SlideShare a Scribd company logo

New Chapter 3 Medical Microbiology (1) 2.pdf

R
RaNI SaBrA

Medical microbiology Chapter 3

1 of 130
Download to read offline
Medical
Dr. Khalil Abujheisha
PhD, Medical Microbiology
1
Chapter 3
Medically important Bacteria
Chapter 3
Medically important Bacteria
”
Gram Negative
“
2
Pathogenic Neisseriae
• Neisseriae: Gram-negative cocci.
• Neisseriae contain endotoxin in their outer
membrane.
** Note that the endotoxin of Neisseriae consist
of lipooligosaccharide (LOS), in contrast to the
lipopolysaccharide (LPS) found in enteric gram-
negative rods.
• N. gonorrhoeae infections (Gonorrhea) have
High prevalence and Low mortality.
• N. meningitidis infections (Meningitis) have Low
prevalence and High mortality.
3
• The growth of both bacteria is inhibited by
toxic trace metals and fatty acids found in
certain culture media (blood agar).
• They are cultured on “chocolate” agar
containing blood heated to 80°C, which
inactivates the inhibitors.
• Neisseriae are oxidase-positive (they possess
the enzyme cytochrome C ).
• It is the terminal enzyme of the respiratory chains,
catalyzes electron transfer from cytochrome c to
molecular oxygen, reducing the latter to water.
• Note: All bacteria that are oxidase positive are aerobic
and can use oxygen as a terminal electron acceptor in
respiration.
4
N. Gonorrhoeae
• First described by A. Neisser in 1879.
• Gram-negative cocci in pairs with adjacent
flattened sides.
5
• Gonococcus.
• Never Normal flora.
• Fragile organism: susceptible to temperature
changes, drying, UV light, and other conditions.
• Fastidious: media containing hemoglobin.
• Cultures:35-36C + 3-10% CO2.
• No growth less than 25 or more than 38.5.
Virulence Factors
• Has no capsule but has multiple serotypes based
on the antigenicity of its pilus protein.
• Attachment by pili.
• Nonpiliated strains are avirulent.
6

More Related Content

Similar to New Chapter 3 Medical Microbiology (1) 2.pdf

Similar to New Chapter 3 Medical Microbiology (1) 2.pdf (20)

meningitis.pdf
meningitis.pdfmeningitis.pdf
meningitis.pdf
 
Central nervous system infections
Central nervous system infectionsCentral nervous system infections
Central nervous system infections
 
Neisseriaceae.pptx
Neisseriaceae.pptxNeisseriaceae.pptx
Neisseriaceae.pptx
 
Infection_of_Central_Nervous_System.ppt
Infection_of_Central_Nervous_System.pptInfection_of_Central_Nervous_System.ppt
Infection_of_Central_Nervous_System.ppt
 
Pyogenic cocci.pptx
Pyogenic cocci.pptxPyogenic cocci.pptx
Pyogenic cocci.pptx
 
4th sem BMLS CNS - Copy.pptx
4th sem BMLS CNS - Copy.pptx4th sem BMLS CNS - Copy.pptx
4th sem BMLS CNS - Copy.pptx
 
Meningitis ppt
Meningitis pptMeningitis ppt
Meningitis ppt
 
Gram Negative Cocci.pptx
Gram Negative Cocci.pptxGram Negative Cocci.pptx
Gram Negative Cocci.pptx
 
Streptococcus pneumoniae 2013.pptx
Streptococcus pneumoniae 2013.pptxStreptococcus pneumoniae 2013.pptx
Streptococcus pneumoniae 2013.pptx
 
meningitis.pdf
meningitis.pdfmeningitis.pdf
meningitis.pdf
 
Lec 3. viral infection
Lec 3. viral infectionLec 3. viral infection
Lec 3. viral infection
 
Bacterial meningitis
Bacterial meningitisBacterial meningitis
Bacterial meningitis
 
Bacterial meningitits
Bacterial meningititsBacterial meningitits
Bacterial meningitits
 
Gram negative cocci - Batch 03.ppt
Gram negative cocci - Batch 03.pptGram negative cocci - Batch 03.ppt
Gram negative cocci - Batch 03.ppt
 
COMP. MENINGITIS.ppt
COMP. MENINGITIS.pptCOMP. MENINGITIS.ppt
COMP. MENINGITIS.ppt
 
Neisseria ppt mahadi
Neisseria ppt mahadiNeisseria ppt mahadi
Neisseria ppt mahadi
 
Neisseria ppt mahadi
Neisseria ppt mahadiNeisseria ppt mahadi
Neisseria ppt mahadi
 
Gram-Negative cocci. Neisseria. Gonococcal & Meningococcal infections
Gram-Negative cocci. Neisseria. Gonococcal & Meningococcal infectionsGram-Negative cocci. Neisseria. Gonococcal & Meningococcal infections
Gram-Negative cocci. Neisseria. Gonococcal & Meningococcal infections
 
06 infectious disease gram negative
06 infectious disease gram negative06 infectious disease gram negative
06 infectious disease gram negative
 
Neisseria and Shigella
Neisseria and ShigellaNeisseria and Shigella
Neisseria and Shigella
 

Recently uploaded

1. GP Chi trên hay lạ khó cần xem nhiều.pdf
1. GP Chi trên hay lạ khó cần xem nhiều.pdf1. GP Chi trên hay lạ khó cần xem nhiều.pdf
1. GP Chi trên hay lạ khó cần xem nhiều.pdfHongBiThi1
 
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptx
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptxArtificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptx
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptxDr. Dheeraj Kumar
 
Seminario Biología Molecular - Susana Cano V.pdf
Seminario Biología Molecular - Susana Cano V.pdfSeminario Biología Molecular - Susana Cano V.pdf
Seminario Biología Molecular - Susana Cano V.pdfsusiedapp
 
Autism and Savant Syndrome|Study|The Good doctor .pptx
Autism and Savant Syndrome|Study|The Good doctor .pptxAutism and Savant Syndrome|Study|The Good doctor .pptx
Autism and Savant Syndrome|Study|The Good doctor .pptxScripted Symptoms
 
Population of India and Family welfare programme.pptx
Population of India and Family welfare programme.pptxPopulation of India and Family welfare programme.pptx
Population of India and Family welfare programme.pptxDr. Dheeraj Kumar
 
Poliomyelitis.pptx Department of Physiotherapy, SHUATS, Prayagraj
Poliomyelitis.pptx Department of Physiotherapy, SHUATS, PrayagrajPoliomyelitis.pptx Department of Physiotherapy, SHUATS, Prayagraj
Poliomyelitis.pptx Department of Physiotherapy, SHUATS, PrayagrajSurabhi Srivastava
 
Namburi phased spot test - NPST To identify bhasma and sindhura - A Qualitat...
Namburi phased spot test - NPST  To identify bhasma and sindhura - A Qualitat...Namburi phased spot test - NPST  To identify bhasma and sindhura - A Qualitat...
Namburi phased spot test - NPST To identify bhasma and sindhura - A Qualitat...Dr. Madduru Muni Haritha
 
