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Premium member Presentation Transcript A 18 years old malewas brought to emergency department : A 18 years old malewas brought to emergency department Presenting Complaint : Presenting Complaint Drowsiness, Sudden onset of fever 104o F , Severe head ache , Chills, Malaise, Myalgia, vomiting, lethargy Physical examination Signs of ; Increased intracranial pressure ( Pappilledema ) and Meningeal irritation ( Kernig’s sign) were +ive and Nuchal rigidity was also noted Physical examination : Physical examination Cerebrospinal fluid (CSF) was examined for;-- : Cerebrospinal fluid (CSF) was examined for;-- 1. Pressure 2. Appearance (clear or turbid ) 3. Wet Mount (TLC) 4. Gram Stain for bacteria. 5. Geimsa stain for Presence of polymorphs , lymphocytes or R.B.C.s. 6. Cell count; Normal 0-5 cells /mm3, Markedly increased in bacterial, tuberculous and viral accordingly. 7. Glucose measurement; Normal 60 % of blood glucose, decreases in bacterial meningitis. 8. Concentration of protein ; Normal 40-60 mg/dl ++++ in bacterial +++in tuberculous ++ in viral. 9. Look for Bacterial antigens in C.S.F by specific Antibodies. 10. Culture Slide 5: 1500 Polymorphs 25 mg/dl 100 mg/dl clear - - - lymphocytes CSF Gram -negative diplococci seen 45-85mg/dl 15-45mg/dl 0- 4 lymphocytes/cmm Turbid (purulent) clear Slide 6: Gram-negative cocci (pairs)-- Neisseria Pus cells neutrophils Slide 7: Diagnosis --- Acute pyogenic Meningitis causative agent was ---Meningococci Rapid diagnosis [latex agglutination test] (capsular polysaccharide in CSF) +ive Culture on Chocolate agar was positive DIFFERENTIAL DIAGNOSIS OF MENINGITIS : DIFFERENTIAL DIAGNOSIS OF MENINGITIS Bacterial Meningitis PMN's outnumber monocytes, papilledema occurs late in disease, acute onset. High lactate, low glucose of CSF Slide 11: 2.Parasitic Meningitis Acanthamoeba or Naegalaria species Entry via contaminated water or in children swimming in Nullahs. Acute onset, slight change in CSF chemistry, presence of IgM in CSF 90% mortality, presence of vegetative forms of amoeba on direct examination of C.S.F. 3. Viral Meningitis : 3. Viral Meningitis acute onset, slight change in CSF chemistry. Monocytes outnumber PMN's. BACTERIAL VS VIRAL MENINGITIS Predictors of bacterial etiology: CSF glucose < 34 CSF: Serum glucose ratio < 0.23 CSF protein > 220 CSF WBC count > 2000 CSF neutrophil count > 1180 [Presence of any ONE of the above findings predicts bacterial etiology with > 99% certainty] Slide 13: CHRONIC MENINGITIS (occur in Immunocompromised patients, insidious onset) 1.Tubercular Meningitis (M. tuberculosis, M. avium ) slight changes in CSF chemistry, positive tuberculin, low chloride. Slide 14: 2.Fungal Meningitis (Cryptococcus neoformans) history of lung infection, yeast cells in CSF, slight changes in CSF chemistry CHRONIC MENINGITIS : CHRONIC MENINGITIS 3. AIDS patients 4. Syphilitic Meningitis (slight change in CSF chemistry, positive RPR test) Risk groups for Meningitis : Risk groups for Meningitis Slide 18: Purulent (Bacterial) meningitisusually begins as an infection by normal body flora / colonizers of Treatment of Acute Bacterial Meningitis : Treatment of Acute Bacterial Meningitis General The risk of death during the early phases of acute bacterial meningitis usually relates to problems other than the infection itself. A combination of fever, dehydration secondary to vomiting , decreased food and fluid intake with subsequent alkalosis often predisposes patients, especially young children to seizures. Respiratory arrest or airway obstruction often follows; if significant CNS or myocardial hypoxia occurs, fatal cardiac arrhythmias or brainstem damage may result. Slide 20: Procedures commonly employed include: 1. Correction of fluid and electrolyte deficits. 2. Provision for adequate oxygenation. 3. Monitoring of cardiovascular function (Give a cardiac-active glycoside if necessary). 