The most common cases of

pneumonia in small ruminants

Presented by
Dr.Ali A.Alhumood
aliabh2006@hotmail.com

Supervised by
Prof. Dr. Taha A. Fouda
Professor of Medicine & Therapeutics
and CLD

Head of Department
Prof. Dr. F.M Housawi

Department of Clinical Studies

College of veterinary medicine and
animal resources
King Faisal University

Second semester 2009

1
Dedication
My thanks primarily to
prof.dr.Taha Fouda and
then to my friends who
helped me to finish this
work.

2
PNEUMONIA
Pneumonia refers to the inflammation of the pulmonary parenchyma usually
accompanied by the inflammation of bronchioles and often pleurisy and, it is
characterised by respiratory embarrassment or sometimes toxaemia. Upper
respiratory infections are accompanied with respiratory abnormalities and very often
they descend to pneumonia. (Lughano; Dominic, 1996)

There is no universal classification of pneumonias in veterinary medicine; But there

are numerous classifications such as :

 Etiological: Viral pneumonia, Mannheimiosis, Histophilosis pneumonia,

distemper pneumonia, allergic pneumonia, etc.
 Epidemiological: Enzootic pneumonia, contagious bovine
pleuropneumonia, etc.
 Exudate: Suppurative, fibrinous, or granulomatous pneumonias.
 Topographical (distribution): Lobar, lobular, diffuse, interstitial, focal,
etc.
 Miscellaneous: Progressive pneumonia, proliferative pneumonia,
atypical pneumonia, pneumonitis, etc. (Alfonso López, 2007)

Classification Of Pneumonia According To Exudate, Texture

And Port Of Entry: (Figure: 1)

1. Suppurative Bronchopneumonia.

2. Fibrinous Bronchopneumonia.

3. Interstitial Pneumonia.

4. Embolic Pneumonia.

5. Granulomatous Pneumonia.

3
 Fig: 1/A: Normal, B:
Bronchopneumonia, C: Fibrinous
pneumonia, Red=consolidation,
Yellow =fibrin, D: Interstitial (diffuse
with rib imprints), E: Embolic, F:
Granulomatous. (Dr. Paulsen, 2009)

1. Suppurative Bronchopneumonia (Lobular pneumonia)

 Distribution: Cranioventral consolidation of lungs .

 Lung texture: Firm
 Port of entry: Aerogenous
 Etiology: Generally caused by bacteria or mycoplasma which produce
mild to moderate injury to the lung (i.e. P. multocida, A. pyogenes,
Bordetella bronchiseptica).

Ovine Enzootic Pneumonia: (clinico-epidemiologic term) / Chronic

Bronchopneumonia (pathologic term): Multifactorial Disease of lambs (less than 1
year old). Environmental stressors, viral infections (PI-3, Adenovirus, RSV, etc),
bacterial (M. haemolytica), Mycoplasmal infection (Mycoplasma ovipneumoniae).
High morbidity, low mortality. Gross lesions: Chronic bronchopneumonia /
bronchointerstitial with mucopurulent exudate in airways.

Ovine Mannheimiosis occurs in two distinct types:

 Pneumonic Mannheimiosis (Mannheimia haemolytica; Lesions and

pathogenesis are similar to shipping fever of cattle: acute fibrinous
pneumonia predisposed by stress, viral infections (PI-3, Adenovirus),
chlamydial infections.
 Septicemic Mannheimiosis (M. haemolytica) in stressed sheep which is
characterized by a fulminating septicemia with DIC, petechial hemorrhages,
lung edema, (sometime necrotizing pharyngitis). M. haemolytica is present
in the tonsils of 95% of normal sheep.

Ovine Verminous Pneumonia (Dictyocaulus filariae; Lungworm). As in calves,

this is a parasitic bronchitis rather than pneumonia. The larval stage causes a
transitory interstitial pneumonia and edema. The adult nematodes live inside the
large airways causing chronic bronchitis and atelectasis, particularly in the dorsal
aspect of the caudal lobes.

4
  Death due to bronchopneumonia occurs when there is more than 60% of
lung involvement in uncomplicated cases.
 Gross lesions: Affected lung is consolidated and the lobular pattern is
accentuated. Color varies from red (acute, hyperaemia) to grey (chronic
inflammation, atelectasis, fibrosis). Typically, purulent/pus exudate can be
expressed from airways; in chronic bronchopneumonia the exudate takes a
mucous appearance. (Figure: 2)

Fig: 2/Lungworms infect several types of animals. The worms irritate the linings of
air passages and cause coughing, which is most noticeable in sheep. It can also cause
weight loss. Lungworm can be treated by drenching. Here, the lungworm
Dictyocaulus filaria is shown in part of a lamb’s lung. (The encyclopedia of New
Zealand, 2008)

 Histopathology: Large number of polymorphonuclear leukocytes in

bronchoalveolar space in acute cases and a mixture of PMN,PAM and mucus
(goblet cell hyperplasia) in the more chronic cases. (Fig: 2 &3)

Fig: 4/ High power of previous

Fig: 3/ Bronchioles filled with
slide showing polymorphnuclear
polymorphnuclear cells.
cells inside alveoli.

5
 Common sequels:

 Abscesses (cranioventral lobes)

 Bronchiecatasis (cranioventral lobes)
 Fibrosis and fibrous pleural adhesions (cranioventral lobes). (Alfonso López,
2007)

2. Fibrinous Bronchopneumonia (Fibrinous pneumonia or Lobar

pneumonia)

Some authors consider fibrinous pneumonia a "peracute and generally fatal form
of bronchopneumonia.

