Membrane of diphtheria lying within a transverse bronchus. Inhaled C. diphtheriae carried in respiratory droplets proliferate at the site of attachment on the mucosa of the nasopharynx, oropharynx, larynx, or trachea. The bacteria also form satellite lesions in the esophagus or lower airways. Release of exotoxin causes necrosis of the epithelium, accompanied by an outpouring of a dense fibrinosuppurative exudate. The coagulation of this exudate on the ulcerated necrotic surface creates a tough, dirty gray to black, superficial membrane, sometimes called pseudo-membrane because it is not formed by viable tissue
Mechanism of action of DT
DT targets an elongation factor-2 (EF-2). ADP-ribosylation prevents EF-2 tRNA-mRNA translocation activity, resulting in inhibition of protein production and host cell death
Whooping cough showing a haze of bacilli entangled with the cilia of bronchial epithelial cells. The inset highlights the haze of bacilli by immunohistochemistry using a monoclonal antibody reactive to the lipooligosaccharide A of Bordetella pertussis
Acute meningitis, microscopic
A neutrophilic exudate involves the meninges on the left, with prominent dilated vessels. Edema and focal inflammation (extending into superficial brain parenchyma through the Virchow-Robin space) are present in the neocortex to the right. This acute meningitis is typical of a bacterial infection. This edema can lead to brain swelling with herniation and death. Resolution of infection may be followed by adhesive arachnoiditis with obliteration of the subarachnoid space leading to obstructive hydrocephalus. Diagnosis is aided by performing lumbar puncture to obtain CSF that typically shows increased leukocytes, mainly neutrophils, decreased glucose, and increased protein. Gram stain, serologies, and culture help identify specific microorganisms.
Acute meningitis, gross
The yellow-tan clouding of the meninges over gyri shown here, which obscures the sulci, is caused by an inflammatory exudate from acute meningitis. This is most often the result of a bacterial (pyogenic) infection. Routes for intracranial infection include hematogenous dissemination (the most common cause), extension from an adjacent paranasal sinus or mastoid air cells, retrograde flow through facial veins into the cavernous sinus, and trauma with direct implantation by a penetrating injury through the skull. Lumbar puncture reveals increased ICP and CSF showing a marked leukocytosis with a preponderance of neutrophils. Patients often have headache, nuchal rigidity, and changes in mental status.
These adrenals have a dark-red to black color from extensive hemorrhage with disseminated intravascular coagulopathy as a consequence of endotoxin release from Neisseria meningitidis organisms causing septicemia. This condition is known as Waterhouse-Friderichsen syndrome and is more likely to complicate infections in children. Infection with N. meningitidis can start initially as a mild pharyngitis but become a florid septicemia with hypotension and shock within hours. Destruction of more than 90% of the adrenal cortex leads to adrenal cortical insufficiency.
Characteristic strawberry (raspberry) tongue, red cheeks and rash of scarlet fever