Microbial Diseases of the Nervous System<br />DR SONNIE P. TALAVERA    08162009 OLFU <br />
How Microbes Enter the Nervous System<br />Skull or backbone fractures<br />Medical procedures<br />Along peripheral nerve...
The Nervous System<br />Figure 22.1<br />
Microbial Diseases of the Nervous System<br />Bacteria can grow in the cerebrospinal fluid in the subarachnoid space of th...
The Meninges and Cerebrospinal Fluid<br />Figure 22.2<br />
Bacterial Meningitis<br />Fever, headache, and stiff neck<br />Followed by nausea and vomiting<br />May progress to convul...
Bacterial Meningitis<br />Figure 22.3<br />
ACUTE BACTERIAL MENINGITIS<br />infection and inflammation of the meninges<br />infection of other parts of the CNS<br />
SYMPTOMS<br />(meningeal symptoms)<br /><ul><li>high fever
  headache
	stiff neck
	irritability (children)
	neurologic dysfunction
lethargy
confusion
	uncharacteristic sleepiness
	vomiting</li></li></ul><li>B.  Agents: - vary depending on the age of the patient<br />	1.  newborns/neonates<br /><ul><l...
E. coli K1
Listeriamonocytogenes</li></ul>	2.  infants and children up to 24 months old<br /><ul><li>Streptococcus pneumoniae
Neisseriameningitidis
(Haemophilusinfluenzae type b – vaccine; </li></ul>                   self study) <br />	3.  Adults<br /><ul><li>Streptoco...
Neisseriameningitidis</li></li></ul><li>
Neisseria Meningitis, Meningococcal Meningitis<br />N. meningitidis<br />Gram-negative aerobic cocci, capsule<br />10% of ...
Neisseria Meningitis, Meningococcal Meningitis<br />N. meningitidis causes meningococcal meningitis. This bacterium is fou...
Neisseria Associated Diseases<br />(ophthalmia neonatorum)<br />
Differential Characteristics of Commonly Isolated Neisseria spp.<br />
General Overview of Neisseriameningitidis<br /><ul><li>Encapsulated small, gram-negative diplococci
Second most common cause (behind S. pneumoniae) of community-acquired meningitis in previously healthy adults
swift progression from good health to life-threatening disease</li></li></ul><li>General Overview of Neisseriameningitidis...
Pili-mediated, receptor-specific colonization of nonciliated cells of nasopharynx
Antiphagocytic polysaccharide capsule
hyperproductionof lipooligosaccharide</li></li></ul><li>Diseases Associated with    Neisseriameningitidis<br /><ul><li>Fol...
Meningitis
Septicemia (meningococcemia) with or without meningitis
Meningoencephalitis
Pneumonia
Arthritis
Urethritis</li></li></ul><li>Neisseria meningitidis in Cerebrospinal Fluid<br />
Epidemiology of Meningococcal Disease<br /><ul><li>Humans only natural hosts
Person-to-person transmission by aerosolization of respiratory tract secretions in crowded conditions
Close contact with infectious person (e.g., family members, day care centers, military barracks, prisons, and other instit...
Commonly colonize nasopharynx of healthy individuals;  highest  oral and nasopharyngeal carriage rates in school-age child...
Organisms are internalized into phagocytic vacuoles, avoid intracellular killing
Replicate intracellularly and migrate to subepithelialspace</li></li></ul><li>Pathogenesis of Meningococcal Disease<br /><...
most clinical manifestations including
diffuse vascular damage,
vasculitis,
thrombosis,
disseminated intravascular coagulation</li></li></ul><li>Skin Lesions of Meningococcemia<br />NOTE:Petechiae have coalesce...
Immunogenicity of Neisseriameningitidis<br /><ul><li>Following colonization of the nasopharynx, protective humoral immunit...
complementsystem is required for clearance of the organisms
Cross-reactive protective immunity acquired with colonization by closely related antigenic strains e.g., E. coli K1)</li><...
Transparent, non-pigmented nonhemolytic colonies on chocolate blood agar with enhanced growth in moist atmosphere with 5% ...
Oxidase-positive
Acid production from glucose and maltose</li></li></ul><li>Prevention and Treatment of Meningococcal Disease<br /><ul><li>...
Chloramphenicolor cephalosporins as alternatives
Chemoprophylaxis of close contacts with rifampin or sulfadiazine (if susceptible)
Polyvalent vaccineis effective in people older than 2 years of age adjunct to chemoprophylaxis</li></li></ul><li>Neisseria...
Haemophilusinfluenzae Meningitis<br />Occurs mostly in children (6 months to 4 years).<br />Gram-negative aerobic bacteria...
Haemophilusinfluenzae Meningitis<br />H. influenzae requires blood factors for growth<br /> there are six types of H. infl...
Differential Characteristics<br />X factor = hemin (hematin)<br />V factor = (NAD or NADP)<br />nicotinamide adenine dinuc...
