Neonatal Meningitis.pptx

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1. Neonatal Meningitis DR. Magdy Shafik Senior Pediatric and neonatology Consultant Diploma, M.S , Ph.D of Pediatrics

2. Outline 1- introduction 2 - Etiology 3- Epidemiology 4- Clinical Presentation 5- Case definition by MOH 6- Complications 7- Laboratory Studies and Radiological investigation 8- case presentation 9- Prevention 10- vaccination for meningitis

3. Although the occurrence of neonatal meningitis is uncommon , it remains a devastating infection with high mortality and high morbidity . Neonatal meningitis is often caused by group B streptococcus  Despite the development of effective vaccines, useful tools for rapid identification of pathogens and potent antimicrobial drugs, neonatal meningitis continues to contribute to neurological disability worldwide

4. The persistence of neonatal meningitis results from increases in the numbers of infants surviving premature delivery. In addition, the absence of specific clinical findings makes diagnosis of meningitis more difficult in neonates than in older children and adults. Moreover, a wide variety of pathogens are seen in infants as a consequence of the immaturity of their immune systems and intimate exposure to possible infection from their mothers .

5. Etiology Common bacterial pathogens group B streptococci (GBS ) are the most commonly identified causes of bacterial meningitis, implicated in roughly 50% of all cases [ 5 ]    . Escherichia coli accounts for another 20% [ 6 ] .  Listeria monocytogenes is the third most common pathogen, accounting for 5–10% of cases ;  [ 6 ] .  Studies suggest that in underdeveloped countries , gram-negative bacilli—specifically,  Klebsiella organisms and E coli —may be more common than GBS [ 7 ] 

6. Epidemiology   The incidence of neonatal meningitis is estimated to be 0.3 per 1000 live births, as observed in the United States , Sweden, The Netherlands, England, and Wales. [4 Reported estimated incidences of neonatal meningitis that ranged from 0.48 per 1000 live births in Hong Kong to 2.4 per 1000 live births in Kuwait . [7]

7. Neonatal Meningitis Clinical Presentation Signs and symptoms of neonatal meningitis are often subtle , making diagnosis difficult that leads to morbidity. Clinical signs of the infection are including but not limited to: Fever or hypothermia Irritability or lethargy Hypotonia Feeding intolerance or vomiting Respiratory distress Apnea Bradycardia Hypotension Poor perfusion Seizures Bulging anterior fontanel Nuchal rigidity Jaundice Hypo- or hyperglycemia Diarrhea

8. Detection of neonatal meningitis is often late , with signs such as nuchal rigidity, bulging anterior fontanel, and convulsions . These symptoms are a predictor for a poor prognosis for the infant . In evaluating a neonate for meningitis, the following 3 key points should be kept in mind: It is important to remain vigilant for maternal infection “setups” ( eg , prolonged rupture of membranes, fever, and chorioamnionitis) while remembering that asymptomatic maternal infection is always a possibility even with screening Early-onset and late-onset bacterial infections have distinctive clinical courses (see below) In herpes simplex virus (HSV) infections, the presence of skin lesions in a meningitic neonate is the exception rather than the rule cluding severe neurological impairments. 

9. Brudzinski sign (hip & knee flexion with neck movement)  Kernig sign (extend knee with hip flexed) The sensitivity and negative predictive value o f Kernig and Brudzinski sign is low in the diagnosis of meningitis and therefore do not contribute to the diagnosis of bacterial meningitis

10. Case definition : suspected case: fever of 38 or more plus one or more of the following: 1- neck stiffness 2– bulging fontanel in children below 2 years

11. Probable case: suspected case with turbidity of C.S.F which means: cells ↑ 80 / m3 protein ↑100 /dl sugar ↓ 40 / dL plus one or more of the following: 1- Gm staing show : - ve : N. meningiococcal (+ Epedmic ) - H.infulnza b + ve : pneumocci 2- antibodies in C .S .F by( latex antigen detection )

12. Confirmed case : confirmed by lab. : 1- C.S. F culture 2- P.C.R

13. Bacterial meningitis Early onset in the first 48 hours of life temperature instability, episodes of apnea or bradycardia, hypotension, feeding difficulty, hepatic dysfunction, and irritability alternating with lethargy. [1]  Respiratory symptoms can become prominent within hours of birth in group B streptococcal (GBS ) infection; however, the symptom complex also is seen with infection by E coli or Listeria species.

