Manifestations of infection may be local (eg, cellulitis, abscess) or systemic (most often fever). Manifestations may develop in multiple organ systems. Severe, generalized infections may have life-threatening manifestations (eg, sepsis and septic shock). Most manifestations resolve with successful treatment of the underlying infection.
Clinical manifestations
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 (relative bradycardia). Hypotension can result from hypovolemia, septic shock, or toxic shock. Hyperventilation and respiratory alkalosis are common.
Alterations in sensorium (encephalopathy) may occur in severe infection regardless of whether central nervous system infection is present. Encephalopathy is most common and serious in older adults and may cause anxiety, confusion, delirium, stupor, seizures, and coma.
Hematologic manifestations
Infectious diseases commonly increase the numbers of mature and immature circulating neutrophils. Mechanisms include demargination and release of immature granulocytes from bone marrow, interleukin-1–mediated and interleukin-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 25,000 to 30,000/mcL (25 to 30 × 109/L).
Conversely, some infections (eg, typhoid fever, brucellosis) commonly cause leukopenia. In overwhelming, severe infections, profound leukopenia 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, it is a normochromic, normocytic anemia characterized by low serum iron, low total iron-binding capacity, and normal to increased serum ferritin.
Serious infection may cause thrombocytopenia and disseminated intravascular coagulation (DIC).
Other organ systems
Pulmonary compliance may decrease, progressing to acute respiratory distress syndrome (ARDS) and respiratory muscle failure (1).
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.
Gastrointestinal (GI) manifestations include upper GI bleeding due to stress ulceration that 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
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 patients with diabetes.
Reference
1. Bos LDJ, Ware LB. Acute respiratory distress syndrome: causes, pathophysiology, and phenotypes. Lancet. 2022;400(10358):1145-1156. doi:10.1016/S0140-6736(22)01485-4
