Bloodlytmphatic disease


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Bloodlytmphatic disease

  1. 1. 23 Microbial Diseases of the Cardiovascular and Lymphatic Systems
  2. 2. The Cardiovascular Systemand Lymphatics System Blood: Transports nutrients to and wastes from cells. WBCs: Defend against infection. Lymphatics: Transport interstitial fluid to blood. Lymph nodes: Contain fixed macrophages.
  3. 3. The Lymphatic System Figure 23.2
  4. 4. Sepsis and Septic Shock Sepsis: Bacteria growing in the blood Severe sepsis: Decrease in blood pressure Septic shock: Low blood pressure cannot be controlled Figure 23.3
  5. 5. Sepsis Gram-negative sepsis  Endotoxins caused blood pressure decrease.  Antibiotics can worsen condition by killing bacteria. Gram-positive sepsis  Nosocomial infections  Staphylococcus aureus  Streptococcus pyogenes  Group B streptococcus  Enterococcus faecium and E. faecalis
  6. 6. Sepsis Puerperal sepsis (childbirth fever)  Streptococcus pyogenes  Transmitted to mother during childbirth by attending physicians and midwives.
  7. 7. Bacterial Infections of the Heart Endocarditis: Inflammation of the endocardium Subacute bacterial endocarditis: Alpha-hemolytic streptococci from mouth Acute bacterial endocarditis: Staphylococcus aureus from mouth Pericarditis: Streptococci
  8. 8. Bacterial Infections of theHeart Figure 23.4
  9. 9. Rheumatic Fever Inflammation of heart valves Autoimmune complication of Streptococcus pyogenes infections Figure 23.5
  10. 10. RF RF is characterized by a constellation of findings major manifestations  (1) migratory polyarthritis of the large joints  (2) carditis,  (3) subcutaneous nodules  (4) erythema marginatum of the skin  (5) Sydenham chorea, a neurologic disorder with involuntary purposeless, rapid movements.
  11. 11. RF minor manifestations (nonspecific signs and symptoms)  fever, arthralgia  elevated blood levels of acute phase reactants CRP, ESR, ASO The diagnosis is established by the so-called Jones criteria:  evidence of a preceding group A streptococcal infection, with the presence of two of the major manifestations listed above or one major and two minor manifestations
  12. 12. RF After an initial attack, there is increased vulnerability to reactivation of the disease with subsequent pharyngeal infections, and the same manifestations are likely to appear with each recurrent attack. Carditis is likely to worsen with each recurrence, and damage is cumulative. valvular disease  cardiac murmurs, cardiac hypertrophy and dilation, and heart failure, arrhythmias (particularly atrial fibrillation in the setting of mitral stenosis), thromboembolic complications, and infective endocarditis.
  13. 13. Tularemia Francisella tularensis, gram-negative rod Transmitted from rabbits and deer by deer flies. Bacteria reproduce in phagocytes. Figure 23.6
  14. 14. Brucellosis (Undulant Fever) Brucella, gram-negative rods that grow in phagocytes. B. abortus (elk, bison, cows) B. suis (swine) B. melitensis (goats, sheep, camels) Undulating fever that spikes to 40°C each evening. Transmitted via milk from infected animals or contact with infected animals.
  15. 15. Anthrax Bacillus anthracis, gram-positive, endospore- forming aerobic rod Is found in soil. Cattle are routinely vaccinated. Treated with ciprofloxacin or doxycycline. Cutaneous anthrax  Endospores enter through minor cut  20% mortality
  16. 16. Anthrax Gastrointestinal anthrax  Ingestion of undercooked food contaminated food  50% mortality. Inhalational anthrax  Inhalation of endospores.  100% mortality. Figure 23.7
  17. 17. Biological Weapons 1346: Plague-ridden bodies used by Tartar army against Kaffa. 1925: Plaque-carrying flea bombs used in the Sino-Japanese War. 1950s: U.S. Army spraying of S. marcescens to test weapons dispersal. 1972: International agreement to not possess biological weapons. 1979: B. anthracis weapons plant explosion in the Soviet Union. 1984: S. enterica used against the people of The Dalles. 2001: B. anthracis distributed in the United States
  18. 18. Biological WeaponsBacteria VirusesBacillus anthracis “Eradicated” polio and measlesBrucella spp. Encephalitis virusesChlamydophila psittaci Hermorrhagic fever virusesClostridium botulinum toxin Influenza A (1918 strain)Coxiella burnetti MonkeypoxFrancisella tularensis Nipah virusRickettsia prowazekii SmallpoxShigella spp. Yellow feverVibrio choleraeYersinia pestis
  19. 19. Gangrene Ischemia: Loss of blood supply to tissue. Necrosis: Death of tissue. Gangrene : Death of soft tissue. Gas gangrene  Clostridium perfringens, gram-positive, endospore- forming anaerobic rod, grows in necrotic tissue  Treatment includes surgical removal of necrotic tissue and/or hyperbaric chamber.