Macquarie Neurosurgery Journal Club 2022 PPT
Macquarie Neurosurgery Journal Club 2022 PPTMacquarie Neurosurgery Journal Club 2022 PPT
Macquarie Neurosurgery Journal Club 2022 PPTMQ_Library
 
Staphylococcus.ppt.........ali.rasool.badr
Staphylococcus.ppt.........ali.rasool.badrStaphylococcus.ppt.........ali.rasool.badr
Staphylococcus.ppt.........ali.rasool.badrssuser06f49d
 
Influenza.pptx Department of Physiotherapy, SHUATS, Prayagraj
Influenza.pptx Department of Physiotherapy, SHUATS, PrayagrajInfluenza.pptx Department of Physiotherapy, SHUATS, Prayagraj
Influenza.pptx Department of Physiotherapy, SHUATS, PrayagrajSurabhi Srivastava
 
Seminario biología molecular Kevin Duque
Seminario biología molecular Kevin DuqueSeminario biología molecular Kevin Duque
Seminario biología molecular Kevin Duquekevinestebanduque
 
USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.
USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.
USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.vrchk912
 
Typhoid.pptx Department of Physiotherapy, SHUATS, Prayagraj
Typhoid.pptx Department of Physiotherapy, SHUATS, PrayagrajTyphoid.pptx Department of Physiotherapy, SHUATS, Prayagraj
Typhoid.pptx Department of Physiotherapy, SHUATS, PrayagrajSurabhi Srivastava
 
Seminario Biología Molecular Manuela Álvarez Ramírez
Seminario Biología Molecular Manuela Álvarez RamírezSeminario Biología Molecular Manuela Álvarez Ramírez
Seminario Biología Molecular Manuela Álvarez Ramírezmanuelaalvarezr
 
Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...
Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...
Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...Abhinav S
 
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...Golden Helix
 
(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj
(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj
(DENGUE).pptx Department of Physiotherapy, SHUATS, PrayagrajSurabhi Srivastava
 
SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...
SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...
SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...Dr. Madduru Muni Haritha
 
Bioavailability & Bioequivalence Studies- Definitions, Methods of Measureme...
Bioavailability & Bioequivalence  Studies- Definitions, Methods  of Measureme...Bioavailability & Bioequivalence  Studies- Definitions, Methods  of Measureme...
Bioavailability & Bioequivalence Studies- Definitions, Methods of Measureme...Rajshri
 
Introducing amazing Healthy habits and fitness
Introducing amazing Healthy habits and fitnessIntroducing amazing Healthy habits and fitness
Introducing amazing Healthy habits and fitnessFredrick Amos
 

Recently uploaded (20)

1. GP Chi trên hay lạ khó cần xem nhiều.pdf
1. GP Chi trên hay lạ khó cần xem nhiều.pdf1. GP Chi trên hay lạ khó cần xem nhiều.pdf
1. GP Chi trên hay lạ khó cần xem nhiều.pdf
 
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptx
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptxArtificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptx
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptx
 
Seminario Biología Molecular - Susana Cano V.pdf
Seminario Biología Molecular - Susana Cano V.pdfSeminario Biología Molecular - Susana Cano V.pdf
Seminario Biología Molecular - Susana Cano V.pdf
 
Autism and Savant Syndrome|Study|The Good doctor .pptx
Autism and Savant Syndrome|Study|The Good doctor .pptxAutism and Savant Syndrome|Study|The Good doctor .pptx
Autism and Savant Syndrome|Study|The Good doctor .pptx
 
Population of India and Family welfare programme.pptx
Population of India and Family welfare programme.pptxPopulation of India and Family welfare programme.pptx
Population of India and Family welfare programme.pptx
 
Poliomyelitis.pptx Department of Physiotherapy, SHUATS, Prayagraj
Poliomyelitis.pptx Department of Physiotherapy, SHUATS, PrayagrajPoliomyelitis.pptx Department of Physiotherapy, SHUATS, Prayagraj
Poliomyelitis.pptx Department of Physiotherapy, SHUATS, Prayagraj
 
Namburi phased spot test - NPST To identify bhasma and sindhura - A Qualitat...
Namburi phased spot test - NPST  To identify bhasma and sindhura - A Qualitat...Namburi phased spot test - NPST  To identify bhasma and sindhura - A Qualitat...
Namburi phased spot test - NPST To identify bhasma and sindhura - A Qualitat...
 
Macquarie Neurosurgery Journal Club 2022 PPT
Macquarie Neurosurgery Journal Club 2022 PPTMacquarie Neurosurgery Journal Club 2022 PPT
Macquarie Neurosurgery Journal Club 2022 PPT
 
Staphylococcus.ppt.........ali.rasool.badr
Staphylococcus.ppt.........ali.rasool.badrStaphylococcus.ppt.........ali.rasool.badr
Staphylococcus.ppt.........ali.rasool.badr
 
Influenza.pptx Department of Physiotherapy, SHUATS, Prayagraj
Influenza.pptx Department of Physiotherapy, SHUATS, PrayagrajInfluenza.pptx Department of Physiotherapy, SHUATS, Prayagraj
Influenza.pptx Department of Physiotherapy, SHUATS, Prayagraj
 
Seminario biología molecular Kevin Duque
Seminario biología molecular Kevin DuqueSeminario biología molecular Kevin Duque
Seminario biología molecular Kevin Duque
 
USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.
USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.
USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS.
 
Typhoid.pptx Department of Physiotherapy, SHUATS, Prayagraj
Typhoid.pptx Department of Physiotherapy, SHUATS, PrayagrajTyphoid.pptx Department of Physiotherapy, SHUATS, Prayagraj
Typhoid.pptx Department of Physiotherapy, SHUATS, Prayagraj
 
Seminario Biología Molecular Manuela Álvarez Ramírez
Seminario Biología Molecular Manuela Álvarez RamírezSeminario Biología Molecular Manuela Álvarez Ramírez
Seminario Biología Molecular Manuela Álvarez Ramírez
 
Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...
Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...
Circulatory shock Cardiogenic Shock Hypovolemic Shock Sepsis, Septic Shock an...
 
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D...
 
(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj
(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj
(DENGUE).pptx Department of Physiotherapy, SHUATS, Prayagraj
 
SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...
SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...
SCIENTIFIC APPROACH OF DIET IN MASANUMASIKA GARBINI PARICHARYA – FOR A HEALTH...
 
Bioavailability & Bioequivalence Studies- Definitions, Methods of Measureme...
Bioavailability & Bioequivalence  Studies- Definitions, Methods  of Measureme...Bioavailability & Bioequivalence  Studies- Definitions, Methods  of Measureme...
Bioavailability & Bioequivalence Studies- Definitions, Methods of Measureme...
 
