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Pathology of Infectious Diseases V. Žampachová
Categories of infectious agents ,[object Object],[object Object],[object Object],[object Object],[object Object]
Categories ,[object Object],[object Object],[object Object],[object Object],[object Object]
RESIDENT FLORA ,[object Object],[object Object],[object Object],[object Object],[object Object]
Table 13.2
OPPORTUNISTIC FLORA ,[object Object],[object Object],[object Object]
TRUE PATHOGENS ,[object Object],[object Object],[object Object]
Extent of  h ost  i nvolvement ,[object Object],[object Object],[object Object]
Extent of Host Involvement ,[object Object],[object Object],[object Object]
Extent of Host Involvement ,[object Object],[object Object],[object Object],[object Object],[object Object]
Host  i nvolvement ,[object Object],[object Object],[object Object]
Host  i nvolvement ,[object Object],[object Object],[object Object],[object Object]
Host  i nvolvement ,[object Object],[object Object]
Host  i nvolvement ,[object Object],[object Object],[object Object],[object Object]
Infection
Epidemic process and epidemic factors of infectious disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Reservoirs of  i nfection ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
TRANSMISSION OF DISEASE ,[object Object],[object Object],[object Object],[object Object],[object Object]
CONTACT TRANSMISSION ,[object Object],[object Object],[object Object],[object Object],[object Object]
VECTORS ,[object Object],[object Object],[object Object]
Pathogen  c haracteristics  f avoring  e nvironmental  t ransmission ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Pathogen  c haracteristics  f avoring  e nvironmental  t ransmission ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Pathogen  c haracteristics  f avoring  e nvironmental  t ransmission ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Virulence  p roperties of  p athogenic  b acteria  f avoring  e nvironmental  t ransmission ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Bacterial pathogenicity and virulence ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
Host  f actors in  p athogen  t ransmission ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Sensitive  p opulations –  i ncreased  i nfectious  d isease  r isks ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Table 13.4
Infection and  i llness  f actors in  p athogen  o ccurrence and  t ransmission ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Characteristics of  p athogen  i nteractions with  h osts   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Outcomes of  i nfection  p rocess Hospitalization Infection Asymptomatic  i nfection Mortality Disease Advanced  i llness,  c hronic  i nfections and  s equelae Acute  s ymptomatic  i llness: s everity and  d ebilitation Exposure Sensitive  p opulations
INFECTIOUS DISEASES ,[object Object],[object Object],[object Object]
Common signs and symptoms ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
Health  o utcomes of  m icrobial  i nfection ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute and  c hronic  o utcomes  a ssociated with  m icrobial  i nfections
Portals of  e ntry ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Attachment ,[object Object],[object Object],[object Object],[object Object],[object Object]
Surviving Host Defenses
Cellular mechanisms of clinical disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
EXOTOXINS ,[object Object],[object Object],[object Object]
EXOTOXINS ,[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],EXOTOXINS
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],MEMBRANE DAMAGING TOXINS
[object Object],[object Object],[object Object],[object Object],MEMBRANE DAMAGING TOXINS
SUPERANTIGENS ,[object Object],[object Object]
SUPERANTIGENS ,[object Object],[object Object]
EXOTOXINS
EXOTOXINS
ENDOTOXINS ,[object Object],[object Object]
ENDOTOXINS ,[object Object],[object Object]
ENDOTOXINS ,[object Object],[object Object],[object Object]
ENDOTOXINS ,[object Object],[object Object]
COMPARISON OF EXOTOXINS AND ENDOTOXINS
COMPARISON OF EXOTOXINS AND ENDOTOXINS
COMPARISON OF EXOTOXINS AND ENDOTOXINS
Additional  Virulence  Factors
 
Virus and host cell reactions ,[object Object],[object Object],[object Object],[object Object],[object Object]
TRANSMISSION ,[object Object],[object Object]
Host defense mechanisms ,[object Object],[object Object],[object Object]
Nonspecific host defenses ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Nonspecific host defenses ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Nonspecific host defenses ,[object Object],[object Object],[object Object],[object Object]
 
