RESPIRATORY DISEASES OF CATTLE

Lecturer: Dr. Don Montgomery

(Note: the links on this page are for interest.  You will NOT be tested on the linked material - DO'T)

In cattle from about six weeks of age up to two years, respiratory diseases are the major causes of illness and death (= morbidity and mortality, respectively). General anatomical considerations, the primary and ancillary functions of the respiratory system, defense mechanisms, and symptoms of respiratory diseases were covered in the last lecture. In contrast to the horse, there are anatomical differences in cattle that deserve mentioning.

First, compared to the horse, cattle have relatively small lung capacity for their body size. Cattle are like Iowans - capable of strenuous physical activity, but only in relatively short bursts. Another deleterious consequence of this is that cattle have little functional reserve, so lung disease can seriously compromise function. At odds with this is the finding that with some types of pneumonia as much as 70-80% of the lung is affected. Cattle compensate for the presence of extensive lung disease by decreasing physical activity. If, however, the affected animals are forced to move or exert themselves, death can follow. Although applicable to all species, this is a major reason why cattle with respiratory disease should be handled deliberately and carefully, with as little stress and exertion as possible.

Second, compared to the horse, the lung of cattle is divided into distinct lobes and lobules. Lobation may help isolate diseases such as bacterial pneumonia to more anterior and ventral lobes.  With some respiratory pathogens, the benefit derived from this is easily overcome.

Third, individual lung lobes are further subdivided into distinct lobules by connective tissue septae. This also potentially isolates pneumonic processes to individual lobules but the caveats of highly virulent organisms apply here as well.  Lobulation does not allow for appreciable collateral ventilation. Another unwanted effect is that the interlobular septae, along with their associated lymphatic vessels, may serve as a conduit to spread some infections in the lung.

As with any of the various species, diseases of the respiratory system can have various etiologies. In contract to the previous lecture on horses where diseases were discussed along anatomical lines, this lecture focuses more on the various causes of respiratory disease in cattle. 

CONGENITAL ANOMALIES

Congenital abnormalities in the development of tissues and organs occur prior to birth. Congenital anomaly is not synonymous with hereditary disease. Some anomalies are hereditary but this is not always the case. Relatively few examples of anomalous tissue or organ development affect the respiratory system; one that may be encountered in all species is cleft palate.

Cleft palate (palatoschisis)

Cleft palate is failure of closure of hard or hard plus soft palates in the roof of the mouth. Defective closure results in communication between oral and nasal cavities. This defect may occur alone or in combination with cleft lip (= cheiloschisis). The cause is often undetermined. In thoroughbred horses, approximately 4% of the congenital anomalies involve a cleft palate; the cause is unknown. In Hereford cattle, palatoschisis may have simple autosomal recessive inheritance. In Charolais cattle, simple autosomal inheritance is suspected. Cleft palate in Charolais calves frequently occurs with arthrogryposis (severely contracted limbs at birth). Cases have also occurred in cattle grazing certain species of lupine plants from 40 - 70 days of gestation. The disorder is uncommon in lambs but when it occurs it may have a hereditary basis. Cases have also been observed with ingestion of the toxic plant Veratrum californicum. This plant is teratogenic (= capable of causing birth defects) and can be associated with cyclopean malformations (= one eye in the center of the face). In pigs, cleft palate may be hereditary (not proven) or be associated with ingestion of plants such as poison hemlock, tree tobacco, and feeds contaminated with Crotalaria seeds. Animals with cleft palate are usually born alive.  Many die of aspiration pneumonia since they inhale food into their lungs due to lack of partition between their mouth and nose.

TRAUMATIC INJURY

Traumatic injury can occur to any of the tissues of the respiratory system. One that is avoidable is traumatic injury to the pharyngeal recess in cattle and small ruminants.

Traumatic pharyngitis

The pharyngeal recesses occur to the left and right sides of the larynx and epiglottis. Injuries occur most commonly with balling or drench guns used by inexperienced or poorly trained operators who violently insert the instrument deep into the oral cavity and penetrate the pharynx. The photo in the PPT lecture is a classic example of this sort of injury. Because the operator usually performs the procedure repetitively, it is common to see multiple animals affected. Clinical signs include pain (difficult to evaluate in many animals) and swelling, usually unilateral in the ventrolateral anterior neck. The swelling may gravitate as far as the thoracic inlet. The swelling is due to a mixed bacterial infection along with reaction to whatever material was introduced by the penetrating injury.  These tend to be dirty wounds since they are contaminated by a mixture of bacteria.  It can be hard to salvage animals with antibiotics.

