what is the cure for f-meningitis? what helps improve the immune system?
Below are some articles to consider:
Painkiller linked to meningitis, FDA says
In a report published in the Archives of Internal Medicine, scientists from the U.S. Food and Drug Administration (FDA) revealed that the popular painkiller Vioxx has been linked to five cases of meningitis.
Vioxx (chemical name: rofecoxib) was approved in May 1999 for the treatment of osteoarthritis, management of acute pain, and treatment of primary dysmenorrhea.
In the U.S. alone, from May 1999 through Feb. 2001, seven cases of aseptic meningitis were reported in patients receiving the drug, the researchers noted. Two cases were not included for further analysis because there was not enough information to assess causality, they explained.
The patients (four females ranging in age from 16 to 67, and one 40-year-old male) had been prescribed the drug for osteoarthritis and rheumatoid arthritis, neck pain, carpal tunnel syndrome, and postoperative inflammation. None had a history of aseptic meningitis but began displaying symptoms within a few days of taking the drug. The symptoms included headache, fever, photophobia, altered mental status and elevated levels of protein, among others.
Although none of the patients died, all required hospitalization. They all improved after discontinuing the Vioxx therapy, the report stated.
This isn't the first time that pain killers have been linked to aseptic meningitis. Previous reports have linked the condition to other nonsteroidal anti-inflammatory drugs such as ibuprofen and naproxen.
As a result of the study, the FDA has ordered Merck to add meningitis to the growing list of potential side effects for Vioxx. Last year, the medical journal The Lancet reported a possible link between Vioxx and kidney damage. In addition, the critics claim the drug is associated with a fourfold increase in the risk of heart attack for women.
SOURCE: "Aseptic Meningitis Associated With Rofecoxib," Archives of Internal Medicine, March 26, 2002.
MENINGITIS THE DEBATE
Bacterial meningitis is a serious, life-threatening disease. There is no debate, dispute or speculation on this matter--it is a fact. However, there is a debate about mass vaccination programs of the meningitis C vaccine.
Is this vaccine warranted for every infant, student and adult in Canada?
Are there side-effects from this vaccine and does it protect against all strains of meningitis2 "The risk Of infection of meningococcal meningitis in Canada is low, with approximately 250 to 750 cases reported each year. Even so, Alberta is presently implementing a province-wide meningitis vaccination campaign costing as much as $25 million. There are concerns about the safety of this endeavour. As a parent, it is important to weigh the risks and benefits of this new vaccine to make an educated decision about the health care of your child.
Meningitis is an infection of the meninges, the three membranes that lie between the brain and skull and surround the spinal cord. There are various forms, including viral and bacterial infections. Viral meningitis, the most common form, is fairly benign and usually lasts between two to three weeks. Signs and symptoms include headaches and fatigue. Antibiotics are ineffective.
The uncommon bacterial meningitis is a more serious, life-threatening 'disease. Classic symptoms include a fever, stiff neck, vomiting, a rash that does not fade with pressure and a headache. There are two main types of bacterial meningitis: H. influenza and mening0coccal meningitis.
Currently all children in North America are vaccinated for the H. influenza bacteria (bib). In a standard immunization schedule, they receive their first of many shots at ages two, four and six months for pertussis, diohtheria. tetanus, polio and hib meningitis.
The other form of bacterial meningitis is meningococcal meningitis, caused by the bacteria Neisseria meningitides. This rare form of meningitis receives a tremendous amount of press due to its fast-moving nature and rate of fatalities. One in 10 dies and one in seven survivors is left with serious handicaps such as brain injury or deafness. Early diagnosis and aggressive antibiotic therapy are critical for proper recovery.
Vaccine Reactions Numerous
The five strains of meningococcal meningitis include types A, B, C, Y and W-135. In North America, type B accounts for 60 per cent of the infections. Type C accounts for the remaining 40 per cent. Last year, Britain introduced a mass vaccination program of the new meningitis C vaccine one year ahead of schedule. Doctors and nurses administered the injections to over 14 million children. So far, 7,742 adverse reactions were reported, .including 12 deaths!
The number of reported reactions equals about one in every 1,800 children receiving the vaccine. The most common reactions reported were dizziness, blackouts, epileptic fits, fainting, nausea and headaches. In comparison, 5,570 reactions have been reported for the whooping cough vaccine in 37 years.
According to Isabella Thomas of the UK vaccination support group JABS (Justice Awareness Basic Support), "We are receiving daily phone calls from parents whose children have had serious reactions. The government introduced the vaccine far too quickly."
