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Viral diseases Slide 1 Viral diseases Slide 2 Viral diseases Slide 3 Viral diseases Slide 4 Viral diseases Slide 5 Viral diseases Slide 6 Viral diseases Slide 7 Viral diseases Slide 8 Viral diseases Slide 9 Viral diseases Slide 10 Viral diseases Slide 11 Viral diseases Slide 12 Viral diseases Slide 13 Viral diseases Slide 14 Viral diseases Slide 15 Viral diseases Slide 16 Viral diseases Slide 17 Viral diseases Slide 18 Viral diseases Slide 19 Viral diseases Slide 20 Viral diseases Slide 21 Viral diseases Slide 22 Viral diseases Slide 23 Viral diseases Slide 24 Viral diseases Slide 25 Viral diseases Slide 26 Viral diseases Slide 27 Viral diseases Slide 28 Viral diseases Slide 29 Viral diseases Slide 30 Viral diseases Slide 31 Viral diseases Slide 32 Viral diseases Slide 33 Viral diseases Slide 34 Viral diseases Slide 35 Viral diseases Slide 36 Viral diseases Slide 37 Viral diseases Slide 38 Viral diseases Slide 39 Viral diseases Slide 40 Viral diseases Slide 41 Viral diseases Slide 42 Viral diseases Slide 43 Viral diseases Slide 44 Viral diseases Slide 45 Viral diseases Slide 46 Viral diseases Slide 47 Viral diseases Slide 48 Viral diseases Slide 49 Viral diseases Slide 50 Viral diseases Slide 51 Viral diseases Slide 52 Viral diseases Slide 53 Viral diseases Slide 54 Viral diseases Slide 55 Viral diseases Slide 56 Viral diseases Slide 57 Viral diseases Slide 58 Viral diseases Slide 59 Viral diseases Slide 60 Viral diseases Slide 61 Viral diseases Slide 62 Viral diseases Slide 63
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Viral diseases

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This file describes Viral Diseases, pathogenesis and their management and trearment.

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Viral diseases

  1. 1. Diseases of viral origin Faraza Javed Ph.D Pharmacology
  2. 2. Viruses  Noncellular genetic elements that use a living cell for their replication and have an extracellular state.Outside host cell, virus is known as a virion.  Viruses vary considerably in size (0.02 μm - 0.3 μm) and shape.Smallpox viruses are among the largest viruses; polio viruses are among the smallest.
  3. 3. Viral structure  Certain viruses contain RNA while other viruses have DNA  The nucleic acid portion of viruses is known as genome.  The genome of virus is surrounded by a protein coat known as a capsid which is formed from a number of individual protein molecules called capsomeres.
  4. 4.  Capsomeres are arranged in a precise and highly repetitive pattern around nucleic acid. The combination of genome and capsid is called nucleocapsid.
  5. 5. Classification Based on morphology 1)Icosahedral  The icosahedron is made up of equilateral triangles fused together in a spherical shape.  The genetic material is fully enclosed inside capsid.  Examples of viruses with an icosahedral structure are poliovirus, rhinovirus, and adenovirus
  6. 6. 2)Helical virus has its capsid shaped into a rod-shaped structure. This type of shape has a central cavity that encloses its nucleic acid. An example is the tobacco mosaic virus.