  20. 20. Animal Bites and Scratches Pasteurella multocida Clostridium Bacteroides Fusobacterium Bartonella hensellae: Cat-scratch disease
  21. 21. Plague Yersinia pestis, gram-negative rod Reservoir: Rats, ground squirrels, and prairie dogs Vector: Xenopsylla cheopsis Bubonic plague: Bacterial growth in blood and lymph Septicemia plague: Septic shock Pneumonic plague: Bacteria in the lungs
  22. 22. Plague Figures 23.10, 23.11
  23. 23. Relapsing Fever Borrelia spp., spirochete Reservoir: Rodents Vector: Ticks Successive relapses are less severe
  24. 24. Lyme Disease Borrelia burgdorferi Reservoir: Deer Vector: Ticks Figures 23.13b–c
  25. 25. Lyme Disease Figure 23.13a
  26. 26. Lyme Disease First symptom: Bulls eye rash Second phase: Irregular heartbeat, encephalitis Third phase: Arthritis Figure 23.14
  27. 27. Figure 23.12
  28. 28. Ehrlichiosis Ehrlichia, gram-negative, obligately intracellular (in white blood cells) Reservoir: Deer, rodents Vector: Ticks Figure 23.15
  29. 29. Typhus Epidemic typhus  Rickettsia prowazekii  Reservoir: Rodents  Vector: Pediculus humanus corporis  Transmitted when louse feces rubbed into bite wound
  30. 30. Typhus Epidemic murine typhus:  Rickettsia typhi  Reservoir: Rodents  Vector: Xenopsylla cheopsis
  31. 31. Spotted Fevers (Rocky MountainSpotted Fever)  Rickettsia rickettsii  Measles-like rash except that the rash appears on palms and soles too. Figure 23.18
  32. 32. Spotted Fevers (Rocky MountainSpotted Fever) Figure 23.16
  33. 33. Tick Life Cycle Figure 23.17
  34. 34. Human Herpes Virus 4 InfectionsEbstein Barr Virus EBVInfectious Mononucleosis  Childhood infections are asymptomatic.  Transmitted via saliva  Characterized by proliferation of monocytesBurkitt’s lymphoma  Nasopharyngeal carcinoma  Cancer in immunosuppressed individuals, and malaria and AIDS patients
  35. 35. Infectious Mononucleosis Figure 23.20
  36. 36. Cytomegalovirus Infections Cytomegalovirus (Human herpesvirus 5) Infected cells swell (cyto-, mega-) Latent in white blood cells May be asymptomatic or mild Transmitted across the placenta; may cause mental retardation Transmitted sexually, by blood, or by transplanted tissue
  37. 37. Viral Hemorrhagic Fevers Pathogen Portal of Reservoir Method of entry transmissionYellow fever Arbovirus Skin Monkeys Aedes aegyptiDengue Arbovirus Skin Humans Aedes aegypti; A. AlbopictusMarburg, Filovirus, Mucous Probably Contact withEbola, arenavirus membranes fruit bats; bloodLassa other mammalsHantavirus Bunyavirus Respiratory Field mice Inhalationpulmonary tractsyndrome
  38. 38. Ebola Virus Figure 23.21
  39. 39. American Trypanosomiasis (Chagas’Disease) Trypanosoma cruzi Reservoir: Rodents, opossums, armadillos Vector: Reduviid bug Figures 23.22, 12.33d
  40. 40. Toxoplasmosis Toxoplasma gondii Figure 23.23
  41. 41. Malaria Plasmodium vivax, P. ovale, P. malariae, P. falciparum Anopheles mosquito Figure 12.31b
  42. 42. Malaria Figure 23.25
  43. 43. Malaria Figure 23.24
  44. 44. Malaria Figure 12.19
  45. 45. OTHER PROTOZOABLOOD and TISSUE PROTOZOA  Plasmodium  Babesia  Trypanosoma brucei  Trypanosoma cruzi  Toxoplasma gondii  Leishmania
  46. 46. PROTOZOA FROM OTHER BODY SITES  Free-living Amebae  Naegleria  Acanthamoeba  Trichomonas vaginalis
