affecting Th17 development or function can produce similar susceptibility.

Acquired abnormalities in this axis may also impair mucosal protection.

Slide 35 · Disease severity reflects pathogen × host

Candida

Neutrophils

Macrophages

Th17 response

Original schematic

Adhesion, phenotypic switching, and biofilm formation increase fungal fitness.

Phagocytes protect against tissue invasion and dissemination.

Th17-associated recruitment is particularly important for mucocutaneous defense.

Slide 36 · Yeast forms: Budding round-to-oval cells

Schematic fungal growth forms

Candida appears as yeast in histologic sections.

Yeast are round-to-oval fungal cells that mainly reproduce by budding.

Yeast may coexist with other Candida growth forms in a specimen.

Slide 37 · Pseudohyphae: Constrictions are the clue

Schematic fungal growth forms

Elongated budding cells remain connected end to end.

Narrowings occur at the junctions of adjacent cells.

Pseudohyphae as a useful diagnostic clue.

Slide 38 · True hyphae show filamentous septated growth

Schematic fungal growth forms

True hyphae are reported less commonly than yeast/pseudohyphae in tissue.

The source identifies septa as a defining structural feature.

Reduced oxygen tension is one associated condition noted.

Slide 39 · A tissue section can contain mixed forms

Budding yeast

Pseudohyphae

Septate hyphae

Schematic fungal growth forms

Yeast, pseudohyphae, and true hyphae can coexist.

One section should not be expected to show only a single morphotype.

Interpret fungal elements alongside the site and tissue reaction.

Slide 40 · Histologic stains make fungal elements visible

Stain

Textbook role

Hematoxylin–eosin

Organisms can be visible in routine tissue sections

Gömöri methenamine silver

Special fungal stain often improves visualization

Periodic acid–Schiff

Special stain often improves visualization

Slide 41 · Oral thrush forms a pseudomembrane

Pseudomembrane: Fungal elements + debris

Congested mucosa

Original schematic

Superficial proliferation produces gray-white, dirty-looking plaques.

The pseudomembrane comprises fungal organisms and inflammatory debris.

This is a characteristic mucosal presentation of candidiasis.

Slide 42 · Thrush is not confined to surface deposits

Surface fungal pseudomembrane

Inflammatory mucosal response

Original schematic

The superficial plaque contains matted organisms and inflammatory material.

Underlying mucosa exhibits congestion and inflammation.

A surface lesion therefore represents both organisms and a host response.

Slide 43 · Settings associated with oral thrush

Host / exposure

Source-defined association

Newborns or debilitated patients

Susceptibility to oropharyngeal candidiasis

Inhaled/oral steroids for asthma

Thrush can occur in treated children

Broad-spectrum antibiotic course

Reduced competing normal bacterial flora

HIV infection

Important setting for oral thrush

Slide 44 · Unexplained thrush requires clinical attention

Robbins advises evaluating unexplained oral thrush for HIV infection.

The inference is prompted by a change in expected host susceptibility.

A thrush lesion alone does not establish an HIV diagnosis.

Slide 45 · Esophageal candidiasis causes swallowing symptoms

Esophageal mucosa

White plaques

Dysphagia / pain

Original schematic

Common clinical contexts include AIDS and hematologic malignancy.

Patients may present with swallowing difficulty or pain and retrosternal pain.

Endoscopy can show white plaques and pseudomembranes.

Slide 46 · Oral versus esophageal candidiasis

Oral thrush

Candida esophagitis

Gray-white mucosal pseudomembranes

White esophageal plaques/pseudomembranes

Risk: newborns, steroids, antibiotic use, HIV

Risk: AIDS, hematologic malignancies

Lesion primarily in oral cavity

Swallowing complaints and retrosternal discomfort

Slide 47 · Vulvovaginal candidiasis has a characteristic syndrome

Predisposition

Pruritus

Curd-like discharge

Original schematic

The source emphasizes diabetes, pregnancy, and oral contraceptive use as associated settings.

