– Dr. Michelle Arnold, DVM, MPH UK Ruminant Extension Veterinarian
Figure 1: Adult cow displaying signs of Acute Respiratory Distress Syndrome (ARDS) due to lungworm larvae migration. Photo courtesy of Thompson Farms.
“Acute Respiratory Distress Syndrome” or “ARDS” is a rapid and dramatic onset of severe breathing difficulty due to lack of oxygen transfer across the air sacs (alveoli) in the lungs to the bloodstream. Affected cattle exhibit open-mouth breathing with the head and neck extended, nostrils dilated, a sway-back appearance, foam coming from the mouth, an open-shouldered stance, and sometimes become aggressive (see Figure 1). Breathing is shallow and rapid (35-75 breaths per minute) and may have a loud grunt associated with exhalation. Temperature is typically normal or mildly elevated depending on severity of the condition. In extreme cases, air pockets can be felt under the skin on the upper portions of the neck, shoulders and back (subcutaneous crepitation). Mild exercise is enough to cause the animal to collapse and die.
Generally, there is no coughing nor signs of infection such as fever or depression. Severely affected animals frequently die within 2-3 days after initial onset of clinical signs.
Figure 2: Lungworm life cycle. Accessed from “COWS – www.cattleparasites.org.uk”
Figure 3: Adult lungworms within the trachea, found on necropsy. Photo Courtesy of UKVDL Photo Archive
There are a variety of “agents” that will directly or indirectly damage the linings of the alveoli and blood vessels in the lungs of cattle, preventing gas exchange and initiating acute respiratory distress. The most common triggers include: 1) 3-methyl indole (3-MI), a toxin produced when cattle are moved from dry to lush pastures containing increased L-tryptophan levels; 2) the ketones from consuming the weed perilla mint; 3) certain respiratory viruses, especially bovine respiratory syncytial virus (BRSV); 4) lungworm infections; and 5) sepsis from bacterial infection. Although most producers recognize the symptoms of respiratory disease in cattle, lungworms are usually left off the list of possible causes. This is because respiratory disease due to lungworms is both uncommon and unpredictable, yet it can be devastating in a herd. Lungworm disease outbreaks are most often seen in grazing calves and yearlings exposed to the parasite for the first time and are therefore completely unprotected. But occasionally outbreaks are seen in adult cattle if their immunity to lungworms has waned from lack of exposure or pasture infectivity is high. The lungworm life cycle (Figure 2) begins when cattle consume infective L3 larvae in the pasture, typically during wet summers or when grazing in swampy areas. After ingestion, larvae penetrate through the intestine, mature to the L4 stage in the mesenteric lymph nodes, then migrate to the lungs and break into the alveoli, all within a week. These larvae continue to migrate to the airways and mature into adult worms inside the bronchi and trachea (Figure 3). From day 26-60 after infection (called the “patent phase”), the mature worms deposit eggs in the airways, where they hatch and the L1 larvae ascend the trachea by causing the animal to cough, called “parasitic bronchitis”. The larvae are then swallowed followed by excretion in the feces. On pasture, the L1 larvae mature to L2 then L3 in the fecal pat, spread to grass and are ingested to begin the cycle anew. The severity and duration of clinical signs depend on the number of larvae and how quickly they are consumed. ARDS develops from a hypersensitivity (allergic reaction) to the larvae migrating through the lungs that causes an overreaction by the immune system that damages the lung tissues. Proteases and enzymes are also released by the larvae that directly damage lung tissue as they travel. Within an affected group of cattle, symptoms of lungworm infection may range from a mild, intermittent cough and weight loss up to severe difficulty breathing and death. Most animals gradually recover although it may take weeks to months. At the cellular level (visible through a microscope), this very distinct pattern of lung injury is called “diffuse alveolar damage” or “DAD” and is the most frequent microscopic finding in animals exhibiting acute respiratory distress. The old name of “Atypical Interstitial Pneumonia” or “AIP” has fallen out of favor due to confusion arising from a similar human disease with the same acronym.
Diagnosis of this type of pneumonia resulting from DAD, known as “interstitial pneumonia”, is easily performed at necropsy because it is a very different pattern from the typical shipping fever pneumonia. “Shipping Fever” or “Bovine Respiratory Disease (BRD)” causes a “bronchopneumonia” that occurs at the junction of the air sacs and the airways leading to them. On postmortem examination, damaged areas of shipping fever lungs are firm, red-tan, and mostly present in the cranioventral lung lobe. With interstitial pneumonia, on the other hand, damage is to the “interstitium” or supporting structures of the lungs including the lining of the air sacs, the lining of the blood vessels and the septa (divisions) between the lung lobes. These structures become filled with fluid and white blood cells, making the lungs feel wet, heavy, and meaty with a firm, rubbery texture and they do not collapse when the chest cavity is opened. The lungs themselves are often emphysematous or over-inflated. The entire lung may be diffusely involved or affected areas are dark red to purple and may be interspersed with normal looking lobules, creating a “patchwork” or “checkerboard” appearance. Cattle often develop secondary bacterial bronchopneumonia after the initial lung injury. Treatment decisions by the veterinarian will depend upon determining the etiology of the clinical signs but, if treatment is attempted, must be handled very cautiously. A dart gun can be used to avoid having to move the animal to a treatment facility as these animals die quickly when exercised. Treatment recommendations typically include diuretics and anti-inflammatory medications to facilitate breathing and antibiotics to prevent secondary bacterial infections.
Figure 4: Ingestion of perilla mint causes acute respiratory distress syndrome as described with fog fever. Animals are frequently found dead with mature cattle most often affected but it can occur in yearlings and calves. Treatment is of limited value and severe cases seldom survive. Photo Courtesy of JD Green
The take-home message to remember is not all pneumonia cases in cattle are truly “shipping fever” that should be treated with antibiotics. As mentioned previously, lung damage can be from ingesting certain toxins such as when grazing cattle are moved from dry to lush pasture and develop “fog fever”, one of the first respiratory diseases known to cause ARDS. Lush pasture contains the amino acid L-tryptophan that can be metabolized by the rumen microbes to 3-methyl indole (3-MI). The 3-MI is absorbed into the bloodstream, transported to the lungs and metabolized to a new compound 3-methyleneindolenine (3MEIN) that causes widespread cellular damage to the lung. Recent studies have questioned the finding that tryptophan levels in pastures associated with fog fever are exceptionally higher than unaffected pastures. Instead, it could be the abrupt change from grazing the poor-quality dry forage to lush pasture that increases the number of rumen microflora capable of metabolizing tryptophan to 3-MI. Brassicas including kale, rape, and green turnip tops are rich sources of tryptophan that can be converted in the rumen to 3-MI and potentially cause ARDS. Cattle mildly affected with fog fever show dramatic improvement within a few days with recovery spanning approximately 10 days. Severely affected animals often die but survivors can have long-term consequences of chronic emphysema or heart failure. Feeding an ionophore such as monensin or lasalocid has been shown to reduce the conversion of tryptophan to 3-MI in the rumen by as much as 90% but the ionophore must be present in the rumen at the time of exposure. Other potential causes of lung damage in animals due to ingested toxins include 4-ipomeanol from consuming Fusarium solani-contaminated moldy sweet potatoes, perilla ketone from grazing the weed purple mint (Perilla frutescens-see Figure 4), ingestion of the herbicide Paraquat, and ingestion of stinkwood (Zieria arborescens). Early involvement with your veterinarian is key to a proper diagnosis and appropriate treatment of any respiratory disorder in cattle. Establish a “daylight relationship” with your veterinarian now so he/she will know who you are when you call with an emergency.