Introducing amazing Healthy habits and fitness
Introducing amazing Healthy habits and fitnessIntroducing amazing Healthy habits and fitness
Introducing amazing Healthy habits and fitness
 

New Chapter 3 Medical Microbiology (1) 2.pdf

  • 1. Medical Dr. Khalil Abujheisha PhD, Medical Microbiology 1
  • 2. Chapter 3 Medically important Bacteria Chapter 3 Medically important Bacteria ” Gram Negative “ 2
  • 3. Pathogenic Neisseriae • Neisseriae: Gram-negative cocci. • Neisseriae contain endotoxin in their outer membrane. ** Note that the endotoxin of Neisseriae consist of lipooligosaccharide (LOS), in contrast to the lipopolysaccharide (LPS) found in enteric gram- negative rods. • N. gonorrhoeae infections (Gonorrhea) have High prevalence and Low mortality. • N. meningitidis infections (Meningitis) have Low prevalence and High mortality. 3
  • 4. • The growth of both bacteria is inhibited by toxic trace metals and fatty acids found in certain culture media (blood agar). • They are cultured on “chocolate” agar containing blood heated to 80°C, which inactivates the inhibitors. • Neisseriae are oxidase-positive (they possess the enzyme cytochrome C ). • It is the terminal enzyme of the respiratory chains, catalyzes electron transfer from cytochrome c to molecular oxygen, reducing the latter to water. • Note: All bacteria that are oxidase positive are aerobic and can use oxygen as a terminal electron acceptor in respiration. 4
  • 5. N. Gonorrhoeae • First described by A. Neisser in 1879. • Gram-negative cocci in pairs with adjacent flattened sides. 5
  • 6. • Gonococcus. • Never Normal flora. • Fragile organism: susceptible to temperature changes, drying, UV light, and other conditions. • Fastidious: media containing hemoglobin. • Cultures:35-36C + 3-10% CO2. • No growth less than 25 or more than 38.5. Virulence Factors • Has no capsule but has multiple serotypes based on the antigenicity of its pilus protein. • Attachment by pili. • Nonpiliated strains are avirulent. 6
  • 7. • Protein P.II: invasion of epithelial cells. • The outer membrane porin/ P.I: to Survive inside of Phagocytes. • The lipooligosaccharide (LOS) of the outer membrane responsible for symptoms. • The organism’s IgA protease can hydrolyze secretory IgA. Disease • Gonococci cause both localized infections, usually in the genital tract, and disseminated infections with seeding of various organs. • Gonococci reach these organs via the bloodstream (gonococcal bacteremia). 7
  • 8. Pathogenic mechanism • Attachment to Non-Ciliated epithelial cells via pili and production of LOS endotoxin. • Gonococci infect primarily the mucosal surfaces (urethra and vagina) resulting in Purulent discharge/ Pus like (Foul smelling). • Symptoms: inflammation, redness, swelling, Dysuria and Burning sensation during urination. 8
  • 9. • Neonatal Conjunctivitis. • Infection in females can result in Pelvic inflammatory disease. If untreated may lead to Infertility. 9 Gonococcal ophthalmia neonatorum develop in 28% of infants born to women with gonorrhea.
  • 10. • The most frequent complication in women is an ascending infection of the uterine tubes, which can result in sterility or ectopic pregnancy. • The incidence of gonococcal ophthalmia has declined greatly in recent years because of the widespread use of prophylactic erythromycin eye ointment (or silver nitrate) applied shortly after birth. • Syphilis and non-gonococcal urethritis caused by Chlamydia trachomatis) can coexist with gonorrhea; therefore, appropriate diagnostic and therapeutic measures must be taken. 10
  • 11. Diagnosis • Signs and symptoms: Purulent (Pus like) discharge. • In men, finding of gram-negative diplococci within PMNs in urethral discharge specimen is sufficient for diagnosis. • In women, use of Gram stain alone can be difficult to interpret; therefore, cultures should be done. • Gram stains on cervical specimens can be falsely positive because of the presence of gram- negative diplococci in the normal flora. 11
  • 12. • It can be also falsely negative because of the inability to see small numbers of gonococci when using the oil immersion lens. Culture Chocolate agar and Thayer-Martin Agar • TMA: 3 antibiotics and nutrients. • Vancomycin: inhibit gram positive. • Polymyxin: Inhibit gram negative bacilli. • Nystatin, which can kill most fungi. 12
  • 14. Treatment and Prevention • Ceftriaxone is the treatment of choice in uncomplicated gonococcal infections. • Because mixed infections with C. trachomatis are common, azithromycin or doxycycline should be prescribed also. • A major problem is the detection of asymptomatic carriers. • Gonococcal conjunctivitis in new-born is prevented most often using erythromycin ointment. • No vaccine is available. 14
  • 15. Neisseria meningitidis • Meningococcus • Identical in staining and morphologicaly to N. gonorrhoeae. • Has antiphagocytic polysaccharide Capsule. • Cultivation in moist chamber containing 5-10% CO2. • All media must be warmed to 37C prior to inoculation as the organism is Susceptible to above or below 37C. 15
  • 16. Meningitis • Inflammation meninges of brain or spinal cord. • Meninges: 3 membranes that envelope brain and spinal cord. • Meningitis: caused by bacteria and viruses. • N. meningitidis, Haemophilus influenzae, E. coli, S. pneumoniae, S. pyogenes, S. aureus. 16
  • 17. Pathogenesis • Humans are the only natural hosts for meningococci. • The organisms are transmitted by airborne droplets; they colonize the membranes of the nasopharynx. • Carriers (5%) are usually asymptomatic. • From the nasopharynx, the organism can enter the bloodstream and spread to specific sites, such as the meninges or joints, or be disseminated throughout the body (meningococcemia). 17
  • 18. Clinical Findings • The two most important manifestations of disease are meningococcemia and meningitis. • The most severe form of meningococcemia is the life-threatening Waterhouse–Friderichsen syndrome, which is characterized by high fever, shock, widespread purpura, disseminated intravascular coagulation and thrombocytopenia. • Petechiae (minute hemorrhagic spots in skin) or Purpura (hemorrhages into skin) in 30-60% of patients with meningococcal disease. 18
  • 19. • Bacteremia can result in the seeding of many organs, especially the meninges. • The symptoms of meningococcal meningitis are those of a typical bacterial meningitis, (Headache, Fever, Stiff neck, Confusion, difficulty in wake) and an increased level of PMNs in spinal fluid. 19
  • 20. Virulence Factors • Fimbriae for attachment. • Polysaccharide capsule: enables the organism to resist phagocytosis by polymorphonuclear leukocytes (PMNs). • Endotoxin: lipooligosaccharide (LOS) and its mechanism is endotoxic which causes fever, shock, and other pathophysiologic changes. • Immunoglobulin A (IgA) protease helps the bacteria attach to the membranes of the upper respiratory tract by cleaving secretory IgA. 20
  • 21. Diagnosis • Sample: Cerebrospinal fluid (CSF). • A presumptive diagnosis of meningococcal meningitis can be made if gram-negative cocci are seen in a smear of spinal fluid. 21
  • 22. • Culture on Chocolate agar and TMA. The organism grows best on chocolate agar incubated at 37°C in 5% CO2. • Oxidase (all Neisseria positive). • N. meningitidis utilize glucose and maltose. • Tests for serum antibodies are not useful for clinical diagnosis. • Rapid diagnosis of meningococcal meningitis is done by “latex agglutination test”, which detects capsular polysaccharide in the spinal fluid. 22
  • 23. CSF findings in different forms of meningitis Type of meningitis Glucose Protein Acute bacterial Low High Acute viral Normal Normal or high 23
