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the only form of prevention from viral infection of the neonate is a caesarean section form of delivery if the mother is showing symptoms of infection.
The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further ten months. Steroids help reduce the risk of death in those without HIV. Steroids can be used in the first six weeks of treatment, A few people may require immunomodulatory agents such as thalidomide. Hydrocephalus occurs as a complication in about a third of people with TB meningitis. The addition of aspirin may reduce or delay mortality, possibly by reducing complications such as infarcts.
Prevention of neonatal meningitis is primarily intrapartum (during labor) antibiotic prophylaxis (prevention) of pregnant mothers to decrease chance of early-onset meningitis by GBS. For late-onset meningitis, prevention is passed onto the caretakers to stop the spread of infectious microorganisms. Proper hygiene habits are first and foremost, while stopping improper antibiotic use; such as over-prescriptions, use of broad spectrum antibiotics, and extended dosing times will aid prevention of late-onset neonatal meningitis. A possible prevention may be vaccination of mothers against GBS and "E. coli", however, this is still under development.
For some causes of meningitis, protection can be provided in the long term through vaccination, or in the short term with antibiotics. Some behavioral measures may also be effective.
Empiric antibiotics (treatment without exact diagnosis) should be started immediately, even before the results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place and population. For instance, in the United Kingdom empirical treatment consists of a third-generation cefalosporin such as cefotaxime or ceftriaxone. In the USA, where resistance to cefalosporins is increasingly found in streptococci, addition of vancomycin to the initial treatment is recommended. Chloramphenicol, either alone or in combination with ampicillin, however, appears to work equally well.
Empirical therapy may be chosen on the basis of the person's age, whether the infection was preceded by a head injury, whether the person has undergone recent neurosurgery and whether or not a cerebral shunt is present. In young children and those over 50 years of age, as well as those who are immunocompromised, the addition of ampicillin is recommended to cover "Listeria monocytogenes". Once the Gram stain results become available, and the broad type of bacterial cause is known, it may be possible to change the antibiotics to those likely to deal with the presumed group of pathogens. The results of the CSF culture generally take longer to become available (24–48 hours). Once they do, empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism and its sensitivities to antibiotics. For an antibiotic to be effective in meningitis it must not only be active against the pathogenic bacterium but also reach the meninges in adequate quantities; some antibiotics have inadequate penetrance and therefore have little use in meningitis. Most of the antibiotics used in meningitis have not been tested directly on people with meningitis in clinical trials. Rather, the relevant knowledge has mostly derived from laboratory studies in rabbits. Tuberculous meningitis requires prolonged treatment with antibiotics. While tuberculosis of the lungs is typically treated for six months, those with tuberculous meningitis are typically treated for a year or longer.
Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for "Candida" meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for "Aspergillus" and coccidioidal infections is poor.
Because it is a bacterial disease, the primary method of treatment for "Haemophilus" meningitis is anti-bacterial therapy. Common antibiotics include ceftriaxone or cefotaxime, both of which can combat the infection and thus reduce inflammation in the meninges, or the membranes that protect the brain and spinal cord. Anti-inflammatories such as corticosteroids, or steroids produced by the body to reduce inflammation, can also be used to fight the meningeal inflammation in an attempt to reduce risk of mortality and reduce the possibility of brain damage.
The treatment includes lowering the increased intracranial pressure and starting intravenous antibiotics (and meanwhile identifying the causative organism mainly by blood culture studies).
Hyperbaric oxygen therapy (HBO2 or HBOT) is indicated as a primary and adjunct treatment which provides four primary functions.
Firstly, HBOT reduces intracranial pressure. Secondly, high partial pressures of oxygen act as a bactericide and thus inhibits the anaerobic and functionally anaerobic flora common in brain abscess. Third, HBOT optimizes the immune function thus enhancing the host defense mechanisms and fourth, HBOT has been found to be of benefit when brain abscess is concomitant with cranial osteomyleitis.
Secondary functions of HBOT include increased stem cell production and up-regulation of VEGF which aid in the healing and recovery process.
Surgical drainage of the abscess remains part of the standard management of bacterial brain abscesses. The location and treatment of the primary lesion also crucial, as is the removal of any foreign material (bone, dirt, bullets, and so forth).
There are few exceptions to this rule: "Haemophilus influenzae" meningitis is often associated with subdural effusions that are mistaken for subdural empyemas. These effusions resolve with antibiotics and require no surgical treatment. Tuberculosis can produce brain abscesses that look identical to conventional bacterial abscesses on CT imaging. Surgical drainage or aspiration is often necessary to identify "Mycobacterium tuberculosis", but once the diagnosis is made no further surgical intervention is necessary.
CT guided stereotactic aspiration is also indicated in the treatment of brain abscess.
