MITE INFESTATION IN
RABBITS
Presented by
Jisha shaji
22- BVM- 037
FUR MITES
•2 genus
Cheyletiella : C. parasitavorax ( most common)
C. yasguri
C. blakei
Listrophorus : L.gibbus
CHEYLETIELLA PARASITAVORAX
Etiology : noninvasive fur mite of rabbits
Transmission: Direct contact, Numerous in intrascapular
region
Pathogenesis:The mite remains in association with the keratin
layer of skin and feeds on tissue fluids.
Clinical signs: Fur falling off in clumps with erythema & flaking
of underlying skin
Diagnosis : Microscopical examination Mites are ovoid or
saddle shaped with large palps and pedal combs.
PSOROTOPES CUNICULI
Etiology: Non burrowing ear mite of rabbits causing “Ear
Canker”
Distribution: External ear canals , spread to face, neck and
legs.
Transmission: Direct contact
Pathogenesis :Live on the surface feeding on lipids, keratin,
crusts and cerumen.
Clinical signs: Light to heavy brown crusts in outer ear canal ,
head shaking, weight loss, decreased productivity, secondary
infection result in torticollis.
Diagnosis: Microscopical examination of ear crusts and swab.
LEPORACARUS GIBBUS
Etiology: small, non- burrowing, obligate parasite.
Distribution: Entire body, concentrated in rump.
Transmission: Direct contact
Pathogenesis: The life cycle of the parasite is characterized by
complete metamorphosis and occurs entirely on rabbit coat. It
feeds on sebum and skin epithelial cells.
Clinical signs: Moist dermatitis in back, groin and ventral
abdomen.
Diagnosis : Microscopical examination
Mites are brown, ovoid with short ventrally directed legs.
Males have posterior clasping organ.
SARCOPTES SCABIEI
Etiology: Small, burrowing mite, also referred as itch or scab
mite
Distribution: Ears, nose, feet and perineal area
Transmission: Direct contact
Pathogenesis: Mite burrows into the skin and feeds on the
host’s serum and epithelial tissues , resulting in severe skin
lesions.
Clinical signs: Intense pruritus, hair loss and abrasions as a
result of scratching, anemia, leukopenia.
Diagnosis: Microscopical examination of skin scrapings
The body of the mite is round and legs are very short.
WEST NILE FEVER IN
WILD ANIMALS
ETIOLOGY
• Family – Flaviviridae
• Genus – Flavivirus
• Single stranded RNA virus
Two Genetic lineage
• Lineage 1: 3 clades ( 1a,1b,1c)
• Lineage 2
TRANSMISSION
• Primary mosquito vector
• Culex sp.
• Tick vectors
• Overwintering of mosquitoes
• Birds
TRANSMISSION CYCLE
SPECIES AFFECTED BY WEST NILE VIRUS
Horses Black Bear Cattle
Goats Wolf Seal
Sheep Alpaca Cat
Dog Mountain goat Deer
Rabbit Alligator
Chipmunk Gray Squirrels
Skunk Bats
Crocodile Llama
PATHOGENESIS
• Virus entry via bite of a mosquito vector
• Replication of the virus occurs in dendritic cells
• Infected dendritic cells transport the virus to regional lymph nodes
• Primary viremia
• Infection of peripheral tissues such as spleen and kidney
• By end of the first week, virus cleared from serum and peripheral
organs
CLINICAL SIGNS
Birds
• Non-specific signs e.g. depression, anorexia, weakness, leg paralysis, weight
loss
• Neurological signs e.g. abnormal head or neck posture, ataxia, tremors,
circling, disorientation, paresis, visual impairment, dysphagia and seizures
Horses
• Neurological signs -weakness, paresis or paralysis, apparent blindness, lip
droop and tooth grinding
Other mammal
• Neurological signs
GROSS LESIONS
• Birds- splenomegaly, meningoencephalitis, and myocarditis
• Horses- oedema of supraorbital fossa, submeningeal edema,
congestion in spinal cord, oral and lingual ulceration,
pulmonary oedema.
• Raptors - Encephalitis, endopthalmitis, endocarditis
• Other mammal - No relevant gross lesions.
HISTOPATHOLOGY
• Birds: mild to severe encephalitis and meningitis, with
infiltrates and perivascular cuffing– mainly lymphocytes and
plasma cells.
• Myocarditis (mild to severe), sometimes nephritis, hepatitis,
pneumonitis
• Horses: Nonsuppurative encephalitis – neuronophagia ,
multifocal gliosis, perivascular cuffing.
• Other mammals: Nonsuppurative encephalitis and
myocarditis.
DIAGNOSIS
• Clinical signs and lesions
• Detection of antibodies: PRNT ( plague reduction neutralization test ),
ELISA
• Detection of antigen: RT- PCR, NASBA ( Nucleic acid sequence based
amplification), VecTest.
