Hemorrhagic fever communti

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Hemorrhagic fever communti

  1. 1. Overview of seminar Introduction Aetiology Epidemiology. Dengue hemorrhagic fever . Ebola fever . Crimean-Congo hemorrhagic fever . Yellow fever . Marburg hemorrhagic fever . Lassa fever . Rift valley hemorrhagic fever . Prevention and control.
  2. 2. Definition:Haemorrhagic disease is term with a very wide spectrum . It comprise the disease caused by organisms and Those due to the other causes (any cause other than organisms ). Here we are going to deal with infectious haemorrhagic disease , which are caused mainly by viruses and rarely by bacteria.
  3. 3. The viral haemorrhagic fevers:Is a term refers to a group of illnesses caused by several distinct families of viruses that effect humans and non -humans primates.
  4. 4. What is Viral Hemorrhagic Fever? • Severe multisystem syndrome • Damage to overall vascular system • Symptoms often accompanied by hemorrhage – Rarely life threatening in itself – Includes conjunctivitis, petechia, echymosis
  5. 5. Classification Arenaviridae Bunyaviridae Filoviridae Flaviviridae Junin CrimeanCongo H.F. Ebola Kyasanur Forest Disease Machupo Hantavirus Marburg Omsk H.F. Sabia Rift Valley fever Guanarito Lassa Yellow Fever Dengue
  6. 6. • Hemorrhagic Fevers viruses . • RNA viruses covered in a lipid coating – Viruses are geographically restricted to areas where host species live – Humans are not natural reservoirs for these viruses . – With few noteworthy exception, there is no cure or established treatment .
  7. 7. History :The term hemorrhagic fever was first used in the 1930s by Soviet and Japanese scientists .to describe an acute febrile disease encountered in eastern Siberia and northern Manchuria.
  8. 8. This syndrome subsequently reported from Korea, Bulgaria, Hungary, European Russia and Northern Scandinavia under several labels including. epidemic hemorrhagic fever, hemorrhagic fever with renal syndrome and hemorrhagic fever nephrosonephritis (HNN).
  9. 9. Since 1940s ,,,,,,, 1-Omsk hemorrhagic fever occurs in Western Siberia. 2-KFD in Mysore state and India . 3-DHF in several large cities in southeast Asia . 4-AFHF in portions of central , eastern and southern Africa. 5-RVF in southern eastern Africa . 6-CrHF. 7-BHF. 8-LF. 9-AHF.
  10. 10. Arenaviridae History • First isolated in 1933 • 1958: Junin virus - Argentina – First to cause hemorrhagic fever – Argentine hemorrhagic fever • 1963: Machupo virus – Bolivia – Bolivian hemorrhagic fever • 1969: Lassa virus – Nigeria – Lassa fever
  11. 11. Bunyaviridae History • 1930: Rift Valley Fever – Kenya – Epizootic in sheep • 1940s: CCHF - Crimean peninsula – Hemorrhagic fever in agricultural workers • 1951: Hantavirus – Korea – Hemorrhagic fever in UN troops • 5 genera with over 350 viruses
  12. 12. Filoviridae History • 1967: Marburg virus – European laboratory workers • 1976: Ebola virus – Ebola Zaire – Ebola Sudan • 1989 and 1992: Ebola Reston – USA and Italy – Imported macaques from Philippines • 1994: Ebola Côte d'Ivoire
  13. 13. Marburg in 1967
  14. 14. Flaviviridae History • 1648 : Yellow Fever described • 17th–20th century – Yellow Fever and Dengue outbreaks • 1927: Yellow Fever virus isolated • 1943: Dengue virus isolated • 1947 – Omsk Hemorrhagic Fever virus isolated • 1957: Kyasanur Forest virus isolated
  15. 15. Why do VHFs make good Bioweapons? • • • • • • • Disseminate through aerosols Low infectious dose High morbidity and mortality Cause fear and panic in the public No effective vaccine Available and can be produced in large quantity Research on weaponization has been conducted
  16. 16. Why do VHFs make good Bioweapons? • • • • • • • Disseminate through aerosols Low infectious dose High morbidity and mortality Cause fear and panic in the public No effective vaccine Available and can be produced in large quantity Research on weaponization has been conducted
  17. 17. VHF Agents as Biological Weapons • Outbreak of undifferentiated febrile illness 2-21 days following attack – Could include • Rash, hemorrhagic diathesis and shock • Diagnosis could be delayed – Unfamiliarity – Lack of diagnostic tests • Ribavirin treatment may be beneficial
  18. 18. etiology
  19. 19. Major causes of haemorrhagi fever  1) 2) 3) 4) 5)  1) 2) 3) Arenaviridae family: Guanarito virus. Junin virus. Machupo virus. Lassa virus. Sabia virus. Bunyaviridae family: Nairo virus. Phlebo virus. Hantaan virus.  1) 2) 3)  1) 2) Flaviviridae family: Yellow fever virus. Dengue virus. Omsk H.f virus. Filoviridae family: Ebola virus. Marburg virus.
