Meningitis encephalitis slides Dr sarfaraz
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Review of Meningitis and encephalitis particularly in poor developing countries. Please review, correct and suggest
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Meningitis encephalitis slides Dr sarfaraz
- 5. Meningitis : Inflammation of pia and arachnoid matter with/ without suppuration of CSF Encephalitis : Inflammation of brain parenchyma
- 6. INFECTIOUS NON- INFECTIOUS VIRUS ( aseptic ) NSAID ( especially ibuprofen ) BACTERIA TRIMETHOPRIM- SULPHAMETHOXAZOLE FUNGUS IV IMMUNOGLOBULINE PARASITES METRONIDAZOLE LEVAMISOLE
- 7. DISEASE USUAL CAUSES Meningitis Viral, bacterial, fungal Encephalitis Mainly viral Brain abscess Mainly bacterial
- 8. MENINGITIS FEVER , HEADACH , STIFF NECK ENCEPHALITIS ( meningo- encephalitis ) CHANGES IN MS, FOCAL SIGNS , SEIZURE BRAIN ABSCESS , SUBDURAL EMPYEMA SIMILAR TO ENCEPHALITIS
- 9. AGE GROUPS ORGANISMS Gram stain /morphology Neonate Strep. agalactiae (Gr B Strep.) E. Coli Listeria monocytogenes Gram pos. cocci Gram neg. rods Gram pos. rods …single/chain Months : 1 - 23 Strep. agalactiae E . Coli Strep. Pneumoniae Neisseria meningitidis Haemophilus influenzae Gram pos. cocci Gram neg. cocci Gram neg. coccobacilli Years : 2 - 50 N. meningitis S. pneumoniae Years : > 50 N. meningitidis S . Pneumoniae L . monocytogenes E . coli
- 10. AGE AGENTS 0 --- 2 months E.coli, Group B strep. , S . aurius , L . Monocytogenes 2 months---- 2 yrs H . Influenzae , S . Pneumoniae , N . Meningitidis 2 yrs ----- 15 + yrs N . meningitidis , S . Pneumoniae , H . Influenzae
- 11. NEONATE YOUNG ADULT OLDER IMMUNOSUP. TRAUMATIC E. Coli Strep Gr B Listeria Meningo cocci Pneumo cocci Meningo cocci Pneumo cocci Cryptococci Listeria Pneumo S. aureus Gram negative
- 18. CLASS OF VIRUS SPECIFIC VIRUS Enterovirus Polio , Echo , Coxsackie Herpesvirus HSV , VZV , EBV Paramyxovirus Mumps , Measles Togavirus Rubella Rhabdovirus Rabies Retrovirus HIV Arbovirus Japanese encephalitis B
- 19. AGE GROUPS VIRUS NEONATES HSV-2 CHILDREN & ADULTS HSV-1
- 20. Cryptococcus neoformans Candida H . Capsulatum
- 24. Free living amoebas Acanthamoeba Balamuthia Naegleria Helminthic eosinophilic meningitis
- 27. ROUTES AGENTS Hematogenous Most of them Contiguous( sinus, ear , face ) Bacteria Direct inoculation ( trauma ) Bacteria Via nerves Virus , Naegleria
- 30. Polysaccharide encapsulation of bacteria Meningococci Pneumococci H .influenzae Colonize in nasopharynx without any local or systemic reaction Viral infection May facilitate the penetration of epithelium by bacteria Polysaccharide capsule prevent opsonization thus inhibit phagocytosis
- 31. BACTERIA PATHOGENIC COMPONENT GRAM POSITIVE TEICOIC ACID GRAM NEGATIVE LIPOPOLYSACCHARIDE ENDOTOXIN
- 32. Event Effect Inflam. of spinal nerves & roots Meningeal irritation signs •Adhesive thickening..arachinoid in basal cystern •Fibrosis … aqueduct / foramina Lushka/ Magendie Hydrocephalus Thrombosis …cortical veins… necrosis of cerebral cortex Cerebral atrophy Cellular electrolyte imbalance…. Depolarization of Seizure
- 34. Inflamed meninges covered with exudates
- 36. virus Neurological affection HSV- 2 Neonates. Acute generalized necrotizing encephalitis ( with systemic infection liver adrenals etc). Neuronal spread HSV- 1 Children & adults. Localized encephalitis. Neurons & glial cells. Dormant within trigeminal and others. Neuronal spread. Togaviruses Flaviviruses Bunyaviruses Diffuse encephalitis. Largely to neurons . Hematogenous spread rabies Anterior horn cells…. CNS neurons Neuronal spread polioviruses Specific motor neuron. Neuronal spread.
