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Tropical diseases.pptx

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Tropical diseases.pptx

  1. 1. M R S S A M I R A A A B D U L L A H I Tropical diseases
  2. 2. Introduction  Some of the organisms that cause tropical diseases are bacteria and viruses, terms that may be familiar to most people since these types of organisms cause illness  many familiar viral and bacterial diseases are spread directly from person to person, by airborne routes of transmission or by sexual contact.  Alternatively, some tropical disease agents are transmitted by an intermediate carrier or vector. The insect or other invertebrate vector picks up the pathogen from an infected person or animal and transmits it to others in the process of feeding
  3. 3. viruses  Viruses are minute infectious agents that generally consist only of genetic material covered by a protein shell. They only replicate within cells, which provide the synthetic machinery necessary to produce new virus particles.
  4. 4. Yellow fever  Yellow fever is a mosquito-borne viral hemorrhagic fever with a high case-fatality rate. Clinical manifestations include hepatic dysfunction, renal failure.  The yellow fever virus belongs to the genus, Flavivirus. Flavivirus species are characterized by having a positive-sense, single-stranded RNA of about 10,000 to 11,000 bases  The genome codes or three structural proteins: capsid protein (C), membrane protein M (prM), and envelope protein (E). It also codes for seven nonstructural protein molecules
  5. 5. .  It makes use of an arthropod as vector. In particular, it utilizes mosquitoes, for its transmission to another host.
  6. 6.  The virus replicates in the lymph node.  The viruses are capable of infecting the dendritic cells. They may also invade the host’s liver and infect the hepatocytes.  Liver damage causes the yellowing of the skin (jaundice) of the host.  This is the reason this condition is called yellow fever. When the viral infection leads to significant liver damage, the disease could become severe and life-threatening to the host. The disease is formerly called black vomit.  It is because bleeding in the mouth, the eyes, and the gastrointestinal tract may result in a vomit containing blood.
  7. 7. Ebola  Ebola virus causes fever, severe headache, backache, vomiting, diarrhea, and severe hemorrhaging.  The method by which Ebola is transmitted in nature, and what animal is its natural host, remains unclear.  Ebola virus (EBOV) is a member of the Filoviridae family and causes severe hemorrhagic fever in humans and nonhuman primates,
  8. 8.  Virus entry and attachment is mediated by a single envelope glycoprotein (GP) as a class I fusion protein, which is proteolytically processed during maturation into two subunits, GP1 and GP2. The GP1 N terminus contains a putative receptor-binding domain (RBD) and the GP2 C terminus contains a fusion peptide .GP1 and GP2 are linked by a disulfide bond (Cys53-Cys609)
  9. 9.  EBOV GP is also extensively glycosylated, especially within a region of GP which contains multiple N- and O-linked glycans. ebolaviruses primarily target antigen-presenting cells such as dendritic cells and macrophages, which are one of the main components of the innate immune system.
  10. 10.  By stander apoptosis of lymphocytes is also observed, and the induction of adaptive immunity is also impaired by a significant reduction in their numbers .Lymphocytes themselves are insensitive to ebolaviruses and marburgviruses, suggesting that direct infection of lymphocytes may not be the cause.
  11. 11. lasa  Lassa virus (LASV) belongs to the family of Arenaviridae. It is the causative agent of Lassa fever, a potentially fatal viral hemorrhagic fever in humans for which only limited treatment options and no licensed vaccine are available  LASV was first isolated in 1969 from a missionary nurse who worked in a clinic in a small town, Lassa, in northeastern Nigeria  The virus particle consists of only four structural proteins and a lipid envelope as well as a segmented single- stranded RNA genome in negative orientation. LASV replicates in the cytoplasm of the host cell..
  12. 12.  The genome consists of a small (s) and a large (l) RNA fragment of 3.4 and 7 kilobases, respectively. The small RNA (sRNA) fragment encodes the viral structural proteins like glycoprotein, precursor protein, and the nucleoprotein. The large RNA fragment on its own encodes for nonstructural proteins including viral polymerase and a small zinc- binding (Z) protein
  13. 13.  It is transmitted by rodents. Symptoms of Lassa fever include sharp backache and/or headache, sore throat, fever, rashes, dehydration, general swelling, skin hemorrhaging, irregular heart beat, and disorientation.
  14. 14. Bacteria  Bacteria (singular = bacterium) are more complex than viruses, containing genetic information and much of the equipment necessary to produce energy and replicate independently.  Some bacteria, however, can only reproduce when growing inside a cell, from which they derive required nutrients
  15. 15. Cholera  Cholera is a diarrheal disease caused by infection with Vibrio cholerae, a bacterium most often found in contaminated water and shellfish, which produces a toxin that upsets the biochemical balance of cells lining the intestine and makes them secrete copious amounts of water and electrolytes.
  16. 16.  Cholera Toxin(CT) is made up of two types of subunits. The larger A subunit (240 amino acids;) is located centrally, while the five B subunits (103 amino acids; each; are located peripherally.
