Lesson 28

Pathomorphology of Sepsis. Emerging Infections

Key Points:

  1. Sepsis as a special form of infection. Differences from other infections.
  2. The concept of SIRS, septic shock.
  3. Clinical-anatomical forms of sepsis (septicemia, septicopiemia, septic (infectious) endocarditis): morphological characteristics.
  4. Plague, tularemia, anthrax: pathomorphology of clinical and morphological forms, complications, causes of death.

Myocardial abscesses

The epicardial surface of the heart shows small yellowish microabscesses that may appear in patients with sepsis and who have hematogenous spread of infection. They may also represent emboli from an infective endocarditis in which small portions of cardiac vegetation have embolized into the coronary arteries. Myocarditis caused by other microorganisms can give a similar pattern of focal inflammation with necrosis. Patients with myocarditis can have fever, chest pain, dyspnea from left-sided heart failure, and peripheral edema from right-sided heart failure. Arrhythmias may lead to sudden death.

Hepatic abscesses

Pyogenic abscesses in liver are often bacterial and result from spread of infection to hepatic parenchyma with septicemia through the arterial supply; or abdominal infection through the portal vein. The left panel shows multiple microabscesses in a patient with septicemia. The right panel shows a microabscess containing numerous neutrophils producing focal liquefactive necrosis, along with the beginning of an organizing abscess wall with some pink fibrin.

Apostematous pyelonephritis

The cut surface of this swollen kidney reveals many small yellowish microabscesses (apostemes) involving cortex and medulla. This pattern of acute pyelonephritis is most typical of hematogenous dissemination of infection to the kidney in patients with septicemia.

Infectious arteritis

Parenchymal tissue infection can spread to vessels, as with pneumonia. Septicemia and septic emboli, as from endocarditis, may also lead to this complication. The infection is typically bacterial or fungal, such as Staphylococcus aureus or Aspergillus species. The infection can weaken or destroy the vascular wall and lead to aneurysm formation or hemorrhage. An aneurysm formed in such a manner is known as a mycotic aneurysm. The bacterial infection involving the muscular artery shown here is leading to necrosis, marked by an irregular luminal outline, along with inflammation and hemorrhage of the media and adventitia.

Cerebral abscess

This coronal section through the superior parietal lobe shows a focal lesion with a liquefactive center containing yellow pus and surrounding thin wall. Cerebral abscesses usually result from hematogenous spread of a bacterial infection, typically from infective endocarditis or from pneumonia, but may also occur from direct penetrating trauma or extension from adjacent infection in paranasal sinuses or mastoid. Patients may have a fever along with focal but progressive neurologic deficits. The mass effect with surrounding edema can increase the ICP, with risk for herniation.

Cerebral abscess

The acute inflammatory cells in the abscess are at the right, with adjacent cerebral cortex at the left. Note the prominent small artery with thickened wall and dilated lumen, which imparts the ring enhancement visible with radiologic scans.

Petechiae

The multiple small nodular red hemorrhages seen here on the hand (Janeway lesions) resulted from peripheral embolization of fragments of a left-sided valvular vegetation in a patient with infective endocarditis. The irregular reddish purple mottled areas of skin represent livedo reticularis from ischemia after embolization to mediumsized arteries. The smaller pinpoint hemorrhages can be termed petechiae and represent bleeding from small vessels. Petechial hemorrhages are classically found when a coagulopathy is caused by a low platelet count. They can also appear after sudden hypoxia.

Infective endocarditis

The aortic valve shows a large, irregular, reddish tan vegetation. Virulent organisms, such as Staphylococcus aureus, produce an acute bacterial endocarditis within days, similar to the lesion shown here, whereas some organisms, such as the viridans group of Streptococcus, produce a more slowly developing subacute bacterial endocarditis. Endocarditis is marked by fever with heart murmur. Predisposing risks for endocarditis include bacteremia and previously damaged or deformed valves, but endocarditis can involve anatomically normal valves.

Infective endocarditis

The more virulent bacteria causing the acute bacterial form of infective endocarditis can lead to serious valvular destruction, as shown here involving the aortic valve. Irregular reddish tan vegetations overlie valve cusps that are being destroyed by the action of the proliferating bacteria. Portions of the vegetation can break off and become septic emboli that travel to other organs, leading to foci of infarction or infection.

Infective endocarditis

The valve leaflet in the left panel has friable vegetations composed of fibrin and platelets (pink) mixed with inflammatory cells and bacterial colonies (blue). The friability explains how portions of the vegetation can break off and embolize. In the right panel a septic embolus fills the lumen of a small artery showing inflammation and necrosis. Left-sided endocarditis can be complicated by embolization to the systemic circulation, whereas right-sided embolization affects the lungs. Cardiac valves are relatively avascular, so high-dose, prolonged antibiotic therapy is needed to eradicate the infection.

Mycotic aneurysm

Septic embolization from infective endocarditis spreads the infection to other parts of the body. Left-sided valvular lesions shower emboli to the systemic circulation, and embolic lesions can subsequently lodge in organs such as the brain, spleen, and kidneys. Shown here is an embolic infarct involving a cerebral hemisphere in the left panel, which microscopically shows features of a mycotic aneurysm in the right panel, with destruction of an arterial wall by the blue bacterial colonies.