- 46. PROFILE COMMON CAUSES Purulent ( PMN’s ) Low Glucose Bacterial Lymphocytic Low Glucose TB , Fungal , Spirochetal , Sarcoidosis Lymphocytic Normal Glucose Viral
- 47. PROFILE ONSET PATHOLOGY Purulent Acute ( 1- 2 days ) Pus over convexities Lymphocytic Low Glucose Subacute Granulomatous Base of Brain Cranial N. palsies ( 3rd , 7th , 8th ) Lymphocytic Normal Glucose Acute / Sub acute Mild inflammation
- 48. Broad-range bacterial polymerase chain reaction (PCR) may allow early detection of bacterial meningitis, PCR testing has clinical utility for diagnosis of enteroviral meningitis While 19 samplings using conventional cerebrospinal fluid (CSF) cultures failed to detect any organisms, fungal DNA was identified in the CSF by a new polymerase chain reaction (PCR)-based method.
- 51. In Neonates Ultrasonic brain examinations helps early changes in hydrocephalus.
- 52. PATHOGENS ANTIBIOTIS DURATION S . pneumoniae Vancomycin + ceftriaxone OR Cefotaxime 14 DAYS N . meningitiditis Penicillin G 7 DAYS H . Influenzae Ceftriaxone OR Cefotaxime 7 DAYS L . monocytogenes Ampicillin Penicillin G Gentamycin Group B streptococci Penicillin G 2 – 4 WEEKS Enterobacteriaceae Ceftriaxone OR Cefotaxime + gentamycin 3 WEEKS Pseudomonas Ceftazidime 21 DAYS
- 55. Dexamethasone : Currently, it is indicated for children with suspected meningitis who are older than 6 weeks and is recommended for treatment of infants and children with H influenzae B meningitis. >2 years: 0.15 mg/kg IV, at or before first antibiotic dose, then q6h for 4 d. No benefit N. meningitidis
- 56. Suspected organism Prophylactic medication. H. influenzae Rifampicin N.meningitidis Rifampicin, Penicillin, Co-tmz, Macrolids, Ceftriaxone, Ciprofloxacin S. pneumoniae Rifampicin, penicillin
- 57. N. meningitidis Quadrivalent vaccine ( A , C , Y , W 135 ) S . pneumoniae 23 valent vaccine H. influenzae Type B ( Hib) conjugate vaccine H . Influenzae type B + Streptococcus pneumonia Conjoint vaccine Japanese encephalitis
- 58. MOSQUITOES / TICKS CONTROL WARM BLOODED RABID ANIMAL/ ANIMAL VACCINATION MIGRATING BIRD WATCH
- 59. Meningitis vs Encephalitis ……. MS changes CSF Profile Purulent : Big 3(N meningitidis, S pneumoniae, H influenzae ) Lympho , Low Glu : Brain base , Cranial N. , Most treatable , Remember TB Lympho , Nrm Glu : Viral Risk groups : Age , immunosuppression The CSF is poorly equipped to control infection …. because type-specific antibodies do not penetrate the blood brain barrier well and complement components are absent or in low concentrations. Viral meningitis is the most common infection of the CNS
- 60. SEPTICEMIA MENINGITIS Hypotension Cyanosis Impaired consciousness in children Raised intra cranial pressure • increased BP • decreased pulse rate • rapid deterioration of consciousness • pupils dilated , unequal & poorly reacting •Tense fontanelle
- 61. Japanese encephalitis B reported vector is culex mosquito Do not miss HSV encephalitis , which has highly effective treatment
- 62. A recent case described a 7-week-old infant with P multocida meningitis after exposure to dog saliva with no wound, emphasizing the need to protect young children from this pathogen Salmonella meningitis should be suspected in any child with this organism grown at any other site in an unwell child or one younger than 6 months. Mothers known to be infected with Salmonella during pregnancy may put their child at risk. As therapy is different for Salmonella meningitis, while rare, it must be considered in the above situations. Antibiotic therapy causes a significant release of mediators of inflammatory response.