  20. 20. Minor causes of haemorrhagic fever 1) 2) A. B. Rickettsia . Spirochaetes : Leptospira. Borrelia .
  21. 21. most serious causes to haemorrhagic fever • • • • • • • 1- yellow fever virus. 2- rift valley virus. 3- Ebola virus. 4- Dengue virus. 5- Crimean congo virus. 6- Lassa virus. 7- Marburg virus.
  22. 22. Yellow fever virus • Is member of the genus Flavivirus of Flaviviridae family • Is spherical virus and is 40 to 50 nm in diamter • Is positive sense single stranded RNA is approximately 11,000 nucleotides long and has single open reading frame encoding polyportein .
  23. 23. Yellow fever virus
  24. 24. Rift valley virus • Is member of genus phlebo virus of family bunyavirid • Is single-stranded RNA viruses , spherical in shape,and 90 to110 nm in diameter, with lipid envelope from which glycoprotein spikes protrude. • It can found in the host membrane system.
  25. 25. Rift valley virus
  26. 26. Ebola virus • Is member of the flioviridae family. • It is may appear in the shape of a shepherd's crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched . • It is an alongated filamentous molecule, which can vary between 800 to 1000 nm in length and can reach up to 14000 nm long, with diameter of 80 nm. • Scientists have identified five types of Ebola virus. Three have been reported to cause disease in humans: Ebola-Zaire virus, Ebola-Sudan virus, and Ebola-Ivory Coast virus .
  27. 27. Dengue virus • Is member of flavivirus group in the family flaviridae. • Is spherical single stranded enveloped RNA virus,is 30 nm in diameter. • Which can grow in variety of mosquitoes and tissue culture.
  28. 28. Crimean congo virus • Is belonging to the genus nariovirus of family bunyaviridae . • Is triple segmented ,single strand ,negative sense RNA . • The virions are spherical ,with 85 to 105 nm in daimeter.
  29. 29. Lassa virus • Is belonging to the genus Arenavirus , family Arenaviridae . • Is Double segmented, single stranded RNA virus. • The viral fragment may be in several distinct shapes (pleomorphic), and is between 80 to 150nm in diameter .
  30. 30. Marburg virus • is a member of the Filoviridae family. • is an elongated filamentous molecule, highly variable in length, but typically around 1000 nm long with a uniform diameter of 80 nm . • may appear in the shape of a "6", a "U", or a circle, and it is contained within a lipid membrane . • Each virion contains one molecule of single stranded, negative sense viral genomic RNA .
  31. 31. EPIDEMIOLOGY 1-Dengue hemorrhagic fever . 2-Ebola &Marburg hemorrhagic fever . 3-Crimean-Congo hemorrhagic fever . 4-Yellow fever . 5-Lassa fever . 6-Rift valley hemorrhagic fever .
  32. 32. Descriptive Studies
  33. 33. Analytical Studies
  34. 34. Dengue Fever • Each year, an (500,000) cases of dengue hemorrhagic fever occur worldwide, with (22,000) deaths (mainly in children). • In the last 50 years, the incidence of dengue has increased 30-fold worldwide. • In Sudan ,there is (168) cases of dengue fever arise to a hospital Port Sudan during the period from November to February, with (6) cases of deaths .
  35. 35. • Agent: Dengue virus. • Host: - Definitive host: Aedes aegypti. Aedes albopictus. - Intermediate hosts: Humans and non-human primates. • Vectors: mosquito-born favivirus.
  36. 36. aegypti albopictus
  37. 37. • Person: Both sexes - Child more common affected. • Period: Biphasic (May- November) peak at June -August. • Place: Tropical and Subtropical Worldwide.
  38. 38. Ebola and Marburg FEVER Year Location Sudan Reported Cases, No. 284 Deaths, No. (%) 151 (53) 1976 1979 Sudan 34 22 (65) 2004 Sudan 17 17 (41) 1976 Englandb 1 0 (0) 2000-2001 Uganda 425 224 (53) 761 414 (54.4) Total
  39. 39. • Agent: Ebola virus . Marburg fever. • Host and vector: -research scientists continue to search for the exact animal host.