  47. 47. PLASMODIUM  Disease: Malaria  P. vivax: Benign tertian malaria  P. malariae: Quartan malaria  P. falciparum: Malignant tertian malaria  P. ovale: Ovale tertian malaria  Lab Dx: Giemsa stained thick and thin blood smears; IFA; PCR
  48. 48.  Infected RBC:  P. vivax and P. ovale: reticulocytes  P. malariae: senescent erythrocytes  P. falciparum: erythrocytes of all ages Cyclic paroxysm of fever:  P. vivax and P. ovale: every 48 hours  P. malariae: every 72 hours  P. falciparum: every 36-48 hours
  49. 49. P. falciparum: Blood Stage Parasites Thin Blood SmearsFig. 1: Normal red cell;Figs. 2-18: Trophozoites(among these, Figs. 2-10correspond to ring-stagetrophozoites);Figs. 19-26: Schizonts (Fig.26 is a ruptured schizont);Figs. 27, 28: Maturemacrogametocytes (female);Figs. 29, 30: Maturemicrogametocytes (male).
  50. 50. Gametocytes of P. falciparum in thin bloodsmears. Note the presence of a “Laveran’s bib”,which is not always visible.
  51. 51. P. falciparum rings have delicate cytoplasm and 1 or 2 smallchromatin dots. Red blood cells (RBCs) that are infected are notenlarged; multiple infection of RBCs more common in P. falciparumthan in other species. Occasional appliqué forms (rings appearingon the periphery of the RBC) can be present.
  52. 52. P. falciparum schizonts: seldom seen in peripheralblood. Mature schizonts have 8 to 24 small merozoites;dark pigment, clumped in one mass.
  53. 53. Plasmodiummalariae: BloodStage ParasitesThin Blood SmearsFig. 1: Normal red cell;Figs. 2-5: Youngtrophozoites (rings);Figs. 6-13: Trophozoites;Figs. 14-22: Schizonts;Fig. 23: Developinggametocyte;Fig. 24: Macrogametocyte(female);Fig. 25: Microgametocyte(male).
  54. 54. P. malariae rings: have sturdy cytoplasm and a largechromatin dot. The red blood cells (RBCs) are normalto smaller than normal (3/4 ×) in size.
  55. 55. P. malariae schizonts: have 6 to 12 merozoites with largenuclei, clustered around a mass of coarse, dark-brownpigment. Merozoites can occasionally be arranged as arosette pattern.
  56. 56. P. malariae trophozoites: have compact cytoplasm and alarge chromatin dot. Occasional band forms and/or"basket" forms with coarse, dark-brown pigment can beseen.
  57. 57. Plasmodiumovale: Blood StageParasitesFig. 1: Normal red cell;Figs. 2-5: Youngtrophozoites (Rings);Figs. 6-15: Trophozoites;Figs. 16-23: Schizonts;Fig. 24:Macrogametocytes(female);Fig. 25: Microgametocyte(male).
  58. 58. P. ovale gametocytes: round to oval, and may almost fillthe red blood cells (RBCs). Pigment is brown and morecoarse than that of P. vivax. RBCs are normal to slightlyenlarged (1 1/4 ×), may be round to oval, and aresometimes fimbriated. Schüffners dots are visibleunder optimal conditions.
  59. 59. Plasmodiumvivax: Blood StageParasitesThin Blood SmearsFig. 1: Normal red cell;Figs. 2-6: Youngtrophozoites (ring stageparasites);Figs. 7-18:Trophozoites;Figs. 19-27: Schizonts;Figs. 28 and29: Macrogametocytes(female);Fig. 30:Microgametocyte (male).
  60. 60. P. vivax gametocytes: round to oval with scatteredbrown pigment and may almost fill the red blood cell(RBC). RBCs are enlarged 1 1/2 to 2 × and may bedistorted. Under optimal conditions, Schüffners dotsmay appear more fine than those seen in P. ovale.