Editor's Notes
- Anatomy and site of infection of the brain and spinal cord.
- Levamisole is used in the treatment of colon cancer. The etiology of aseptic meningitis caused by drugs is not well understood. This form of meningitis is infrequent in the pediatric population.
- The frequency of Hib infections in patients with asplenia, splenectomy, sickle cell disease, malignancies, and congenital or acquired immunodeficiencies is higher than in individuals without these conditions.
- In general, Hib infections are rare in patients older than 6 years because of the acquisition of secondary immunity; however, immunocompromised individuals remain susceptible.
- Major causes of acute meningitis (all ages, worldwide). "Other" viruses include herpes simplex virus type 2, arthropod-borne viruses, Epstein-Barr virus, influenza virus, and measles virus, as well as infections caused by Mycoplasma pneumoniae, M tuberculosis, Leptospira, fungi and rickettsiae that may be difficult to differentiate from viral meningitis.
- Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic diplococcus aerotolerant anaerobe. Both H. influenzae and S. pneumoniae can be found in the upper respiratory system of humans. A study of competition in a laboratory revealed that, in a petri dish, S. pneumoniae always overpowered H. influenzae by attacking it with hydrogen peroxide and stripping off the surface molecules that H. influenzae needs for survival.
- H. influenzae was mistakenly considered to be the cause of influenza until 1933, when the viral etiology of the flu became apparent. Still, H. influenzae is responsible for a wide range of clinical diseases. It is a non-motile Gram-negative coccobacillus first described in 1892 by Richard Pfeiffer during an influenza pandemic.
- It is known that meningococci only infects human and never been reported from animals because the bacterium cannot get iron other than human source (transferrin and lactoferrin)[3] and it exists as normal flora in the nasopharynx of up to 40% of adults. It causes the only form of bacterial meningitis known to cause epidemics.
- It is a gram negative bacterium that is commonly found in the lower intestine of warm-blooded animals. E. coli is Gram-negative, facultative anaerobic and non-sporulating. Virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for hæmolytic-uremic syndrome (HUS), peritonitis, mastitis, septicemia and Gram-negative pneumonia.
- Studies suggest that up to 10% of human gastrointestinal tracts may be colonized by L. monocytogenes. Due to its frequent pathogenicity causing meningitis in newborns (acquired transvaginally), pregnant mothers are often advised not to eat soft cheeses such as Brie, Camembert, feta and queso blanco fresco, which may be contaminated with and permit growth of L. monocytogenes.[3] It is the third most common cause of meningitis in newborns. Its ability to grow at temperatures as low as 0°C permits multiplication in refrigerated foods. In refrigeration temperature such as 4°C the amount of ferric iron promotes the growth of L. monocytogenes.
- Most aseptic meningitis . Culex as vector to transmit arbovirus from domestic pigs and birds. Major viral causes are enteroviruses, mumps virus and lymphocytic choriomeningitis virus. Many viruses, including enteroviruses, mumps, and lymphocytic choriomeningitis viruses, cause mild forms of encephalitis. Life-threatening viral encephalitis is due primarily to herpes simplex viruses and arboviruses.
