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Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
Viral & Bacterial  Infections 2
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Viral & Bacterial Infections 2

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  • 1. VIRAL INFECTION
  • 2. VIRAL INFECTIONS
  • 3. Transient Viremia
  • 4. Measles- Rubeola virus
    • Measles virus is an RNA virus of the paramyxovirus
    • 5. There is only one strain of measles virus with Envelope
  • PATHOPHYSIOLOGY
  • 6. Clinical Manifestation
  • 7.
    • Antibody-protects against reinfection
    • 8. T cell-mediated immunity  controls the viral infection  skin rash ( hypersensitivity reaction to viral antigen )
    • 9. PathognomonicKoplik spots Ulcerated mucosal lesions in the oral cavity near the opening of Stensen ducts
    • 10. LN  Follicular Hyperplasia & multi- nucleate giant cells, called Warthin-Finkeldey cells, which have eosinophilic nuclear and cytoplasmic inclusion bodies.
  • Mumps
    • Transient inflammation of the parotid glands and, less often, of the testes, pancreas and central nervous system
  • 11. Clinical Manifestation
    • Mumps parotitis, which is bilateral in 70% of cases
    • 12. Mumps orchitis,  swelling  local hemorrhages  Infarction Sterility due to scars and atrophy of the testis
    • 13. Pancreasdestructive lesion  causing parenchymal and fat necrosis & pmns
    • 14. Mumps encephalitis causes perivenousdemyelinization and perivascular mononuclear cuffing.
  • Poliovirus
    Unencapsulated RNA virus of Enterovirus
    Transmitted by fecal-oral route
    3 major strains
    Infects people but not other animals
    Briefly shed
    Do not undergo antigenic variation
    EFFECTIVELY PREVENTED BY IMMUNIZATION
  • 15. Poliovirus
  • 16. Special Consideration
    1 : 100 infected invades the CNS
    Due to VIREMIA or RETROGRADE TRANSPORT VIA AXONS TO MOTOR NEURONS
    Motor Neurons of Spinal Cord
    SPINAL POLIOMYELITIS
    Brain Stem
    BULBAR POLIOMYELITIS
  • 17. CHRONIC LATENT INFECTIONS- Herpesvirus infections
  • 18. Features:
    Cause Acute Infection  Followed by Latent Infection 
    Viruses persist in a Non-Infectious Form
    With Periodic Reactivation & Shedding of Infectious Virus
    Latency defined
    Inability to recover Infectious particles from cells that harbor the virus
  • 19. Herpesvirus infections
  • 20. Pathophysiology of Latency
    Viral DNA remains w/in Nucleus of Sensory Neurons
    No viral protein are produced
    Only Latency–Associated viral RNA transcripts are synthesized ( LATS )
    Confer Resistance to Apoptosis
    Contribute to viral persistence in sensory neurons
    Reactivation may occur in presence of host immunity
    Virus Developed ways to avoid Immune Recognition
  • 21. ESCAPE or Elude Immune System
    DownModulating MHC class I & II molecules
    Hide from immune system
    Producing Homologues of TNF receptor, IL-10 and MHC class I receptors
    Actively Suppress immune response
  • 22. Herpes Simplex Virus
  • 23. Herpesvirus Blister - Mucosa
  • 24. Herpes Virus
  • 25. Cytomegalovirus
    Usually produce Asymptomatic infxn except Immunocompromised
