Circulating and storage neutrophil changes in experimental type II group B streptococcal sepsis

Abstract

The availibility of neutrophils is an important factor in host resistance to bacterial infection. Therefore, circulating and storage neutrophil quantification was carried out on groups of neonatal rats intranasally inoculated with type II group B streptococci. The dose of type II group B streptococci used produced 56% mortality in 48 neonatal rats with death being due to pneumonia and sepsis. Neutropenia (1300 ± 150/mm3 versus 2300 ± 170/mm3; mean ± S.D.; P < 0.01) and an elevation in band/polymorphonuclear ratio (0.98 ± 0.04 versus 0.30 ± 0.04; P < 0.01) were observed in infected neonatal rats 24 hr following inoculation. Femoral marrow as well as splenic and hepatic neutrophil storage compartment quantification revealed dimunition of postmitotic (polymorphonuclear, band, and metamyelocyte) neutrophils in the infected group (P < 0.01) with sparing of the proliferative neutrophils (myeloblasts, promyelocytes, and myelocytes). Repletion of the myeloid but not the splenic or hepatic neutrophil storage compartments with normalization of the neutrophil count and band/polymorphonuclear ratio occurred in animals surviving 72 hr. These studies establish that neutropenia and neutrophil storage pool depletion are prominent features of experimental type II group B streptococci infection in neonates. Speculation: Although neutrophil storage pool depletion is rare in infected adult animals or humans, its presence can be correlated with an increased mortality. It appears that neutrophil storage pool depletion is a prominent feature of experimental neonatal type II group B streptococci infection. The resulting deficiency of phagocytic cell supply probably represents diminution in the already compromised host defense mechanism of the neonate. Thus, it is postulated that neutrophil storage pool depletion represents a pathophysiologic factor contributing to the high mortality rate observed in neonatal type II group B streptococci infection. © 1980 International Pediatric Research Foundation, Inc.