Pneumonia in Sheep and Goat

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The most common cases of pneumonia in small ruminants Presented by Dr.Ali A.Alhumood [email protected] 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 1

Transcript of Pneumonia in Sheep and Goat

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The most common cases of pneumonia in small ruminants

Presented by

Dr.Ali [email protected]

Supervised by

Prof. Dr. Taha A. FoudaProfessor of Medicine & Therapeutics

and CLD

Head of Department

Prof. Dr. F.M Housawi

Department of Clinical StudiesCollege of veterinary medicine and

animal resourcesKing Faisal University

Second semester 2009

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Dedication

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

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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.

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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.

Death due to bronchopneumonia occurs when there is more than 60% of lung involvement in uncomplicated cases.

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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: 3/ Bronchioles filled with polymorphnuclear

Fig: 4/ High power of previous slide showing

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cells.polymorphnuclear cells

inside alveoli.

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) 

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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.

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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).

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 normal lung

tissue

Fig: 9/ Microscopic appearance of OPP-affected lung tissue (Cynthia,

1998)

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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. 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

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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:

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.

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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:

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(The RVC/FAO, 2004)

Tail

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

Fig: 11/ Sheep/goat lungworm larvae: Cysto- caulus

Cystocaulus (The RVC/FAO, 2004)

Tail

d. Dictyocaulus filaria. (Figure: 12)

Fig: 12/ Sheep/goat lungworm larvae: Dictyocaulus Dictyocaulus filarial(The RVC/FAO, 2004).

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

Fig: 13/ Sheep/goat lungworm larvae: Protostrongylus

Protostrongylus (The RVC/FAO, 2004).

Tail

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

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1) Ganskweek (Lasiospermum bipinnatum). (Figure:14, 15 &16)

Fig: 14/ Lasiospermum

bipinnatum (seed)

Fig: 15/ Lasiospermum bipinnatum (flower and seed)

Fig: 16/ Lasiospermum bipinnatum (plant)

2) Springbokbos (Hertia pallens). (Figure: 17, 18 & 19)

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

Fig: 19/ Hertia pallens (plant)

(UPSpace, 2002)

Signs: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)

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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)

Fig: 21/ Chlorine. (Virtual Chembook,

2003)

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

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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 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

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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)

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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,

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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: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 thedisease. Oxytetracycline (15 mg/kg), tiamulin, chloramphenicol and penicillinstreptomycincan 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,

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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)

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

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mg/head/day for 3 weeks has been recommended and appears to be effective. (Maria, 2006)

Control:

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.

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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: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)

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

Control: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:

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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:

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.

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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.

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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)

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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-

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conversion is variable and may be as long as one or more years. Some infected animals remain seronegative. (Vein, 2009)

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:

1 )Isolation the infected animals because this disease are spread by the respiratory route, 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.

2 )Disinfection: The respiratory secretions of sheep with pulmonary adenomatosis are contagious. Retroviruses are generally fragile in the environment and are susceptible to most common disinfectants. (oie, 2005)

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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.

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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:

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.

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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)

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_SmallRuminantRespiratoryDz_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.

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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, 1999.21. The RVC/FAO Guide to Veterinary Diagnostic Parasitology,

http://www.rvc.ac.uk/review/Parasitology/LungwormSheepGoat/Dictyocaulus.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/DiseasesOfSheepCattleAndDeer/2/ENZ-Resources/Standard/1/en, 2008.

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