Articles "Respiratory Tract Diseases" Article Index

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By: "Goat Handbook, United States, 1992"
Original Document: Web Site
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Rated 3.3 by 46 responses.

Clinical pneumonia in goats is almost invariably preceeded by some event or set of circumstances commonly referred to as stress. This very broad term, stress includes such factors as weaning, long distance hauling, weather factors including sudden temperature changes or low nightime with high daytime temperatures, poorly ventilated barns especially those heated in extremely cold weather, overcrowding, malnutrition, feed changes, parasitism and worming. The microorganisms (germs) which produce the actual disease process are often normal inhabitants of the respiratory tract. These microorganisms are prevented from causing disease by the normal animal's body defense mechanisms. The relationship between the body and the microorganism is sometimes a very delicate balance especially in the very young animal. Stressing factors can tip the balance in favor of the microorgansim and against the young animal.

Barn ventilation in extremely cold weather deserves special comment because it is often overlooked. Warming a barn increases the relative humidity, thus producing a stressful situation. Moisture should never be allowed to accumulate on the walls, ceilings and floors. The rule to follow, especially in barns where the bedding is allowed to accumulate and help maintain the warmth, is if the inside temperature is 5F above the outside temperature, an exhaust fan of adequate capacity to prevent moisture condensation must be used. Goats kept in well ventilated barns, which protect them from drafts and becoming wet, can readily tolerate temperatures below -25F.

3) Acute Pasteurella Pneumonia
In the United States of America the most common cause of pneumonia in goats is Pasteurella multocida and P. hemplytica. It is an acute disease causing extreme debilitation and often death. It occasionally has a systemic form in which the gastro-intestinal tract is the other primarily involved system.

In sheep and presumably in goats, up to 400f normal animals contain one of the above species of bacteria in their nasal passages.

5) Clinical Signs
While herd outbreaks do occur, individual cases also occur in goats. Morbidity and mortality figures are not available for goats. Depression, lack of appetite, mucopurulent (''pussy'') discharge from the nose and occasionally the eyes, occasional coughing (but not as consistent as in cattle and sheep), fever (104 to 107F) are usually present. Difficult or increased breathing is often not noticed unless the animal is forced to exercise; in this case, panting and coughing occurs.

6) Tissue Changes
Small (petechial) hemorrhages may be present on the lining of the body cavities especially of the heart. The bronchiole lymph nodes are usually swollen and hemorrhagic.

The most consistent and striking change is seen immediately upon opening the chest and completely reflecting the ribs, especially of the right side. First there are marked adhesions of the visceral and parietal pleura (chest cavity lining) and pericardium. The heart and lung may be covered with yellow-gray gelatinous or clotted fluid, fibrin and fibrous connective tissue. This may completely or partially hide the underlying apical and cardiac lung lobe exposure of which reveals a very angry red or purple appearance. The lobes are necrotic, friable and often contain purulent exudate or even abscesses. The fluid may be dirty-yellow and have a fetid odor. When cut, the lungs may have a sharp line of demarcation between the less angry looking (merely consolidated or nearly normal) lung and the necrotic portion. A dark hemorrhagic band of 2 to 3 millimeters may separate the two zones. There are often necrotic cavitations containing purulent exudate or necrotic debris.

8) Diagnosis
Diagnosis is based upon the history, signs and necropsy lesions and is confirmed by isolation and identification of P. multocida or P. hemolytica. Because of the presence of the organism in normal animals, diagnosis cannot be made by culturing the organism without the signs and lesions. Differentiation from mycoplasma pneumonia (Mycoplasma mycoides subspecies mycoides) can be tentatively assumed at necropsy by the severe, angry appearance with marked necrosis which is characteristic of caprine pasteurellosis. Differentiation is important because treatment of pasteurellosis and mycoplasmosis is different.

9) Prevention and Treatment
Reducing stressful circumstances or giving antibiotics preventively when stress cannot be avoided, will help reduce the severity and the incidence of the disease.

Penicillin and sulfamethazine are approved for treatment by injection and sulfamethazine is approved for oral administration.

However, oxytetracycline and the long acting sulfonamide, sulfadimethoxine are also effective against the organism. The major limitation in using these antimicrobial drugs comes from the very short but severe course of the disease. It is difficult to detect, diagnose and treat before the severe necrotizing tissue changes occur. However, in an outbreak, an alert herdsman can detect additional new cases early.

12) Acute Mycoplasmal Pneumonia
The mycoplasmal diseases of goats have taken some time for scientists to sort, classify and understand. The explanation is far beyond the scope of this article, but suffice to say, in the US there is a rather common disease characterized by acute pneumonia and arthritis. This disease is caused by Mycoplasma mycoides ss mycoides and is the most common cause of pneumonia in Arizona goats. The organism with the same name, but with very slight differences in growth characteristics (colony size), is the one which causes the dreaded Contagious Bovine Pleuropneumonia, eradicated from US cattle in the 19th century.

The disease occurs primarily in 2 to 10 week old kids. Two Arizona outbreaks were associated with the spring weather change of warm days but continued cool (30 to 40F) nights. The acute stage of severe disease and death loss lasted about one week. Sick animals which survived were ill about 3 weeks. The morbidity (percentage of the herd affected) was 70and the mortality was 36

14) Clinical Signs
The most prominent signs were swollen joints, especially the carpi and stifles (front and rear knees) with or without lameness, fever (106 to 108F) and dyspnea. Coughing is not consistent unless ellicited by forced exercise or laryngeal pressure. Swelling of the face or head is infrequently seen and results from mandibular or atlanto-occipital joint involvement.