- In neonates, the disease is predominantly due to HSV-2 virus, and irrespective of serotype, the acute generalized necrotizing encephalitis is often accompanied by evidence of systemic infection of the liver, adrenals, and other organs. In children and adults, however, encephalitis is caused by HSV-1 virus and is usually localized.
- High risks in AIDS , immunodeficient , immunosuppresed
- THIS YEAST CROSS BBB WHILE ENCLOSED WITHIN MACROPHAGES / MONOCYTES
- Cryptococcus neoformans is an encapsulated yeast-like fungus that can live in both plants and animals
- H. capsulatum grows in soil and material contaminated with bat or bird droppings. Spores become airborne when contaminated soil is disturbed. Breathing the spores causes infection.
- Infrequent , life threatening , in underdeveloped states , parasites found in water, food and soil
- Free-living amebae belonging to the genera Acanthamoeba, Balamuthia, and Naegleria are important causes of disease in humans and animals. Naegleria fowleri produces an acute, and usually lethal, central nervous system (CNS) disease called primary amebic meingoencephalitis (PAM). Trophozoites infect humans or animals by entering the olfactory neuroepithelium and reaching the brain. N. fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while flagellated forms are found in CSF. Acanthamoeba spp. and Balamuthia mandrillaris are opportunistic free-living amebae capable of causing granulomatous amebic encephalitis (GAE) in individuals with compromised immune systems. B. mandrillaris however, has not been isolated from the environment but has been isolated from autopsy specimens of infected humans and animals. The trophozoites are the infective forms and are believed to gain entry into the body through the lower respiratory tract, ulcerated or broken skin and invade the central nervous system by hematogenous dissemination .
- Acanthamoeba in brain tissue
- Naegleria ( free living amoeba )
- Most agents invade from blood. Bacteria grow rapidly in cerebrospinal fluid; viruses infect meningeal and ependymal cells.
- The most common causative organisms (eg, N meningitidis, S pneumoniae, H influenzae) contain a polysaccharide capsule that allows them to colonize the nasopharynx of healthy children without any systemic or local reaction. A concurrent viral infection may facilitate the penetration of the nasopharyngeal epithelium by the bacteria. Once in the bloodstream, the polysaccharide capsule allows the bacteria to resist opsonization by the classical complement pathway and, thus, inhibit phagocytosis.
- In the gram-positive bacteria, teichoic acid is considered the major pathogenic component. In gram-negative bacteria, lipopolysaccharide or endotoxin is the major pathogenic component.
- Autopsy: Brain surrounded by pus (the yellow-greyish coat around the brain, under the dura lifted by the forceps), the result of bacterial meningitis. A brain autopsy demonstrating signs of meningitis. The forceps (center) are retracting the dura mater (white). Underneath the dura mater are the leptomeninges, which appear to be edematous and have multiple small hemorrhagic foci(red).
- Marked in Pneumococcal meningitis
- This is an inferior view of a brain infected with Gram-negative en:Haemophilus influenzae bacteria. In the U.S. and other industrialized countries, more than 50% of H. influenzae serotype b cases present as en:meningitis with fever, headache, and stiff neck. 3%-6% of cases are fatal; up to 20% of surviving patients have permanent hearing loss.
- The pathogenesis of encephalitis due to herpes simplex virus, arboviruses, and rabies virus is different for each virus. In neonates, the disease is predominantly due to HSV-2 virus, and irrespective of serotype, the acute generalized necrotizing encephalitis is often accompanied by evidence of systemic infection of the liver, adrenals, and other organs. In children and adults, however, encephalitis is caused by HSV-1 virus and is usually localized. This virus, which is acquired in childhood, remains latent within the trigeminal and other ganglia. It may reactivate to cause cold sores. Encephalitis in an immune host results either from the entry of a new virus, possibly across the olfactory mucosa, or from reactivation of latent virus in the trigeminal ganglia, which spread along sensory nerve fibers to the base of the anterior and middle fossa. In either case, infection is localized to the orbital frontal and medial temporal lobes. Because the host is immune, virus presumably spreads from cell to cell over a contiguous localized area, infecting neurons and glial cells. In contrast, arboviruses (mainly togaviruses, flaviviruses, and bunyaviruses) spread to the brain from the blood. The encephalitis is diffuse, but is localized largely to neurons. Rabies, in contrast, is usually acquired through the bite of a rabid warm-blooded animal. This virus spreads by axonal transport from the inoculated skin or muscle to the corresponding dorsal root ganglion or anterior horn cells and then to populations of neurons throughout the CNS. The early involvement of neurons of the limbic system cause the typical behavioral changes of clinical rabies. Polioviruses also show a selective infection of specific motor neuron populations which explains the asymmetrical flaccid motor paralysis of poliomyelitis.