14. Late-onset bacterial meningitis  onset after 48 hours of life) associated with neurological symptoms . stupor and irritability, more than 75 % of affected neonates. Between 25% and 50% of neonates will exhibit the following neurological signs: Seizures Bulging anterior fontanel Extensor posturing or opisthotonos Focal cerebral signs including gaze deviation and hemiparesis Cranial nerve palsies Nuchal rigidity is the least common sign in neonatal bacterial meningitis, occurring in fewer than 25% of affected neonates.  [ 1

15. HSV meningitis Early features of HSV meningitis may mimic with bacterial meningitis, including pallor, irritability, high-pitched cry, respiratory distress, fever, or jaundice, progressing to pneumonitis, seizures, hepatic dysfunction, and disseminated intravascular coagulopathy (DIC). [16]

16. Complications cerebral edema, hydrocephalus , hemorrhage , ventriculitis (especially with bacterial infection), abscess formation, and cerebral infarction . Cerebral edema , hydrocephalus, and hemorrhage each may cause increased intracranial pressure, with potential for secondary ischemic injury to the brain because of decreased brain perfusion : Cerebral edema results from vasogenic changes, cytotoxic cell injury , and, at times, inappropriate antidiuretic hormone (ADH) secretion Hydrocephalus results from debris obstructing the flow of cerebrospinal fluid (CSF) through the ventricular system or from dysfunction of arachnoid villi; it occurs in as many as 24% of neonates with bacterial meningitis [22] Hemorrhage occurs in regions of infarction or necrosis and should be suspected in a neonate with new focal neurological findings or clinical deterioration

17. Ventriculitis results in sequestration of infection to areas that are poorly accessible to systemic antimicrobial drugs . Inflammation of the ependymal lining of ventricles often obstructs CSF flow. Thus, all of these complications are interactive, making effective management difficult. Ventriculitis occurs in as many as 20% of infected neonates . [23]  Failure to respond to appropriate antibiotic therapy and signs of elevated intracranial pressure (ICP) may suggest the diagnosis. [24]  Intraventricular administration of antibiotics may be necessary in cases of ventriculitis.

18. Cerebral abscess occurs in as many as 13% of neonates with meningitis. [22]  New seizures, signs of elevated ICP , or new focal neurological signs suggest the diagnosis. Brain imaging with contrast is essential for making the definitive diagnosis. Surgical intervention may be required.

19. Cerebral abscess occurs in as many as 13% of neonates with meningitis. [22]  New seizures, signs of elevated ICP , or new focal neurological signs suggest the diagnosis. Brain imaging with contrast is essential for making the definitive diagnosis. Surgical intervention may be required.

20. Cerebral infarction , both focal (arterial) and diffuse (venous), may complicate recovery. Autopsy studies have found evidence of infarction in 30-50% of specimens studied. [1]  Imaging studies suggest that the actual incidence of infarction may be even higher. [25]  Meningitis has been shown to be associated with 1.6% of all cases of neonatal arterial stroke and 7.7% of venous infarcts . [26] Necrotizing lesions secondary to HSV meningitis can be deleterious to the developing brain.

21. longer-term complications that may develop include residual epilepsy , cognitive impairment , hearing loss , visual impairment, spastic paresis , and microcephaly. Some of these disorders may be difficult to detect during infancy. Hearing , for example, is difficult to evaluate without the child’s cooperation, and even then, assessment may be limited to behavioral response to sounds. Brainstem auditory evoked response (BAER) testing does not evaluate all dimensions of hearing, but this test, which can be performed reliably in sedated infants, only slightly overestimates hearing loss, which occurs in 30% of survivors of bacterial meningitis and 14% of survivors of nonbacterial meningitis. [27] Subtle impairment of sound discrimination may not be readily apparent.