Typical symptoms include intense itching.

A thick curd-like discharge is described.

Slide 48 · Cutaneous candidiasis: Nail and follicular disease

Pattern

Site

Onychomycosis

Nail plate

Paronychia

Nail folds

Folliculitis

Hair follicles

Slide 49 · Intertrigo follows the anatomy of moist folds

Opposing skin folds

Moist environment

Candidal intertrigo

Original schematic

Candidal intertrigo affects moist, opposing skin surfaces.

Examples include axillae and interdigital webs.

Anatomical site is an important clue to the superficial pattern.

Slide 50 · Other cutaneous presentations are site-defined

Lesion

Characteristic site

Balanitis

Penile skin

Diaper rash

Infant perineum in contact with wet diapers

Intertrigo

Axillae and finger/toe web spaces

Slide 51 · Mucocutaneous patterns form a location map

Oral cavity

Esophagus

Vagina

Skin + nails

Schematic site map

Mouth and esophagus: Pseudomembranous disease.

Vagina: Pruritus and curd-like discharge.

Skin, nails, folds, follicles, and perineum: Named cutaneous patterns.

Slide 52 · Bloodstream spread seeds distant organs

Bloodstream Candida

Vascular dissemination

Tissue localization

Focal invasive disease

Robbins specifically describes invasive candidiasis as hematogenous.

The organs involved determine the pathology and clinical consequences.

Slide 53 · Deep-organ candidiasis: Focal suppurative disease

Organ

Reported lesion

Kidney

Renal abscesses

Liver

Hepatic abscesses

Myocardium

Myocardial abscesses

Brain

Microabscesses

Slide 54 · Cardiac infection includes endocarditis

Myocardial abscess

Endocarditis

Valvular context

Original schematic

Disseminated disease may involve myocardial abscesses.

Candida can infect valves and cause endocarditis.

Robbins characterizes Candida spp. As the leading cause of fungal endocarditis.

Slide 55 · CNS and ocular involvement extend the differential

Brain microabscesses

Meningitis

Endophthalmitis

Original schematic

Brain lesions include microabscesses and meningitis.

Endophthalmitis may involve virtually any ocular structure.

In high-risk hosts, distant fungal seeding should be clinically considered.

Slide 56 · Tissue inflammation is host-dependent

Minimal

Suppurative

Granulomatous

Host immune state changes the tissue response

Original schematic

Candida may elicit little inflammation in some immunocompromised patients.

A suppurative reaction is a common inflammatory pattern.

Granulomatous inflammation occurs occasionally.

Slide 57 · Candida endocarditis: Clinical contexts

Clinical setting

Textbook emphasis

Prosthetic heart valve

Important predisposing substrate

Intravenous drug use

Tricuspid valve involvement is highlighted

Slide 58 · Dissemination is especially dangerous in acute leukemia

Profound neutropenia after chemotherapy is a high-risk state.

The burden may be multiorgan rather than restricted to a mucosal site.

Severe disseminated disease can be accompanied by shock and DIC.

Slide 59 · Candida auris is an emerging healthcare pathogen

Critical illness

Antifungal resistance

Healthcare outbreaks

Original schematic

Disease disproportionately affects critically ill and immunocompromised patients.

Reported infections can involve blood, gastrointestinal tract, wounds, or other sites.

The source emphasizes antimicrobial resistance, colonization, and nosocomial outbreaks.

Slide 60 · Invasive C. Auris disease carries high severity

30%–60% mortality in patients with invasive C. Auris infection.

This is an historical textbook summary, not an individualized prognosis.

Severity must be interpreted in the context of critical illness and comorbidity.

Reported textbook estimate; Not a contemporary surveillance update.