Haemophilus General Overview<br /><ul><li>Gram-negative bacilli liking blood (as per genus name)
Obligate Parasites of Man and Animals
Major pathogens for which humans are natural hosts
Haemophilusinfluenzae
Acute pyogenic, normally invasive infections
Chronic infections with H. influenzae as 2opathogen
Haemophilusducreyi
True pathogen (i.e., not found in healthy individuals)
STD;  Soft chancre (chancroid)</li></li></ul><li>Haemophilus Diseases<br />
Haemophilusinfluenzae Diseases<br />
HIB VACCINE <br /><ul><li>humoralIgG to capsule prevents systemic infection by opsonization
new vaccine composed of type b carbohydrate coupled to protein has drastically reduced meningitis by Hib
the vaccine is now part of the standard infant/childhood regimen</li></li></ul><li>Streptococcus pneumoniae Meningitis, Pn...
Streptococcus pneumoniae Meningitis, Pneumococcal Meningitis<br />Hospitalized patients and young children are most suscep...
Listeriosis<br />Listeria monocytogenes<br />Gram-negative aerobic rod<br />Usually foodborne; it can be transmitted to fe...
Listeriosis<br />causes meningitis in newborns, the immunosuppressed, pregnant women, and cancer patients.<br />Acquired b...
Listeriamonocytogenes<br /><ul><li>Gram-positive beta-hemolytic bacillus
Multiply at refrigerator temperatures (4oC)
Tumbling motility at room temperature
CAMP Test positive (like Group B Streptococcus)</li></li></ul><li>Where do we find Listeria?<br /><ul><li>Intestinal tract...
Persists in soil
Soft cheeses & unwashed raw vegetables
Raw or undercooked food of animal origin
 Luncheon meats
 Hot dogs
Large scale food recalls have become common</li></li></ul><li>Epidemiology of     Listeriosis<br />
Natural Reservoirs<br />Common Routes for Human Exposure<br />Population at Greatest Risk<br />Epidemiology of Listeria In...
Listeriosis<br /><ul><li>Neonates, elderly & immunocompromised
Granulomatosisinfantiseptica
Transmitted to fetus transplacentally
 Early septicemic form: 1-5 days post-partum
 Delayed meningitic form: 10-20 days following birth
Intracellular pathogen
Cell-mediated and humoralimmunity develop
 Only cell-mediated immunity is protective </li></li></ul><li>Methods That Circumvent Phagocytic Killing<br />See Chpt. 19...
Tetanus<br />Clostridium tetani<br />Gram-positive, endospore-forming, obligate anaerobe<br />Grows in deep wounds.<br />T...
Tetanus<br />produces the neurotoxin tetanospasmin, which causes the symptoms of tetanus: <br />Spasms<br />contraction of...
Tetanus<br />grow in deep, unclean wounds and wounds with little bleeding.<br />Acquired immunity results from DPT immuniz...
Tetanus<br />Figure 22.6<br />
Summary of   C. tetani Infections<br />
Summary of Clostridium tetani Infections(cont.)<br />
Clostridium tetani Gram Stain<br />NOTE:  Round terminal spores give cells a “drumstick” or “tennis racket” appearance.<br />
Clinical Forms of Tetanus<br />
Opisthotonos in Tetanus Patient<br />
RisusSardonicus in Tetanus Patient<br />
Mechanism of Action of Tetanus Toxin<br />
Botulism<br />Clostridium botulinum<br />Gram-positive, endospore-forming, obligate anaerobe<br />Intoxication comes from ...
Botulism<br />Botulism is caused by an exotoxin produced by C. botulinum growing in foods.<br />Serological types of botul...
Botulism<br />Type A<br />60-70% fatality, most heat resistant and proteolytic<br />Found in CA, WA, CO, OR, NM.<br />Type...
Botulism<br />Blurred vision occurs in 1 to 2 days<br />progressive flaccid paralysis follows for 1 to 10 days<br />possib...
Botulism<br />C. botulinum will not grow in acidic foods or in an aerobic environment.<br />Endospores are killed by prope...
Summary of   C. botulinum Infections<br />
Summary of   C. botulinum Infections (cont.)<br />
Mechanism of Action of Botulinum Toxin<br />
Botulism<br />Treatment: Supportive care and antitoxin.<br />Infant botulism results from C. botulinum growing in intestin...
Botulism<br />For diagnosis, mice protected with antitoxin are inoculated with toxin from the patient or foods.<br />
Diagnosis<br />Figure 22.8<br />
Leprosy<br />Mycobacterium leprae<br />causes leprosy, or Hansen’s disease.<br />Acid-fast rod that grows best at 30°C.<br...
Mycobacterial Clinical Syndromes<br />
Leprosy<br />Leprosy is not highly contagious and is spread by prolonged contact with exudates.<br />Untreated individuals...