Thank you

Power point presentations related to mite

  • 1.
    MITE INFESTATION IN RABBITS Presentedby Jisha shaji 22- BVM- 037
  • 2.
    FUR MITES •2 genus Cheyletiella: C. parasitavorax ( most common) C. yasguri C. blakei Listrophorus : L.gibbus
  • 3.
    CHEYLETIELLA PARASITAVORAX Etiology :noninvasive fur mite of rabbits Transmission: Direct contact, Numerous in intrascapular region Pathogenesis:The mite remains in association with the keratin layer of skin and feeds on tissue fluids. Clinical signs: Fur falling off in clumps with erythema & flaking of underlying skin Diagnosis : Microscopical examination Mites are ovoid or saddle shaped with large palps and pedal combs.
  • 5.
    PSOROTOPES CUNICULI Etiology: Nonburrowing ear mite of rabbits causing “Ear Canker” Distribution: External ear canals , spread to face, neck and legs. Transmission: Direct contact Pathogenesis :Live on the surface feeding on lipids, keratin, crusts and cerumen. Clinical signs: Light to heavy brown crusts in outer ear canal , head shaking, weight loss, decreased productivity, secondary infection result in torticollis. Diagnosis: Microscopical examination of ear crusts and swab.
  • 7.
    LEPORACARUS GIBBUS Etiology: small,non- burrowing, obligate parasite. Distribution: Entire body, concentrated in rump. Transmission: Direct contact Pathogenesis: The life cycle of the parasite is characterized by complete metamorphosis and occurs entirely on rabbit coat. It feeds on sebum and skin epithelial cells. Clinical signs: Moist dermatitis in back, groin and ventral abdomen. Diagnosis : Microscopical examination Mites are brown, ovoid with short ventrally directed legs. Males have posterior clasping organ.
  • 9.
    SARCOPTES SCABIEI Etiology: Small,burrowing mite, also referred as itch or scab mite Distribution: Ears, nose, feet and perineal area Transmission: Direct contact Pathogenesis: Mite burrows into the skin and feeds on the host’s serum and epithelial tissues , resulting in severe skin lesions. Clinical signs: Intense pruritus, hair loss and abrasions as a result of scratching, anemia, leukopenia. Diagnosis: Microscopical examination of skin scrapings The body of the mite is round and legs are very short.
  • 11.
    WEST NILE FEVERIN WILD ANIMALS
  • 12.
    ETIOLOGY • Family –Flaviviridae • Genus – Flavivirus • Single stranded RNA virus Two Genetic lineage • Lineage 1: 3 clades ( 1a,1b,1c) • Lineage 2
  • 13.
    TRANSMISSION • Primary mosquitovector • Culex sp. • Tick vectors • Overwintering of mosquitoes • Birds
  • 14.
  • 15.
    SPECIES AFFECTED BYWEST NILE VIRUS Horses Black Bear Cattle Goats Wolf Seal Sheep Alpaca Cat Dog Mountain goat Deer Rabbit Alligator Chipmunk Gray Squirrels Skunk Bats Crocodile Llama
  • 16.
    PATHOGENESIS • Virus entryvia bite of a mosquito vector • Replication of the virus occurs in dendritic cells • Infected dendritic cells transport the virus to regional lymph nodes • Primary viremia • Infection of peripheral tissues such as spleen and kidney • By end of the first week, virus cleared from serum and peripheral organs
  • 17.
    CLINICAL SIGNS Birds • Non-specificsigns e.g. depression, anorexia, weakness, leg paralysis, weight loss • Neurological signs e.g. abnormal head or neck posture, ataxia, tremors, circling, disorientation, paresis, visual impairment, dysphagia and seizures Horses • Neurological signs -weakness, paresis or paralysis, apparent blindness, lip droop and tooth grinding Other mammal • Neurological signs
  • 18.
    GROSS LESIONS • Birds-splenomegaly, meningoencephalitis, and myocarditis • Horses- oedema of supraorbital fossa, submeningeal edema, congestion in spinal cord, oral and lingual ulceration, pulmonary oedema. • Raptors - Encephalitis, endopthalmitis, endocarditis • Other mammal - No relevant gross lesions.
  • 19.
    HISTOPATHOLOGY • Birds: mildto severe encephalitis and meningitis, with infiltrates and perivascular cuffing– mainly lymphocytes and plasma cells. • Myocarditis (mild to severe), sometimes nephritis, hepatitis, pneumonitis • Horses: Nonsuppurative encephalitis – neuronophagia , multifocal gliosis, perivascular cuffing. • Other mammals: Nonsuppurative encephalitis and myocarditis.
  • 20.
    DIAGNOSIS • Clinical signsand lesions • Detection of antibodies: PRNT ( plague reduction neutralization test ), ELISA • Detection of antigen: RT- PCR, NASBA ( Nucleic acid sequence based amplification), VecTest.
  • 21.