Britain's Committee on Safety of Medicines denied reports that any of the deaths reported were attributed to the vaccine. They concluded seven deaths were due to sudden infant death syndrome (SIDS), one from pneumococcal septicemia, one from bronchiolitis, one from pneumonia and two from meningitis B infections. Scientific research indicates a possible correlation between childhood vaccinations and SIDS. This vaccine does not provide protection against the meningitis B strain, the most common form of meningitis.
The long-term effects of this vaccine are not yet known. It's recommended that individuals sensitive to mercury or other components of the vaccine should not be vaccinated. There are natural steps that can be taken to help guard against potential infection.
Building Body Defences
It's well known that the bacteria that cause meningococcal and pneumococcal meningitis .live in the back of the nose and throat of one or two out of every 10 adults, without causing infection. People of any age can carry these germs for days, weeks or months and not become ill. In fact, being a carrier helps to boost natural immunity. Only rarely do the bacteria overcome the body's defences. Those with weakened immune systems are less resistant and more likely to develop the infection.
It's important to support your immune system by eating a balanced diet consisting .of raw fruits and vegetables, whole grains, nuts and seeds. In addition, a garlic supplement can be taken for its natural antibiotic properties. Following the acute phase of the illness, Lactobacilli acidophilus and bifidus are very good supplements to restore bowel health after taking a regimen of potent antibiotics. Vitamin C and bioflavonoids will also help to stimulate the immune system and cleanse the blood (see alive #220).
The best. insurance factor to guard against the disease is a healthy, energetic lifestyle and whole food nutrition, not the prick of a needle. The potholes surrounding this vaccine raise serious questions about the side-effects reported, the low prevalence of infection in Canada and the lack of protection it provides. Mass vaccination programs are extremely controversial and even dangerous. Derive all the facts from your doctor or public health nurse, both the pros and .cons, before you make a vaccine decision for either you or your family.
Mass Vaccinations Rejected
Public health officials in Saskatchewan have ruled out a mass vaccination program even though a Saskatoon-area teenager died from meningococcal disease after attending a rave in February. The provincial health officer, Dr. Gary Neudorf, said the case was isolated and did not merit mass vaccinations.
By Joey Shulman, DC
Eosinophilic meningitis: a case report
ABSTRACT. Parasitic infection by the rat lungworm Angiostrongylus cantonensis is recognized as the major cause of eosinophilic meningitis in man. The diagnosis is based on clinical presentation, cerebral spinal fluid analysis, and travel to endemic regions. While Angiostrongylus cantonensis is considered to have tropical distribution, widespread patient travel to endemic areas and the recent identification of the parasite in the continental U.S.A. increases the likelihood of patients presenting to chiropractors with signs and symptoms of this form of meningitis. The diagnostic challenge lies in differentiating the signs and symptoms of this and other benign self-limiting forms of meningitis from acute, potentially fatal bacterial meningitis. The case of a 28-year-old male presenting to a chiropractic office with signs and symptoms associated with eosinophilic meningitis is described. The life cycle of the parasite, pathogenesis, clinical manifestations, prognosis, and treatment are highlighted. A brief comparative review of viral and bacterial meningitis is conducted.
KEY WORDS: Chiropractic -- Meningitis -- Eosinophilic Meningitis -- Parasitic Infection -- Angiostrongylus cantonensis
EOSINOPHILIA IS OFTEN ASSOCIATED with a wide variety of disease states including acute allergic reactions, extensive chronic skin disorders such as psoriasis and pemphigus, and to a lesser extent, collagen disorders. However, eosinophilic reactions are singularly responsible for host defenses against invasive parasitic infections. Rarely, parasites invade the central nervous system of the human host and trigger a dramatic eosinophilic response within the meninges. Although there are several different parasitic organisms that can initiate this "eosinophilic meningitis," it is almost exclusively associated with infection by the rat lungworm Angiostrongylus cantonensis.
Angiostrongylus cantonensis was first recognized as a cause of parasitic lung disease in Cantonese rats by Chen in 1935 [ 1]. It was not until 1945, when Namura and Lin reported the recovery of the site from the cerebral spinal fluid (CSF) of a Japanese patient, that it was suspected as a possible source of human disease [ 2]. This was confirmed in 1962 when Rosen et al. isolated the parasite from the brain tissue of two patients diagnosed with fatal eosinophilic meningitis [ 3]. Since then, additional case reports and studies have shown A. cantonensis to be the major cause of eosinophilic meningitis in humans [ 4, 5].