4. Monitoring intracranial pressure - administer urea or mannitol to reduce cerebral edema. Slide 21: Administration of antibiotics Empiric regimen ; Neonate (up to 1m) (Ampicillin + Cefotoxime) or (Ampicillin + Gentamycin) Neonate (1-3 m) (Ampicillin + Dexamethazone) or (Ampicillin + Dexamethazone + Cefotoxime) Other (3 m- 50 yrs) Cefotoxime + Vancomycin (Over 50 yrs Old or Alcoholics) Ampicillin + Cefotoxime Slide 22: Neisseria Meningitidis (Meningococci) More than 80 % of bacterial meningitis in children over 02 months is caused by Meningococci and Pneumococci . Meningococci Gp A cause epidemics of meningitis. Overall Neisseria meningitidis ranges 2nd to S. pneumoniae as a cause of meningitis, but most common cause at the ages of 2-18 yrs. Slide 23: Meningococcal meningitis has been recognized as a serious problem for almost 200 years. Meningococcal disease still is associated with a high mortality rate and persistent neurological defects, particularly among infants and young children. Neisseria Meningitidis : Neisseria Meningitidis Meningococci comprise at least 13 serogroups based on the composition of their polysaccharide capsular antigens. They differ in their agglutination reactions to sera directed against polysaccharide antigens. More than 99% of meningococcal infections are caused by serogroups A, B, C, 29E, or W-135. There is currently no vaccine to prevent group B , however there are some in the near future. Slide 25: · Virulence factors ; Polysaccharide capsule, Endotoxin, IgA protease The natural habitat and reservoir for meningococci mucosal surfaces of the human nasopharynx and, to a lesser extent, the urogenital tract and anal canal. Approximately 5-10% of adults are asymptomatic nasopharyngeal carriers. But that number increases to as many as 60-80% of members of closed populations (eg, military recruits in camps, boarding schools, dormitories, crowded living conditions, youth camps, daycares . Pathogenesis Pathogenesis : Pathogenesis Humans are the natural hosts. The mode of infection; Transmission: airborne droplets. Colonize: upper resp tract, nasopharyx. Carriers: asymptomatic chronic carriers 5 to 35%. The incubation period; averages 3-4 days (range 1-10 days), which is the period of communicability. Slide 27: INFECTION OCCURS IN THREE STAGES leading to subclinical infection 1. 2. 10-20% of cases, N. meningitidis enters the bloodstream. 3. SYSTEMIC DISEASE; appears with the development of meningococcemia and usually precedes meningitis by 24-48 hours. or joints Clinical Manifestations : Clinical Manifestations Meningitis (Inflammation of the meninges. Pathogen reach the meninges in the bloodstream or from nearby sites such as middle ear, sinuses or nasopharynx) Meningococcemia. (Its severe form is called as Water-house-Friderichen syndrome.) Slide 29: Water-house-Friderichen syndrome is characterized by high fever ,shock, widespread purpura, disseminated intravascular coagulation,& adrenal insufficiency. Acute fulminating form , patient dies in few hours of circulatory collapse due to adrenal cortical failure caused by hemorrhage into the adrenals Slide 30: Skin rashes occur in meningococcemia, with or without meningitis. From the first to the third day, at least one-third of patients with meningococcal meningitis develop petechiae, most prominently in areas subjected to pressure . Slide 31: Specimens; Blood, CSF Direct microscopy Gram staining of blood & c.s.f. Gram negative diplococci . 2.Isolation of organisms: Media: chocolate agar. Incubation: 37o c x 5% Co 2 x 24 hrs oxidase positive sugar fermentation test meningococci gonococci maltose + - glucose + + 3. Detection of capsular polysaccharide by latex agglutination test. Laboratory diagnosis Slide 32: Penicillin – G. is the treatment of choice for meningococci PREVENTION Chemoprophylaxis and immunization Rifampin is used for prophylaxis in household and other close contacts. · Vaccine contains capsular polysaccharides of group A, C, Y and W – 135 strains Effective in preventing epidemics of meningitis. Treatment: Slide 33: Other Gram negative cocci Gonococci Veillonella Consists of small anaerobic, gram-negative cocci growing in masses, they are sometimes isolated from suppurative lesions. Moraxella catarrhalis A part of normal throat flora & an occasional opportunistic cause of pneumonia. learning objectives : learning objectives Types of meningitis depending upon causative organisms. Pathogenesis of Meningococcal (pyogenic) meningitis Describe the findings of normal CSF Describe the CSF findings in different types of meningitis Interpretation of Laboratory reports in case of meningitis Treatment of meningitis Lab diagnosis of meningococcal meningitis You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