  40. 40. • Person: Adult more exposure both sexes. • Period: DRY SEASONS. • Place: Sub-Saharan Africa.
  41. 41. Crimean Congo fever • Agent: Criminal Congo virus. • Host: - Definitive host: Adult Tics. - Intermediate host: human • Vectors: Tics of genus Hyalomma.
  42. 42. • Person: All ages- man more exposed • Period: June- August • Place: Africa – East china.
  43. 43. Yellow fever • The case-fatality rate of yellow fever in Africa approximates 20%. • The Federal Ministry of Health reported to WHO an outbreak of yellow fever in the South Kordofan State. In16 November 2005, 404 cases and 118 deaths in ( Abu Gebiha , Rashad , Dilling , Kadugli , Talodi ).
  44. 44. • Agent: Yellow fever virus. • Host: -Definitive host: Aedes aegypti. -Intermediate host: Human. • Vectors: Wild mosquitoes ( Aedes aegypti ,Haemogogus).
  45. 45. Haemogogus
  46. 46. • Person: Both sexes affected, Adult more exposed (and Infants and children are at highest risk). • Period: Rainy season. • Place: Africa-south America .
  47. 47. Lassa fever. • Lassa fever occur yearly (300, 000 )– (500 ,000) people and (5000) deaths among those in the West African region. • Case-fatality rate of 1% to 15% among patients treated in hospitals.
  48. 48. • Agent: Lassa virus. • Host: - Definitive host: rodent - ( Mastomys natalensis ). - Intermediate host: Human Vector: Not proven yet.
  49. 49. • Person: All ages and Both sexes. • Period: No mark peak. • Place: west Africa.
  50. 50. Rift valley Fever. • Until 14 November 2007,WHO reported (329) human cases of Rift Valley Fever in Sudan has led to (96) deaths and that in the states of White Nile, Sennar and Gezira. • The cases reported in Khartoum State is not endemic in the state cases, but cases are coming from one of the other affected States.
  51. 51. • Countries with endemic disease and outbreaks of RVF:• South Africa. • Sudan…. • Zambia. • Kenya. • Egypt and Madagascar. • Saudi Arabia and Yemen.
  52. 52. • Agent: Rift valley virus. • Host: - Definitive host: Aedes - culex pipiens. -Intermediate host: Human , sheep , cattle . • Vectors: Arthropod-blood born.
  53. 53. culex pipiens
  54. 54. • Person: All ages and Both sexes (man more affect). • Period: In late summer. • Place: -sub-Saharan African and Madagascar - Egypt.
  55. 55. Dengue fever
  56. 56. Contents 1. What is dengue fever 2. Dengue virus 3.Symptoms of dengue fever 4.Characteristics of the Aedes mosquito 5.Life cycle of the Aedes mosquito 6.How the Aedes mosquito transmit diseases 7.What is the lab diagnosis 8.How to prevent the spread of dengue fever
  57. 57. What is dengue fever? Dengue Fever is an illness caused by infection with a virus transmitted by the Aedes mosquito.
  58. 58. Dengue Virus 1.Causes dengue and dengue hemorrhagic fever 2. It is an arbovirus 3.Transmitted by mosquitoes Aedes aegypti
  59. 59. Symptoms of Dengue Fever Example of a skin rash due to dengue fever
  60. 60. Do you know… Dengue Fever (DF) and Dengue Haemorrhagic Fever (DHF) are the most common mosquito-borne viral disease in the world. It can be fatal.
  61. 61. The most common epidemic vector of dengue in the world is the Aedes aegypti mosquito. It can be identified by : the white bands or scale patterns on its legs and thorax.
  62. 62. Characteristics of the Aedes Mosquito One distinct physical feature – black and white stripes on its body and legs. Bites during the day. Lays its eggs in clean, stagnant water. Close-up of an Aedes mosquito
  63. 63. Do you know… Only the female Aedes mosquito feeds on blood. This is because they need the protein found in blood to produce eggs. Male mosquitoes feed only on plant nectar. On average, a female Aedes mosquito can lay about 300 eggs during her life span of 14 to 21 days.
  64. 64. Life cycle of the Aedes Mosquito 1-2 days Larvae Pupae 4-5 days Stagnant water Eggs 2-3 days
  65. 65. How Do Aedes Mosquitoes Transmit Diseases... Mosquito bites and sucks blood containing the virus from an infected person. And passes the virus to healthy people when it bites them. Virus is carried in its body.