  61. 61. P. vivax rings: have large chromatin dots and can showamoeboid cytoplasm as they develop. RBCs can be normalto enlarged up to 1 1/2 × and may be distorted. Underoptimal conditions, Schüffners dots may be seen.
  62. 62. P. vivax schizonts: large, have 12 to 24 merozoites,yellowish-brown, coalesced pigment, and may fill thered blood cell (RBC).
  63. 63. P. vivax trophozoites: show amoeboid cytoplasm, largechromatin dots, and have fine, yellowish-brown pigment.
  64. 64. Positive IFA result with P. malariae schizont antigen.
  65. 65. TRYPANOSOMA BRUCEI  Disease: African trypanosomiasis  T. b. gambiense: Gambian trypanosomiasis, West & Mid-African sleeping sickness  T. b. rhodesiense: Rhodesian trypanosomiasis, East African sleeping sickness  Lab Dx: Giemsa stained thick and thin blood smears or lymph exudate (early stage); Giemsa stained smears of CSF (late stage)
  66. 66.  Site in host: lymph glands, blood stream, brain Portal of entry: skin Source of infection: tsetse fly Winterbottom’s sign: enlargement of posterior cervical LNs
  67. 67. Trypomastigote: slender to fat and stumpy forms; inGiemsa stained films – C or U shaped forms NOT seen;small, oval kinetoplast located posterior to the nucleus; acentrally located nucleus, an undulating membrane, and ananterior flagellum. The trypanosomes length range is 14-33 µm
  68. 68. A dividing parasite is seen at the right. Dividing formsare seen in African trypanosomiasis, but not in Americantrypanosomiasis (Chagas disease)
  69. 69. Tsetse fly. The vector of African trypanosomiasis
  70. 70. Winterbottoms sign
  71. 71. TRYPANOSOMA CRUZI  Disease: American trypanosomiasis, Chaga’s disease  Lab Dx: Giemsa stained thick and thin blood smears for the trypomastigote; histopath exam for the amastigote  Site in host: Tissues – heart; blood  Portal of entry: skin  Source of infection: Kissing bug Triatomidae
  72. 72. Trypomastigote: shape is short & stubby to long &slender; in Giemsa stained blood films – C or U shaped;kinetoplast is large, oval & located posterior to thenucleus; anterior long free flagellum
  73. 73. Trypanosoma cruzi crithidia
  74. 74. Trypanosoma cruzi: Leishmanial form
  75. 75. Riduviid bug: the vector of Americantrypanosomiasis
  76. 76. Ramanas sign: unilateralconjunctivitis and orbitaledema
  77. 77. TOXOPLASMA GONDII  Disease: Toxoplasmosis  Site in host: All organs  Portal of entry:  Ingestion of oocyst contaminated water  Aerosolization of oocyst contaminated dust or litter  Consumption of raw or undercooked cyst infected meat  Transplacental passage of the tachyzoite
  78. 78. - Definitive host: domestic cats - Intermediate host: infected rodents Accidental intermediate host: humans Lab Dx: IFAT and ELISA; Giemsa-stained smears of exudates, aspirates or tissues
  79. 79. T. gondii tachyzoites: crescentic to pyriformshaped with a prominent, centrally placed nucleus.
  80. 80. Toxoplasma gondii cyst in brain tissue stained withhematoxylin and eosin (100×).
  81. 81. T. gondii oocysts in a fecal floatation (100×).
  82. 82. A: Positive reaction (tachyzoites + human antibodies toToxoplasma + FITC-labelled antihuman IgG = fluorescence.)B: Negative IFA for antibodies to T. gondii.