Slide 61 · C. Auris: Documented emergence milestones

2009

Identified in Japan as a cause of ear infection

2016

CDC clinical alert following multicontinental emergence

2022

2,377 US clinical cases

Slide 62 · C. Auris colonization is not synonymous with infection

Colonization

Invasive / clinical infection

Sites: nostrils, groin, axilla, rectum

Sites include bloodstream, gut, wounds, others

Most colonized individuals do not become ill

Severe invasive illness can occur

Carriage is epidemiologically significant

Clinical syndrome requires separate interpretation

Slide 63 · C. Auris colonizes multiple body surfaces

Nostrils

Axilla

Groin

Rectum

Schematic site map

Colonization is reported in nostrils, groin, axilla, and rectum.

Most colonized patients do not develop clinical disease.

Carriage and healthcare environmental persistence create outbreak concerns.

Slide 64 · Catheter-associated C. Auris outbreaks are a concern

Critically ill patient

Central venous / urinary catheter

Possible biofilm formation

ICU transmission / infection

ICU outbreaks occur among catheterized patients.

The source suggests, rather than conclusively establishes, biofilm formation as a virulence mechanism.

Slide 65 · Environmental persistence complicates control

Dry / moist surfaces

Survival up to 14 days

Cleaning challenge

Original schematic

Survival on dry and moist surfaces for up to 14 days.

Elimination of environmental sources is challenging in healthcare facilities.

The value is source-specific and should not be generalized to all cleaning conditions.

Slide 66 · C. Auris: Source-reported antifungal resistance

Historical resistance percentages reported in the source textbook

Fluconazole

90%

Amphotericin B

30%

Echinocandins

5%

Figures reflect Robbins (2026), not a live susceptibility surveillance database.

Slide 67 · Broad antifungal resistance changes risk assessment

The source reports resistance to several major antifungal classes.

Pan-resistant strains have also been reported.

Specific susceptibility determination is distinct from identifying Candida in tissue.

Slide 68 · C. Albicans and C. Auris pose different challenges

C. albicans

C. auris

Usually commensal on host surfaces

Often colonizes critically ill healthcare patients

Broad mucocutaneous and invasive patterns

Outbreaks and device-associated infection emphasized

Host barrier / Th17 / neutrophil mechanisms elaborated

Resistance and environmental persistence highlighted

Slide 69 · Diagnosis: Integrate specimen, morphology, and setting

Evidence level

Interpretation

Tissue morphology

Candida yeast and pseudohyphae can support tissue recognition

Stains

H&E, PAS, and GMS aid visualization

Species determination

Histology alone may not definitively identify fungal species

Clinical context

Host immunity and evidence of tissue invasion matter

Slide 70 · Clinical application: White oral plaques

An otherwise healthy adult develops gray-white oral plaques after a broad-spectrum antibiotic course.

What mechanism links the exposure to thrush?

Antibiotics can reduce competing normal bacterial microbiota, permitting florid Candida proliferation.

Slide 71 · Clinical application: Catheter and neutropenia

A patient receiving induction chemotherapy for acute leukemia has profound neutropenia and an indwelling venous catheter.

What disease pattern must remain in the differential?

Bloodstream and disseminated candidiasis, with potential abscesses, valve involvement, and other organ disease.

Slide 72 · Clinical application: Persistent hospital colonization

A critically ill ICU patient is colonized with C. Auris in the axilla and has a urinary catheter.

Does colonization alone establish invasive infection?

No. Most colonized patients do not become sick; Catheter risk and possible environmental spread require context-specific assessment.

Slide 73 · Integrative summary: Connect form, host, and site

Candida disease begins with commensal overgrowth or barrier breach and is promoted by adhesins, enzymes, and biofilms.

Yeast and pseudohyphae provide diagnostic morphology; Th17 cells and phagocytes provide major host protection.

Mucocutaneous disease differs from hematogenous dissemination; C. Auris additionally raises outbreak and resistance concerns.

Slide 74 · Primary reference

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th ed. (2026), Chapter 8, pages 348–350.

Foundational fungal classification, Candida albicans pathogenesis and morphology, clinical candidiasis, and Candida auris.

Original textbook Figure 8.43 was not reproduced; morphologic illustrations in this deck are explicitly schematic.