- Herpes encephalitis is a fulminant necrotizing infection localized to temporal lobes. The space between cells in the brain parenchyma is too small to permit passage even of a virus. However, tetanus toxin and some viruses travel through the CNS by axoplasmic flow.
- This coronal section focuses on the cingulate gyrus showing patchy hemorrhagic necrosis in a case of herpes simplex encephalitis.
- Besides doing all routine blood investigations,blood gases, urine , stool analysis and chest x-ray look specially source of infection . Don’t forget drugs history. PCR..polymerase chain reaction genetic detection.
- Cerebrospinal fluid findings are critical in differential diagnosis. Viruses, such as enteroviruses and mumps virus, can be grown from the CSF, but this requires special viral cultures.
- CT scan : multiple cystic lesions. Many are calcified. Typical of neurocysticercosis. Among about 20 helminths that can cause neurologic disorders, the pork tapeworm Taenia solium causes by far the most cases in the Western Hemisphere. The resulting disorder is neurocysticercosis
- The CT findings of bacterial meningitis are commonly nonspecific and even normal in the majority of cases.
- Infants younger than 30 days, ampicillin and an aminoglycoside or a cephalosporin (cefotaxime) are recommended. Children 30-60 days old, ampicillin and a cephalosporin (ceftriaxone or cefotaxime) can be used. Since S pneumoniae occasionally occurs in this age range, vancomycin should be considered instead of ampicillin. In older children, a cephalosporin (eg, cefotaxime, ceftriaxone) or ampicillin plus chloramphenicol can be used. Cefotaxime (Claforan) Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms. Arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. Ceftazidime (Fortaz) Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins. Ceftriaxone (Rocephin) Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins. Gentamicin (Garamycin) Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Chloramphenicol (Chloromycetin) Not used frequently since introduction of third-generation cephalosporins. Binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria. Vancomycin (Vancocin) Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci.
- Cryptococcal meningitis should be treated for two weeks with intravenous Amphotericin B 0.7–1.0 (mg/kg)/day and oral flucytosine 100 (mg/kg)/day (or intravenous flucytosine 75 (mg/kg)/day if the patient is unable to swallow). This should then be followed by oral fluconazole 200mg daily for ten weeks[4] and then 200 mg daily until the patient's CD4 count is above 100 for three months and, if infected, his HIV viral load is undetectable.[5][6]
- Brain damage in meningitis is caused not only by bacteria but probably more by host responses. These responses have a protective purpose (to eliminate bacteria) but are excessive and indiscriminate and set in motion destructive cascades that damage everything in their way, mostly host tissues. Modulating these reactions, in addition to killing bacteria, can reduce the morbidity and mortality of meningitis.
- No indication for prophylaxis of pneumococcal meningitis. Ceftriaxone is safe in pregnancy.
- The incidence of Hemophilus influenzae and Streptococcus pneumoniae meningitis in children has decreased significantly after the introduction of conjugated vaccines against these organisms. Jap encph…The usual schedule is three injections of this vaccine. The second dose is given seven days after the first. The third dose is given 28 days after the first. Full immunity takes up to a month to develop. The course of injections should be completed at least two weeks before departure. So, you should see your practice nurse well in advance of your travel date. Children between one and three years should receive half the adult dose.