22. Long-Term Monitoring Because of the potential for hearing loss, neonates with meningitis should undergo brainstem auditory evoked response (BAER) testing at 4-6 weeks after discharge. [40]  Survivors of neonatal meningitis require long-term surveillance not only for disorders of hearing but also for disorders of vision, motor, or cognitive function. Developmental delay is a frequent complication of neonatal meningitis. Early intervention services should be employed to maximize developmental gains

23. cognitive impairment may not be evident until the child has started school or advanced into higher grades where more complex analysis of information is necessary. [20]  Careful screening for neurological, cognitive, and developmental deficits must be conducted as part of routine pediatric care over a period of many years , and the responsible physician should be attentive to possible problems with perception, learning, or behavior that may result from neonatal infection.

24. Laboratory Studies Lumbar Puncture Lumbar puncture  is indicated for evaluation of the CSF in all neonates suspected of having sepsis or meningitis, even in the absence of neurological signs. Many clinicians are reluctant to perform this procedure on a critically ill infant. Although the theoretical complications of lumbar puncture include trauma, brain-stem herniation, introduction of infection, and hypoxic stress, none of these complications were reported in a meta-analysis of more than 10,000 infants who underwent lumbar puncture. [29] .

25. Meningitis, however, increases the risk of death in neonates. Stoll et al reported a mortality of 23% in babies with CSF-proven meningitis, compared with a mortality of 9% in neonates whose lumbar puncture results were not consistent with meningitis. [35]  Additionally, many infants who had negative blood cultures had positive CSF cultures , suggesting that cases of meningitis may be missed. In cases of bacterial meningitis, repeat lumbar puncture should be performed 24-48 hours after initiation of therapy to ensure sterilization of the CSF. After a full course of therapy for PCR-proven HSV, repeat lumbar puncture should be undertaken to rule out incompletely treated infections

26. It should be kept in mind that interpretation of CSF findings is more difficult in neonates than in older children , especially in premature infants whose more permeable blood-brain barrier causes higher levels of glucose and protein. The number of white blood cells (WBCs ) found in the CSF in healthy neonates varies according to gestational age .1 The classic finding of decreased CSF glucose , elevated CSF protein, and pleocytosis is seen more with gram-negative meningitis and with late gram-positive meningitis ; this combination also is suggestive of viral meningitis, especially HSV.

27. Many authors use a cutoff value of 20-30/µL . Bacterial meningitis commonly causes CSF pleocytosis greater than 100/µL, with predominantly polymorphonuclear leukocytes (PMNs) gradually evolving to lymphocytes. In neonates with viral meningitis , the picture may be similar but with a less dramatic pleocytosis. HSV meningitis may be particularly associated with a large number of red blood cells (RBCs) in the CSF . If the mother is symptomatic, maternal investigation may be warranted; bacterial or viral cultures can provide valuable adjunctive information.

28. Polymerase chain reaction (PCR) assay is a powerful diagnostic tool with excellent sensitivity and specificity . It permits identification of group B streptococcal ( GBS) antigen in urine or CSF , and it is the standard for identification of herpes simplex virus (HSV) and enterovirus in CSF . In neonates, PCR is 71-100% sensitive for HSV but 98-99% specific. [16

29. Magnetic Resonance Imaging Magnetic resonance imaging (MRI) is the neuroimaging modality of choice for identifying focal areas of infection, infarction , secondary hemorrhage, cerebral edema, hydrocephalus, or, rarely, abscess formation. Sinovenous occlusions, ventriculitis, and subdural collections are best diagnosed with MRI. Follow-up MRI scans are useful for following the resolution of the infection, as well as for contributing to prognostication. If available, magnetic resonance spectroscopy can add important information on the metabolic function of the neonatal brain. Several studies have documented periventricular white matter abnormalities on MRI in infants with neonatal meningitis. [31]  Newer MRI technologies, including diffusion-weighted and diffusion tensor imaging, have allowed this association to be evaluated in more detail, and such evaluation may prove to have prognostic implications.  [ 32 ]

30. MR Angiography (MRA) In magnetic resonance angiography (MRA), a powerful magnetic field, radio frequency waves and a computer are used to evaluate blood vessels and help identify abnormalities1 Magnetic Resonance Venography (MRV) An MRV uses magnetic resonance technology and intravenous (IV) contrast dye to visualize the veins . Contrast dye causes the blood vessels to appear opaque on the X-ray image, allowing the physician to visualize the blood vessels being evaluated.