  • 24. Normal CSF !!!! Normal CSF !!!!  Appearance:  WBCs count:  RBCs:  Bacteria:  Protein and Glucose: 24
  • 25. Treatment and Prevention • Penicillin G is the treatment of choice for meningococcal infections. • A third-generation cephalosporin such as ceftriaxone can also be used. • Ciprofloxacin can be used for prophylaxis in people who have had close contact with the index case. • Menomune, unconjugated vaccine, contains only the four polysaccharides (not conjugated to a carrier protein). 25
  • 26. What are the difference between N. gonorrhoeae and N. meningitidis What are the difference between N. gonorrhoeae and N. meningitidis ???????????? 26
  • 27. Haemophilus influenzae • Small gram-negative rod (coccobacillus) with a polysaccharide capsule. • It is one of the three important encapsulated pyogens, along with the pneumococcus and the meningococcus. • Serologic typing is based on the antigenicity of the capsular polysaccharide. • Of the 6 serotypes, type b causes most of the severe, invasive diseases, such as meningitis and sepsis. 27
  • 28. • Unencapsulated strains can also cause disease, especially of the upper respiratory tract such as sinusitis and otitis media, but usually non- invasive. • Growth of the organism on laboratory media requires the addition of two components, heme (factor X) and NAD (factor V), for adequate energy production. Diseases • H. influenzae used to be the leading cause of meningitis in young children, but the use of the highly effective “conjugate” vaccine has greatly reduced the incidence of meningitis. 28
  • 29. • It is still an important cause of upper respiratory tract infections (otitis media, sinusitis) and sepsis in children. • It also causes pneumonia in adults, particularly in those with chronic obstructive lung disease. Pathogenesis • H. influenzae infects only humans; there is no animal reservoir. • It enters the body by airborne droplets into the respiratory tract, resulting in either asymptomatic colonization or infections such as otitis media, sinusitis, or pneumonia. 29
  • 30. • The organism produces IgA protease that degrades secretory IgA, thus facilitating attachment to the respiratory mucosa. • After becoming established in the upper respiratory tract, the organism can enter the bloodstream (bacteremia) and spread to the meninges. Clinical Findings • Meningitis caused by H. influenzae cannot be distinguished on clinical grounds from that caused by pneumococci or meningococci). • The rapid onset of fever, headache, and stiff neck, along with drowsiness, is typical. 30
  • 31. • Sinusitis and otitis media cause pain in the affected area. • Other serious infections include septic arthritis, cellulitis, and sepsis. • A swollen “cherry-red” epiglottis is seen. Laboratory Diagnosis • It depends on the isolation of the organism on heated-blood (“chocolate”) agar enriched with two growth factors required for bacterial respiration (factor X ( heme compound) and factor V (NAD)). 31
  • 32. • The blood used in chocolate agar is heated to inactivate nonspecific inhibitors of H. influenzae growth. • An organism that grows only in the presence of both growth factors is presumptively identified as H. influenzae. 32
  • 33. 33
  • 34. • Other species of Haemophilus, such as H. parainfluenzae, do not require both factors. • Definitive identification can be made with either biochemical tests or the capsular swelling (quellung) reaction. 34
  • 35. Treatment • The treatment of choice for meningitis or other serious systemic infections caused by H. influenzae is ceftriaxone. • 20-30% of H. influenzae type b isolates produce β-lactamase that degrades ampicillin but not ceftriaxone. • Untreated H. influenzae meningitis has a fatality rate of approximately 90%. 35
  • 36. Prevention • The vaccine contains capsular polysaccharide of H. influenzae type b conjugated to diphtheria toxoid or other carrier protein. • This vaccine is much more effective in young children than the unconjugated vaccine. • Meningitis in close contacts of the patient can be prevented by rifampin. • Rifampin decreases respiratory carriage of the organism, thereby reducing transmission. 36
  • 37. Bordetella pertussis • Pertussis = Whooping cough caused by Bordetella pertussis. • Toxin mediated infection. • Symptoms are initially mild, and then develop into severe coughing fits, which produce the namesake "whoop" sound in infected babies and children when they inhale air after coughing. • Despite the severity of the symptoms, the organism is restricted to the respiratory tract and blood cultures are negative. 37
  • 38. • In adults, the characteristic whoop is often absent, leading to difficulty in recognizing the cough as caused by this organism. • B. pertussis: Gram-negative, aerobic coccobacillus, non-motile. • Encapsulated. • Fastidious. • Preschool children (severe under 12 months). Pathogenesis • B. pertussis, pathogen only for humans, is transmitted by airborne droplets. 38
  • 39. • The organisms attach to the ciliated epithelium of the upper respiratory tract but do not invade the underlying tissue. • Decreased cilia activity and subsequent death of the ciliated epithelial cells are important aspects of pathogenesis. • Pertussis is a highly contagious disease that occurs primarily in infants and young children and has a worldwide distribution. 39
  • 40. • Several factors play a role in the pathogenesis: (1) Attachment to the cilia of the epithelial cells is mediated by a protein on the pili called filamentous hemagglutinin. Antibody against the filamentous hemagglutinin inhibits attachment and protects against disease. (2) Pertussis toxin: Leading to edema of the respiratory mucosa that contributes to the severe cough of pertussis. Pertussis toxin also causes a striking lymphocytosis in the blood. 40
  • 41. (3) The organisms also synthesize, and export adenylate cyclase. This enzyme, when taken up by phagocytic cells (neutrophils), can inhibit their bactericidal activity. Bacterial mutants that lack cyclase activity are avirulent. (4) Tracheal cytotoxin is a fragment of the bacterial peptidoglycan that damages ciliated cells of the respiratory tract. 41
  • 42. Laboratory Diagnosis • The bacteria can be isolated from nasopharyngeal swabs. • Bordet-Gengou medium: Slow growing. • Identification of the isolated organism can be made by agglutination with specific antiserum or by fluorescent-antibody staining. 42
  • 43. • However, the organism grows very slowly in culture, so direct fluorescent-antibody staining of the nasopharyngeal specimens can be used for diagnosis. • Polymerase chain reaction–based tests are highly specific and sensitive. • Isolation of the organism in patients with a prolonged cough is often difficult. • Serologic tests that detect antibody in the patient’s serum can be used. 43
  • 44. Treatment • Azithromycin is the drug of choice. • Azithromycin reduces the number of organisms in the throat and decreases the risk of secondary complications but has little effect on the course of the disease at the “prolonged cough” stage because the toxins have already damaged the respiratory mucosa. • Supportive care (oxygen therapy and suction of mucus) during the paroxysmal stage is important, especially in infants. 44
  • 45. Prevention • There are two types of vaccines: acellular vaccine containing purified proteins from the organism and killed vaccine containing inactivated B. pertussis organisms. • The acellular vaccine contains five antigens purified from the organism. • The main immunogen in this vaccine is inactivated pertussis toxin (pertussis toxoid). • To protect new-borns, pregnant women should receive pertussis vaccine. • Anti-pertussis IgG will pass the placenta and protect the new-born. 45