    Found in All Secretions include Milk
    Can carry the usual dormant virus for life
    Transmission
    1. Transplacental 4. Venereal Route
    2. Cervical or Birth Canal 5. Organ transplant
    3. Breast Milk 6. Blood transfusion
    4. Saliva (children-day care)
  • 26. Diseases:
    Congenital CMV- acquired in Utero
    95% asymptomatic
    Mother w/ primary infection  CID develops
    Classic cytomegalic inclusion disease CID
    Similar to erythroblastosisfetalis
  • 27. Diseases:
    Perinatal Infections
    Passage birth canal/breast milk
    Majority asymptomatic due to ( +) Ig from mother
    Many continue excrete CMV in urine/saliva x years
    Pneumonitis Later in life  Hearing loss noted
    CMV- mononucleosis like illness
    Fever, atypical lymphos, mild hepatitis, Lymphadenopathy
    CMV in Immunocompromised
    Disseminated CMV- lungs, GIT, Retina
  • 28. Varicella – Zoster Virus
    Acute Infection – Chickenpox
    Infects mucous membrane, skin, neurons
    Reactivation – Herpes zoster / shingles
    Self-limiting  Latent infxn in Sensory Ganglia
    Transmitted by Aerosols
    Disseminates Hematogenously
    Cause widespread vesicular skin lesions
  • 29. Varicella-Zoster Virus
  • 30. Chronic Productive Infections
    HIV AND HBV
  • 31. Features of Chronic Productive Infections
  • 32. Hepatitis B Virus- Hepadna
  • 33. HBV- Pathogenesis
    HBV integrate in host genome
    Cause Hepatic injury is due to immune response not cytopathic effect of virus
    Cytotoxic T lymphocytes eliminate infected cells
    Evasion of immune system
    Inhibiting IFN-beta  downregulation of viral gene expression
    High mutation rate
  • 34. HBV- Pathogenesis
    Chronic Infxn
    5-10% Adults
    Up to 90 % Perinatally infected Children
    Carrier State
    Occur when CTL response is Dormant
  • 35. Transforming Viruses
  • 36. Transforming infection
    EBV ,HPV, HBV, HTLV-1
  • 37. Epstein – Barr Virus
  • 38. Epstein – Barr Virus
  • 39. Atypical lymphocytes- Reactive T lymphocytes
  • 40. Immune Response to EBV
  • 41. Some
    Ac quired Defects in Cellular Immunity
  • 42. Human Papilloma Virus
  • 43. HPV
  • 44. Malignant Transformation
  • 45. Bacterial infection
  • 46. Gram Positive Bacteria
  • 47. Staphylococcus aureusInfection
    Skin Lesions
    Abscesses
    Sepsis
    Osteomyelitis
    Pneumonia
    Endocarditis
    Food Poisoning
    Toxic Shock Syndrome
  • 48. Other Staph species
    Opportunistic infection
    Prosthetic valves
    Catheter
    D rug addicts
    Polysaccharide capsule – attach artificial materials
    UTI in young women
    Staph epidermidis
    Staph saprophyticus
  • 49. Pathogenesis- Staph aureus
    Clumping Factor
    Binds fibrinogen, Fibronectin,
    Use as bridge
    Adhere host Endothelial cells
    Enzymes - Lipase
    Degrade skin lipids
    Protein A
    Binds the Fc portion of immunoglobulins – Escape Ab-mediated killing
  • 50. Pathogenesis- Staph aureus
    Superantigens
    Stimulate 2 0 % of Lymphos Release of large amounts of TNF, IL-1  Septic Shock
    Toxins –Damage host cell
    Membrane damaging toxins
  • 51. Exfoliative Toxins
  • 52. staph food poisoning
  • 53. Diseases Causesd by Staphy.