Death occurs in about 10% of cases and people do well about 70% of the time. This is a large improvement from the 1960s due to improved ability to image the head, better neurosurgery and better antibiotics.
Fungal meningitis is treated with long courses of high dose antifungal medications. The duration of treatment is dependent upon the causal pathogen and the patient's ability to stave off the infection; for patients with a weaker immune system or diabetes, treatment will often take longer.
Before the widespread use of the Hib vaccine, "Haemophilus" meningitis accounted for 40%-60% of all meningitis cases in children under the age of fifteen, and 90% of all meningitis cases in children under the age of five. Vaccination can reduce incidence. Vaccination has reduced the occurrences of "Haemophilus" meningitis by 87-90% in countries with widespread access to the Hib vaccine. Rates are still high in areas with limited levels of vaccination. Less-developed countries as well as countries with medical infrastructure that has been damaged in any way, such as from warfare, do not have such widespread access to the vaccine and thus experience higher rates of meningitis cases. Multiple conjugate Hib vaccines are available for use, though, and are extremely effective when given to infants. Additionally, the vaccine has only the side effects of reddened skin and swelling at the location of the injection.
The presence of bacteria in the blood almost always requires treatment with antibiotics. This is because there are high mortality rates from progression to sepsis if antibiotics are delayed.
The treatment of bacteremia should begin with empiric antibiotic coverage. Any patient presenting with signs or symptoms of bacteremia or a positive blood culture should be started on intravenous antibiotics. The choice of antibiotic is determined by the most likely source of infection and by the characteristic organisms that typically cause that infection. Other important considerations include the patient's past history of antibiotic use, the severity of the presenting symptoms, and any allergies to antibiotics. Empiric antibiotics should be narrowed, preferably to a single antibiotic, once the blood culture returns with a particular bacteria that has been isolated.
Bacterial infections of the orbit have long been associated with a risk of catastrophic local
sequelae and intracranial spread.
The natural course of the disease, as documented by Gamble (1933), in the pre-antibiotic era,
resulted in death in 17% of patients and permanent blindness in 20%.
Immediate treatment is very important for someone with orbital cellulitis. Treatment typically involves intravenous (IV) antibiotics in the hospital and frequent observation (every 4–6 hours). Along with this several laboratory tests are run including a complete blood count, differential, and blood culture.
- Antibiotic therapy – Since orbital cellulitis is commonly caused by "Staphylococcus" and "Streptococcus" species both penicillins and cephalosporins are typically the best choices for IV antibiotics. However, due to the increasing rise of MRSA (methicillin-resistant "Staphylococcus aureus") orbital cellulitis can also be treated with Vancomycin, Clindamycin, or Doxycycline. If improvement is noted after 48 hours of IV antibiotics, healthcare professions can then consider switching a patient to oral antibiotics (which must be used for 2–3 weeks).
- Surgical intervention – An abscess can threaten the vision or neurological status of a patient with orbital cellulitis, therefore sometimes surgical intervention is necessary. Surgery typically requires drainage of the sinuses and if a subperiosteal abscess is present in the medial orbit, drainage can be performed endoscopically. Post-operatively, patients must follow up regularly with their surgeon and remain under close observation.
The disease is associated with high rates of mortality and severe morbidity.
Aseptic meningitis, or sterile meningitis, is a condition in which the layers lining the brain, the meninges, become inflamed and a pyogenic bacterial source is not to blame. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g., Kernig's sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF) obtained via lumbar puncture (normally being fewer than five visible leukocytes per microscopic high-power field).
The term "aseptic" is frequently a misnomer, implying a lack of infection. On the contrary, many cases of aseptic meningitis represent infection with viruses or mycobacteria that cannot be detected with routine methods. While the advent of polymerase chain reaction has increased the ability of clinicians to detect viruses such as enterovirus, cytomegalovirus, and herpes virus in the CSF, many viruses can still escape detection. Additionally, mycobacteria frequently require special stains and culture methods that make their detection difficult. When CSF findings are consistent with meningitis, and microbiologic testing is unrevealing, clinicians typically assign the diagnosis of aseptic meningitis—making it a relative diagnosis of exclusion.
Aseptic meningitis can result from non-infectious causes as well. it can be a relatively infrequent side effect of medications, or be a result of an autoimmune disease. There is no formal classification system of aseptic meningitis except to state the underlying cause, if known. The absence of bacteria found in the spinal fluid upon spinal tap, either through microscopic examination or by culture, usually differentiates aseptic meningitis from its pyogenic counterpart.
"Aseptic meningitis", like non-gonococcal urethritis, non-Hodgkin lymphoma and atypical pneumonia, merely states what the condition is not, rather than what it is. Terms such as viral meningitis, bacterial meningitis, fungal meningitis, neoplastic meningitis and drug-induced aseptic meningitis can provide more information about the condition, and without using one of these more specific terms, it is difficult to describe treatment options or prognosis.