 Distribution: Cranioventral consolidation (except Porcine

Pleuropneumonia (Actinobacillus pleuropneumonia)
 Lung texure: Hard
 Color of affected lung: Red -> yellow -> grey / Fibrin on pleura /
necrosis of cut surface
 Port of entry: Aerogenous
 Etiology: Caused by agents that produce severe injury to the lung (i.e.,
Mannheimia haemolytica, Actinobacillus pleuropneumonia, etc). There is
severe toxemia due to bacterial toxins and tissue necrosis. Also aspiration of
harsh material.
 Sequels: Survivors can develop large pulmonary sequestra (pieces of
necrotic lung surrounded by connective tissue.
 Histopathology: Notable dilation and thrombosis of lymphatic vessels,
massive exudation of fibrin and polymorphonuclear leukocytes into the
bronchoalveolar space and pleural, areas of coagulative necrosis. (Figure: 5)

6
 Fig: 5/ M. haemolytica pneumonia (Dr. Paulsen, 2009)

 Common sequela: Pulmonary sequestra, pleural adhesions, fibrosis.

 Examples of disease causing fibrinous bronchopneumonia:
Pneumonic Mannheimiosis (shipping fever), Porcine Pleuropneumonia,
Contagious Bovine Pleuropneumonia (does not occur in the American
continent). (Alfonso López, 2007)

3. Interstitial Pneumonia (Pneumonitis)

 Distribution: Diffuse, lungs fail to collapse.

 Texture: Elastic with rib imprints. Cut surface has a meaty and often
edematous appearance.
 Port of Entry: Aerogenous or hematoagenous
 Etiology: viremia, airborne-viruses, septicemia, blood-borne toxins,
systemic toxicants, allergy, and inhaled gases. The disease can be
Transmitted through respiratory route.
 Gross lesions: The lungs fail to collapse when the thorax is opened;
occasional costal imprints are visible on the pleural surface. The color
depends on blood: tissue ratio and type of exudate or fibrous scarring.
Histopathology: Changes are often subtle and difficult to diagnose grossly
generally requiring histopathologic confirmation. Interstitial pneumonia may
coexist with edema, emphysema or bronchopneumonia (Broncho-interstitial
pneumonia). (Figure: 6). Ovine Progressive Pneumonia (Maedi-
Visna / Lymphoid Interstitial Pneumonia). In Iceland, "Maedi"
means shortness of breath. Clinical disease only in sheep older than 2 years;
it is caused by a retrovirus. Gross lesions: Lungs fail to collapse, heavy, elastic
texture and prominent rib imprints typical of a severe interstitial pneumonia
(Figure: 7).

7
 Fig: 6/ Ovine progressive interstitial
pneumonia. Cross section of the lung
parenchyma. The lungs are enlarged,
non collapsible and have a meaty
appearance
Fig: 7/ Lung sheep Maedi/Visna :
lung enlarged graybrown & of tens
tippled with dark grey spots
(Dr.khaled fujairah municipality,
2008)

 Histopathology: The primary lesion is centered in the alveolar wall.

Thickening of alveolar walls. Interstitial exudation or proliferation of type II
pneumonocytes. In chronic interstitial pneumonia there is alveolar
fibrosis. (Fig: 7&8). Histopathology of (OPP): Interstitial lymphocytic
infiltrates with notable hyperplasia of bronchial associated lymphoid tissue
(BALT) and smooth muscle.

Fig: 8/Microscopic appearance of Fig: 9/ Microscopic appearance of OPP-

normal lung tissue affected lung tissue (Cynthia, 1998)

 Bronchointerstitial pneumonia is a term currently used in veterinary

pathology to describe the microscopic lesions caused by viral infections.
Some respiratory viruses cause necrosis and inflammation of the
bronchial/bronchiolar epithelium (bronchopneumonia) and also interstitial
necrosis and proliferation of pneumonocytes (interstitial pneumonia). Most
viral pneumonias are transient unless complicated with bacteria.

8
  Common sequels: Pulmonary fibrosis, interstitial emphysema. (Alfonso
López, 2007)

4. Embolic Pneumonia.

 Distribution: Multiple foci or small nodules randomly distributed in all

pulmonary lobes.
 Texture: Nodular.
 Port of entry: Always Hematogenous.
 Etiology: Endocarditis, ruptured hepatic abscess (vena cava thrombosis in
cattle), omphalophlebitis.
 Gross lesions: Variable number of foci, often with a white center and red
hemorrhagic margins. Eventually embolic lesions may progress to abscesses.
 Histopathology: Septic emboli attached to pulmonary capillaries,
pulmonary edema, microabscesses.
 Common sequels: Abscesses in all pulmonary lobes. (Alfonso López,
2007)

5. Granulomatous Pneumonia

 Distribution: Randomly distributed nodules.