Leprosy<br />
Leprosy<br />Laboratory diagnosis is based on observations of acid-fast rods in lesions or fluids and the lepromin test.<b...
Acid-Fast (Kinyoun) Stain of Mycobacterium<br />NOTE: cord growth (serpentine arrangement)of virulent strains<br />
Eight Week Growth of Mycobacterium tuberculosis on Lowenstein-Jensen Agar<br />
Mycobacterium leprae Infections (cont.)<br />
Tuberculoid vs. Lepromatous Leprosy<br />Clinical Manifestations and Immunogenicity<br />
Lepromatous vs. Tuberculoid Leprosy<br />
Lepromatous Leprosy (Early/Late Stages)<br />
Lepromatous Leprosy Pre- and Post-Treatment<br />
Clinical Progression of Leprosy<br />
Leprosy<br />Figure 22.9<br />
Poliomyelitis<br />Poliovirus<br />Transmitted by ingestion.<br />Initial symptoms: Sore throat and nausea<br />Viremia ma...
Poliomyelitis<br />The symptoms of poliomyelitis <br /> headache<br /> sore throat<br /> fever<br />stiffness of the back ...
Poliomyelitis<br />Poliovirus first invades lymph nodes of the neck and small intestine. <br />Viremia and spinal cord inv...
Poliomyelitis<br />The Salk vaccine (an inactivated polio vaccine, or IPV)<br /> involves the injection of formalin-inacti...
Poliomyelitis<br />Figure 22.11<br />
Rabies Virus (Rhabdovirus)<br />Transmitted by animal bite.<br />Virus multiplies in skeletal muscles, then brain cells ca...
RABIES<br />Rabies virus (a rhabdovirus) causes an acute, usually fatal, encephalitis called rabies.<br />Rabies may be co...
RABIES<br />Encephalitis occurs when the virus moves along peripheral nerves to the CNS.<br />Symptoms of rabies include <...
RABIES<br />Laboratory diagnosis may be made by direct FA tests of saliva, serum, and CSF or brain smears.<br />Reservoirs...
How Is Rabies Transmitted?<br />
How Is Rabies Transmitted?<br />
How Is Rabies Transmitted?<br />
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  1. 1. Microbial Diseases of the Nervous System<br />DR SONNIE P. TALAVERA 08162009 OLFU <br />
  2. 2. How Microbes Enter the Nervous System<br />Skull or backbone fractures<br />Medical procedures<br />Along peripheral nerves<br />Blood or lymph<br />
  3. 3. The Nervous System<br />Figure 22.1<br />
  4. 4. Microbial Diseases of the Nervous System<br />Bacteria can grow in the cerebrospinal fluid in the subarachnoid space of the CNS.<br />The blood brain barrier (capillaries) prevents passage of some materials (such as antimicrobial drugs) into the CNS.<br />Meningitis: Inflammation of meninges.<br />Encephalitis: Inflammation of the brain.<br />
  5. 5. The Meninges and Cerebrospinal Fluid<br />Figure 22.2<br />
  6. 6. Bacterial Meningitis<br />Fever, headache, and stiff neck<br />Followed by nausea and vomiting<br />May progress to convulsions and coma<br />Diagnosis by Gram stain or latex agglutination of CSF<br />Treated with cephalosporins<br />
  7. 7. Bacterial Meningitis<br />Figure 22.3<br />
  8. 8. ACUTE BACTERIAL MENINGITIS<br />infection and inflammation of the meninges<br />infection of other parts of the CNS<br />
  9. 9. SYMPTOMS<br />(meningeal symptoms)<br /><ul><li>high fever
  10. 10. headache
  11. 11. stiff neck
  12. 12. irritability (children)
  13. 13. neurologic dysfunction
  14. 14. lethargy
  15. 15. confusion
  16. 16. uncharacteristic sleepiness
  17. 17. vomiting</li></li></ul><li>B. Agents: - vary depending on the age of the patient<br /> 1. newborns/neonates<br /><ul><li>Group B streptococci
  18. 18. E. coli K1
  19. 19. Listeriamonocytogenes</li></ul> 2. infants and children up to 24 months old<br /><ul><li>Streptococcus pneumoniae
  20. 20. Neisseriameningitidis
  21. 21. (Haemophilusinfluenzae type b – vaccine; </li></ul> self study) <br /> 3. Adults<br /><ul><li>Streptococcus pneumoniae
  22. 22. Neisseriameningitidis</li></li></ul><li>
  23. 23. Neisseria Meningitis, Meningococcal Meningitis<br />N. meningitidis<br />Gram-negative aerobic cocci, capsule<br />10% of people are healthy nasopharyngeal carriers<br />Begins as throat infection, rash<br />Serotype B is most common in the United States<br />Vaccination recommended for college students.<br />
  24. 24. Neisseria Meningitis, Meningococcal Meningitis<br />N. meningitidis causes meningococcal meningitis. This bacterium is found in the throats of healthy carriers.<br />The bacteria probably gain access to the meninges through the bloodstream. The bacteria may be found in leukocytes in CSF.<br />Symptoms are due to endotoxin. The disease occurs most often in young children.<br />Purified capsular polysaccharide vaccine against serotypes A, C, Y, and W-135 is available.<br />