15) Tissue Changes
The lung changes always occur on the right side and usually on the left. They consist of red-purple consolidation of the dependent or entire portions of the apical and cardiac and occasionally the diaphragmatic lobes. These portions are friable and moderate amounts of mucopurulent exudate can often be squeezed from them. Depending on the stage of the disease process, cut sections of affected lung vary from dark reddish-purple homogeneous tissue to a varigated color pattern of hepatized to necrotic lobules separated by interlobular edema or fibrosis. Occasionally thin walled abscesses are present from which the organism can be isolated in pure culture.

The copious yellow pleural exudate often contain large quantities of soft fibrin lightly adhering to the surfaces. Bronchial and mediastinal lymph nodes are generally enlarged and on cut section, very moist.

The major diarthrodial joints are most often affected. The inflammatory reaction varies from increased cloudy joint fluid with fibrin clots to marked erosions of articular cartilage with fibrosis of the joint capsule. Periarticular tissues in acute cases were often edematous and congested, with extensive fibrosis occurring in chronic cases.

18) Diagnosis
As with acute pasteurellosis, diagnosis is based on history, signs, necropsy lesions and isolation of the causative organism. However, the knowledge of which disease usually occurs in a particular area is of practical importance while awaiting laboratory confirmation. As previously stated, pasteurellosis usually produces a much more severe or angry appearance than mycoplasmosis; this is a subjective determination and subject to error.

The organism will grow on ordinary blood agar but many inexperienced technicians may not keep the plate long enough to notice the tiny areas of hemolysis in which a colony can only be seen under magnification. Ideally a special mycoplasma medium should be used, and if typical colonies are found, sent by the diagnostic laboratory to one of the few mycoplasma reference laboratories.

20) Prevention and Treatment
Tylosin is the drug of choice for mycoplasmosis. Prevention is as difficult as preventing the change in the weather. If outbreaks recur, the use of tylosin before an outbreak occurs may possibly prevent it. In the face of severe outbreaks, massive does of tylosin seem to be necessary to appreciably affect the disease process. Two grams of injectable tylosin given intravenously (slowly) followed by 1 gram given subcutaneously twice daily for 14 days appear to reduce the severity of an outbreak. It must be stated that tylosin in any dose is not approved for use in goats and inclusion in this section cannot be construed as a recommendation of its use. Indeed, at these high does, there may be a risk of killing the animal. This must be weighed against the possibility of losing the animal without this treatment and needs to be discussed by the owner and the veterinarian. The author gratefully acknowledges Dr. Dale Brooks of the University of California at Davis as the initiator of the massive dose system. The above dosage schedule may not be the same as currently recommended by Dr. Brooks.

21) Mycoplasmal Pneumonia of Spanish and Angora Goats
A pneumonia disease of Spanish and Angora goats caused by Mycoplasma ovipneumoniae has been reported from Texas. The time changes are apparently quite similar to those produced by M. mycoides ss mycoides.

Further, the affected animals were subjected to extreme stress of inadequate handling, inclement weather and disease. In two of the four cases, only M. ovipneumoniae was isolated. The occurance of the disease is associated with pasturing cows, sheep and goats together; transmission may take place from sheep to goats.

23) Chronic Progressive Pneumonia
This poorly documented pulmonary disease of goats has many of the characteristics of Progressive Pneumonia of sheep. It may be caused by a virus but it is complicated by the common pneumonia producing bacteria. It is found in breeding goats and invariably associated with the stress of bad ventilation or close confinement in dirty pens, especially kidding pens. Presumably the kids acquire the etiologic agent early, perhaps at birth from an infected mother. Each time the animal is stressed, another episode of acute pneumonia and more and more debilitation occurs; finally an acute episode causes death, often not until 6 or 7 years of age.

24) Clinical Signs
During each acute episode the animal is anorexic (won't eat), stands by itself with its ears down, acts completely lifeless. Auscultation of the lungs reveals some rales; however, in the advanced case, so little air moves through the lungs that the lung sounds are muffled. Difficult breathing (dyspnea) is present and worsens with repeated episodes. Hypoxia with blue tinting of the mucous membranes of the mouth, vulva or sheath continually worsen.

25) Tissues Changes
If an animal dies at a young age, lesions similar to but milder than acute pasteurella pneumonia may be seen. As the disease progresses, very small (miliary) foci containing mucous or mucopurulent exudate occupy more and more of the lung. Eventually the lung becomes essentially filled by these foci and by old fibrous connective tissue (scars) and abscesses. The lungs and bronchiolar and mediastinal lymph nodes become 3 to 5 times as heavy as normal. The animal has become extremely debilitated and has very little body fat.

26) Diagnosis
The history of chronic, recurring pulmonary illness and necropsy findings of chronic lung changes facilitate a diagnosis. Because the disease in goats is not well documented, and the real etiologic agent has not been identified, definitive diagnosis is not yet possible.

27) Prevention and Treatment
Treatment has been unsuccessful. This fact gives evidence for a viral etiology. Preventive measures should give good results. All does with a chronic cough and having acute pulmonary episodes should be culled from the herd. Kidding barns and all other types of winter housing should be kept clean and well ventilated.

About the author: Extension Goat Handbook - This material was contributed from collections at the National Agricultural Library. However, users should direct all inquires about the contents to authors or originating agencies.
J. L. Ayers; Los Olivos, CA
S. B. Guss; Pennsylvania State U., Unversity Park.

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