Many poultry farmers see pericarditis, perihepatitis, and three-serositis lesions and immediately assume Escherichia coli, starting antibiotics right away. But after treating an entire batch, they still can’t control the deaths, and losses keep recurring.
The core reason is simple: the same pericarditis and perihepatitis can be caused either by a primary Escherichia coli infection or by a secondary infection in which influenza first damages the immune barrier, allowing Escherichia coli to take advantage. The disease processes, necropsy characteristics, and approaches to medication are completely different. Misdiagnosis is the biggest hidden loss in poultry farming.
This article brings together practical necropsy experience from the front lines. It shows you how to quickly distinguish the two by examining five aspects: odor, exudate, appearance, trachea, and the condition of birds that have died. Avoid detours and unnecessary spending on medication.
One. Odor: the first check when opening the abdominal cavity, and the one least likely to be wrong
The first step in a post-mortem examination is to smell the abdominal cavity. This is a signal that many experienced veterinarians check first.
Influenza with secondary E. coli infection: The abdominal cavity has no odor, or only a faint fishy smell. The influenza virus mainly attacks the respiratory tract and immune organs, first causing the body's immune system to collapse. E. coli is a “secondary invader”; bacterial growth is limited, tissue breakdown is mild, and large amounts of foul-smelling gases such as ammonia and hydrogen sulfide are not produced.
Primary E. coli infection alone: When the cavity is opened, there is a sharp, foul odor that can be smelled even from across the dissection table. Pathogenic E. coli proliferates in large numbers and continuously breaks down abdominal organs and tissues, producing irritating toxic gases through metabolism. A strong odor is a characteristic sign of primary E. coli infection.
In short: A strong odor points first to primary E. coli infection; little to no odor calls for vigilance for a viral infection with a secondary bacterial infection.
II. Compare the nature of the exudates in the three inflammations: pericarditis and perihepatitis look different
Even when both pericarditis and perihepatitis are present, their texture and color differ greatly.
Exudate from secondary E. coli infection following influenza: white or milky-white, curd-like, crumbly caseous material. It is brittle and lacks toughness; it crumbles at a touch and comes away with a gentle scrape. This exudate forms from a mixture of systemic inflammation caused by the virus, large numbers of disintegrating immune cells, and protein leakage, and has a low fibrin content.
Exudate from uncomplicated primary E. coli infection: a yellow or yellowish-white fibrinous membrane that is dense and elastic, highly tough, and not easily broken; when peeled away, it comes off as one intact sheet. Primary E. coli infection produces large amounts of fibrin, which envelops the heart and liver—what is commonly called typical fibrinous polyserositis.
Three. Check the external appearance: facial swelling and tearing are important warning signs
E. coli secondary to influenza: In large flocks, it is often accompanied by swelling of the head and face, tearing, and redness of the conjunctiva; some individual chickens have swelling on one side of the face. The influenza virus directly damages the nasal cavity, eye sockets, and respiratory mucosa. Edema and tearing are characteristic effects of the virus itself.
Primary E. coli infection alone: Facial swelling and tearing are very rare. Primary E. coli mainly attacks the abdominal cavity and intestines and generally does not target the upper respiratory tract or eye tissue. Respiratory abnormalities occur only when it is co-infected with Mycoplasma; E. coli alone generally does not cause facial swelling.
Four. Check lesions inside the trachea to distinguish the source of the respiratory disease
E. coli secondary to influenza: Diffuse bleeding in the trachea, with the entire trachea appearing red. The lumen is often blocked by milky-white, tofu-curd-like caseous plugs. The virus damages blood vessels in the tracheal mucosa, causing extensive bleeding. Inflammatory exudate coagulates rapidly, forming caseous plugs that obstruct the trachea; this is also an important reason these chickens are prone to suffocation and death.
E. coli alone: When it occurs as a single infection, tracheal lesions are very mild, with extensive bleeding rarely seen. Ring-shaped tracheal hemorrhages and sticky, clear mucus inside the trachea are more commonly seen only with a mixed E. coli and Mycoplasma infection; typical white caseous plugs do not form.
Five. Look at the body condition of dead chickens: the speed of the disease is reflected in how thin or well-fleshed the chickens are
Chickens that die from E. coli secondary to influenza: These are mostly medium-sized to larger, robust chickens. Influenza spreads quickly and causes rapid illness. No matter how good a chicken’s immunity is, once the virus invades, illness and death can occur within a short time, before the chicken has had time to lose weight. Losses in the flock can occur suddenly, with robust chickens often dying first.
Chickens that die from primary E. coli infection alone: deaths are mostly due to chronic wasting. The chickens are thin, with prominent keels and dry, dehydrated feet. Primary E. coli disease runs a prolonged course: feed intake continues to decline, and the chickens gradually become thin and debilitated, with intermittent, sporadic deaths occurring at a gradual pace.
Six. Distinguish the cause of disease to keep prevention, control, and medication strategies on track
Influenza with secondary E. coli infection: the root cause is immune damage caused by the virus. Using only antibiotics to kill E. coli treats the symptoms, not the underlying cause, and the condition rebounds as soon as treatment stops. The core of the plan is to control the virus first, repair the respiratory mucosa, and improve the body's resistance, while using sensitive antibiotics to control secondary bacterial infection. At the same time, ensure proper ventilation and manage temperature differences to reduce stress.
Primary E. coli infection alone: the root cause is contamination of the environment, drinking water, or feed lines, or vertical transmission of bacteria from chicks. The core of the plan is to use sensitive antibiotics as the main treatment, prioritizing susceptibility testing to avoid resistance caused by indiscriminate medication; at the same time, clean the water lines and strengthen disinfection to reduce the pathogen load in the environment and cut off the source of transmission.
Final summary
A wrapped, congested intestine ≠ E. coli; it is simply an inflammatory finding. Combining these five checks—smelling for an odor, assessing the consistency of the exudate, checking for facial swelling and watery eyes, examining the pattern of tracheal bleeding, and observing whether dead chickens are thin or fat—can greatly reduce the likelihood of misdiagnosis.
Successful farming is about more than just administering medication; it is about understanding the disease process behind the lesions. Accurate diagnosis ensures medication is used where it is needed, helps keep losses under control, and improves farming returns.