  25. 25. Neisseria Associated Diseases<br />(ophthalmia neonatorum)<br />
  26. 26. Differential Characteristics of Commonly Isolated Neisseria spp.<br />
  27. 27. General Overview of Neisseriameningitidis<br /><ul><li>Encapsulated small, gram-negative diplococci
  28. 28. Second most common cause (behind S. pneumoniae) of community-acquired meningitis in previously healthy adults
  29. 29. swift progression from good health to life-threatening disease</li></li></ul><li>General Overview of Neisseriameningitidis<br /><ul><li>Pathogenicity:
  30. 30. Pili-mediated, receptor-specific colonization of nonciliated cells of nasopharynx
  31. 31. Antiphagocytic polysaccharide capsule
  32. 32. hyperproductionof lipooligosaccharide</li></li></ul><li>Diseases Associated with Neisseriameningitidis<br /><ul><li>Following dissemination of virulent organisms from the nasopharynx:
  33. 33. Meningitis
  34. 34. Septicemia (meningococcemia) with or without meningitis
  35. 35. Meningoencephalitis
  36. 36. Pneumonia
  37. 37. Arthritis
  38. 38. Urethritis</li></li></ul><li>Neisseria meningitidis in Cerebrospinal Fluid<br />
  39. 39. Epidemiology of Meningococcal Disease<br /><ul><li>Humans only natural hosts
  40. 40. Person-to-person transmission by aerosolization of respiratory tract secretions in crowded conditions
  41. 41. Close contact with infectious person (e.g., family members, day care centers, military barracks, prisons, and other institutional settings) </li></li></ul><li>Epidemiology of Meningococcal Disease<br /><ul><li>Highest incidence in children younger than 5 years and particularly those younger than 1 year of age as passive maternal antibody declines and as infants immune system matures
  42. 42. Commonly colonize nasopharynx of healthy individuals; highest oral and nasopharyngeal carriage rates in school-age children, young adults and lower socioeconomic groups </li></li></ul><li>Pathogenesis of Meningococcal Disease<br /><ul><li>Specific receptors (GD1 ganglioside) for bacterial fimbriae on nonciliatedcolumnar epithelialcells innasopharynx of host
  43. 43. Organisms are internalized into phagocytic vacuoles, avoid intracellular killing
  44. 44. Replicate intracellularly and migrate to subepithelialspace</li></li></ul><li>Pathogenesis of Meningococcal Disease<br /><ul><li>Hyperproduction of endotoxinand blebbing into surrounding environment (e.g., subepithelial spaces, bloodstream)
  45. 45. most clinical manifestations including
  46. 46. diffuse vascular damage,
  47. 47. vasculitis,
  48. 48. thrombosis,
  49. 49. disseminated intravascular coagulation</li></li></ul><li>Skin Lesions of Meningococcemia<br />NOTE:Petechiae have coalesced into hemorrhagic bullae.<br />
  50. 50. Immunogenicity of Neisseriameningitidis<br /><ul><li>Following colonization of the nasopharynx, protective humoral immunity develops against the same or closely related organisms of the same serogroup
  51. 51. complementsystem is required for clearance of the organisms
  52. 52. Cross-reactive protective immunity acquired with colonization by closely related antigenic strains e.g., E. coli K1)</li></li></ul><li>Laboratory Characterization of Neisseriameningitidis<br /><ul><li>Large numbers of encapsulated, small, gram-negative diplococciand PMN seen in cerebrospinal fluid
  53. 53. Transparent, non-pigmented nonhemolytic colonies on chocolate blood agar with enhanced growth in moist atmosphere with 5% CO2
  54. 54. Oxidase-positive
  55. 55. Acid production from glucose and maltose</li></li></ul><li>Prevention and Treatment of Meningococcal Disease<br /><ul><li>Penicillin is drug of choice for treatment in adjunct with supportive therapy for meningeal symptoms
  56. 56. Chloramphenicolor cephalosporins as alternatives
  57. 57. Chemoprophylaxis of close contacts with rifampin or sulfadiazine (if susceptible)
  58. 58. Polyvalent vaccineis effective in people older than 2 years of age adjunct to chemoprophylaxis</li></li></ul><li>Neisseria Meningitis, Meningococcal Meningitis<br />Figure 22.4<br />
  59. 59. Haemophilusinfluenzae Meningitis<br />Occurs mostly in children (6 months to 4 years).<br />Gram-negative aerobic bacteria, normal throat microbiota<br />Capsule antigen type b<br />Prevented by Hib vaccine<br />
  60. 60. Haemophilusinfluenzae Meningitis<br />H. influenzae requires blood factors for growth<br /> there are six types of H. influenzae based on capsule differences.<br />H. influenzae type b <br />the most common cause of meningitis in children under 4 years old.<br />A conjugated vaccine directed against the capsular polysaccharide antigen is available.<br />