 Texture: Nodular. Cut surface: granulomas
 Port of entry: Aerogenous or hematogenous.
 Etiology: Tuberculosis, systemic mycosis, some parasites (Muellerius
capillaris; larva migrans). Usually caused by microorganisms, parasites
(ova, larvae) or foreign material (inhaled food particles) difficult to eliminate
by phagocytosis. Muellerius capillaris (Nodular lung worm): Some
parasites induced granulomatous reaction in the lungs. Muellerius capillaria
is an Important parasitic disease of sheep and goats that induces multifocal
sub-pleural calcified granulomas mainly in the dorsal caudal lobes. It is
generally an incidental finding except for severe parasitic infections. The
granulomas contain dead larvae, parasitic eggs and many eosinophils.
 Gross lesions: Granulomas in the lung and sometimes in other organs too.
Be aware that granulomatous pneumonia can resemble lung cancer and may
require histopathological confirmation.
 Histopathology: Variable size nodules with a necrotic center infiltrated by
macrophages and giant cells and surrounded by connective tissue mixed with
lymphocytes and plasma cells.
 Common sequels: Cachexia (wasting) in chronic cases. (Alfonso López,
2007)

Etiology of pneumonia:

9
A. Microbial:
1. Bacterial Infections:

I. Chlamydia e.g. Chlamydia pecorum. (Rodolakis, 2001)

II. Mycoplasma

a. Mycoplasma dispar. (Carter, 2003)

b. Ureaplasma. (Thomas, Ronald, Norval, 1997)
c. Mycoplasma arginini. (Kathryn, 2006)
d. Mycoplasma agalactiae. (Kathryn, 2006)
e. Mycoplasma bovirhinis. (Thomas, Ronald, Norval, 1997)
f. Mycoplasma mycoides. (mycoplasm mycoides ssp.capri).
g. Mycoplasma ovipneumonia. (Kathryn, 2006)
h. Mycoplasma capricolum subsp. (Thomas, Ronald, Norval, 1997)

III. Pasteurella

a. Pasteurella hemolytica.
b. Pasteurella multocida. (Michael, Donald, Marie, 2008)

IV. Other bacteria

a. Corynebacterium pyogenes.
b. Streptococcus spp.
c. Staphylococcus aureus.
d. Proteus mirabilis.
e. Pseudomonas aeruginosa.
f. Escherichia coli. (Lughano; Dominic, 1996)
g. Corynebacterium pseudotuberculosis.(Sheep&rabbits). (Thomas,
Ronald, Norval, 1997)

2. Viral infection

a. Bovine mucosal disease. (Thomas, Ronald, Norval, 1997)

b. Bovine viral diarrhea. (Frederick, 1999)
c. Bovine respiratory syncytial virus.
d. Para influenza. (Keith 2000)
e. Retroviridae i.e Maedi/Visna (Ovine Progressive Pneumonia).
f. Retroviridae jaagsiekte sheep retrovirus (JSRV); type D reovirus.
(Thomas, Ronald, Norval, 1997)

3. Parasitic infestation:

10
Lung worms occur in the windpipe and windpipe branches of sheep and
goats worldwide. They are also seen in antelopes. The problem is
common in cooler parts of the country, where it is very moist. (Mashishi,
2007)

Etiology:
a. Muellerius capillaries. (Figure: 10)

Fig: 10/ Sheep/goat lungworm larvae:

Muellerius Muellerius capillaries Tail
(The RVC/FAO, 2004)

b. Bicaulus spp.
c. Cystocaulus ocreatus and Cystocaulus nigrescens. (Figure: 11)

Fig: 11/ Sheep/goat lungworm

larvae: Cysto- caulus Cystocaulus Tail
(The RVC/FAO, 2004)

11
d. Dictyocaulus filaria. (Figure: 12)

Fig: 12/ Sheep/goat lungworm

larvae: Dictyocaulus Dictyocaulus
filarial
(The RVC/FAO, 2004).

e. Neostrongylus linearis.
f. Protostrongylus rufescens. (Figure 13)

Fig: 13/ Sheep/goat lungworm larvae: Protostrongylus Tail

Protostrongylus (The RVC/FAO, 2004).

g. Spirocaulus spp. (Gracey, Collins, Robert, 1999)

12
Pathogenesis:

Food & water Animal Intestine Lymph

Pulmonary capillaries Bronchi Verminuos bronchitis
Producing its action partly A . Metabolic. B. Mechanical.

Signs:

Infected animals show shallow breathing with the head raised, coughing, mucous
from the nose, loss of weight and death may occur.

P.M:

1- Adult worms are seen in the windpipe branches. There is froth in the lungs.
2- Most of the windpipe branches contain plugs of mucous and pus.
Some parts of the lungs are sunken, some have crackling sounds when touching them
and others show dark red or grey patches. (Mashishi, 2007)

B. Poisonous plants:

1) Ganskweek (Lasiospermum bipinnatum).

(Figure:14, 15 &16)

Fig: 14/ Lasiospermum Fig: 15/ Lasiospermum

bipinnatum (seed) bipinnatum (flower and seed)

13
 Fig: 16/ Lasiospermum
bipinnatum (plant)

2) Springbokbos (Hertia pallens). (Figure: 17,

18 & 19)

Fig: 17/ Hertia pallens (flowers) Fig: 18/ Hertia pallens (branch)

Fig: 19/ Hertia

pallens (plant)

(UPSpace, 2002)

Signs:

14
Difficult in breathing.

P.M:
1. Fluid collects in the lungs and makes a crackling sound when
touched.
2. The liver may be yellow. (Mashishi, 2007)

