Manifestations may be local (eg, cellulitis, abscess) or systemic, most often fever (see Biology of Infectious Disease: Fever). Manifestations may develop in multiple organ systems. Severe, generalized infections may have life-threatening manifestations (eg, sepsis, septic shock—see Sepsis and Septic Shock). Most manifestations resolve with successful treatment of the underlying infection.

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Clinical: Most infections increase the pulse rate and body temperature, but others (eg, typhoid fever, tularemia, brucellosis, dengue) may not elevate the pulse rate commensurate with the degree of fever. Hypotension can result from hypovolemia or septic shock. Hyperventilation and respiratory alkalosis are common.

Alterations in sensorium (encephalopathy) may occur in severe infection regardless of whether CNS infection is present. Encephalopathy is most common and serious in the elderly and may cause anxiety, confusion, delirium, stupor, seizures, and coma.

Hematologic: Infectious diseases commonly increase the numbers of mature and immature circulating neutrophils. Mechanisms include demargination and release of immature granulocytes from bone marrow, IL-1- and IL-6-mediated release of neutrophils from bone marrow, and colony-stimulating factors elaborated by macrophages, lymphocytes, and other tissues. Exaggeration of these phenomena (eg, in trauma, inflammation, and similar stresses) can result in release of excessive numbers of immature leukocytes into the circulation (leukemoid reaction), with leukocyte counts up to 25 to 30 × 10⁹/L.

Conversely, some infections (eg, typhoid fever, brucellosis) commonly cause neutropenia. In overwhelming, severe infections, profound neutropenia is often a poor prognostic sign. Characteristic morphologic changes in the neutrophils of septic patients include Döhle bodies, toxic granulations, and vacuolization.

Anemia can develop despite adequate tissue iron stores. If anemia is chronic, plasma iron and total iron-binding capacity may be decreased. Serious infection, particularly with gram-negative organisms, may cause disseminated intravascular coagulation (DIC—see Coagulation Disorders: Disseminated Intravascular Coagulation (DIC)).

Other organ systems: Pulmonary compliance may decrease, progressing to acute respiratory distress syndrome (ARDS) and respiratory muscle failure.

Renal manifestations range from minimal proteinuria to acute renal failure, which can result from shock and acute tubular necrosis, glomerulonephritis, or tubulointerstitial disease.

Hepatic dysfunction, including cholestatic jaundice (often a poor prognostic sign) or hepatocellular dysfunction, occurs with many infections, even though the infection does not localize to the liver. Upper GI bleeding due to stress ulceration may occur during sepsis.

Endocrinologic dysfunctions include increased production of thyroid-stimulating hormone, vasopressin, insulin, and glucagon; breakdown of skeletal muscle proteins and muscle wasting secondary to increased metabolic demands; and bone demineralization. Hypoglycemia occurs infrequently in sepsis, but adrenal insufficiency should be considered in patients with hypoglycemia and sepsis. Hyperglycemia may be an early sign of infection in diabetics.

Last full review/revision October 2012 by Allan R. Tunkel, MD, PhD

Content last modified November 2012