4meningococci--LECTURE.pptIMDC 4 ppt aSGuest40434 Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 247 Category: Education License: Some Rights Reserved Like it (2) Dislike it (0) Added: March 13, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript A 18 years old malewas brought to emergency department : A 18 years old malewas brought to emergency department Presenting Complaint : Presenting Complaint Drowsiness, Sudden onset of fever 104o F , Severe head ache , Chills, Malaise, Myalgia, vomiting, lethargy Physical examination Signs of ; Increased intracranial pressure ( Pappilledema ) and Meningeal irritation ( Kernig’s sign) were +ive and Nuchal rigidity was also noted Physical examination : Physical examination Cerebrospinal fluid (CSF) was examined for;-- : Cerebrospinal fluid (CSF) was examined for;-- 1. Pressure 2. Appearance (clear or turbid ) 3. Wet Mount (TLC) 4. Gram Stain for bacteria. 5. Geimsa stain for Presence of polymorphs , lymphocytes or R.B.C.s. 6. Cell count; Normal 0-5 cells /mm3, Markedly increased in bacterial, tuberculous and viral accordingly. 7. Glucose measurement; Normal 60 % of blood glucose, decreases in bacterial meningitis. 8. Concentration of protein ; Normal 40-60 mg/dl ++++ in bacterial +++in tuberculous ++ in viral. 9. Look for Bacterial antigens in C.S.F by specific Antibodies. 10. Culture Slide 5: 1500 Polymorphs 25 mg/dl 100 mg/dl clear - - - lymphocytes CSF Gram -negative diplococci seen 45-85mg/dl 15-45mg/dl 0- 4 lymphocytes/cmm Turbid (purulent) clear Slide 6: Gram-negative cocci (pairs)-- Neisseria Pus cells neutrophils Slide 7: Diagnosis --- Acute pyogenic Meningitis causative agent was ---Meningococci Rapid diagnosis [latex agglutination test] (capsular polysaccharide in CSF) +ive Culture on Chocolate agar was positive DIFFERENTIAL DIAGNOSIS OF MENINGITIS : DIFFERENTIAL DIAGNOSIS OF MENINGITIS Bacterial Meningitis PMN's outnumber monocytes, papilledema occurs late in disease, acute onset. High lactate, low glucose of CSF Slide 11: 2.Parasitic Meningitis Acanthamoeba or Naegalaria species Entry via contaminated water or in children swimming in Nullahs. Acute onset, slight change in CSF chemistry, presence of IgM in CSF 90% mortality, presence of vegetative forms of amoeba on direct examination of C.S.F. 3. Viral Meningitis : 3. Viral Meningitis acute onset, slight change in CSF chemistry. Monocytes outnumber PMN's. BACTERIAL VS VIRAL MENINGITIS Predictors of bacterial etiology: CSF glucose < 34 CSF: Serum glucose ratio < 0.23 CSF protein > 220 CSF WBC count > 2000 CSF neutrophil count > 1180 [Presence of any ONE of the above findings predicts bacterial etiology with > 99% certainty] Slide 13: CHRONIC MENINGITIS (occur in Immunocompromised patients, insidious onset) 1.Tubercular Meningitis (M. tuberculosis, M. avium ) slight changes in CSF chemistry, positive tuberculin, low chloride. Slide 14: 2.Fungal Meningitis (Cryptococcus neoformans) history of lung infection, yeast cells in CSF, slight changes in CSF chemistry CHRONIC MENINGITIS : CHRONIC MENINGITIS 3. AIDS patients 4. Syphilitic Meningitis (slight change in CSF chemistry, positive RPR test) Risk groups for Meningitis : Risk groups for Meningitis Slide 18: Purulent (Bacterial) meningitisusually begins as an infection by normal body flora / colonizers of Treatment of Acute Bacterial Meningitis : Treatment of Acute Bacterial Meningitis General The risk of death during the early phases of acute bacterial meningitis usually relates to problems other than the infection itself. A combination of fever, dehydration secondary to vomiting , decreased food and fluid intake with subsequent alkalosis often predisposes patients, especially young children to seizures. Respiratory arrest or airway obstruction often follows; if significant CNS or myocardial hypoxia occurs, fatal cardiac arrhythmias or brainstem damage may result. Slide 20: Procedures commonly employed include: 1. Correction of fluid and electrolyte deficits. 2. Provision for adequate oxygenation. 3. Monitoring of cardiovascular function (Give a cardiac-active glycoside if necessary). 