Contagious Bovine Pleuro pneumonia / Mycoplasmosis

 

Contagious Bovine Pleuropneumonia / Mycoplasmosis

Introduction:-

Effects mainly cattle

Two types of mycoplasma involve

1: Mycoplasma mycoid sub species mycoides

2: Mycoplasma bovine group-7, cause arthritis of bovine mastitis

Other species which is antigenicuae related are Mycoplasma capricolum subspecies pneumoniae (in caprines)

4 other strains of mycoplasma---- causes agalactia complexin caprines

M.mycoids, Agalactiae, M. capricola, M.putrifaueres

According to OIE, list a disease contagious of trade important in socio-economic importance (FMD, PPR, HS...)

Route of infection:-

Inhalation (aerosol) ---5m-45m spread

This bacteria is resistant to immune system but environmental susceptic

Mycoplasma---- not produce endotoxin & no cell wall so poor age of immune system does not recognize it (gram +ve and has more glycerol in the membrane)

Pathogenesis:-

Not clear

Gets entry through inhalation ---- enters lumen and causes sequester formation  (localized of cause persistent infection) and localized in bronchial--- cause septicemia (no blood supply) and effect various type of organ and affects kidneys, brain, joints result in the death of the patient due to thrombi formation in pulmonary vessels and death due to anoxia

Clinical Finding:-

Per acute: Sudden death without signs within one week

Acute: common in cattle

Incubation period: 3-6 weeks

• The sudden rise of body temperature 105°F (40°C)
• Agalactiae
• Cessations of ruminal movements
• Anorexia
• The animal feels severe depression and lays behind the flock

Respiratory sign:-

• Exercise-induced coxyniry and thoracic pair
• Animal reluctant to move and stand with abduction elbows (chest pain)
• Arches back and head extended forward
• Respiration will increase and shallow respiration
• Grunting sound on the expiration
• On percussion of the test, animal feel pain
• Initially, pleuritic frictional sounds and later on which fluid accumulates then furyliry sound
• Edematous swelling at throat area, joints, dewlaps (in septicemic and cause confusion with HS but in HS 6-72 hour’s death

Morbidity: 75%

Case Fertility: 50%

Chronic/Sub-acute form:-

• Clinically animal normal but there is sequester formation in lumps
• In sequester necrotic center of sufficient size burst when immune decreases and cause septicemia and later toxemia
• Chronic cough is an indication
• No antibodies formation but in HS LPS so most acute death

Diagnosis:-

• Isolation and culturing difficult----- grow lately
• serological CFT and ELISA
• for culturing: PPlO agar is used to contain glycerol

In capricolum no glycerol phosphatase but in mycoides glycerol phosphatase present

Control:-

• Vaccination
• DDX
• HS
• Anthrax
• TB
• BEF
• FMD

Treatment:-

• Tylosine drug of choice 20mg/kg (20%, L.A) tylogent, tylopen, Fertylo, Tylo 20, G-Tylo
• Chloramphenicol 20mg/kg repeated 48 hours
• Oxytetra 10mg/kg 24 hour, 20mg/kg 48 hour

In thiamphenicol sulphur replace it in chloramphenicol because there were side effects of aplastic pneumonia

Caseous lymphadenitis

 

Caseous lymphadenitis

Etiology:-

Corynebacterium pseudotuberculosis

·         Common in sheep and goat

·         Also exist in a horse called ulcerative lymphadenitis

·         It also causes contagious acne in horse

·         ulcerative lymphadenitis clinically similar to Glander in horse

Bacterial characteristics:-

Highly resistance bacteria

It produces the toxin phospholipase, which hydrolyzes the sphingomyelin sheath of macrophages due to which survive the phagocytosis that’s why resistance to immune and environment

Pathogenesis:-

Those animals which are grazing

↓ 

Get the injury and common inhabitant (Corynebacterium) cause the infection

↓  

Prefemoral nodules

↓  

Pus formation

↓  

Caseous yellowish in color

 ↓ 

Swell the nymph nodes of heard area.

            Mostly in cervical in goat but in sheep effect any gland (because shearing occurs, injury at any site.

Common inhabitant is skin and soil and survives for four months.

In fomites survive for two months.

 Shed in nasal and oral secretions

Discharge from the rupture lymph node.

Clinical finding:-

·         Enlargement of superficial lymph node (mainly cervical) sub-maxillary pre-scapular parotid lymph node in other animals pre-femoral and supra-mammary lymph node also enlargement.

