Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার

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  Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার  Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরকার Muhammad Shakil Sarker| Md. Shakil Sarker| Sajek Valley|মো: শাকিল সরক...

Diseases of Goat | ছাগলের রোগসমূহ

 



PPR (Peste des Petits Ruminants)

Introduction 

Peste des petits ruminants(PPR) is also known as ‘ovine rinderpest’,‘Goat plague’. It is an acute, highly contagious viral disease of goat and sheep. It is characterized by the fever, sores in mouth, diarrhoea, pneumonia and sometimes death. 


Cause 

It is caused by a morbillivirus (ssRNA) in the family of paramyxoviridae, that is related to Rinderpest, Measles and Canine distemper. Incubation period 3-6 days. 


Transmission 

The virus is secreted in tears, nasal discharge, secretions from coughing, and in the faeces of infected animals. Water, feed, and bedding can also be contaminated with secretions. Since animals excrete the virus before showing signs of the disease, it can spread by movement of infected animals. Virus also present in semen and embryo. Offspring can also affected from the infected mother through milk 


Clinical Signs/ Symptoms

Hyper acute cases: Hyper acute cases are found dead without previous symptoms. They die with a serous, foamy or haemorrhagic discharge coming out of the nose.

Acute cases at onset 

1. Body temperature is high (40.5 to 41°C) 

2. Loss of appetite 

3. Depression 

4. Ulcers in the gums (lower), dental pad, hard palate, cheeks and tongue 

Evolution of acute cases: 

• Nasal discharge become mucopurulent and may obstruct the nose 

• Dry coughing develop 

• pneumonia 

• Death occur from 5-10 days after the onset of fever 

• Some animals may recover but the dry, stertorous coughing often persist for some days 

• Pregnant may abort 

Post Mortem Lesion

  • Carcase will be dehydrated with faecal soiling 

  • Congestion of the ileo-ceacal valve

  • Engorgement and blackening of the folds in the caecum, colon and rectum(‘zebra striping’) 

  • Enlarged spleen 

  • Oedematous lymph nodes 

  • Bronchopneumonia 


Diagnosis 

1. Based on the clinical signs. 

2. Histo-pathological changes in the lungs. 

3. Bronchopneumonia with antero-ventral consolidation. 

4. Virus can be isolated from lymphoid tissue at necropsy, including lymph nodes, Peyer’s patches and spleen. 

5. Blood examination 

6. Serological test: 

• AGI 

• PCR 

• ELISA 

• cDNA probe 


Treatment  

  • There is no specific treatment, supportive therapy.  

  • Symptomatic treatment for diarrhoea and respiratory problem  

  • Gentamycin can be used 

  • Hyper immune rinderpest serum  

  • OTC- 10ml mg/kg b.wt with levamisole 2.5 mg/kg b.wt for 3 days followed by repetition at 3 days interval recommended for secondary bacterial invaders  

  • Lemon juice effective against scab formation 


Prevention and Control 

• Disease is prevented in many countries by strict quarantine controls. 

• Introduced disease has been eradicated from countries by compulsory slaughter of affected flocks/herds. 

• Sanitation and hygienic measures 

• Do not introduce of new animal especially from areas where the disease is prevalent 

• Affected isolated and treated 

Vaccine 

• Tissue culture rinderpest vaccine, given at 3-4 months 

• PPR culture vaccine (I.V.R.I)- 1ml s/c annually 

• Raksha PPR- 1 ml s/c 

• Live attenuated RP vaccine protection for one year only 

• PPRV attenuated vaccine commercially available 

• Genetically engineered recombinant vaccine is under trial (OIE, 2002) 

• French attenuated PPR vaccine- immunity for at least 3 years 21





Pneumonia 

Pneumonia is inflammation of the pulmonary parenchyma accompanied by inflammation of the bronchioles and may bethe pleura. It is manifested by fever, increase in respiratory rate, cough and abnormal sounds on auscultation. 


Cause 

Causes of pneumonia are often classified into primary and secondary, but differentiation is difficult because the uncertain role of viruses in many bacterial pneumonia.

1. Bacterial causes: Other bacteria that are incriminated to cause pneumonia in sheep is considered as secondary invaders to viral infections and the enteric bacteria invade the lungs tissues when the general health conditions are lowered after digestive tract involvement. 

A. Pasteurella haemolytica and. Pasteurella multocida types 2 and 4(A&B)

B. Mycoplasma mycoides.

C. Pseudomonas pseudomallei.

D. Corynebacterium spp.

E. Staphylococci and streptococci.

F. Salmonella and Klebsiella.


2. Viral causes

A. ACUTE VIRAL RESPIRATORY DISEASES: 

1) Virus pneumonia of lambs. 

2) IBR. 

3) Parainfluenza. 

4) Bovine respiratory synceteal virus (BRSV). 

