WNF zoonoses


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WNF zoonoses

  1. 1. Dr. Heba Ahmed Sunday, 17 th , April, 2011
  2. 3. Introduction <ul><li>WNV is a mosquito-borne flavivirus originally isolated from the blood of a febrile woman in the West Nile province in Uganda. </li></ul><ul><li>Neuro-invasiveness is a common feature of flavivirus infections </li></ul>
  3. 4. Etiology <ul><li>The virus belongs to Family Flaviridae and genus Flavivirus </li></ul><ul><li>Single stranded positive sense RNA virus </li></ul><ul><li>Phylogenetic studies revealed the existence of two main lineages </li></ul><ul><li>1- Lineage I </li></ul><ul><li>2- Lineage II </li></ul>
  4. 5. Animal Reservoir <ul><li>Avian species and wild birds </li></ul><ul><li>Reptiles </li></ul><ul><li>Equines </li></ul><ul><li>Other animals: bats, cats, dogs, camels, rabbits, squirrels and chipmunks </li></ul>
  5. 6. Insect vector <ul><li>Mosquitoes: 43 species </li></ul><ul><li>Culex </li></ul><ul><li>Ticks </li></ul>
  6. 7. Transmission in humans
  7. 8. Transmission in humans <ul><li>Mosquito bites </li></ul><ul><li>Blood transfusion </li></ul><ul><li>Transplantation </li></ul><ul><li>Breast feeding </li></ul><ul><li>Intrauterine transmission </li></ul>
  8. 9. Occurrence <ul><li>Before 1994 , outbreaks of West Nile fever were sporadic and occurred primarily in the Mediterranean region, Africa and east Europe. </li></ul><ul><li>Since 1994 , outbreaks have occurred with higher incidence of severe human disease </li></ul><ul><li>Since 1999 , the disease has spread rapidly to the western hemisphere, including USA, Canada, Mexico, Central and South America </li></ul>
  9. 10. Occurrence <ul><li>In Egypt: </li></ul><ul><li>WNV was first recognized in Egypt in 1950s where a sero-survey revealed that 22% of children and 61% of adults had antibodies to WNV </li></ul><ul><li>In 1968 , a study in Alexandria showed that 14.6% of children admitted to a hospital with a febrile illness had WNV </li></ul><ul><li>In 1989 , a seroprevalence study in Nile Delta showed only 3% prevalence of WNV in school children </li></ul><ul><li>In 1999 , a study showed that WNV was widely distributed in Egypt </li></ul><ul><li>In 2010 , a study revealed that WNV was actively circulating in different areas in Egypt (humans, birds and mosquitoes) </li></ul>
  10. 11. Clinical Picture In Humans <ul><li>Most individuals are asymptomatic </li></ul><ul><li>Symptoms may develop in 20-40% of people with West Nile virus infection </li></ul><ul><li>Less than 1% of infected individuals develop severe neuroinvasive syndromes: </li></ul><ul><li>1- West Nile meningitis </li></ul><ul><li>2- West Nile encephalitis </li></ul><ul><li>3- Acute flaccid paralysis </li></ul>
  11. 12. Prevention and Control <ul><li>1- Surveillance: </li></ul><ul><li>Importance </li></ul><ul><li>Methods </li></ul><ul><li>2- Vaccination: </li></ul><ul><li>A- An inactivated vaccine </li></ul><ul><li>B- Chimeric vaccines </li></ul><ul><li>C- Kunjin vaccine </li></ul><ul><li>3- Vector Control </li></ul>
  12. 14. Introduction <ul><li>Toxoplasmosis is a protozoan disease of warm blooded animals including humans </li></ul><ul><li>Worldwide distributed </li></ul>
  13. 15. Etiology <ul><li>Toxoplasma gondii </li></ul><ul><li>Obligate intracellular parasite </li></ul><ul><li>Toxo </li></ul><ul><li>Plasma </li></ul><ul><li>Different strains </li></ul>
  14. 16. Etiology <ul><li>Toxoplasma gondii </li></ul><ul><li>Has three forms: </li></ul><ul><li>1- Oocyst </li></ul><ul><li>2- Tachyzoites </li></ul><ul><li>3- Tissue cyst </li></ul>
  15. 17. Etiology <ul><li>1- Oocyst </li></ul>
  16. 18. Etiology <ul><li>2- Tachyzoites </li></ul>
  17. 19. Etiology <ul><li>3- Tissue cyst </li></ul>
  18. 20. Reservoir <ul><li>1- Definitive host: Cats </li></ul><ul><li>2- Intermediate host: </li></ul><ul><li>Pigs </li></ul><ul><li>Sheep </li></ul><ul><li>Goats </li></ul><ul><li>Cattle </li></ul><ul><li>Poultry </li></ul><ul><li>Rodents </li></ul><ul><li>Humans </li></ul>
  19. 21. Occurrence <ul><li>One-third of the world population is infected </li></ul><ul><li>What are the reasons of the high environmental contamination with the oocysts? </li></ul>
  20. 22. Transmission cycle
  21. 23. Clinical manifistaion <ul><li>1- Acute infection in immunocompetents </li></ul><ul><li>Mainly asymptomatic </li></ul><ul><li>Signs: </li></ul><ul><li>Localized or generalized lymphadenopathy </li></ul><ul><li>Low grade of fever </li></ul><ul><li>Lethargy </li></ul><ul><li>Headache </li></ul><ul><li>Most symptoms resolve in few weeks </li></ul>
  22. 24. Clinical manifistaion <ul><li>2- Occular toxoplasmosis </li></ul><ul><li>Headlight in the fog appearance </li></ul><ul><li>Blurred vision </li></ul><ul><li>Photophobia </li></ul>
  23. 25. Clinical manifistaion <ul><li>3- Infection of immunocompromised patients </li></ul><ul><li>Mainly due to recurrence of chronic infection </li></ul><ul><li>Signs: </li></ul><ul><li>CNS abnormalities </li></ul><ul><li>Chorioretinitis </li></ul><ul><li>Dyspenia </li></ul><ul><li>Diarrhea </li></ul>
  24. 26. Clinical manifistaion <ul><li>4- Infection during pregnancy and congenital toxoplasmosis </li></ul><ul><li>In pregnancy </li></ul><ul><li>Congenital: </li></ul><ul><li>Manifested directly after birth or many years later </li></ul><ul><li>Hydrocephalus </li></ul><ul><li>Microcephalus </li></ul><ul><li>Chorioretinitis </li></ul><ul><li>Blindness </li></ul><ul><li>Epilepsy </li></ul><ul><li>Mental retardation </li></ul>
  25. 27. Prevention and control <ul><li>1- Treatment </li></ul><ul><li>Combination of pyrimethamine, sulfadiazine and folinic acid for 4-6 weeks </li></ul><ul><li>Spiramycin </li></ul><ul><li>2- Vaccination </li></ul><ul><li>Animal vaccine: TOXOVAX ® </li></ul><ul><li>Vaccine candidates (SAG1 antigen) </li></ul><ul><li>3- Hygienic measures </li></ul>