Candidiasis

Etiology and pathogenesis

The infection is caused by yeast-like fungi of the genus Candida. About 200 species of this microorganism are known in medical mycology, but Candida albicans remains the traditional dominant pathogen.

In the vast majority of clinical cases, an endogenous route of infection occurs. Fungi of this genus are natural representatives of the normal human mucous membrane microflora. Upon the development of immunosuppression, they rapidly acquire pathogenic properties, deeply invade surrounding tissues, and provoke autoinfection.

Exogenous routes of transmission are significantly less common in practice:

• Vertical: infection of the newborn infant directly during childbirth or during breastfeeding.
• Contact: transmission of the pathogen sexually, which naturally leads to the development of urogenital candidiasis.

Predictors of development (risk factors)

The development of candidiasis is always triggered by conditions that disrupt local or systemic homeostasis. The optimal environment for the active multiplication of fungi is warm and moist body surfaces.

Key triggers of the disease:

• Immunodeficiency states: HIV infection, T-cell immunity defects, and neutrophilic leukocytopenia. Extremely severe disseminated forms are characteristic of patients with leukemia and individuals receiving immunosuppressive treatment for organ transplantation.
• Iatrogenic dysbiosis: disruption of the natural microbiocenosis against the background of prolonged antibiotic therapy.
• Endocrine and metabolic disorders: polyendocrine deficiency, including hypothyroidism, hypoparathyroidism, and decreased adrenal function.
• Mechanical factors: damage to the skin and mucous membranes, especially under conditions of high humidity and maceration. In newborn infants, defects in basic care serve as a major factor.

Classification and clinical manifestations

The disease is conventionally classified by the depth of tissue involvement:

1. Localized forms. Cover mucous membranes (esophagitis, vaginitis) and skin (candidal dermatitis). In immunocompetent individuals, the infection presents as superficial "thrush" with hyperemia, exudation, pruritus, and characteristic white plaques. Skin lesions are eczematous in nature and are localized in moist areas: inguinal folds, interdigital spaces, under the mammary glands, and in the perianal region. This form is often associated with antibiotic use and is characterized by rapid involution after their withdrawal.
2. Invasive forms. Include severe involvement of internal organs (endocarditis, endophthalmitis) and systemic circulation of the pathogen in the blood (fungemia).

In HIV-infected patients, the clinical picture strictly correlates with the stage of the disease and the degree of CD4 lymphocyte depletion. The spectrum varies from persistent skin and nail lesions to visceral forms (involvement of the gastrointestinal tract, respiratory, and urogenital systems) and multiorgan sepsis.

Candidal stomatitis (thrush)

This is one of the most common mucocutaneous forms of the infection. In newborns, it often manifests against a background of somatic weakness or banal care defects.

• Symptomatology: specific, slightly raised whitish plaques, spots, or coatings form on the mucous membrane of the cheeks, lips, or tongue.
• Diagnostic criterion: upon an attempt to mechanically remove the coating, a hyperemic, inflamed, and easily bleeding surface is always revealed underneath.
• Complications: as the process progresses, the inflammation may spread from the oral cavity downward into the esophagus.
• Therapy: 2–4% sodium bicarbonate solution (to create an alkaline environment detrimental to fungi), aqueous solutions of aniline dyes, or 0.1% hexetidine solution are used topically. For recurrent courses, systemic oral antimycotics (fluconazole) are indicated. Creams with clotrimazole or isoconazole are used for extraoral foci.

Visceral lesions and pathomorphology

In severe immunodeficiencies or direct entry of fungi into the bloodstream (e.g., in injection drug users), generalized forms develop. Microscopically, acute or chronic inflammation with the formation of small abscesses and small granulomas is detected in the affected tissues.

• Heart: severe endocarditis develops with the formation of massive friable deposits on valve cusps (the aortic valve is affected particularly often).
• Kidneys: multiple microabscesses form in the renal tissue, and the pathogens themselves can be visualized directly within the glomerular capillaries.
• Lungs: multiple foci of necrosis are formed, accompanied by the development of hemorrhagic perifocal pneumonia.
• Hematogenous dissemination: systemic spread of the infection leads to the development of meningitis, brain and liver abscesses, multiple subcutaneous abscesses, osteomyelitis, arthritis, and enteritis.

Class and exam questions

What else to study on this topic

• Pathomorphological picture of visceral candidiasis (kidneys, heart, lungs)
• Features of the course of diaper dermatitis with secondary fungal flora
• Regimens of local and systemic antimycotic therapy for relapses
• Differential diagnosis of candidiasis and allergic bronchopulmonary aspergillosis

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.