  • 47. Brucella • The brucellae are obligate parasites of animals and humans and are characteristically located intracellularly. • Brucella melitensis typically infects goats; Brucella suis, swine; Brucella abortus, cattle. • The disease in humans, brucellosis (undulant fever, Malta fever), is characterized by an acute bacteremic phase followed by a chronic stage that may extend over many years and may involve many tissues. 47 from swine pika Revision
  • 48. Morphology and Identification • The appearance in young cultures varies from cocci to rods 1.2 μm in length (Short coccobacillary forms). • They are gram negative but often stain irregularly. • They are aerobic. • Nonmotile, and non-spore forming. • Catalase and oxidase are produced by the four species that infect humans. 48 8940481 am catalase oxidase positive
  • 49. Culture • Brucellae nutritional requirements are complex. • Fresh specimens from animal or human sources are usually inoculated on trypticase-soy agar or blood culture media. • B. abortus requires 5–10% CO2 for growth, the other three species grow in air. • Small, convex, smooth colonies appear on enriched media in 2–5 days. • Hydrogen sulfide is produced by many strains. 49 a culture characteristics
  • 50. • Brucellae use carbohydrates but produce neither acid nor gas in amounts sufficient for classification. • They are killed in milk by pasteurization. • Differentiation among Brucella species is made by their characteristic sensitivity to dyes and their production of H2S. • Because brucellae are hazardous in the laboratory, tests to classify them should be performed only in reference public health laboratories using appropriate biosafety precautions. 50 nogas youcan'tuse fermentation to identification DEAL
  • 51. Pathogenesis • Although each species of Brucella has a preferred host, all can infect a wide range of animals and humans. • The common routes of infection in humans are ingestion of infected milk, mucous membranes (droplets), and skin (contact with infected tissues of animals). • Cheese made from unpasteurized goats’ milk is a particularly common vehicle. 51
  • 52. • The organisms progress from the portal of entry via lymphatic channels and regional lymph nodes to the thoracic duct and the bloodstream, which distributes them to the kidneys, adrenal glands, liver, spleen, and pancreas. • Granulomatous nodules that may develop into abscesses form. • In such lesions, the brucellae are principally intracellular. • Osteomyelitis, meningitis also occasionally occurs. 52
  • 53. • The main histologic reaction in brucellosis consists of proliferation of mononuclear cells, exudation of fibrin, coagulation necrosis, and fibrosis. • The granulomas consist of epithelioid and giant cells, with central necrosis and peripheral fibrosis. • B. abortus usually causes mild disease without suppurative complications. • B. melitensis infection is more acute and severe. 53 HE
  • 54. • Placentas and fetal membranes of cattle, swine, sheep, and goats contain erythritol, a growth factor for brucellae. • The proliferation of organisms in pregnant animals leads to placentitis and abortion in these species. • There is no erythritol in human placentas, and abortion is not part of Brucella infection of humans. 54 erythritol Jiva goats die Nsb
  • 55. Clinical Findings • The incubation period ranges from 1–4 weeks. • The onset is insidious, with malaise, fever, weakness, and sweats. • The fever usually rises in the afternoon; its fall during the night is accompanied by sweat. • There may be gastrointestinal and nervous symptoms. • Lymph nodes enlarge, and the spleen becomes palpable. • Hepatitis may be accompanied by jaundice. 55
  • 56. • Deep pain and disturbances of motion, particularly in vertebral bodies, suggest osteomyelitis. • These symptoms of generalized Brucella infection generally subside in weeks or months, although localized lesions and symptoms may continue. • After the initial infection, a chronic stage may develop, characterized by weakness and pains, low-grade fever, nervousness, and other nonspecific manifestations. 56
  • 57. Diagnostic Laboratory Tests • Blood should be taken for culture, biopsy material for culture (lymph nodes, bone), and serum for serologic tests. • Brucella agar was specifically designed to culture Brucella species. • In oxygenated form, the medium grows Brucella species very well. • 8–10% CO2 at 35–37°C should be observed for 3 weeks before being discarded as being negative results; liquid media cultures should be blindly subcultured during this time. 57 liquid I subculture 45049media 14
  • 58. • Brucella grow on trypticase-soy medium with or without 5% sheep blood, brain–heart infusion medium, and chocolate agar. • Blood culture media readily grow Brucella. • Liquid medium used to culture Mycobacterium tuberculosis also supports the growth of at least some strains. • They are nonhemolytic. • The observation of tiny gram-negative coccobacilli that are catalase positive and oxidase positive suggests Brucella species. 58 9
  • 59. • A positive urease test result is characteristic of Brucella species. Serology • (IgM) antibody levels rise during the first week of acute illness, peak at 3 months, and may persist during chronic disease. • IgG antibody levels rise about 3 weeks after onset of acute disease, peak at 6–8 weeks, and remain high during chronic disease. • IgA levels parallel the IgG levels. • ELISA assays—IgG, IgA, and IgM antibodies may be detected using enzyme-linked immunosorbent assay (ELISA), which use cytoplasmic proteins as antigens. 59 314hm affrgyweak 76 monthafter thiswill beni gan centra
  • 60. Treatment • Brucellae may be susceptible to tetracyclines, rifampin, aminoglycosides, and some quinolones. • Symptomatic relief may occur within a few days after treatment with these drugs. • However, because of their intracellular location, the organisms are not readily eradicated completely from the host. • For best results, treatment must be prolonged. • Combined treatment with a tetracycline (eg, doxycycline) and either streptomycin for 2–3 weeks or rifampin for 6 weeks is recommended. 60
  • 61. Prevention, and Control • Because of occupational contact, Brucella infection is much more frequent in men. • Most infections remain asymptomatic (latent). • Infection rates vary greatly with different animals and in different countries. • Active immunization of humans against Brucella infection is experimental. • Control rests on limitation of spread and possible eradication of animal infection, pasteurization of milk and milk products, and reduction of occupational hazards wherever possible. 61 51 5441 D8 more thanWomen
  • 62. Enterobacteriaceae • Most encountered bacteria in Microbiology Lab. • Gram-negative rods (Bacilli). • Do not form spores. • Motile by Peritrichous flagella or Nonmotile. 62
  • 63. • They found primarily in the colon of humans and other animals, many as part of the normal flora. • These organisms are present in relatively small numbers compared with anaerobes such as Bacteroides. • Grow aerobically and anaerobically. • Active biochemically, ferment glucose and other sugars with gas production. • Catalase positive and Oxidase negative. • Grow well on MacConkey agar and EMB. • They cause a variety of diseases with different pathogenetic mechanisms. 63