B. CHRONIC VIRAL RESPIRATORY DISEASES: 

1) Maedi. 

2) Jaajsiekte. 

3) Poxvirus.


3. Parasitic causes: 

Members of the family Metastrongylidae. 

A. Dictyocaulus filaria 

B. Cystocaulus ocreatus

C. Protostrongylus rufescens

D. Neostrongylus dinearis

E. Muellerius capillaris

4. Mycotic causes: 

Aspergillus fumigatus

5. Mechanical causes of pneumonia in case of faulty dosing or drenching medications.


Clinical signs 

  • The problem starts with high rise of temperature (40– 41°C). 

  • Followed by anorexia, inappetance, dullness, depression. 

  • Dyspnea and dry cough. 

  • Nasal and/or ocular discharge changed frommucoid to mucopurulent and purulent. 

  • Abnormal respiratory rales. 

  • Abdominal respiration is evident. 


Diagnosis 

  • Clinical signs. 

  • Isolation and identification of the causative agents.


Treatment and Control 

  • Remove the real cause.

  • Prevent or avoid the stress predisposing factors. 

  • Rest the animal and present a plenty of fresh water. 

  • Streptopen is used to treat pneumonia 

  • Broad spectrum antibiotics should be used as: Oxytetracycline: 3-5 mg/Kg. OR Kanamycin: 6-8 mg/Kg. OR Penicillin- streptomycin OR Lincospectin. 

  • Vaccination against contagious and infectious diseases. 

  • Regular Antiparasitic dosing against lung worm. 

  • Careful drenching of sheep to avoid drenching pneumonia.



Diarrhea (Scours) 

Diarrhea is defined as an increased frequency, fluidity, or volume of fecal excretion. The feces may contain blood or mucous and be smelly


Cause  

Scours are not a disease.  Scours are a symptom.  There are many causes: 

1. Infectious 

2. Non-infectious

NON-INFECTIOUS   

  • Parasitic  

    • Worms

  • Nutritional 

    • Dietary changes

    • Simple indigestion or allergy

    • Poor quality feed

    • High moisture content of feed

    • Toxins in feed

  • Management

    • Poor sanitation

    • Overcrowding


  • Stress

    • Weaning

    • Weather

    • Shipping/transportation

INFECTIOUS

  • Bacterial

    • E. coli

    • Salmonella

    • Clostridial diseases

    • Johne's disease

  • Viral

    • Rotavirus

    • Coronavirus

  • Protozoan

    • Eimeria (coccidia)

    • Cryptosporidia

    • Giardia


CLINICAL SIGNS  

  • Increased frequency, fluidity, or volume of feces. May have mucous or blood  

  • Dehydration  

  • Dirty legs and hocks  

  • Soiled wool  

  • Rough hair coat  

  • Ill thrift  

  • Poor performance


Diagnosis 

  • Clinical signs. 

  • Isolation and identification of the causative agents.


TREATMENT  

Depends upon underlying cause (and age of animal). It is treated by sulpha-III

  • Non-infectious 

    1. Bismuth Subsalicylate [OTC] 

    2. Kaolin-Pectin [OTC] 

    3. Probiotics [OTC] 

    4. Fluid therapy 


  • Infectious

    • Antibiotics

      • Penicillin [OTC]

      • Spectinomycin® [Rx]

      • Corid, sulfa drugs [Rx]


PREVENTION

  • Gradual changes in diet 

  • Roughage (dry) in diet 

  • Good sanitation 

  • Coccidiostats




Coccidiosis 

Disease situation when large numbers of the infective form of the protozoa (oocysts) are ingested – overwhelming the animal’s immune system. Most common in growing lambs/kids, age 1 to 6 months. Outbreaks are most common around time of weaning (due to stress), but disease outbreaks can occur at other times. Most common in intensively reared (housed or grazed) lambs and kids. Adults are highly resistant to disease (goats less). There are two kinds of coccidiosis. 

  • SUB-CLINICAL 

  • Clinical


Cause 

Coccidia are microscopic parasites called protozoa from the genus Eimeria. Several species of Eimeria affect sheep and goats, but not all are pathogenic. Sheep and goats harbor their own species of Eimeria and there is no cross-infection. Coccidia develop in the intestinal tract and produce oocysts (eggs) that pass in the manure.


Transmission

  • Transmission is oral; ingestion of infective oocysts.

  • Adult animals pass infective stage of the parasite into their manure.

  • Then, there is fecal contamination of the environment: hay, grain, bedding, pasture, teats, feeders, waterers, etc. 