The Infectious Disease Society of America (IDSA) recommends treating uncomplicated methicillin resistant staph aureus (MRSA) bacteremia with a 14-day course of intravenous vancomycin. Uncomplicated bacteremia is defined as having positive blood cultures for MRSA, but having no evidence of endocarditis, no implanted prostheses, negative blood cultures after 2–4 days of treatment, and signs of clinical improvement after 72 hrs.
The antibiotic treatment of choice for streptococcal and enteroccal infections differs by species. However, it is important to look at the antibiotic resistance pattern for each species from the blood culture to better treat infections caused by resistant organisms.
Throughout history treatment relied primarily on β-lactam antibiotics. In the 1960s nearly all strains of "S. pneumoniae" were susceptible to penicillin, but more recently there has been an increasing prevalence of penicillin resistance especially in areas of high antibiotic use. A varying proportion of strains may also be resistant to cephalosporins, macrolides (such as erythromycin), tetracycline, clindamycin and the quinolones. Penicillin-resistant strains are more likely to be resistant to other antibiotics. Most isolates remain susceptible to vancomycin, though its use in a β-lactam-susceptible isolate is less desirable because of tissue distribution of the drug and concerns of development of vancomycin resistance. More advanced beta-lactam antibiotics (cephalosporins) are commonly used in combination with other drugs to treat meningitis and community-acquired pneumonia. In adults recently developed fluoroquinolones such as levofloxacin and moxifloxacin are often used to provide empiric coverage for patients with pneumonia, but in parts of the world where these drugs are used to treat tuberculosis resistance has been described.
Susceptibility testing should be routine with empiric antibiotic treatment guided by resistance patterns in the community in which the organism was acquired. There is currently debate as to how relevant the results of susceptibility testing are to clinical outcome. There is slight clinical evidence that penicillins may act synergistically with macrolides to improve outcomes.
Treatment is generally supportive. Rest, hydration, antipyretics, and pain or anti-inflammatory medications may be given as needed.
Herpes simplex virus, varicella zoster virus and cytomegalovirus have a specific antiviral therapy. For herpes the treatment of choice is aciclovir.
Surgical management is indicated where there is extremely increased intracranial pressure, infection of an adjacent bony structure (e.g. mastoiditis), skull fracture, or abscess formation.
The majority of people that have viral meningitis get better within 7-10 days.
It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall.
The Meningitis Research Foundation is conducting a study to see if new genomic techniques can the speed, accuracy and cost of diagnosing meningitis in children in the UK. The research team will develop a new method to be used for the diagnosis of meningitis, analysing the genetic material of microorganisms found in CSF (cerebrospinal fluid). The new method will first be developed using CSF samples where the microorganism is known, but then will be applied to CSF samples where the microorganism is unknown (estimated at around 40%) to try and identify a cause.
Antiviral therapy: as early as possible
10~15mg/kg every 8 hours for 14~21d
5~10mg/kg every 12hours for 14~21d
immune therapy: interferon
symptomatic therapy
High fever: physical regulation of body temperature
Seizure: antiepileptic drugs
high intracranial pressure-20%mannitol
Infections: antibiotic drugs
When properly diagnosed, the mortality of Lemierre's syndrome is about 4.6%. Since this disease is not well known and often remains undiagnosed, mortality might be much higher.
Due to the importance of disease caused by "S. pneumoniae" several vaccines have been developed to protect against invasive infection. The World Health Organization recommend routine childhood pneumococcal vaccination; it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom, United States, and South Africa.
Persons with component deficiencies in the final common complement pathway (C3,C5-C9) are more susceptible to "N. meningitidis" infection than complement-satisfactory persons, and it was estimated that the risk of infection is 7000 times higher in such individuals. In addition, complement component-deficient populations frequently experience frequent meningococcal disease since their immune response to natural infection may be less complete than that of complement non-deficient persons.
Inherited properdin deficiency also is related, with an increased risk of contracting meningococcal disease. Persons with functional or anatomic asplenia may not efficiently clear encapsulated "Neisseria meningitidis" from the bloodstream Persons with other conditions associated with immunosuppression also may be at increased risk of developing meningococcal disease.
The basic method for control of the conjunctivitis includes proper hygiene and care for the affected eye. If the conjunctivitis is found to be caused by "H. aegyptius" Biogroup III then prompt antibiotic treatment preferably with rifampin has been shown to prevent progression to BPF. If the infected person resides in Brazil, it is mandatory that the infection is reported to the health authority so that a proper investigation of the contacts can be completed. This investigation will help to determine the probable source of the infection.