Pneumothorax

Trauma with perforation of the thoracic wall occasionally occurs in cattle and sheep.   In the normal thoracic cavity, the lungs are helped stay inflated by negative pressure in the pleural sacs, which surround the lungs.  When the thorax or diaphragm is perforated, negative pressure is lost and one or both lungs collapse.  Affected animals are in considerable pain and have respiratory distress.  You should suspect pneumothorax if you see a deep wound in the chest wall and the animal is showing pain with each breath.  The major complication is infection entering and resulting in inflammation of the pleural sac (= pleuritis).  If an animal if found gored or with some other perforating wound in the thorax, the best option may be emergency slaughter.

Perforating wound in muscles between ribs (through intercostal muscles) following a goring, resulting in pneumothorax and death.   You are looking at it from the inside of the chest. This can occur in horned animals after they are mixed and they fight to establish social hierarchy. WSVL 09N1111

IRRITANT / ALLERGIC / TOXIC INJURY

Multiple different disorders will be covered under this heading. Although a specific cause may be alluded to for some of the diseases, in some cases it is conjectural.

Allergic rhinitis (‘nasal granuloma’)

This disorder of cattle and sheep is thought to be due to inhaled allergens (pollen or fungal spores).  There may be a familial predisposition in certain breeds or bloodlines. The most common occurrence is in summer and many animals in a herd or flock may be affected. Clinical signs include sneezing, itchy-runny eyes, and nasal discharge (can you see similarities with ‘hay’ fever in humans?). Nasal granuloma is considered a chronic form of allergic rhinitis.

Necrotic laryngitis (calf diphtheria) and laryngeal contact (or 'kissing') ulcers

Necrotic laryngitis ("calf diphtheria") is common in feedlots.  It also occurs in cow-calf operations.  As the name suggests, it occurs predominantly in calves, usually >3 months old.  Diphtheria is derived from the Greek word for leather, due to the type of exudate that forms.  In truth. the pus that forms in affected cattle is more like curds.  You have probably heard the term diphtheria, due to an unrelated bacterial disease in children. Both diseases have in common their occurrence in upper respiratory tract, formation of a tenacious exudate that bleeds when removed, and a capacity to suffocate the hapless child or calf.   The cause of bovine necrotic laryngitis is the bacterium Fusobacterium necrophorum.  This organism is a normal inhabitant of the gut and is widely distributed in the environment around cattle.  The same agent is responsible for a common form of liver abscesses in older cattle, and for bovine footrot.  How it becomes established to cause or exacerbate laryngeal ulcers is unclear.  A clue may be that it tends to occur in dirty crowded conditions, often in feedlots after animals are on feed for >30 days.  One cause is thought to be chronic irritation from dusty environments or allergens, complicated by persistent vocalization, resulting in traumatic injury ('kissing ulcers') in vocal folds.   Low grade infections by some infectious agents of BRD (see below) may play a role.   Many calves with calf diphtheria have additional lesions in cheek, tongue, pharynx and trachea.  In crowded conditions, calves can spread infection via feed buckets.

Calf diphtheria.  The larynx has been opened dorsally, exposing its lateral walls and floor.  Note cheese-like material (white arrows) on vocal folds of the larynx.  Fusobacterium necrophorum can be cultured from these lesions.  Such lesions account for a) the characteristic guttural sound as the calf breaths and b) the distinctive bad smell.  This exudate can fill the lumen of the larynx and suffocate the calf. Noah image F01700 Dr. Don McGavin

Affected calves have difficulty breathing due to constriction of the larynx - the result is an audible sound as the calf breaths, open mouth breathing, and distinct halitosis.  Calves have a fever and are depressed. Pain while trying to swallow is common.  Calves may die due to obstruction of the larynx, and/or due to inhalation pneumonia.  If they recover, they may have abnormal breathing sounds and a dry cough due to chronic laryngeal injury.  