C. Management mistakes:
1. Incorrect dosing.
2. Overcrowding; Figure: 20.
3. When animals are stressed, for example, when there is a change of diet
or during extreme weather conditions, especially cold and wind. (Mashishi,
2007)
4. Bad sanitary.
5. Severe fatigue and traveling for a long distance.
6. Food insufficient specially with vitamin C .
7. Sudden exposure from hot to cold and air droughts. (Fouda, 2006)

Fig: 20/ Overcrowding.(Superstock, 2009)

D. Chemical irritants:

a. Sulfur dioxide. (Fouda, 2006)

b. Chlorine. (Figure: 21)
c. Carbon dioxide.
d. Mustard gas.
e. Ether vapor used as an anesthetic.
f. Various irritating medicinal substances accidentally
introduced via the trachea. (Thomas, Ronald, Norval, 1997)

15
 Fig: 21/ Chlorine. (Virtual
Chembook, 2003)

Clinical Signs, Diagnosis, Treatment and Control Of

Pneumonia:
1. Bacterial pneumonia:
A. pasteurella and Mannheimia Pneumonias:
P. haemolytica biotype A is the commonest isolate from pneumonic pasteurellosis
although P. haemolytica biotype T and P. multocida may also be encountered. Other
bacteria isolated from pneumonic lungs of goats and sheep in sub-Saharan Africa
include Corynebacterium pyogenes, Streptococcus spp, Staphylococcus aureus,
Proteus mirabilis, Pseudomonas aeruginosa and Escherichia coli. The clinical signs
as the following:

 Outbreaks in groups of sheep and goats usually occur 10-14 days after a
stress.
 Early clinical signs may be observation of sudden death in a few
animals or a decline in feed consumption within a group.
 Harsh lung sounds, especially in the cranioventral portions of the lung
field, may be auscultated.
 Fever with temperature of 104 degrees F (40 degrees C) to 106 degrees
F (41 degrees C)
 Moist, painful cough, lacrimation, dyspnea (difficulty in breathing).
Examination of the lungs may reveal cracklelike sounds, along with nasal and
ocular mucopurulent discharge. (Figure: 22; A, B, &C)
 Anorexia (loss of appetite)
 Depression.

16
  Morbidity and mortality rates are variable. (The Merck Veterinary
Manua, 2008)

B
C

Fig: 22/ Goat with nasal mucopurulent discharge as A &B (Maria, 2007). Sheep with
nasal mucopurulent discharge as C. (The Merck Veterinary Manual, 2008)

Diagnosis:
In acute cases, cultures obtained from tracheal swabs or washes or from lung lesions
will be diagnostic. Histopathologic examination is useful, especially if other types of
pneumonia (eg, retrovirus interstitial pneumonia in adult sheep and goats) are also
suspected. In chronic cases, bacterial cultures may be less rewarding; Pasteurella or
Mannheimia may have been the initial problem, but results of cultures taken later
may reveal Arcanobacterium pyogenes , a common causative agent of lung abscesses.
(The Merck Veterinary Manual, 2008)

Treatment:
Medicines effective in treating pneumonia in goats include penicillin, ampicillin,
tetracycline (Figure: 23), oxytetracycline (Figure: 24), tylosin, florfenicol, and
ceftiofur. Ceftiofur is the only antibiotic approved by the Food and Drug
Administration (FDA) to treat Caprine pneumonia. The daily dosage is 0.5 to 1.0
mg/lb body weight injected intramuscularly for three days. Consult the

17
manufacturer's guide for complete product usage and storage instructions. Probiotics
are recommended after antibiotics to promote regrowth of the normal rumen
microflora (bacteria and protozoa populations). With the exception of ceftiofur, the
FDA has not approved the antibiotics discussed for treating goats. Their use is
considered extra-labeled, requiring consultation with a veterinarian for product
usage and guidance. The treatment should be repeated after 4-6 days because
relapses may occur. (Maria, 2007)

Fig: 23/ Oxytetracycline Fig: 24/ Tetracycline

Control:
 Vaccinate the herd, a systematic vaccination of the entire herd is
advised. The FDA (Food and drug administration) has approved a P.
multocida - M. hemolyticum vaccine for use in goats from the Colorado
Serum Company (Fig: 28) or Poly Serum from Novartis company (Fig:
29). The product label provides recommendations for vaccinating goat
kids up to six months of age. For complete product usage and storage
consult the manufacturer's guide. This vaccine may cause temporary
limping in a few goats.
 Improve management practices by providing optimal sanitation and air
quality in housing.
 Minimize transportation stress.
 Quarantine new animals before introducing them into the existing
herd.
 Administer trace minerals, such as Cu, Se, and Zn, to enhance immune
function. Adding vitamin E to receiving diets at pharmacological levels
(e.g., > 1,000 IU/animal daily) also seems to be beneficial.
 Provide good quality hay and water, and supplement as appropriate.
Consult a veterinarian to prescribe and administer a decongestant and
anti-histaminic drugs to reduce lung congestion.
 Keep sick goats in a dry, wellventilated location away from the rest of
the herd. (Maria, 2007)

18
 Fig: 28/ (Colorado Serum) For
vaccination of healthy cattle, sheep and
goats against pasteurellosis caused by
the micro-organisms named. Inject 2
ml SQ. Administer a 2nd dose at 2 to 4
weeks. Animals vaccinated at less than
3 months of age should be revaccinated
at weaning or at 4 to 6 months of age.
(Valleyvet, 2009)