Early reports from Hawaii [ 3], Thailand [ 6], and Samoa [ 7], in addition to the first documented Japanese report, indicated that the parasite was confined to Western Pacific Rim countries. In 1981, the identification of the parasite and five reported cases of eosinophilic meningitis in Cuba suggested that the geographic distribution was far greater than originally thought [ 8, 9]. Angiostrongylus cantonensis has been subsequently identified in Puerto Rico in 1986 [ 10] and in New Orleans in 1988 [ 11]. This latter identification suggests the recent establishment of the parasite in North America since earlier investigations between 1962 and 1976 failed to identify A. cantonensis in the continental United States [ 11, 12].
The clinical presentation of eosinophilic meningitis secondary to infection by A. cantonensis is very similar to that of aseptic or viral meningitis. After a flu-like prodrome, patients present with headache, nausea, vomiting, nuchal rigidity, and low grade fever. Within several weeks symptoms subside and most patients experience a full and uneventful recovery. Like viral meningitis the diagnostic challenge lies in differentiating benign, self-limiting forms of meningitis from acute, potentially fatal bacterial meningitis.
This case of a 28-year-old male chiropractor presenting to a chiropractic office with signs and symptoms of eosinophilic meningitis secondary to A. cantonensis is significant for several reasons. First, it serves to highlight the major clinical differences in meningitis of viral, bacterial, or parasitic origin. Second, it challenges our concepts of international travel and tropical disease. Patients routinely travel to Caribbean and Pacific regions; so routinely, in fact, that as clinicians it is easily forgotten that patients are traveling to endemic areas of tropical disease and infection. Third, in clinical settings dominated by biomechanical disorders, the unusual and bizarre does present itself.
After the case presentation the life cycle of the parasite in both the rodent and human hosts is highlighted. Pathogenesis, common clinical manifestations, prognosis, and treatment are described. A comparative review of bacterial and viral meningitis, types more likely to be encountered in a chiropractic office, is undertaken.
A 28-year-old male chiropractor presented with bilateral occipital headache with pain radiating into the temporal and frontal regions of 2 days' duration. The pain was described as constant and dull and aggravated by forward flexion of the cervical spine. He also complained of ocular pain on the extremes of right and left lateral gaze. General, diffuse myalgia and arthralgia had been present several weeks prior to the onset of headache. A review of current life situation revealed high levels of stress as a result of recent graduation from chiropractic college and marriage. The patient reported travel to Hawaii 4 weeks prior to the onset of symptoms.
On examination the patient did not appear to be in any physical distress. Vital signs including temperature were normal. Range of motion of the cervical spine was limited in forward flexion and accompanied by generalized, mid-line pain in the cervical and thoracic regions. Motion palpation demonstrated painful restrictions in movement at the occiput-C1 and C1-C2 levels. Neurologic examination was unremarkable. Although the patient reported discomfort on both fight and left lateral gaze, there was no obvious evidence of nystagmus or dysfunction of the medial or lateral rectus muscles. Brudzinski's test was positive for meningeal irritation.
Based on patient history and physical examination findings, a tentative diagnosis of aseptic or viral meningitis was made. The painful restrictions of movement in the upper cervical spine were adjusted and the patient discharged with instructions to rest and consult his medical doctor should his symptoms increase.
In the following 48 hours the patient developed additional symptoms of nausea and vomiting while headache and neck rigidity intensified. He presented to a local hospital where he was admitted for further examination and observation. Chest radiographs to rule out lung infection were normal. Sputum analysis for beta hemolytic streptococci were negative reducing the suspicion of streptococcal meningitis. CT scans of the skull were normal. Abdominal and stool analysis for ova and parasites were negative while urinalysis was unremarkable. Blood test failed to demonstrate any increase in acute phase reactants, a sign of infectious, inflammatory response. Although the white blood cell count of 10,000 cells per mm( 3) was within the upper range of normal, white blood cell differential count revealed an elevated eosinophil differential count of 6.1% (normal value 3%). A lumbar puncture was performed and the CSF analyzed revealing an elevated leukocyte count of 83,000/mm( 3) (normal, 0.5/mm( 3)), with 32% of the cell count being eosinophils.
A second set of blood tests were performed the following day and white blood cell differential count indicated a further increase in eosinophils to 10.4%. Although a second lumbar puncture demonstrated a reduction in the number of leukocytes to 51,900/mm( 3), the overall percentage of eosinophils increased to 61%. Protein concentration, a general sign of the degree of CSF leukocytosis, unavailable in the first analysis was 955 mg/100 ml (normal 15.40 mg/100 ml) on the second analysis.
Based on the presence of elevated eosinophil counts in both the blood tests and cerebral spinal fluid, absence of any readily identifiable disease, clinical presentation and travel to an endemic area of Angiostrongylus cantonensis the diagnosis of eosinophilic meningitis was made. The patient remained in hospital for 10 days, where he was treated symptomatically and then discharged. Subsequent follow-up 2 months later demonstrated no residual affects secondary to the parasitic infection.