31. Other Imaging Modalities (CT ) carries the risk of exposing the neonatal brain to radiation, the rapidity and ease with which it can be obtained (in comparison with MRI) makes it useful in decision-making for potential neurosurgical interventions, such as ventriculostomy for hydrocephalus or surgical drainage of empyema or abscess . It may be particularly appropriate for a critically ill neonate being considered for neurosurgery. Cranial ultrasonography provides an alternative imaging modality for critically ill neonates , but it does not provide optimal detail in all circumstances. However, it is a low-risk and thus is useful in monitoring ventricular size for hydrocephalus during the acute phase of meningitis. Chest radiography provides important information about the lung parenchyma and the cardiac silhouette. Meningitis or sepsis may occur with pneumonia but may be indistinguishable from surfactant deficiency, pulmonary hypertension, and obstructive cardiac disease.

32. Electroencephalography (EEG) is not an essential part of the initial diagnostic process. However, in neonates who are unresponsive or have seizures presenting as episodes of apnea, bradycardia, or rhythmic focal movements, EEG monitoring provides useful information to guide treatment with anticonvulsant drugs. EEG also has some prognostic utility

33. Neonatal Meningitis Treatment & Management early initiation of antimicrobial drugs is essential Aggressive antimicrobial intervention is lifesaving in neonates with suspected meningitis. \Because distinguishing viral from bacterial meningitis is difficult early in the clinical course, a combination of agents is often necessary, providing coverage for both types of infection. The duration of therapy for bacterial and herpes simplex virus (HSV) meningitis with an appropriate agent is typically 14-21 days Although there is a consensus that acyclovir is the preferred antiviral therapy, there remains some disagreement with respect to what constitutes optimal antibacterial therapy.

34. The choice of an antibiotic regimen should be based on the likely pathogen , the local patterns of antibacterial drug sensitivities , and the policies of the hospital. Corticosteroids have been shown to reduce long-term sequelae, particularly hearing loss, in older infants with  Haemophilus influenzae type B meningitis and S pneumoniae infection. However, use of corticosteroids is not recommended for neonates with meningitis management of seizures is a common challenge in neonates with meningitis. Phenobarbital and phenytoin remain the current drugs of choice, with benzodiazepines utilized as adjunctive therapy

35. Assessment of response to therapy Lumbar puncture , should be repeated 24-48 hours after the initial study to monitor the course of the infection and guide further treatment decisions. If the patient has persistent infection in the lumbar CSF or clinical deterioration that is not explained by other complications, imaging studies to investigate for abscess formation should be performed. A diagnostic tap of the lateral ventricle should be considered to assess for ventriculitis if no focal abscess is noted on imaging. Ventriculitis may occur, especially with gram-negative bacteria , in the absence of pleocytosis in the lumbar CSF or with sterile CSF.

36. infants with partially treated bacterial meningitis should be managed on a case-by-case basis in accordance with their clinical presentation . These infants should be observed for at least 48 hours after treatment is discontinued. C-reactive protein levels can be useful in identifying the presence of a systemic anti-inflammatory response and can be used serially to track the response to treatment.

37. Ventriculostomy Ventriculostomy with external drainage may be required in cases where acute hydrocephalus develops secondary to obstruction of CSF flow. Administration of intraventricular antibiotics is recommended in cases of ventriculitis, but is no longer recommended as a routine treatment for gram-negative meningitis

38. Prognosis 25-50% have significant problems with language, motor function, hearing, vision, and cognition [18, 3] ; 5-20% have future epilepsy . [19, 20] Survivors are also more likely to have subtle problems, including visual deficits, middle-ear disease, and behavioral problems. [21] As many as 20% of children identified as normal at 5-year follow-up may have significant educational difficulties lasting into late adolescence. [18]