  • Clinical disease develops, 14-17 days after infection with pathogenic levels of oocysts


Symptoms

Clinical signs 

  • Diarrhea (not always) 

  • Dirty tails, hocks 

  • Lack of appetite 

  • Depression 

  • Weight loss 

  • Poor hair coat 

  • Thin, loss of body condition 

  • Straining and pain 

  • Dehydration 

  • Weakness 

  • Death 

Subclinical signs

  • Not observed immediately and long-term infection 

  • Lower feed consumption 

  • Poor growth and weight loss 

  • Poor utilization of nutrients from feed 

  • Soft feces

 

Diagnosis

  • Observation of clinical symptoms 

  • Fecal oocyte count

    • Quantitative way of diagnosis 

    • High number of oocyte eggs can be found in feces 

    • Animals may shed oocysts without showing signs of infection 

    • Counts may vary drastically between animals (low FOC does not meant not infected) 


  • Detection of lesions in small intestine

  • Farm history 

  • Microscopic evaluation

  • Post-mortem examination


Prevention

GOOD ANIMAL HUSBANDRY 

  • Hygienic conditions 

  • Good nutrition 

  • Reduce stress factors 

ANTICOCCIDIAL THERAPY 

  • Feed 

  • Minerals 

  • Water 

  • Milk replacer 

  • Drench



TREATMENT

  • Treat all animals sharing space with infected animals 

  • No Drugs are FDA-Approved to Treat Coccidiosis in Sheep and Goats in the U.S. 

  • Drugs used for treatment include: 

    • Amprolium (Corid®) – both treatment and preventative 

    • Sulfonamides (Sulfamethazine, Sulfadimethoxine and Sulfaquinoxaline) 

    • Toltrazuril (Baycox®)– approved outside the U.S. 

    • Diclazuril (Vecoxan®) – approved outside the U.S. 

    • Ponazuril – approved for use in horses but no other animal in the U.S. 



Metabolic Disease 


Hypomagnesemia/ GRASS TETANY/ Lactation Tetany

There may be a partial dietary deficiency of Mg, but nutritional or metabolic factors reduce the availability of increase body loss of magnesium. Highly fatal metabolic diseases of lactating ruminants, characterized clinically by hyperaesthesia, tetany and convulsions and biochemically by hypomagnesaemia.


Cause

  • Low blood Mg and in many cases low blood Ca 

  • Cattle grazing on lush grass pastures in latter stages of gestation or early lactation 


Clinical signs 

Nervousness, staggering, convulsions, coma and death

(A) Acute form:  

1- Sudden onset of hyperaesthesia and muscle twitching .  

2- staggering in gait followed by falls down with tetany and convulsions. 

3- During episodes (attack) there are:  

  • a) Opithotonus (back-head).  

  • b) Pricking of ears. 

  • c) Nystagmus (Rotation of eye ball).  

  • d ) Retraction of eye lids.  

  • e) Champing of jaw. 

  • f) Frothing at from mouth.

4- Between episodes animal lie quiet but any noise or touch starting other attack .  

5- Pulse and respiration accelerated.  

6- Temperature moderatly elevated (due to muscular spasm).  

7- Death from respiratory failure. 

(B) Subacute form :  Same signs of acute but onset gradual and course longer. 

(C) Chronic form :  Animal have low serum magnesium but shows no symptoms.


Diagnosis  

  1. History

  2. Clinical signs

  3. Laboratory diagnosis:  

  • (a) Serum magnesium level commonly between  1-2mg % (normal 2.5-3 mg%).  

  • (b) Low urine magnesium level.  

  • (c) Low CSF magnesium level.  

  • (d) Bone biopsy from ribs commonly revealed disturbed Ca: Mag. ratio. 

  1. Diagnostic therapy (Therapeutic diagnosis):  Diseased animals respond well to calcium-magnesium therapy.


Treatment  

  • Contraindicated to use Mg compounds alone (may cause cardiac arrest).  

  • Safe therapy to use combined calcium- magnesium preparations as follow:  

    • 1- Calcium borogluconate 15% (I/V 500 ml).  

    • 2- Followed by: Magnesium lactate 15% (S/C 250 ml).  

    • 3- Followed by: Magnesium sulphate (oral 125 gram).


  • Preparations: Cal-D-Mg (Pfizar). Calphomag (Vibrac).  

  • Tranquilizer e.g: Chloropromazine HCl (Neurazine) used and useful before calcium- magnesium therapy in severe cases.


Prevention  

  • 1- Magnesium supplementation of diet with crude magnesium 60 gm/head which can be mixed with molasses:  

  • 2- Magnesium Bullets placed in reticulum for slow liberation of constant traces of magnesium daily for long period as long as several months or even years.



Hypoglycemia / Pregnancy Toxemia

It is highly fatal disease occurring in late pregnancy characterized by Hypoglycaemia, ketoneaemia and low liver glycogen content. Negative energy balance and multiple fetuses predispose the disease.


Cause

  • Low blood sugar  

  • Energy imbalance 

  • Breakdown of energy into ketone bodies which overwhelm liver capacity. 

