2. Aspiration Pneumonia
Definition:
•It is an inflammation of lung tissue
caused by inhalation or aspiration of large
amounts of foreign material, often liquids.
•Causes:
(1) Careless drenching or passage of stomach tube to lung during
administration of milk or liquid medication.
(2) Animals with pharyngeal paresis or abscess and cattle with
parturient paresis or laryngeal paralysis or obstruction.
(3) Sheep that are dipped and cattle that ingests crud oils or
anesthetized animals
(4) Meconium aspiration secondary to fetal distress.
(5) Vomiting.
3. Pathogenesis:
(1)If drenching substances are large in quantities , asphyxia
& death may occur.
(2) Drenching o f soluble small quantities (e.g. chloral
hydrate or Mg sulphate) will exert their systemic
pharmacological effects.
(3) Drenching o f non soluble small quantities (e.g. liquid
paraffin or vomitus material), death may occur within 48- 72
hours.
(4) Drenching of bacterial infection will cause suppuration &
gangrenous pneumonia, resulting in death.
(5) When animal survive from acute stage, chronic ill health
& pulmonary abscesses will occur.
4.
5. Clinical symptoms:
(1) Mild diffuse alveolitis that results in hypoxia and
acidosis.
(2) If large quantities of fluid are aspirated, death may
occur.
(3) Gangrenous bronchopneumonia develops as a result of
infection and the irritating properties of the inhaled material.
(4) Depression, polypnea, dyspnea, coughing and fever.
(5) Putrid breath in suppuration and gangrenous
pneumonia.
(6) Moist rales and continuous cough.
Diagnosis:
It based on the history, sudden onset, sever signs.
Differential diagnosis:
It includes acute bronchopneumonia and septicemia.
6.
7. Lungworm infestation (Verminous
broncho-pneumonia)
Definition:
Lung worm infestation is an enzootic or epizootic affection
manifested by bronchitis and broncho-pneumonia caused
by parasitic infestation of the lung.
Causes:
(1) Dictycolous filaria (Strongylus filaria): in sheep and goat.
(2) Dictycoluus vivparous: in cattle.
(3) Dictycolous arnfeld: in equines.
(4) Dictycolous cameli: in camel.
(5) Hemotrongylus vasorum: in dog.
8. Pathogenesis:
(1) The larvae ingested with the food (grass stem) or water
enter lymph stream from the intestine then they reach the
pulmonary capillaries from which they enter the alveoli and
bronchi.
(2) The larvae invading the pulmonary alveoli and bronchi,
damage them, causing bronchitis. Bacteria also play a
secondary part in producing pneumonia.
(3) Occlusion of individual bronchi may be caused by
exudate and or clumps of worms lead to collapse of portion
of lung.
(4) Incubation period between infestation and appearance
of symptoms average between 4-8 weeks.
9. Clinical findings
(1) In sheep and goats:
1) Paroxysmal cough is often accompanied by
expectoration of masses o f mucous containing sometimes
adult worms or larvae.
AIB: Paroxysmal cough: when sputum reach pharynx after
cough animal try to swallow it.
10. 2) Sero-mucoid nasal discharge. This causes severe itching of the
skin around the nares.
3) Respiration is labored with moderate dyspnea.
4) Temperature may reach 41 °C if lung is involved.
5) Emaciation, anemia and frequent diarrhea.
6) Edema o f the submaxillary region, eyelids and or the whole o f
the anterior part o f the head.
(2) In cattle (mostly calves 4-6 months age and yearlings):
1) Acute form:
1- Sudden cough, accompanied by protrusion o f tongue and the
expectoration o f masses o f mucus, sometimes mixed with worms.
2- Sudden onset o f rapid swallow respiration is accelerated up to
100/minute and later becomes labored.
3- Increase vascular and bronchial sounds on auscultation all over
parts o f the lungs. Moist rales are heard over the bronchial tree.
4- High temperature 40.5°C.
5- Heart rate increases to 100-200/min.
11. 6- A slight nasal discharge.
7- Very severe dyspnoea, cyanosis and recumbence.
8- Severe infestation may kill the animal in 3 to 8 days
(mortality rats 70-80%) proceeded by a period of
emaciation, anaemia and severe diarrhoea.
2) Subacute verminous pneumonia is more common in
calves than the acute form:
1- The onset is usually sudden.
2- Evidence o f recent diarrhea.
12. 3- The temperature is normal or slightly elevated.
4- Increase in the rate (60-70/min) and depth of
respiration.
5- Expiratory grunt and expiration may be
relatively prolonged.
6- Frequent paroxysmal o f coughing.