39. case presentation En Rawan Saad Esmaail , from Dareen Villlage , Dakhalia governement , F.T . B.OB 16-3-2022 , C.S , admiited to AL- Rawada NICU (private hospital ) because of respiratory distress grade IV since birth . NO maternal history of D.M or HTN OR PROM . By examination : wt 3.1 kg , chest show diminished air entery for which baby put on M.V for 7 days , then HFNC then NC . on 28/3/2022 baby transferred to Nabrou NICU, ON examination , baby was moderate general condition , chest : diminished air entry ,fine chest crepitation was improved by nebulization, heart :no murmur , CNS: fontanelle at level , intact reflexes there was oedema lower limb feeding : 15 ml Ryle /3h

40. antibiotic given in private NICU was: Unasyn - cefotax then shifted to vancomymcin - meronam then Tavanic - zithero . investigation done on day of transfer was: CBC: HB: 9 , WBC:9.2 , PLT 18 S. CR 0 .6 CRP 172 , blood culture was taken on30/3/2022: new born poor activity, weak reflexes , bad general condition , baby developed convulsions for which epanutin was given as loading dose then maintenance . packed RBS , plasama , plt was infused . feeding :NPO Antibiotic : levo - Vanco - Meronam neublization with farcolin , atrovent , plumocort on 31-3-2022: new born poor activity, weak reflexes , bad general condition , fits continue , A.F bulging , there was neck rigidity and opisthotonos , tem . 39.5 , we add somoni Leta as loading then maintaince to epanuotin

41. Antibiotic : levo - Vanco - Meronam strat 2ml full term forumla /3 h by Ryle on HFNC , neublization with farcolin , atrovent , plumocort L.P was taken and sent for Lab ON 1/4/2022 Antibiotic : levo - Vanco - Meronam epanutoin - Somonilta + CA on HFNC , neublization with farcolin , atrovent , plumocort NPO 2/4/2022 NO more convulsion on epanuotin and somonilta Antibiotic : levo - Vanco - Meronam neublization with farcolin , atrovent , plumocort NPO on NC

42. C.S.F reprt : chemical examination: Ref.Range protein : 230 mg/dl (high) (15.0 - 45.0 ) white blood cells : 150.00 cmm (high) (up to 50.00) RBCs : over 100 / HPF ( 0-1 ) Choloride :107 mEq/L (110 -130 ) LDH : 84 U/L (Less than 20 ) ADA : 7.8 U/L ( up to 50 U/L )

43. 3/4/2022: NO more convulsion on epanuotin and somonilta c ontiue same treatment CBC: HB: 10.8 , WBC :6.9 , plt 38 , CRP 96 4/4/2022: CBC: HB: 12.2 , WBC :11.1 , plt 42 . 5 and 6 /4 /2022 same treatment 7/4/2022 full anterior fontanelli , good reflexes , opthitonous , limitation of movement of lower limb stop epanutoin , only sommonilta stop levofloxacin , antibiotic given was vancom . + Meronaum + Tazocin feeding : 15 ml ryle with 5 ml increase /3h

44. CBC : HB: 10.6 , WBC :13 , plt 35 , CRP 96 one unit of plalteltes was transfused and Vitammin K was given for 3 days 8/4/2022 feeding : 45 ml ryle /3h antibiotics : tazocin - vanco - meronam one unit of plalteltes was transfused and Vitammin K 9/4/2022: stiffeness of both lower limb , more arching of the back CBC : HB: 10.6 , WBC :7.2 , plt 38 , CRP 96 , Na 133, K 4.6 one unit of plalteltes was transfused and Vitammin K 11/4/2022 baby very poor activity , severe limitation of movement of both left hip and knee with arching of the back

45. Blood Culture , hip and knee US and MRI brain was requasted CBC : HB: 7.9, WBC :15.6 , plt 95 packed RBS was given 12/4/2022: red urine discoulouration , S. cr 0.3 feeding : feeding : 60 ml ryle /3h 13/4/2022: feeding as desire CBC : HB: 14.1 , WBC :26 , plt 213 , CRP 96 14/4/2022: open O2