Fig: 29/ Poly Serum is the specific

antibody supplement for the prevention
of scours and pneumonia in calves and
sheep. Serum is recommended for the
prevention and treatment of infections
caused by Arcanobacterium pyogenes,
Escherichia coli, Mannheimia
haemolytica, Pasteurella multocida
and Salmonella typhimurium. It
fortifies treatment programs when used
with antibiotics or other drugs for
treatment of diarrhea and pneumonia.
(Novartis, 2008)

B. Mycoplasma: (Contagious Caprine Pleuropneumonia)

Clinical signs:
Weakness, anorexia, cough, hyperpnea, and nasal discharge accompanied by fever
(41.6-41.7°C) are often found. Exercise intolerance and eventually respiratory
distress develop. A septicemic form of the disease without specific respiratory tract
involvement has been described. Death may occur within 2 days of the onset of the
clinical signs. Morbidity may reach 100 % and mortality ranges from 60% to 100%.
In endemic areas animals may suffer a chronic disease which is characterised by
catarrhal nasal discharges, debility, emaciation and sometimes enteritis. Recovered
animals serve as carriers. (The Merck Veterinary Manual, 2008)

Diagnosis:
The clinical signs, epidemiology, and necropsy findings are used to establish a
diagnosis. The causative organism should be isolated and identified, but isolation
may be difficult and special media is required for culture. Serological methods of
diagnosis include complement fixation, ELISA and agar gel immunodiffusion. Latex
agglutination test is very useful in field diagnosis of CCPP. Monoclonal antibodies are
also employed in the diagnosis of CCPP.

Note:

19
Morbidity can be 100 PERCENT and mortality may be in the range of 70 percent to
100 percent (19). Gathering or increased confinement of animals facilitates the
spread of the disease. (The Merck Veterinary Manual, 2008)

Treatment:
Tylosin (11 mg/kg) is effective in the treatment of CCPP when used in early stages of
the
disease. Oxytetracycline (15 mg/kg), tiamulin, chloramphenicol and
penicillinstreptomycin
can also be used. (Lughano; Dominic, 1996)

Control:
Contagious caprine pleuropneumonia is most likely to enter a country in infected animals. It
is uncertain whether long-term subclinical carriers exist; however, some outbreaks in
endemic areas have occurred when apparently healthy goats were introduced into flocks.
Outbreaks can be eradicated with quarantines, movement controls, slaughter of infected and
exposed animals, and cleaning and disinfection of the premises. Some countries have
.included vaccination in their eradication procedures
In endemic areas, care should be taken when introducing new animals into the flock. Flock
testing, slaughter, and on-site quarantine may be helpful in controlling the spread of disease.
Vaccines help prevent disease in some countries. Some antibiotics, such as tetracyclines or
.tylosin, can be effective if given early
The outbreak of CCPP in wild goats, ibex, mouflon and gerenuk suggests that this
disease could be a threat to some wildlife and/or captive wild animals. Vaccination
was helpful in ending this outbreak. In endemic areas, susceptible species should be
kept from contact with goats. Mycoplasma screening should also be considered
before animals are released into a zoo or other site, but M. capripneumoniae
infections are difficult to detect. (oie, 2008)

C. Chlamydia: (Chlamydial Pneumonia)

Chlamydiae have been identified in various parts of the world as a cause of enzootic
pneumonia in cats, calves, mice, sheep, piglets, foals, and goats. (The Merck
Veterinary Manual, 2008)

Clinical signs:

They develop a serous and later mucopurulent nasal discharge with a dry hacking
cough. Abortions occur without previous clinical specificsigns even if some goats may
develop persistent cough without breathlessness, or arthritis and
keratoconjunctivitis. In experimental infections, slight vaginal discharge was
observed the day before abortion on some goats (Figure: 25). (The Merck Veterinary
Manual, 2008)

20
 Fig: 25/ Early aborted foetuses (enzootic abortion). (ARC.LNR, 2008)

Diagnosis:
Chlamydia abortion may be diagnosed in several ways. Signs in the flock are often
enough to raise suspicion but are not reliable because they are often very similar to
those of "vibrionic" and coxiella (Q Fever) abortion. Three types of laboratory tests
are used in diagnosis. The first involves examination of the fetus, its stomach
content, and especially the placenta under the microscope. Even a fragment of
placenta may be useful. The second involves the growth of the bacteria in incubating
hens eggs. The best material to use for this test is also placenta. Third, a blood test is
available. Two clotted blood samples are needed, one taken at the time of abortion
and the other taken two to three weeks later. A positive result is indicated by a "rising
antibody titre" i.e. an increase in the level of blood antibody from the first to the
second sample. The blood test must be used along with one of the other tests and
several ewes (aborting and nonaborting) should be tested. (GoatWorld Goat Articles
Master 1999-2009)

Treatment:

Infected does should be treated with tetracycline, oxytetracycline, and

chlortetracycline. The injection of 20 mg/kg of oxytetracycline given by
intramuscular route at 105 and 120 days of pregnancy can prevent abortion but
cannot prevent chlamydial shedding at kidding. Tetracyclines affect the replication of
chlamydia and can be effective in preventing abortions. Chlamydia psittaci are
susceptible to chlortetracycline. In an infected herd, abortion can be prevented by
administrating 80 mg/head/day during pregnancy. In an outbreak, 250
mg/head/day for 3 weeks has been recommended and appears to be effective.
(Maria, 2006)

Control:

21
Formalin-inactivated suspension of Chlamydia organisms emulsified in an oil
emulsion for the immunisation of sheep against enzootic abortion.(Figure: 30).