  66. 66. Pathogensis(mechanism) 1.The virus is inoculated into humans with the mosquito saliva. 2.The virus localizes and replicates in various target organs, for example, local lymph nodes and the liver. 3.The virus is then released from these tissues and spreads through the blood to infect white blood cells and other lymphatic tissues. 4.The virus is then released from these tissues and circulates in the blood.
  67. 67. 5.The mosquito ingests blood containing the virus. 6.The virus replicates in the mosquito midgut, the ovaries, nerve tissue and fat body. It then escapes into the body cavity, and later infects the salivary glands. 7.The virus replicates in the salivary glands and when the mosquito bites another human, the cycle continues.
  68. 68. diagnosis
  69. 69. TREATMENT • The are no specfic treatment for dengue fever • Supportive treatment • 1-rehydration • 2-blood transfusion • 3-admission in present of warning signs • 4-avoidence of NGT IM injection NSAID
  70. 70. • 5-pracatamol for fever • 6-Analgesic for headache
  71. 71. Prevent Aedes from Breeding! Remove ALL sources of stagnant water. Deny the Aedes mosquito of any chance to breed.
  72. 72. Do the 10-Minute Mozzie Wipe-out everyday. Change water in vases on alternate days.
  73. 73. Do the 10-Minute Mozzie Wipe-out everyday. Remove water from flowerpot plates on alternate days.
  74. 74. Do the 10-Minute Mozzie Wipe-out everyday. Turn over all pails and water storage containers.
  75. 75. Do the 10-Minute Mozzie Wipe-out everyday. Clear blockages and put Bti insecticide in roof gutters monthly.
  76. 76. Unwanted items Do not litter. Rubbish such as cups and bottles can collect rain water and breed mosquitoes.
  77. 77. Spread the dengue prevention message to others… Let your family, friends and neighbours know about the dangers of breeding Mozzies!!
  78. 78. Ebola
  79. 79. Ebola • Ebola hemorrhagic fever is a severe and often deadly illness that can occur in humans and primates (monkeys, gorillas).
  80. 80. Cause Ebola hemorrhagic fever is caused by a virus belonging to the family called Filoviridae. Scientists have identified five types of Ebola virus. Three have been reported to cause disease in humans: EbolaZaire virus, Ebola-Sudan virus, and Ebola-Ivory Coast virus. The human disease has so far been limited to parts of Africa. The Reston type of Ebola virus has recently been found in the Philippines.
  81. 81. MODE OF TRANSMTION -The disease can be passed to humans from infected animals and animal materials. - Ebola can also be spread between humans by close contact with infected body fluids or through infected needles in the hospital.
  82. 82. PATHOGENESIS *The specific mechanism of pathogenicity is poorly understood due to difficulty obtaining samples and study the disease in areas of outbreaks.
  83. 83. • Endothelial cells, mononuclear phagocytes, and hepatocytes are the main targets of infection. After infection, in a secreted glycoprotein (sGP) the Ebola virus glycoprotein (GP) is synthesized. Ebola replication overwhelms protein synthesis of infected cells. The GP forms a trimetric complex, which binds the virus to the endothelial cells lining the interior surface of blood vessels.
  84. 84. • The sGP forms a dimetric complex which interferes with the signaling of neutrophils, , which allows the virus to evade the immune system by inhibiting early steps of neutrophil activation. These white blood cells also serve as carriers to transport the virus throughout the entire body to places such as the lymph nodes, liver, lungs, and spleen.] The presence of viral particles and cell damage resulting from causes the release of cytokines (specificallyTNF , IL 6, IL 8, etc.), which are the signaling molecules for fever and inflammation.
  85. 85. • The CYTOPATHIC effect, from infection in the endothelial cells, results in a loss of vascular integrity. This loss in vascular integrity is furthered with synthesis of GP, which reduces specific integrins responsible for cell adhesion to the inter-cellular structure, and damage to the liver, which leads to coagulopathy.
  86. 86. -During the incubation period, which can last about one week after infection, symptoms include: -Arthritis. -Chills. -Fatigue. -Headache -Nausea. -Vomiting. -Backache. -Diarrhea. -Fever. -Malaise. - Sore throat
  87. 87. Late symptoms include: *Bleeding from eyes, ears, and nose *Gastrointestinal bleeding. *Eye swelling &conjunctivitis. *Genital swelling (labia and scrotum). *Hemorrhagic skin rash. *Depression
  88. 88. COMPLICATION • DIC. • Perfuse bleeding. • Shock. • Survivors may have unusual problems, such as hair loss and sensory change
  89. 89. LABROTARY DIAGNOSIS
  90. 90. *Tests used to diagnose Ebola fever include: 1-CBC. -Thrombocytopenia. 2-IFA. 3-ELISA. 4-Detection of specific Abs (IgM).