46. 15/4/2022: poor activity , paracetamol infusion given for elevated body temperature . stop vancomymcin as it was taken 18 days , we add Diphlocan as mainintance therpy for proloned course of antibiotic antibiotics : Tazocin-Targocid - Meronam to follow up head circumference daily 17/4/2022 : BL. Cult. result : candidiasis S. Cr 0.5 ulcer of the left foot 18/4/2022 CRP : 48

47. MRI Brain show multiple bilateral subacute brain infarcts Diffuse brain atrophy

48. Knee US normal both RT and LF knee

49. Hip US LF hip joint septic arthritis

50. 19/4/2022: till 22/4 S.cr 0.4 , CBC: HB: 9.9, WBC :15.1 , plt 142 baby off O2 , feeding as desire ,lf hip, lf shoulder septic arthritis , improved arching of the back .still hypertonic chest: mild wheezes Drugs : Tazocin-Targocid - Meronam, diphlocan, phenobaribitone , Nebulization /6h 23/4/2022: S.cr 0.4 , CRP 48 Duration of drugs : Tazocin 19 day-Targocid 8 days - Meronam 25 day , diphlocan 11 day , phenobaribitone ( till discharge ), epanuotin 7 days , vancomycin 18 day , levo 8 days Diagnosis: N. Sepsis,left hip and shoulder septic artheritis , N.meningitis , subacute multiple brain infarct , N. Candidiasis

51. 0n 24/4/2022: We consultation from Aswan University Hospital by Tellimedicine avaible in our hospital which they cosult us to do: 1- antibiotics: change to ciprofloxacin , linozolid, Fortum . 2 -I.V.IG for 2 days 3- no plasma infusion as it increase sepsis 4- breast feeding is essential for the baby 5- repeat L.P for follow up now 6- newborn must be still isolated till CRP decease at least 12 7- follow up of platellts because of linozolid 8- baby must be consulted by ped. orthopedic , ped. neurology . ped ophalomologest and E.N.T .

52. 25/4- 1/5/2022: CBC: HB: 9.8 WBC :16.8 , plt 158 . CRP 48 baby off O2 , feeding as desire , lf hip, lf shoulder septic arthritis , improved arching of the back .still hypertonic chest: mild wheezes Drugs : ciprofloxacin , linozolid , Fortum, diphlocan , phenobaribitone , Nebulization /6h I.V.IG : 2.5 gm in 50 ml ( 2 times 24 hour apart )1

53. 1/5/20221 Second LP sample CSF was clear

54. 3/5- 4/5 /2022 1 ESR : 1 ST h 30 Drugs : ciprofloxacin day 11, linozolid day11, Fortum day 11, diphlocan 22, phenobaribitone (still) We consultation from Aswan University Hospital by Tellimedicine who advised us to discharg the baby for consultation of ped. orth. ped. neuro and MRI brain for follow up of postmeninigitc sequale of brain infarct . 5/5/2022: baby discharged with moderate condition medication of discharge : Averozolid syrp ., suprax susp. , germnia drops, l-carnitine drops, vi drops

55. Follow up after discharge : On Saturday 7/5/2022: Newborn went to pediatric orthopedic who advised to do US of left shoulder

56. On 8/5/2022 pediatric neurological consultant

57. 0N 11/5/2022 By consultation of prdiatri nurologist from BENI SEOF University Hospital : who advisesd us to : MRA ( Brain angiography) to detect any arterial thormosis MRV ( Magnetic Resonance Venography (MRV ) to detect ventriculits to do ECHO to continue phenobarbitone syrp till 6 months without convuslion , if it occurs change to tritam and do EEG TO strat physioyherpy

58. 0n 15/5/2022 : MRA , of cerebral arteries ( internal carotid , anterior and middle cerebral and basilar ) show Normal course, caliber and flow . MRV: Normal all parts of the venous drainage system of the whole brain , no signs of inflammation or disturbed flow. Commentary axial images of the brain revealed : Reduction of the area of brain atrophy . There are areas of hyperdensity ?? Suggesting area of calcification at the sites of brain infarction .