This vaccine can be immunised at any age but it is preferable to inoculate young ewes
at least four weeks before the first mating season. The vaccine will not prevent
abortions in pregnant or non-pregnant ewes which have become infected prior to
immunisation.
Apart from abortions the natural disease may also cause polyarthritis, pneumonia,
nervous symptoms and gastro-intestinal disturbances in young lambs. Lambs may be
immunised during the first week after birth but there is as yet no guarantee that the
vaccine will protect against these manifestations.

DOSAGE: 1 ml subcutaneously. (Obpvaccines, 1869)

Fig: 30/ Formalin-inactivated suspension. (Obpvaccines, 1869)

2. Lung worm infestation: (Verminous broncho pneumonia)

Clinical signs:
 The first symptom is cough.
 Cough is accompanied by expectoration of masses of mucous containing adult
worms or larvae.
 Seromucoid nasal discharge which cause irritation & itching around the nares.
 Respiration is labored.
 Severe rise of body temperature reaching to 42 when the lung is involved.
 Emaciation.
 Anaemia.
 Frequent diarrhea.
 Enlargement & swelling of submaxillany region, lips & eye lids & sometimes
all of the anterioventral part of the head. (Fouda, 2006)

Diagnosis:

22
Diagnosis of helminthosis is based on history, epidemiological, clinical and
pathological findings and laboratory analysis of appropriate samples. The most
commonly used laboratory methods for diagnosis of gastrointestinal nematodes are
faecal egg counts, faecal cultures, determination of infective larvae on herbage and
worm counts at post mortem. (Alfonso López, 2007)

Treatment:
Many anthelmintics which are effective against different species of helminths
affecting small ruminants have been developed. Benzimidazoles, imidazothiazoles,
tretrahydropyrimidines, organophosphates and ivermectins form the major classes
of anthelmintics.

The following benzimidazoles are used to treat gastrointestinal nematodes,

lungworms and some tapeworms; albendazole (5.0-10 mg/kg), fenbendazole (5.0-7.5
mg/kg), mebendazole (12.5 mg/kg) and oxfendazole (4.5-5.0 mg/kg), oxibendazole
(15 mg/kg), parbendazole (20 mg/kg) and thiabendazole (80 mg/kg).

Fenbantel and thiophanate are effective against gastrointestinal nematodes,

lungworms and anoplocephalid tapeworms.

Ivermectin 0.2 mg/kg is very effective against gastrointestinal nematodes and

immature stages of lungworms in goats, (Figure: 26). (Alfonso López, 2007)

Fig: 26/ Ivermectin is effective treatment for lung worms.

Control:

23
The control of helminthosis is designed to eliminate or reduce the prevalence of
helminths and improve the productivity of the livestock industry. The eradication of
helminthosis in animals is difficult and the aim of control is therefore to limit the
infection by minimising the challenge to an economically justifiable level. It is
therefore important to accurately assess the cost-benefit effectiveness of any
helminth control programme if production from the animals is to be optimised.
Effective control of helminthoses can be achieved by judicious use of anthelmintics
and good management. The methods of control of helminthosis can be grouped into
four main categories;

1. Control by use of anthelmintics.

2. Control through management.
3. Control by breeding resistant stocks.
4. Control by immunization. (Alfonso López, 2007)

3. Viruses:
A. Ovine progressive pneumonia:

Clinical signs:

Maedi-visna is a chronic, progressive viral infection characterised by a prolonged

incubation period and predominantly two clinical manifestations; pneumonia
(Maedi means dyspnoea) and encephalomyelitis (Visna means wasting in Icelandic).

Animals with maedi are listless, emaciated and dyspnoeic. Respirations are laboured
and rapid; 80 per minute or higher. There is coughing and nasal discharge but most
affected sheep retain their appetite. Udder induration, hind-limb paralysis and, in
some cases, swollen joints with or without lameness, may also be present in the flock.
Clinical signs last for 3 to 12 months but the disease is inevitably fatal. (Vein, 2009)

Diagnosis:

Differential diagnoses of progressive pneumonia include pulmonary adenomatosis

( jaagsiekte), verminous pneumonia, and pulmonary caseous lymphadenitis.
Necropsy with histopathologic examination of affected lung tissue is very useful in
differentiating these various types of pneumonias. Listeriosis, scrapie, louping ill,
rabies, cerebrospinal nematodiasis, and space-occupying lesions should be
considered when the neurologic form (visna) of the disease is seen. (The Merck
Veterinary Manual, 2008)

Treatment:

There is no effective treatment or vaccine for OPP. The future holds promise for the
development of a vaccine. (Cynthia, 1998)

Control:

24
The OPP virus can best be eradicated from flocks by either of two methods (Figure:
40). One is to test and remove all positive sheep every six to twelve months until
three negative flock tests are achieved at six-month intervals or in two consecutive
years. An alternative method is to separate lambs from infected ewes at birth, before
the lambs nurse or are licked by the ewe.

Method 1: Test and remove (Figure: 40)

This method usually takes at least three or more years to achieve a negative status,
and can only be advised in flocks that on initial testing are already less than 50%
infected.

Note: Random testing 10% of the flock every year will help insure that the flock is
remaining free of the virus.

Method 2: Isolate and artificially rear progeny (Figure: 40)

This method requires 24-hour lambing supervision in order to be successful. Thus, when
considering this method, it is important to manage the flock's breeding program
accordingly.

