Infectious diseases commonly invoke leukocytosis, with an increased number of neutrophils and immature circulating neutrophils. The sustained neutrophilia that accompanies chronic infections appears to be mediated by colony-stimulating factors elaborated by macrophages, lymphocytes, and other tissues. Exaggeration of these phenomena can result in leukemoid reactions, with release of immature leukocytes into the circulation. In overwhelming, severe infections, the bone marrow may be incapable of keeping up with peripheral use of neutrophils, leading to a profound neutropenia, often a poor prognostic sign. Eosinophilia suggests a nonbacterial cause, usually allergy or parasitic infection.
Anemia develops despite adequate iron stores.
Tumor necrosis factor may play an integral role in promoting DIC by inducing endothelial cells to express tissue factor procoagulant activity. Isolated thrombocytopenia may also signal bacterial sepsis and may be useful in observing the patient's response to therapy. Cardiac manifestations of infection range from tachycardia and increased cardiac output to failing myocardial function. While most infections increase the pulse rate, others, such as typhoid fever, tularemia, brucellosis, and dengue, may not elevate the pulse rate as one would expect with the degree of fever shown. Respiratory manifestations include hyperventilation, commonly with a marked respiratory alkalosis.