  • 64. Escherichia coli • Escherichia coli = E. coli. • It’s discoverer - Theodor Escherich). • Commonly found in the Lower Intestine. • E. coli normally colonizes an infant's gastrointestinal tract within 40 hours of birth, arriving with food or water or with the individuals handling the child. • Most E. coli strains are harmless.  Benefit hosts by producing Vitamin K.  Preventing establishment of Pathogenic bacteria within intestine. 64
  • 65. • Contamination of the public water supply system by sewage is detected by the presence of coliforms in the water. • In a general sense, the term coliform includes not only E. coli, but also other inhabitants of the colon such as Enterobacter and Klebsiella. • Because E. coli is a large intestine organism, It is used as the indicator of fecal contamination. • E. coli and the enteric pathogens are killed by chlorination of the drinking water. 65
  • 66. Pathogenesis of E. coli • Intestinal diseases (Gastroenteritis) O157:H7. “traveler’s diarrhea,” a watery diarrhea. Some strains of E. coli are enterohemorrhagic and cause bloody diarrhea. • Neonatal meningitis. capsular antigen K1. • Urinary tract infections (UTI) Uropathogenic E. coli (UPEC). • It has three antigens that are used to identify the organism in epidemiologic investigations: O, or cell wall antigen; H, or flagellar antigen; and K, or capsular antigen. 66
  • 67. Virulence factors E. coli components that contribute to its ability to cause disease: • Pili. • Capsule. • Flagella. • Endotoxin. • Three exotoxins (enterotoxins), two that cause watery diarrhea and one that causes bloody diarrhea and hemolytic–uremic syndrome. 67
  • 68. Intestinal Tract Infection • The enterotoxin-producing strains do not cause inflammation, do not invade the intestinal mucosa, and cause watery, non- bloody diarrhea. • Certain strains of E. coli are enteropathic (enteroinvasive) and cause disease by invasion of the epithelium of the large intestine, causing bloody diarrhea (dysentery) accompanied by inflammatory cells (neutrophils) in the stool. 68
  • 69. • Certain enterohemorrhagic strains of E. coli (those with the O157:H7 serotype) also cause bloody diarrhea by producing exotoxin called Shiga toxin, so called because it is very similar to that produced by Shigella species. • Some patients with bloody diarrhea caused by O157:H7 strains also have life-threatening complication called hemolytic–uremic syndrome (HUS). • It occurs when Shiga toxin enters the bloodstream. • This syndrome consists of hemolytic anemia, thrombocytopenia, and acute renal failure. 69
  • 70. • The hemolytic anemia and renal failure occur because there are receptors for Shiga toxin on the surface of the endothelium of small blood vessels and on the surface of kidney epithelium. • Treatment of diarrhea caused by O157:H7 strains with antibiotics, such as ciprofloxacin, increases the risk of developing HUS by increasing the amount of Shiga toxin released by the dying bacteria. • For this reason, antibiotics should not be used to treat diarrhea caused by EHEC. 70
  • 71. Clinical findings • Diarrhea caused by enterotoxigenic E.coli is usually watery, non-bloody, self-limited, and of short duration (1–3 days). • It is frequently associated with travel (Traveler’s diarrhea). • Infection with enterohemorrhagic E. coli (EHEC) results in a dysentery-like syndrome characterized by bloody diarrhea, abdominal cramping, and fever similar to that caused by Shigella. 71
  • 72. UTI • Bacterial infection that affects any part of the Urinary tract. • Symptoms include frequent feeling to urinate, pain during urination (Dysuria), and burning sensation in the urethra. • Although urine contains a variety of fluids, salts, and waste products, it does not usually have bacteria in it. • The most common type of UTI is acute Cystitis: referred to Bladder infection. • An infection of the upper urinary tract or Kidney known as Pyelonephritis: is potentially more serious. (Fever and Abdominal pain). 72
  • 73. 73
  • 74. Risk factors SEX Intercourse • In young sexually active women. • “Honeymoon cystitis": frequent UTIs during early marriage. • Spermicide use increases risk of UTIs. Sex/Gender: Women are more prone to UTIs than men due to:  Much shorter length of Urethra.  Women lack the bacteriostatic properties of prostatic secretions.  Among elderly, UTI frequency is roughly equal proportions in women and men. 74
  • 75. Urinary catheters • It can be decreased by only using aseptic technique for insertion. UTI Causative Microbes Gram negative E. coli, Klebsiella pneumoniae (Lactose fermentors). Proteus spp., Pseudomonas aeroginosa (NLF). Gram Positive S. saprophyticus, Group B streptococci. Fungi: Candida albicans. Viruses: Rare. 75
  • 76. Diagnosis • Multiple bacilli (rod-shaped bacteria, shown as black between white cells at urinary microscopy. • This is called Bacteriuria and Pyuria, respectively. 76
  • 77. • Samples: depending on the infection. • Culture: MacConkey agar + EMB. • Gram stain. • Ferment all sugars with Gas. Indole +ve. 77
  • 78. 78 Lactose Catalase Oxidase Indole Citrate Urease S 2 H Escherichia coli + + _ + _ _ _
  • 79. Treatment • Uncomplicated lower UTI (cystitis) can be treated using oral trimethoprim- sulfamethoxazole or nitrofurantoin. • Pyelonephritis can be treated with ciprofloxacin or ceftriaxone. • E. coli sepsis requires treatment with third generation cephalosporin, such as cefotaxime, with or without an aminoglycoside, such as gentamicin. • For the treatment of neonatal meningitis, a combination of ampicillin and cefotaxime. 79
  • 80. Prevention • There is no specific prevention for E. coli infections, such as active or passive immunization. • However, various general measures can be taken to prevent certain infections caused by E. coli and other organisms. 80
  • 81. pneumoniae K. • German microbiologist Edwin Klebs. • They can be found in water, soil, plants, animals and humans. • Non-motile. • They are usually opportunistic pathogens that cause nosocomial infections, especially pneumonia and urinary tract infections. • K. pneumoniae is important respiratory tract pathogen outside hospitals as well. • It has very large polysaccharide capsule, which gives its colonies striking mucoid appearance. 81
  • 82. Pathogenesis • Predisposing conditions for K. pneumoniae infections include advanced age, chronic respiratory disease, diabetes, or alcoholism. • UTI and pneumonia are the usual clinical entities associated with the bacteria, but bacteremia and secondary spread to other areas such as the meninges and liver occur. • Pneumonia caused by Klebsiella, which produces a thick sputum (“currant-jelly”) and can progress to necrosis and abscess formation. 82
  • 83. Diagnosis • Form large sticky colonies. • Ferment sugars (glucose, lactose, sucrose, and mannitol) with abundant gas. • Citrate positive. • Indole negative. • Urease positive. 83
  • 84. 84 Bacteria Lactose Sucrose Catalas e Oxidase Indole Citrate Urease S 2 H Klebsiella pneumoniae + + + _ _ d + _
  • 85. Treatment • Because of antibiotic resistance, the choice of drug depends on sensitivity testing. • Isolates from hospital-acquired infections are frequently resistant to multiple antibiotics. • Carbapenem-resistant strains are an important cause of hospital-acquired infections and are resistant to almost all antibiotics. • An aminoglycoside (gentamicin) and cephalosporin (cefotaxime) are used empirically until the results of testing are known. 85
  • 86. Salmonella • Salmonella parasitise intestines of large number of vertebrate species. • Transmission = uncooked meats and eggs. • Chickens: are major reservoir of Salmonella. • Most Salmonella are carried by animals, S. typhi is unique because it is only carried by humans. • Cause Typhoid fever (Enteric fever). • S. typhimurium causes Gastroenteritis in humans and other mammals. 86