The life cycle of A. cantonensis in its natural host, the rat, has been well documented [ 13]. The adult worm measures between 17 and 25 mm and can have a maximum diameter of 0.36 mm. Adult females migrate to the lungs of the rodent host and deposit up to 15,000 eggs per day. After an incubation period of i week, the eggs hatch and the first stage larvae travel from the alveolar air space to the trachea, where they are swallowed into the gastro-intestinal tract and excreted in the feces. If they are deposited inca dry environment the larvae can remain viable for only several hours; if excreted into a watery environment they can remain infectious for several weeks. In watery environments, intermediate hosts such as land crabs, African giant land snails, mollusks, and freshwater prawns ingest the first stage larvae. The first stage larvae undergo two successive molts to become third stage larvae. These intermediate hosts with their third stage larvae are then ingested by the rat (or man) and enter the host's portal system by burrowing through the lining of the gastrointestinal tract. From the portal system the larvae journey through the inferior vena cava, right ventricle, pulmonary arteries, and left ventricle into the peripheral vascular system. During this period the third stage larvae undergo a third molt to become fourth stage larvae. The fourth stage larvae then disseminate through the kidneys, muscle, spinal cord, and brain. For larvae reaching the spinal cord and brain, a final molt takes place within the gray matter and the immature adults measuring 2 mm in length begin to migrate toward the surface of the brain. In the rodent host the mature adults enter the vascular system through walls of the cerebral veins and the subarachnoid space and return to the lung where, eggs are deposited and the cycle repeats.
In man the third stage larvae gain access to the gastrointestinal tract following ingestion of infected intermediate hosts or fecal soiled plants. A similar migration from the gastrointestinal tract to spinal cord and brain takes place. As in the rodent host, the adult parasites attempt to reenter the vascular system through the cerebral veins and subarachnoid space. Here, the human host's eosinophilic mediated immune response renders the adult nonviable and the life cycle is terminated. A rare, bizarre migration phenomenon has been observed when the parasite travels through the optic tract to the eye where it is visible in the aqueous and vitreous humor of the human host [ 13].
Pathogenesis of A. cantonensis in man is due primarily to mechanical damage during migration of the parasite within the central nervous system and subsequent inflammatory response to dead worm tissue. Thangchai et al., after autopsy of a 28-year-old Thai woman with eosinophilic meningitis, described four specific types of lesions [ 6]. First, migratory tracts 0.9 mm in diameter caused mechanical derangement and damage to nerve fibers with Wallerian or secondary axonal degeneration present around all migratory tracts within the brain and spinal cord. Second, dilation and inflammation of all blood vessels and the veins in the subarachnoid space were observed. It is felt that this is likely a reaction to the attempted migration of the parasite from the brain parenchyma into the subarachnoid space. Third, extensive eosinophilic reactions were observed in worm tracts and about dead parasites. Strangely, no eosinophilic reactions were seen around live parasites. Fourth, extensive granulomatous inflammatory reaction developed around dead parasites and accompanying necrotic debris within the brain.
In most cases of eosinophilic meningitis, onset of symptoms occurs within 20 to 36 days of parasitic infection [ 4]. Signs and symptoms of infection are those most often associated with meningeal irritation. Punyagupta et al. [ 4] in a review of 424 cases of eosinophilic meningitis found headache to be the primary complaint in 99% of all cases. Neck stiffness, vomiting, nausea, blurred vision, paraesthesia, and low grade fever were also common. Less frequently, aching of body and extremities, impairment of sensorium, facial paralysis, high fever, and weakness were experienced. A review of the most common presenting signs and symptoms is found in Table 1.
For the large majority of infected patients prognosis is excellent. Headache, neck stiffness, nausea, and vomiting usually subside within 1 week. More obscure symptoms such as paraesthesia, altered sensorium and paralysis may require 6 to 8 weeks to abate. Reid and Wallis [ 7] have reported three rare cases where symptoms have remained for up to 4 months but this is unusual. Almost all patients experience full and complete recovery with no residual effects. Death due to infection is quite rare. In Punyagupta's study [ 4] the mortality rate was determined to be less than 1%. The major factors affecting mortality are thought to be age (very young or old), health status prior to infection and the number of parasites within the CNS.