  61. 61. Differential Characteristics<br />X factor = hemin (hematin)<br />V factor = (NAD or NADP)<br />nicotinamide adenine dinucleotide<br />
  62. 62. Haemophilus General Overview<br /><ul><li>Gram-negative bacilli liking blood (as per genus name)
  63. 63. Obligate Parasites of Man and Animals
  64. 64. Major pathogens for which humans are natural hosts
  65. 65. Haemophilusinfluenzae
  66. 66. Acute pyogenic, normally invasive infections
  67. 67. Chronic infections with H. influenzae as 2opathogen
  68. 68. Haemophilusducreyi
  69. 69. True pathogen (i.e., not found in healthy individuals)
  70. 70. STD; Soft chancre (chancroid)</li></li></ul><li>Haemophilus Diseases<br />
  71. 71. Haemophilusinfluenzae Diseases<br />
  72. 72. HIB VACCINE <br /><ul><li>humoralIgG to capsule prevents systemic infection by opsonization
  73. 73. new vaccine composed of type b carbohydrate coupled to protein has drastically reduced meningitis by Hib
  74. 74. the vaccine is now part of the standard infant/childhood regimen</li></li></ul><li>Streptococcus pneumoniae Meningitis, Pneumococcal Meningitis<br />Gram-positive diplococci<br />70% of people are healthy nasopharyngeal carriers<br />Most common in children (1 month to 4 years)<br />Mortality: 30% in children, 80% in elderly<br />Prevented by vaccination<br />
  75. 75. Streptococcus pneumoniae Meningitis, Pneumococcal Meningitis<br />Hospitalized patients and young children are most susceptible to S. pneumoniae meningitis.<br /> It is rare but has a high mortality rate.<br />A conjugated vaccine is available.<br />
  76. 76.
  77. 77. Listeriosis<br />Listeria monocytogenes<br />Gram-negative aerobic rod<br />Usually foodborne; it can be transmitted to fetus.<br />Reproduce in phagocytes.<br />Figure 22.5<br />
  78. 78. Listeriosis<br />causes meningitis in newborns, the immunosuppressed, pregnant women, and cancer patients.<br />Acquired by ingestion of contaminated food, it may be asymptomatic in healthy adults.<br />L. monocytogenes can cross the placenta and cause spontaneous abortion and stillbirth.<br />Figure 22.5<br />
  79. 79. Listeriamonocytogenes<br /><ul><li>Gram-positive beta-hemolytic bacillus
  80. 80. Multiply at refrigerator temperatures (4oC)
  81. 81. Tumbling motility at room temperature
  82. 82. CAMP Test positive (like Group B Streptococcus)</li></li></ul><li>Where do we find Listeria?<br /><ul><li>Intestinal tract of mammals & birds (especially chickens)
  83. 83. Persists in soil
  84. 84. Soft cheeses & unwashed raw vegetables
  85. 85. Raw or undercooked food of animal origin
  86. 86. Luncheon meats
  87. 87. Hot dogs
  88. 88. Large scale food recalls have become common</li></li></ul><li>Epidemiology of Listeriosis<br />
  89. 89.
  90. 90.
  91. 91. Natural Reservoirs<br />Common Routes for Human Exposure<br />Population at Greatest Risk<br />Epidemiology of Listeria Infections<br />
  92. 92. Listeriosis<br /><ul><li>Neonates, elderly & immunocompromised
  93. 93. Granulomatosisinfantiseptica
  94. 94. Transmitted to fetus transplacentally
  95. 95. Early septicemic form: 1-5 days post-partum
  96. 96. Delayed meningitic form: 10-20 days following birth
  97. 97. Intracellular pathogen
  98. 98. Cell-mediated and humoralimmunity develop
  99. 99. Only cell-mediated immunity is protective </li></li></ul><li>Methods That Circumvent Phagocytic Killing<br />See Chpt. 19<br />
  100. 100. Tetanus<br />Clostridium tetani<br />Gram-positive, endospore-forming, obligate anaerobe<br />Grows in deep wounds.<br />Tetanospasmin released from dead cells blocks relaxation pathway in muscles.<br />Prevention by vaccination with tetanus toxoid (DTP) and booster (dT).<br />Treatment with tetanus immune globulin.<br />
  101. 101. Tetanus<br />produces the neurotoxin tetanospasmin, which causes the symptoms of tetanus: <br />Spasms<br />contraction of muscles controlling the jaw<br />death resulting from spasms of respiratory muscles.<br />
  102. 102. Tetanus<br />grow in deep, unclean wounds and wounds with little bleeding.<br />Acquired immunity results from DPT immunization that includes tetanus toxoid.<br />Following an injury, an immunized person may receive a booster of tetanus toxoid. <br />An unimmunized person may receive (human) tetanus immune globulin.<br />Debridement (removal of tissue) and antibiotics may be used to control the infection.<br />
  103. 103.