Note: This method is more costly and labor-intensive in the short run, but will
result in a virus-free flock more quickly than method 1.

25
 Fig: 40/ This method requires 24-hour lambing supervision in order to be
successful. Thus, when considering this method, it is important to manage the flock's
breeding program accordingly. (Cynthia, 1998)

26
B. Ovine pulmonary carcinoma (OPC):

Sheep pulmonary adenomatosis (SPA, Jaagsiekte)

Clinical signs:

The adenomatous ingrowths encroach on the alveolar space and lead to anoxic
anoxia. Coughing occurs but is not a prominent sign. Emaciation, dyspnoea and
panting after exercise, profuse watery discharge from the nose are characteristic
signs (Figure: 27). Moist rales are audible over affected areas of lung. The disease is
inevitably fatal. Necropsy finding: The lungs are enlarged, heavy, consolidated and
there is frothy fluid in the bronchi. Histopathology is characteristic. (Vein, 2009)

Fig: 27/ profuse watery discharge from the nose. (Gary, 2004)

Diagnosis:

Sheep pulmonary adenomatosis (Jaagsiekte) can produce similar clinical signs with
similar flock history and, in some countries, can be simultaneously present in the
same flock and the same sheep. Pulmonary adenomatosis is characterised by a
profuse nasal discharge and a shorter clinical course. The two diseases can be readily
differentiated histopathologically. Parasitic pneumonia and melioidosis also have
signs of chronic respiratory disease.

Clinical pathology can aid in diagnosis, either by one of a number of techniques for
virus identification or by serology. Serology is used as a flock diagnosis but negative
serology in individual cases is not reliable evidence of freedom from infection. The
time between infection and sero-conversion is variable and may be as long as one or
more years. Some infected animals remain seronegative. (Vein, 2009)

27
Treatment:

There is no treatment. A vaccine is used successfully in Kenya. (Vein, 2009)

Control:

This disease can be controlling through many main ways; such as:

Isolation the infected animals because this disease are spread by the respiratory route, (1
probably by aerosol or droplet infection. Infectious virus can be found in the respiratory
exudates of infected sheep. There is no evidence of transmission in utero; however, neonates
.seem to be particularly susceptible to infection
Disinfection: The respiratory secretions of sheep with pulmonary adenomatosis are (2
contagious. Retroviruses are generally fragile in the environment and are susceptible to most
(common disinfectants. (oie, 2005

28
Summary

Pneumonia is an inflammation of the lung caused by infection with bacteria,

viruses, or other organisms. Pneumonia is usually triggered when a person's defense
system is weakened, most often by a simple viral upper respiratory tract infection or
a case of influenza (the flu). Such infections or other triggers do not cause
pneumonia directly, but they alter the protective blanket of mucous in the lungs
(which prevents foreign substances from getting into the lungs), thus encouraging
bacterial growth. Other factors can also make specific people susceptible to bacterial
growth in the lungs and pneumonia. (adam, 2009)

Most cases of pneumonia are caused by bacterial, viral, and parasitic infections.
Pasteurella haemolytica and Pasteurella multocida are bacterial organisms carried
in the respiratory tract of many normal animals.
Viral agents such as parainfluenza-3 (PI3) are common in sheep and goats and can
increase susceptibility to infection by causing inflammation of the respiratory tract.
Certain infections of ovine progressive pneumonia (OPP) and caprine arthritis
encephalitis (CAE) can cause pneumonia in sheep and goats.
Other organisms, including Mycoplasma, Dictyocaulus (lung worms), and Eimeria
can also cause lung problems.
In many cases, high humidity, dust, damp bedding, excessive heat, tight buildings
with inadequate ventilation, and irritating gases such as ammonia compromise
disease resistance and natural defense mechanisms in the sheep or goat, allowing
pneumonia to develop.

Clinical signs of pneumonia in young nursing animals that develop pneumonia

commonly lose weight, become gaunt and lethargic, fail to nurse, and usually have a
moderate fever. If the pneumonia remains undetected, serious lung damage will
result and treatment will not be effective. Additional clinical signs include the
following:

1. Clear to yellow, runny to thick nasal discharge.

2. Coughing and/or rapid breathing.
3. Harsh lung sounds heard when listening with a stethoscope.
4. Fever (temp. >103.5°).

Young animals that recover are susceptible to relapse during the feeding period and
are more likely to suffer from heat stress and chronic cough. Coughing can lead to
serious problems with rectal prolapse in feeder lambs.

Diagnosis of pneumonia is more important because lethargy and fever in

sheep and goats may have several causes, a careful physical examination is required.
In many cases, an exact (definitive) diagnosis is made by post-mortem (necropsy)
examination. Three main points to get an accurate determine diagnosis; as a
following:

29
 1. The initial diagnosis can be made from general appearance and
physical exam. The information on page C888 show regions of the lungs that
should be listened to when using a stethoscope.
2. Culture and sensitivity performed on nasal secretions or on samples
taken at necropsy can help identify the specific cause of the infection.
3. To accurately identify an infectious cause of pneumonia, a
transtracheal wash performed by a veterinarian, with culture and sensitivity,
may be necessary.

