Purulent inflammation is a term applied to acute inflammatory responses that evolve a large amount of pus. This occurs when the agent inducing the inflammation is particularly irritating and induces a powerful chemotactic signal for neutrophils.

When neutrophils swarm to the defense of the body they have the ability to inadvertently cause a great deal of "collateral damage." Pus is a fluid consisting of a liquid phase, containing leukocytes and the debris of dead cells and tissue elements. These materials are liqufied by the lytic action of proteolytic and histolytic enzymes liberated when neutrophils die and lose them into the external environment. The terms "suppurative" and "purulent" denote the production of pus; it's common to speak of a "suppurative lesion," i.e., one oozing pus. And yes, this is a variation on the theme of liquefactive necrosis.

There's a subtle difference between a "region of purulent inflammation" and an "abscess," in that the regional accumulation of pus is more diffuse and not isolated to a certain site, nor encapsulated by CT. If pus becomes walled-off by granulation tissue or fibrous tissue, we use the term "abscess." If a hollow viscus fills with pus, this is called an empyema, for example, empyema of the gall bladder or of the appendix.

Purulent inflammatory lesions can be difficult to resolve and can quickly lead to complications, such as fibrous scarring or (if this involves the peritoneum) adhesions.

You are inspecting livestock one Spring at a large feedlot operation when one of the hands calls your attention to twelve steers. The steers are all about a year old, and from a group that arrived from a stocker operation just one week before.

The steers appear listless and depressed. Half of them show ataxia, tremors, knuckling and stumbling. Three of the most affected are severely depressed and their eyelids are drooping. These steers appear to be all but asleep on their feet. Of the steers that do not show ataxia, all are experiencing dyspnea and three have conjunctivitis. You condemn the cattle and isolate them for further examination.

All twelve have a very high fever, two reaching higher that 107 degrees. In the isolation lot one collapses and remains recumbent. Three others fall and have great difficulty standing again. You draw blood from one of the ataxic steers and from one of the steers with respiratory signs. The recumbent steer is all but unconscious, a serous discharge dribbling from its nostrils. You decide to euthanize this steer and take samples for necropsy and bacterial culture. The condition of the steers does not improve over the next six hours and they're all condemned.


When the cultures come back they confirm your diagnosis: you're faced with an outbreak of Haemophilus somnus infection. H. somnus is a gram-negative, spore forming coccobacillus that typically affects cattle on feedlots. A feedlot is a far cry from the pastures of the typical beef cattle operation. These animals are under severe stress: and they're encountering cattle from other operations.

Stressed animals are immunocompromised, often to the point where they can't deal with the onslaught of foreign organisms carried by the other cattle. This infection scenario isn't unique to H. somnus infection; many diseases, (particularly Pasteurella, colloquially called "shipping fever") are encountered in cattle in this situation.

Haemophilus is true to its name: it "loves blood." That is, it loves the endothelium (where it replicates) and it loves the bloodstream (where it migrates). Exactly how H. somnus gets to the bloodstream is a matter of some conjecture; it's known that the bacterium can gain entry through mucous membranes and the lungs, but the exact pathogenesis is not well understood. A typical scenario would be aerosol infection through the lungs or mucosal infection from naso-genital contact. A feedlot is just about as ideal an environment for this sort of transmission as could be imagined.

H. somnus can cause an impressive array of lesions in the affected animal. Clinical signs can include high fever, mastitis, abortion, retinal necrosis, pneumonia, myocarditis, convulsions, paralysis, and death. This makes for a difficult diagnosis, especially if the signs are vague and mild. The two more commonly encountered syndromes associated with the organism are pneumonia and thrombotic meningoencephalitis (TME).

Pneumonia is a result of the organism's entry via the lungs. An example of a lung from a necropsy specimen is shown above left. H. somnus adheres to the pulmonary parenchyma, causing a diffuse inflammatory response and subsequent necrosis. This is pretty evident in the photo above. An inflamed meningeal covering is shown at right: this is due to coccidial infection. You can see the hemorrhagic areas quite easily.