59. Prevention The use of intrapartum antibiotic prophylaxis in pregnant mothers who are positive for group B streptococcal (GBS) colonization on screening or have risk factors for GBS colonization has reduced the incidence of neonatal early-onset GBS meningitis from approximately 1.8 cases to 0.3 cases per 1000 live births. [9]  Screening and risk factor assessment should be included universally in routine prenatal care. Cesarean delivery decreases , but does not eliminate, transmission of HSV from the mother’s genital tract to the neonate in cases of known infection. Suppressive antiviral therapy for HSV-infected women during the third trimester may prevent recurrent infectious episodes and thereby minimize the infant’s exposure to the virus during delivery. [16]

60. Diet Listeria monocytogenes and Escherichia coli are bacteria found in contaminated foods that can cause neonatal meningitis. [43]  By avoiding certain foods and safely preparing produce, pregnant mothers can reduce the risk of neonatal meningitis caused by these bacteria. Foods to avoid that may be contaminated by listeria include: Soft cheeses made with unpasteurized milk Smoked seafood that is not canned or shelf-stable Raw ( unpasteurized) milk Foods that must be safely prepared to prevent the growth of listeria and E. coli include: Raw sprouts Melons الشمام Hot dogs, deli meat, and cold cuts  اللحوم الباردة

61. عند اكتشاف حالة مؤكدة 1- حصر جميع المخالطين المباشرين للحالة ومراقبتهم صحيا لمدة 10 ايام. اعطاء المخالطين ريفامبيسين لمدة يومين للقضاء علي حامل الميكروب . عند اكتشاف حالة داخل تجمع مثل مدرسة - معسكر – حضانة يتم اعطاء جميع المخالطين ريفامبيسين

62. How to give Rifampicin Adult: 600 mg twice daily for 2 days Infant more than 2 months of age : 10 mg/kg twice daily for 2 days neonates less than one month : 5 mg/kg twice daily for 2 days N.B ciprofloxacin and cefotriaxone can be given

63. Vaccinations for Meningitis

64. The five most common types (or serogroups ) of meningococcal bacteria found are A, B, C, W and Y. No single vaccine protects against all serogroups ; there are separate vaccines against meningococcal ACWY serogroups and the meniningococcal B serogroup

65. A smaller yet steady rise in the occurrence of meningococcal Y disease has also been seen since 2016. Together, meningococcal W and Y disease cause approximately half of the cases of IMD in Australia. Meningococcal B , which historically caused the majority of meningococcal disease in Australia , continues to cause around half of all reported cases of IMD

66. Meningococcal vaccines available for use Quadrivalent meningococcal ( MenACWY ) conjugate vaccines against A, C, W and Y serogroups Registered age group Formulation Trade name 9 month- 55 years Quadrivalent diphtheria toxoid conjugate Menactra® ≥2 months Quadrivalent CRM conjugate Menveo® ≥6 weeks Quadrivalent tetanus toxoid conjugate Nimenrix®

67. 2 types of meningococcal vaccine in Egypt : 1- A,C V accine : ( polysaccraide ) ويعطي جرعة من اللقاح للفئات العمرية الاتية: السنة الاولي من الحضانة اولي ابتدائي اولي اعدادي اولي ثانوي ينصح بعدم اعطاء التطعيم قبل سنتين

68. 2- Quadirivalent vaccine A,C,W,Y ويعطي للمسافرين والحجاج والمعتمرين

69. Meningococcal (Menactra) Polysaccharide Diphtheria Toxoid (D T)Conjugate Vaccine DOSAGE AND ADMINISTRATION Primary Vaccination • Children 9 month through 23 months of age: Two doses, three months apart. • Individuals 2 through 55 years of age: A single dose Booster Vaccination:  A single booster dose may be given to individuals 15 through 55 years of age at continued risk for meningococcal disease, if at least 4 years have elapsed since the prior dose .

70. Nimenrix

71. Nimenrix is   Meningococcal polysaccharide vaccine serogroups A, C, W-135 & Y conjugate vaccine  ( TT )which is used to prevent . meningococcal infections INDICATIONS AND CLINICAL USE: active immunization of individuals from 6 weeks to 55 years of age

72. THANK YOU