EXTENT OF HOST INVOLVEMENT ,[object Object],[object Object],[object Object]
EXTENT OF HOST INVOLVEMENT ,[object Object],[object Object],[object Object]
DAMAGE TO THE HOST ,[object Object],[object Object]
 
Nosocomial  i nfections Figure 14.9
Nosocomial  i nfections
Common Causes of Nosocomial Infections Percentage of Total Infections Percentage Resistant to Antibiotics Coagulase-negative staphylococci 25% 89% S.  a ureus  ( MRSA) 16% 80% Enterococcus   (vancomycin-res.) 10% 29% Gram-negative rods 23% 5-32% C. difficile 13% None
Nosocomial  i nfections ,[object Object],[object Object],[object Object],[object Object]
Most important risk   p rocedure s MRSA
Staphylococcus aureus ,[object Object],[object Object],[object Object]
General  c linical  s ignificance ,[object Object],[object Object]
P redisposing factors ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
S. aureus  is a problem ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
S. aureus pneumonia ,[object Object],[object Object]
Skin  + mucous membranes infections  / wounds ,[object Object],[object Object],[object Object]
Skin  + mucous membranes infections  / wounds ,[object Object],[object Object],[object Object]
Food poisoning ,[object Object],[object Object],[object Object],[object Object]
S. aureus  – other pathology   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Emerging  i nfectious  d iseases ,[object Object],[object Object],[object Object]
Emerging  i nfectious  d iseases ,[object Object],[object Object],[object Object]
Emerging  i nfectious  d iseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Emerging  i nfectious  d iseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Emerging  i nfectious  d iseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Crossing the Species Barrier Clinical Focus, p. 371
Lower respiratory tract ,[object Object],[object Object],[object Object],[object Object]
 
FLORA of the RESPIRATORY SYSTEM
FLORA of the UPPER RESPIRATORY SYSTEM ,[object Object],[object Object]
FLORA of the LOWER RESPIRATORY SYSTEM ,[object Object]
Respiratory tract infections ,[object Object],[object Object],[object Object]
Respiratory tract infections ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Upper respiratory tract ,[object Object],[object Object]
Upper respiratory tract   ,[object Object],[object Object],[object Object]
Lower respiratory tract ,[object Object],[object Object],[object Object]
Lower respiratory tract ,[object Object],[object Object],[object Object],[object Object],[object Object]
Influenza ,[object Object],[object Object],[object Object]
Influenza   e pidemiology ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Influenza   p athogenesis ,[object Object],[object Object],[object Object],[object Object]
Influenza m anifestations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Influenza m anifestations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Influenza m anifestations ,[object Object],[object Object],[object Object],[object Object]
Perez-Padilla R et al. N Engl J Med 2009;10.1056/NEJMoa0904252 Initial Radiograph of the Lung and Lung-Tissue Sample from Patient 3
Influenza m anifestations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Influenza c omplications ,[object Object],[object Object],[object Object]
Influenza c omplications ,[object Object],[object Object],[object Object],[object Object],[object Object]
Differential diagnosis ,[object Object],[object Object],[object Object]
Avian influenza ,[object Object],[object Object],[object Object],[object Object]
 
 
Laboratory findings The 1st day after the admission The 2nd day after the admission
The 4th day after the admission
GIT infections
GIT infections ,[object Object],[object Object],[object Object],[object Object]
FLORA of the ORAL CAVITY ,[object Object],[object Object],[object Object]
Oral cavity and oesophagus infections ,[object Object],[object Object],[object Object]
Infectious Mononucleosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Stomach infections ,[object Object],[object Object],[object Object]
FLORA of the LARGE INTESTINES ,[object Object],[object Object],[object Object],[object Object]
Intestinal infections ,[object Object],[object Object],[object Object]
Infectious diarrhea ,[object Object],[object Object],[object Object]
Types of diarrhea ,[object Object],[object Object],[object Object],[object Object]
Entamoeba histolytica  pathology 1. COLONIZATION OF THE LARGE INTESTINE primary ulcer:   Mucosa submucosa