  • 54. Streptococcal infection
  • 55. Beta Hemolytic Strep
  • 56. Strep Pharingitis
    Epiglottal swelling & abscess
    Cervical LN
    Strep Pyogenes
    Major antecedent of PoststrepGlomerulonephritis
    Ag-Ab complex deposit in glomerulus
    Poststrep Rheumatic fever
    Antistreptococcal M protein antibodies & T cells that cross react with cardiac myosin
  • 57. Strep pyogenes:VirulenceFactors
    Capsules
    M proteins – prevents phagocytosis
    C5a peptidase – Degrade chemotactic C5
    Antistreptococcal M protein – Ab that cross react w/ cardiac Myosin ( RHD)
  • 58. Other Streptococcal Infection
    Strep. Pneumoniae
    Common cause of CAP & Adult Meningitis
    Lobar Pneumonia
    Otitis media, Sinusitis
    Often preceded by viral infection that injure ciliated epithelium
    Has capsule- prevent phagocytosis
    Pneumolysin
    Inserts on target cell membrane  Lysis
    Activates Classical pathway Reducing complement available for Opsinization
  • 59. Beta Hemolytic Strep
  • 60. Other Streptococcal Infection
    Strep. Mutans
    Major cause of Dental Caries
    Sucrose  Lactic acid  Demineralization of Tooth enamel
    Secrete HMW Glucans Promote Bacterial Aggregation  Plaque formation
  • 61. Gram negative bacteria
    Salmonella
    Neisserialinfxn
    Whooping cough
    Pseudomonas
    Chancroid
    Granulomainguinale
  • 62. Salmonella Typhi
    Enteric fever
    Transmitted
    From person to person
    Food or Contaminated water
    GB colonization may be associated with
    Gallstones
    Chronic Carrier State
  • 63. Pathogenesis
    Survive gastric acid
    In the SI  Taken by M cells
    Engulf by macrophages in the underlying LN Reactive LN hyperplasia
    Disseminate by blood & Lymphatic
    Unlike S. enteriditidis
  • 64. Clinical manifestation of Typhoid Fever
  • 65. Pathogenesis- Salmonella
  • 66. Typhoid fever
    Blood Culture
    >90% in the Febrile State
    Relapse may occur
    Systemic dissemination
    Encephalopathy
    Meningitis
    Seizures
    Endocarditis
    Myocarditis
    Pneumonia
    Cholecystitis
    Osteomyeltis
  • 67. Neisseria Infections
    2 Clinically significant species
    N. meningitidis
    N. gonorrhea
  • 68. Neisseriameningitidis
    13 serotypes
    • Common Colonizes Oropharynx
    • 69. Spread by respiratory route
    Only small fraction develop Cause Bacterial Meningitis
    Children less than 2 years old
  • 70. Pathophysiology- N. meningitidis -
  • 71. Neisseria gonorrhea
    Surface pili that form barrier against phagocytosis
    Encapsulated gm(-) diplococci
    STI – Men - Urethritis, Pharyngitis, Proctitis
    Urethral strictures, chronic infection of Male genitals
    STI – Women - Salpingitis Tubo-ovarian abscess  Scar  Sterility or Ectopic pregnancy
    Perinatal Ophthalmic infxn
  • 72. Neisseria gonorrhea
  • 73. Neisseria - Evasion of immune response
    Use antigenic variation of OPA proteins to escape immune response
    A single clone of bacteria  several multiple antigenic types
    Pili Protein are altered by genetic recombination
  • 74. Whooping cough
    Gram (-) coccobacilli
    Acute highly communicable
    Paroxysm of violent cough followed by loud inspiratory whoop
    Colonizes the brush border of bronchial epithelium
    Laryngotracheobronchitis
    Virulence is regulated by BVG locus
  • 75. Virulence factor :Regulated by Bordetella virulence gene locus (bvg)
    PertusisExotoxins paralyze cilia
  • 76. Pseudomonas Infection
    Opportunistic gram-negative bacterium
    Frequent, deadly pathogen of patients with cystic fibrosis, severe burns, or neutropenia.
    Coregulatedpili
    Adherence proteins that mediate adherence to epithelial cells and lung mucin
    Endotoxinthat causes the symptoms and signs of gram-negative sepsis.
  • 77. Distinctive Virulence Factor
  • 78. Distinctive Virulence Factor
  • 79. Distinctive Virulence Factor
  • 80. Syphilis- Treponemapallidum
    Sexual intercourse is the usual mode of transmission
    Transplacental transmission of T. pallidum occurs readily, & active disease during pregnancy results in congenital syphilis.
  • 81. Pathology - syphilis
  • 82. Chancre
    Sensored
    A single firm, nontender, raised, red lesion
    3 weeks after contact
    Heals in a few weeks with or without therapy
  • 83.