  7. 7. 3)Complex  Have a combination of icosahedral and helical shape and may have a complex outer wall or head-tail morphology.  The head-tail morphology structure is unique to viruses that only infect bacteria and are known as bacteriophages. The head of the virus has an icosahedral shape with a helical shaped tail.  An example is Poxvirus
  8. 8. 4)Enveloped  This virus structure is a conventional icosahedral or helical structure that is surrounded by a lipid bilayer membrane, meaning virus is encased or enveloped.  Examples are Influenza virus, Hepatitis C and HIV
  9. 9. Based on genome replication The Baltimore Classification System  Class I viruses, double-stranded DNA genomes: the genome is double-stranded DNA, so mRNA is synthesized in the normal fashion using negative-strand DNA as a template. Examples: Adenovirus, Hepatitis B virus
  10. 10.  Class II viruses, single-stranded DNA genones: the genome is single-stranded DNA. Form a double stranded DNA intermediate during replication and this intermediate used for transcription. Examples: parvovirus, maize streak virus.  Class III viruses, double-stranded RNA genomes: genome is double-stranded RNA, one strand of which is therefore equivalent to mRNA.Examples: reovirus, rotavirus
  11. 11.  Class IV viruses, positive-strand RNA genomes: genome is single-stranded RNA that can serve as mRNA directly, so these are positive-strand viruses. Examples: poliovirus,  Class V viruses, negative-strand RNA genomes: the genome is single-stranded RNA that serve as template for synthesis of viral mRNA. Since genome is complementary to mRNAs, these are negative-strand viruses. Therefore, complementary positive strand is synthesized by RNA polymerase and used as mRNA. Examples: rabies virus,mumps virus
  12. 12.  Class VI viruses, retroviruses:the genome is positive-strand RNA.This RNA virus require reverse transcriptase to copy the information found in RNA to DNA but its expression and replication require synthesis of a double- stranded DNA molecule Example: Human Immunodeficiency Virus (HIV).  Class VII viruses: double-stranded DNA with RNA intermediate: Double-stranded DNA genome that replicates with RNA intermediate. Required reverse transcriptase.
  13. 13. Viral diseases 1) AIDS  Human immunodeficiency virus infection / acquired immunodeficiency syndrome (HIV/AIDS) is a disease of human immune system caused by infection with HIV.  During the initial infection, a person may experience a brief period of influenza-like illness. This is typically followed by a prolonged period without symptoms.
  14. 14.  As illness progresses, it interferes more and more with the immune system, making the person much more likely to get infections, including opportunistic infections (e.g. Pneumocystis pneumonia, central nervous system lymphoma) and tumors.
  15. 15. Modes of HIV/AIDS transmission  Through blood products  Intravenous drug abuse Sharing needles Unsterilized blades  Through sexual contact  From mother to baby
  16. 16. Pathogenesis
  17. 17.  Natural course of HIV/AIDS Stage 1 – Primary  Short,occurs 1-6 weeks after infection  Mild symptoms(flu like illness)  Infected person can infect other people Stage 2 - Asymptomatic  Lasts for an average of ten years  This stage is free from symptoms  There may be swollen glands  The level of HIV in blood drops to low levels
  18. 18. Stage 3 – Symptomatic  The immune system deteriorates  Opportunistic infections and cancers start to appear. Stage 4 - HIV  AIDS  The immune system weakens too much as CD4 cells decrease in number
  19. 19. Treatment HAART = highly active anti-retroviral treatment  Nucleoside Reverse Transcriptase inhibitors Zidovudine  Non-Nucleoside Transcriptase inhibitors Nevirapine  Protease inhibitors Ritonavir
  20. 20. 2)Hepatitis  Is a medical condition defined by inflammation of liver and characterized by presence of inflammatory cells in the tissue of organ,caused by viruses i.e. Hepatitis A,B,C,D,E. Hepatitis A Pathogenesis  HAV invade into human body by fecal-oral route, and replicates in the liver. After 10–12 days, virus is present in blood and is excreted via the biliary system into the feces.
  21. 21. Symptoms  Influenza like symptoms (anorexia,nausea,vomitting,fatigue)  Headcahe and low grade fever  Dark colored urine,Abdominal pain Treatment  No specific medicine  Take rest, increase fluid intake ,  Vaccine is available(Haverix,Vaqta)
  22. 22. Hepatitis B Pathogenesis  It is transmitted pareterally,perinatally and sexualy. Virus enters hepatocytes via blood. Immune response (cytotoxic T cell) to viral antigens expressed on hepatocyte cell surface responsible for clinical syndrome Symptoms  same as Hepatitis A
  23. 23. Treatment  Interferon (3 injections per week)or PEG interferon alpha-2a( once in a week) for 6 months  OR Ribavirin+ Lamivudine or Adevofir  Vaccine is available(Engirex)
  24. 24. Hepatitis C Symptoms  Influenza like symptoms  Pruritis  Severe joint pain  Ascites  Abdominal pain Treatment  Interferon (3 injections per week)or PEG interferon alpha-2a( once in a week) for 6 months  If it is not effective then PEG interferon+Ribavirine OR IFN+ Silymarin
  25. 25. 3)Dengue fever  Also know as breakbone fever, is an acute communicable disease caused by Dengue viruses (categorize into types 1,2,3,4) transmitted by mosquitoe Aedes aegypti ,Aedes albopictus.