  • 87. Important Properties • Salmonellae do not ferment lactose but produce H2S—features used in their lab identification. • Their antigens—cell wall O, flagellar H, and capsular Vi (virulence)—are important for taxonomic and epidemiologic purposes. • The Vi antigens (capsular polysaccharides) are antiphagocytic and are important virulence factor for S. typhi. • The Vi antigens are also used for the serotyping of S. typhi in the clinical laboratory. 87
  • 88. • Clinically, Salmonella species are in two distinct categories, namely, typhoidal species (cause typhoid fever) and nontyphoidal species (cause diarrhea [enterocolitis]. • The typhoidal species are S. typhi and S. paratyphi. • The non-typhoidal species are the serotypes of S. enterica. Pathogenesis The three types of Salmonella infections (enterocolitis, enteric fevers, and septicemia) have different pathogenic features. 88
  • 89. 1. Enterocolitis • Characterized by invasion of the epithelial and subepithelial tissue of the small and large intestines with resulting inflammation and diarrhea. • Neutrophils limit the infection to the gut. • Bacteremia is infrequent in enterocolitis. (2) Typhoid and other enteric fevers: • Infection begins in the small intestine, but few gastrointestinal symptoms occur. 89
  • 90. • The organisms enter, multiply in the mononuclear phagocytes of Peyer’s patches, and then spread to the phagocytes of the liver, gallbladder, and spleen. • This leads to bacteremia, which is associated with the onset of fever and other symptoms, probably caused by endotoxin. • Survival and growth of the organism within phagosomes in phagocytic cells are a striking feature of this disease, as is the predilection for invasion of the gallbladder, which can result in establishment of the carrier state and excretion of the bacteria in the feces for long periods. 90
  • 91. (3) Septicemia • Accounts for only about 5-10% of Salmonella infections and occurs in one of two settings:  A patient with an underlying chronic disease, such as sickle cell anemia or cancer.  A child with enterocolitis. • Osteomyelitis in a child with sickle cell anemia is an important example of this type of salmonella infection. 91
  • 92. Clinical Findings • Incubation period of 12 to 48 hours. Enterocolitis: begins with nausea, vomiting and then progresses to abdominal pain and diarrhea, which can vary from mild to severe, with or without blood. • Usually the disease lasts a few days, is self- limited, causes non-bloody diarrhea, and does not require medical care except in very young and very old. • S. typhimurium is the most common species of Salmonella to cause enterocolitis. 92
  • 93. • Typhoid fever: caused by S. typhi, and in enteric fever, caused by S. paratyphi A, B, and C the onset of illness is slow, with fever and constipation rather than vomiting and diarrhea predominating (almost). • Diarrhea may occur early but usually disappears by the time the fever and bacteremia occur. • After the first week, as the bacteremia becomes sustained, high fever, tender abdomen, and enlarged spleen occur. • Rose spots (rose-colored macules on the abdomen) are associated with typhoid fever but occur rarely. 93
  • 94. • Leukopenia and anemia are often seen. • Liver function tests are often abnormal, indicating hepatic involvement. • The disease begins to resolve by the third week, but severe complications such as intestinal hemorrhage or perforation (hole) can occur. • About 3% of typhoid fever patients become chronic carriers which is higher among women, especially those with previous gallbladder disease and gallstones. 94
  • 95. Diagnosis • The clinical picture together with information on travel. • Samples: Stool, Blood. • Media are differential and slightly selective, i.e., in addition to lactose and a pH indicator, they contain an inhibitor for non-enterics. • (e.g., MacConkey agar and Eosin-methylene blue agar - EMB). 95
  • 96. • Selective for Salmonella are SS agar. • Xylose-Lisine-Deoxycholate (XLD) agar. 96
  • 97. • Gram stain: Gram-negative bacilli. • Sugar fermentation: Lactose negative; acid and gas from glucose, mannitol, maltose. • Biochemical tests  Citrate positive.  H2S produced from Sodium Thiosulfate. • On TSI agar, an alkaline slant and acid butt with both gas and H2S, are produced. 97
  • 98. 98
  • 99. Treatment • Enterocolitis caused by Salmonella is self- limited that resolves without treatment. • Fluid and electrolyte replacement may be required. • Antibiotic treatment does not shorten the illness or reduce the symptoms; in fact, it may prolong excretion of the organisms, increase the frequency of the carrier state, and select mutants resistant to the antibiotic. 99
  • 100. • Antimicrobial agents are indicated only for neonates or persons with chronic diseases who are at risk for septicemia and disseminated abscesses. • The treatment of choice for typhoid fever and septicaemia with metastatic infection is either ceftriaxone or ciprofloxacin. • Ampicillin or ciprofloxacin should be used in patients who are chronic carriers of S. typhi. 100
  • 101. Prevention • Two vaccines are available, but they confer limited (50 –80%) protection against S. typhi. • One contains Vi capsular polysaccharide of S. typhi (intramuscularly), and the other contains a live, attenuated strain (Ty21a) of S. typhi (orally). • A new conjugate vaccine containing capsular polysaccharide (Vi) antigen coupled to a carrier protein is safe and immunogenic in young children. 101
  • 102. Shigella • Discovered over 100 years ago. • Japanese microbiologist - Shiga. • Related to Escherichia and considered another strain of E. coli. • Shigella species cause enterocolitis (bacillary dysentery). • The term dysentery refers to bloody diarrhea. • Shigellae are non–lactose-fermenting. 102
  • 103. • Shigellae can be distinguished from salmonellae by three criteria:  Do not produce gas from the fermentation of Glucose.  They do not produce H2S.  Nonmotile. • All Shigella have O antigens (polysaccharide) in their cell walls, and these antigens are used to divide the genus into four groups:  Serotype A- S. dysenteriae.  Serotype B- S. flexneri.  Serotype C- S. boydii.  Serotype D- S. sonnei. 103
  • 104. Pathogenesis • Shigellae are the most effective pathogens among the enteric bacteria. • They have very low ID. Ingestion of as few as 100 organisms causes disease, whereas at least 105 V. cholerae or Salmonella are required to produce symptoms. • Shigellosis is only human disease (there is no animal reservoir). • The organism is transmitted by fecal–oral route. The four (Fs—fingers, flies, food, feces). 104
  • 105. • There is no prolonged carrier state with Shigella infections, unlike that seen with S. typhi. • Shigella cause bloody diarrhea (dysentery) by invading the cells of the mucosa of the distal ileum and colon. • Local inflammation accompanied by ulceration occurs, but the organisms rarely penetrate through the wall or enter the bloodstream, unlike Salmonellae. • Shiga toxins very similar to those produced by Shigella are produced by enterohemorrhagic E. coli O157:H7 strains that cause enterocolitis and HUS. 105
  • 106. Clinical Findings • After an incubation period of 1 to 4 days, symptoms begin with fever and abdominal cramps, followed by diarrhea, which may be watery at first but later contains blood and mucus. • The disease varies from mild to severe depending on two major factors: the species of Shigella and the age of the patient, with young children and elderly people being the most severely affected. 106