Entamoeba histolytica  trophozoites
Entamoeba histolytica  mature   cysts quadrinucleate or mature cysts – diagnostic in feces
Entamoeba histolytica  pathology 3.  EXTRA-INTESTINAL LESIONS occur in 3 ECTOPIC SITES A.  HEPATIC AMEBIASIS  Trophozoites in submucosa are carried by hepatic portal vein to the liver  -> abscess   B.  PULMONARY AMEBIASIS  following l iver abscess rupture  C.  CEREBRAL AMEBIASIS  Trophozoites in bloodstream   
2 Groups of Parasitic Amebae ____________________parasites  – can only exist as parasites - amebae in the family Entamoebidae - occur in the digestive tracts of vertebrates ____________________parasites –  free-living soil and water amebae that can become parasitic if they enter vertebrate tissues
Entamoeba histolytica  pathology 1. COLONIZATION OF THE LARGE INTESTINE flask-shaped lesions: proteolytic enzymes : Symptoms: Ulcers may form sinuses and extend into the submucosa  
Liver abscess Diagram of pathology from text on page 112 Shows movement of trophozoites from large intestine to lungs via hepatic portal vein
Pathology of  Ascaris lumbricoides Roundworm, 1 billion patients infected worldwide, larval migration into systemic circulation -> hepatic abscess, eosinophilic pneumonitis. Adults in large numbers  -> intestinal obstruction
Pathology of  Ascaris lumbricoides Larvae  cause  problems in the lungs  when they break through the lung capillaries to enter the respiratory tree. S mall hemorrhages ,   inflammatory response ->   pneumonia-like symptoms  The more eggs ingested, the more migrating larvae, the greater the pathology.   larva Inflammatory cells
Pathology of Visceral Larva Migrans ,[object Object],[object Object],[object Object],[object Object],[object Object],Scar tissue in retina L 3  in retina
Pathology of  Enterobius vermicularis   Pinworms do not invade any tissue , live intraluminally. Nightly egg deposition on the perirectal mucosa ->  irritation of the anal region , itching, possible s econdary bacterial infection in scratched .
Pathology of  Enterobius vermicularis ,[object Object],[object Object],[object Object]
Trematodes of medical importance ,[object Object],[object Object],[object Object],[object Object]
Schistosomiasis ,[object Object],[object Object],[object Object]
Human liver fluke disease ,[object Object],[object Object],[object Object]
Human liver fluke disease ,[object Object],[object Object],[object Object]
Human lung fluke disease ,[object Object],[object Object],[object Object],[object Object]
Infectious hepatitis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Viral hepatitis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Urogenital tract infections
 
FLORA of the URINARY SYSTEM ,[object Object],[object Object],[object Object]
FLORA of the REPRODUCTIVE SYSTEM ,[object Object],[object Object],[object Object]
Urogenital tract infections ,[object Object],[object Object],[object Object]
Urogenital tract infections ,[object Object],[object Object],[object Object],[object Object]
Sexually Transmitted Infections ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
STD ,[object Object],[object Object],[object Object],[object Object],[object Object]
Chlamydia: Manifestations ,[object Object],[object Object],[object Object]
Chlamydia: Complications ,[object Object],[object Object],[object Object],[object Object]
Genital Herpes: Pathophysiology ,[object Object],[object Object],[object Object],[object Object],[object Object]
Genital Herpes: Pathophysiology ,[object Object],[object Object]
Genital Herpes: Pathophysiology ,[object Object],[object Object],[object Object]
Genital Warts ,[object Object],[object Object],[object Object],[object Object]
Genital Warts ,[object Object],[object Object],[object Object],[object Object],[object Object]
Genital Warts: Complications ,[object Object],[object Object],[object Object],[object Object]
Gonorrhea ,[object Object],[object Object],[object Object],[object Object]
Gonorrhea ,[object Object],[object Object],[object Object],[object Object],[object Object]
Syphilis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Syphilis:  P rimary   s tage ,[object Object],[object Object],[object Object],[object Object]
Syphilis:  Secondary  s tage ,[object Object],[object Object],[object Object],[object Object],[object Object]
Syphilis: Latency  p eriod ,[object Object],[object Object],[object Object],[object Object]
Syphilis:  Tertiary  s tage ,[object Object],[object Object],[object Object]
 
FLORA of the SKIN ,[object Object],[object Object],[object Object],[object Object],[object Object]
