Report on Report on Hemorrhagic fevers, Report prepared by 1. Dr. Sajid Mahmood, MD (EU), Accident & Emergency Department, NHS Royal infirmary Liverpool United Kingdom. 2. Dr. Adnan Akram, MD (EU), Department of Infectious Diseases. University Hospital Ri
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Report on Hemorrhagic fevers: - etiology, clinic, prophylaxis
HF syndrome associated with vascular instability & ↓ vascular integrity.
Direct or indirect attack on micro
vascular permeability (esp.
when PLT function is ↓ ) to...
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pg-1
Report on Hemorrhagic fevers: - etiology, clinic, prophylaxis
HF syndrome associated with vascular instability & ↓ vascular integrity.
Direct or indirect attack on micro
vascular permeability (esp.
when PLT function is ↓ ) to actual disruption and local hemorrhage.
Pathogenesis is
poorly understood and varies among the viruses that are involved.
The acute phase in the most of the HF’s are
associated with virus replication and viraemia .
except hanta virus and dengue fever in which the immune response
plays a main pathogenic role.
Yello fever:Etiology:- Flavi virus ( in Africa and in south America) .
transmitted from monkey to human by mosquito.
Clinics:- IP 3-6 days.
In mild cases the disease is indistinguishable from other viral infections as influenza or
dengue.
Classically jaundice, protienuria, hemorrhage can occur
Initial phase:- acute high fever 39 – 40 deg C (normalize in 4-5 days), Head ache, Retro bulbar pain, myalgia,
arthralgia, flushed face, suffused conjunctivae are common, epigastric discomfort & vomiting.
In severe cases
relative brady cardia (fagets sign) from the second day of the disease.
Second phase: - Pt feels well for several days, apparent recovery ( Calm phase)
Third phase:- Again pt develops fever, ↑jaundice, hepato megaly, ecchymosis, bleeding from gums, hematamesis
& melena may occur.
Coma, usually a result of uremia or hemorrhagic shock.
then death.
Dg:-I>isolating virus from blood during first 3days of illness.
Antibody titers are ↑.
II> typical histological lesions
on liver biopsy (mid zone necrosis, fatty degeneration, intracellular hyaline necrosis councilman bodies)
Treatment:- Supportive, Bed rest, analgesic, Fluid & electrolyte balance.
Prevention:- Vaccine (chick embryo vaccine)& eradication of the breeding places of the vectors.
Dengu:Etiology-Flava virus (Asia & Africa).
4 diff antigenic varieties are recognized.
Transmitted by Aegisa aegypti day
time biting.
Humans are infective during first 3 days of the disease (viraemic stage).
Mosquito’s become infective
abt 2 wks after feeding on an infected individual and remain so for the rest of the life.
Clinics:- Ip 5-6 days.
2 clinical forms are recognized
I.
Classical dengue fever: abrupt fever, malaise, head ache, retro bulbar pain(↑ on eye movements) suffused
conjunctivae, severe back ache which is a prominent symptom.
Lymphadeno pathy, petechiae on the soft
palate, and skin rashes appears on the limbs and to trunk.
The rash is transient and morbilli form.
Desquamation occurs subsequently.
Fever subsides in 3-4 days.
Temp normal or couple of days then fever
reoccur with above mentioned features but milder.
This biphasic or saddle back pattern is characteristic for
dengue.
Severe fatigue, feeling ill, depression even after fever subsides.
II.
Dengue hemorrhagic fever: severe form and is believed to be the result of the 2 or more sequential infec with
different dengue serotypes.
Mostly in children (in south east Asia ).
This has mild start, often with symptoms
of an upper respiratory tract infection( fever, head ache, cough, nausea, vomiting).
Then its followed by abrupt
onset shock and hemorrhage in skin, ear, epitasis, hematomesis, and melena known as dengue shock
syndrome.
Dg:- Dengue virus isolation in tissue culture in sera obtained during first 2 days of the illness.
Most specific is
demonstrating the rising antibody titers by neutralization, hemagglutination inhibition or compliment fixing AB in
sequential serum samples .
↓ compliments, thrombocytopenia,↑ PT , + tourniquet test.
Treatment:- symptomatic
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