7- The course o f the disease is long, 3-4 weeks.
8- By auscultation, there is consolidation and
bronchitis ventrally and marked emphysema
dorsally.
9- Affected animals loss weight very quickly.
10- The mortality rate is much less than in acute
form.
13. (3) In the horse:
1) The symptoms are nearly the same as in calves.
2) It is more common in donkeys than horses.
Diagnosis:
(1) By the microscopic examination o f the feces (larvae). The larvae
may not present in the early stage of symptoms because the worm in
the bronchi aren’t yet mature.
(2) Eosinophilia is present in subacute cases.
(3) Lung worm is easily confused clinically with bacterial
bronchopneumonia or viral pneumonia.
•Treatment:
(1) Broad spectrum anthelmentics as Ivermectin (1 cc/50 kg S/C). It is
effective against mature and immature stage.
(2) Antihistaminic to reduce the severity o f the reaction on the larvae.
(3) Antibiotic for secondary infection.
(4) Vitamin A and C.
14.
15. Pulmonary Abscess
It is circumscribed suppurative foci
involving the lung parenchyma. It may
cause suppurative bronchopneumonia.
It may be primary or secondary or
acute or chronic in nature. It has been
recorded in cattle, dog and cat.
Pyogenic abscess of liver may extend
to adjacent lung
parenchyma and cause lung abscess.
16.
17. •Systemic fungal infection
(Aspergillus, Cryptococcus) may
cause lung abscess.
•Causative organisms o f pneumonia
(Streptococcus, Mycoplasma,
Klebsiella, TB) etc. may produce lung
abscess
18. Causes:
(1) Aspiration o f infectious material in the lungs is the most
common cause of lung abscess. Faulty drenching or during
milk fever, ephemeral fever, neurologic condition, general
anaesthesia or feeding in orphan c a lf may lead to this
condition.
(2) Penetration o f lung parenchyma as a consequence of
traumatic reticule pericarditis may set up lung abscess.
19. Pathogenesis:
There are three stages in the production of lung
abscess.
(1) Stage o f consolidation: Inflammatory
exudate fills up the
alveoli and convert the lung into a solid mass.
(2) Stage o f liquefaction: Due to virulence o f
the organism and low resistance o f the host,
necrosis o f the lung occurs. The necrosis
material and exudate get liquefied by the toxin
of the bacteria. The liquid materials are the pus.
20. (3) Stage of rupture and cavity formation:
Pus, thus formed increases the tension and thereby cause
rupture of the abscess. Pus is then drained out leaving
behind a cavity containing exudate and air.
Clinical findings:
(1) Loss o f appetite, dullness and depression.
(2) Loss of body weight.
(3) Reduction in milk yield.
(4) Intermittent (fluctuating) temperature.
(5) Productive cough and respiratory distress (dyspnea).
(6) Foul smelling discharge from nose and occasional
hemoptysis.
(7) Area of dullness on auscultation.
(8) Fine or medium rales on the involved area.
21. Diagnosis:
•This is based on clinical findings and laboratory
investigations.
(1) Blood examination: Neutrophilic leukocytosis.
It is more in acute cases than chronic cases.
(2) Nasal exudate, pus lung tissues, culture for
isolation of causative organisms.
(3) Radiological examination: It is helpful in
small animal. Xray will show a dense
homogenous radio dense shadow with
rarefication in the centre and later on cavity
containing fluid surrounded by alveolar infiltrate.
22.
23. Prognosis:
It is bad due to rupture o f this
abscess resulting in fatal broncho-
pneumonia.
Treatment:
Antibiotic (after sensitivity test),
vitamin C and A.
24. Pulmonary Congestion and Edema
(Hyperemia of Lung)
(1) Pulmonary Congestion:
It is abnormal engorgement o f pulmonary vessels with
blood due to active (increase out flow) or passive
hyperemia (diminished out flow) with normal or increased in
flow of blood.
(2) Pulmonary edema:
It is abnormal accumulation o f liquid and solute in the
pulmonary tissue, air ways. It occurs from exudation of
serous fluid into the alveoli and bronchioles and then into
the interalveolar tissue.
25.
26. Causes:
(1) Early stage o f pneumonia.
(2) Hypostatic congestion in recumbent animals.
(3) Anaphylactic reactions.
(4) An increase capillary hydrostatic pressure.
(5) A loss o f negative interstitial hydrostatic pressure.
(6) Increase of capillary permeability to protein.
(7) Insufficient lymphatic drainage.
27. •Clinical finding:
(1)Dyspnoea and dilated nostrils.
(2)Mouth breathing.