FLORA of the SKIN ,[object Object],[object Object],[object Object],[object Object],[object Object]
Skin infections ,[object Object],[object Object],[object Object],[object Object],[object Object]
Human Anthrax Infections ,[object Object],[object Object],[object Object]
Common  c hildhood  v iral  i nfections ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Measles ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Measles ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Rubella ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Rubella ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Rubella
Erythema infectiosum ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Erythema infectiosum ,[object Object],[object Object],[object Object],[object Object],[object Object]
Fifth Disease
Fifth disease
Mumps ,[object Object],[object Object],[object Object],[object Object]
Mumps ,[object Object],[object Object],[object Object],[object Object],[object Object]
Chickenpox Varicella-zoster virus ,[object Object],[object Object],[object Object],[object Object],[object Object]
Chickenpox (varicella) ,[object Object],[object Object],[object Object],[object Object],[object Object]
Complications of chickenpox ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Shingles (varicella zoster) ,[object Object],[object Object],[object Object],[object Object]
Coxsackieviruses and Echoviruses ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Coxsackieviruses and Echoviruses ,[object Object],[object Object],[object Object]
 
CNS infections ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
CNS infections ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Transmission of infection to  C NS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Bacterial infections ,[object Object],[object Object]
Meningitis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Pachymeningitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Meningitis (i.e. leptomeningitis) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Meningitis ,[object Object],[object Object],[object Object],[object Object]
Pathology of bacterial meningitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Meningococcal meningitis ,[object Object],[object Object],[object Object],[object Object]
Suppurative meningitis
Cerebral abscess ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Cerebral abscess ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Cerebral abscess
Cerebral Abscess
C NS tuberculosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
C NS syphilis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral infections of  C NS ,[object Object],[object Object],[object Object],[object Object]
Effects of viral infections ,[object Object],[object Object],[object Object],[object Object],[object Object]
Viral meningitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral meningitis ,[object Object],[object Object]
Viral encephalitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral encephalitis ,[object Object],[object Object],[object Object],[object Object]
Herpes Simplex Encephalitis
Herpes simplex encephalitis
Perivascular cuffing in viral encephalitis
West Nile Encephalitis Virus - Epidemiology ,[object Object],[object Object],[object Object],[object Object]
West Nile Virus Transmission ,[object Object],[object Object],[object Object]
Clinical Features of WNV Infection ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],Clinical Features of WNV Infection West Nile virus found in brain and spinal cord  on autopsy
West Nile Virus - Differential Diagnosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Fetal  C NS infections ,[object Object],[object Object],[object Object],[object Object],[object Object]
Congenital and childhood viral disease ,[object Object],[object Object],[object Object],[object Object]
Parasitic inf. -  Naegleria fowleri After entering the nose and nasal cavities, the trophozoites  actively  migrate  to  the brain and cause  purulent meningoencephalitis - abscess. Symptoms :  headache, fever, neck rigidity, and mental confusion followed by coma and death
Facultative Amebae Facultative amebae are normal inhabitants of soil and water where they feed on bacteria.  A few members have the ability to become parasitic   when an opportunity to enter a vertebrate exists. Three are able to infect humans: Naegleria fowleri This ameba is responsible for over 200 cases of _____________________________________________________ During 1989-2000, CDC documented 24 fatal cases of PAM in the United States.  Only 7 cases were successfully treated; all others were fatal!
