The humoral and cellular contributions to PMN motility in vitro were studied in 37 malnourished (PCM) pediatric patients. Early-phase directed migration to BCF and to ZANS was diminished significantly (p less than 0.001) in severe PCM patients as compared to healthy adult or age-matched controls or respective nutritionally restored patients. Abnormalities were reversible after nutritional restoration and unrelated to occurrence of clinical infection. To determine the pathogenic mechanism of impaired PMN mobility in PCM, studies of cell morphology and adhesive function were performed. Abnormalities observed in severe PCM suspensions included significantly (p less than 0.001) increased baseline (unstimulated) adherence values and impaired CF modulation of adhesive function. Diminished enhancement of PMN adherence or decreased (relative to baseline) adherence values were observed in response to BCF (mean % delta = +5) or f-Met-Leu-Phe (mean % delta = -6) as compared to adult PMN values of +28% delta and +31% delta, respectively. That these abnormalities may result from in vivo CF prestimulation was suggested by findings of "activated" PMN morphology in suspensions prior to in vitro stimulation, and abnormalities of the distribution of PMN surface adhesion sites under conditions of chemotactic stimulation. Further investigations will be required to determine the underlying pathogenic mechanism(s) accounting for our observations.