Tracheal edema syndrome (‘honkers’)

This is another disorder of feedlot cattle. Tracheal edema syndrome can occur in two forms, an acute syndrome that can lead to acute or sudden death, and a more chronic syndrome. The acute syndrome is covered at the end of the ‘Sudden Death’ lecture. You will be responsible for knowing the little bit of information given here. The acute syndrome occurs in the latter part of the feeding period in ‘fat’ cattle. The cause is unknown. The incidence is somewhat seasonal. Clinical signs, if observed, include open-mouth breathing, extension of the head and neck, cyanosis, rapid recumbency and death. Lesions are marked edema and hemorrhage distending the soft tissues of the dorsal part of the trachea. The trachea may rupture with extensive hemorrhage and accumulation of blood clots in the tracheal lumen.

The chronic form of tracheal edema occurs in lightweight feedlot calves. The syndrome is less seasonal than the acute form. The cause is unknown. The major clinical symptom is a persistent, continuous dry hacking cough. The lesions are similar to the acute form but often less dramatic with edema distending the dorsal tracheal soft tissue. Hemorrhage can occur due to labored forceful respiration.

‘Atypical’ interstitial pneumonia (AIP)

Atypical interstitial pneumonia is not an appropriate term for this disease but is in common usage. Synonyms include ‘acute bovine edema and emphysema’ and ‘fog fever’. A more descriptive and appropriate moniker fwould be ‘bovine exudative and proliferative interstitial pneumonia’, but it may be a while before that catches on! Various causes are recognized.  In Wyoming the most common cause is grazing on lush forages high in the amino acid tryptophan, resulting in toxic lung damage. The disorder occurs when cattle are abruptly moved from sparse dry summer pastures to lush irrigated pastures in the fall. AIP commonly occurs as a herd outbreak with as many as 50% of cattle showing acute onset of respiratory distress. Outbreaks typically occur during the first 2 weeks of a pasture change, generally during the first few days. Clinical signs are rapid, labored respiration with head extended and held low. Adults are more susceptible than yearlings. Death occurs at any time during the course of clinical illness. Pathogenesis (mechanism): See PPT lecture. During the acute phase, lesions consists of alveolar septal thickening and a massive outpouring of fibrin-rich proteinaceous fluid into alveolar spaces with formation of hyaline alveolar membranes mixed with few leukocytes (white blood cells). At about three days, proliferation of the epithelial cells (pneumocyte proliferation) lining alveoli commences and at this stage, there may be a mix of hyalin membranes and pneumocyte proliferation. As the lesions progress, pneumocyte proliferation dominates. During these stages, gross lesions include failure of the lungs to collapse when the chest cavity is opened; the lungs have a meaty texture, and edema and/or emphysema (gas bubbles) distend interlobular septae. Treatment regimens vary. Handle and move cattle only if necessary. Excessive movement will precipitate additional death loss. If cattle are moved to another pasture, do it slowly and with little stress. Give access to good quality free-choice hay. Various medical treatments have been used with little evidence of effectiveness. Flunixin meglumine (Flunixamine®), a non-steroidal anti-inflammatory drug, given intravenously has achieved some success. Preventive measures: See PPT lecture.

As an aside, the sort of emphysema we see in AIP is sometimes found at necropsy in adult cows that are found dead in the spring.  If you open an animal and find these changes (see picture) it may represent terminal (agonal) change and/or be associated with hypomagnesemic tetany.  

One of several cattle were found acutely dead in April 2008.   All animals were in good condition and the most consistent change seen at necropsy was emphysema (gas bubbles in tissue; the blue vein-like lines in picture) in the lungs.  The cause was tetany.  These changes are characteristic of, but not diagnostic for, tetany. Dr. Marshall Kohr, Gillette, WY

THE BOVINE RESPIRATORY DISEASE (BRD) COMPLEX

“Complex” is an appropriate term. BRD is a complex multifactoral disease process, with inter-related variables, that eventually leads to bacterial pneumonia and high morbidity and appreciable mortality in the cattle industry across diverse production systems. The complicated chart shown in the classroom presentation illustrates the interactions of these variables. Some apply mainly to the feedlot situation, but many are applicable to other production systems.   Below is a cartoon showing the various pre-weaning and post-weaning factors that can increase or decrease the risk of BRD in cattle in beef cattle (from J Anim Sci 2007. 85:823-840)

Pre- and post-weaning factors affecting bovine respiratory disease (BRD) in beef cattle and resulting outcomes of the disease. + = i incidence or consequence; – = h increased incidence or consequence; ? = effects not fully understood based on the available data. BVD = bovine viral diarrhea virus.  Source: J. Anim Sci. 2007. 85:823-840

Classical pasteurellosis in lung of a steer.  The white-yellow material on the surface of the lung is fibrin - pleuritis is common in pasteurellosis, and probably accounts for much of the pain affected animals exhibit.