  91. 91. Treatment *Supportive treatment: -ICU. - Correct The body fluids & Electrolytes. - Give Analgesics.
  92. 92. Prognosis *Patients usually die from low blood pressure (shock) rather than from blood loss. *Completely bad prognosis.
  93. 93. • The disease was first characterized in the Crimea • Then occurs in the Central Asia, and regions of AFRICA. • (CCHF) is caused by:• a tick-borne virus (Nairovirus) in the family Bunyaviridae .
  94. 94. Enveloped, spherical. Diameter from 80 to 120nmNairovirus Nairovirus
  95. 95. Hyalomma ticks vector
  96. 96. Route of transmition • xodid (hard) ticks, especially those of the genus, Hyalomma, are both a reservoir and a vector for the CCHF virus. Numerous wild and domestic animals, such as cattle, goats, sheep and hares, serve as amplifying hosts for the virus. • Transmission :• Zoonotic • human to human • Documented spread of CCHF
  97. 97. Site of infection
  98. 98. Risk factor • • • • Animal herders livestock workers slaughter houses in endemic areas Healthcare workers in endemic areas
  99. 99. Animal herders
  100. 100. Cilinical features • (a) Incubation:• 1-3 days after ticks bite • 5-6 days after contact to blood and tissue Of infected livestock or human patient
  101. 101. • (b) pre hemorrhagic phase(3-6 days):• Sudden onset of fever(39-41c’) • sever headache • Dizziness • hyperemia of face • vomiting • abdominal pain • low blood pressure • neuropsychological changes:mood and feeling of confusion aggression
  102. 102. (c) hemorrhagic phase(12-14days):.Ecchymoses .intestinal hamorrhagis . epistaxis . puncture sites . hematemesis . melena . hematuria . leucopenia .thrombocytopenia . Hepatosplenomegaly
  103. 103. Lab diagnosis • Laboratory tests that are used to diagnose CCHF include:• antigen-capture enzyme-linked ELISA • RT-PCR • virus isolation attempts • detection of antibody by ELISA (IgG and IgM). • Immunohistochemical staining can also show evidence of viral antigen in formalin-fixed tissues.
  104. 104. treatment .primarily supportive. Care should include careful attention to fluid balance and correction of electrolyte abnormalities, • oxygenation and hemodynamic support • appropriate treatment of secondary infections. • The virus is sensitive in vitro to the antiviral drug ribavirin.
  105. 105. Complications • • • • complications may include:Organic failure intraabdominal abscess acute cholecystitis
  106. 106. Yellow fever
  107. 107. Definition:•Yellow fever is an acute viral hemorrhagic disease transmitted by infected mosquitoes. The "yellow" in the name refers to the jaundice that affects some patients. •The virus is endemic in tropical areas of Africa and Latin America.
  108. 108. •The number of yellow fever cases has increased over the past two decades due to declining population immunity to infection, deforestation, urbanization, population movements and climate change. •There is no cure for yellow fever. Treatment is symptomatic.
  109. 109. Morphology of the virus . RNA virus . Spherical. . Envelope with spikes. envelope Lipoprotein. spikes glycoprotein. . Spherical capsid .
  110. 110. Transmission The yellow fever virus is an arbovirus of the flavivirus genus. The mosquito is the primary vector. It carries the virus from one host to another, primarily between monkeys, from monkeys to humans, and from person to person.
  111. 111. • Several different species of the Aedes and haemogogus mosquitoes transmit the virus. • The mosquitoes either breed around houses (domestic), in the jungle (wild) or in both habitats (semi-domestic).
  112. 112. Aedes Aegypti Yellow fever mosquito
  113. 113. There are three types of transmission • cycles:- 1 Sylvatic yellow fever: •Take place in tropical rainforests. •Wild mosquitoes ………bite monkeys ……infected mosquitoes ……….bite human entering the forest …..resulting in yellow fever. •The majority of infection occur in young men working in the forest.
  114. 114. •2 Intermediate yellow fever: •Take place in humid and semi-humid parts of Africa. •Semi –domestic mosquitoes ……bite human and monkey…..resulting in yellow fever …..small out break. •Increased contact between people and infected mesquite lead to transmission. • 3 Urban yellow fever: • Large epidemics occur in populated area with a high number of non-immune people and aedes mosquitoes.
