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

pg2 Hemorrhagic fever with renal syndrome (HRFS) Et: hanta virus, Epidemiology:- Transmission to humans by aerosolized excretes of rodents( Korea , China common in spring n fall), IP- 10-25 days. Clinics:- 5 phases I. Febrile (invasive) phase: ↑fever 41 deg C for 3-4 days then ↓, chills, relative bradycardia. Head ache, back ache, generalized myalgia, abdominal pain, nausea, vomiting, diffuse reddening of the skin, mostly over face and “V” of the neck, Hemorrhage starts from palates, Petachiaes in conjunctiva , axillary folds, hips, thighs II. Hypotensive phase : During last 24-48 hrs BP starts to drop and shock develops.. cool skin, moist, bradycardia is replaced by tachy cardia. III. Oliguric phase : BUN ↑, Creatinine↑, hyperkalaemia, Pressure starts to increase. ↑ hematamesis, melena, hemoptysis, haematuria. Haemorrhages in CNS. In urine protein, RBC, cylinders. IV. Diuretic phase… finally V. Convalescing phase Dg:- Specific Ig M , Ig G ↑, ELISA Treatment :- Non specific Ribavirin 1g/4X/d / 4Days or 0.5 g/4X/d/ 6 Days Prophylaxis:- Nonspecific - ↑ in old age (DD – Malaria, shigellosis , typhoid, leptosprosis. Leptosprosis Et:- Leptospira interrogans – icterohemorrhagia (L.tavasa, L.pomoni, L.fevani) Epidemiology :- Zoonotic dis. Transmitted by pigs, cattle, cat, rat and other animals. Veterinarians, farmers, sewage workers are at special risk. The infection is transmited by urine or urine contaminated food or water → portal of entry is damaged skin (feet or exposed nasopharyngeal mucosa) IP 10 days. Clinics :- 3 main stages Leptospiraemic pahse:- 4-9 days Leptospira is in the blood and in csf. Symptoms ;- fever ↑ instepladder fashion, chills(frontal), Severe muscle aches (thighs and lumbar area) Muscles are painful in palpation. Anorexia, nausea, vomiting (mostly), Cough, chest pain, conjunctival suffusion, photophobia. Haemorrhage from palatum mucosa and in axillaries region. Asymptomatic phase:- 1-3 days Immune phase:- IgM levels↑, Meningismus may develop( in less severe forms this is the only symptomatic) Symptoms of weils syndrome:- All symptoms above + jaundice+ hepatic involvement+ hemorrhages+ kidney involvement. Jaundice +/- temp(DD hepatitis fever ↓, jaundice appears) hepatomegaly and tenderness. Hemorrhages GIT bleedings, Haematuria, hemoptysis, subarachnoidal hemorrhage. Renal proteinuria, pyuria, haematuria, azothemia. Complications:- ARF, myocarditis, encephalitis. Dg:- blood- leucocytosis, thrombocytopenia, anemia, compensatory reticulocytosis. Biochemical- 1.bilirubin ↑ 2.ALAT ↑ 3.Creatinine ↑ 4.Urea ↑ 5.↑K+ 6.↑ HCO3 – (3456 indicates ARF) Urine- protienuria, hematuria, cylinduria. Specific tests – I. Culture (urine, blood) II. Serology ↑ IgM III.CSFLymphocytic pleocytosis, increased proteins. Treatment:- etiologic- Penicillin (if meningitis) iv 2-4 ml/6X/d and tetracycline 500 mg X3/day Pathogenetic – Disintoxication iv 5 % glucose, haemodialysis (ARF) if oligo or anuria , Blood infusion FFP, vit K if hemorrhage….H2 blocker gastric mucosa protection. Prophylaxis:- Vaccines for risk group , farmers, veterinarians, non specific measures gloves, boots. DD:- fever- Influenza, typhoid, paratyphoid, sepsis. Jaundice- viral and toxic hepatitis.. if myalgia then trichomonasis. Hepatomegaly –hepatitis, malaria, chronic liver disease, parasitic disease. Renal damage- hemorrhagic fever, sallmonellosis, cholera, food poisoning.

Report on Report on Hemorrhagic fevers: - etiology, clinic, prophylaxis 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 Riga Latvia. 3. Dr. Aftab Ahmed, MD (EU), Infection Control Department, Kaunas Medical University Clinic. Lithuania. Contact: publications [at] infekcijas.eu