Treatment is directed toward the chief symptomatic complaints of headache, nausea, and vomiting. Many patients report a dramatic improvement in these symptoms following diagnostic lumbar puncture and secondary reduction in intracranial pressure [ 1]. Steroids and antibiotics have not been shown to significantly alter the clinical course of the condition [ 4]. Paradoxically antihelminthic drugs are contraindicated. Although live parasites within the brain do not appear to initiate the hosts immune response, extensive eosinophilic reactions are seen in association with dead parasites and necrotic debris. It is felt that the simultaneous death of many worms within the CNS may initiate an intense, fatal, immune reaction.
The most significant differential diagnosis in patients presenting with signs of meningeal irritation is acute bacterial meningitis. The incidence of bacterial meningitis is currently thought to be between 4.6 and 10 cases per 100,000 persons per year [ 14]. Eighty percent of all cases of bacterial meningitis are a result of infections by Meningococcus, Pneumococcus, and Hemophilus influenzae. These infectious agents, commonly found throughout the respiratory tract, typically gain access to the meninges through hematogenous spread or, less frequently, through extensions of surface structures, sinuses, osteomyelytic foci within the skull, penetrating cranial injuries, or subsequent to neurosurgical procedures.
After a short prodromal respiratory illness or sore throat, patients become exceedingly ill within 24 hours. Early signs of high fever, headache, nausea, vomiting, and nuchal rigidity very quickly give way to confusion, stupor, seizure, and death secondary to respiratory and circulatory collapse and necrosis of brain tissue. In infants and children the course can be shorter and symptoms less defined. Fever, vomiting, and convulsions are usually present but nuchal rigidity may be absent.
Diagnosis of bacterial meningitis is confirmed following lumbar puncture and CSF analysis. In most cases the infectious agent can be quickly identified on microscopic examination of the fluid. Leukocyte count typically averages between 5,000 and 20,000 cells per mm( 3) with a preponderance of neutrophils. Protein levels are elevated to 150 to 500 mg/dl.
In patients where bacterial meningitis is even remotely suspected, referral for further diagnostic procedures and treatment is mandatory. It is estimated that 14% of all bacterial meningitis cases are fatal. In nonfatal cases the incidence of complication and neurologic sequelae, such as deafness, epilepsy and mental retardation in children, is directly related to the duration of the meningitis and response to treatment. Although the diagnosis is confirmed through CSF examination, early aggressive antibiotic therapy will be initiated on the basis of clinical findings alone.
In contrast to bacterial meningitis, aseptic or viral meningitis is a benign, self-limiting illness. When the causative agent, usually the picorno-virus or enterovirus, is known the infection is termed vital meningitis; when the agent is unknown it is termed aseptic. A flu-like prodrome may proceed the onset of signs and symptoms by several weeks. Intense frontal, retro-orbital headache, malaise, nausea, vomiting, low-grade fever, and nuchal rigidity develop. Unlike bacterial meningitis, confusion, stupor, and seizure are rare. On examination temperatures may be elevated to as high as 40C, with Bruclzinkski's and Kemig's signs positive for meningeal irritation. Cerebral spinal fluid analysis demonstrates mild leukocytosis between 100 and 3,000 cells per mm( 3) with lymphocytosis as high as 75%. CSF protein is within normal limits.
Treatment of viral meningitis is primarily symptomatic with symptoms disappearing within 3 to 5 days and full resolution within 2 weeks.
A review of presenting signs and symptoms associated with eosinophilic meningitis illustrates a very similar clinical presentation to aseptic or vital meningitis. The patient had experienced a similar flu-like prodrome of myalgia and arthralgia prior to the onset of frontal headache, nuchal rigidity, nausea, and vomiting. Unlike bacterial meningitis there was no elevated temperature, stupor, seizure, or coma. Definitive diagnosis was made when CSF analysis demonstrated leukocytosis with a preponderance of eosinophils. An elevated lymphocytic count would have been indicative of viral meningitis; neutrophils of bacterial meningitis.
The case of a 28-year-old male chiropractor who presented with signs and symptoms of meningitis following travel to an area endemic to A. cantonensis has been presented. As described, the presenting signs and symptoms of eosinophilic meningitis and viral or aseptic meningitis can be very similar. For the primary contact practitioner, the diagnostic challenge lies in differentiating benign, self-limiting forms of meningitis from the potentially fatal, acute forms of bacterial meningitis.
In patients who present with headache, nausea, vomiting, and nuchal rigidity, a thorough history and physical examination should be performed to ensure that the presence of meningitis is not overlooked. If there is the remotest suspicion of bacterial meningitis, the patient should be referred immediately for further examination and medical treatment. Aggressive antibiotic therapy is often instituted on the basis of clinical presentation even before a definitive diagnosis is made. Failure to institute early treatment may increase morbidity and mortality.
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The National College of Chiropractic.
By Edward R. Crowther
Answer by prokopton