(3) Abdominal and thoracic movement during inspiration and
expiration.
(4) Abducted elbow.
(5) Increase respiratory rate and pulse.
(6) Bright red nasal mucous membrane.
(7) Compensatory emphysema in the dorsal parts of the
lung.
(8) Cough (soft and moist).
(9) Slight nasal discharge.
(10) Auscultation reveals bubbling sound with movement of
air.
28. •Diagnosis:
•By clinical symptoms
•Treatment:
(1) Complete rest of the animal and correct the respiratory cause.
(2) Oxygen therapy in cases o f dyspnoea.
(3) SC injection of camphor or caffeine.
(4) Cardiac tonic.
(5) Antihistaminic (IM) in conjugation with adrenaline (SC).
(6) Diuretic.
29. Respiratory emphysema
•Definition:
•It is an over distention of the
alveoli with air without any
change in the pulmonary tissue.
•In this disease, the pulmonary
alveoli are over distended with
air resulting in loosing of their
elasticity.
30.
31. (1) Acute alveolar emphysema
Causes:
(1)Persisting coughing.
(2)Acute bronchiolitis.
(3) Forced expiration and inspiration due to obstruction by foreign body,
larvae of worms or worms (Dictycollus).
Symptoms:
(1) Dyspnea.
(2) Exaggerated vesicular sound by auscultation.
(3) By percussion, hyperresonant sound is heard.
Diagnosis:
•By history and symptoms.
Treatment:
•Treat the primary cause.
32. Chronic alveolar emphysema
(Poor man disease - Heaves — Broken
wind — Asthma )
Definition:
•It is a permanent dilatation and over
distension of the alveoli without any
change in the lung tissue. It is involve
one lobe or both lobes. It is mainly
disease of horses and in sporting dogs.
33.
34. •Causes:
The main cause is unknown but there are some
predisposing factors such as:
(1) Over exertion (heavy work).
(2) Supplying the animal with non-nourished food
containing dust for long time as dusty rice straw (Poor man
disease). This dust will cause irritation and continuous
coughing and consequently dilatation o f the alveoli.
(3) Chronic bronchitis or chronic coughing or chronic
edema.
(4) Traumatic perforation of the lung and pulmonary
abscess.(5) Allergic.
(6) Sensitivity o f some horse to mouldy and dusty food
(Aspergillus fumigatus).
35. Pathogenesis:
(1) The primary deficiency in the strength of
the supporting
tissue.
(2) The stenosis in the bronchial tree in cases
of chronic bronchitis, bronchiolitis or bronchial
spasms lead to accumulation of air in the
alveoli.
36. (3) The previous two parameters (1&2)
resulting in over stretching o f the elastic
tissues ( supporting tissues ) of the
pulmonary parenchyma resulting in excessive
dilatation leads to loss o f elasticity causing:
1) Chronic alveolar emphysema.
2) Weakness o f alveolar wall, which rupture
resulting in
interstitial emphysema.
37. Symptoms:
(1) Prolonged cough which is weak and low
(usually at morning).
(2) Difficulty in breathing (expiratory
dyspnea).
(3) Double expiratory movement. The first is
costoabdominal (normal) while the second is
wholly abdominal because the animal tries to
get rid of the rest o f the expiratory air (Broken
wind) by the only movement o f its abdominal
muscles.
(4) Percussion give hyper-resonant sound.
38. (5) Heave’s line: It is development of
a grooves in the flank along the line of the
costal-arch due to the action of the
abdominal muscles in trail for getting rid
the rest of the air.
(6) The abdomen of the affected horse is
barrel-shaped.
(7) Increase the area of lung (the posterior
border of the lung area will cut the 14th rib
in its middle (in disease) instead of the
11th rib (in normal horse).
39.
40. •Course and prognosis:
It is a chronic, low progressive and incurable
disease.
Diagnosis:
(1) Clinical symptoms
(2) Respiratory rate test:
1) Counting the number of respiration/m before
exercise.
2) Exercises the horse for 5-10 minutes.
3) Rest the animal for 5 minutes.
4) Count respiratory rate each 5 minutes till
become normal.
41. •In normal horse, the respiratory rate
return to normal (10- 14 m) after
15-20 minutes rest, but in
emphysema, respiration reach
80-120/m lasts 30-60 m to return
normal.
42. Treatment
•No direct treatment but stop the progress
of the disease by symptomatic relief. Full
recovery cannot be expected.
(1)Oxygen supply for life threating phase
in valuable animals.
(2)Good nourished food free from dust.
(3) Administration of belladonna.
(4) Bronchodilator.
(5) Expectorant.
(6) Vitamin A and C.