Naegleria fowleri ,[object Object],[object Object],[object Object]
 
Parasitic infections - toxoplasmosis ,[object Object],[object Object],[object Object],[object Object]
Cerebral toxoplasmosis
Parasitic infections - neurocystocercosis ,[object Object],[object Object],[object Object],[object Object]
Cerebral malaria ,[object Object],[object Object],[object Object],[object Object],[object Object]
Cerebral malaria – parasites in vessels
Other parasitic infections ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Fungal infections of NS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Prion disease ,[object Object],[object Object]
CJD (Creuzfeldt-Jakob disease)  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Prion plaques in variant CJD
Variant CJD ,[object Object],[object Object],[object Object]
BACTERIA of the EYE ,[object Object],[object Object],[object Object]
Complications ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Differential diagnosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Malaria ,[object Object],[object Object],[object Object],[object Object],[object Object]
Malaria’s Range (cross hatching) Science : Volume 289,  Number 5485 (2000),  p. 1763
General Malaria Pathology …more later. ,[object Object],[object Object],[object Object],[object Object]
Tertian Malaria ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malaria ,[object Object],[object Object],[object Object],[object Object],[object Object]
P. falciparum  - malignant tertian malaria ,[object Object],[object Object],[object Object],“ knobs” Knobs promote cell clumping… clogging veins and arteries.
Ascarid Nematodes – Chapter 26 Ascaris lumbricoides Common parasite of humans.  Disease is called ______________________________ Cosmopolitan in distribution.   - flourishes in warm, moist climates where the eggs may remain viable in warm soil for many years.   - use of ___________________________ to fertilize vegetables is common source of infection.   - Children are most likely to become infected by ingesting eggs by eating dirt or placing soiled fingers or toys into the mouth.
FUNGI ,[object Object],[object Object],[object Object],[object Object]
MYCOSES ,[object Object],[object Object],[object Object]
MYCOSES ,[object Object],[object Object]
MYCOSES ,[object Object],[object Object],[object Object],[object Object]
MYCOSES ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Candida albicans  and other  Candida  species ,[object Object],[object Object]
MAIN DEFENSE MECHANISMS AGAINST CANDIDA I. ,[object Object],[object Object]
MAIN DEFENSE MECHANISMS AGAINST CANDIDA II. ,[object Object],[object Object],[object Object]
THE MOST IMPORTANT RISK FACTORS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
THE MOST IMPORTANT RISK FACTORS 7. Indwelling catethers 8. Major surgery 9. Organ transplantation 10. Neonates 11. Severity of any illness 12. Intravenous drug addicts
CLINICAL FORMS OF CANDIDIASIS ,[object Object],[object Object]
INVASIVE CANDIDIASIS ,[object Object],[object Object]
INVASIVE CANDIDIASIS ,[object Object],[object Object]
Pneumocystis carinii ,[object Object]
Pneumocystis carinii ,[object Object],[object Object],[object Object]
Cryptococcus neoformans ,[object Object],[object Object]
Aspergillus  species ,[object Object]
The most frequent syndromes are: - aspergilloma -  invasive aspergillosis   (high mortality rate) Treatment : amphotericin B,  itraconazole, flucytosine  and surgery Prevention : avoid exposure  to conidia  (new buildings in the hospital!)
ZYGOMYCETES ,[object Object],[object Object],[object Object]
Major clinical syndrome is: Rhinocerebral mucormycosis  (infection of nasal passages, sinuses, eyes, cranial bones  and brain) Treatment : surgery and amphotericin B Prognosis : very poor
OPPORTUNISTIC FUNGAL INFECTIONS ARE: ,[object Object],[object Object],[object Object],[object Object],[object Object]
Upper respiratory tract  ,[object Object],[object Object],[object Object]

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Infectious diseases20

  • 1. Pathology of Infectious Diseases V. Žampachová
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  • 32. Outcomes of i nfection p rocess Hospitalization Infection Asymptomatic i nfection Mortality Disease Advanced i llness, c hronic i nfections and s equelae Acute s ymptomatic i llness: s everity and d ebilitation Exposure Sensitive p opulations
  • 33.
