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Contemporary review of Charles West's third edition (1854), published January 1855. Locators: pp. 109–112, primary atelectasis, secondary collapse, inflation and the historical misidentification of lobular pneumonia.

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]

“Atelectasis pulmonum” means incomplete expansion or collapse of lung air spaces; in the newborn it classically describes portions that have not expanded adequately after birth. Modern atelectasis also includes collapse of previously aerated lung. The older distinction between primary non-expansion and secondary collapse is useful when reading this paper.

The affected lung is airless, often dark and firm, with reduced volume, a depressed surface and little or no crepitation. Failure of inspiratory effort, obstruction of a bronchus by secretions, and external compression are different routes to this appearance. Modern physiology adds the role of pulmonary surfactant in opposing alveolar collapse; deficiency in premature infants belongs to neonatal respiratory distress syndrome, not an explanation the 1867 question itself supplies.^[ref]

The main historical confusion was with pneumonia. A pre-1867 review of Charles West's work distinguishes primary non-expansion from secondary collapse, and contrasts both with pneumonic hepatization. A collapsed region loses air and volume; inflammatory pulmonary consolidation fills air spaces with exudate. Both can look solid.^[ref]

The classical experiment introduces air through the trachea or an appropriate bronchus while the affected region is observed. Uncomplicated collapsed lobules can expand and regain buoyancy; inflation does not simply remove inflammatory exudate. The historical review describes this distinction.^[ref] The experiment's interpretation requires more than one observation: whether a region takes air, whether its volume changes, and whether its contents show inflammation are different measurements. Cut-surface inspection and histology test the last point directly. Floating or sinking alone cannot distinguish all mixtures of collapse, fluid and pneumonia, and cannot reliably establish whether an infant was born alive.

Other potential confusions include pulmonary oedema, pulmonary haemorrhage, and compressed lung beside a pleural effusion or pneumothorax. Fluid or blood in the air spaces differs from collapse alone, although the conditions can coexist; external compression can actually cause atelectasis. Pulmonary hypoplasia is different again: an underdeveloped organ is not merely an otherwise normally formed organ awaiting inflation.^[ref]

Reduced aeration is the observation; non-expansion, obstruction, compression and inflammatory consolidation are competing or coexisting explanations. Gross inspection, controlled inflation and histology help discriminate them.