  104. 104. Tetanus<br />Figure 22.6<br />
  105. 105. Summary of C. tetani Infections<br />
  106. 106. Summary of Clostridium tetani Infections(cont.)<br />
  107. 107. Clostridium tetani Gram Stain<br />NOTE: Round terminal spores give cells a “drumstick” or “tennis racket” appearance.<br />
  108. 108. Clinical Forms of Tetanus<br />
  109. 109.
  110. 110.
  111. 111. Opisthotonos in Tetanus Patient<br />
  112. 112. RisusSardonicus in Tetanus Patient<br />
  113. 113. Mechanism of Action of Tetanus Toxin<br />
  114. 114. Botulism<br />Clostridium botulinum<br />Gram-positive, endospore-forming, obligate anaerobe<br />Intoxication comes from ingesting botulinal toxin.<br />Botulinal toxin blocks release of neurotransmitter causing flaccid paralysis.<br />Prevention<br />Proper canning<br />Nitrites prevent endospore germination in sausages.<br />
  115. 115.
  116. 116. Botulism<br />Botulism is caused by an exotoxin produced by C. botulinum growing in foods.<br />Serological types of botulinum toxin vary in virulence, with type A being the most virulent.<br />The toxin is a neurotoxin that inhibits the transmission of nerve impulses.<br />
  117. 117.
  118. 118.
  119. 119. Botulism<br />Type A<br />60-70% fatality, most heat resistant and proteolytic<br />Found in CA, WA, CO, OR, NM.<br />Type B<br />25% fatality,; proteolytic and nonproteolytic<br />Europe and eastern United States<br />Type E<br />Found in marine and lake sediments<br />Pacific Northwest, Alaska, Great Lakes area<br />Non proteolytic, grow in ref temp and less anaerobic condition<br />
  120. 120. Botulism<br />Blurred vision occurs in 1 to 2 days<br />progressive flaccid paralysis follows for 1 to 10 days<br />possibly resulting in death from respiratory and cardiac failure.<br />
  121. 121. Botulism<br />C. botulinum will not grow in acidic foods or in an aerobic environment.<br />Endospores are killed by proper canning. The addition of nitrites to foods inhibits growth after endospore germination.<br />The toxin is heat labile and is destroyed by boiling (100°C) for 5 minutes<br />
  122. 122.
  123. 123. Summary of C. botulinum Infections<br />
  124. 124. Summary of C. botulinum Infections (cont.)<br />
  125. 125. Mechanism of Action of Botulinum Toxin<br />
  126. 126.
  127. 127. Botulism<br />Treatment: Supportive care and antitoxin.<br />Infant botulism results from C. botulinum growing in intestines.<br />Wound botulism results from growth of C. botulinumin wounds.<br />
  128. 128. Botulism<br />For diagnosis, mice protected with antitoxin are inoculated with toxin from the patient or foods.<br />
  129. 129. Diagnosis<br />Figure 22.8<br />
  130. 130. Leprosy<br />Mycobacterium leprae<br />causes leprosy, or Hansen’s disease.<br />Acid-fast rod that grows best at 30°C.<br />Grows in peripheral nerves and skin cells.<br />Transmission requires prolonged contact with an infected person.<br />
  131. 131. Mycobacterial Clinical Syndromes<br />
  132. 132. Leprosy<br />Leprosy is not highly contagious and is spread by prolonged contact with exudates.<br />Untreated individuals often die of secondary bacterial complications, such as tuberculosis.<br />Patients with leprosy are made noncontagious within 4 to 5 days with sulfone drugs and then treated as outpatients.<br />Leprosy occurs primarily in the tropics.<br />
  133. 133. Leprosy<br />
  134. 134. Leprosy<br />Laboratory diagnosis is based on observations of acid-fast rods in lesions or fluids and the lepromin test.<br />
  135. 135. Acid-Fast (Kinyoun) Stain of Mycobacterium<br />NOTE: cord growth (serpentine arrangement)of virulent strains<br />
  136. 136. Eight Week Growth of Mycobacterium tuberculosis on Lowenstein-Jensen Agar<br />
  137. 137. Mycobacterium leprae Infections (cont.)<br />
  138. 138. Tuberculoid vs. Lepromatous Leprosy<br />Clinical Manifestations and Immunogenicity<br />
  139. 139. Lepromatous vs. Tuberculoid Leprosy<br />
  140. 140. Lepromatous Leprosy (Early/Late Stages)<br />
  141. 141. Lepromatous Leprosy Pre- and Post-Treatment<br />
  142. 142. Clinical Progression of Leprosy<br />
  143. 143. Leprosy<br />Figure 22.9<br />
  144. 144.
