Rabies

Disease of all warm-blooded animals

Etiology:

·        Rabdoviridae/Genus/Lysa Virus

Clinical Importance:

·        Zoonotic and acute type of encephalomyelitis

Characteristics of Virus:

·        Bullet shaped

·        RNA

·        Capsid Proteins

·        Surface glycopeptide serve as a neurotoxin for this virus, its helps to enter virus in nerves due to presence of surface glycopeptide receptor on nerves (Lipid receptors)

Transmission:

·      Always through bite of infected or carrier animal

·     Mainly dogs, wild carnivores particularly foxes, racoons are important while rodents (rate bite in KPK) and bats (not common in our area, Important in America and African continents)

·     Saliva is rich in rabies virus

·  Its present in world wide but countries are considered rabies free like Australia, New-zeland, Norway, England and Sweden.

Pathogenesis:

·        Virus enters through bite (Saliva inject virus)

·        Initial replication occurs in local tissues

·        Virus reaches at neuromuscular junction

·    Enter into peripheral nerves, from nerves travel in axons via retrograde manner and then reach spinal cord and brain affected (Specially forebrain), then moves centrifugally through trigeminal nerve (Cranial Nerve) to salivary gland and comes in saliva. (Rabies also occur through wound, where dog lick, cats pawing on skin and has licking habit, In USA cats are major carrier)

·  Bats which cause rabies not in Pakistan, vampire virus responsible transmission of this disease in nerves.

Incubation period vary depends upon;

·        Distance from site of bite

·        Intensity of innervation

·        Amount of virus in inoculum

·       Speed of rabies in nerves is 100mm/day, if area more nervated then speed is 400mm/day.

·        No aerosol transmission

·      Rabies 2^nd name is death because when virus enter in nerves then there is no recovery

·      Negri bodies formed in brain

• Before appearing nerves signs, virus began to shed from saliva

Clinical Findings:

·        Clinically course 3-10 days

·        Incubation period is 4-24 weeks in dogs, 2-6 weeks in cats, years in human (up to 17 years)

·        Acute behavioral changes

·        Sudden onset of anorexia (esophageal obstruction leads to drooling of saliva)

·        Nervousness

·        Hyperexcitability

·        Changes in temperament

·        All above signs in esophageal shocking but not enter mouth of animal

Phases:

1.     Prodromal

2.     Dumb/Paralytic

3.     Furious

Prodromal Phase:

·        Nervousness

·        Anxiety

·        Variable fever

·        Erratic behavior

·        Loneliness and solitude

·        Corneal and palpebral reflexes are very slow

·        Pupillary dilation

·   Licking at site of wound (If excessive chewing either self-mutilation in rabies)

Furious Form:

·        Vigor in movement and forebrain effected

·        Incubation period is 2-4 days

·        Restlessness

·        Irritated behavior

• Include auditory and visual response

Photophobia:

·        Hyperexcitation

·        Barking at inanimate objects and pica like behavior

·        Muscular incoordination

·        Seizure and death

Paralytic/dumb form:

·        Incubation period is 2-4 days

·        Whole nervous system involved

·    Progressive motor lower nerve paralysis (ascending paralysis). It starts where bite, limbs and head paralysis

·        Laryngeal paralysis which leads to horror sounds

·        Dyspnea due to laryngealparalysis

·        Change in bark, hoarse sound due to laryngealparalysis

·        Pharyngeal paralysis leading to hypersalivation and dysphagia

·        Lockjaw

·        Masticatory paralysis or dropped jaw

·        Paralysis of respiratory muscles and cause comma and death

·       In cattle there is frequent urination and bellowing which is confused with estrous. In estrous not continuous bellowing, in paralysis continuously and sounds heavy

Diagnosis:

·        Case history

·        Stole test in which Fluorescent Ab technique is used (standard test)

·        In cats there is hyperexcitation and no carrier stage

Treatment:

·        No treatment, prophylactic vaccine, canvac, Rabisin and hexadoy

·        First vaccine at day zero- post exposure

·        If mother vaccinated, then 6th week pup

·        At 4 weeks age, first deworming then first shot after 3 weeks, 2nd shot. 6, 9, 12th and15th week then annual booster which depends on manufacturer

·        3 weeks 3 months, annual+ then 3 years in book

·        Serological titer does not show complete protection

Post exposure or of vaccinated:

·        Day zero            1 ml s/c

·        Day 7                  1ml s/c

In Non-vaccinated:

·        Zero-day             1ml S.c

·        7-day                   1ml S.c

·        14-day                 1ml S.c

·        21-day                1ml S.c

·        28-day                 1ml S.c

 

·        In buffalo: 4ml, 2cc IM, 2cc s/c, 7, 14, 21 days 3ml each

·        In horse: 3ml initially and then 2,2 ml

·  IGs and vaccine must be given, after exposure 2-8 weeks disease disappear

·     In vaccine 3 weeks takes for Abs, so no immediate treatment; so, IGs given but not available so keep it under observation. If behavioral abnormality then euthanizes it immediately

·        In humans: 5 injections, only 18% chances of death if vaccinated

·        In donkey, if dog bite then rabies occurs

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.