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Muguet denotes the adherent white fungal coating of oral thrush, now oral candidiasis; it is not simply any white tongue or any mouth ulcer. Patches occur on the tongue and oral mucosa and may merge into broader plaques. The underlying surface can be red, sore and liable to bleed when a plaque is disturbed. An infant may feed poorly because the mouth hurts. Milk residue lacks the same persistent inflamed adherent lesion, while an aphthous ulcer is a focal ulcer rather than a confluent fungal plaque. ^[ref]

Cause and nature. The modern explanation is opportunistic overgrowth of Candida, commonly Candida albicans, on a susceptible mucosal surface. An immature or impaired immune system, illness and altered local conditions favour it. Antibiotics, corticosteroids, diabetes and other causes of reduced host defence are relevant modern risk factors. These were not all understood in 1865, and exposure to the organism alone does not explain every case. Local oral candidiasis also does not, by itself, establish invasive fungal disease. ^[ref]

Evidence available in the nineteenth century. Fungal forms could already be observed with a microscope. A contemporary 1849 review reports Charles West's suggestion that the organisms could be transferred by shared cups and spoons, while the reviewer preferred an explanation involving decomposition and acidity. The review is evidence of the disagreement, not authority for spontaneous generation of a fungus. It also illustrates why historical “aphthae”, ulceration and Muguet should not all be treated as identical modern diagnoses. ^[ref]

Diagnosis and treatment. Clinical inspection is often sufficient; when uncertain or atypical, material from the lesion can be examined microscopically for fungal forms, with further laboratory testing when needed. Repeated or unusually severe disease calls for attention to underlying illness and host defence, rather than simply repeating local cleansing. ^[ref]

The historically defensible measures include maintaining adequate feeding, gentle mouth care and clean feeding utensils. Harsh scraping and treating every white patch as the same disease are inappropriate. Present-day treatment adds an age-appropriate antifungal drug, such as a suitable topical nystatin preparation; more extensive or resistant disease may require systemic treatment such as fluconazole. Drug choice and formulation depend on the patient's age and clinical state. Those agents are later additions and must not be placed in an 1865 prescription. Hygiene and correction of predisposing factors accompany, rather than replace, effective antifungal treatment. ^[ref]

The historical common principle was to identify and destroy a superficial fungal parasite, remove material harbouring it and prevent reinfection. Modern diagnosis preserves this principle for genuine fungal infection, but rejects its indiscriminate application to “tinea decalvans”. The three labels must therefore be discussed separately.

In pityriasis versicolor, look for finely scaling patches of altered skin pigmentation, commonly on the trunk. Examine superficial skin scrapings by microscopy when uncertain. Historically, washing, removal of loose scale and a topical “parasiticide” aimed to reach the organism in the outer epidermis. Today pityriasis versicolor is associated with overgrowth of Malassezia yeasts already present on the skin; it is not ordinary contagious ringworm and is not evidence of poor cleanliness.^[ref] Topical ketoconazole or selenium sulfide can control it. Extensive or recurrent disease sometimes needs other treatment. Loss of scale and control of the yeast need not immediately restore skin pigmentation; residual colour can persist for weeks or months. A Wood's lamp can assist examination, but is not a substitute for the whole clinical assessment.^[ref]

“Tinea decalvans” is the critical historical trap. Some nineteenth-century writers interpreted patchy baldness as parasitic and advocated extraction of affected hairs followed by prolonged topical treatment. A January–June 1867 digest explicitly calls the condition contagious and reports a mercury(II) chloride preparation. That is evidence of a contemporary belief, not evidence that the proposed organism caused every case of patchy baldness.^[ref] The label often covered what is now called alopecia areata, an immune-mediated form of hair loss. Smooth bald patches require differentiation from scaly patches with broken hairs and demonstrated fungal infection. Confirm the diagnosis before treating. In established alopecia areata, a period “parasiticide” is inappropriate: observation or diagnosis-specific treatment, including local corticosteroids in suitable cases, is considered instead. Neither mercury(II) chloride nor destructive epilation is a modern treatment for alopecia areata.^[ref]

For contagious ringworm, establish the site and extent. An enlarging scaly ring on bare skin suggests tinea corporis; scaly bald areas with broken hairs suggest tinea capitis. Examine scrapings or hairs by microscopy and, where appropriate, fungal culture. Clean clothing, towels, combs and brushes; avoid sharing them and investigate relevant human or animal sources. These measures address transmission, while an antifungal drug treats the affected tissue.^[ref] Limited tinea corporis can often be treated topically. Tinea capitis needs an oral antifungal drug, such as griseofulvin or terbinafine chosen for the circumstances, because a cream alone does not clear the infected hair-bearing site. An adjunctive shampoo can reduce spread but does not replace systemic treatment. Unsupervised corticosteroid cream can mask or worsen ringworm.^[ref][ref]

Thus the useful unifying idea is cause-directed treatment that reaches the affected tissue, with transmission control when infection is transmissible. It does not follow that all three nineteenth-century names denote the same class of disease, or that every bald patch requires killing a parasite.