  145. 145. Poliomyelitis<br />Poliovirus<br />Transmitted by ingestion.<br />Initial symptoms: Sore throat and nausea<br />Viremia may occur; if persistent, virus can enter the CNS; destruction of motor cells and paralysis occurs in <1% of cases.<br />Prevention is by vaccination (enhanced-inactivated polio vaccine).<br />
  146. 146. Poliomyelitis<br />The symptoms of poliomyelitis <br /> headache<br /> sore throat<br /> fever<br />stiffness of the back and neck<br /> occasionally paralysis (fewer than 1% of cases)<br />Poliovirus is transmitted by the ingestion of water contaminated with feces.<br />
  147. 147. Poliomyelitis<br />Poliovirus first invades lymph nodes of the neck and small intestine. <br />Viremia and spinal cord involvement may follow.<br />Diagnosis is based on isolation of the virus from feces and throat secretions.<br />
  148. 148. Poliomyelitis<br />The Salk vaccine (an inactivated polio vaccine, or IPV)<br /> involves the injection of formalin-inactivated viruses and boosters every few years<br />The Sabin vaccine (an oral polio vaccine, or OPV)<br /> contains three live, attenuated strains of poliovirus and is administered orally.<br />Polio is a good candidate for elimination through vaccination.<br />
  149. 149. Poliomyelitis<br />Figure 22.11<br />
  150. 150.
  151. 151. Rabies Virus (Rhabdovirus)<br />Transmitted by animal bite.<br />Virus multiplies in skeletal muscles, then brain cells causing encephalitis.<br />Initial symptoms may include muscle spasms of the mouth and pharynx and hydrophobia.<br />Furious rabies: Animals are restless then highly excitable.<br />Paralytic rabies: Animals seem unaware of surroundings.<br />Preexposure prophylaxis: Infection of human diploid cells vaccine.<br />Postexposure treatment: Vaccine plus immune globulin.<br />
  152. 152. RABIES<br />Rabies virus (a rhabdovirus) causes an acute, usually fatal, encephalitis called rabies.<br />Rabies may be contracted through bite of a rabid animal<br /> by inhalation of aerosols<br /> invasion through minute skin abrasions<br />The virus multiplies in skeletal muscle and connective tissue.<br />
  153. 153.
  154. 154.
  155. 155. RABIES<br />Encephalitis occurs when the virus moves along peripheral nerves to the CNS.<br />Symptoms of rabies include <br />spasms of mouth and throat muscles followed by extensive brain and spinal cord damage<br />death.<br />
  156. 156. RABIES<br />Laboratory diagnosis may be made by direct FA tests of saliva, serum, and CSF or brain smears.<br />Reservoirs for rabies in the United States include skunks, bats, foxes, and raccoons. Domestic cattle, dogs, and cats may get rabies. Rodents and rabbits seldom get rabies.<br />Current postexposure treatment includes administration of human rabies immune globulin (RIG) along with multiple intramuscular injections of vaccine.<br />Preexposure treatment consists of vaccination.<br />Other genotypes of Lyssavirus cause rabies-like diseases.<br />
  157. 157. How Is Rabies Transmitted?<br />
  158. 158. How Is Rabies Transmitted?<br />
  159. 159. How Is Rabies Transmitted?<br />
  160. 160.
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  178. 178. Rabies Virus (Rhabdovirus)<br />Figure 22.12<br />
  179. 179. Rabies Virus (Rhabdovirus)<br />Figure 22.13<br />
  180. 180. Arboviral Encephalitis<br />Arboviruses are arthropod-borne viruses that belong to several families.<br />Prevention is by controlling mosquitoes.<br />Figure 22.14<br />
  181. 181. Arboviral Encephalitis<br />Symptoms of encephalitis are <br />Chills<br />Headache<br />Fever<br />Coma<br />Many types of viruses (called arboviruses) transmitted by mosquitoes cause encephalitis.<br />
  182. 182. Arboviral Encephalitis<br />The incidence of arboviral encephalitis increases in the summer months, when mosquitoes are most numerous.<br />Notifiablearboviral infections are <br />eastern equine encephalitis (EEE), <br />western equine encephalitis (WEE), <br />St. Louis encephalitis (SLE), <br />California encephalitis (CE), <br />West Nile virus (WNV).<br />
  183. 183. Arboviral Encephalitis<br />Diagnosis is based on serological tests.<br />Control of the mosquito vector is the most effective way to control encephalitis.<br />
  184. 184. Arboviral Encephalitis<br />
  185. 185. Cryptococcus Neoformans Meningitis (Cryptococcosis)<br />Figure 22.15<br />
  186. 186. Cryptococcus Neoformans Meningitis (Cryptococcosis)<br />Soil fungus associated with pigeon and chicken droppings.<br />Transmitted by the respiratory route; spreads through blood to the CNS.<br />Mortality up to 30%.<br />Treatment: Amphotericin B and flucytosine.<br />
  187. 187. Cryptococcus Neoformans Meningitis (Cryptococcosis<br />Cryptococcus neoformans is an encapsulated yeastlike fungus that causes cryptococcosis.<br />The disease may be contracted by inhalation of dried infected pigeon or chicken droppings.<br />The disease begins as a lung infection and may spread to the brain and meninges.<br />
  188. 188.