  26. 26. Pathogenesis  Once virus is in body, immune system produces antibodies against it that adhere to structural proteins and inactivate virus, which inhibits it from infecting macrophages. This stage is when a primary infection occurs, also known as febrile illness, or dengue fever  Upon exposure to a different serotype of dengue, immune system attacks in same way it did to first serotype.
  27. 27.  However, because surface proteins of each serotype differ slightly, antibody adherence does not inactivate virus  It invades macrophages and induces release of cytokines which causes a more severe secondary infection, such as DHF.  In addition, dengue viruses have M proteins that aid in apoptosis of their target cell
  28. 28. Symptoms  Dengue starts with chills, headache, pain upon moving the eyes, and low backache  Painful aching in legs and joints  The temperature rises quickly as high as 104 F (40 C), with relatively low heart rate and low blood pressure
  29. 29.  Dengue hemorrhagic fever is a more severe form of viral illness.  Symptoms include headache, fever, rash, and evidence of hemorrhage in the body.  Petechiae (small red or purple splotches or blisters under the skin), bleeding in the nose or gums, black stools are all possible signs of hemorrhage.
  30. 30. Management of DF Fever  Is mainly symptomatic and supportive. 1)Bed rest 2)Antipyretics and Analgesics for control of fever and pain 3)Oral fluid and electrolyte therepy for excessive sweating and vomiting.
  31. 31. Management of DHF Fever 1)Antipyretics and Analgesics for control of fever and pain 2) Oral fluid and electrolyte therapy for excessive sweating and vomiting 3) IV fluid therapy to control plasma loss and impending shock like Iv Colloid, Crystalloid.
  32. 32. 4)Chicken pox  An infectious disease causing a mild fever and a rash of itchy inflamed pimples which turn to blisters and then loose scabs. It is caused by the Varicella zoster virus(VZV) and mainly affects children.
  33. 33. Pathogenesis  VZV enters through respiratory tract  It replicate at the site of entry in nasopharynx and in regional lymph nodes.  A primary viremia occurs 4 to 6 days after infection and disseminates virus to other organs,e.g. liver, spleen, and sensory ganglia.  Further replication, causes secondary viremia, with viral infection of skin.
  34. 34. Symptoms  Rash that turns into itchy, fluid-filled blisters that eventually turn into scabs.  High fever  Tiredness  Loss of appetite  Headache
  35. 35. Treatment  Acyclovir can shorten or combat varicella infection if it is started within 24 hours of rash development.
  36. 36. Prevention  CDC recommends two doses of chickenpox vaccine.  Children should receive two doses—the first dose at 12 -15 months and a second dose at 4- 6 years of age.  Varicella-zoster immunoglobulin (VZIG) contains antibodies to the chickenpox virus.
  37. 37. 5)Rabies  It is acute viral disease of CNS. The causative agent of rabies is rabies virus (RV), a negative-stranded RNA virus of the rhabdovirus family
  38. 38. Mode of Transmission  Animal bite,Licks  Persin to person Pathogenesis Is an acute infection of CNS .Following inoculation, virus replicates in striated or connective tissue at site of inoculation and enters peripheral nerves through neuromuscular junction.  It then spreads to CNS.