  • 84.
  • 85. Immune response to Syphlis
  • 86. Pathogenesis of Syphilis
  • 87. Obliterative endarteritis
  • 88. Anaerobic Bacteria
    Clostridia Infection
  • 89. Clostridial Infections
    Clostridium species are gram-positive bacilli
    There are four types of Clostridium that cause human disease:
    1.Clostridium perfringens (welchii), septicum
    2.Clostridium tetani
    3.Clostridium botulinum
    4.Costridium difficile
  • 90. Clostridium perfringens (welchii)
    Anaerobic cellulitis – foul , thin discolored exudate, quick tissue destruction ( versus pyogenic )
    Myonecrosis (gas gangrene)- 1to 3 days after infection
    Invade traumatic and surgical wounds
    Contaminate illegal abortions
    Cause uterine myonecrosis,
    Cause mild food poisoning,
    Infect the small bowel of ischemic or neutropenic patients to produce severe sepsis.
  • 91. Clostridium tetani
    Proliferates in:
    puncture wounds
    umbilical stump of newborn infants
    Releases a potent neurotoxin, called tetanospasmin
    causes convulsive contractions of skeletal muscles (lockjaw).
  • 92. Clostridium botulinum
    Grows in inadequately sterilized canned foods
    Releases a potent neurotoxin that blocks synaptic release of acetylcholine
    Causes a severe paralysis of respiratory and skeletal muscles (botulism).
  • 93. Clostridium difficile
    Overgrows other intestinal flora in antibiotic-treated patients
    Releases multiple toxin
    Causes pseudomembranous colitis
  • 94. Pathogenesis- Clostridium Perfringens
  • 95. Alpha Toxin- Properties
  • 96. Beta toxin
  • 97. O Toxins
  • 98. Clostridium tetani
  • 99. Clostridium Botulinum- Neurotoxin
    Are released when the organisms die and autolyse
    Act at the peripheral nerve endings,
    Cleaving either synaptobrevin (as described for tetanus toxin) or synapse-associated proteins, called SNAP-25 and syntaxin.
  • 100. Unable to release acetylcholine at the neuromuscular junction and at the synaptic ganglia and parasympathetic motor end-plates of the autonomic nervous system
    Descending paralysis from the cranial nerves down to the extremities.
  • 101. Clostridium difficile
    Produces toxin A
    Which is an enterotoxin
    a potent chemoattractant for granulocytes
    toxin B
    a cytotoxin,
    which causes distinctive cytopathic effects in cultured cells and is used in the diagnosis of C. difficile infections
  • 102. Obligate Intracellular Bacteria
    Chlamydia trachomatis is an obligate intracellular pathogen
    Venereal urethritis, lymphogranulomavenereum, and trachoma
    Lymphogranulomavenereum
    results in granulomatous inflammation of the inguinal and rectal lymph nodes.
    Trachoma or chronic keratoconjunctivitis, a leading global cause of blindness, is a disease of poverty and overcrowding, transmitted from eye to eye by aerosols or by hand contact.
  • 103. Malaria
    Intracellular protozoan parasite
    Plasmodium falciparum is a worldwide infection that affects 100 million and kills 1 to 1.5 million persons per year and so is the major parasitic cause of death.
    Other types (P. vivax, P. ovale, P. malariae)
    Transmitted by more than a dozen species of Anopheles mosquitoes widely distributed throughout Africa, Asia, and Latin America.
  • 104. Malaria
    P. vivax and P. malariae
    mild anemia
    in rare instances, splenic rupture and nephrotic syndrome.
    Acute P. falciparum infections
    produce high parasitemias,
    severe anemia,
    cerebral symptoms,
    renal failure,
    pulmonary edema, and death.
