This form of inflammation occurs most often in body cavities and affecting the lungs, pleura, mesenteric fat, pericardium, and viscera. It occurs when inflammatory damage has been done to the vasculature that allows leakage of large proteins, including fibrinogen, into the lesion.
Fibrinogen is the soluble precursor of the fibrillar element of blood, fibrin. Fibrin is normally polymerized into fibrin under the influence of platelets, to form clots. But leakage of fibrinogen into the extravascular spaces causes it to poymerize into the sticky strands of fibrin where it's not supposed to, forming a thickened coating on the affected tissues.
If the inflammation is not resolved quickly, the fibrin strands organize and are replaced with collagenous connective tissue: scarring by fibrosis is the result. This can commonly be seen in cases of bovine foreign body pericarditis (hardware disease).
You're performing a routine inspection of cattle coming to a feedlot outside of Tulsa, Oklahoma. One cattle car that has arrived from coastal Alabama by way of Texas; the train was forced to wait for two days in Galveston when a hurricane blew through.
You have the cattle walked off of the train and you immediately notice that there is something wrong. All of the cattle are slow and awkward as they leave the car. You hear a rough grunting sound when they breathe and many of them are coughing. You immediately have them isolated and detained for closer inspection.
Many of the cattle have crusty, mucopurulent discharge from their noses as well as a pronounced serous discharge from their eyes. One has a temperature of 105 degrees and is experiencing rapid, shallow respiration. This animal occasionally coughs and you can hear lung crackles without your stethoscope.
This is a classic scenario for the presentation and circumstances of "shipping fever." Anytime you encounter coughing, congested, depressed, and febrile cattle or horses that have been transported from one place to another, you can say "shipping fever" and have an excellent chance of being right.
The common causative agent of this disease is bacteria of the genus Pasteurella. The two most common isolates are P. haemolytica and P. multocida, both inhabitants of the upper respiratory tracts of healthy animals. The cattle have succumbed to an opportunistic infection because of the stress of transit. The sudden susceptibility after shipping is the major clue to the diagnosis. P. haemolytica is the more common causative agent of the two; it's associated with coagulative necrosis of the lung parenchyma.
Pasteurellosis has several classic signs: Affected animals are depressed and lethargic. They may be inappetant and off feed. Soon they present with a high fever, occasionally as high as 106 degrees. Nasal discharge comes next: it may be serous but is usually mucopurulent, the typical character of discharges in bacterial infections. Straightforward respiratory symptoms include dyspnea and a mild cough, the latter rapidly become harsher and more severe.
Severe cases may involve pleuritis, a very painful condition that causes grunting and much respiratory discomfort. On auscultation, the lungs will wheeze and crackle. As the infection progresses, the lungs become consolidated and lung sounds become muffled and difficult to discern. This is due to the sounds refracting on the fluid-air interface in the infected lungs.
Acute cases can be treated successfully with antibiotic and fluid therapy. As expected, the prognosis is better the earlier the treatment begins. Some animals harbor subclinical infections and never show signs: these tend to be "poor-doers," failing to thrive and gain weight at the same rate as their herd mates.
This is a section of lung from one of the cattle. The major airways are obtunded with blue staining inflamamtory infiltrate and the alveoli are occluded by a faint pink fibrinous matrix. The vasculature is diffusely congested and hyperRemic, the interstitium is edematous, and there are multiple foci of interstitial and intralveolar hemorrhage.
This field shows why this process is called "fibrinopurulent" inflammation. The pink matix seen within the alveoli and small airways is fibrin, and there's a collection of pus at the left side of the field. Pus has filled small bronchioles as well. As you can imagine, filling the lumina of alveoli with a solid plug of fibrin makes oxygen exchange difficult. The area of pus at left is a small abscess consisting of mixed inflammatory cells and necrotic debris.
Pasteurella infection induces a marked inflammatory response: many neutrophils have been drawn to the lungs. Between the damage caused by the bacterium and the damage caused by the neutrophils, a fair amount of hemorrhage has resulted and throughout the lung there are congested blood vessels where there isn't hemorrhage.
At high magnification the fibrillar nature of the fibrin can more easily be seen. These small individual strands can be made out at the edge of the purulent areas and in the alveoli. Note that in addition to the numerous neutrophils, there's a fair number of macrophages who are coming in to clean up. If this infection is cleared, and the process of resolution begun, these macrophages will eventually clear the fibrin away to restore more or less complete lung function: though if areas have been heavily damaged they'll be replaced by scarring (fibrosis) and non-functional.
In pre-antibiotic days, a diagnosis of bacterial pneumonia that was as bad as this one was often a death sentence: either the body fought it off or it didn't, and if it didn't the animal died from anoxia, drowned in its own pus. Nowadays deaths from pneumonia do happen but they're not so common because intervention with anti-bacterial and anti-inflammatory drugs can help the system heal itself.
These fields are from the lobe of a lung undergoing resolution of fibrinopurulent inflammation. Although there is still congestion in blood vessels that's quite obvious, there isn't any hemorrhage visible, and it's recognizably lung tissue. It's markedly less pathological than the example above. Note also that the load of fibrillar material in the lumina of the alveoli is considerably reduced, thanks to macrophage action.
The later stages of inflammation involve the arrival of macrophages, who are capable of phagocytosing the components of the pus (dead neutrophils and cellular debris) and also the fibrin threads that have formed. In this field the macrophages (arrows) have been busy, and the reduction of fibrin in the alveoli will permit the exchange of gasses much more freely than in the full-blown condition. The small bronchiole at right is also more or less cleared of pus, and the architecture of its lining has been restored.
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