  115. 115. Pathogenesis •After transmission of the virus from a mosquito the viruses replicate in the lymph nodes and infect dendritic cells in particular. From there they reach the liver and infect hepatocytes (probably indirectly via Kupffer cells), which leads to eosinophilic degradation of these cells and to the release of cytokines. Necrotic masses (Councilman bodies) appear in the cytoplasm of hepatocytes.
  116. 116. • When the disease takes a deadly course, a cardiovascular shock and multi organ failure with strongly increased cytokine levels.
  117. 117. Signs and symptoms • The incubation period (3—6days). • Acute phase:• Fever. • Muscle pain. • Backache. • Headache. • Loss of appetite. • Nausea and vomiting. • Most patient improve and their symptoms disappear after(3---4)days.
  118. 118. toxic phase:• Occurred within 24 hours of the initial remission with: • High fever. • jaundice • abdominal pain with vomiting. • Bleeding from the mouth, nose, eyes. blood in the vomits and faeces. • Kidney function deteriorates. • Half of the patients who enter the toxic phase die within 10 to 14 days, the rest recover without significant organ damage.
  119. 119. Lab diagnosis virus isolation : - from blood or liver either :- Intra cerebrally in mice. -Tissue :- culture of chick embryo. 2 Serology :- the best is neutralization test:Plague reduction . if the patient have anti bodies . In his serum ,the virus will not produce plague in the serum . 1 3 ELISA : IgM 4 Histology :- is the patient dies 5 P.C.R
  120. 120. Treatment There is no specific treatment for yellow fever, only supportive care to treat dehydration and fever. Associated bacterial infections can be treated with antibiotics. Supportive care may improve outcomes for seriously ill patients, but it is rarely available in poorer areas.
  121. 121. MARBURG hemorrhagic fever
  122. 122. Definition *Acute infectious of VHF which effect both human and non human( primates) *Marburg virus are bacilliform in morphology and can be pleomorphic when grown in tissue culture *The culture as either long filamentous or branching
  123. 123. *Marburg virus is enveloped and single strand *non segmental negative sense RNA *the reservoir for Marburg virus is still un know but can be found in bat ,monkey ,spider and ticks
  124. 124. Mode of Transmission: 1zoonotic Avectors BWaste products 2Person to person Afluid excretion BSexual transmission 3Nosocomial infection A Reuse of needle BExposure to infection tissue CHospital waste 4Aerosol has been observed in primates
  125. 125. PATHOGENESIS: Virion are contain surface spikes (large glycoprotein) Attachment structure in binding cell receptor molecules in the infection process Mediated entry into susceptible cell lead to systemic inflammatory response(tumor necrosis factor) Injury to microvasculature and endothelial permeability lead to coagulation effect (DIC) impairment adaptive immunity Tissue damage and shock
  126. 126. Risk factor: 1Travel to Africa 2Contact with animals 3Prepare people for burial . Still contagious .
  127. 127. Clinical feature: ICP usually 5-7days but can rang form 3-10 days *mortality rate around 25%-30% * *Early signs and symptoms include: -Sudden onset Fever - Severe headache -Joint and muscle aches -Chills -Weakness -Maculopapular rash
  128. 128. late symptoms become increasingly severe and may Uveitis include: Hearing loss ,psychosis pericarditis blindness bleeding *Ecchomyoses *Petechial hemorrhagic Chest pain cough orchitis Rectal bleeding Vomiting nausea diarrhea stomach pain hepatitis
  129. 129. complication: -Multiple organ failure -Severe bleeding -Jaundice -Delirium -Seizures -Coma -Shock
  130. 130. *Differential diagnosis: shigellosis typhoid malaria leptospirosis *Investigation: - ELISA -reverse transcriptase polymerase chain reaction (PCR) -can detect specific genes or the virus or antibodies to them
  131. 131. -CBC -liver function test Management: *No specific antiviral therapy exists *isolate patient *notify local and state community department *Supportive hospital care
  132. 132. Lassa Fever
  133. 133. Lassa fever (LF) is a severe hemorrhagic fever (HF) caused by the arenavirus( Lassa viru), it causes an acute hemorrhagic disease and sometimes it may be fatal in humans and nonhuman primates.
  134. 134. Mode of transmission : • Lassa virus is zoonotic Which is can be by tow ways :
  135. 135. Rodent to human
  136. 136. The virus is shed in rodent excreta (urine, feces and saliva ), which could be ingested by human or can be aerosolized.
  137. 137. by catching and repapering it as a meal or by host bite
  138. 138. Human to human by: Direct contact with blood , tissues, secretions or excretion s of infected humans
  139. 139. Needle stick or cut Inhalation of aerosolized virus
  140. 140. The virus is excreted in semen for three months so it STD and it excreted in urine for three to nine weeks.