  • 105. Features of P. falciparum
    Infect rbc of all ages Versus young rbc for other species
    High parasite burden
    Profound Anemia
    Infected rbc clump together  Stick to Endothelial lining of small blood vessels ( Sequestration )  Block blood flow
    Form KNOBs on rbc surface (PfEMP 1)
    Plasmodium falc. Eryhtrocytememb protein
    Bind Ligands on blood vessel wall
    Cause poor perfusion to the brain ( Cerebral malaria )
  • 106. Life cycle of P. falciparum
  • 107. Features of P. falciparum
    Stimulates production of HIGH levels of Cytokines
    Induce fever
    Suppress rbc production
    NO prodn Tissue damage
    Induce expression of endothelial receptors for PfEMP 1
    Increasing sequestration
  • 108. Morphology
    P. falciparum initially  Splenic congestion and enlargement of the spleen
    Infected rbc taken byreticuloendothelial cells.
    The liver becomes progressively enlarged and pigmented with progression of malaria.
    Kidneys  often enlarged and congested
     pigment in the glomeruli and hemoglobin
    casts in the tubules.
  • 109. Addendum
    Sporozoites – Infectious stage
    During feeding SporozoitesReleased in blood w/in minutes Bind to and invade liver cells
    by binding to the hepatocyte receptor for the serum proteins thrombospondin and properdin, located on the basolateral surface of hepatocytes
    The binding is accomplished because of the presence of sporozoite surface proteins that contain a domain homologous to the binding domain of thrombospondin.
    Within liver cells, malaria parasites multiply rapidly, so as many as 30,000 merozoites (asexual, haploid blood forms)
    Merozoites released when the hepatocyte ruptures
  • 110. Addendum
    Merozoites bind by a parasite lectin-like molecule to sialic residues on glycophorin molecules on the surface of red blood cells.
    Merozoitesrelease multiple proteases from a special organelle called the rhoptry.
    Within the red blood cells, the parasites multiply in a membrane-bound digestive vacuole,
    Hydrolyzing hemoglobin through secreted enzymes that include an aspartate protease
    Most malaria parasites  rupture the cell  infect new red blood cells
    Some parasites sexual forms called gametocytes  infect the mosquito when it takes its blood meal.
  • 111. Addendum
    Maturation  change morphologic  from ring to schizont form  secrete proteins that form 100-nm bumps on the red blood cell surface, called knobs called sequestrins
    Sequestrins bind to endothelial cells by ICAM-1, the thrombospondin receptor, and the glycophorin CD46
    cause malaria-infected red blood cells to be removed from circulation
    Red blood cells containing immature ring forms of the parasite  flexible  pass through the spleen, circulate in the blood
    Red blood cells containing mature schizonts, 
    rigid  sequestration in the spleen.
  • 112. Schistosoma
  • 113. Schistosoma
    S. mansoni / japonicum eggs  liver disease.
    1. Substances released from schistosome eggs
    Are directly hepatotoxic,
    2. Carbohydrate antigens from eggs induce Granuloma formation
    mediated by TNF and TH 1 and TH 2 helper cells.
    TH 2 helper T cells  secrete IL-4 Induce IgE synthesis eosinophilia, mastocytosis, and high levels of serum IgE in human schistosomiasis
    Resistance to reinfection by schistosomes after treatment correlates with IgE levels
    Whereas eosinophil major basic protein may destroy larval schistosomula
  • 114. 3. Eggs release factors that stimulate lymphocytes secrete a fibrogeniclymphokine
    Stimulates fibroblast proliferation and portal fibrosis.
    This exuberant periportal fibrosis, which is out of proportion to the injury caused by the eggs and granulomas,
    Pipestem Fibrosis
    Occurs in 5% - 10% of persons heavuly infected with schistosomes
    Hallmarks of severe schistosomiasis:
    Portal hypertension
    Esophageal varices,
    Ascites
  • 115. Pipestem Fibrosis - Liver
  • 116. S. haematobium infection,
    Bladder inflammatory patches due to massive egg deposition and granulomas
    cause hematuria
    The most frequent complication is inflammation and fibrosis of the ureteral walls
    leading to obstruction, hydronephrosis, and chronic pyelonephritis.
  • 117. Schisoma eggs

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