4. Monitoring intracranial pressure - administer urea or mannitol to reduce cerebral edema. Slide 21: Administration of antibiotics Empiric regimen ; Neonate (up to 1m) (Ampicillin + Cefotoxime) or (Ampicillin + Gentamycin) Neonate (1-3 m) (Ampicillin + Dexamethazone) or (Ampicillin + Dexamethazone + Cefotoxime) Other (3 m- 50 yrs) Cefotoxime + Vancomycin (Over 50 yrs Old or Alcoholics) Ampicillin + Cefotoxime Slide 22: Neisseria Meningitidis (Meningococci) More than 80 % of bacterial meningitis in children over 02 months is caused by Meningococci and Pneumococci . Meningococci Gp A cause epidemics of meningitis. Overall Neisseria meningitidis ranges 2nd to S. pneumoniae as a cause of meningitis, but most common cause at the ages of 2-18 yrs. Slide 23: Meningococcal meningitis has been recognized as a serious problem for almost 200 years. Meningococcal disease still is associated with a high mortality rate and persistent neurological defects, particularly among infants and young children. Neisseria Meningitidis : Neisseria Meningitidis Meningococci comprise at least 13 serogroups based on the composition of their polysaccharide capsular antigens. They differ in their agglutination reactions to sera directed against polysaccharide antigens. More than 99% of meningococcal infections are caused by serogroups A, B, C, 29E, or W-135. There is currently no vaccine to prevent group B , however there are some in the near future. Slide 25: · Virulence factors ; Polysaccharide capsule, Endotoxin, IgA protease The natural habitat and reservoir for meningococci mucosal surfaces of the human nasopharynx and, to a lesser extent, the urogenital tract and anal canal. Approximately 5-10% of adults are asymptomatic nasopharyngeal carriers. But that number increases to as many as 60-80% of members of closed populations (eg, military recruits in camps, boarding schools, dormitories, crowded living conditions, youth camps, daycares . Pathogenesis Pathogenesis : Pathogenesis Humans are the natural hosts. The mode of infection; Transmission: airborne droplets. Colonize: upper resp tract, nasopharyx. Carriers: asymptomatic chronic carriers 5 to 35%. The incubation period; averages 3-4 days (range 1-10 days), which is the period of communicability. Slide 27: INFECTION OCCURS IN THREE STAGES leading to subclinical infection 1. 2. 10-20% of cases, N. meningitidis enters the bloodstream. 3. SYSTEMIC DISEASE; appears with the development of meningococcemia and usually precedes meningitis by 24-48 hours. or joints Clinical Manifestations : Clinical Manifestations Meningitis (Inflammation of the meninges. Pathogen reach the meninges in the bloodstream or from nearby sites such as middle ear, sinuses or nasopharynx) Meningococcemia. (Its severe form is called as Water-house-Friderichen syndrome.) Slide 29: Water-house-Friderichen syndrome is characterized by high fever ,shock, widespread purpura, disseminated intravascular coagulation,& adrenal insufficiency. Acute fulminating form , patient dies in few hours of circulatory collapse due to adrenal cortical failure caused by hemorrhage into the adrenals Slide 30: Skin rashes occur in meningococcemia, with or without meningitis. From the first to the third day, at least one-third of patients with meningococcal meningitis develop petechiae, most prominently in areas subjected to pressure . Slide 31: Specimens; Blood, CSF Direct microscopy Gram staining of blood & c.s.f. Gram negative diplococci . 2.Isolation of organisms: Media: chocolate agar. Incubation: 37o c x 5% Co 2 x 24 hrs oxidase positive sugar fermentation test meningococci gonococci maltose + - glucose + + 3. Detection of capsular polysaccharide by latex agglutination test. Laboratory diagnosis Slide 32: Penicillin – G. is the treatment of choice for meningococci PREVENTION Chemoprophylaxis and immunization Rifampin is used for prophylaxis in household and other close contacts. · Vaccine contains capsular polysaccharides of group A, C, Y and W – 135 strains Effective in preventing epidemics of meningitis. Treatment: Slide 33: Other Gram negative cocci Gonococci Veillonella Consists of small anaerobic, gram-negative cocci growing in masses, they are sometimes isolated from suppurative lesions. Moraxella catarrhalis A part of normal throat flora & an occasional opportunistic cause of pneumonia. learning objectives : learning objectives Types of meningitis depending upon causative organisms. Pathogenesis of Meningococcal (pyogenic) meningitis Describe the findings of normal CSF Describe the CSF findings in different types of meningitis Interpretation of Laboratory reports in case of meningitis Treatment of meningitis Lab diagnosis of meningococcal meningitis