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Hemorrhagic fevers
They include acute feverish of viral etiology of zoonostic origin.
Classification by French classification includes Leptospirosis in this group.
In animals these disease cause latent (non-manifested) forms.
Classification:
Several types of classification.
According to clinical- epidemiologic classification of “Simpsons” 3 epidemologic groups.
a- Tickborne hemorrhagic fevers
b- Mosquito borne Hemorrhagic fevers
c- Contagious hemorrhagic fevers.
Most of these disease take name from geographical regions.
Tick-borne Hemorrhagic fever:
Includes:
1- Crimiao Congo hemorrhagic fevers
2- Omsks (Russian) Hemorrhagic fever / Siberian Hemorrhagic fever
3- Disease of Kiasani Forest
Crimia Congo Hemorrhagic fever is rather frequently last 2 years.
Large number of cases is seen.
Mortality rate 10 – 15%.
Omsk HF not registered in last 10 years.
Disease of Kiasanu forest spread in South west territory of India. Morality ratio is
1 = 10%.
Main Resevior of this infection is monkeys.
All mosquito disease are tropical disease. Include:
1- Yellow fever
2- Dengue fever
3- Rift valley fever
4- Chichungunya fever
Dengue fever
Most wide spread in China, Vietnama, Cuba, Thailand.
Usually registered is 1 million cases/ year.
Specific feature is Myelgia (pain in muscles).
Rift valley fever: in Africa; Uganda, Suclan.
Last year some cases in some Arabian countries.
Usually mechanism with transmission of mosquitoes but also but direct contact with meat of domestic animals.
Chichyngunya fever
5% of cases causes with hemorrhagic syndrome.
Contagious HF
With contact way of mechanism.
Main mosological form is carrier fever with or without hemorrhagic fever and renal failure.
A.k.a. as Endemic nephropathy.
Occurs in Russian, Saint Petersburg à Registered 10 – 20 cases/ year.
Finland: 100 cases/ year.
Pathogen is Hantan virus.
Seous – registers high mortality rate > 10%.
Europe – Puumola type of virus – less severe form severity depends on presence of hemorrhagic fever. Reason of death is severe bleeding. Less severe forms see Renal failure as reason of death.
Scandinavian fever
In central Europe with see most severe forms:
By Dobrawa Belgrad type of virus mice excrete virus with urine that contaminates environment including food.
In Saint Petersburg category are people who live in villages.
Routes of transmission – inhalation (during working with hay)
Inhalation with water from small lakes
Contact with contaminated objects Haemacontact
Specific Clinical manifest:
Incubation 3 – 4 weeks.
4 main periods.
1- Innitial
2- Period of Oligourea
3- Period of Polyurea
4- Period of Reconvalesense.
Onset is acute during several hours body temperature rises to 39- 40°C with headache, muscle pans and vomiting.
Duration of initial period: 3 – 5 days.
Appearance of patient:
All other signs are non specific
At this period temperature decrease, myelgia disappears but on this from headache and vomiting becomes severe due to oedema of Brain.
Symptoms of hemorrhagic syndrome appears – petechial rash, microhematurea, intestinal bleeding.
Period of polyurea begins from 9th day – 11th day of disease. Daily diuresis approximately 5 liters or more. This period is also dangerous, patient’s disease due to electrolyte disturbances.
Therefore must restore electrolytes.
Treatment of this disease is difficult only pathogenic.
Therapy is used:
1- Detoxication
2- Prednosolone
3- Diuretics
4- Electrolytes
Yellow fever
Described in yr 1684.
Mosquito transmission proved in beginning of 20th century.
In 1927year virus was isolated.
Vector of transmission à Mosquito ladez.
Improved sanitation and water system, use of vaccines.
Reduced medical importance of yellow fewer but still occur in tropical parts of southern America, African. But it doesn’t occur in Asia anymore.
Pathogenesis:
Was started by expirements with monkeys. After rounds of replication, liver becomes principle localization of affection.
Damage of kuffer cells is due to direct viral injury and inflammation.
Hemorrhagic syndrome is characterized by thrombocytopenia due to liver failure, lower reduction of clotting factors and due to DIC syndrome.
~ 1/ 20 cases results in jaundice as clinical sign.
Onset of disease is sudden, incubation 3 – 6 days.
Early phase is period of infection with virus blood (fever, chills, headache, backpains, myelgias, nausea, severe, malaise, frustration).
Physical examination reveals signs of:
Within several days, patients may recover transitionally but fever disturb patient patient again and this is period of intoxication with systemic signs (jaundice, hemorrhagic manifestations, oligourea).
Hemorrhagic manifestations seen as Black vomit.
Patients die from acidosis with toxic shock.
Prognosis without have jaundice is poor.
Patients duration after 6- 7 days after onset.
Necessary to differentiate with hemorrhagic disease + disease with jaundice (Leptospirosis, Hepatitis).
Specific diagnostics is isolation of virus from blood by biological methods, serological methods, ELIZA + PCR.
Ab’s appear in 5 – 7 days but serological diagnosis is complicated by post reactions of other viruses.
More easy is prevention rather than treat the infection. Treatment is only symptomatic (bleeding, headache) blood replacement is useful.
Detoxication for prevention of toxic shock.
Prevention:
Vaccines. All children vaccinated in endemic regions and all people trailing to endemic regions.
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Robert Morgan Pigg | | | Higher Education in the USA |