The Role of Viruses in BRD

Viral infections are an important, but not the sole, component of the BRD complex. Some viruses are capable of causing mild or subclinical infection.  They are important since, as in people with influenza, they predispose animals to secondary bacterial infections. Other viruses are capable of causing severe clinical illness and death.  This capacity depends in large part on the immune status of the animal. Clinical signs of disease, lesions, and vaccination will be covered in the classroom lectures.

• Parainfluenza 3 virus (PI-3): PI-3 is an RNA virus in the paramyxovirus family. Infection is common in cattle throughout the world.  Clinical disease is usually mild or subclinical. The virus, however, predisposes to bacterial pneumonia by infecting epithelial cells lining the respiratory tract.

• Respiratory syncytial virus (BRSV): BRSV is an RNA virus in the paramyxovirus family. Infection is common but overt clinical disease and death are not. Much is unknown concerning the role of this virus in BRD and there seems to be variability in different geographic regions and different production systems. In some cases, BRSV infection alone is sufficient to cause outbreaks of severe respiratory disease and death in individual animals. The virus can infected and kill epithelial cells lining airways. At the same time and in the process of killing epithelial cells, the virus has a fusion protein that, when expressed on the surface of the infected cells, causes fusion and formation of multinucleated ‘syncytial’ cells. Similar lesions, generally milder, can be seen with PI-3 virus.

• Infectious bovine rhinotracheitis (IBR, bovine herpesvirus 1, BHV-1): BHV-1 is a DNA virus in the alphaherpesvirus family. Herpesviruses in this family can also cause genital infections in breeding cattle (infectious pustular vulvovaginitis, balanoposthitis), abortion, keratoconjunctivitis, and encephalitis. It is unusual to see these manifestations of bovine herpesvirus infections all at one time. It is likely that strains of this virus that are more likely to infect some tissues and not others. IBR can cause a fatal rhinitis, pharyngitis, laryngitis, and tracheitis alone.  A bacterial pneumonia is at least contributory in most cases.

• The role of other viruses in the BRD complex is not fully understood but, at least with some such as bovine virus diarrhea virus, there seems to be at least a contributory or complimentary effect. With other viruses, a specific contribution is unknown at this time (coronavirus) or disease manifestations are rare (adenovirus). These unknowns may not prevent some vaccine manufacturers from eventually including the viruses in their products.

The Role of Bacteria in BRD   

Bacterial infection of the lung, leading to pneumonia, is the ultimate cause of death in the majority of cases. Bacterial pathogens cultured from cases of fatal pneumonia include Mannheimia haemolytica, Pasteurella multocida, Histophilus somni, and Arcanobacter pyogenes.

• Mannheimia haemolytica: This is a Gram-negative bacillus that can inhabit of the nasal passages of healthy cattle.  Under conditions of stress, the bacterium can go into the lower airways and cause a virulent, fulminant pneumonia with deaths commonly occurring from 2-3 or up to 7 or 8 days following onset depending on timing and efficacy of treatment and level of immunity. M. haemolytica produces a potent toxin that affects neutrophils and macrophages.

• Pasteurella multocida: This is also a Gram-negative bacillus that is a normal inhabitant of the nasal passages. The pneumonia caused by P. multocida is typically less fulminant than that induced by M. haemolytica. During the initial stages of the pneumonia, it is difficult to detect these calves as clinically ill. By the time treatment is started, the pneumonia is commonly advanced and most feedlot calves dying from P. multocida pneumonia are in the chronic stages. This organism can also be associated with joint infections (septic arthritis).

• Histophilus somni (old name still used on most vaccines: Haemophilus somnus). This is a Gram-negative bacterium. It is a normal inhabitant of the nasal passages and lower urogenital tract in cattle. It can cause either an acute fulminant pneumonia resembling M. haemolytica or more chronic pneumonia similar to P. multocida. Commonly, there are features of both when the lesions are examined. H. somnus can cause a severe myocarditis (inflammation of the heart; see Sudden Death & ‘Feedlot’ lectures), encephalitis (see Sudden Death & ‘Feedlot’ lectures), as well as genital and joint infections.  We occasionally see it as a cause of abortion in cattle.  One of us (DO'T) is doing a study of the cardiac form of the disease with a student who took this class last year.