Clinical Signs

  • Weakness, dull attitude, and poor appetite. 

  • Separation from the flock or herd. Inability to rise. 

  • Apparent blindness, staring off into space. 

  • Constipation is usual, the faeces are dry and scanty.

  • There is grinding of the teeth.

  • In later stages, marked drowsiness develops and episodes of more severe nervous signs occur. In these episodes, tremors of the muscles of the head cause twitching of the lips, champing of the jaws and salivation.  

  • The muscle tremor usually spreads to involve the whole body and the ewe falls with tonic-clonic convulsions.

  • Abnormal postures.

  • Recumbent in 3-4 days and remain in a state of profound depression or coma for a further 3-4 days.

  • The respirations are rapid, there may be an expiratory grunt 

  • Foetal death occurs commonly and is followed by transient recovery of the ewe, but the toxaemia caused by the decomposing foetus soon causes a relapse.  

  • Rumen contractions are weak or absent .


Diagnosis 

  • History of pregnancy 

  • Clinical signs

  •  Ketone bodies high in blood and in urine

  •  Blood glucose below 25mg/dl.

DIFFERENTIAL DIAGNOSIS 

  • Listeriosis 

  • Cerebral abscess 

  • Acidosis  

  • Uterine torsion or impending abortion 

  • Rabies.


Treatment

  • Get rid of the nutritional drain 

    • 1. Induce labor with steroids [Rx] 

    • 2. Caesarian section [Vx]

  • Glucose replacement 

1. Oral propylene glycol Alternatives: Karo™ syrup, molasses 

2. SQ glucose 

3. IV glucose 

  • Other Tx’s 

    • 1. Calcium 

    • 2. Lactated ringers 

    • 3. Sodium bicarbonate

  • Parentral therapy 

  1. Electrolytes and glucose (5% dextrose) given over a prolonged period of time

  2. Corticosteroids isoflupredone/ ISOFLUD 

  3. Trenbolone acetate 30mg i/m daily. 

  4. Triamcinolone

  • Oral therapy

  1. propylene glycol or glycerine (110 g/day) given orally is used to support parentral glucose therapy.

  • Caesarean section

  • Cal-D-mag


PREVENTION  

  • Sufficient energy in diet of females during late pregnancy  

    • Concentrates 

    • Better quality forage  

  • Identify females carrying twins and triplets and feed them accordingly.  

  • Moderate body condition.  

  • Avoid stress  

  • Encourage exercise  

  • Adequate feeder space




Hypocalcemia / Milk Fever 

A disease of cattle, sheep, and goats occurring around the time of parturition and caused by hypocalcemia and characterized by weakness, recumbency, and ultimately shock and death  “Fever” is a misnomer, as body temperature during the disease is usually below normal


Cause

  • Low level of blood calcium    

  • Insufficient intake or absorption of calcium to meet fetal or lactation demands.  

  • Occurs anywhere from six weeks prior to parturition to 10 weeks after parturition.  

    • Non-dairy (before parturition)

    • Dairy (after parturition)


CLINICAL SIGNS  

  • Fever  

  • Sudden onset of symptoms  

    • Uncoordinated  

    • Nervous 

    • Hyperactivity  

    • Sluggish  

    • Cold ears  

    • Rear legs splayed out  

    • Recumbency  

    • Comatose  

    • Death  


  • Clinical signs are similar to pregnancy toxemia; diagnosis is based on the response to treatment (calcium).


Diagnosis  

  • I) History.  

  • II) Clinical signs. 

  • III) Diagnostic therapy: Estimation of serum calcium level usually below 6 mg %, sometimes, as low as, 3 mg % (normal around 10 mg %). 

  • IV) Diagnostic therapy: (therapeutic diagnosis)

Milk fever is a dramatic disease, due to treatment with calcium borogluconate usually followed by a dramatic recovery within few minutes.


TREATMENT  

  • Calcium  

    • Oral Calcium gluconate  

    • Subcutaneous 

    • Calcium gluconate  

    • Intravenous Calcium borogluconate  

  • Other Tx’s  

    • B-complex vitamins

    • Glucose  

    • Dextrose  

    • Magnesium

  • Cal-D-mag


PREVENTION  

  • Proper levels of calcium in late gestation diet and over the long run.  

    • Addition of limestone to the grain diet.  

    • Feed better quality hay - part legume

    • Avoid stressing females.



References 

  1. Goodman & Gilman's Pharmacological Basis of Therapeutics: Hardman, Joel G

  2. Pharmacology & Pharmacotherapeutics: R.S. Satosker, Paperback

  3. Veterinary Pharmacology: Gupta & Misra

  4. Internet sources: https://en.m.wikipedia.org/ ; https://www.slideshare.net/;




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