  17. 17.  Cholera toxin, by acting as a classical A-B type toxin, leads to ADP-ribosylation of G protein, and constitutive activation of AC(adenylatecyclase enzyme) , thereby giving rise to increased levels of cyclic AMP within the host cell . As a result, electrolyte imbalance occurs due to a rapid efflux of chloride ions and decreased influx of sodium ions, leading to massive water efflux through the intestinal cells, thereby causing severe diarrhoea and vomiting, the cardinal clinical signs of cholera. Diarrhoea, if untreated, leads to severe dehydration, electrolyte abnormalities and metabolic acidosis15, almost inevitably resulting in death.
  18. 18. Tuberculosis  Caused primarily by the bacterium Mycobacterium tuberculos.this is an infection that can last a lifetime, resulting in disease to virtually every organ in the body but primarily affecting the lungs. Tuberculosis occurs all over the world.  It is treatable and preventable. Several factors like human immunodeficiency virus (HIV) co-infection and other may affect outcome if not properly addressed
  19. 19.  TB was associated with biochemical changes namely low serum sodium, low serum albumin, low/high serum calcium, low/high serum potassium, among others
  20. 20.  lungs are more commonly affected by tuberculosis than any other organ, partly because inhalation is the commonest mode of infection and partly because lung tissue provides a favorable environment for the growth of the organism  globulin formation increases in the body as a result of increased immune response where antibodies are produced.
  21. 21. Parasites  Parasites are organisms that live within or on another organism, the host, at whose expense they obtain some advantage such as nourishment. This group of pathogens includes the protozoa (single- celled organisms more complex than bacteria) and the helminths(multicellular organisms commonly referred to as worms).
  22. 22. malaria Over 300 million people develop clinical cases of malaria each year, and one to three million of them die. Many of these are children living in Sub-Saharan Africa.  Almost half of the world's population lives in an area where they are at risk of contracting the disease. Malaria is caused by protozoa of genus Plasmodium.
  23. 23.  the parasites are transmitted to humans by female anopheline mosquitoes. When the mosquito takes a blood meal on the host, she injects the parasites along with her saliva. The parasites develop first in liver cells and then infect red blood cells (erythrocytes), where they consume hemoglobin, the oxygen-carrying component of the blood.  The parasites divide in the red cell, and at the completion of development the red cell ruptures releasing parasites that can infect many other erythrocytes. The typical symptoms of malaria, cycles of chills, fever and sweating, are experienced by patients at these times.
  24. 24.  Parasites also became resistant to the widely used drug chloroquine and other antimalarials.  Part of the complex life cycle of the malaria parasite Plasmodium Falciparum involves invasion and occupation of a red blood cell. There it catabolizes hemoglobin in its digestive vacuole in order to grow and asexually multiply into a new generation of parasites that can subsequently invade new healthy red blood cells.
  25. 25.  A byproduct of the degraded hemoglobin is heme, a porphyrin ring with a central iron (Fe) atom, which is precipitated into hemozoin crystals consisting of dimers of the heme molecule. Monomers of heme in solution in the digestive vacuole cytosol would be toxic to the parasite as they are highly reactive, but in form of hemozoin crystals the heme is harmless4. Obvious targets for drug design would be impedement either of hemozoin crystal growth, or of the protein assisted dimerization of heme6, 7.
  26. 26.  The folate pathway of Plasmodium falciparum is a well-established malaria drug target with proven benefits in treatment and prophylaxis These antifolate compounds target two different enzymes in the folate pathway of P. falciparum, with pyrimethamine and sulphadoxine inhibiting dihydrofolate reductase (DHFR) and dihydropteroate synthase (DHPS)
  27. 27.  The inhibition of the folate pathway cuts down the amount of folate derivatives that act as one-carbon carriers in nucleotide synthesis and amino acid metabolism.  The malaria parasites became resistant to antifolates by gaining mutations at the dhfr and dhps genes .  The changes decrease the binding affinity of the drugs to the targeted enzyme.  The interest in antifolates has been renewed in recent years with the development of new lead compounds and the novel applications in malaria treatment
  28. 28. Trypanosomiasis  Trypanosomiasis The protozoa causing trypanosomiasis are closely related to leishmania parasites. In humans, different species of the genus Trypanosoma are responsible for diseases
  29. 29.  Unlike malaria and leishmaniasis, the parasites are not injected during feeding; rather they are deposited by defecating bugs. The parasite enters the host through the eyes, nose or mouth, or through breaks in the skin. Symptoms may appear as acute disease shortly after infection or as chronic disease years later.  Acute disease involves fever, swelling of the lymph nodes and, sometimes, inflammation of the heart muscle and of the brain. Although the acute stage may be fatal, especially in children, most infected individuals survive.  One quarter or more will develop cardiac damage that may result in heart failure and sudden

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