• Arcanobacter pyogenes: This is a Gram-positive coccobacillus or bacillus. This bacterium is commonly a ‘late’ lung pathogen occurring in mixed infections with other bacteria during the later stages of pneumonia. Arcanobacter causes extensive liquifactive necrosis and abscesses (nasty looking, smelly lung).

• Mycoplasma spp.: The role of Mycoplasmas in BRD is still debated. If you believe some individuals, it is a major pathogen; others assign it a minor role. There is evidence that more pathogenic species such as M. bovis may be contributory, often as late secondary invaders. This confusion is due in part to the fact that mycoplasmas are prominent in some parts of the country and certain production systems, and not in others. Additionally, studies of M. bovis in pneumonic lesions have attributed some lesions to this organism that are also commonly seen in pneumonias caused by other pathogens (P. multocida, Hemophilus somnus). Additionally, specific immunohistochemical staining for this organism is evident in areas of the lung with as well as without pneumonia leading some pathologists to question its role in the disease process. Mycoplasmas can also be cultured, or identified by other means, in lungs with no evidence of pneumonia. The role for Mycoplasmas is better documented as a cause of chronic infection of joints and tendons and in some genital infections and abortions.

Other considerations:

• It is common to see mixed bacterial infections in fatal cases of BRD. When this occurs, all bets are off when trying to incriminate a specific cause based on gross observations.

• A severe fibrinous pleuritis (inflammation of the lining of the chest) with minimal or no involvement of lung may be observed with M. haemolytica and P. multocida and occasionally with Histophilus. Why this occurs is not understood. It may be a mild pneumonia and pleuritis resolved with appropriate antibiotic therapy. The thoracic lining is difficult to treat successfully with antibiotics, particularly when an inflammatory membrane forms.  Failure of antibiotics to reach effective concentrations at this site may have allowed persistence of the infection.

• Pneumonia may occur acutely, with animals are dull one day and dead the next.  This is particularly the case when animals are stressed by weather or transportation.  We periodically see acute death loss in well-nourished heifers and bulls.  Owners refuse to believe it's "just" pneumonia, even when presented with gross and microscopic evidence, and supporting microbiology.  Take home: pneumonia can be very acute and kill adult well fed animals with little warning.  If you are alert, you should however be able to identify and treat most animals affected with pneumonia.  The trick is being able to spot animals early in the course of the disease.

Vaccines to Aid in the Prevention of BRD

There are eight major companies producing over 60 vaccines for the aid in prevention of BRD. Most are multivalent, containing IBR, PI-3, BRSV, and/or BVD in various modified live, attenuated, or killed virus combinations. To this are added bacterins for M. haemolytica, P. multocida and/or Histophilus in various products. A vaccine is now available for Mycoplasma. The use of these products can be confusing.  Not all products are appropriate for all production systems, farms, or ranches.

The best source of information concerning what vaccine or combination of vaccines to use in your area or production system, how and when to use them safely and to provide the best protection, and other guidelines is your local veterinarian.

Use of Medications for the Treatment of BRD

A variety of medications with various treatment schedules and philosophies are used in the medical management of cattle with BRD. Given here are some simple guidelines.

1.  Antibiotics

• Early, accurate diagnosis
• Selection of appropriate antibiotics
• Proper dosage, route, and schedule for treatments

2.  Analgesics/anti-inflammatory drugs – provide some benefit by getting cattle to eat, as well as lessening the consequences of pulmonary inflammation

3.  Metaphylaxis (mass medication) – for potentially problem cattle, treating the entire group can be more effective and efficient than identifying and treating individual sick animals. Some indications for mass medication include (applies mainly to feedlots but same principles may be applicable to other production systems):

• Past history of high morbidity and death (cattle from a particular ranch, sale barn, etc. Cattle transported long distances.
• Over 10% pulled for treatment + death loss on any one day
• Over 25% pulled for treatment + death loss in any 3 to 5 day period

There are now some highly effective antibiotics on the market such as cetiofur (Excede^®) that are specifically designed to reach high therapeutic concentrations in the lungs of cattle and to kill the three major bacteria responsible for BRD (M haemolytica; P mutocida; Histophilus somni).  Care is needed with some of these products since they can ONLY be given in a particular location such within or at the base of the ear, or due to residue concerns  There is a recent report of sudden death in cattle due to inadvertent injection into aural arteries.