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  • 35.  
  • 36.
  • 37. Acute and c hronic o utcomes a ssociated with m icrobial i nfections
  • 38.
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  • 55. COMPARISON OF EXOTOXINS AND ENDOTOXINS
  • 56. COMPARISON OF EXOTOXINS AND ENDOTOXINS
  • 57. COMPARISON OF EXOTOXINS AND ENDOTOXINS
  • 59.  
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  • 70.  
  • 71. Nosocomial i nfections Figure 14.9
  • 72. Nosocomial i nfections
  • 73. Common Causes of Nosocomial Infections Percentage of Total Infections Percentage Resistant to Antibiotics Coagulase-negative staphylococci 25% 89% S. a ureus ( MRSA) 16% 80% Enterococcus (vancomycin-res.) 10% 29% Gram-negative rods 23% 5-32% C. difficile 13% None
  • 74.
  • 75. Most important risk p rocedure s MRSA
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  • 91. Crossing the Species Barrier Clinical Focus, p. 371
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  • 94. FLORA of the RESPIRATORY SYSTEM
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  • 109. Perez-Padilla R et al. N Engl J Med 2009;10.1056/NEJMoa0904252 Initial Radiograph of the Lung and Lung-Tissue Sample from Patient 3
  • 110.
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  • 117. Laboratory findings The 1st day after the admission The 2nd day after the admission
  • 118. The 4th day after the admission
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  • 132. Entamoeba histolytica pathology 1. COLONIZATION OF THE LARGE INTESTINE primary ulcer:   Mucosa submucosa
  • 133. Entamoeba histolytica trophozoites
  • 134. Entamoeba histolytica mature cysts quadrinucleate or mature cysts – diagnostic in feces
  • 135. Entamoeba histolytica pathology 3. EXTRA-INTESTINAL LESIONS occur in 3 ECTOPIC SITES A. HEPATIC AMEBIASIS Trophozoites in submucosa are carried by hepatic portal vein to the liver -> abscess B. PULMONARY AMEBIASIS following l iver abscess rupture C. CEREBRAL AMEBIASIS Trophozoites in bloodstream  
  • 136. 2 Groups of Parasitic Amebae ____________________parasites – can only exist as parasites - amebae in the family Entamoebidae - occur in the digestive tracts of vertebrates ____________________parasites – free-living soil and water amebae that can become parasitic if they enter vertebrate tissues
  • 137. Entamoeba histolytica pathology 1. COLONIZATION OF THE LARGE INTESTINE flask-shaped lesions: proteolytic enzymes : Symptoms: Ulcers may form sinuses and extend into the submucosa  
  • 138. Liver abscess Diagram of pathology from text on page 112 Shows movement of trophozoites from large intestine to lungs via hepatic portal vein
  • 139. Pathology of Ascaris lumbricoides Roundworm, 1 billion patients infected worldwide, larval migration into systemic circulation -> hepatic abscess, eosinophilic pneumonitis. Adults in large numbers -> intestinal obstruction
  • 140. Pathology of Ascaris lumbricoides Larvae cause problems in the lungs when they break through the lung capillaries to enter the respiratory tree. S mall hemorrhages , inflammatory response -> pneumonia-like symptoms The more eggs ingested, the more migrating larvae, the greater the pathology.   larva Inflammatory cells
  • 141.
  • 142. Pathology of Enterobius vermicularis Pinworms do not invade any tissue , live intraluminally. Nightly egg deposition on the perirectal mucosa -> irritation of the anal region , itching, possible s econdary bacterial infection in scratched .
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  • 223. Perivascular cuffing in viral encephalitis
  • 224.
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  • 230.
