It is double stranded DNA virus HSV1,HSV2 Herpes simplex It is double stranded DNA virus HSV1,HSV2

CLINICAL FEATURES HSV1 cause infection to upper part of body above the waist; herpes of skin and mucosa ;herpes labialis, herpetic whitlow of fingers, herpitic gingivostomatitis .these are primary infections. recurrence of lesion at same site is by reactivation of latent virus in the sensory gangila. CNS infection leads to encephalitis focal lesion (focal).

HSV2 is mainly genital . It infects the newborn leads to either local lesions or generalized disseminated including CNS . Inta- uterine infection by herpes simplex is rare, but it is perinatal infection. Treatment by acyclovir is indicated to neonatal infection ,primary encephalitis , Others are usually not needed acyclovir.

Meningitis Bacterial and viral

ETIOLOGY inflammation of the leptomeninges, can be caused by bacteria, viruses, or, rarely, fungi. Bacterial meningitis is readily diagnosed by gram stain or culture for bacteria while aseptic M. means negative culture and m.o. not seen by gram stain. The term aseptic meningitis refers principally to viral meningitis or other agents that not grow in usual bacterial culture media and time like spirochete, tuberculosis,amebic,or partialiy treated meningitis.

Bacterial Causes of Meningitis

Bacterial meningitis 1m-12yr 1. S. pneumonia 2. N. meningitidis 3-H Bacterial meningitis 1m-12yr 1.S.pneumonia 2.N.meningitidis 3-H.influenza type b H.influenza b. is most common cause for meningitis younger than 4 yr before vaccine introduced. usually the source is hematological; preceded by viral URTI for few days then bacteria infect the URT and spread by blood so as to colonize in the meninges. Staph.epidermidis is common cause of meningitis in ventriculoperitonial shunt. Staph aureus in open neural tube defect. Pneumococal M.is common in CSF leaks caused by cribriform plate fracture and in mastoiditis or sinusitis. 3]

Viral meningitis is caused principally by entero-viruses, including coxsackie viruses, echoviruses, and, in unvaccinated individuals, polioviruses . Other viruses that cause meningitis include HSV, EBV, CMV, lymphocytic choriomeningitis virus, and HIV. Mumps virus is a common cause of viral meningitis in unvaccinated children

EPIDEMIOLOGY Risk factors The incidence of bacterial meningitis is highest among children younger than 1 year of age .Highly infectious is patients with H.influenza, and Niesseria Meningitis patient wit pneumococcal m. is not infectious Risk factors acquired or congenital immunodeficiencies: recurrent meningitis Contact to highly infectious patients with N.meningitidis , H.influenza .

3. Hyposplenism as in sickle cell dis or surgical asplenia ; by pneumococcal bact. 4. crowding such as occurs in some households, daycare centers, or college and military dormitories. 5. A CSF leak resulting from congenital skull anomaly or after fracture base of the skull, increases the risk for meningitis, especially caused by S. pneumoniae ;Recurrent meningitis. 6. Osteomyelitis of the skull as in mastoidits

CLINICAL MANIFESTATIONS Preceding upper respiratory tract symptoms are common Indications of meningeal inflammation include headache, irritability, nausea, nuchal rigidity, lethargy, photophobia, and vomiting. Fever usually is present

Kernig and Brudzinski signs of meningeal irritation usually are positive in children older than 12 months of age. In young infants, signs of meningeal inflammation may be minimal with only irritability, restlessness, depressed mental status, and poor feeding. Focal neurologic signs, seizures, arthralgia, myalgia, petechial or purpuric lesions, sepsis, shock, and coma may occur.

Increased intracranial pressure is reflected in complaints of headache, diplopia, and vomiting. A bulging fontanel may be present in infants. Ptosis, sixth nerve palsy, bradycardia with hypertension, and apnea are signs of increased intracranial pressure with brain herniation. Papilledema may occur 48-72 hr after onset and it indicates intracranial hypertension and it contraindicates LP. It is usually due to venous sinuses occlusion ,subdural empyema or brain abscess.

LABORATORY AND IMAGING STUDIES If bacterial meningitis is suspected, a lumbar puncture should be performed. A lumbar puncture should be avoided in the presence of cardiovascular instability or signs of increased intracranial pressure, other than a bulging fontanel, because of the risk of herniation.

CSF EXAMINATION Routine CSF examination includes WBC count, differential, protein and glucose levels, and Gram stain 90% positive in bacterial M. . Bacterial meningitis is characterized by neutrophilic pleocytosis, moderately to markedly elevated protein, and low glucose. Latex agglutination test for bacterial antigens helps when the CSF become sterile with partial treatment Viral meningitis is characterized by mild to moderate lymphocytic pleocytosis, normal or slightly elevated protein, and normal glucose.

CSF should be cultured for bacteria and, when appropriate, fungi, viruses, and mycobacteria. PCR is used to diagnose enteroviruses and HSV; it is more sensitive and more rapid than viral culture. Leukocytosis is common in bacterial . Blood cultures are positive in 50- 90% of cases of bacterial meningitis. An electroencephalogram (EEG) may confirm an encephalitis component

TREATMENT

Duration of treatment is 10 to 14 days for S Duration of treatment is 10 to 14 days for S. pneumoniae, 5 to 7 days for N. meningitidis, and 7 to 10 days for H. influenzae Supportive therapy involves treatment of dehydration with replacement fluids and treatment of shock, disseminated intravascular coagulation, inappropriate antidiuretic hormone secretion, seizures, increased intracranial pressure, apnea, arrhythmias, and coma. Supportive therapy also involves the maintenance of adequate cerebral perfusion in the presence of cerebral edema.

prognosis Even with appropriate antibiotic therapy, the mortality rate for bacterial meningitis in children is significant: 25% for S. pneumoniae, 15% for N. meningitidis, and 8% for Hib. Of survivors, 35% have some complications, particularly after pneumococcal infection, including deafness, seizures, learning disabilities, blindness, paresis, ataxia, or hydrocephalus.

Tuberculous meningitis most commonly occurs in children younger than 5 years old and often within 6 months of the primary infection. Tubercle bacilli that seed the meninges during the primary infection; after few months start to replicate, triggering an inflammatory response. This features may have an insidious onset, initially characterized by low-grade fever, headache, and subtle personality change.

Progression of the infection results in basilar meningitis with involvement of the cranial nerves and is manifested by meningeal irritation, nuchal rigidity ,cranial nerve palsies ,seizures and eventually increased intracranial pressure, deterioration of mental status, and coma

Investigations CSF analysis reveals increased cell number (50 to 500/cmm leukocytes), which early in the course of disease may be either lymphocytes or polymorphonuclear leukocytes. Glucose is low, and protein is significantly elevated. Acid-fast bacilli may be seen in the CSF by either routine or fluorescent staining procedures. Although culture is the gold standard for diagnosis, PCR for M. tuberculosis is useful to make this diagnosis.

treatment 2 mo of isoniazid, rifampicin, pyrazinamide, and streptomycin once a day with steroids dexamethazone to lower increased intracranial hypertension; followed by 7-10 mo of isoniazid and rifampicin, once a day or twice a week (9-12 mo total)