Source: Cattle Treatment Guide

MISCELLANEOUS RESPIRATORY DISEASES OF CATTLE

Many diseases affect the respiratory system. Some are important to producers in Wyoming.  Others impact cattle production in other areas or throughout the country. A few are noted below.

Anaphylaxis (anaphylactic reactions)

Anaphylaxis was covered in the lecture on ‘Sudden Death’. With the many medications and vaccines that cattle are given during their lifespan, it is not surprising that anaphylactic reactions occur. Most diagnoses are made in the field based on clinical history of cattle being given an injectable medication or vaccine, then developing acute onset severe respiratory distress, progressing to death within 10 – 20 minutes. Less severe degrees of anaphylactic reactions also occur.  Drugs are not, however, the only cause of anaphylaxis. Insect bites or stings and reactions to decomposing parasites (Hypoderma spp. grubs) in the tissues can lead to anaphylactic reactions.  These are difficult to diagnose in field cases. The cause of death with anaphylaxis in cattle is due typically to marked, rapid-onset fulminating laryngeal and pulmonary edema leading to asphyxiation. Of the two lesions, pulmonary edema can be seen in a variety of situations and is more nonspecific. Severe laryngeal edema is more definitive in the absence of other identifiable causes. Treatment of anaphylaxis can be an emergency. When it occurs, there is little time to decide how to treat it, dig through the medicine closet, and decide on the correct dosage. Prior preparation is inadequate in most cases. The drug of choice to treat anaphylaxis is epinephrine. The drug can be given subcutaneously and intramuscularly (4 to 8 ml of a 1:1000 solution) or intravenously (1 to 5 ml of a 1:1000 solution) for a 500 kg cow. Epinephrine has a short half-life in the body and relapses can occur, necessitating further treatment. Other ancillary treatments include corticosteroids or other anti-inflammatory drugs and fluids.

Short piece on anaphylaxis by veterinarian with Colorado Serum Company

Brisket disease ('brisket', mountain sickness, high mountain disease)

High mountain disease (HMD) is a concern for producers in Wyoming and the region (CO, NM, UT) who run cattle above 5,000 feet (1524 m).  We see this condition particularly in Angus cattle, but bloodlines in all breeds of cattle are susceptible.  We recently looked at a syndrome that resembles 'brisket' in Holstein cattle along the Colorado Front Range, although we are still unsure whether it is HMD.  One of the students in the 2010 class had images of a Holstein cow with a brisket-like disease (thumbnail below).  There is a form of brisket that occurs in feedlots in Nebraska, the Dakotas and Kansas - cattle come in looking healthy, and develop brisket on feed.  Perhaps these animals developed cardiac injury before coming into the yard and, in spite of being at below the cutoff altitude of 5,000 feet,  develop HMD because rapid weight gain puts additional stress on a heart of marginal efficiency.  A group in the University of Nebraska at Lincoln is investigating this problem.

Some cattle at high altitude develop inappropriately high vascular resistance in lungs.  Small intra-pulmonary arteries develop permanent changes and place increased workload on the heart, specifically that portion which pumps blood to the lungs (right ventricular myocardium).  The end result is heart failure.  Losses in affected operations can be 3 - 5% of the calf crop.  We occasionally see higher rates on some ranches.  Deaths tend to be seen when cattle are moved up or down from high altitudes.  It may appear counter-intuitive that they die moving to lower altitudes but signs occur because the forced exercise of trailing is too much for animals and their weak hearts.  Interestingly, we don't see a brisket-like disease in sheep and horses.  This is because of peculiar anatomic features of arteries in the lungs of cattle that predispose them to HMD.  People at high altitudes, like cattle, may develop cardiac disease with HMD-like features.

Clinical signs: Affected calves (typically >2 weeks) and adults with HMD will have clinical signs due to failure of the right side of the heart: weakness, collapse, diarrhea, bulging eyes, distended and/or pulsating jugular veins, and pitting edema in ventral parts of the body. Edema develops because elevated blood pressure forces fluid out of vessels into surrounding tissues.  Terminally, cattle are lethargic, do not eat and are unable to rise.  Affected calves have a normal body temperature.  Changes in affected calves at necropsy are characteristic.  The right side of the heart is large, there is excessive clear fluid in the abdominal cavity (= ascites), and the liver is large and firm due to congestion and fibrosis.

HMD is seen in the following scenarios:

• After a group of lowland adult cattle is purchased and moved to high altitude.  The higher the altitude, the bigger the risk.