  • 231. Parasitic inf. - Naegleria fowleri After entering the nose and nasal cavities, the trophozoites actively migrate to the brain and cause purulent meningoencephalitis - abscess. Symptoms : headache, fever, neck rigidity, and mental confusion followed by coma and death
  • 232. Facultative Amebae Facultative amebae are normal inhabitants of soil and water where they feed on bacteria. A few members have the ability to become parasitic when an opportunity to enter a vertebrate exists. Three are able to infect humans: Naegleria fowleri This ameba is responsible for over 200 cases of _____________________________________________________ During 1989-2000, CDC documented 24 fatal cases of PAM in the United States. Only 7 cases were successfully treated; all others were fatal!
  • 233.
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  • 239. Cerebral malaria – parasites in vessels
  • 240.
  • 241.
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  • 244. Prion plaques in variant CJD
  • 245.
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  • 249.  
  • 250.
  • 251. Malaria’s Range (cross hatching) Science : Volume 289, Number 5485 (2000), p. 1763
  • 252.
  • 253.
  • 254.
  • 255.
  • 256. Ascarid Nematodes – Chapter 26 Ascaris lumbricoides Common parasite of humans. Disease is called ______________________________ Cosmopolitan in distribution.   - flourishes in warm, moist climates where the eggs may remain viable in warm soil for many years.   - use of ___________________________ to fertilize vegetables is common source of infection.   - Children are most likely to become infected by ingesting eggs by eating dirt or placing soiled fingers or toys into the mouth.
  • 257.
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  • 266. THE MOST IMPORTANT RISK FACTORS 7. Indwelling catethers 8. Major surgery 9. Organ transplantation 10. Neonates 11. Severity of any illness 12. Intravenous drug addicts
  • 267.
  • 268.
  • 269.
  • 270.
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  • 272.
  • 273.
  • 274. The most frequent syndromes are: - aspergilloma - invasive aspergillosis (high mortality rate) Treatment : amphotericin B, itraconazole, flucytosine and surgery Prevention : avoid exposure to conidia (new buildings in the hospital!)
  • 275.
  • 276. Major clinical syndrome is: Rhinocerebral mucormycosis (infection of nasal passages, sinuses, eyes, cranial bones and brain) Treatment : surgery and amphotericin B Prognosis : very poor
  • 277.
  • 278.

Editor's Notes

  1. Figure 3. Initial Radiograph of the Lung and Lung-Tissue Sample from Patient 3. The radiograph (Panel A) shows bilateral alveolar opacities in the base of both lungs that progressed and became confluent. The specimen (Panel B, hematoxylin and eosin) shows necrosis of bronchiolar walls (top arrow), a neutrophilic infiltrate (middle arrow), and diffuse alveolar damage with prominent hyaline membranes (bottom arrow). Bacterial cultures were negative on admission, and no evidence of bacterial infection of the lungs was found. The patient ultimately died.
  2. Yeasts are unicellular organisms, reproducing by budding and division; molds are multicellular organisms growing in filaments called hyphae, forming mycelium and reproducing by conidia and spores. Both yeasts and molds have sexual and asexual reproduction. Rare fungi have other forms (cysts, spherulas). Fungi have a rigid cell wall with mannans, glucans and chitin in it, and with ergosterol in the cell membrane.
  3. 1. Affects stratum corneum only; Malassezia furfur rarely causes opportunistic fungemia 2. Affects superficial keratinized tissue only (about 40 related fungi) 3. Fungi from soil or vegetation, reach subcutaneous tissue by traumatic inoculation; rarely cause systemic disease.
  4. 4. Fungi geographically restricted to specific endemic areas. They are primary pathogens (true pathogenic fungi), living in soil mixed with guano ( H. capsulatum, C. immitis ), or not clearly defined soil ( B. dermatitidis , P. brasiliensis ). They cause pneumonia and systemic disease in a previously healthy persons.
  5. “ Endogenous” means that the fungus is a part of a normal human flora. “Exogenous”(see next slide) means that the fungus does not normaly live in/on human body, although it can transiently contaminate human body surfaces (especially respiratory tract). P.carinii is most probably a part of normal flora of lungs of many mammals, including humans.