TME is a common result when the animal becomes bacteremic. The organism adheres to the endothelium which causes contraction, exposure of the basement membrane, acute vasculitis, and thrombic embolism of small venules. The brain, retinas, and kidneys are exquisitely sensitive to this kind of insult, and neural, visual, and metabolic deficits are the result. Cattle affected to the point of TME become depressed and lethargic; ataxia and high fever are typical as well. Severe cases are somnolent, hence the organism's name. Paralysis and opisthotonus occur as the brain is more severely affected. Death can occur within hours of the onset of signs or the animal may linger. Once the disease has progressed to TME, treatment is not often successful. Humane slaughter is typically the best option for the animal and for the producer.


The steers in this case received their initial infections via the respiratory portal, and thanks to stress, it quickly became systemically distributed: it moved from the respiratory form to the CNS form, a shower of septic debris has created numerous microabscesses in the cerebrum.

First, of course, in order to reach the brain proper, the bacteria had to travel via the blood vessels of the meninges. Thus a suppurative meningitis will be caused by this infection before it actually reaches the interior space of the brain.

Here you see it in the meningeal covering of the cerebrum. The meningeal spaces are filled with neutrophils and inflammatory fluid, seen as a dense infiltrate of blue-staining cells. Blood vessels are extensively dilated and very congested, and there's a reactive zone in the cortex itself. The inflammation proper appears to be contained entirely within the meninges, so this is "meningitis"; once it's extended to include the substance of the cerebrum, it's termed "meningoencephalitis."

There's a mixed population of inflammatory cells within this exudate. Some lymphocytes are present (not marked) and there are neutrophils (N) and macrophages (M) as well. Notice the weblike, eosinophilic fibrin within the subarachnoid space. Fibrin is a component of all inflammatory processes; here it's present in mild to moderate amounts. A small amount of hemorrhage is present as well.


Assuming the infection continues to be present, sooner or later the bacteria will get past the meninges and the blood-brain barrier. Here's a field in which you can see several areas of necrosis, where escape from the blood vessels has led to bacterial colonization and consequent attack by the immune system. The bacteria in this field have formed what amount to bacterial colonies, in the brain tissue, leading to abscesses. Abcesses are essentially localized foci of purulent inflammation, septic pockets of dead neutrophils and fluid sequestered within the infected tissue. An abscess forms when a pyogenic stimulus invades a tissue and can't be eliminated quickly.

(The vigorous neutrophil response actually serves to protect the infecting agents, particularly if they're resistant to phagocytosis. By crowding the site of infection with dead neutrophils, the bacteria make it more difficult for new neutrophils or macrophages to actually reach them. What results is a sustained infection with an ongoing signal for ever more neutrophils to gather. The recruited neutrophils pile up around the source of the signal: et voila, an abscess forms.)

In addition to abscess formation in situ in brain tissue, the presence of bacteria in the blood may lead to the development of clots (emboli) of bacteria and reacting inflammatory cells, as the body desperately tries to deal with a generalized infection. These septic emboli (below) are very bad news, indeed.

Septic emboli continue to seed the brain with bacteria, neutrophils, and necrotic debris. They cause disruption of the blood brain barrier, triggering more necrosis of cerebral tissue, and more attempts by the immune system to deal with the infection by sending in more neutrophils. The oxidative activity of the neutrophils, since the blood-brain barrier is breached, affects the animal's own neural tissue causing further tissue injury. This "collateral damage" is one of the most dangerous aspects of brain infections.

It gets worse. Another dangerous aspect of brain infections is the possibility of an abscess creating a space-occupying lesion that can compress brain tissue. A growing abscess can quickly impinge on the integrity of the surrounding tissue, triggering severe neurological signs and worse, more necrosis from compression. And...septic emboli cause localized ischemia and that adds fuel to the fire, so to speak: oxygen-deprived tissue isn't capable of maintaining itself and dealing with the damage from the inflammation.

These images make it easier to understand the gross appearance, and the nature of the symptoms of this condition. Inflammation of the meninges and the brain is a very serious situation, because the destruction and damage wrought by the inflammatory cells impairs the normal homeostasis: neural tissue is a very delicate type, and fiddling with things like temperature, pH, osmotic balance, and ionic composition of brain fluid (not to mention destruction of the blood-brain barrier and the invasion of the interior space by lytic enzymes) is bound to have grave consequences. Thombotic meningoencephalitis is usually fatal.

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