Equine Viral Encephalitis

 

Equine Viral Encephalitis

Introduction:-

This disease is not present in Pakistan.

It has three types:

1. Eastern equine encephalitis (EEE)   →    Sporadic
2. Western equine encephalitis (WEE) →   Least virulent virus
3. Venezuelan equine encephalitis (VEE)  → Most virulent virus (epidemic)

Epidemiology:-

The virus belongs to α-viruses of the family Togaviridae. They need arthropod vectors for their transfer. All vectors are susceptible to Equine viral encephalitis. It disappears within hours in infected tissue. This disease is more prevalent in the USA and the arthropod vector is mosquitoes. Mammals like a horse are accidental hosts. It is zoonotic in nature and causes mild type infection or clinical encephalitis in human beings. In human’s infection occurs two weeks after visiting an infected horse.

Mild types:-

1. Mild Influenza
2. Anorexia

Clinical encephalomyelitis

Clinical encephalomyelitis is seen in those having an immunocompromised system such as young ones and old animals.

Mild influenza pathogenesis:-

At first there is transitory viremia. Then the virus reaches the brain and affects the grey matter which may lead to blindness. The white matter is myelinated. The spinal cord is affected leading to paralysis.

Clinical findings:-

The incubation period in different types is as follows.

In Venezuelan  →  1-6 days

WEE    →   1-9 days

EEE   →      2-3 days

The following clinical signs may be found in animals with Equine viral encephalitis.

• High rise of temperature which persists for 24-48 hours
• Hypersensitive to touch
• Involuntary muscle contraction
• Erection of the penis in male horses
• Effected horse severally depressed with head down
• Absence of proper chewing. Half chewed food structure in the mouth
• Paralysis and animal go to recombinant position
• Incoordination in movement
• Caseation of urine and defecation
• Complete Paralysis at the end

Treatment:-

• No specific treatment.
• Culling of animal suggested.

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