  6. Some of many other opportunistic fungi are: Penicillium marneffei , Fusarium, Bipolaris, Exophiala, Scedosporium, Sporothrix, Pseudallescheria. True pathogenic (endemic) fungi cause more severe infections in compromised host than in otherwise healthy people. If a patient, undergoing therapy which will compromise him/her, was exposed, he/she has to take fluconazole for the reactivation prevention.
  7. As Candida is present in practically all humans, it has many opportunities to cause endogenous infections in compromised host - so, Candida infections are the most frequent opportunistic fungal infections. Other Candida species are: C.tropicalis, C.krusei, C.parapsilosis, C.glabrata, C.gullermondii, C.lusitaniae, C.kefyr and many more.
  8. If normal bacterial flora is disturbed by antimicrobial therapy, then Candida overgrowths on mucosal surfaces, and with its pseudohyphae internalizes (translocates) itself to deeper layers and causes mucosal infections. The same happens if skin and mucous membranes integrity is broken.
  9. Neutrophil leukocytes are probably responsible for resistance to invasive candidiasis, and CD4 T-cells are responsible for resistance to mucocutaneous candidiasis. If neutrophil number or function is disturbed, after translocation, Candida goes to lymphatic and blood, spreading throughout the body and causing infection in virtually all organs.
  10. 1. The most profound neutropenia (less than 100 neutrophils/L) is seen in bone marrow and hematopoietic stem cells transplant patients, but occurs also in patients with malignancies treated with intensive chemotherapy. 2. In diabetic patients, fusion of lysosome in phagocytes is greatly impaired. 3.,4. CD4 T-cells defects are important risk factors.
  11. Oral trush, oezophagitis (AIDS patients, diabetic patients, patients on corticosteroid therapy, T-cell deficiency); vulvovaginal infection (diabetes, pregnancy, antibiotic therapy); cutaneous candidiasis (skin trauma, burns, maceration); onychomycosis; mucocutaneous candidiasis in SCID patients
  12. Most cases of candidemia in surgical patients end this way. C.albicans is found in over 75% in blood culture of non-neutropenic and non-cancer patients, while other species are found in more than 50% of neutropenic and cancer patients.
  13. The most frequent organs involved are kidney, skin (maculonodular lesions), eye, heart, liver, meninges. Prevention of candida infections in severely immunocompromised patient can be done by use of peroral fluconazole (azole antifungal drug) during deepest immunosupression
  14. P.carinii is present worldwide and seroepidemiological studies show that most humans are infected in early childhood. Natural reservoir, the source and mode of transmission are not known, possibly P.carinii spreads by aerosols.
  15. Main risk factors are AIDS, transplantation, corticosteroid and antineoplastic therapy. About 20% of AIDS patients will develop P.carinii pneumonia despite prophylaxis, if CD4 count is >100 mm 3 . Diagnosis is made from bronchoalveolar fluid, induced sputum or lung biopsy - smears are stained with special stains, and the presence of cysts and trophozoits is diagnostic. P.carinii has not yet been isolated.
  16. Cryptococci are found in large numbers in dry pigeon feces. In macrophages Cryptococci can survive and grow easily.
  17. Most frequent species causing infections in compromised patients are: A.fumigatus, A.flavus, A.niger, A.terreus , A.nidulans and many other species. Especially abundant are aspergilli conidia when buildings are done and various dusts are spread around.
  18. Aspergilloma is formed when conidia are inhaled in a preexisting lung cavity (tuberculosis, emphysema); if there is not a cavity, aspergilli develop in lung tissue causing invasive infection (spreading through the tissue and involving blood vessels); then spread can occur to other organs. Diagnosis of aspergilloma is radiological (CT scan); invasive aspergillosis can be diagnosed from respiratory secretions or lung biopsy; test for circulating galactomannan is also diagnostic
  19. Most frequent genera in the class Zygomycetes, causing disease in compromised host, are: rhisopus, rhizomucor, absidia, mucor, cunningamella.
  20. Pulmonary infection can also occur, with very high mortality rate. Diagnosis is made by direct smear and by isolation of molds from respiratory secretions or biopsy specimens.