• When pairs are trailed long distances in the fall.  Losses mostly seen in calves.

• When AI semen from sires that are not PAP tested (see below) is used in a herd: progeny over the following breeding seasons may have HMD calves.

• Feedlot cattle.  Presumably, as these animals gain weight, the workload on lungs (and therefore the heart) increases.  Right-sided heart failure develops.  Sometimes these cattle are found dead overnight

Avoidance and control: Recommendations have not changed much from those of Glover and Newsom (1915), who suggested that Colorado ranchers use selective breeding to get away from carriers.  Although brisket disease has a big genetic component, we still do not know the genes involved.  As a result, we lack a genetic test to screen bulls and cows for the disease.  In the past, control was done by culling females that gave birth to HMD calves, and being careful about introducing breeding stock from lower elevations. This traditional approach, which works well over multiple generations, can be supplemented and accelerated with an invasive procedure known as the pulmonary arterial pressure ("PAP") test, which should be done on all bulls and - ideally - replacement heifers.  This involves inserting a catheter with a pressure transducer into one jugular vein, threading it into the right side of the heart, and passing it into the pulmonary trunk (the main artery going to the lungs).  This allows the operator to measure the pressure in the pulmonary trunk/pulmonary arteries.  A PAP test can be done quickly and easily, but requires: 1. good working facilities (chute with head catch and body squeeze) and competent help and 2. a veterinarian familiar with the procedure and its interpretation.  Cattle prods and use of herding dogs should be avoided when breeding stock are evaluated since excitement can cause artifactual jumps in PAP.

	Holstein with ventral and brisket edema.  I don't know whether this Holstein had classical brisket.  Nevertheless this gives you a good idea of what the disease in an extreme form looks like in an Angus.  Image: Claire B. Tousley
	Typical brisket disease heart.  This one is from a 550-lb 10-month old Angus steer that was found dead on pasture.  The right side of the heart (RVFW = right ventricular free wall) is markedly enlarged relative to the left side (LVFW = left ventricular free wall).  In healthy animals the left side of the heart wall is heavier than the right, as it has to pump blood to the entire body, with the exception of the lungs.  The right side is lighter, since it only has to pump blood to the lungs.  In brisket disease, the extra workload on the right side of the heart causes that side to initially undergo get bigger.  Eventually, this side of the heart fails.  WSVL case 09B172
	Liver from above calf.  As a result of the right sided heart failure, blood backs up in the liver, causing the liver to enlarge.  Fluid accumulates in the abdominal cavity (ascites).  The liver has a characteristic reticulated pattern that resembles a cross-section of a nutmeg, hence the term "nutmeg liver", one of the hallmarks of brisket.  WSVL case 09B172

The test works best when it is done when animals are 12 months or older.  It can be done at younger ages since a high PAP (>49 mm Hg) is strongly predictive of high PAP later in life.  But a low PAP in young animals does not necessarily predict a low PAP in adulthood.  The PAP test is best done at elevations of 6,500 feet or above.  Cattle recently introduced from low altitudes should be acclimated for 3 - 6 weeks before being tested.  There is a marketing advantages in identifying bulls with low PAP (<41 mm Mg); they can attract a premium of $2 - $5K when sold in high mountain states.  The only number I expect you to know is the safe cut off number: a PAP of <41 mm Hg.  Other numbers in the table are for information only.

Lungworms (will cover all species)

Lungworms are not common in Wyoming cattle. Lungworms that affect the various species will be mentioned in lecture as will the diagnosis of these infections. Dr. O’Toole will briefly cover this topic in his lectures on internal parasitism.

Tuberculosis

Tuberculosis is an ancient disease, and has been seen in mummies dating from the fourth millennium BC - in other words, in humans older than the lecturers in this course. In Victorian England, 20% of all human deaths were estimated to be due to tuberculosis - "the white plague." In 1900, it is estimated that the infection rate in humans was as high as 90%, based on skin testing.  Most were subclinical or transient infections.  The disease in people is now largely treatable, but it is costly, lengthy and complex.  Recently, multi-drug resistant forms of the organism (= MDR TB) emerged.  That, and the advent of AIDS, deterioration in the national infrastructure for testing for and treating TB, and the rise in homelessness/prison populations, led to a rise in TB cases.  In the United States in 1977, the mortality rate was 13.9/100,000 population.  It is now less than 1.4/100,000.  The disease causes about 2 million human deaths worldwide.  There are ~8.9 million new cases of TB annually  Bottom line: this is historically one of the most important infectious diseases of people.  The most important cause of human TB is Mycobacterium tuberculosis.  An important secondary cause, particularly in immunocompromised individuals, is the related organism of cattle, Mycobacterium bovis.  In the past it infected people through ingestion of cow's milk.  Bovine TB is now virtually eliminated in the national herd, and exposure of people to infected milk in the US is virtually zero, thanks to pasteurization.  Yet it continues to pop up in various states. 

