MICRO Flashcards
RHABDOVIRUS
-Lyassavirus > Rhabdoviridae
-Bullet-shaped
-Enveloped RNA genome
-Single-stranded non-segmented RNA
-helical symmetry
-Zoonotic disease
(severe fatal encephalitis)
Mode of infection- of rabies:
-Animal bite
-inhalation or Licks
—corneal transplantation
-wounds on the face have a shorter incubation period than wounds in the leg.
-virus moves towards other parts of body (salivary gland skeletal muscle , myocardial muscle & skin)
CLINICAL COURSE OF rabies DISEASE Four stages
•Prodrome stage:
nonspecific flu-like symptoms such as fever, malaise, headache and nausea
•Acute encephalitic phase:
- Acute neurologic syndrome after the onset of prodrome
- Includes (dysphagia, excessive salivation, vertigo, agitation, visual and auditory hallucinations,
hydrophobia (Pathognomonic feature)
•Coma
•Death - Due to respiratory arrest.
LABORATORY DIAGNOSIS of rabies:
ANTEMORTEM
Negri bodies
(Intracytoplasmic inclusion neurons in cerebellum and hippocampus)
Sample:
-Corneal impression smear, Facial skin biopsy, Saliva, CSF Investigations:
• Virus isolation
• Immunofluorescence to demonstrate antigen, RT PCR
Prevention of Rabies
Pre-exposure prevention (Killed vaccine )
Post-exposure prevention ( passive immunizationby immunoglobulin), (Active immunization HDC)
Prion
- small proteinaceous infectious material devoid of nucleic acid
- Prions onsist of single type of protein-(Prion Protein (PrP)
(PRNP) of human reside in short arm of chromosome 20
• The gene which encodes it are also found in normal ‘uninfected’ cells.
• The agent may be recovered from different organs, but the disease is confined to the CNS
-Sporadic mostly
-Normal prions (PrPc) is found on the membrane of cells.
PrPsc is abnormal
Which aggregates to form amyloid fibrilsoutside brain cells leading to tissue damage in the form of vacuole formation in neurons - spongiform changes
-diagnosis clinically and confirmed by post-mortem
Features of Prion disease
-Called transmissible spongiform encephalopathies (TSEs)
-Long incubation period ( years )
-neurodegeneration and spongiform changes.
-No effect on host B and T cell response.
-Disease is fatal with no cases of remission or recovery
-dementia, convulsions & ataxia.
-untreatable & fatal
-Leads to incoordination and dementia, ending fatally. مو بالتحديد
-corneal transplant and injection of pituitary
growth hormone, cadaveric transplant of dura mater
CREUTZFELDT-JAKOB DISEASE
Infection due to cannibalism
cerebellar ataxia and tremors. مو ب
KURU
Keratoconjunctivitis
Trachoma is an infection of the conjunctiva by the bacterium
-Chlamydia trachomatis ( A- C)
-Transmission by
-contact, contaminated flies, fingers and towels.
-40 % of blindness cases.
Pathogenesis of Trachoma
-symptomless،، inflammation with fluid discharge and eyelid irritation
-inside of the eyelid may become red, swollen, and thickened.
-Scarring follicles occur on underside of eyelid and in the tear ducts.
-chronic infection, scarring distorts shape of upper lid, causing
it to contract - lashes rub against the eyeball (Trichiasis)
-Scarring increases susceptibility to secondary infections by other bacteria or fungi.
Progress of untreated C. trachomatis infection
(1) Eyelid congestion
(2) Trachoma follicles
(3) Conjunctival scarring
(4) Corneal opacity
Lab diagnosis of C. trachomatis
• Specimen: swab from eye discharge
• Giemsa stain: shows inclusion bodies
• Fluorescent antibody test, PCR
Otitis Externa
In fection of the ear canal, may be caused by:
Ba cteria: (90%)
Pseudomonas aeruginosa (common)
Staph aureus
Proetus, Klebsiella, E. coli
-Fungi (10%)
Aspergillus niger
Candida albicans
Otitis Externa
Swimmer’s ear or Mediterranean ear
Severe form is called malignant otitis externa
Overgrowth in an ear canal subjected to excess moisture or to local trauma.