  83. 83. LEISHMANIA- Disease: - L. tropica complex: Old Word Cutaneous leishmaniasis (oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil) - L. mexicana complex: New Word Cutaneous leishmaniasis (chiclero ulcer, bay sore) - L. braziliensis complex: Mucocutaneus leishmaniasis (espundia, uta) - L. donovani: Visceral leishmaniasis (kala-azar or black disease, Dumdum fever)
  84. 84. - Lab Dx: Giemsa stained tissue sections or impression smears- Site in host: Monocytes/macrophages of skin & mucosa- Portal of entry: Skin- Source of infection: Phlebotomus or Lutzomiya fly
  85. 85. L. tropica amastigotes: ovoid in shape; large & eccentricnucleus; small, rodlike kinetoplast positioned oppositethe nucleus; rodlike axoneme perpendicular to thekinetoplast
  86. 86. LeishmaniasisDisease Visceral Cutaneous Mucocutaneous Babesiosis leishmaniasis leishmaniasis leishmaniasis Fatal if Papule that Disfiguring Replicates in untreated ulcerates and RBCs scarsCausative Leishmania L. Tropica L. Braziliensis Babesiaagent donovani microtiVector Sandflies Sandflies Sandflies Ixodes ticksReservoir Small Small mammals Small Rodents mammals mammalsTreatment Amphotericin Amphotericin B Amphotericin B Atovaquone + B or or miltefosine or miltefosine azithromycin miltefosineGeographic Asia, Africa, Asia, Africa, Rain forests of United Statesdistribution Southeast Mediterranean, Yucatan, South Asia Central America, America South America
  87. 87. BABESIA  Disease: Babesiosis  Lab Dx: Giemsa stained thick and thin blood smears
  88. 88. Babesiosis Figures 23.26, 12.32
  89. 89. Babesia microti infection, Giemsa stained thin smear. Theorganisms resemble P. falciparum; however Babesiaparasites present several distinguishing features: theyvary more in shape and in size; and they do not producepigment.
  90. 90. Infection with Babesia. Giemsa stained thin smearsshowing the tetrad, a dividing form pathognomonic forBabesia. Note also the variation in size and shape of thering stage parasites and the absence of pigment.
  91. 91. Schistosomiasis Figure 23.28
  92. 92. Schistosomiasis Tissue damage (granulomas) in response to eggs lodging in tissuesS. haemotobium Granulomas in urinary Africa, Middle East bladder wallS. japonicum Granulomas in intestinal East Asia wallS. mansoni Granulomas in intestinal African, Middle East, wall South American, CaribbeanSwimmer’s itch Cutaneous allergic U.S. parasite of reaction to cercariae wildfowl
  93. 93. Schistosomiasis Figure 23.27a
  94. 94. SCHISTOSOMA MANSONI- Disease: Schistosomiasis, intestinal schistosomiasis, bilharziasis “snail fever”- Site in host: veins of LI- Portal of entry: skin- Definitive host: humans, baboons & rodents- Intermediate host: snail (Biomphalaria sp & Tropicorbis sp)- Infective stage: cercariae- Lab Dx: eggs in stool; rectal or liver biopsy
  95. 95. Biomphalaria spp.
  96. 96. Schistosoma mansoni eggs: large (length 114 to 180 µm)and have a characteristic shape, with a prominent lateralspine near the posterior end. The anterior end is taperedand slightly curved. When the eggs are excreted, theycontain a mature miracidium
  97. 97. Male and female schistosomes.
  98. 98. SCHISTOSOMA HAEMATOBIUM- Disease: Urinary schistosomiasis, schistosomal hematuria, urinary bilharziasis- Site in host: veins of urinary bladder- Portal of entry: skin- Definitive host: humans, monkeys & baboons- Intermediate host: snail (Bulinus, Physopsis, and Biomphalaria sp)- Infective stage: cercariae- Lab Dx: eggs in stool; cystoscopy
  99. 99. Bulinus spp.
  100. 100. S. haematobium eggs: large and have a prominentterminal spine at the posterior end
  101. 101. S.haematobium: adult schistosomes live in pairs in the pelvic veins(especially in the venous plexus surrounding the bladder); males are10-15 mm in lenght by 0,8-1 mm in diameter, and have a ventralinfolding from the ventral sucker to the posterior end forming thegynecophoric canal. Adult male with female in the copulatory groove.
  102. 102. SCHISTOSOMA JAPONICUM- Disease: Schistosomiasis, Katayama fever- Site in host: veins of SI- Portal of entry: skin- Definitive host: humans, dogs, cats, horses, pigs, cattle, deer, caribou & rodents- Intermediate host: snail (Oncomelania)- Infective stage: cercariae- Lab Dx: eggs in stool; liver biopsy
  103. 103. Onchomelania, hupensis spp.
  104. 104. S. japonicum egg: typically oval or subspherical, andhas a vestigial spine (smaller than those of the otherspecies)
  105. 105. Cercaria
  106. 106. Schistosomiasis Figure 23.27b