The effect of toxic agents commonly ingested by children on antibacterial defenses in the lung

Abstract

405 this report to describe the changes in the coagulation mechanism in 4 children with severe varicella infection, 3 of whom had hemorrhagic chickenpox. All cases had a malignant disease at the time of their viral infection; 2 with acute leukemia in remission, 1 acute leukemia in relapse, and 1 with metastatic retinoblastoma. All were receiving an antineoplastic drug but none were on corticosteroids. None had bacterial sepsis or shock at the time of their chickenpox. Hemorrhagic varicella only occurred in the 3 leukemic patients, and all 3 died. The non-hemorrhagic case survived. The coagulation data revealed that the patients with the hemorrhagic form demonstrated thrombocytopenia, reduced levels of coagulation factors II, V, and VIII, hypofibrinogenemia, positive fibrin split products, and normal euglobulin lysis. In the non-hemorrhagic patient all studies were normal. Heparin therapy was given to one patient with questionable improvement only noted in the fibrinogen level. Although hepatic necrosis may be found in fatal cases of varicella the coagulation data suggest that the multiple defects were due to DIC. In addition, the data further suggest that the mechanism by which this virus elicits DIC is different from bacterial sepsis since the DIC was clearly present in the absense of hypotension or shock. Kerosene ingestion, a common cause of accidental poisoning in children, is often followed by serious bacterial pulmonary infection. The effect of kerosene ingestion (10 ml/kg) on pulmonary antibacterial defense mechanisms was studied acutely (4 hr) and subacutely (24 hr) in pretreated mice exposed to an aerosol inocu-lum of radiotracer-tagged (32 P) Staphylococcus aureus. Intrapul-monary bacterial inactivation was determined by quantitating the change in bacterial viability and isotope clearance in the lungs of each animal. Controls inactivated 86.6 ± 1.0% of the inoculum. Kerosene ingestion resulted acutely in a depression of host defenses, with only 59.1 ± 4.5% of the inhaled bacteria cleared. In animals challenged with aerosolized bacteria 24 hours after kerosene ingestion, intrapulmonary bacterial replication exceeded inactivation and bacterial clearance did not return to normal until 96 hours after ingestion. Pulmonary histology, correlated with bacterial clearance, revealed a chemical pneumonitis, with alveolar hemorrhage, bronchial necrosis and pulmonary edema. Aspiration of the ingested kerosene increased the severity of the anatomical and functional alterations. Similar structural and functional responses were demonstrated following ingestion of other toxic agents commonly ingested by children, with acute and subacute inactivation values of 70.5 ± 3.9% and 32.2 ± 11.7% for linseed oil, 46.3 ± 5.6% and 70.4 ± 4.8% for gasoline, 73.4 ± 2.9% and 70.6 ± 5.7% for lighter fluid and 54.3 ± 6.5% and 71.3 ± 3.2% for turpentine. The unusual severity of mycoplasmal pneumonia in children with sickle cell disease.