  39. 39. Pathogenesis
  40. 40. Prevention 1)Human rabies bilogical products  Rabies immune globulin 2)Vaccine  Human diploid cell vaccine (HDCV)  Purified chick embryo cell vaccine (PCEC)  Purified Vero cell vaccine (PVRV)  Purified duck embryo vaccine (PDEV)
  41. 41. Pre exposure prophylaxis 1)Active immunization (Vaccine) On days: 0, 7, 21,28 2)Booster doses  Post exposure prophylaxis 1)Wound cleaning 2)Passive immunization HRIG 20IU/Kg IM on day 0 3)Active immunization On day :0,3,7,14,28
  42. 42. 6)Poliomyelitis  Polio  gray matter  Myelitis  inflammation of the spinal cord  This disease result in destruction of motor neurons caused by polio virus.It attacks the nerve cells of the brain & spinal cord
  43. 43. Pathogenesis  Poliovirus enters body through mouth, infecting pharynx and intestinal mucosa.  The virus then hijacks the host cell's own machinery, and begins to replicate.  Divides within GIT ,from where it spreads to tonsils,intestinal lymphoid tissue where it multiplies.  The virus is subsequently absorbed into the bloodstream.(viremia)
  44. 44.  It can survive and multiply within blood and lymphatics  This sustained replication causes a major viremia  Rarely, this may progress and virus may invade central nervous system, provoking a local inflammatory response.  In most cases, this causes a self-limiting inflammation of meninges,which is known as nonparalytic aseptic meningitis
  45. 45. Symptoms  Many include fever, pharyngitis, headache, anorexia, nausea, and vomiting. Ilness may progress to aseptic meningitis and menigoencephalitis .  These patients develop a higher fever and sever headache with stiffness of neck and back.  Paralysis of respiratory muscles can occur or from cardiac arrest if the neurons in the medulla oblongata are destroyed.
  46. 46. Treatment  Bed rest with close monitoring of respiratory and cardiovascular functioning is essential during the acute stage of poliomyelitis along with fever control and muscle relexants.Mechanical ventilation, respiratory therapy may be needed depending on severity of patients. Vaccine  There are two types of vaccine that protect against polio: inactivated polio vaccine (IPV) and oral polio vaccine (OPV). IPV is given as an injection in the leg or arm.
  47. 47. 7)Measles (Rubeola)  It is an acute viral infection characterized by a final stage with a maculopapular rash erupting successively over the neck and face, trunk, arms, and legs, and accompanied by a high fever. It is caused by infection with the Rubeola virus, a paramyxovirus of the genus Morbillivirus.
  48. 48. Pathogenesis and clinical features  Virus infects epithelial cells of nose and conjunctiva. Virus multiplies in them and then extends to regional lymph nodes.  Primary viraemia occurs 2 to 3 days after infection, and virus continues to replicate in epithelial and reticuloendothelial system tissue over next few days.  Secondary viraemia occurs on days 5 to 7, and infection becomes established in skin and other tissues including respiratory tract on days 7 to 11
  49. 49.  The prodromal phase, which lasts 2 to 4 days, occurs at this time with fever, malaise, cough, coryza, and conjunctivitis.  Koplik's spots(very small grayish-white spots with bluish-white centers in the mouth, insides of cheeks, and throat)may develop on buccal mucosa about 1 to 2 days before rash and may be apparent for 1 to 2 days after rash onset.
  50. 50.  The rash then develops at about 14 days after infection; at this time virus can be found in blood, skin, respiratory tract, and other organs.  Over next few days, viraemia gradually decreases as rash gradually resolves along with other signs and symptoms.  Viraemia and presence of virus in tissue and organs ceases by days 15 to 17 corresponding to appearance of antibody
  51. 51. Treatment  It is an acute self-limiting disease .However immunocompromised and undernourished, patients can be protected by  Administration of human anti-measles gamma globulin if given within the first 3 days after exposure.  Alternatively, exposed individual can simply be vaccinated within 72 hours of exposure.  Treatment for symptoms includes plenty of fluids and paracetamol for the fever
  52. 52. Vaccine  The initial measles immunization, usually as measles-mumps-rubella ( MMR ) vaccine , is recommended at 12-15 month of age  MMR vaccine may be given for Measles post exposure  A second immunization , also as MMR, is recommended routinely at 4-6 year of age
  53. 53. Reference  Warren Levinson(2012). Review of Medical Microbiology and Immunology(12th edition)  classification-of-virus   sheets/19/73/the-hiv-life-cycle
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