  • 107. • The diarrhea frequently resolves in 2 or 3 days; in severe cases, antibiotics can shorten the course. Diagnosis 107 XLD
  • 108. • No utilise Citrate as source of carbon. • Do not form H2S. • (Comparing to Salmonella). 108 Shigella on XLD Salmonella on XLD
  • 109. Proteus • Distinguished from other members of the Enterobacteriaceae by their ability to produce the enzyme phenylalanine deaminase. • They produce enzyme urease, which cleaves urea to form NH3 and CO2. 109
  • 110. • Certain species are very motile and produce a striking swarming effect on blood agar, characterized by expanding rings (waves) of organisms over the surface of the agar. 110
  • 111. • Proteus species are found in the human intestinal tract as part of normal intestinal flora, along with E. coli and Klebsiella species. Pathogenesis • It causes UTI due to their presence in the colon and to colonization of the urethra, especially in women. • The motility of Proteus may contribute to their ability to invade the urinary tract. • Proteus species possess extracytoplasmic outer membrane, contains lipid bilayer, lipoproteins, polysaccharides, and lipopolysaccharides. 111
  • 112. • Fimbriae facilitate adherence and thus enhance the capacity of the organism to produce disease. Specific chemicals located on the tips of pili enable organisms to attach to selected host tissue sites (eg, urinary tract endothelium). • The ability of Proteus to produce urease and to alkalinize urine by hydrolyzing urea to ammonia makes it effective in producing an environment in which it can survive. • This leads to precipitation of organic and inorganic compounds, which leads to Struvite Stone formation. pH / Alkaline. 112
  • 113. • Stones in the urinary tract obstruct urine flow, damage urinary epithelium, and serve as a nidus for recurrent infection by trapping bacteria within the stone. • Because alkaline urine also favors growth of the organisms and more extensive renal damage, treatment involves keeping the urine at a low pH. 113
  • 114. Clinical Findings • The signs and symptoms of urinary tract infections caused by these organisms cannot be distinguished from those caused by E. coli or other members of the Enterobacteriaceae. • Proteus species can also cause pneumonia, wound infections, and septicemia. • P. mirabilis causes 90% of Proteus infections.  Those with structural abnormalities of the urinary tract.  Those who have had urethral instrumentation. • Another species is Proteus vulgaris. 114
  • 115. Laboratory Studies • Proteus organisms are easily recovered through routine laboratory cultures. • Most strains are lactose-negative. • Demonstrate Swarming motility on agar plates. • Growth on blood agar containing phenylethyl alcohol inhibits swarming. 115
  • 116. 116 Bacteria Lactose Sucro se Catalase Oxida se Indole Citrate Urease S 2 H Proteus vulgaris _ + + _ + _ + + Proteus mirabilis _ Slow + + _ _ d + +
  • 117. Other Enterobacteria • Enterobacter. • Serratia. • Citrobacter. • Yersinia. 117
  • 118. Pseudomonas aeruginosa • Gram-negative bacilli and aerobic. • Motile by single polar flagellum. • Has Capsule. Diseases • P. aeruginosa causes infections (sepsis, pneumonia, and UTI) primarily in patients with lowered host defenses. • It also causes chronic lower respiratory tract infections in patients with cystic fibrosis, wound infections (cellulitis) in burn patients and malignant otitis externa in diabetic patients. 118
  • 119. • It is the most common cause of ventilator- associated pneumonia. Important Properties • Pseudomonads are gram-negative rods that resemble the members of the Enterobacteriaceae but differ in that they are strict aerobes (derive their energy only by oxidation of sugars rather than by fermentation). 119
  • 120. • Because they do not ferment glucose, they are called non-fermenters,in contrast to the members of the Enterobacteriaceae, which do ferment glucose. • Oxidation involves electron transport by cytochrome c (oxidase-positive). • Pseudomonads are able to grow in water containing only traces of nutrients (tap water), and this favors their persistence in the hospital environment. • It withstands disinfectants; this accounts in part for their role in hospital-acquired infections. 120
  • 121. • P. aeruginosa produces two pigments useful in clinical and laboratory diagnosis: (1) Pyocyanin: color the pus in a wound blue. (2) Pyoverdin (fluorescein): yellow-green pigment that fluoresces under ultraviolet light, a property that can be used in the early detection of skin infection in burn patients. • In the laboratory, these pigments diffuse into the agar, imparting blue-green color that is useful in identification. • P. aeruginosa is the only species of Pseudomonas that synthesizes pyocyanin. 121
  • 122. • Its optimum temperature for growth is 37C and able to grow at 42C. • Strains of P. aeruginosa isolated from cystic fibrosis patients have a prominent slime layer (glycocalyx), which gives their colonies a very mucoid appearance. • The slime layer mediates adherence of the organism to mucous membranes of the respiratory tract and prevents antibody from binding to the organism. 122
  • 123. Pathogenesis • P. aeruginosa is found chiefly in soil and water, although approximately 10% of people carry it in the normal flora of the colon. • It is found on the skin in moist areas and can colonize the upper respiratory tract of hospitalized patients. • Its ability to grow in simple aqueous solutions has resulted in contamination of respiratory therapy and anesthesia equipment, intravenous fluids, and even distilled water. 123
  • 124. P. aeruginosa is primarily opportunistic pathogen:  Those with extensive burns, in whom the skin host defenses are destroyed.  Those with chronic respiratory disease (cystic fibrosis), in whom the normal clearance mechanisms are impaired.  Those who are immunosuppressed.  In those with indwelling catheters. • The most common cause of gram-negative nosocomial pneumonia, especially ventilator- associated pneumonia. 124
  • 125. • Pathogenesis is based on multiple virulence factors: endotoxin, exotoxins, and enzymes.  Its endotoxin like that of other gram-negative bacteria, causes the symptoms of sepsis and septic shock. • The best known of the exotoxins is exotoxin A, which causes tissue necrosis.  It inhibits eukaryotic protein synthesis by the same mechanism as diphtheria exotoxin.  It also produces proteases that are histotoxic and facilitate invasion of the organism into the bloodstream. • Pyocyanin damages the cilia and mucosal cells of the respiratory tract. 125
  • 126. Diagnosis • Symotoms and sample depend on infection. • Gram stain: gram negative bacilli. • No ferment glucose and Lactose. • Catalase positive. • Oxidase Positive. • Fruity odor colonies. • Ability to grow at 42°C. 126
  • 127. • Confirmatory tests: production of blue-green pigment on Cetrimide agar. • Cetrimide has bactericidal activity against Gram- positive and certain Gram-negative organisms, including species of pseudomonas other than Pseudomonas aeruginosa . 127
  • 128. 128 Bacteria Lactose Sucrose Catalase Oxidas e Indole Citrate Urease S 2 H Pseudomon as aeruginosa _ _ + + _ + d _
  • 129. Treatment and Prevention • P. aeruginosa is resistant to many antibiotics. • For infections caused by highly resistant strains, colistin (polymyxin E) is useful. • The drug of choice for UTI is ciprofloxacin. • Removing indwelling catheters promptly. • Taking special care of burned skin. 129
  • 130. 130