  141. 141. Pathogenesis pathologic descriptions of Lassa virus in human are limited to a few cases . common gross finding at postmortem examination include ; _ petechial hemorrhages in separate parts of the body
  142. 142. pleural effusion, pericardial effusion and ascites microscopically : Congestion and variable degree of necrosis in all organ systems hepatocellular necrosis s with cytoplasmic eosinophilia inflammatory cell in necrotic area
  143. 143. pneumonitis , myocarditis ,acute renal tubular necrosis is not part of pathogenesis of lassa fever
  144. 144. CLINICAL MANIFESTATION
  145. 145. Symptoms • Incubation period of 6-21 days • 80% of human infections are asyptomatic the pt notes the insidious onset of : • Onset is slow: fever, weakness, & malaise
  146. 146. • Few days: headache, pharyngitis, muscle pain, retrostinal & abdominal pain, nausea, vomiting, diarrhea, cough, & proteinuria – Neurological problems: tremors, encephalitis, hair loss, gait disturbance, deafness • 95% deathrate among pregnant women & spontaneous abortion
  147. 147. • present with classic symptoms of bleeding ( mucoprpular bleeding )
  148. 148. conjunctival bleeding
  149. 149. Sensorineural Hearing Deficit in Lassa Fever • Typically appears during early convalescence • Not related to severity of acute illness • Occurs in one-third of cases • May be bilateral or unilateral • May persist for life in up to one-third of those affected
  150. 150. Clinically, Lassa fever infections are difficult to distinguish from other viral hemorrhagic fevers such as Ebola and Marburg, and from more common febrile illnesses such as malaria
  151. 151. Lassa fever in pregnancy and pediatric
  152. 152. lSV in pregnant woman a significantly elevated risk for both the mother and the fetus ,maternal mortality elevated during 3rd trimester fetal death approaches 100%
  153. 153. pediatric lassa fever is less well described but produce a spectrum of disease “swollen baby syndrome “ comprised of anasarca , abd. distention and bleeding.
  154. 154. Diagnosis: There is a range of laboratory investigations that are performed to diagnose the disease and assess its course and complications
  155. 155. • . ELISA test for antigen and IgM antibodies gives 88% sensitivity and 90% specificity for the presence of the infection. Other laboratory findings in Lassa fever include lymphopenia (low white blood cell count), thrombocytopenia (low platelets), and elevated aspartate aminotransferase (AST) levels in the blood
  156. 156. TREATMENT • 1-supportive treatment • 2-virus specific therapy Lassa fever can be treated with the ribavirin
  157. 157. Rift valley fever
  158. 158. • Rift Valley fever (RVF) is An acute febrile viral zoonosis that affects human and livestock (such as cattle, buffalo, sheep, goats, and camels) • Infection can cause severe disease in both animals and humans. The disease also results in significant economic losses due to death and abortion among RVF-infected livestock… • Currently RVF is one of the notifiable group A of Exotic Diseases.
  159. 159. Route of transmission 1-Blood feeding arthropod:(Mosquitoes) • Aedes • Anopheles • Culex • Mansonia
  160. 160. • 2-Contact with blood or other body fluids of infected animals. • 3-Consumption of infected milk. • 4-Airborne transmission. *Note No person-to-person transmission.
  161. 161. PATHOGENESIS
  162. 162. Clinical features (I)-In animals:- RVF has been found to infect many species of animals, however the most commonly affected are sheep, goats and cattle….
  163. 163. Sheep and Goats • Incubation period: less than 3 days – Asymptomatic – Foul diarrhea – mucopurulent nasal discharge – High rate of abortion (5-100%) Any stage of gestation – Acute death (20-30%)
  164. 164. Lambs • Incubation period: 12-36 hrs • High fever (105.8 oF) • • • • restlessness Anorexia Death Mortality rate: • Less than 1 week old:90% • over 2 weeks old:20%
  165. 165. Cattle – Incubation period : 3 days. – Fever. – weakness. – Anorexia. – fetid diarrhea. – excessive salivation – Death - Mortality 10% – Abortion can be up to 100%
  166. 166. Clinical features (II)In human:Incubation period 2-6 days -Asymptomatic or flu like illness (Fever, headache, myalgia, nausea, vomiting) -Abdominal pain _Photophobia *Recovery in 4-7 days
  167. 167. complication *RVF associated with 3 main complications:(i)-Encephalitis:(1 week after febrile phase Confusion, vertigo ,stupor, coma). (ii)-Optic neuropathy:(7-20 days decrease visual acuity, retinitis, permanent loss of vision). (iii) )- Hemorrhage (Epistaxis , Hematemsis , Melena , Ecchymoses)DIC, Shock.