Treatment of pneumonia is must be based on early identification of affected

individuals and depends on whether the cause is bacterial, viral, or parasitic. Fluid
therapy, if practical, often helps the recovery rate. Producers should be sure that sick
newborns are nursing or that they are provided supplemental milk via stomach tube.
In serious outbreaks, it is often advisable to treat all exposed animals with a
therapeutic dose of antibiotics for several days.

1. Bacterial Causes -

 Treatment with antibiotics such as penicillin, tetracycline, Albon,

Gallimycin and even LA-200 may be considered. Like most bacterial
infections, culture and sensitivity testing is recommended.

2. Viral Causes -

 Treatment for all viruses involves treating the symptoms, not killing the
virus. With this in mind, fluids, anti-inflammatory agents (Banamine),
and antibiotics for secondary bacterial infections are recommended.

3. Parasitic Causes -

 Most parasites can be treated using ivermectin or doramectin. Routine

de-worming will also help prevent the parasitic causes of pneumonia.

The most accurate control of pneumonia; good management is the key to preventing
respiratory problems. Producers with young animals that have pneumonia often have
ventilation problems in the lambing/kidding and nursing facilities.
Newborn animals should be provided supplemental heat only until they are dry and
have nursed. Avoid overcrowding and do not keep the birthing areas too warm.

If an animal has an infectious cause of pneumonia, it should be isolated from the

rest of the flock/herd. No matter the cause of the pneumonia, caution should be
used to prevent additional spread of the disease by contaminated clothing, hands,
buckets, troughs, etc. (Cody, 1998)

30
References:
1. Infovets, Dr. Cody W. Faerber,
http://www.infovets.com/healthysmrm/F640.htm, 2998.
2. A.D.A.M., http://www.adam.com/, 2009.
3. Institute for InternationalCooperation in Animal Biologics,
www.oie.com, 2005.
4. Vein,
http://vein.library.usyd.edu.au/sheephealth/Chapter20.html, 2009.
5. Small ruminants ; respiratory diseases, GaryA.Sod,
rover.vetmed.lsu.edu/student/2010/y2s2files/FANML_Sod_SmallRumi
nantRespiratoryDz_NeonateWeanling.pdf, 2004.
6. University of Minnesota, Cynthia B. Wolf,
http://www.extension.umn.edu/distribution/livestocksystems/DI5750.html,
1998.
7. Manual Veterinary,
http://www.merckvetmanual.com/mvm/index.jsp, 2008.
8. DISEASES OF SMALL RUMINANTS: A HANDBOOK; Common
Diseases of Sheep and Goats in Sub-Saharan Africa by Lughano
Kusiluka and Dominic Kambarage, 1996.
9. Essentials of Veterinary Medicine Fouda, T.A.& Youssef, M.A,
2006.
10. Obpvaccines, http://www.obpvaccines.co.za/prods/47.htm,
1869.
11. Alabama A&M University, Maria Lenira Leite-Browning,
http://www.aces.edu/pubs/docs/U/UNP-0079/, 2006.
12. GoatWorld Goat Articles Master Index,
http://www.goatworld.com/articles/index.shtml, 2009.
13. ARC.LNR, http://www.arc.agric.za/home.asp?pid=3971, 2008.
14. Valleyvet, http://www.valleyvet.com/ct_detail.html?
pgguid=2dae75b3-7a7e-4fd8-82f4-38d5a4b248db, 2009.
15. Novartis,
http://www.livestock.novartis.com/polyserum_beef.html, 2008.
16. Maria Leite-Browning, DVM, MS, Extension Animal Scientist,
Alabama A&M University, www.aces.edu/urban, 2009.
17. Virtual Chembook,
http://www.elmhurst.edu/~chm/vchembook/102chlorine.html 18.
TeAra, 2003.
18. Veterinary Pathology (Thomas Carlyle Jones B.S., D.V.M, D.Sc.)
(Ronald Duncan Hunt B.S, D.V.M.) (Norval William King B.S., D.V.M.),
1997.
19. UPSpace, https://www.up.ac.za/dspace/, 2002.
20. Meat Hygiene J. F. Gracey, D. S. Collins, Robert J. Huey, 1999.

31
21. The RVC/FAO Guide to Veterinary Diagnostic Parasitology,
http://www.rvc.ac.uk/review/Parasitology/LungwormSheepGoat/Dict
yocaulus.htm, 2004.
22. Veterinary virology Frederick A. MurphySchool of Veterinary
Medicine University of California, Davis Davis, California, 1999.
23. History of bighorn sheep Respiration in Montana Keith Aune
Montana Dept. Fish, Wildlife and Parks Helena, Montana, 2000.
24. Pneumonia and pleurisy in sheep: Studies of prevalence, risk
factors, vaccine efficacy and economic impact Kathryn Anne
Goodwin-Ray, 2006.
25. In: Recent Advances in Goat Diseases, Tempesta M.(Ed.)
Publisher: International Veterinary Information Service, A. Rodolakis,
www.ivis.org, 2001.
26. Pathology of the respiratory system (Handout), Zachary Eds. Mosby,
http://people.upei.ca/lopez/respiratory/Notes-respi-2007.htm, 2007.
27. Sheep meat inspection chapter 1&2; By Dr.khaled fujairah
municipality, 2008.
28. Lower Respiratory Pathology; by Dr. Paulsen, 2009.
29. The encyclopedia of New Zealand,
http://www.teara.govt.nz/TheSettledLandscape/AnimalFarming/Dise
asesOfSheepCattleAndDeer/2/ENZ-Resources/Standard/1/en, 2008.

32