Respiratory Diseases

18 September, 2015rodster385Comments (0)

1 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.

2 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.

4 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.

7 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.

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

11 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.

13 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.

16 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.

17 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.

19 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.

22 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 Tissue 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.