  168. 168. Diagnosis • Antibody detection: Serological test: ELISA EIA virus detection: » PCR – Tissue culture – (the laboratory should be notified that specimens originate from HF patient !!so appropriate biologic safety measures can be taken)
  169. 169. Management • General Supportive Measures:* Isolation in negative airway pressure room. * Blood transfusion. *Antiviral drugs( Ribavirin . Interferon). * Immune Modulators. * Introduction to ICU if indicated.
  170. 170. • Hospital discharge after:*Improvement in general status. *Decline in liver symptoms. *Recovery from DIC. • Follow-up in ophthalmology and medical clinics for 6 weeks .
  171. 171. *Safe burial practice for dead cases
  172. 172. Prevention and Control
  173. 173. That mean any activity which reduces morbidity and mortality of diseases .
  174. 174. Levels of Prevention: Primary Level Secondary Level Tertiary Level education, bed nets, Vaccines
  175. 175. Levels of Prevention: Primary Level Secondary Level Tertiary Level Early diagnosis and adequate treatment
  176. 176. Levels of Prevention: Primary Level Secondary Level Tertiary Level Medical, Occupational, Social and Psychological rehabilitation
  177. 177. Prevention (I)Avoid contact with host species (III) Protective clothing (II) Vaccine available (IV) Disinfect and dispose of instruments
  178. 178. Prevention (I)Avoid contact with host species (II) Vaccine available 1-Rodents 2-Insects 3-cattle 4-in human (III) Protective clothing (IV) Disinfect and dispose of instruments
  179. 179. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects A-Control rodent populations 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  180. 180. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects B-prevent the rodents from enteringor living in human populations 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  181. 181. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects C-Safe clean up of rodent nests and droppings 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  182. 182. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects A-Use insect repellents 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  183. 183. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects B-Proper clothing and bed nets 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  184. 184. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects C-Window screens and othe barriers to insects 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  185. 185. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects D-Use anti mosquito lotion 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  186. 186. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects E-Avoid the replication of mosquito in there different outburst . 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  187. 187. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects A-Disposal of infected cattle (Burning & buried) 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  188. 188. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects B-Vaccination of cattle 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  189. 189. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects C-avoid to contact with infected cattle blood 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  190. 190. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects D-Cook the meat well 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  191. 191. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects A-Isolation of infected individuals. 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  192. 192. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects B-Avoid direct contact 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  193. 193. Prevention (I)Avoid contact with host species 1-Rodents (II) Vaccine available 2-Insects C-Avoid use the material of the infected individuals 3-cattle (III) Protective clothing 4-in human (IV) Disinfect and dispose of instruments
  194. 194. Prevention (I)Avoid contact with host species (II) Vaccine available 1-Rodents 2-Insects 3-cattle 4-in human (III) Protective clothing (IV) Disinfect and dispose of instruments
  195. 195. Prevention (I)Avoid contact with host species (II) Vaccine available Yellow fever Which have duration of: (3 to 9 years) (III) Protective clothing (IV) Disinfect and dispose of instruments
  196. 196. Prevention (I)Avoid contact with host species (II) Vaccine available Experimental vaccines under study Argentine HF Rift Valley Fever Dengue HF (III) Protective clothing (IV) Disinfect and dispose of instruments
  197. 197. Prevention (I)Avoid contact with host species (III) Protective clothing (II) Vaccine available (IV) Disinfect and dispose of instruments
  198. 198. Prevention (I)Avoid contact with host species (II) Vaccine available -Disposable gowns -gloves -masks and shoe covers -protective eyewear (III) Protective clothing (IV) Disinfect and dispose of instruments
  199. 199. Prevention (I)Avoid contact with host species (III) Protective clothing (II) Vaccine available (IV) Disinfect and dispose of instruments
  200. 200. Prevention (I)Avoid contact with host species (II) Vaccine available Use a 0.5% solution of sodium hypochlorite (1:10 dilution of bleach) (III) Protective clothing (IV) Disinfect and dispose of instruments
  201. 201. Prevention (I)Avoid contact with host species (III) Protective clothing (II) Vaccine available (IV) Disinfect and dispose of instruments
  202. 202. Disease Control • An ongoing operations aimed at reducing: – The incidence of disease – The duration of disease – Complication of the disease – The financial burden to the community • It concentrates on primary and secondary prevention

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