·         Rupture of mature abscesses and discharge of various consistency on rupture, caseous pus discharge without any smell.

·         Loss of hair at that site

·         In systemic cases   when lymph node attach with organ

·         Chronic pneumonia pyelonephritis

·         Ataxia

·         Paraplegia (paralysis of single side)

·         Poor body condition (in the chronic form called the thin ewe syndrome)

·         Enlargement of supra-mammary lymph node

·         A decrease in milk production 

Treatment:-

·         Highly resistance bacteria

·         Mature abscess by iodex and hot therapy

·         Penicillin + tetracycline are used

Bovine Tuberculosis

 

Bovine Tuberculosis

Introduction:-

·         It is a zoonotic disease caused by mycobacterium (myco. tuberculosis)

·         John’s disease is caused by myco. paratuberclosis

·         It is a disease of mammals and most susceptible hosts are cattle, goats, pigs, horse, and deer

·         Sheep’s are naturally resistant to this disease

Source of Infection:-

·         Secreted in all the secretions, exhaled air, sputum, feces, semen, milk, vaginal and urine discharge, nasal discharges, and ocular discharges

·         TB affects all the body organs but bovine TB most commonly to the digestive tract and in the human’s respiratory system

·         Mainly through ingestion, inhalation, intra-uterine, during coitus, intramammary during passing contaminated siphon, in young dairy during suckling and milk ingestion

Pathogenesis:-

2 stages

1. Primary complex formation

2. Post-primary dissemination

1. Primary complex form

Formation of granulomatous lesions on the site of injury, regional lymph nodes, and mostly through inhalation.

When through ingestion not necessarily lesions formation, it mainly affects tonsils and mucosa

Primary foci form 8 days after entry then start of calcification of lesion starts 2 wks. Later surrounded by granular tissues, monocytes, plasma cells and result in the formation of pathognomonic signs of tuberculosis

2. Post-primary dissemination form

Bacteria inter to the other organs and produce some lesion

In 90 % of cases of cattle lesions formation on the caudal lobe of the lung and in calves it occurs in pharyngeal lymph nodes

Clinical Finding:-

·         Emaciation

·         Capricious appetite

·         Fluctuating body temperature

·         Roughness of body coat

·         And overall animal become sluggish and docile

Pulmonary Tuberculosis

·         In this case chronic cough of more than 2 wks. and more intensive at night time

·         Bronchopneumonia and moist cough

·         Coughing is induced by pressing the trachea or after exercise (exercise intolerance)

·         Coughing at night only in a cold environment

·         When pulmonary tissues destroyed then advance stages then dyspnea characterized by increased respiratory rate, consolidation of lungs, fibrosis of lungs, there will be dull sounds

·         In further advanced stages crackle because of pleurisy

·         There is the involvement of bronchial and mediastinum and due to enlargement of mediastinal lymph nodes recurrent tympany

·         In the case of the alimentary tract

·         There should be diarrhea but diarrhea is very rare in TB cases

·         Enlargement of retropharyngeal and tonsillar lymph nodes hence dyspnea and rise in breathing

·         Chronic painful swelling of submaxillary lymph nodes

Uterine Tuberculosis

Not common in cattle, otherwise bursitis, salpingitis peritonitis

Metritis leading to infertility may or may not, when conception occurs then concurrent abortion in late stages of pregnancy.

Newborn calf borne but immediately died after birth.

In males very less in metritis purulent discharges.

Mastitis

Residue in other tissues marked in duration and hypertrophy of udder. Mostly rare quarters are involved. Enlargement of supra memory lymph nodes.

In TB follicles appear in milk in the last portion. If in test tube follicles descend down and leave behind umber color fluid.

Diagnosis:-

1 SCID:

Ø  Tuberculin PPD inj 0.1 ml in a skin fold.

Ø  Observe reaction 12 to 48 hours later.

Ø  Swelling measured by Vernier caliper if more than 4 mm then the test is positive.

2 Short thermal test:

Ø  Temperature measured 4 ml of tuberculin inj ID into the neck of an animal.

Ø  Rectal temperature of the animal is 102 F but after 24hour body temperature rises up to 108 F.

Ø  20 mg / kg body weight PO ionized for 4 to 9 months.

Ø  Streptomycin 5g / animal prolong therapy.

Ø  30% human cases from bovine.

3 Double ID Test:

Avian and mammalian tuberculin injected to check either bovine or avian origin. Screening is most important.

Those bacteria when giving false-positive result with tuberculin