Tubercles in bovine lung - there are the discreet yellow nodules in the image. Source: Noah's Archive image #F02463.  Dr. Mosier

Elsewhere in the world, bovine TB infects an estimated 50 million cattle resulting in annual economic losses of ~$3 billion.  Other tuberculosis organisms exist - birds have their own agent called M. avium and it too can infect immunocompromised humans and dogs.  As an aside, M. tuberculosis occasionally infect cattle - a reverse zoonosis

The natural host range of M. bovis is extensive.  It has the potential to infect virtually all warm–blooded vertebrates. During the early 1900s in the U.S., it is estimated that tuberculosis caused more death losses in farm animals than all other infectious diseases combined. In the recent past, TB has been a problem in herds in NM, MN, MI and CA.  In a typical recent episode (July 2008), >1,000 exposed cattle were slaughtered in Fresno, CA when TB was found at three dairies.   Federal officials quarantined >12,000 cattle there to protect the country's largest milk-producing region.  The government paid dairy operators $3,000 for each slaughtered animal. As with brucellosis, cattle owners have the option to quarantine their herds until tests prove the herd is TB-free.

Mycobacterium bovis and M. tuberculosis are closely related. By convention and to avoid confusion, the disease cause by these pathogens is called tuberculosis.   Diseases cause by other Mycobacterium spp. are termed mycobacteriosis.

In animals, an eradication program for bovine TB has been in place in the USA since 1917. There are differences in species susceptibility. Cattle and goats are highly susceptible.  The disease occurs in horses, rarely.   Sheep are regarded as relatively resistant although outbreaks have been reported in New Zealand.

Tuberculosis lesions in the lung of a deer harvested in Michigan.  TB due to M. bovis is now largely eliminated in the US, but it still circulates in wildlife reservoirs, particularly when wildlife are artificially concentrated by artificial winter feeding and bating. For other images, click here.

In the United States, the disease occurs in free-ranging cervid species, and in cattle imported from Mexico, particularly roping steers.   Virtually any tissue of the body can be infected.  Lesions are most common in lungs and lymph nodes.  As in people, this is a slowly progressive process that results in tumor-like, space occupying inflammatory lesions.  The route of exposure is commonly by ingestion but aerosol transmission can occur. Bovine TB causes mastitis, which is how the organism is transmitted in milk.  The disease in cattle is untreatable.  Control of an outbreak in a herd is by test and slaughter.  Control of transmission of the disease to people from cattle is by pasteurization of dairy products and by meat inspection - you have TB to thank or curse for the advent of pasteurization.

For additional information, interested students are referred to the following websites:

USDA summary on bovine TB

CONDITIONS THAT MIGHT BE MISTAKEN FOR BOVINE RESPIRATORY DISEASE

It is not unusual in clinical veterinary or pathology practice to be presented with a dead animal for autopsy that had been treated extensively for pneumonia, only to find that there is no pneumonia. The reason for this is that some of the clinical signs of respiratory disease such as rapid or labored respiration can be caused by miscellaneous abnormalities including disease in other organ systems.

• Acidosis: As mentioned in the overview last lecture, the lung is one organ involved in controlling acid-base balance. With severe acidosis (decrease in pH), a compensatory mechanism is elimination of C0₂ via the lungs. In such cases, respiration may be rapid (60 to 90/minute) and shallow that can be mistaken for evidence of pneumonia

• Pain and hyperthermia: Both can lead to rapid, shallow respiration but usually not to the same extent as in acidosis.

• Anemia: Animals with anemia are commonly hypoxic.  This can increase the respiratory rate markedly.

• Nervous system dysfunction: Abnormalities of the nervous system can result in alterations from normal of the rate and depth of respiration.

• Heart disease: Heart disease can directly lead to congestion and accumulation of serous fluid (edema) in the lungs, resulting in respiratory difficulty.

Drs. Don Montgomery and Donal O'Toole

Updated: 01/25/2010