  189. 189. Cryptococcus Neoformans Meningitis (Cryptococcosis<br />Immunosuppressedindividuals are most susceptible to Cryptococcus neoformans meningitis.<br />Diagnosis is based on latex agglutination tests for cryptococcal antigens in serum or CSF.<br />
  190. 190. African Trypanosomiasis<br />Trypanosoma brucei gambiense infection is chronic (2 to 4 years).<br />T. b. rhodesiense infection is more acute (few months).<br />Transmitted from animals to humans by tsetse fly.<br />Prevention: Elimination of the vector.<br />Treatment: Eflornithine blocks an enzyme necessary for the parasite.<br />Parasite evades the antibodies through antigenic variation.<br />
  191. 191. Tsetse fly.The vector of African trypanosomiasis<br />
  192. 192. African Trypanosomiasis<br />African trypanosomiasis is caused by the protozoa Trypanosomabruceigambiense and T. b. rhodesiense and transmitted by the bite of the tsetse fly.<br />The disease affects the nervous system of the human host, causing lethargy and eventually coma. It is commonly called sleeping sickness.<br />Vaccine development is hindered by the protozoan’s ability to change its surface antigens.<br />
  193. 193. African Trypanosomiasis<br />Figure 22.16<br />
  194. 194. TRYPANOSOMA BRUCEI<br />
  195. 195. TRYPANOSOMA BRUCEI<br />Lab Dx: <br />Giemsa stained thick and thin blood smears or lymph exudate (early stage); Giemsa stained smears of CSF (late stage)<br />
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  197. 197. A dividing parasite is seen at the right. Dividing forms are seen in African trypanosomiasis, but not in American trypanosomiasis (Chagas' disease)<br />
  198. 198. Winterbottoms sign<br />
  199. 199. Ramana's sign: unilateral conjunctivitis and orbital edema  <br />
  200. 200.
  201. 201. Naegleriafowleri<br />Protozoan infects nasal mucosa from swimming water.<br />Figure 22.17<br />
  202. 202. Naegleriafowleri<br />Encephalitis caused by the protozoan Naegleriafowleri is almost always fatal.<br />Granulomatous amebic encephalitis, caused by Acanthamoeba spp. and Balamuthiamandrillaris, is a chronic disease.<br />
  203. 203. PROTOZOA FROM OTHER BODY SITES<br />FREE LIVING AMEBAE<br /><ul><li>Disease:
  204. 204. Naegleria: Primary Amebic Meningoencephalitis (PAM)
  205. 205. Acanthamoeba: Chronic Granulomatous Amebic Encephalitis and keratitis
  206. 206. Lab Dx: Direct microscopic exam (Wheatley’s trichrome stain); culture of organism by inoculation of sample onto nonnutritive agar seeded w/ E. coli or E. aerogenes</li></li></ul><li>FREE LIVING AMEBAE<br /><ul><li>Portal of Entry:
  207. 207. Naegleria: nose
  208. 208. Acanthamoeba: respiratory tract or ulcers in skin or mucosa / direct invasion of eye
  209. 209. Source of infection:
  210. 210. Naegleria: warm lakes, streams, ponds or inadequately chlorinated swimming pools
  211. 211. Acanthamoeba: immunocompromised or debilitated host </li></li></ul><li>
  212. 212. N. fowleri trophozoites cultured from cerebrospinal fluid: cells have characteristically large nuclei, with a large, dark staining karyosome.  The amebae are very active and extend and retract broad pseudopods. Trichrome stain. <br />
  213. 213. Naegleria spp.: trophozoite stained with Greenstein’s five dye stain And observed under dark field microscope.<br />                                                                                                                                                 <br />
  214. 214. PRIONS<br />Diseases of the CNS that progress slowly and cause spongiform degeneration are caused by prions.<br />Sheep scrapie and bovine spongiform encephalopathy (BSE) are examples of diseases caused by prions that are transferable from one animal to another.<br />Creutzfeldt-Jakob disease and kuru are human diseases similar to scrapie. They are transmitted between humans.<br />Prions are self-replicating proteins with no detectable nucleic acid.<br />
  215. 215. Transmissible Spongiform Encephalopathies<br />Caused by prions<br />Sheep scrapie<br />Creutzfeldt-Jakob disease<br />Kuru<br />Bovine spongiform encephalopathy<br />Transmitted by ingestion or transplant or inherited.<br />Chronic and fatal<br />
  216. 216. Transmissible Spongiform Encephalopathies<br />Figure 22.18<br />

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